diff --git a/stage1/manifest.json b/stage1/manifest.json
index ebb25643fb3e805a6fc93496798e136927fd4c52..b0fd610708765269017446e23cc9804e91568f0a 100644
--- a/stage1/manifest.json
+++ b/stage1/manifest.json
@@ -1,5 +1,5 @@
 {
-  "generated_at": "2025-11-12T14:09:36.063429Z",
+  "generated_at": "2025-11-12T14:20:47.587309Z",
   "stage": "extract",
   "dataset": {
     "name": "HuggingFaceM4/FineVision",
diff --git a/stage1/sample_00000/document.md b/stage1/sample_00000/document.md
index 3ff0d4f5a40f168826bb8ece99c7e8a978922062..7ad8650623c657a51626fed02a7bd05c0bdd6c19 100644
--- a/stage1/sample_00000/document.md
+++ b/stage1/sample_00000/document.md
@@ -1,60 +1,82 @@
 21 April 2023 Accepted: 03 June 2023 Published: 07 June 2023  
 
-sub_title[[95, 89, 366, 101]]
+sub_title[[93, 88, 366, 100]]
 ## Ethics approval and consent to participate  
 
-text[[94, 99, 483, 202]]
+text[[93, 100, 481, 203]]
 The study was conducted in accordance with the ethical principles of the Declaration of Helsinki (2013). Ethical approval was obtained from Sakhiya Skin Clinic, Surat, Gujarat, India. (Approval No: 2023/06). Consent forms were signed by patient. He was informed that he had the right to withdraw from the study at any time without any consequences. All pictures reported in this case- report study belong to Sakhiya Skin Clinic, Surat- 395003, Gujarat, India.  
 
-sub_title[[94, 216, 245, 227]]
+sub_title[[93, 216, 248, 228]]
 ## Consent for publication  
 
-text[[94, 229, 171, 241]]
+text[[93, 228, 180, 240]]
 Not applicable  
 
-sub_title[[94, 255, 218, 267]]
+sub_title[[93, 256, 218, 268]]
 ## Competing interest  
 
-text[[94, 267, 443, 280]]
+text[[93, 268, 444, 281]]
 The authors declare that they have no competing interests.  
 
-sub_title[[94, 294, 177, 305]]
+sub_title[[93, 294, 179, 306]]
 ## Open Access  
 
-text[[94, 307, 483, 434]]
+text[[93, 308, 481, 432]]
 This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article unless otherwise stated.  
 
-sub_title[[94, 448, 191, 460]]
+sub_title[[93, 446, 192, 458]]
 ## Author Details  
 
-text[[94, 462, 463, 514]]
-1 Department of Dermatology, Sakhiya Skin Clinic, Surat, Gujarat, India. 2Department of Medical Writing, Sakhiya Skin Clinic, Surat, Gujarat, India  
+text[[93, 459, 461, 512]]
+1Department of Dermatology, Sakhiya Skin Clinic, Surat, Gujarat, India. 2Department of Medical Writing, Sakhiya Skin Clinic, Surat, Gujarat, India  
 
-sub_title[[94, 529, 169, 540]]
+sub_title[[93, 527, 169, 539]]
 ## Article Info  
 
-text[[94, 542, 242, 579]]
-Received: 21 April 2023  Accepted: 03 June 2023  Published: 07 June 2023  
+text[[93, 540, 242, 577]]
+Received: 21 April 2023 Accepted: 03 June 2023 Published: 07 June 2023  
 
-sub_title[[94, 594, 166, 605]]
+sub_title[[93, 594, 167, 606]]
 ## References  
 
-text[[93, 607, 483, 786]]
-1. Grando SA. Pemphigus autoimmunity: hypotheses and realities. Autoimmunity. 2012 Feb;45(1):7-35. doi 10.3109/08916934.2011.606444.  
-2. Lever WF, Schaumburg-Lever G. Immunosuppressants and prednisone in pemphigus vulgaris: therapeutic results obtained in 63 patients between 1961 and 1975. Arch Dermatol. 1977 Sep;113(9):1236-41. doi: 10.1001/archderm.1977.016400900084013.  
-3. Pasricha JS, Gupta R. Pulse therapy with dexamethasone-cyclophosphamide in pemphigus. Indian J Dermatol Venereol Leprol. 1984; 50:199-203.  
+text[[93, 607, 481, 782]]
+1. Grando SA. Pemphigus autoimmune: hypotheses and realities. Autoimmunity. 2012 Feb;45(1):7-35. doi 10.3109/08916934.2011.606444.  
+2. Lever WF, Schaumburg-Lever G. Immunosuppressants and prednisone in pemphigus vulgaris: therapeutic results obtained in 63 patients between 1961 and 1975. Arch Dermatol. 1977 Sep;113(9):1236-41. doi: 10.1001/archderm.1977.01640090084013.  
+3. Pasricha JS, Gupta R. Pulse therapy with dexamethasonecyclophosphamide in pemphigus. Indian J Dermatol Venereol Leprol. 1984; 50:199-203.  
 4. Bystryn JC, Steinman NM. The adjuvant therapy of pemphigus. An update. Arch Dermatol. 1996 Sep;132(2):203-12.  
 
-text[[514, 74, 905, 782]]
-5. Heizmann M, Itin P, Wernli M, Borradori L, Bargetzi MJ. Successful treatment of paraneoplastic pemphigus in follicular NHL with rituximab: report of a case and review of treatment for paraneoplastic pemphigus in NHL and CLL. Am J Hematol. Feb 2001;66(2):142-4. doi: 10.1002/1096-8652(200102)66:2<142::AID-AJH1032>3.0. CO;2-0.  
-6. Food and Drug Administration. Rituxan label; 2012 [cited Feb 2, 2021]. Available from: http://www.accessdata.fda.gov/drugs/afd/datasheet/2012/103705s5373lbl.pdf.  
+text[[516, 79, 905, 205]]
+5. Heizmann M, Itin P, Wernli M, Borradori L, Bargetzi MJ. Successful treatment of paraneoplastic pemphigus in follicular NHL with rituximab: report of a case and review of treatment for paraneoplastic pemphigus in NHL and CLL. Am J Hematol. Feb 2001;66(2):142-4. doi: 10.1002/1096-8652(200102)66:2<142::AID-AJH1032>3.0.00;2-0.  
+
+text[[516, 207, 905, 258]]
+6. Food and Drug Administration. Rituxan label; 2012 [cited Feb 2, 2021]. Available from: http://www.accessdata.fda.gov/drugsatfda_docs/label/2012 /103705s5373lb.pdf.  
+
+text[[516, 200, 906, 270]]
 7. Belgi AS, Azeez M, Hoyle C, Williams REA. Response of pemphigus vulgaris to anti-CD20 antibody therapy (rituximab) may be delayed. Clin Exp Dermatol. 2006 Jan;31(1):143. doi: 10.1111/j.1365-2230.2005.01941.x.  
-8. Schmidt E, Seitz CS, Benoit S, Brucker EB, Goebeler M. Rituximab in autoimmune bullous diseases: mixed responses and adverse effects. Br J Dermatol. 2007 Feb;156(2):352-6. doi: 10.1111/j.1365-2133.2006.07646.x.  
-9. Barrera MV, Mendiola MV, Bosch RJ, Herrera E. Prolonged treatment with rituximab in patients with refractory pemphigus vulgaris. J Dermatolog Treat. 2007 Jan;18(5):312-4. doi: 10.1080/09546630701323988.  
-10. Fauschou A, Gniadecki R. Two courses of rituximab (anti-CD20 monoclonal antibody) for recalcitrant pemphigus vulgaris. Int J Dermatol. 2008 Mar;47(3):292-4. doi: 10.1111/j.1365-4632.2008.03423.x.  
+
+text[[516, 272, 906, 313]]
+8. Schmidt E, Seitz CS, Benoit S, Bröcker EB, Goebelier M. Rituximab in autoimmune bullous diseases: mixed responses and adverse effects. Br J Dermatol. 2007 Feb;156(2):352-6. doi: 10.1111/j.1365-2133.2006.07646.x.  
+
+text[[516, 314, 905, 367]]
+9. Barrera MV, Mendiola MV, Bosch RJ, Herrera E. Prolonged treatment with rituximab in patients with refractory pemphigus vulgaris. J Dermatol Treat. 2007 Jan;18(5):312-4. doi: 10.1080/09546630701323988.  
+
+text[[516, 368, 905, 420]]
+10. Faurschou A, Gniadecki R. Two courses of rituximab (anti-CD20 monoclonal antibody) for recalcitrant pemphigus vulgaris. Int J Dermatol. 2008 Mar;47(3):292-4. doi: 10.1111/j.1365-4632.2008.03423.x.  
+
+text[[516, 421, 905, 473]]
 11. Craythorne EE, Mufti G, DuVivier AW. Rituximab used as a first-line single agent in the treatment of pemphigus vulgaris. J Am Acad Dermatol. 2011 Nov;65(5):1064-5. doi: 10.1016/j.jaad.2010.06.033.  
-12. Horvath B, Huizinga J, Pas HH, Mulder A, Jonkman MF. Low-dose rituximab is effective in pemphigus. Br J Dermatol. 2012 Feb;166(2):405-12. doi: 10.1111/j.1365-2133.2011.10663.x.  
-13. Craythorne E, Du Vivier A, Mufti GJ, Warnakulasuriya S. Rituximab for the treatment of corticosteroid—refractory pemphigus vulgaris with oral and skin manifestations. J Oral Pathol Med. 2011 Sep;40(8):616-20. doi: 10.1111/j.1600-0714.2011.01017.x  
-14. Kim JH, Kim YH, Kim MR, Kim SC. Clinical efficacy of different doses of rituximab in the treatment of pemphigus: a retrospective study of 27 patients. Br J Dermatol. 2011Sep;165(3):646-51. doi: 10.1111/j.1365-2133.2011.10411.x  
+
+text[[516, 474, 905, 525]]
+12. Horvath B, Huizinga J, Pas HH, Mulder A B, Jonkman MF. Low-dose rituximab is effective in pemphigus. Br J Dermatol. 2012 Feb;166(2):405-12. doi: 10.1111/j.1365-2133.2011.10663.x.  
+
+text[[516, 526, 905, 592]]
+13. Craythorne E, Du Vivier A, Mufti GJ, Warnakulasuriya S. Rituximab for the treatment of corticosteroid—refractory pemphigus vulgaris with oral and skin manifestations. J Oral Pathol Med. 2011 Sep;40(8):616-20. doi: 10.1111/j.1600-0714.2011.01017.x.  
+
+text[[516, 593, 905, 644]]
+14. Kim JH, Kim YH, Kim MR, Kim SC. Clinical efficacy of different doses of rituximab in the treatment of pemphigus: a retrospective study of 27 patients. Br J Dermatol. 2011Sep;165(3):646-51. doi: 10.1111/j.1365-2133.2011.10411.x.  
+
+text[[516, 645, 905, 698]]
 15. Kasperkiewicz M, Shimanovich I, Ludwig RJ, Rose C, Zillikens D, Schmidt E. Rituximab for treatment-refractory pemphigus and pemphigoid: a case series of 17 patients. J Am Acad Dermatol. 2011 Sep;65(3):552-8. doi: 10.1016/j.jaad.2010.07.032  
-16. Investor update. Basel; June 12, 2019. [cited Feb 5, 2021]. Available from: https://www.roche.com/investors/updates/inv-update-2019-06-12. htm.
\ No newline at end of file
+
+text[[516, 698, 905, 736]]
+16. Investor update. Basel; June 12, 2019. [cited Feb 5, 2021]. Available from: https://www.roche.com/investors/updates/inv-update-2019-06-12.htm.
\ No newline at end of file
diff --git a/stage1/sample_00000/raw_response.md b/stage1/sample_00000/raw_response.md
index 3ff0d4f5a40f168826bb8ece99c7e8a978922062..7ad8650623c657a51626fed02a7bd05c0bdd6c19 100644
--- a/stage1/sample_00000/raw_response.md
+++ b/stage1/sample_00000/raw_response.md
@@ -1,60 +1,82 @@
 21 April 2023 Accepted: 03 June 2023 Published: 07 June 2023  
 
-sub_title[[95, 89, 366, 101]]
+sub_title[[93, 88, 366, 100]]
 ## Ethics approval and consent to participate  
 
-text[[94, 99, 483, 202]]
+text[[93, 100, 481, 203]]
 The study was conducted in accordance with the ethical principles of the Declaration of Helsinki (2013). Ethical approval was obtained from Sakhiya Skin Clinic, Surat, Gujarat, India. (Approval No: 2023/06). Consent forms were signed by patient. He was informed that he had the right to withdraw from the study at any time without any consequences. All pictures reported in this case- report study belong to Sakhiya Skin Clinic, Surat- 395003, Gujarat, India.  
 
-sub_title[[94, 216, 245, 227]]
+sub_title[[93, 216, 248, 228]]
 ## Consent for publication  
 
-text[[94, 229, 171, 241]]
+text[[93, 228, 180, 240]]
 Not applicable  
 
-sub_title[[94, 255, 218, 267]]
+sub_title[[93, 256, 218, 268]]
 ## Competing interest  
 
-text[[94, 267, 443, 280]]
+text[[93, 268, 444, 281]]
 The authors declare that they have no competing interests.  
 
-sub_title[[94, 294, 177, 305]]
+sub_title[[93, 294, 179, 306]]
 ## Open Access  
 
-text[[94, 307, 483, 434]]
+text[[93, 308, 481, 432]]
 This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article unless otherwise stated.  
 
-sub_title[[94, 448, 191, 460]]
+sub_title[[93, 446, 192, 458]]
 ## Author Details  
 
-text[[94, 462, 463, 514]]
-1 Department of Dermatology, Sakhiya Skin Clinic, Surat, Gujarat, India. 2Department of Medical Writing, Sakhiya Skin Clinic, Surat, Gujarat, India  
+text[[93, 459, 461, 512]]
+1Department of Dermatology, Sakhiya Skin Clinic, Surat, Gujarat, India. 2Department of Medical Writing, Sakhiya Skin Clinic, Surat, Gujarat, India  
 
-sub_title[[94, 529, 169, 540]]
+sub_title[[93, 527, 169, 539]]
 ## Article Info  
 
-text[[94, 542, 242, 579]]
-Received: 21 April 2023  Accepted: 03 June 2023  Published: 07 June 2023  
+text[[93, 540, 242, 577]]
+Received: 21 April 2023 Accepted: 03 June 2023 Published: 07 June 2023  
 
-sub_title[[94, 594, 166, 605]]
+sub_title[[93, 594, 167, 606]]
 ## References  
 
-text[[93, 607, 483, 786]]
-1. Grando SA. Pemphigus autoimmunity: hypotheses and realities. Autoimmunity. 2012 Feb;45(1):7-35. doi 10.3109/08916934.2011.606444.  
-2. Lever WF, Schaumburg-Lever G. Immunosuppressants and prednisone in pemphigus vulgaris: therapeutic results obtained in 63 patients between 1961 and 1975. Arch Dermatol. 1977 Sep;113(9):1236-41. doi: 10.1001/archderm.1977.016400900084013.  
-3. Pasricha JS, Gupta R. Pulse therapy with dexamethasone-cyclophosphamide in pemphigus. Indian J Dermatol Venereol Leprol. 1984; 50:199-203.  
+text[[93, 607, 481, 782]]
+1. Grando SA. Pemphigus autoimmune: hypotheses and realities. Autoimmunity. 2012 Feb;45(1):7-35. doi 10.3109/08916934.2011.606444.  
+2. Lever WF, Schaumburg-Lever G. Immunosuppressants and prednisone in pemphigus vulgaris: therapeutic results obtained in 63 patients between 1961 and 1975. Arch Dermatol. 1977 Sep;113(9):1236-41. doi: 10.1001/archderm.1977.01640090084013.  
+3. Pasricha JS, Gupta R. Pulse therapy with dexamethasonecyclophosphamide in pemphigus. Indian J Dermatol Venereol Leprol. 1984; 50:199-203.  
 4. Bystryn JC, Steinman NM. The adjuvant therapy of pemphigus. An update. Arch Dermatol. 1996 Sep;132(2):203-12.  
 
-text[[514, 74, 905, 782]]
-5. Heizmann M, Itin P, Wernli M, Borradori L, Bargetzi MJ. Successful treatment of paraneoplastic pemphigus in follicular NHL with rituximab: report of a case and review of treatment for paraneoplastic pemphigus in NHL and CLL. Am J Hematol. Feb 2001;66(2):142-4. doi: 10.1002/1096-8652(200102)66:2<142::AID-AJH1032>3.0. CO;2-0.  
-6. Food and Drug Administration. Rituxan label; 2012 [cited Feb 2, 2021]. Available from: http://www.accessdata.fda.gov/drugs/afd/datasheet/2012/103705s5373lbl.pdf.  
+text[[516, 79, 905, 205]]
+5. Heizmann M, Itin P, Wernli M, Borradori L, Bargetzi MJ. Successful treatment of paraneoplastic pemphigus in follicular NHL with rituximab: report of a case and review of treatment for paraneoplastic pemphigus in NHL and CLL. Am J Hematol. Feb 2001;66(2):142-4. doi: 10.1002/1096-8652(200102)66:2<142::AID-AJH1032>3.0.00;2-0.  
+
+text[[516, 207, 905, 258]]
+6. Food and Drug Administration. Rituxan label; 2012 [cited Feb 2, 2021]. Available from: http://www.accessdata.fda.gov/drugsatfda_docs/label/2012 /103705s5373lb.pdf.  
+
+text[[516, 200, 906, 270]]
 7. Belgi AS, Azeez M, Hoyle C, Williams REA. Response of pemphigus vulgaris to anti-CD20 antibody therapy (rituximab) may be delayed. Clin Exp Dermatol. 2006 Jan;31(1):143. doi: 10.1111/j.1365-2230.2005.01941.x.  
-8. Schmidt E, Seitz CS, Benoit S, Brucker EB, Goebeler M. Rituximab in autoimmune bullous diseases: mixed responses and adverse effects. Br J Dermatol. 2007 Feb;156(2):352-6. doi: 10.1111/j.1365-2133.2006.07646.x.  
-9. Barrera MV, Mendiola MV, Bosch RJ, Herrera E. Prolonged treatment with rituximab in patients with refractory pemphigus vulgaris. J Dermatolog Treat. 2007 Jan;18(5):312-4. doi: 10.1080/09546630701323988.  
-10. Fauschou A, Gniadecki R. Two courses of rituximab (anti-CD20 monoclonal antibody) for recalcitrant pemphigus vulgaris. Int J Dermatol. 2008 Mar;47(3):292-4. doi: 10.1111/j.1365-4632.2008.03423.x.  
+
+text[[516, 272, 906, 313]]
+8. Schmidt E, Seitz CS, Benoit S, Bröcker EB, Goebelier M. Rituximab in autoimmune bullous diseases: mixed responses and adverse effects. Br J Dermatol. 2007 Feb;156(2):352-6. doi: 10.1111/j.1365-2133.2006.07646.x.  
+
+text[[516, 314, 905, 367]]
+9. Barrera MV, Mendiola MV, Bosch RJ, Herrera E. Prolonged treatment with rituximab in patients with refractory pemphigus vulgaris. J Dermatol Treat. 2007 Jan;18(5):312-4. doi: 10.1080/09546630701323988.  
+
+text[[516, 368, 905, 420]]
+10. Faurschou A, Gniadecki R. Two courses of rituximab (anti-CD20 monoclonal antibody) for recalcitrant pemphigus vulgaris. Int J Dermatol. 2008 Mar;47(3):292-4. doi: 10.1111/j.1365-4632.2008.03423.x.  
+
+text[[516, 421, 905, 473]]
 11. Craythorne EE, Mufti G, DuVivier AW. Rituximab used as a first-line single agent in the treatment of pemphigus vulgaris. J Am Acad Dermatol. 2011 Nov;65(5):1064-5. doi: 10.1016/j.jaad.2010.06.033.  
-12. Horvath B, Huizinga J, Pas HH, Mulder A, Jonkman MF. Low-dose rituximab is effective in pemphigus. Br J Dermatol. 2012 Feb;166(2):405-12. doi: 10.1111/j.1365-2133.2011.10663.x.  
-13. Craythorne E, Du Vivier A, Mufti GJ, Warnakulasuriya S. Rituximab for the treatment of corticosteroid—refractory pemphigus vulgaris with oral and skin manifestations. J Oral Pathol Med. 2011 Sep;40(8):616-20. doi: 10.1111/j.1600-0714.2011.01017.x  
-14. Kim JH, Kim YH, Kim MR, Kim SC. Clinical efficacy of different doses of rituximab in the treatment of pemphigus: a retrospective study of 27 patients. Br J Dermatol. 2011Sep;165(3):646-51. doi: 10.1111/j.1365-2133.2011.10411.x  
+
+text[[516, 474, 905, 525]]
+12. Horvath B, Huizinga J, Pas HH, Mulder A B, Jonkman MF. Low-dose rituximab is effective in pemphigus. Br J Dermatol. 2012 Feb;166(2):405-12. doi: 10.1111/j.1365-2133.2011.10663.x.  
+
+text[[516, 526, 905, 592]]
+13. Craythorne E, Du Vivier A, Mufti GJ, Warnakulasuriya S. Rituximab for the treatment of corticosteroid—refractory pemphigus vulgaris with oral and skin manifestations. J Oral Pathol Med. 2011 Sep;40(8):616-20. doi: 10.1111/j.1600-0714.2011.01017.x.  
+
+text[[516, 593, 905, 644]]
+14. Kim JH, Kim YH, Kim MR, Kim SC. Clinical efficacy of different doses of rituximab in the treatment of pemphigus: a retrospective study of 27 patients. Br J Dermatol. 2011Sep;165(3):646-51. doi: 10.1111/j.1365-2133.2011.10411.x.  
+
+text[[516, 645, 905, 698]]
 15. Kasperkiewicz M, Shimanovich I, Ludwig RJ, Rose C, Zillikens D, Schmidt E. Rituximab for treatment-refractory pemphigus and pemphigoid: a case series of 17 patients. J Am Acad Dermatol. 2011 Sep;65(3):552-8. doi: 10.1016/j.jaad.2010.07.032  
-16. Investor update. Basel; June 12, 2019. [cited Feb 5, 2021]. Available from: https://www.roche.com/investors/updates/inv-update-2019-06-12. htm.
\ No newline at end of file
+
+text[[516, 698, 905, 736]]
+16. Investor update. Basel; June 12, 2019. [cited Feb 5, 2021]. Available from: https://www.roche.com/investors/updates/inv-update-2019-06-12.htm.
\ No newline at end of file
diff --git a/stage1/sample_00001/document.md b/stage1/sample_00001/document.md
index 1b2869e49a8289c2eff519af2ca10eaff08276a9..622e73427d0ba0b894f784f8906c5ac1bc7af7c5 100644
--- a/stage1/sample_00001/document.md
+++ b/stage1/sample_00001/document.md
@@ -1,24 +1,27 @@
-3- month history of painful ulcerated lesions in the oral cavity. On enquiring about the patient's history, we came to know that initially, the patient had difficulty chewing food and the severity increased gradually. The ulcerations caused considerable discomfort, affecting his normal oral functions. Subsequently, fluid-filled lesions developed involving the scalp, trunk, limbs, and axilla. Lesions were increasing in size and number and had little tendency to heal. Blisters were flaccid and burst on their own to form erosions within 2-3 days. Medical and family history was non- contributory. No history of fever, joint pain, malaise, and photosensitivity. He had weak oral hygiene due to the bad habit of taking betel quid with tobacco five times a day and smoking seven- - - - days per day for the past 12 years. Further, he consumes two- quarters of alcohol on an alternative day for the last 12 years. History of any drug intake before the appearance of lesions was also absent. Intraoral examination revealed that approximately \(1.0 \times 1.5\) dimensions ulceration lesions were present on the buccal mucosa. Dermatological examination revealed multiple vesicular lesions ranging from \(0.3 \times 0.3\) to \(1.5 \times 1.5\) involving the face, trunk, upper limbs, and dorsum of the penis (Figure 1a-1).  
+3- month history of painful ulcerated lesions in the oral cavity. On enquiring about the patient's history, we came to know that initially, the patient had difficulty chewing food and the severity increased gradually. The ulcerations caused considerable discomfort, affecting his normal oral functions. Subsequently, fluid-filled lesions developed involving the scalp, trunk, limbs, and axilla. Lesions were increasing in size and number and had little tendency to heal. Blisters were flaccid and burst on their own to form erosions within 2-3 days. Medical and family history was non- contributory. No history of fever, joint pain, malaise, and photosensitivity. He had weak oral hygiene due to the bad habit of taking betel quid with tobacco five times a day and smoking seven bidi per day for the past 12 years. Further, he consumes two- quarters of alcohol on an alternative day for the last 12 years. History of any drug intake before the appearance of lesions was also absent. Intraoral examination revealed that approximately \(1.0 \times 1.5\) dimensions ulceration lesions were present on the buccal mucosa. Dermatological examination revealed multiple vesicular lesions ranging from \(0.3 \times 0.3\) to 1.5 \(\times 1.5\) involving the face, trunk, upper limbs, and dorsum of the penis (Figure 1a-1i).  
 
-text[[91, 72, 484, 140]]
+text[[93, 73, 482, 141]]
 to tumor necrosis factor alpha (TNF- \(\alpha\) ) inhibitors. Rituximab is off- label and used for various autoimmune disorders including, PV due to potential therapeutic effects in the modulation of pathogenic B cells [5]. We report a case of generalized PV, treated with rituximab.  
 
-sub_title[[91, 157, 235, 170]]
+sub_title[[93, 158, 235, 171]]
 ## Case presentation  
 
-text[[91, 172, 484, 499]]
-A 39- year- old male patient who lives in Surat, Gujarat, was referred with a 3- month history of painful ulcerated lesions in the oral cavity. On enquiring about the patient's history, we came to know that initially, the patient had difficulty chewing food and the severity increased gradually. The ulcerations caused considerable discomfort, affecting his normal oral functions. Subsequently, fluid- filled lesions developed involving the scalp, trunk, limbs, and axilla. Lesions were increasing in size and number and had little tendency to heal. Blisters were flaccid and burst on their own to form erosions within 2- 3 days. Medical and family history was non- contributory. No history of fever, joint pain, malaise, and photosensitivity. He had weak oral hygiene due to the bad habit of taking betel quid with tobacco five times a day and smoking seven- - days per day for the past 12 years. Further, he consumes two- quarters of alcohol on an alternative day for the last 12 years. History of any drug intake before the appearance of lesions was also absent. Intraoral examination revealed that approximately \(1.0 \times 1.5\) dimensions ulceration lesions were present on the buccal mucosa. Dermatological examination revealed multiple vesicular lesions ranging from \(0.3 \times 0.3\) to \(1.5 \times 1.5\) involving the face, trunk, upper limbs, and dorsum of the penis (Figure 1a- 1).  
+text[[93, 174, 482, 496]]
+A 39- year- old male patient who lives in Surat, Gujarat, was referred with a 3- month history of painful ulcerated lesions in the oral cavity. On enquiring about the patient's history, we came to know that initially, the patient had difficulty chewing food and the severity increased gradually. The ulcerations caused considerable discomfort, affecting his normal oral functions. Subsequently, fluid- filled lesions developed involving the scalp, trunk, limbs, and axilla. Lesions were increasing in size and number and had little tendency to heal. Blisters were flaccid and burst on their own to form erosions within 2- 3 days. Medical and family history was non- contributory. No history of fever, joint pain, malaise, and photosensitivity. He had weak oral hygiene due to the bad habit of taking betel quid with tobacco five times a day and smoking seven bidi per day for the past 12 years. Further, he consumes two- quarters of alcohol on an alternative day for the last 12 years. History of any drug intake before the appearance of lesions was also absent. Intraoral examination revealed that approximately \(1.0 \times 1.5\) dimensions ulceration lesions were present on the buccal mucosa. Dermatological examination revealed multiple vesicular lesions ranging from \(0.3 \times 0.3\) to 1.5 \(\times 1.5\) involving the face, trunk, upper limbs, and dorsum of the penis (Figure 1a- 1i).  
 
-image[[94, 511, 484, 796]]
-image_caption[[91, 799, 484, 865]]
+image[[94, 509, 483, 795]]
+image_caption[[92, 799, 483, 862]]
 <center>Figure 1: Showing (a) ulcerative lesions present on the buccal mucosa (b) multiple vesicular lesions present on the face (c) multiple vesicular lesions with erosion present on the lower neck (d) multiple vesicular lesions present on the umbilicus (e) multiple vesicular lesions with erosion present on the upper limb (f) multiple vesicular lesions with erosion present on the back (g) multiple vesicular lesions with erosion on the axilla (h) flaccid blister lesions on the scalp (i) multiple vesicular lesions present on the dorsum of the penis. </center>  
 
-text[[92, 878, 484, 918], [513, 71, 904, 255]]
-There was a positive Nikolsky sign and a bulla spread sign. The clinical manifestations of oral ulcers, flaccid bullae, and positive Nikolsky sign hinted at the provisional diagnosis of PV. Mucous membrane pemphigoid, bullous lichen planus, paraneoplastic pemphigus, chronic ulcerative stomatitis, recurrent herpes lesions in immunocompromised patients, and erythema multiforme were the potential differential diagnosis of this condition. Regarding this, a biopsy was performed from a new vesicle to confirm the diagnosis. Histopathological examination revealed an intraepidermal supraslab acantholytic blister. Several acantholytic cells and neutrophils could be seen in the blister. The floor of the blister showed a tombstone pattern with occasional acantholytic cells. A moderately dense superficial perivascular mixed infiltrate was present in the dermis. Mild spongiosis with neutrophils was present at the periphery of the blister (Figure 2).   
+text[[92, 877, 484, 918]]
+There was a positive Nikolsky sign and a bulla spread sign. The clinical manifestations of oral ulcers, flaccid bullae, and positive Nikolsky sign hinted at the provisional diagnosis of  
 
-image[[513, 269, 905, 507]]
-image_caption[[512, 511, 904, 550]]
-<center>Figure 2: Photomicrograph showing acantholysis of the keratinocytes, tombstone appearance, epithelium exhibiting spongiosis, and superficial perivascular mixed infiltrate (H & E stain, x5). </center>  
+text[[513, 72, 903, 254]]
+PV. Mucous membrane pemphigoid, bullous lichen planus, paraneoplastic pemphigus, chronic ulcerative stomatitis, recurrent herpes lesions in immunocompromised patients, and erythema multiforme were the potential differential diagnosis of this condition. Regarding this, a biopsy was performed from a new vesicle to confirm the diagnosis. Histopathological examination revealed an intraepidermal subparabasal acantholytic blister. Several acantholytic cells and neutrophils could be seen in the blister. The floor of the blister showed a tombstone pattern with occasional acantholytic cells. A moderately dense superficial perivascular mixed infiltrate was present in the dermis. Mild spongiosis with neutrophils was present at the periphery of the blister (Figure 2).  
 
-text[[512, 568, 905, 924]]
+image[[515, 269, 904, 505]]
+image_caption[[513, 511, 904, 552]]
+<center>Figure 2: Photomicrograph showing acantholysis of the keratinocytes, tombstone appearance, epithelium exhibiting spongiosis, and superficial perivascular mixed infiltrate (H & E stain, \(\times 5\) ). </center>  
+
+text[[513, 569, 904, 923]]
 The hematological test had all findings within standard limits and, routine urine examination was unremarkable. In accordance with these findings, the definite diagnosis of PV was made and the treatment with oral cefuroxime (500mg twice a day) and oral prednisolone (20mg twice a day) with azathioprine (50mg twice a day) was started. Topical antibiotics and triamcinolone gel are advised for local application in the oral cavity. The dose of oral prednisolone was gradually tapered to 20mg, 10mg, 5mg, and 2.5mg (twice a day) every 30 days. The patient was maintained on the same dose of azathioprine (50mg twice a day) for one year. With the given therapy, complete remission was not achieved. Also, azathioprine was discontinued due to an elevated level of liver enzymes. Hence, the patient was shifted to rituximab therapy. The patient was initially given three doses of rituximab 1 gm each on days 1, 15, and 45. As premedication, ceftriaxone 1gm intravenously, hydrocortisone 100mg intravenously, paracetamol 650mg stat orally, and pheniramine maleate 2cc stat intravenously were given, sequentially on the day of infusion. After 30 minutes of these premedications rituximab (1gm) intravenously in 500ml of normal saline was given slowly over six to eight hours. The last dosage of rituximab was given after 3 months. A administration of rituximab lead to decrease Dsg 3 antibody levels which in turn resulted in the complete remission of the skin lesions within the next year (Figure 3a- g).
\ No newline at end of file
diff --git a/stage1/sample_00001/raw_response.md b/stage1/sample_00001/raw_response.md
index 1b2869e49a8289c2eff519af2ca10eaff08276a9..622e73427d0ba0b894f784f8906c5ac1bc7af7c5 100644
--- a/stage1/sample_00001/raw_response.md
+++ b/stage1/sample_00001/raw_response.md
@@ -1,24 +1,27 @@
-3- month history of painful ulcerated lesions in the oral cavity. On enquiring about the patient's history, we came to know that initially, the patient had difficulty chewing food and the severity increased gradually. The ulcerations caused considerable discomfort, affecting his normal oral functions. Subsequently, fluid-filled lesions developed involving the scalp, trunk, limbs, and axilla. Lesions were increasing in size and number and had little tendency to heal. Blisters were flaccid and burst on their own to form erosions within 2-3 days. Medical and family history was non- contributory. No history of fever, joint pain, malaise, and photosensitivity. He had weak oral hygiene due to the bad habit of taking betel quid with tobacco five times a day and smoking seven- - - - days per day for the past 12 years. Further, he consumes two- quarters of alcohol on an alternative day for the last 12 years. History of any drug intake before the appearance of lesions was also absent. Intraoral examination revealed that approximately \(1.0 \times 1.5\) dimensions ulceration lesions were present on the buccal mucosa. Dermatological examination revealed multiple vesicular lesions ranging from \(0.3 \times 0.3\) to \(1.5 \times 1.5\) involving the face, trunk, upper limbs, and dorsum of the penis (Figure 1a-1).  
+3- month history of painful ulcerated lesions in the oral cavity. On enquiring about the patient's history, we came to know that initially, the patient had difficulty chewing food and the severity increased gradually. The ulcerations caused considerable discomfort, affecting his normal oral functions. Subsequently, fluid-filled lesions developed involving the scalp, trunk, limbs, and axilla. Lesions were increasing in size and number and had little tendency to heal. Blisters were flaccid and burst on their own to form erosions within 2-3 days. Medical and family history was non- contributory. No history of fever, joint pain, malaise, and photosensitivity. He had weak oral hygiene due to the bad habit of taking betel quid with tobacco five times a day and smoking seven bidi per day for the past 12 years. Further, he consumes two- quarters of alcohol on an alternative day for the last 12 years. History of any drug intake before the appearance of lesions was also absent. Intraoral examination revealed that approximately \(1.0 \times 1.5\) dimensions ulceration lesions were present on the buccal mucosa. Dermatological examination revealed multiple vesicular lesions ranging from \(0.3 \times 0.3\) to 1.5 \(\times 1.5\) involving the face, trunk, upper limbs, and dorsum of the penis (Figure 1a-1i).  
 
-text[[91, 72, 484, 140]]
+text[[93, 73, 482, 141]]
 to tumor necrosis factor alpha (TNF- \(\alpha\) ) inhibitors. Rituximab is off- label and used for various autoimmune disorders including, PV due to potential therapeutic effects in the modulation of pathogenic B cells [5]. We report a case of generalized PV, treated with rituximab.  
 
-sub_title[[91, 157, 235, 170]]
+sub_title[[93, 158, 235, 171]]
 ## Case presentation  
 
-text[[91, 172, 484, 499]]
-A 39- year- old male patient who lives in Surat, Gujarat, was referred with a 3- month history of painful ulcerated lesions in the oral cavity. On enquiring about the patient's history, we came to know that initially, the patient had difficulty chewing food and the severity increased gradually. The ulcerations caused considerable discomfort, affecting his normal oral functions. Subsequently, fluid- filled lesions developed involving the scalp, trunk, limbs, and axilla. Lesions were increasing in size and number and had little tendency to heal. Blisters were flaccid and burst on their own to form erosions within 2- 3 days. Medical and family history was non- contributory. No history of fever, joint pain, malaise, and photosensitivity. He had weak oral hygiene due to the bad habit of taking betel quid with tobacco five times a day and smoking seven- - days per day for the past 12 years. Further, he consumes two- quarters of alcohol on an alternative day for the last 12 years. History of any drug intake before the appearance of lesions was also absent. Intraoral examination revealed that approximately \(1.0 \times 1.5\) dimensions ulceration lesions were present on the buccal mucosa. Dermatological examination revealed multiple vesicular lesions ranging from \(0.3 \times 0.3\) to \(1.5 \times 1.5\) involving the face, trunk, upper limbs, and dorsum of the penis (Figure 1a- 1).  
+text[[93, 174, 482, 496]]
+A 39- year- old male patient who lives in Surat, Gujarat, was referred with a 3- month history of painful ulcerated lesions in the oral cavity. On enquiring about the patient's history, we came to know that initially, the patient had difficulty chewing food and the severity increased gradually. The ulcerations caused considerable discomfort, affecting his normal oral functions. Subsequently, fluid- filled lesions developed involving the scalp, trunk, limbs, and axilla. Lesions were increasing in size and number and had little tendency to heal. Blisters were flaccid and burst on their own to form erosions within 2- 3 days. Medical and family history was non- contributory. No history of fever, joint pain, malaise, and photosensitivity. He had weak oral hygiene due to the bad habit of taking betel quid with tobacco five times a day and smoking seven bidi per day for the past 12 years. Further, he consumes two- quarters of alcohol on an alternative day for the last 12 years. History of any drug intake before the appearance of lesions was also absent. Intraoral examination revealed that approximately \(1.0 \times 1.5\) dimensions ulceration lesions were present on the buccal mucosa. Dermatological examination revealed multiple vesicular lesions ranging from \(0.3 \times 0.3\) to 1.5 \(\times 1.5\) involving the face, trunk, upper limbs, and dorsum of the penis (Figure 1a- 1i).  
 
-image[[94, 511, 484, 796]]
-image_caption[[91, 799, 484, 865]]
+image[[94, 509, 483, 795]]
+image_caption[[92, 799, 483, 862]]
 <center>Figure 1: Showing (a) ulcerative lesions present on the buccal mucosa (b) multiple vesicular lesions present on the face (c) multiple vesicular lesions with erosion present on the lower neck (d) multiple vesicular lesions present on the umbilicus (e) multiple vesicular lesions with erosion present on the upper limb (f) multiple vesicular lesions with erosion present on the back (g) multiple vesicular lesions with erosion on the axilla (h) flaccid blister lesions on the scalp (i) multiple vesicular lesions present on the dorsum of the penis. </center>  
 
-text[[92, 878, 484, 918], [513, 71, 904, 255]]
-There was a positive Nikolsky sign and a bulla spread sign. The clinical manifestations of oral ulcers, flaccid bullae, and positive Nikolsky sign hinted at the provisional diagnosis of PV. Mucous membrane pemphigoid, bullous lichen planus, paraneoplastic pemphigus, chronic ulcerative stomatitis, recurrent herpes lesions in immunocompromised patients, and erythema multiforme were the potential differential diagnosis of this condition. Regarding this, a biopsy was performed from a new vesicle to confirm the diagnosis. Histopathological examination revealed an intraepidermal supraslab acantholytic blister. Several acantholytic cells and neutrophils could be seen in the blister. The floor of the blister showed a tombstone pattern with occasional acantholytic cells. A moderately dense superficial perivascular mixed infiltrate was present in the dermis. Mild spongiosis with neutrophils was present at the periphery of the blister (Figure 2).   
+text[[92, 877, 484, 918]]
+There was a positive Nikolsky sign and a bulla spread sign. The clinical manifestations of oral ulcers, flaccid bullae, and positive Nikolsky sign hinted at the provisional diagnosis of  
 
-image[[513, 269, 905, 507]]
-image_caption[[512, 511, 904, 550]]
-<center>Figure 2: Photomicrograph showing acantholysis of the keratinocytes, tombstone appearance, epithelium exhibiting spongiosis, and superficial perivascular mixed infiltrate (H & E stain, x5). </center>  
+text[[513, 72, 903, 254]]
+PV. Mucous membrane pemphigoid, bullous lichen planus, paraneoplastic pemphigus, chronic ulcerative stomatitis, recurrent herpes lesions in immunocompromised patients, and erythema multiforme were the potential differential diagnosis of this condition. Regarding this, a biopsy was performed from a new vesicle to confirm the diagnosis. Histopathological examination revealed an intraepidermal subparabasal acantholytic blister. Several acantholytic cells and neutrophils could be seen in the blister. The floor of the blister showed a tombstone pattern with occasional acantholytic cells. A moderately dense superficial perivascular mixed infiltrate was present in the dermis. Mild spongiosis with neutrophils was present at the periphery of the blister (Figure 2).  
 
-text[[512, 568, 905, 924]]
+image[[515, 269, 904, 505]]
+image_caption[[513, 511, 904, 552]]
+<center>Figure 2: Photomicrograph showing acantholysis of the keratinocytes, tombstone appearance, epithelium exhibiting spongiosis, and superficial perivascular mixed infiltrate (H & E stain, \(\times 5\) ). </center>  
+
+text[[513, 569, 904, 923]]
 The hematological test had all findings within standard limits and, routine urine examination was unremarkable. In accordance with these findings, the definite diagnosis of PV was made and the treatment with oral cefuroxime (500mg twice a day) and oral prednisolone (20mg twice a day) with azathioprine (50mg twice a day) was started. Topical antibiotics and triamcinolone gel are advised for local application in the oral cavity. The dose of oral prednisolone was gradually tapered to 20mg, 10mg, 5mg, and 2.5mg (twice a day) every 30 days. The patient was maintained on the same dose of azathioprine (50mg twice a day) for one year. With the given therapy, complete remission was not achieved. Also, azathioprine was discontinued due to an elevated level of liver enzymes. Hence, the patient was shifted to rituximab therapy. The patient was initially given three doses of rituximab 1 gm each on days 1, 15, and 45. As premedication, ceftriaxone 1gm intravenously, hydrocortisone 100mg intravenously, paracetamol 650mg stat orally, and pheniramine maleate 2cc stat intravenously were given, sequentially on the day of infusion. After 30 minutes of these premedications rituximab (1gm) intravenously in 500ml of normal saline was given slowly over six to eight hours. The last dosage of rituximab was given after 3 months. A administration of rituximab lead to decrease Dsg 3 antibody levels which in turn resulted in the complete remission of the skin lesions within the next year (Figure 3a- g).
\ No newline at end of file
diff --git a/stage1/sample_00002/document.md b/stage1/sample_00002/document.md
index 3f9e2a23f31ef2322a578b21351d4e0256c51afe..185276cbbdd0cf2bea2104fd581a01c772b2b596 100644
--- a/stage1/sample_00002/document.md
+++ b/stage1/sample_00002/document.md
@@ -1,28 +1,25 @@
-1\\*, Dhruv J agdish Sakhiya1, J ashmine Mukeshbhai Gandhi1, Feral Ravi Daruwala2  
+2645-9248 Journal homepage: www.jidhealth.com Open A ccess Original Article A case report on generalized pemphigus vulgaris treated with rituximaba J agdish J adavbhai S akhiya<sup>1</sup>\*, Dhruv J agdish S akhiya<sup>1</sup>, J ashmine Mukeshbhai Gandhi<sup>1</sup>, F eral R avi Daruwala<sup>2</sup>  
 
-sub_title[[99, 348, 176, 362]]
+sub_title[[100, 347, 174, 362]]
 ## Abstract  
 
-text[[100, 365, 876, 405]]
-Background: P emphigus vulgaris has an obscure etiology; the presence of autoantibodies is coherent with an autoimmune disease. R ituximab a monoclonal antibody that specifically targets the CD20 antigen of B lymphocytes, has arisen as a novel treatment approach for pemphigus vulgaris.  
+text[[100, 364, 873, 404]]
+Background: Pemphigus vulgaris has an obscure etiology; the presence of autoantibodies is coherent with an autoimmune disease. Rituximab a monoclonal antibody that specifically targets the CD20 antigen of B lymphocytes, has arisen as a novel treatment approach for pemphigus vulgaris.  
 
-text[[100, 412, 888, 477]]
+text[[100, 411, 885, 476]]
 Case presentation: A 39- year- old male patient presented with a three- month history of mouth ulcers, poor oral hygiene accompanied with heavy tobacco smoking and alcohol consumption. He was diagnosed with pemphigus vulgaris. The disease gradually progressed to involve other body parts. The patient had shown partial improvement after conventional therapy (oral cefuroxime, oral prednisolone with azathioprine) and was later on successfully treated with rituximab. After 90 days of follow- up, no future recurrence was observed.  
 
-text[[100, 485, 893, 514]]
+text[[100, 484, 891, 513]]
 Conclusion: With this case, the authors would like to aware other clinicians of the potential use of rituximab in treating pemphigus vulgaris, especially when the conventional therapy fails.  
 
-text[[102, 523, 814, 539]]
-Keywords: Autoantibodies; Pemphigus, Rituximab, Oral Hygiene, Ulceration, Tobacco Smoking, Alcohol  
+text[[100, 521, 812, 555]]
+Keywords: Autoantibodies; Pemphigus, Rituximab, Oral Hygiene, Ulceration, Tobacco Smoking, Alcohol consumption, India  
 
-text[[100, 543, 229, 557]]
-consumption, India  
-
-sub_title[[92, 594, 193, 609]]
+sub_title[[93, 594, 193, 609]]
 ## Background  
 
-text[[92, 610, 484, 835]]
-The term pemphigus implies a group of autoimmune, mucocutaneous blistering diseases, in which the keratinocyte antigens are the target of the autoantibodies, prompting acantholysis and the formation of blisters. Main variants of pemphigus include pemphigus vulgaris (PV) and pemphigus folicaceus (PF). PV is the most common subtype and represents well over \(80\%\) of cases. As being a serious and potentially lifethreatening condition, early treatment is of utmost importance [1]. The advent of corticosteroids in the amelioration of pemphigus has dramatically changed the outlook of this perpetually disastrous disease; thus, corticosteroids have become the cornerstone of pemphigus therapy. One case reported favorable outcomes with combined therapy of high- dose corticosteroids and other immunosuppressants. However, such a high dose of corticosteroids can cause serious adverse events such as several metabolic problems, global reduction of  
+text[[93, 610, 484, 834]]
+The term pemphigus implies a group of autoimmune, mucocutaneous blistering diseases, in which the keratinocyte antigens are the target of the autoantibodies, prompting acantholysis and the formation of blisters. Main variants of pemphigus include pemphigus vulgaris (PV) and pemphigus foliaceus (PF). PV is the most common subtype and represents well over \(80\%\) of cases. As being a serious and potentially lifethreatening condition, early treatment is of utmost importance [1]. The advent of corticosteroids in the amelioration of pemphigus has dramatically changed the outlook of this perpetually disastrous disease; thus, corticosteroids have become the cornerstone of pemphigus therapy. One case reported favorable outcomes with combined therapy of highdose corticosteroids and other immunosuppressants. However, such a high dose of corticosteroids can cause serious adverse events such as several metabolic problems, global reduction of  
 
-text[[513, 595, 905, 902]]
+text[[514, 595, 905, 901]]
 immune system efficacy, antecedent risk of serious infections, and mortality [2]. To overcome these long- term events, Pasricha and Gupta introduced dexamethasone cyclophosphamide pulse (DCP) therapy in 1984 [3]. Later on, DCP and oral corticosteroids with or without adjuvant immunosuppressants (azathioprine, cyclophosphamide, mycophenolate mofetil, and cyclosporine) have emerged as the backbone of pemphigus treatment, however, they are associated with the high death rate in pemphigus [4]. With these conventional treatments, some patients fail to improve or some have contraindications for their usage, or some encounter relapse. Hence, advanced research has continuously been going on for finding newer molecules in pemphigus. In 2001, Heizmann et al. [5] first used rituximab for the therapy of autoimmune bullous diseases. He reported a case of paraneoplastic pemphigus favorably managed with rituximab, since then there was a drastic development in the pemphigus treatment era. Rituximab chimeric monoclonal antibody selectively acts on the CD20 expressing B cells, which are known to secrete auto- antibodies targeting the epidermal desmogleins (DSG). It has been used nearly in one million patients for treating lymphoma worldwide. Recently, rituximab has been approved for rheumatoid arthritis that is unresponsive
\ No newline at end of file
diff --git a/stage1/sample_00002/raw_response.md b/stage1/sample_00002/raw_response.md
index 3f9e2a23f31ef2322a578b21351d4e0256c51afe..185276cbbdd0cf2bea2104fd581a01c772b2b596 100644
--- a/stage1/sample_00002/raw_response.md
+++ b/stage1/sample_00002/raw_response.md
@@ -1,28 +1,25 @@
-1\\*, Dhruv J agdish Sakhiya1, J ashmine Mukeshbhai Gandhi1, Feral Ravi Daruwala2  
+2645-9248 Journal homepage: www.jidhealth.com Open A ccess Original Article A case report on generalized pemphigus vulgaris treated with rituximaba J agdish J adavbhai S akhiya<sup>1</sup>\*, Dhruv J agdish S akhiya<sup>1</sup>, J ashmine Mukeshbhai Gandhi<sup>1</sup>, F eral R avi Daruwala<sup>2</sup>  
 
-sub_title[[99, 348, 176, 362]]
+sub_title[[100, 347, 174, 362]]
 ## Abstract  
 
-text[[100, 365, 876, 405]]
-Background: P emphigus vulgaris has an obscure etiology; the presence of autoantibodies is coherent with an autoimmune disease. R ituximab a monoclonal antibody that specifically targets the CD20 antigen of B lymphocytes, has arisen as a novel treatment approach for pemphigus vulgaris.  
+text[[100, 364, 873, 404]]
+Background: Pemphigus vulgaris has an obscure etiology; the presence of autoantibodies is coherent with an autoimmune disease. Rituximab a monoclonal antibody that specifically targets the CD20 antigen of B lymphocytes, has arisen as a novel treatment approach for pemphigus vulgaris.  
 
-text[[100, 412, 888, 477]]
+text[[100, 411, 885, 476]]
 Case presentation: A 39- year- old male patient presented with a three- month history of mouth ulcers, poor oral hygiene accompanied with heavy tobacco smoking and alcohol consumption. He was diagnosed with pemphigus vulgaris. The disease gradually progressed to involve other body parts. The patient had shown partial improvement after conventional therapy (oral cefuroxime, oral prednisolone with azathioprine) and was later on successfully treated with rituximab. After 90 days of follow- up, no future recurrence was observed.  
 
-text[[100, 485, 893, 514]]
+text[[100, 484, 891, 513]]
 Conclusion: With this case, the authors would like to aware other clinicians of the potential use of rituximab in treating pemphigus vulgaris, especially when the conventional therapy fails.  
 
-text[[102, 523, 814, 539]]
-Keywords: Autoantibodies; Pemphigus, Rituximab, Oral Hygiene, Ulceration, Tobacco Smoking, Alcohol  
+text[[100, 521, 812, 555]]
+Keywords: Autoantibodies; Pemphigus, Rituximab, Oral Hygiene, Ulceration, Tobacco Smoking, Alcohol consumption, India  
 
-text[[100, 543, 229, 557]]
-consumption, India  
-
-sub_title[[92, 594, 193, 609]]
+sub_title[[93, 594, 193, 609]]
 ## Background  
 
-text[[92, 610, 484, 835]]
-The term pemphigus implies a group of autoimmune, mucocutaneous blistering diseases, in which the keratinocyte antigens are the target of the autoantibodies, prompting acantholysis and the formation of blisters. Main variants of pemphigus include pemphigus vulgaris (PV) and pemphigus folicaceus (PF). PV is the most common subtype and represents well over \(80\%\) of cases. As being a serious and potentially lifethreatening condition, early treatment is of utmost importance [1]. The advent of corticosteroids in the amelioration of pemphigus has dramatically changed the outlook of this perpetually disastrous disease; thus, corticosteroids have become the cornerstone of pemphigus therapy. One case reported favorable outcomes with combined therapy of high- dose corticosteroids and other immunosuppressants. However, such a high dose of corticosteroids can cause serious adverse events such as several metabolic problems, global reduction of  
+text[[93, 610, 484, 834]]
+The term pemphigus implies a group of autoimmune, mucocutaneous blistering diseases, in which the keratinocyte antigens are the target of the autoantibodies, prompting acantholysis and the formation of blisters. Main variants of pemphigus include pemphigus vulgaris (PV) and pemphigus foliaceus (PF). PV is the most common subtype and represents well over \(80\%\) of cases. As being a serious and potentially lifethreatening condition, early treatment is of utmost importance [1]. The advent of corticosteroids in the amelioration of pemphigus has dramatically changed the outlook of this perpetually disastrous disease; thus, corticosteroids have become the cornerstone of pemphigus therapy. One case reported favorable outcomes with combined therapy of highdose corticosteroids and other immunosuppressants. However, such a high dose of corticosteroids can cause serious adverse events such as several metabolic problems, global reduction of  
 
-text[[513, 595, 905, 902]]
+text[[514, 595, 905, 901]]
 immune system efficacy, antecedent risk of serious infections, and mortality [2]. To overcome these long- term events, Pasricha and Gupta introduced dexamethasone cyclophosphamide pulse (DCP) therapy in 1984 [3]. Later on, DCP and oral corticosteroids with or without adjuvant immunosuppressants (azathioprine, cyclophosphamide, mycophenolate mofetil, and cyclosporine) have emerged as the backbone of pemphigus treatment, however, they are associated with the high death rate in pemphigus [4]. With these conventional treatments, some patients fail to improve or some have contraindications for their usage, or some encounter relapse. Hence, advanced research has continuously been going on for finding newer molecules in pemphigus. In 2001, Heizmann et al. [5] first used rituximab for the therapy of autoimmune bullous diseases. He reported a case of paraneoplastic pemphigus favorably managed with rituximab, since then there was a drastic development in the pemphigus treatment era. Rituximab chimeric monoclonal antibody selectively acts on the CD20 expressing B cells, which are known to secrete auto- antibodies targeting the epidermal desmogleins (DSG). It has been used nearly in one million patients for treating lymphoma worldwide. Recently, rituximab has been approved for rheumatoid arthritis that is unresponsive
\ No newline at end of file
diff --git a/stage1/sample_00003/document.md b/stage1/sample_00003/document.md
index 2a5a1ea46e3b87926861aa3500214e0d05afa2bd..7581f4715744f14f1ac9705abff69368efbdf3f3 100644
--- a/stage1/sample_00003/document.md
+++ b/stage1/sample_00003/document.md
@@ -1,73 +1,68 @@
-1? (X) Enty for the Engineers Ireland Biomedical Research Medal? (X) 1? (X) Enty for the Engineers Ireland Biomedical Research Medal? (X) Post-Doctoral Researcher/Senior Researcher/PI N 
+1) \(\mathbf{Y}\)  
 
-sub_title[[217, 113, 794, 147]]
-LOAD INDUCED CHANGES IN COLLAGEN FIBRE ARCHITECTURE IN ARTERIES CHARACTERISED BY SMALL ANGLE LIGHT SCATTERING 
+text[[149, 74, 341, 97]]
+Entry for the Engineers Ireland Biomedical Research Medal? (X)  
 
-text[[392, 171, 588, 190]]
-Gaul, R.1,2, Lally, C.1,2 
+sub_title[[217, 112, 793, 146]]
+## LOAD INDUCED CHANGES IN COLLAGEN FIBRE ARCHITECTURE IN ARTERIES CHARACTERISED BY SMALL ANGLE LIGHT SCATTERING  
 
-text[[292, 184, 766, 228]]
-1Trinity Centre for Bioengineering, Trinity College Dublin, Dublin, Ireland.
-2School of Engineering, Trinity College Dublin, Dublin, Ireland.
-email: rgaul@tcd.ie 
+text[[240, 168, 768, 231]]
+Gaul, R. \(^{1,2}\) , Lally, C. \(^{1,2}\) \(^{\text {Trinity Centre for Bioengineering, Trinity College Dublin, Dublin, Ireland.}\) \(^{2}\) School of Engineering, Trinity College Dublin, Dublin, Ireland. email: rgau@tcd.ie  
 
-sub_title[[143, 237, 273, 252]]
-INTRODUCTION 
+sub_title[[145, 237, 271, 252]]
+## INTRODUCTION  
 
-text[[143, 260, 471, 362]]
-The structural strength of arteries is governed by reinforcing collagen fibres present in the vessel wall. Although healthy vessels are capable of fibre remodelling, unhealthy fibre remodelling patterns may be associated with disease [1]. A greater understanding of the remodelling of these fibres may provide greater insight into arteries at risk of disease and how arterial repair may be induced. 
+text[[145, 258, 469, 362]]
+The structural strength of arteries is governed by reinforcing collagen fibres present in the vessel wall. Although healthy vessels are capable of fibre remodelling, unhealthy fibre remodelling patterns may be associated with disease [1]. A greater understanding of the remodelling of these fibres may provide greater insight into arteries at risk of disease and how arterial repair may be induced.  
 
-text[[143, 366, 471, 433]]
-Small angle light scattering (SALS) is a technique which has previously been used to determine the structure of thin, highly organised tissue structures, such as bovine pericardium and porcine aortic valve tissue [2]. 
+text[[144, 364, 469, 430]]
+Small angle light scattering (SALS) is a technique which has previously been used to determine the structure of thin, highly organised tissue structures, such as bovine pericardium and porcine aortic valve tissue [2].  
 
-text[[143, 436, 471, 489]]
-The aim of the present study is to design and develop a fully automated SALS system capable of determining the changes in arterial fibre architecture in response to strain. 
+text[[144, 434, 469, 488]]
+The aim of the present study is to design and develop a fully automated SALS system capable of determining the changes in arterial fibre architecture in response to strain.  
 
-sub_title[[143, 502, 368, 517]]
-MATERIALS AND METHODS 
+sub_title[[145, 501, 366, 516]]
+## MATERIALS AND METHODS  
 
-text[[143, 525, 471, 682]]
-An in-house SALS system has been developed making use of an unpolarised 5mW HeNe laser (λ = 632.8 nm) and two focusing lenses in order to pass light through a tissue sample held in an automated sample positioner. The sample positioner incorporates two stepper motors controlled by LabVIEW to allow movement of the sample in the x and y plane with a resolution of 5 μm. The sample is interrogated sequentially in 250 x 250 μm regions. The resulting scattered light pattern is recorded by a CMOS camera and analysed through a custom Matlab code to determine predominant collagen fibre directions. 
+text[[144, 523, 469, 679]]
+An in- house SALS system has been developed making use of an unpolarised \(5\mathrm{mW}\) HeNe laser \((\lambda = 632.8\mathrm{nm})\) and two focusing lenses in order to pass light through a tissue sample held in an automated sample positioner. The sample positioner incorporates two stepper motors controlled by LabVIEW to allow movement of the sample in the x and y plane with a resolution of \(5\mu \mathrm{m}\) . The sample is interrogated sequentially in \(250\times 250\mu \mathrm{m}\) regions. The resulting scattered light pattern is recorded by a CMOS camera and analysed through a custom Matlab code to determine predominant collagen fibre directions.  
 
-text[[143, 686, 471, 790]]
-To validate the system, testing was conducted on test plates with known printed configurations. Once validated, SALS testing was carried out on flat porcine carotid artery wall sections fixed at different stretch ratios. Carotid artery samples were fixed and processed using a standard histological tissue sectioning protocol. Validation of the results was achieved through histological staining of the sections. 
+text[[144, 681, 469, 787]]
+To validate the system, testing was conducted on test plates with known printed configurations. Once validated, SALS testing was carried out on flat porcine carotid artery wall sections fixed at different stretch ratios. Carotid artery samples were fixed and processed using a standard histological tissue sectioning protocol. Validation of the results was achieved through histological staining of the sections.  
 
-sub_title[[143, 802, 224, 816]]
-RESULTS 
+sub_title[[146, 800, 223, 814]]
+## RESULTS  
 
-text[[143, 824, 471, 902]]
-Figure 1a displays the collagen fibre directions in an unstretched carotid artery section, as predicted by SALS, overlaid on picrosirius red stained histological images. Figure 1b shows the reorganisation of the constituent collagen fibres under circumferential stretch (λ=1.25). 
+text[[144, 822, 469, 900]]
+Figure 1a displays the collagen fibre directions in an unstretched carotid artery section, as predicted by SALS, overlaid on picrosirius red stained histological images. Figure 1b shows the reorganisation of the constituent collagen fibres under circumferential stretch \((\lambda = 1.25)\) .  
 
-text[[526, 236, 852, 277]]
-Collagen fibre patterns in the artery were also obtained through the thickness of the artery wall using SALS, for both strained and unstrained configurations. 
+text[[527, 238, 853, 277]]
+Collagen fibre patterns in the artery were also obtained through the thickness of the artery wall using SALS, for both strained and unstrained configurations.  
 
-image[[525, 289, 837, 411]]
- 
+image[[527, 288, 839, 414]]
+image_caption[[525, 415, 853, 452]]
+<center>Figure 1 Fibre orientation as determined by SALS overlaid on histological carotid wall images. a) unstretched \((\lambda = 1)\) and b) stretched circumferentially \((\lambda = 1.25)\) . </center>  
 
-image_caption[[525, 414, 852, 450]]
-<center>Figure 1 Fibre orientation as determined by SALS overlaid on histological carotid wall images. a) unstretched (λ=1) and b) stretched circumferentially (λ=1.25).</center> 
+sub_title[[527, 464, 630, 477]]
+## DISCUSSION  
 
-sub_title[[526, 464, 631, 478]]
-DISCUSSION 
+text[[527, 486, 853, 577]]
+Results shown in Figure 1 highlight the dependence of fibre orientation on the levels of stretch experienced by the artery wall. A clear realignment of collagen fibres in the direction of loading is visible from Figure 1a and 1b. Although these results are widely known and shown in literature, this is the first time they have been resolved through SALS.  
 
-text[[526, 487, 852, 578]]
-Results shown in Figure 1 highlight the dependence of fibre orientation on the levels of stretch experienced by the artery wall. A clear realignment of collagen fibres in the direction of loading is visible from Figure 1a and 1b. Although these results are widely known and shown in literature, this is the first time they have been resolved through SALS. 
+text[[527, 579, 853, 647]]
+Although SALS is limited to thin samples, time consuming staining protocols are not required for fibre characterisation. The speed, accuracy and ease of use of this system make it a powerful system for providing insights into the response of arterial tissue to load.  
 
-text[[526, 582, 852, 649]]
-Although SALS is limited to thin samples, time consuming staining protocols are not required for fibre characterisation. The speed, accuracy and ease of use of this system make it a powerful system for providing insights into the response of arterial tissue to load. 
+text[[526, 650, 853, 689]]
+Future work aims to fully identify load induced tissue changes in healthy and diseased arterial tissue using SALS.  
 
-text[[526, 652, 852, 692]]
-Future work aims to fully identify load induced tissue changes in healthy and diseased arterial tissue using SALS. 
+sub_title[[527, 705, 640, 718]]
+## REFERENCES  
 
-sub_title[[526, 706, 641, 721]]
-REFERENCES 
+text[[526, 726, 853, 780]]
+[1] Creanee et al., Biomech Model Mechanobil, 10: 831- 843, 2011 [2] Billiar, K., and Sacks, M., J. Biomech. 30: 753- 7 56, 1997  
 
-text[[526, 729, 852, 780]]
-[1] Creane et al., Biomech Model Mechanobiol., 10: 831-843, 2011
-[2] Billiar, K., and Sacks, M., J. Biomech. 30: 753-7 56, 1997 
+sub_title[[527, 792, 717, 806]]
+## ACKNOWLEDGEMENTS  
 
-sub_title[[526, 794, 717, 808]]
-ACKNOWLEDGEMENTS 
-
-text[[526, 816, 852, 856]]
+text[[526, 813, 853, 852]]
 This research was part funded by Science Foundation Ireland (SFI/13/ERC/B2775) and the Irish Research Council (GOIPG/2014/515).
\ No newline at end of file
diff --git a/stage1/sample_00003/raw_response.md b/stage1/sample_00003/raw_response.md
index 2a5a1ea46e3b87926861aa3500214e0d05afa2bd..7581f4715744f14f1ac9705abff69368efbdf3f3 100644
--- a/stage1/sample_00003/raw_response.md
+++ b/stage1/sample_00003/raw_response.md
@@ -1,73 +1,68 @@
-1? (X) Enty for the Engineers Ireland Biomedical Research Medal? (X) 1? (X) Enty for the Engineers Ireland Biomedical Research Medal? (X) Post-Doctoral Researcher/Senior Researcher/PI N 
+1) \(\mathbf{Y}\)  
 
-sub_title[[217, 113, 794, 147]]
-LOAD INDUCED CHANGES IN COLLAGEN FIBRE ARCHITECTURE IN ARTERIES CHARACTERISED BY SMALL ANGLE LIGHT SCATTERING 
+text[[149, 74, 341, 97]]
+Entry for the Engineers Ireland Biomedical Research Medal? (X)  
 
-text[[392, 171, 588, 190]]
-Gaul, R.1,2, Lally, C.1,2 
+sub_title[[217, 112, 793, 146]]
+## LOAD INDUCED CHANGES IN COLLAGEN FIBRE ARCHITECTURE IN ARTERIES CHARACTERISED BY SMALL ANGLE LIGHT SCATTERING  
 
-text[[292, 184, 766, 228]]
-1Trinity Centre for Bioengineering, Trinity College Dublin, Dublin, Ireland.
-2School of Engineering, Trinity College Dublin, Dublin, Ireland.
-email: rgaul@tcd.ie 
+text[[240, 168, 768, 231]]
+Gaul, R. \(^{1,2}\) , Lally, C. \(^{1,2}\) \(^{\text {Trinity Centre for Bioengineering, Trinity College Dublin, Dublin, Ireland.}\) \(^{2}\) School of Engineering, Trinity College Dublin, Dublin, Ireland. email: rgau@tcd.ie  
 
-sub_title[[143, 237, 273, 252]]
-INTRODUCTION 
+sub_title[[145, 237, 271, 252]]
+## INTRODUCTION  
 
-text[[143, 260, 471, 362]]
-The structural strength of arteries is governed by reinforcing collagen fibres present in the vessel wall. Although healthy vessels are capable of fibre remodelling, unhealthy fibre remodelling patterns may be associated with disease [1]. A greater understanding of the remodelling of these fibres may provide greater insight into arteries at risk of disease and how arterial repair may be induced. 
+text[[145, 258, 469, 362]]
+The structural strength of arteries is governed by reinforcing collagen fibres present in the vessel wall. Although healthy vessels are capable of fibre remodelling, unhealthy fibre remodelling patterns may be associated with disease [1]. A greater understanding of the remodelling of these fibres may provide greater insight into arteries at risk of disease and how arterial repair may be induced.  
 
-text[[143, 366, 471, 433]]
-Small angle light scattering (SALS) is a technique which has previously been used to determine the structure of thin, highly organised tissue structures, such as bovine pericardium and porcine aortic valve tissue [2]. 
+text[[144, 364, 469, 430]]
+Small angle light scattering (SALS) is a technique which has previously been used to determine the structure of thin, highly organised tissue structures, such as bovine pericardium and porcine aortic valve tissue [2].  
 
-text[[143, 436, 471, 489]]
-The aim of the present study is to design and develop a fully automated SALS system capable of determining the changes in arterial fibre architecture in response to strain. 
+text[[144, 434, 469, 488]]
+The aim of the present study is to design and develop a fully automated SALS system capable of determining the changes in arterial fibre architecture in response to strain.  
 
-sub_title[[143, 502, 368, 517]]
-MATERIALS AND METHODS 
+sub_title[[145, 501, 366, 516]]
+## MATERIALS AND METHODS  
 
-text[[143, 525, 471, 682]]
-An in-house SALS system has been developed making use of an unpolarised 5mW HeNe laser (λ = 632.8 nm) and two focusing lenses in order to pass light through a tissue sample held in an automated sample positioner. The sample positioner incorporates two stepper motors controlled by LabVIEW to allow movement of the sample in the x and y plane with a resolution of 5 μm. The sample is interrogated sequentially in 250 x 250 μm regions. The resulting scattered light pattern is recorded by a CMOS camera and analysed through a custom Matlab code to determine predominant collagen fibre directions. 
+text[[144, 523, 469, 679]]
+An in- house SALS system has been developed making use of an unpolarised \(5\mathrm{mW}\) HeNe laser \((\lambda = 632.8\mathrm{nm})\) and two focusing lenses in order to pass light through a tissue sample held in an automated sample positioner. The sample positioner incorporates two stepper motors controlled by LabVIEW to allow movement of the sample in the x and y plane with a resolution of \(5\mu \mathrm{m}\) . The sample is interrogated sequentially in \(250\times 250\mu \mathrm{m}\) regions. The resulting scattered light pattern is recorded by a CMOS camera and analysed through a custom Matlab code to determine predominant collagen fibre directions.  
 
-text[[143, 686, 471, 790]]
-To validate the system, testing was conducted on test plates with known printed configurations. Once validated, SALS testing was carried out on flat porcine carotid artery wall sections fixed at different stretch ratios. Carotid artery samples were fixed and processed using a standard histological tissue sectioning protocol. Validation of the results was achieved through histological staining of the sections. 
+text[[144, 681, 469, 787]]
+To validate the system, testing was conducted on test plates with known printed configurations. Once validated, SALS testing was carried out on flat porcine carotid artery wall sections fixed at different stretch ratios. Carotid artery samples were fixed and processed using a standard histological tissue sectioning protocol. Validation of the results was achieved through histological staining of the sections.  
 
-sub_title[[143, 802, 224, 816]]
-RESULTS 
+sub_title[[146, 800, 223, 814]]
+## RESULTS  
 
-text[[143, 824, 471, 902]]
-Figure 1a displays the collagen fibre directions in an unstretched carotid artery section, as predicted by SALS, overlaid on picrosirius red stained histological images. Figure 1b shows the reorganisation of the constituent collagen fibres under circumferential stretch (λ=1.25). 
+text[[144, 822, 469, 900]]
+Figure 1a displays the collagen fibre directions in an unstretched carotid artery section, as predicted by SALS, overlaid on picrosirius red stained histological images. Figure 1b shows the reorganisation of the constituent collagen fibres under circumferential stretch \((\lambda = 1.25)\) .  
 
-text[[526, 236, 852, 277]]
-Collagen fibre patterns in the artery were also obtained through the thickness of the artery wall using SALS, for both strained and unstrained configurations. 
+text[[527, 238, 853, 277]]
+Collagen fibre patterns in the artery were also obtained through the thickness of the artery wall using SALS, for both strained and unstrained configurations.  
 
-image[[525, 289, 837, 411]]
- 
+image[[527, 288, 839, 414]]
+image_caption[[525, 415, 853, 452]]
+<center>Figure 1 Fibre orientation as determined by SALS overlaid on histological carotid wall images. a) unstretched \((\lambda = 1)\) and b) stretched circumferentially \((\lambda = 1.25)\) . </center>  
 
-image_caption[[525, 414, 852, 450]]
-<center>Figure 1 Fibre orientation as determined by SALS overlaid on histological carotid wall images. a) unstretched (λ=1) and b) stretched circumferentially (λ=1.25).</center> 
+sub_title[[527, 464, 630, 477]]
+## DISCUSSION  
 
-sub_title[[526, 464, 631, 478]]
-DISCUSSION 
+text[[527, 486, 853, 577]]
+Results shown in Figure 1 highlight the dependence of fibre orientation on the levels of stretch experienced by the artery wall. A clear realignment of collagen fibres in the direction of loading is visible from Figure 1a and 1b. Although these results are widely known and shown in literature, this is the first time they have been resolved through SALS.  
 
-text[[526, 487, 852, 578]]
-Results shown in Figure 1 highlight the dependence of fibre orientation on the levels of stretch experienced by the artery wall. A clear realignment of collagen fibres in the direction of loading is visible from Figure 1a and 1b. Although these results are widely known and shown in literature, this is the first time they have been resolved through SALS. 
+text[[527, 579, 853, 647]]
+Although SALS is limited to thin samples, time consuming staining protocols are not required for fibre characterisation. The speed, accuracy and ease of use of this system make it a powerful system for providing insights into the response of arterial tissue to load.  
 
-text[[526, 582, 852, 649]]
-Although SALS is limited to thin samples, time consuming staining protocols are not required for fibre characterisation. The speed, accuracy and ease of use of this system make it a powerful system for providing insights into the response of arterial tissue to load. 
+text[[526, 650, 853, 689]]
+Future work aims to fully identify load induced tissue changes in healthy and diseased arterial tissue using SALS.  
 
-text[[526, 652, 852, 692]]
-Future work aims to fully identify load induced tissue changes in healthy and diseased arterial tissue using SALS. 
+sub_title[[527, 705, 640, 718]]
+## REFERENCES  
 
-sub_title[[526, 706, 641, 721]]
-REFERENCES 
+text[[526, 726, 853, 780]]
+[1] Creanee et al., Biomech Model Mechanobil, 10: 831- 843, 2011 [2] Billiar, K., and Sacks, M., J. Biomech. 30: 753- 7 56, 1997  
 
-text[[526, 729, 852, 780]]
-[1] Creane et al., Biomech Model Mechanobiol., 10: 831-843, 2011
-[2] Billiar, K., and Sacks, M., J. Biomech. 30: 753-7 56, 1997 
+sub_title[[527, 792, 717, 806]]
+## ACKNOWLEDGEMENTS  
 
-sub_title[[526, 794, 717, 808]]
-ACKNOWLEDGEMENTS 
-
-text[[526, 816, 852, 856]]
+text[[526, 813, 853, 852]]
 This research was part funded by Science Foundation Ireland (SFI/13/ERC/B2775) and the Irish Research Council (GOIPG/2014/515).
\ No newline at end of file
diff --git a/stage1/sample_00004/document.md b/stage1/sample_00004/document.md
index ddd0d460d9b7b9aa8a255f37d821aeca83eec44d..b55fd358f754360295b9f2576020c6fd546e87fd 100644
--- a/stage1/sample_00004/document.md
+++ b/stage1/sample_00004/document.md
@@ -1,26 +1,26 @@
-text[[90, 80, 861, 107]]
+text[[89, 80, 862, 109]]
 The parametric equations for a projectile with constant gravity g: 
 
-equation[[153, 109, 425, 140]]
-\[ x = v_0 t \cos \theta + x_0 \]
+equation[[152, 108, 426, 140]]
+\[x = \nu_0 t \cos \Theta + x_0\]
 
-equation[[152, 155, 566, 225]]
-\[ y = -\frac{1}{2} gt^2 + v_0 t \sin \theta + y_0 \]
+equation[[152, 151, 565, 227]]
+\[y = -\frac{1}{2} gt^2 + \nu_0 t \sin \Theta + y_0\]
 
-text[[89, 255, 867, 307]]
+text[[89, 255, 869, 307]]
 ex. A shell is fired from ground level with an initial speed of 768 ft/sec. at an angle of 30°. Find: 
 
-text[[91, 310, 184, 352]]
+text[[92, 307, 182, 353]]
 1. \(\vec{r}(t)\) 
 
-text[[91, 359, 483, 382]]
+text[[91, 357, 484, 382]]
 2. the maximum altitude attained 
 
-text[[91, 385, 372, 408]]
+text[[91, 384, 372, 408]]
 3. the range of the shell 
 
 text[[91, 411, 360, 434]]
 4. the speed on impact 
 
-text[[91, 437, 607, 461]]
+text[[91, 438, 608, 462]]
 5. the horizontal distance when \(y = 2240\) ft.
\ No newline at end of file
diff --git a/stage1/sample_00004/raw_response.md b/stage1/sample_00004/raw_response.md
index ddd0d460d9b7b9aa8a255f37d821aeca83eec44d..b55fd358f754360295b9f2576020c6fd546e87fd 100644
--- a/stage1/sample_00004/raw_response.md
+++ b/stage1/sample_00004/raw_response.md
@@ -1,26 +1,26 @@
-text[[90, 80, 861, 107]]
+text[[89, 80, 862, 109]]
 The parametric equations for a projectile with constant gravity g: 
 
-equation[[153, 109, 425, 140]]
-\[ x = v_0 t \cos \theta + x_0 \]
+equation[[152, 108, 426, 140]]
+\[x = \nu_0 t \cos \Theta + x_0\]
 
-equation[[152, 155, 566, 225]]
-\[ y = -\frac{1}{2} gt^2 + v_0 t \sin \theta + y_0 \]
+equation[[152, 151, 565, 227]]
+\[y = -\frac{1}{2} gt^2 + \nu_0 t \sin \Theta + y_0\]
 
-text[[89, 255, 867, 307]]
+text[[89, 255, 869, 307]]
 ex. A shell is fired from ground level with an initial speed of 768 ft/sec. at an angle of 30°. Find: 
 
-text[[91, 310, 184, 352]]
+text[[92, 307, 182, 353]]
 1. \(\vec{r}(t)\) 
 
-text[[91, 359, 483, 382]]
+text[[91, 357, 484, 382]]
 2. the maximum altitude attained 
 
-text[[91, 385, 372, 408]]
+text[[91, 384, 372, 408]]
 3. the range of the shell 
 
 text[[91, 411, 360, 434]]
 4. the speed on impact 
 
-text[[91, 437, 607, 461]]
+text[[91, 438, 608, 462]]
 5. the horizontal distance when \(y = 2240\) ft.
\ No newline at end of file
diff --git a/stage1/sample_00005/document.md b/stage1/sample_00005/document.md
index 288d5a4b5b32eaf988382967d0f9d474704035d3..7cd5965c33b3c4ac96a5127c864c4d0a82569083 100644
--- a/stage1/sample_00005/document.md
+++ b/stage1/sample_00005/document.md
@@ -1,4 +1 @@
-An electron in a TV tube is beamed horizontally at a speed of 5 x 10<sup>6</sup> m/sec. toward the face of the tube 40 cm away. To determine how far the electron drops before it hits, which equation would be used?  
-
-text[[87, 212, 421, 355]]
-a. \(y = -4.9t^2\) b. \(y = -4.9t^2 - 5 \times 10^6 t\) c. \(5 \times 10^6 t = 4\) d. \(5 \times 10^6 t = 40\)
\ No newline at end of file
+1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 47. 48. 49. 50. 51. 52. 53. 54. 55. 56. 57. 58. 59. 60. 61. 62. 63. 64. 65. 66. 67. 68. 69. 70. 71. 72. 73. 74. 75. 76. 77. 78. 79. 80. 81. 82. 83. 84. 85. 86. 87. 88. 89. 90. 91. 92. 93. 94. 95. 96. 97. 98. 99. 100. 101. 102. 103. 104. 105. 106. 107. 108. 109. 110. 111. 112. 113. 114. 115. 116. 117. 118. 119. 120. 121. 122. 123. 124. 125. 126. 127. 128. 129. 130. 131. 132. 133. 134. 135. 136. 137. 138. 139. 140. 141. 142. 143. 144. 145. 146. 147. 148. 149. 150. 151. 152. 153. 154. 155. 156. 157. 158. 159. 160. 161. 162. 163. 164. 165. 166. 167. 168. 169. 170. 171. 172. 173. 174. 175. 176. 177. 178. 179. 180. 181. 182. 183. 184. 185. 186. 187. 188. 189. 190. 191. 192. 193. 194. 195. 196. 197. 198. 199. 200. 201. 202. 203. 204. 205. 206. 207. 208. 209. 210. 211. 212. 213. 214. 215. 216. 217. 218. 219. 220. 221. 222. 223. 224. 225. 226. 227. 228. 229. 230. 231. 232. 233. 234. 235. 236. 237. 238. 239. 240. 241. 242. 243. 244. 245. 246.
\ No newline at end of file
diff --git a/stage1/sample_00005/raw_response.md b/stage1/sample_00005/raw_response.md
index 288d5a4b5b32eaf988382967d0f9d474704035d3..7cd5965c33b3c4ac96a5127c864c4d0a82569083 100644
--- a/stage1/sample_00005/raw_response.md
+++ b/stage1/sample_00005/raw_response.md
@@ -1,4 +1 @@
-An electron in a TV tube is beamed horizontally at a speed of 5 x 10<sup>6</sup> m/sec. toward the face of the tube 40 cm away. To determine how far the electron drops before it hits, which equation would be used?  
-
-text[[87, 212, 421, 355]]
-a. \(y = -4.9t^2\) b. \(y = -4.9t^2 - 5 \times 10^6 t\) c. \(5 \times 10^6 t = 4\) d. \(5 \times 10^6 t = 40\)
\ No newline at end of file
+1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 47. 48. 49. 50. 51. 52. 53. 54. 55. 56. 57. 58. 59. 60. 61. 62. 63. 64. 65. 66. 67. 68. 69. 70. 71. 72. 73. 74. 75. 76. 77. 78. 79. 80. 81. 82. 83. 84. 85. 86. 87. 88. 89. 90. 91. 92. 93. 94. 95. 96. 97. 98. 99. 100. 101. 102. 103. 104. 105. 106. 107. 108. 109. 110. 111. 112. 113. 114. 115. 116. 117. 118. 119. 120. 121. 122. 123. 124. 125. 126. 127. 128. 129. 130. 131. 132. 133. 134. 135. 136. 137. 138. 139. 140. 141. 142. 143. 144. 145. 146. 147. 148. 149. 150. 151. 152. 153. 154. 155. 156. 157. 158. 159. 160. 161. 162. 163. 164. 165. 166. 167. 168. 169. 170. 171. 172. 173. 174. 175. 176. 177. 178. 179. 180. 181. 182. 183. 184. 185. 186. 187. 188. 189. 190. 191. 192. 193. 194. 195. 196. 197. 198. 199. 200. 201. 202. 203. 204. 205. 206. 207. 208. 209. 210. 211. 212. 213. 214. 215. 216. 217. 218. 219. 220. 221. 222. 223. 224. 225. 226. 227. 228. 229. 230. 231. 232. 233. 234. 235. 236. 237. 238. 239. 240. 241. 242. 243. 244. 245. 246.
\ No newline at end of file
diff --git a/stage1/sample_00006/document.md b/stage1/sample_00006/document.md
index 6a95245acd2bd88d001033911ac721cbf4e25dfc..b8982bcb447d1704b090c7bb34733e812030e5c1 100644
--- a/stage1/sample_00006/document.md
+++ b/stage1/sample_00006/document.md
@@ -1 +1 @@
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index 6a95245acd2bd88d001033911ac721cbf4e25dfc..b8982bcb447d1704b090c7bb34733e812030e5c1 100644
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diff --git a/stage1/sample_00007/document.md b/stage1/sample_00007/document.md
index 470e839cdf554aa81bd5f466ef36523ed12babd8..25133a2d55d11447db98799ed1d638f9a212b2d7 100644
--- a/stage1/sample_00007/document.md
+++ b/stage1/sample_00007/document.md
@@ -1 +1 @@
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diff --git a/stage1/sample_00007/raw_response.md b/stage1/sample_00007/raw_response.md
index 470e839cdf554aa81bd5f466ef36523ed12babd8..25133a2d55d11447db98799ed1d638f9a212b2d7 100644
--- a/stage1/sample_00007/raw_response.md
+++ b/stage1/sample_00007/raw_response.md
@@ -1 +1 @@
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diff --git a/stage1/sample_00008/document.md b/stage1/sample_00008/document.md
index 767ec452cfbce1c09b4438c8b0fbba3e0691890f..a94dfceb84691d2ce16f93704e03e6faf645a7e4 100644
--- a/stage1/sample_00008/document.md
+++ b/stage1/sample_00008/document.md
@@ -1,67 +1,67 @@
-The Arab Family in Kuwait: Size and Structure (1)
+75% of Iraqi families belong to the extended type grouping three generations living under one roof²) Dr. Sana Khawli's investigation, condensed in Al-Raida (no. 9, vol. 11, p. 15), leads her to conclude that the Arab family is evolving into a non-isolated nuclear family.  
 
-text[[21, 215, 470, 319]]
-Recent studies dealing with family status in the Arab world are few and sometimes contradictory. While some researchers, such as Dr. Madeeha Naser (1972), assume that 75% of Iraqi families belong to the extended type groupin three generations living under one roof(2), Dr. Sana Khawli's investigation, condensed in Al-Raida (no. 9, vol. II, p. 15), leads her to conclude that the Arab family is evolving into a non-isolated nuclear family.
+text[[20, 306, 466, 422]]
+Some researchers adopt a middle course by recognizing the existence of differences between country and town regarding family type and affirming that the extended family exists in a larger proportion in the country than in town and city. Good, another sociologist, asserts that for economic and other reasons, the extended family has not been the rule in Arab countries. Peterson says that demographic factors have prevented the extensive spread of the extended family in Egypt and that the large family of six members or more formed \(40\%\) of Egyptian families since the beginning of the twentieth century.  
 
-text[[21, 321, 470, 467]]
-Some researchers adopt a middle course by recognizing the existence of differences between country and town regarding family type and affirming that the extended family exists in a larger proportion in the country than in town and city. Good, another sociologist, asserts that for economic and other reasons, the extended family has not been the rule in Arab countries. Peterson says that demographic factors have prevented the extensive spread of the extended family in Egypt and that the large family of six members or more formed 40% of Egyptian families since the beginning of the twentieth century.
+text[[20, 421, 466, 473]]
+A study prepared by Dr. Fahd al- Thaqeb aims to show that even if economic and demographic conditions should favor the spread of the extended family, as is the case in Kuwait, this family type is bound to remain a minority.  
 
-text[[21, 469, 470, 522]]
-A study prepared by Dr. Fahd al-Thaqeb aims to show that even if economic and demographic conditions should favor the spread of the extended family, as is the case in Kuwait, this family type is bound to remain a minority.
+text[[20, 471, 466, 524]]
+A study prepared by Dr. Fahd al- Thaqeb aims to show that even if economic and demographic conditions should favor the spread of the extended family, as is the case in Kuwait, this family type is bound to remain a minority.  
 
-text[[21, 523, 470, 564]]
-This study is based on statistics derived from interviews between 1965 and 1970 with a random sample of Kuwaiti families representing various social levels.
+text[[20, 523, 466, 564]]
+This study is based on statistics derived from interviews between 1965 and 1970 with a random sample of Kuwaiti families representing various social levels.  
 
-title[[23, 580, 113, 591]]
-# Family Size
+sub_title[[22, 578, 110, 592]]
+## Family Size  
 
-text[[21, 602, 470, 738]]
-Between 1965 and 1970, the majority of families in Kuwait were made up of six or more members per family. This proportion decreased among university graduates from 67.4% in 1965 to 56.9% in 1970. The data reveal that the number of family members tends to decrease in proportion with the cultural, economic and social status of the family.For example, while 33% of family heads with secondary education have limited the number of their families to five or less, only 12% of illiterate family heads have adhered to this number.
+text[[22, 600, 468, 740]]
+Between 1965 and 1970, the majority of families in Kuwait were made up of six or more members per family. This proportion decreased among university graduates from \(67.4\%\) in 1965 to \(56.9\%\) in 1970. The data reveal that the number of family members tends to decrease in proportion with the cultural, economic and social status of the family. For example, while \(33\%\) of family heads with secondary education have limited the number of their families to five or less, only \(12\%\) of illiterate family heads have adhered to this number.  
 
-text[[21, 741, 470, 806]]
-Large-sized families are characteristic of higher middle and lower middle classes. Small-sized families of 1-5 members exist at the rate of 38% in **less privileged** classes,while 72% of the **lower** **middle** class are made up of eight ore more each.
+text[[22, 739, 468, 806]]
+Large- sized families are characteristic of higher middle and lower middle classes. Small- sized families of 1- 5 members exist at the rate of \(38\%\) in less privileged classes, while \(72\%\) of the lower middle class are made up of eight or more each.  
 
-title[[23, 821, 156, 833]]
-# Family Structure
+sub_title[[23, 818, 153, 833]]
+## Family Structure  
 
-text[[23, 848, 470, 875]]
-Three family types have been singled out: the nuclear,the quasi-extended and the extended family. The first
+text[[22, 847, 468, 875]]
+Three family types have been singled out: the nuclear, the quasi- extended and the extended family. The first  
 
-text[[23, 897, 472, 931]]
-(1)Condensed from Dr. Fahd Al-Thaqeb, "Size and Structure of the Arab and Kuwaiti Family," **Journal of Social Sciences,** No 12,Year IV, July 1976 (Arabic), pp. 81-91.
+text[[23, 897, 469, 935]]
+(1) Condensed from Dr. Fahd Al-Thaqeb, "Size and Structure of the Arab and Kuwaiti Family," Journal of Social Sciences, No 12, Year IV, July 1976 (Arabic), pp. 81-91.  
 
-text[[23, 938, 123, 948]]
-(2) Ibid. p. 81.
+text[[24, 938, 120, 951]]
+(2) Ibid. p. 81.  
 
-text[[524, 213, 972, 267]]
-comprises the parents and children; the third includes two or more families living in the same house, joined by blood ties. The quasi-extended family is a small sized extended family.
+text[[522, 209, 970, 269]]
+comprises the parents and children; the third includes two or more families living in the same house, joined by blood ties. The quasi- extended family is a small sized extended family.  
 
-text[[524, 268, 970, 295]]
-In Kuwait, the nuclear family forms 59.2%, the quasi-extended 18.4%, and the extended family 22.4%.
+text[[525, 266, 968, 295]]
+In Kuwait, the nuclear family forms \(59.2\%\) , the quasi- extended \(18.4\%\) , and the extended family \(22.4\%\) .  
 
-text[[524, 299, 972, 366]]
-The size of the family is not a sound indicator of its type, though it may have some connection with it. It was found that only 26% of the nuclear families interviewed were made up of six members each, while 70% of them had 6-12 members per unit.
+text[[525, 296, 970, 363]]
+The size of the family is not a sound indicator of its type, though it may have some connection with it. It was found that only \(26\%\) of the nuclear families interviewed were made up of six members each, while \(70\%\) of them had 6- 12 members per unit.  
 
-text[[524, 368, 972, 460]]
-The study has shown that the nuclear family, while it is not the ideal type, is most common among urban,educated, young people and among the middle class. This type is less common in lower and lower middle class. About 31% of families of the lower class are quasi-extended while in the upper socio-economic group, the quasi-extended type reaches only 15%.
+text[[526, 363, 970, 457]]
+The study has shown that the nuclear family, while it is not the ideal type, is most common among urban, educated, young people and among the middle class. This type is less common in lower and lower middle class. About \(31\%\) of families of the lower class are quasi- extended while in the upper socio- economic group, the quasi- extended type reaches only \(15\%\) .  
 
-text[[524, 459, 972, 499]]
-The proportion of the extended family type is higher among illiterate groups: 30% for illiterate against 17% for university people.
+text[[526, 457, 970, 498]]
+The proportion of the extended family type is higher among illiterate groups: \(30\%\) for illiterate against \(17\%\) for university people.  
 
-title[[524, 515, 676, 527]]
-# Age of Respondents
+sub_title[[528, 513, 678, 526]]
+## Age of Respondents  
 
-text[[524, 542, 972, 650]]
-The family type differed according to the age of people interviewed. Around 50% of the young lived in nuclear families. Many of them lived in quasi-nuclear ones and did not break communication with their relatives. The ages of 65% of nuclear family people ranged between 30 and 39 years, while the highest proportion of the extended family type existed among those who were 50 years of age or above.
+text[[527, 540, 972, 649]]
+The family type differed according to the age of people interviewed. Around \(50\%\) of the young lived in nuclear families. Many of them lived in quasi- nuclear ones and did not break communication with their relatives. The ages of \(65\%\) of nuclear family people ranged between 30 and 39 years, while the highest proportion of the extended family type existed among those who were 50 years of age or above.  
 
-title[[525, 666, 612, 677]]
-# Conclusion
+sub_title[[528, 663, 612, 678]]
+## Conclusion  
 
-text[[524, 693, 972, 760]]
-The majority of families forming the random sample of this survey belonged to the nuclear family type. The extended family, though it should be favored by social and demographic conditions in a country like Kuwait, is likely to form a minority.
+text[[528, 693, 972, 760]]
+The majority of families forming the random sample of this survey belonged to the nuclear family type. The extended family, though it should be favored by social and demographic conditions in a country like Kuwait, is likely to form a minority.  
 
-text[[524, 761, 972, 854]]
-The data show a steady increase in the average number of family members during the last few years. In 1957 the average was 6.8 per family; in 1965 it rose to 7.3;and in 1970, to 7.6. The rise is due to improved economic and demographic conditions in Kuwait. Also, the proportion of families numbering 6 or more each, rose from 66.4% in 1965 to 70.2% in 1970.
+text[[528, 760, 972, 853]]
+The data show a steady increase in the average number of family members during the last few years. In 1957 the average was 6.8 per family; in 1965 it rose to 7.3 ; and in 1970, to 7.6. The rise is due to improved economic and demographic conditions in Kuwait. Also, the proportion of families numbering 6 or more each, rose from \(66.4\%\) in 1965 to \(70.2\%\) in 1970.  
 
-text[[524, 856, 972, 948]]
-The family size is also an indicator of the fertility rate and bears no relation to family structure. It is noteworthy that extended families joining together three generations formed only 17% of the bulk of extended families. This result coincides with Good's theory that traditional, extended families have been and remain a minority in the Arab world.
\ No newline at end of file
+text[[528, 853, 972, 947]]
+The family size is also an indicator of the fertility rate and bears no relation to family structure. It is noteworthy that extended families joining together three generations formed only \(17\%\) of the bulk of extended families. This result coincides with Good's theory that traditional, extended families have been and remain a minority in the Arab world.
\ No newline at end of file
diff --git a/stage1/sample_00008/raw_response.md b/stage1/sample_00008/raw_response.md
index 767ec452cfbce1c09b4438c8b0fbba3e0691890f..a94dfceb84691d2ce16f93704e03e6faf645a7e4 100644
--- a/stage1/sample_00008/raw_response.md
+++ b/stage1/sample_00008/raw_response.md
@@ -1,67 +1,67 @@
-The Arab Family in Kuwait: Size and Structure (1)
+75% of Iraqi families belong to the extended type grouping three generations living under one roof²) Dr. Sana Khawli's investigation, condensed in Al-Raida (no. 9, vol. 11, p. 15), leads her to conclude that the Arab family is evolving into a non-isolated nuclear family.  
 
-text[[21, 215, 470, 319]]
-Recent studies dealing with family status in the Arab world are few and sometimes contradictory. While some researchers, such as Dr. Madeeha Naser (1972), assume that 75% of Iraqi families belong to the extended type groupin three generations living under one roof(2), Dr. Sana Khawli's investigation, condensed in Al-Raida (no. 9, vol. II, p. 15), leads her to conclude that the Arab family is evolving into a non-isolated nuclear family.
+text[[20, 306, 466, 422]]
+Some researchers adopt a middle course by recognizing the existence of differences between country and town regarding family type and affirming that the extended family exists in a larger proportion in the country than in town and city. Good, another sociologist, asserts that for economic and other reasons, the extended family has not been the rule in Arab countries. Peterson says that demographic factors have prevented the extensive spread of the extended family in Egypt and that the large family of six members or more formed \(40\%\) of Egyptian families since the beginning of the twentieth century.  
 
-text[[21, 321, 470, 467]]
-Some researchers adopt a middle course by recognizing the existence of differences between country and town regarding family type and affirming that the extended family exists in a larger proportion in the country than in town and city. Good, another sociologist, asserts that for economic and other reasons, the extended family has not been the rule in Arab countries. Peterson says that demographic factors have prevented the extensive spread of the extended family in Egypt and that the large family of six members or more formed 40% of Egyptian families since the beginning of the twentieth century.
+text[[20, 421, 466, 473]]
+A study prepared by Dr. Fahd al- Thaqeb aims to show that even if economic and demographic conditions should favor the spread of the extended family, as is the case in Kuwait, this family type is bound to remain a minority.  
 
-text[[21, 469, 470, 522]]
-A study prepared by Dr. Fahd al-Thaqeb aims to show that even if economic and demographic conditions should favor the spread of the extended family, as is the case in Kuwait, this family type is bound to remain a minority.
+text[[20, 471, 466, 524]]
+A study prepared by Dr. Fahd al- Thaqeb aims to show that even if economic and demographic conditions should favor the spread of the extended family, as is the case in Kuwait, this family type is bound to remain a minority.  
 
-text[[21, 523, 470, 564]]
-This study is based on statistics derived from interviews between 1965 and 1970 with a random sample of Kuwaiti families representing various social levels.
+text[[20, 523, 466, 564]]
+This study is based on statistics derived from interviews between 1965 and 1970 with a random sample of Kuwaiti families representing various social levels.  
 
-title[[23, 580, 113, 591]]
-# Family Size
+sub_title[[22, 578, 110, 592]]
+## Family Size  
 
-text[[21, 602, 470, 738]]
-Between 1965 and 1970, the majority of families in Kuwait were made up of six or more members per family. This proportion decreased among university graduates from 67.4% in 1965 to 56.9% in 1970. The data reveal that the number of family members tends to decrease in proportion with the cultural, economic and social status of the family.For example, while 33% of family heads with secondary education have limited the number of their families to five or less, only 12% of illiterate family heads have adhered to this number.
+text[[22, 600, 468, 740]]
+Between 1965 and 1970, the majority of families in Kuwait were made up of six or more members per family. This proportion decreased among university graduates from \(67.4\%\) in 1965 to \(56.9\%\) in 1970. The data reveal that the number of family members tends to decrease in proportion with the cultural, economic and social status of the family. For example, while \(33\%\) of family heads with secondary education have limited the number of their families to five or less, only \(12\%\) of illiterate family heads have adhered to this number.  
 
-text[[21, 741, 470, 806]]
-Large-sized families are characteristic of higher middle and lower middle classes. Small-sized families of 1-5 members exist at the rate of 38% in **less privileged** classes,while 72% of the **lower** **middle** class are made up of eight ore more each.
+text[[22, 739, 468, 806]]
+Large- sized families are characteristic of higher middle and lower middle classes. Small- sized families of 1- 5 members exist at the rate of \(38\%\) in less privileged classes, while \(72\%\) of the lower middle class are made up of eight or more each.  
 
-title[[23, 821, 156, 833]]
-# Family Structure
+sub_title[[23, 818, 153, 833]]
+## Family Structure  
 
-text[[23, 848, 470, 875]]
-Three family types have been singled out: the nuclear,the quasi-extended and the extended family. The first
+text[[22, 847, 468, 875]]
+Three family types have been singled out: the nuclear, the quasi- extended and the extended family. The first  
 
-text[[23, 897, 472, 931]]
-(1)Condensed from Dr. Fahd Al-Thaqeb, "Size and Structure of the Arab and Kuwaiti Family," **Journal of Social Sciences,** No 12,Year IV, July 1976 (Arabic), pp. 81-91.
+text[[23, 897, 469, 935]]
+(1) Condensed from Dr. Fahd Al-Thaqeb, "Size and Structure of the Arab and Kuwaiti Family," Journal of Social Sciences, No 12, Year IV, July 1976 (Arabic), pp. 81-91.  
 
-text[[23, 938, 123, 948]]
-(2) Ibid. p. 81.
+text[[24, 938, 120, 951]]
+(2) Ibid. p. 81.  
 
-text[[524, 213, 972, 267]]
-comprises the parents and children; the third includes two or more families living in the same house, joined by blood ties. The quasi-extended family is a small sized extended family.
+text[[522, 209, 970, 269]]
+comprises the parents and children; the third includes two or more families living in the same house, joined by blood ties. The quasi- extended family is a small sized extended family.  
 
-text[[524, 268, 970, 295]]
-In Kuwait, the nuclear family forms 59.2%, the quasi-extended 18.4%, and the extended family 22.4%.
+text[[525, 266, 968, 295]]
+In Kuwait, the nuclear family forms \(59.2\%\) , the quasi- extended \(18.4\%\) , and the extended family \(22.4\%\) .  
 
-text[[524, 299, 972, 366]]
-The size of the family is not a sound indicator of its type, though it may have some connection with it. It was found that only 26% of the nuclear families interviewed were made up of six members each, while 70% of them had 6-12 members per unit.
+text[[525, 296, 970, 363]]
+The size of the family is not a sound indicator of its type, though it may have some connection with it. It was found that only \(26\%\) of the nuclear families interviewed were made up of six members each, while \(70\%\) of them had 6- 12 members per unit.  
 
-text[[524, 368, 972, 460]]
-The study has shown that the nuclear family, while it is not the ideal type, is most common among urban,educated, young people and among the middle class. This type is less common in lower and lower middle class. About 31% of families of the lower class are quasi-extended while in the upper socio-economic group, the quasi-extended type reaches only 15%.
+text[[526, 363, 970, 457]]
+The study has shown that the nuclear family, while it is not the ideal type, is most common among urban, educated, young people and among the middle class. This type is less common in lower and lower middle class. About \(31\%\) of families of the lower class are quasi- extended while in the upper socio- economic group, the quasi- extended type reaches only \(15\%\) .  
 
-text[[524, 459, 972, 499]]
-The proportion of the extended family type is higher among illiterate groups: 30% for illiterate against 17% for university people.
+text[[526, 457, 970, 498]]
+The proportion of the extended family type is higher among illiterate groups: \(30\%\) for illiterate against \(17\%\) for university people.  
 
-title[[524, 515, 676, 527]]
-# Age of Respondents
+sub_title[[528, 513, 678, 526]]
+## Age of Respondents  
 
-text[[524, 542, 972, 650]]
-The family type differed according to the age of people interviewed. Around 50% of the young lived in nuclear families. Many of them lived in quasi-nuclear ones and did not break communication with their relatives. The ages of 65% of nuclear family people ranged between 30 and 39 years, while the highest proportion of the extended family type existed among those who were 50 years of age or above.
+text[[527, 540, 972, 649]]
+The family type differed according to the age of people interviewed. Around \(50\%\) of the young lived in nuclear families. Many of them lived in quasi- nuclear ones and did not break communication with their relatives. The ages of \(65\%\) of nuclear family people ranged between 30 and 39 years, while the highest proportion of the extended family type existed among those who were 50 years of age or above.  
 
-title[[525, 666, 612, 677]]
-# Conclusion
+sub_title[[528, 663, 612, 678]]
+## Conclusion  
 
-text[[524, 693, 972, 760]]
-The majority of families forming the random sample of this survey belonged to the nuclear family type. The extended family, though it should be favored by social and demographic conditions in a country like Kuwait, is likely to form a minority.
+text[[528, 693, 972, 760]]
+The majority of families forming the random sample of this survey belonged to the nuclear family type. The extended family, though it should be favored by social and demographic conditions in a country like Kuwait, is likely to form a minority.  
 
-text[[524, 761, 972, 854]]
-The data show a steady increase in the average number of family members during the last few years. In 1957 the average was 6.8 per family; in 1965 it rose to 7.3;and in 1970, to 7.6. The rise is due to improved economic and demographic conditions in Kuwait. Also, the proportion of families numbering 6 or more each, rose from 66.4% in 1965 to 70.2% in 1970.
+text[[528, 760, 972, 853]]
+The data show a steady increase in the average number of family members during the last few years. In 1957 the average was 6.8 per family; in 1965 it rose to 7.3 ; and in 1970, to 7.6. The rise is due to improved economic and demographic conditions in Kuwait. Also, the proportion of families numbering 6 or more each, rose from \(66.4\%\) in 1965 to \(70.2\%\) in 1970.  
 
-text[[524, 856, 972, 948]]
-The family size is also an indicator of the fertility rate and bears no relation to family structure. It is noteworthy that extended families joining together three generations formed only 17% of the bulk of extended families. This result coincides with Good's theory that traditional, extended families have been and remain a minority in the Arab world.
\ No newline at end of file
+text[[528, 853, 972, 947]]
+The family size is also an indicator of the fertility rate and bears no relation to family structure. It is noteworthy that extended families joining together three generations formed only \(17\%\) of the bulk of extended families. This result coincides with Good's theory that traditional, extended families have been and remain a minority in the Arab world.
\ No newline at end of file
diff --git a/stage1/sample_00009/document.md b/stage1/sample_00009/document.md
index 6590b97ba0632f9bf338fb2ef5fc58eef5e90905..81f8618adfcfdb16dad78425ce67cdba6aa10ecc 100644
--- a/stage1/sample_00009/document.md
+++ b/stage1/sample_00009/document.md
@@ -1,41 +1,40 @@
-24 baseline demographics and disease characteristics. Significant (p<0.1) variables in univariate were included in multivariate models. Last, multivariate models were selected based on model fit statistics (Akaike information criterion and \(\mathrm {R}^{2}\)) and clinical significance. Adjusted OR and 95% CIs for selected baseline variables were calculated.
+24 baseline demographics and disease characteristics. Significant (p<0.1) variables in univariate were included in multivariate models. Last, multivariate models were selected based on model fit statistics (Akaike information criterion and \(\mathrm {r}^{2}\)) and clinical significance. Adjusted OR and 95% CIs for selected baseline variables were calculated.  
 
-title[[67, 180, 130, 191]]
-# RESULTS
+sub_title[[68, 178, 127, 191]]
+## RESULTS  
 
-text[[67, 194, 485, 368]]
-Overall, 334 patients were randomised to treatment and received adalimumab+MTX ( \(\mathrm {n}=171\) ) or MTX alone \(\mathrm {n}=163\) ), and 148 (86.5%) and 128 (78.5%) patients completed the double-blind portion of the study, respectively (figure 1). Demographics and baseline characteristics were well matched between treatment groups (table 1). The mean RA disease duration was 0.3 years, and the majority of patients had ≥1 erosion at baseline and high disease activity. The mean MTX dose during the 26-week study was \(6.2\pm 0.8\mathrm {mg}/\mathrm {week}\) in the adalimumab+MTX group and \(6.6\pm 0.6\mathrm {mg}/\mathrm {week}\) in the MTX alone group ( \(\mathrm {p}<0.001\) ). After 26 weeks of treatment, 34.5% (59/171) of adalimumab+MTX patients were receiving MTX 8 mg/week versus 65.0% (106/163) of MTX alone patients ( \(\mathrm {p}<0.001\) ).
+text[[68, 193, 486, 368]]
+Overall, 334 patients were randomised to treatment and received adalimumab+MTX \((\mathrm {n}=171)\) or MTX alone \((\mathrm {n}=163)\) 1 and 148 \((86.5\%)\) and 128 \((78.5\%)\) patients completed the double- blind portion of the study, respectively (figure 1). Demographics and baseline characteristics were well matched between treatment groups (table 1). The mean RA disease duration was 0.3 years, and the majority of patients had \(\ge 1\) erosion at baseline and high disease activity. The mean MTX dose during the 26- week study was \(6.2\pm 0.8\mathrm {mg}/\mathrm {week}\) in the adalimumab+MTX group and \(6.6\pm 0.6\mathrm {mg}/\mathrm {week}\) in the MTX alone group \((\mathrm {p}< 0.001)\) . After 26 weeks of treatment, \(34.5\%\) \((59/171)\) of adalimumab+MTX patients were receiving MTX 8 mg/week versus \(65.0\%\) (106/163) of MTX alone patients \((\mathrm {p}< 0.001)\)  
 
-table_caption[[67, 387, 485, 405]]
-Radiographic progression
+sub_title[[68, 382, 240, 398]]
+## Radiographic progression  
 
-text[[67, 400, 485, 677]]
-Treatment with adalimumab+MTX significantly inhibited radiographic progression (figure 2A) at week 26 versus MTX alone (mean change±SD, \(1.5\pm 6.1\mathrm {vs}2.4\pm 3.2\) , respectively; \(\mathrm {p}{<}0.001\) ). Results were confirmed by an LE analysis (figure 2A). Changes in radiographic progression during 26 weeks of treatment were also assessed by a cumulative probability plot of \(\Delta \mathrm {mTSS}\)  (figure 2B). Fewer adalimumab+MTX patients exhibited radiographic progression \((\Delta \mathrm {mTSS}>0.5)\) , with 62.0% (106/171) of patients showing no radiographic progression versus 35.4% (57/161) of MTX alone patients ( \(\mathrm {p}<0.001\) ). Furthermore, only 14.0% (24/171) of adalimumab+MTX patients exhibited clinically relevant radiographic progression \((\Delta \mathrm {mTSS}>3)\)  versus 37.3% (60/161) of MTX alone patients ( \(\mathrm {p}<0.001\) ). In addition, a significantly higher percentage of adalimumab+MTX patients did not experience worsening (≤0.5) in erosion score (73.7% (126/171)) versus MTX alone patients (42.2% (68/161); \(\mathrm {p}<0.001\) ). In patients who lacked baseline erosive damage, the continued absence of erosions was reported in more adalimumab+MTX patients versus MTX alone patients (9/9 vs 2/6 patients, respectively; \(\mathrm {p}=0.01\) ).
+text[[68, 396, 486, 677]]
+Treatment with adalimumab+MTX significantly inhibited radiographic progression (figure 2A) at week 26 versus MTX alone (mean change \(\pm \mathrm {SD}\) \(1.5\pm 6.1\) vs \(2.4\pm 3.2\) , respectively; \(\mathrm {p}< 0.001\) ). Results were confirmed by an LE analysis (figure 2A). Changes in radiographic progression during 26 weeks of treatment were also assessed by a cumulative probability plot of \(\Delta \mathrm {mTSS}\) (figure 2B). Fewer adalimumab+MTX patients exhibited radiographic progression \((\Delta \mathrm {mTS}5>0.5)\) with \(62.0\%\) (106/171) of patients showing no radiographic progression versus \(35.4\%\) \((57/161)\) of MTX alone patients \((\mathrm {p}< 0.001)\) . Furthermore, only \(14.0\%\) \((24/171)\) of adalimumab+MTX patients exhibited clinically relevant radiographic progression \((\Delta \mathrm {mTSS}>3)\) versus \(37.3\%\) (60/161) of MTX alone patients \((\mathrm {p}< 0.001)\) . In addition, a significantly higher percentage of adalimumab+MTX patients did not experience worsening \((\leq 0.5)\) in erosion score \((73.7\%)\) (126/171)) versus MTX alone patients \((42.2\% (68/161)\) \(\mathrm {p}< 0.001\) ). In patients who lacked baseline erosive damage, the continued absence of erosions was reported in more adalimumab+MTX patients versus MTX alone patients \((9/9\) vs \(2/6\) patients, respectively; \(\mathrm {p}=0.01)\)  
 
-title[[67, 694, 188, 707]]
-# Clinical response
+sub_title[[68, 692, 182, 706]]
+## Clinical response  
 
-text[[67, 708, 485, 950]]
-A significantly higher percentage of adalimumab+MTX patients achieved ACR responses versus MTX alone patients at each assessment (figure 3A-C). Significant differences between treatment groups, observed as early as week 2, were maintained through week 26. At week 26, a significantly larger percentage of adalimumab+MTX patients versus MTX alone patients achieved ACR20, ACR50 and ACR70 (figure 3A-C) and ACR90 (12.9% vs 5.5%; \(\mathrm {p}=0.02\) ) responses. Significant differences in favour of adalimumab+MTX were also observed from week 2 to 26 for DAS28-ESR, DAS28-CRP, SDAI and CDAI (see online supplementary figure 1A-D). A larger percentage of adalimumab+MTX patients than MTX alone patients demonstrated good or moderate European League Against Rheumatism responses (figure 3D) and were in states of low disease activity or remission after 26 weeks of treatment (figure 3E). Furthermore, a significantly larger percentage of adalimumab+MTX patients versus MTX alone patients satisfied Boolean remission criteria (19.3% vs 8.6%, \(\mathrm {p}=0.007\) ). Adalimumab+MTX achieved a 1.8-
+text[[68, 706, 486, 950]]
+A significantly higher percentage of adalimumab+MTX patients achieved ACR responses versus MTX alone patients at each assessment (figure 3A- C). Significant differences between treatment groups, observed as early as week 2, were maintained through week 26. At week 26, a significantly larger percentage of adalimumab+MTX patients versus MTX alone patients achieved ACR20, ACR50 and ACR70 (figure 3A- C) and ACR90 \((12.9\%\) \(\mathrm {vs}5.5\%\) \(\mathrm {p}=0.02)\) responses. Significant differences in favour of adalimumab+MTX were also observed from week 2 to 26 for DAS28- ESR, DAS28- CRP, SDAI and CDAI (see online supplementary figure 1A- D). A larger percentage of adalimumab+MTX patients than MTX alone patients demonstrated good or moderate European League Against Rheumatism responses (figure 3D) and were in states of low disease activity or remission after 26 weeks of treatment (figure 3E). Furthermore, a significantly larger percentage of adalimumab+MTX patients versus MTX alone patients satisfied Boolean remission criteria \((19.3\%\) \(\mathrm {vs}8.6\% ,\mathrm {p}=0.007)\) . Adalimumab+MTX achieved a 1.8-  
 
-table[[520, 92, 918, 562]]
+table[[520, 89, 921, 566]]
+table_caption[[523, 74, 829, 89]]
+Table 1 Demographics and baseline characteristics   
 
-<table><td colspan="3">Table 1 Demographics and baseline characteristicsParameter*Adalimumab+MTX<br>(n=171)MTX(n=163)Age±SD (year)54.0±13.154.0±13.2Females (n %)144 (84.2)128 (78.5)RA duration±SD (year)0.3±0.40.3±0.4Weight±SD (kg)54.4±9.756.1±12.3Previous DMARD use (n %)74 (43.3)87 (53.4)1 DMARD57 (33.3)69 (42.3)2 DMARDs17 (9.9)18 (11.0)Corticosteroid use at baseline (n %)58 (33.9)49 (30.1)RF positive (n %)146 (85.4)136 (83.4)Mean titre±SD (IU/ml)154.5±202.3163.7±362.8Anti-CCP positive (n %)145 (84.8)136 (83.4)Mean titre±SD (IU/ml)386.2±694.2241.3±367.2ESR (mm/h)59.9±30.161.8±29.0CRP (mg/dl)2.9±3.03.1±3.3Swollen joint count (n±SD)0-2811.5±4.711.8±5.30-6616.5±6.217.3±7.7Tender joint count (n±SD)0-2813.2±5.813.2±6.10-6820.7±9.421.1±10.2mTSS13.6±22.313.6±17.4Erosion score7.5±11.67.3±9.2Joint space narrowing score6.2±11.46.2±9.4DAS28-ESR6.6±0.96.6±1.0DAS28-CRP5.8±1.05.9±1.0HAQ-DI score1.1±0.71.3±0.8SDAI score40.7±12.041.4±13.8CDAI score37.8±10.938.3±12.4Physician's global assessment of disease activity±SD (mm)65.8±18.466.2±18.8Patient's global assessment of disease activity±SD (mm)64.1±24.866.4±23.7</table>
+<table>Parameter*Adalimumab+MTX (n=171)MTX (n=163)Age±SD (year)54.0±13.154.0±13.2Females (n (%))144 (84.2)128 (78.5)RA duration±SD (year)0.3±0.40.3±0.4Weight±SD (kg)54.4±9.756.1±12.3Previous DMARD use (n (%))74 (43.3)87 (53.4)1 DMARD57 (33.3)69 (42.3)2 DMARDs17 (9.9)18 (11.0)Corticosteroid use at baseline (n (%))58 (33.9)49 (30.1)RF positive (n (%))146 (85.4)136 (83.4)Mean titre±SD (IU/ml)154.5±202.3163.7±362.8Anti-CCP positive (n (%))145 (84.8)136 (83.4)Mean titre±SD (IU/ml)386.2±694.2241.3±367.2ESR (mm/h)59.9±30.161.8±29.0CRP (mg/dl)2.9±3.03.1±3.3Swollen joint count (n±SD)0-2811.5±4.711.8±5.30-6616.5±6.217.3±7.7Tender joint count (n±SD)0-2813.2±5.813.2±6.10-6820.7±9.421.1±10.2mTSS13.6±22.313.6±17.4Erosion score7.5±11.67.3±9.2Joint space narrowing score6.2±11.46.2±9.4DAS28-ESR6.6±0.96.6±1.0DAS28-CRP5.8±1.05.9±1.0HAQ-DI score1.1±0.71.3±0.8SDAI score40.7±12.041.4±13.8CDAI score37.8±10.938.3±12.4Physician&#x27;s global assessment of disease activity±SD (mm)65.8±18.466.2±18.8Patient&#x27;s global assessment of disease activity±SD (mm)64.1±24.866.4±23.7</table>
 
-text[[521, 573, 741, 583]]
-*Data are mean±SD unless otherwise indicated.
+table_footnote[[526, 569, 918, 653]]
+Data are mean±SD unless otherwise indicated. CCP, cyclic citrullinated peptide; DDAI, clinical disease activity index; CRP, C reactive protein; DAS28-CRP, disease activity score using a 28-joint count and CRP level; DAS28-ESR, disease activity score using a 28-joint count and ESR; DMARD, disease-modifying antirheumatic drug; ESR, erythrocyte sedimentation rate; HAQ-DI, Health Assessment Questionnaire disability index; mTSS, modified total Sharp score; MTX, methotrexate; RA, rheumatoid arthritis; RF, rheumatoid factor; SDAI, simplified disease activity index.  
 
-text[[520, 584, 929, 649]]
-CCP, cyclic citrullinated peptide; CDAI, clinical disease activity index; CRP, C reactive protein; DAS28-CRP, disease activity score using a 28-joint count and CRP level; DAS28-ESR, disease activity score using a 28-joint count and ESR; DMARD, disease-modifying antirheumatic drug; ESR, erythrocyte sedimentation rate; HAQ-DI, Health Assessment Questionnaire disability index; mTSS, modified total Sharp score; MTX, methotrexate; RA, rheumatoid arthritis; RF, rheumatoid factor; SDAI, simplified disease activity index.
+text[[519, 679, 927, 720]]
+to 2.2- fold increase in the percentage of patients achieving clinical remission, across all definitions of clinical remission evaluated, versus MTX alone.  
 
-text[[512, 680, 927, 719]]
-to 2.2-fold increase in the percentage of patients achieving clin-ical remission, across all definitions of clinical remission evalu-ated, versus MTX alone.
+text[[519, 721, 927, 827]]
+A significantly larger decrease from baseline in mean HAQ- DI score, indicative of an improvement in physical function, was observed for adalimumab+MTX patients versus MTX alone patients at week 26 \((- 0.6\pm 0.6\) vs \(- 0.4\pm 0.6\) \(\mathrm {p}< 0.001\) ). Although the significant difference between the two groups was small (0.2 units), the percentage of patients achieving normal functionality (HAQ- DI score \(< 0.5\) ) after 26 weeks of treatment was also significantly higher with adalimumab+MTX (figure 3F).  
 
-text[[512, 723, 928, 827]]
-A significantly larger decrease from baseline in mean HAQ-DI score, indicative of an improvement in physical function, was observed for adalimumab+MTX patients versus MTX alone patients at week 26 \((-0.6\pm 0.6\mathrm {vs}-0.4\pm 0.6\) ; \(\mathrm {p}<0.001\) ). Although the significant difference between the two groups was small (0.2 units), the percentage of patients achieving normal functional-ity (HAQ-DI score\(<0.5\) ) after 26 weeks of treatment was also sig-nificantly higher with adalimumab+MTX (figure 3F).
+sub_title[[519, 857, 862, 887]]
+## Factors associated with the absence of radiographic progression or with clinical remission  
 
-title[[512, 859, 861, 884]]
-# Factors associated with the absence of radiographic progression or with clinical remission
-
-text[[512, 886, 928, 950]]
-Disease activity or function baseline variables generally were associated with the absence of radiographic progression \((\mathrm {AmTSS}\le 0.5)\)  and with clinical remission (DAS28-ESR&lt;2.6) in both treatment groups (see online supplementary text and online supplementary table 1).
\ No newline at end of file
+text[[519, 887, 927, 951]]
+Disease activity or function baseline variables generally were associated with the absence of radiographic progression \((\Delta \mathrm {mTSS}\leq 0.5)\) and with clinical remission (DAS28- ESR \(< 2.6)\) in both treatment groups (see online supplementary text and online supplementary table 1).
\ No newline at end of file
diff --git a/stage1/sample_00009/raw_response.md b/stage1/sample_00009/raw_response.md
index 6590b97ba0632f9bf338fb2ef5fc58eef5e90905..81f8618adfcfdb16dad78425ce67cdba6aa10ecc 100644
--- a/stage1/sample_00009/raw_response.md
+++ b/stage1/sample_00009/raw_response.md
@@ -1,41 +1,40 @@
-24 baseline demographics and disease characteristics. Significant (p<0.1) variables in univariate were included in multivariate models. Last, multivariate models were selected based on model fit statistics (Akaike information criterion and \(\mathrm {R}^{2}\)) and clinical significance. Adjusted OR and 95% CIs for selected baseline variables were calculated.
+24 baseline demographics and disease characteristics. Significant (p<0.1) variables in univariate were included in multivariate models. Last, multivariate models were selected based on model fit statistics (Akaike information criterion and \(\mathrm {r}^{2}\)) and clinical significance. Adjusted OR and 95% CIs for selected baseline variables were calculated.  
 
-title[[67, 180, 130, 191]]
-# RESULTS
+sub_title[[68, 178, 127, 191]]
+## RESULTS  
 
-text[[67, 194, 485, 368]]
-Overall, 334 patients were randomised to treatment and received adalimumab+MTX ( \(\mathrm {n}=171\) ) or MTX alone \(\mathrm {n}=163\) ), and 148 (86.5%) and 128 (78.5%) patients completed the double-blind portion of the study, respectively (figure 1). Demographics and baseline characteristics were well matched between treatment groups (table 1). The mean RA disease duration was 0.3 years, and the majority of patients had ≥1 erosion at baseline and high disease activity. The mean MTX dose during the 26-week study was \(6.2\pm 0.8\mathrm {mg}/\mathrm {week}\) in the adalimumab+MTX group and \(6.6\pm 0.6\mathrm {mg}/\mathrm {week}\) in the MTX alone group ( \(\mathrm {p}<0.001\) ). After 26 weeks of treatment, 34.5% (59/171) of adalimumab+MTX patients were receiving MTX 8 mg/week versus 65.0% (106/163) of MTX alone patients ( \(\mathrm {p}<0.001\) ).
+text[[68, 193, 486, 368]]
+Overall, 334 patients were randomised to treatment and received adalimumab+MTX \((\mathrm {n}=171)\) or MTX alone \((\mathrm {n}=163)\) 1 and 148 \((86.5\%)\) and 128 \((78.5\%)\) patients completed the double- blind portion of the study, respectively (figure 1). Demographics and baseline characteristics were well matched between treatment groups (table 1). The mean RA disease duration was 0.3 years, and the majority of patients had \(\ge 1\) erosion at baseline and high disease activity. The mean MTX dose during the 26- week study was \(6.2\pm 0.8\mathrm {mg}/\mathrm {week}\) in the adalimumab+MTX group and \(6.6\pm 0.6\mathrm {mg}/\mathrm {week}\) in the MTX alone group \((\mathrm {p}< 0.001)\) . After 26 weeks of treatment, \(34.5\%\) \((59/171)\) of adalimumab+MTX patients were receiving MTX 8 mg/week versus \(65.0\%\) (106/163) of MTX alone patients \((\mathrm {p}< 0.001)\)  
 
-table_caption[[67, 387, 485, 405]]
-Radiographic progression
+sub_title[[68, 382, 240, 398]]
+## Radiographic progression  
 
-text[[67, 400, 485, 677]]
-Treatment with adalimumab+MTX significantly inhibited radiographic progression (figure 2A) at week 26 versus MTX alone (mean change±SD, \(1.5\pm 6.1\mathrm {vs}2.4\pm 3.2\) , respectively; \(\mathrm {p}{<}0.001\) ). Results were confirmed by an LE analysis (figure 2A). Changes in radiographic progression during 26 weeks of treatment were also assessed by a cumulative probability plot of \(\Delta \mathrm {mTSS}\)  (figure 2B). Fewer adalimumab+MTX patients exhibited radiographic progression \((\Delta \mathrm {mTSS}>0.5)\) , with 62.0% (106/171) of patients showing no radiographic progression versus 35.4% (57/161) of MTX alone patients ( \(\mathrm {p}<0.001\) ). Furthermore, only 14.0% (24/171) of adalimumab+MTX patients exhibited clinically relevant radiographic progression \((\Delta \mathrm {mTSS}>3)\)  versus 37.3% (60/161) of MTX alone patients ( \(\mathrm {p}<0.001\) ). In addition, a significantly higher percentage of adalimumab+MTX patients did not experience worsening (≤0.5) in erosion score (73.7% (126/171)) versus MTX alone patients (42.2% (68/161); \(\mathrm {p}<0.001\) ). In patients who lacked baseline erosive damage, the continued absence of erosions was reported in more adalimumab+MTX patients versus MTX alone patients (9/9 vs 2/6 patients, respectively; \(\mathrm {p}=0.01\) ).
+text[[68, 396, 486, 677]]
+Treatment with adalimumab+MTX significantly inhibited radiographic progression (figure 2A) at week 26 versus MTX alone (mean change \(\pm \mathrm {SD}\) \(1.5\pm 6.1\) vs \(2.4\pm 3.2\) , respectively; \(\mathrm {p}< 0.001\) ). Results were confirmed by an LE analysis (figure 2A). Changes in radiographic progression during 26 weeks of treatment were also assessed by a cumulative probability plot of \(\Delta \mathrm {mTSS}\) (figure 2B). Fewer adalimumab+MTX patients exhibited radiographic progression \((\Delta \mathrm {mTS}5>0.5)\) with \(62.0\%\) (106/171) of patients showing no radiographic progression versus \(35.4\%\) \((57/161)\) of MTX alone patients \((\mathrm {p}< 0.001)\) . Furthermore, only \(14.0\%\) \((24/171)\) of adalimumab+MTX patients exhibited clinically relevant radiographic progression \((\Delta \mathrm {mTSS}>3)\) versus \(37.3\%\) (60/161) of MTX alone patients \((\mathrm {p}< 0.001)\) . In addition, a significantly higher percentage of adalimumab+MTX patients did not experience worsening \((\leq 0.5)\) in erosion score \((73.7\%)\) (126/171)) versus MTX alone patients \((42.2\% (68/161)\) \(\mathrm {p}< 0.001\) ). In patients who lacked baseline erosive damage, the continued absence of erosions was reported in more adalimumab+MTX patients versus MTX alone patients \((9/9\) vs \(2/6\) patients, respectively; \(\mathrm {p}=0.01)\)  
 
-title[[67, 694, 188, 707]]
-# Clinical response
+sub_title[[68, 692, 182, 706]]
+## Clinical response  
 
-text[[67, 708, 485, 950]]
-A significantly higher percentage of adalimumab+MTX patients achieved ACR responses versus MTX alone patients at each assessment (figure 3A-C). Significant differences between treatment groups, observed as early as week 2, were maintained through week 26. At week 26, a significantly larger percentage of adalimumab+MTX patients versus MTX alone patients achieved ACR20, ACR50 and ACR70 (figure 3A-C) and ACR90 (12.9% vs 5.5%; \(\mathrm {p}=0.02\) ) responses. Significant differences in favour of adalimumab+MTX were also observed from week 2 to 26 for DAS28-ESR, DAS28-CRP, SDAI and CDAI (see online supplementary figure 1A-D). A larger percentage of adalimumab+MTX patients than MTX alone patients demonstrated good or moderate European League Against Rheumatism responses (figure 3D) and were in states of low disease activity or remission after 26 weeks of treatment (figure 3E). Furthermore, a significantly larger percentage of adalimumab+MTX patients versus MTX alone patients satisfied Boolean remission criteria (19.3% vs 8.6%, \(\mathrm {p}=0.007\) ). Adalimumab+MTX achieved a 1.8-
+text[[68, 706, 486, 950]]
+A significantly higher percentage of adalimumab+MTX patients achieved ACR responses versus MTX alone patients at each assessment (figure 3A- C). Significant differences between treatment groups, observed as early as week 2, were maintained through week 26. At week 26, a significantly larger percentage of adalimumab+MTX patients versus MTX alone patients achieved ACR20, ACR50 and ACR70 (figure 3A- C) and ACR90 \((12.9\%\) \(\mathrm {vs}5.5\%\) \(\mathrm {p}=0.02)\) responses. Significant differences in favour of adalimumab+MTX were also observed from week 2 to 26 for DAS28- ESR, DAS28- CRP, SDAI and CDAI (see online supplementary figure 1A- D). A larger percentage of adalimumab+MTX patients than MTX alone patients demonstrated good or moderate European League Against Rheumatism responses (figure 3D) and were in states of low disease activity or remission after 26 weeks of treatment (figure 3E). Furthermore, a significantly larger percentage of adalimumab+MTX patients versus MTX alone patients satisfied Boolean remission criteria \((19.3\%\) \(\mathrm {vs}8.6\% ,\mathrm {p}=0.007)\) . Adalimumab+MTX achieved a 1.8-  
 
-table[[520, 92, 918, 562]]
+table[[520, 89, 921, 566]]
+table_caption[[523, 74, 829, 89]]
+Table 1 Demographics and baseline characteristics   
 
-<table><td colspan="3">Table 1 Demographics and baseline characteristicsParameter*Adalimumab+MTX<br>(n=171)MTX(n=163)Age±SD (year)54.0±13.154.0±13.2Females (n %)144 (84.2)128 (78.5)RA duration±SD (year)0.3±0.40.3±0.4Weight±SD (kg)54.4±9.756.1±12.3Previous DMARD use (n %)74 (43.3)87 (53.4)1 DMARD57 (33.3)69 (42.3)2 DMARDs17 (9.9)18 (11.0)Corticosteroid use at baseline (n %)58 (33.9)49 (30.1)RF positive (n %)146 (85.4)136 (83.4)Mean titre±SD (IU/ml)154.5±202.3163.7±362.8Anti-CCP positive (n %)145 (84.8)136 (83.4)Mean titre±SD (IU/ml)386.2±694.2241.3±367.2ESR (mm/h)59.9±30.161.8±29.0CRP (mg/dl)2.9±3.03.1±3.3Swollen joint count (n±SD)0-2811.5±4.711.8±5.30-6616.5±6.217.3±7.7Tender joint count (n±SD)0-2813.2±5.813.2±6.10-6820.7±9.421.1±10.2mTSS13.6±22.313.6±17.4Erosion score7.5±11.67.3±9.2Joint space narrowing score6.2±11.46.2±9.4DAS28-ESR6.6±0.96.6±1.0DAS28-CRP5.8±1.05.9±1.0HAQ-DI score1.1±0.71.3±0.8SDAI score40.7±12.041.4±13.8CDAI score37.8±10.938.3±12.4Physician's global assessment of disease activity±SD (mm)65.8±18.466.2±18.8Patient's global assessment of disease activity±SD (mm)64.1±24.866.4±23.7</table>
+<table>Parameter*Adalimumab+MTX (n=171)MTX (n=163)Age±SD (year)54.0±13.154.0±13.2Females (n (%))144 (84.2)128 (78.5)RA duration±SD (year)0.3±0.40.3±0.4Weight±SD (kg)54.4±9.756.1±12.3Previous DMARD use (n (%))74 (43.3)87 (53.4)1 DMARD57 (33.3)69 (42.3)2 DMARDs17 (9.9)18 (11.0)Corticosteroid use at baseline (n (%))58 (33.9)49 (30.1)RF positive (n (%))146 (85.4)136 (83.4)Mean titre±SD (IU/ml)154.5±202.3163.7±362.8Anti-CCP positive (n (%))145 (84.8)136 (83.4)Mean titre±SD (IU/ml)386.2±694.2241.3±367.2ESR (mm/h)59.9±30.161.8±29.0CRP (mg/dl)2.9±3.03.1±3.3Swollen joint count (n±SD)0-2811.5±4.711.8±5.30-6616.5±6.217.3±7.7Tender joint count (n±SD)0-2813.2±5.813.2±6.10-6820.7±9.421.1±10.2mTSS13.6±22.313.6±17.4Erosion score7.5±11.67.3±9.2Joint space narrowing score6.2±11.46.2±9.4DAS28-ESR6.6±0.96.6±1.0DAS28-CRP5.8±1.05.9±1.0HAQ-DI score1.1±0.71.3±0.8SDAI score40.7±12.041.4±13.8CDAI score37.8±10.938.3±12.4Physician&#x27;s global assessment of disease activity±SD (mm)65.8±18.466.2±18.8Patient&#x27;s global assessment of disease activity±SD (mm)64.1±24.866.4±23.7</table>
 
-text[[521, 573, 741, 583]]
-*Data are mean±SD unless otherwise indicated.
+table_footnote[[526, 569, 918, 653]]
+Data are mean±SD unless otherwise indicated. CCP, cyclic citrullinated peptide; DDAI, clinical disease activity index; CRP, C reactive protein; DAS28-CRP, disease activity score using a 28-joint count and CRP level; DAS28-ESR, disease activity score using a 28-joint count and ESR; DMARD, disease-modifying antirheumatic drug; ESR, erythrocyte sedimentation rate; HAQ-DI, Health Assessment Questionnaire disability index; mTSS, modified total Sharp score; MTX, methotrexate; RA, rheumatoid arthritis; RF, rheumatoid factor; SDAI, simplified disease activity index.  
 
-text[[520, 584, 929, 649]]
-CCP, cyclic citrullinated peptide; CDAI, clinical disease activity index; CRP, C reactive protein; DAS28-CRP, disease activity score using a 28-joint count and CRP level; DAS28-ESR, disease activity score using a 28-joint count and ESR; DMARD, disease-modifying antirheumatic drug; ESR, erythrocyte sedimentation rate; HAQ-DI, Health Assessment Questionnaire disability index; mTSS, modified total Sharp score; MTX, methotrexate; RA, rheumatoid arthritis; RF, rheumatoid factor; SDAI, simplified disease activity index.
+text[[519, 679, 927, 720]]
+to 2.2- fold increase in the percentage of patients achieving clinical remission, across all definitions of clinical remission evaluated, versus MTX alone.  
 
-text[[512, 680, 927, 719]]
-to 2.2-fold increase in the percentage of patients achieving clin-ical remission, across all definitions of clinical remission evalu-ated, versus MTX alone.
+text[[519, 721, 927, 827]]
+A significantly larger decrease from baseline in mean HAQ- DI score, indicative of an improvement in physical function, was observed for adalimumab+MTX patients versus MTX alone patients at week 26 \((- 0.6\pm 0.6\) vs \(- 0.4\pm 0.6\) \(\mathrm {p}< 0.001\) ). Although the significant difference between the two groups was small (0.2 units), the percentage of patients achieving normal functionality (HAQ- DI score \(< 0.5\) ) after 26 weeks of treatment was also significantly higher with adalimumab+MTX (figure 3F).  
 
-text[[512, 723, 928, 827]]
-A significantly larger decrease from baseline in mean HAQ-DI score, indicative of an improvement in physical function, was observed for adalimumab+MTX patients versus MTX alone patients at week 26 \((-0.6\pm 0.6\mathrm {vs}-0.4\pm 0.6\) ; \(\mathrm {p}<0.001\) ). Although the significant difference between the two groups was small (0.2 units), the percentage of patients achieving normal functional-ity (HAQ-DI score\(<0.5\) ) after 26 weeks of treatment was also sig-nificantly higher with adalimumab+MTX (figure 3F).
+sub_title[[519, 857, 862, 887]]
+## Factors associated with the absence of radiographic progression or with clinical remission  
 
-title[[512, 859, 861, 884]]
-# Factors associated with the absence of radiographic progression or with clinical remission
-
-text[[512, 886, 928, 950]]
-Disease activity or function baseline variables generally were associated with the absence of radiographic progression \((\mathrm {AmTSS}\le 0.5)\)  and with clinical remission (DAS28-ESR&lt;2.6) in both treatment groups (see online supplementary text and online supplementary table 1).
\ No newline at end of file
+text[[519, 887, 927, 951]]
+Disease activity or function baseline variables generally were associated with the absence of radiographic progression \((\Delta \mathrm {mTSS}\leq 0.5)\) and with clinical remission (DAS28- ESR \(< 2.6)\) in both treatment groups (see online supplementary text and online supplementary table 1).
\ No newline at end of file
diff --git a/stage1/sample_00010/document.md b/stage1/sample_00010/document.md
index de68ceb34e543fc03be688d5e5cfd787b9a2b025..5087dd5f60bd24b40d787548d2422f03c5ed0621 100644
--- a/stage1/sample_00010/document.md
+++ b/stage1/sample_00010/document.md
@@ -1 +1 @@
-1995;38:44-8. 22 Fries JF, Spitz P, Kraines RG, et al. Measurement of patient outcome in arthritis. Arthritis Rheum 1980;23:137-45. 23 Smolen JS, Breedveld FC, Schiff MH, et al. A simplified disease activity index for rheumatoid arthritis for use in clinical practice. Rheumatology (Oxford) 2003;42:244-57. 24 Aletaha D, Noll VPK, Stamm T, et al. Acute phase reactants add little to composite disease activity indices for rheumatoid arthritis: validation of a clinical activity score. Arthritis Res Ther 2005;7:R796-806. 25 van Gestel AM, Prevoo MLL, van't Hof MA, et al. Development and validation of the European League Against Rheumatism response criteria for rheumatoid arthritis. Comparison with the preliminary American College of Rheumatology and the World Health Organization/International League Against Rheumatism criteria. Arthritis Rheum 1996;39:34-40. 26 Wells G, Becker J-C, Teng J, et al. Validation of the 28-joint Disease Activity Score (DAS28) and European League Against Rheumatism response criteria based on C-reactive protein against disease progression in patients with rheumatoid arthritis, and comparison with the DAS28 based on erythrocyte sedimentation rate. Ann Rheum Dis 2009;68:954-60. 27 Felson DT, Smolen JS, Wells G, et al. American College of Rheumatology/European League Against Rheumatism provisional definition of remission in rheumatoid arthritis for clinical trials. Ann Rheum Dis 2011;70:404-13. 28 Aletaha D, Smolen J. The Simplified Disease Activity Index (SDAI) and the Clinical Disease Activity Index (CDAI): a review of their usefulness and validity in rheumatoid arthritis. Clin Exp Rheumatol 2005;23(5 suppl 39):S100-8.
\ No newline at end of file
+1995;38:44-8. 22 Fries JF, Spitz P, Kraines RG, et al. Measurement of patient outcome in arthritis. Arthritis Rheum 1980;23:137-45. 23 Smolen JS, Breedveld FC, Schiff MH, et al. A simplified disease activity index for rheumatoid arthritis for use in clinical practice. Rheumatology (Oxford) 2003;42:244-57. 24 Aletaha D, Nell VPK, Stamm T, et al. Acute phase reactants add little to composite disease activity indices for rheumatoid arthritis: validation of a clinical activity score. Arthritis Res Ther 2005;7:R796-806. 25 van Gestel AM, Prevoo MLL, van't Hof MA, et al. Development and validation of the European League Against Rheumatism response criteria for rheumatoid arthritis. Comparison with the preliminary American College of Rheumatology and the World Health Organization/International League Against Rheumatism criteria. Arthritis Rheum 1996;39:34-40. 26 Wells G, Becker J-C, Teng J, et al. Validation of the 28- joint Disease Activity Score (DAS28) and European League Against Rheumatism response criteria based on C-reactive protein against disease progression in patients with rheumatoid arthritis, and comparison with the DAS28 based on erythrocyte sedimentation rate. Ann Rheum Dis 2009;68:954-60. 27 Felson DT, Smolen JS, Wells G, et al. American College of Rheumatology/European League Against Rheumatism provisional definition of remission in rheumatoid arthritis for clinical trials. Ann Rheum Dis 2011;70:404-13. 28 Aletaha D, Smolen J. The Simplified Disease Activity Index (SDAI) and the Clinical Disease Activity Index (CDAI): a review of their usefulness and validity in rheumatoid arthritis. Clin Exp Rheumatol 2005;23(5 suppl 39):S100-8.
\ No newline at end of file
diff --git a/stage1/sample_00010/raw_response.md b/stage1/sample_00010/raw_response.md
index de68ceb34e543fc03be688d5e5cfd787b9a2b025..5087dd5f60bd24b40d787548d2422f03c5ed0621 100644
--- a/stage1/sample_00010/raw_response.md
+++ b/stage1/sample_00010/raw_response.md
@@ -1 +1 @@
-1995;38:44-8. 22 Fries JF, Spitz P, Kraines RG, et al. Measurement of patient outcome in arthritis. Arthritis Rheum 1980;23:137-45. 23 Smolen JS, Breedveld FC, Schiff MH, et al. A simplified disease activity index for rheumatoid arthritis for use in clinical practice. Rheumatology (Oxford) 2003;42:244-57. 24 Aletaha D, Noll VPK, Stamm T, et al. Acute phase reactants add little to composite disease activity indices for rheumatoid arthritis: validation of a clinical activity score. Arthritis Res Ther 2005;7:R796-806. 25 van Gestel AM, Prevoo MLL, van't Hof MA, et al. Development and validation of the European League Against Rheumatism response criteria for rheumatoid arthritis. Comparison with the preliminary American College of Rheumatology and the World Health Organization/International League Against Rheumatism criteria. Arthritis Rheum 1996;39:34-40. 26 Wells G, Becker J-C, Teng J, et al. Validation of the 28-joint Disease Activity Score (DAS28) and European League Against Rheumatism response criteria based on C-reactive protein against disease progression in patients with rheumatoid arthritis, and comparison with the DAS28 based on erythrocyte sedimentation rate. Ann Rheum Dis 2009;68:954-60. 27 Felson DT, Smolen JS, Wells G, et al. American College of Rheumatology/European League Against Rheumatism provisional definition of remission in rheumatoid arthritis for clinical trials. Ann Rheum Dis 2011;70:404-13. 28 Aletaha D, Smolen J. The Simplified Disease Activity Index (SDAI) and the Clinical Disease Activity Index (CDAI): a review of their usefulness and validity in rheumatoid arthritis. Clin Exp Rheumatol 2005;23(5 suppl 39):S100-8.
\ No newline at end of file
+1995;38:44-8. 22 Fries JF, Spitz P, Kraines RG, et al. Measurement of patient outcome in arthritis. Arthritis Rheum 1980;23:137-45. 23 Smolen JS, Breedveld FC, Schiff MH, et al. A simplified disease activity index for rheumatoid arthritis for use in clinical practice. Rheumatology (Oxford) 2003;42:244-57. 24 Aletaha D, Nell VPK, Stamm T, et al. Acute phase reactants add little to composite disease activity indices for rheumatoid arthritis: validation of a clinical activity score. Arthritis Res Ther 2005;7:R796-806. 25 van Gestel AM, Prevoo MLL, van't Hof MA, et al. Development and validation of the European League Against Rheumatism response criteria for rheumatoid arthritis. Comparison with the preliminary American College of Rheumatology and the World Health Organization/International League Against Rheumatism criteria. Arthritis Rheum 1996;39:34-40. 26 Wells G, Becker J-C, Teng J, et al. Validation of the 28- joint Disease Activity Score (DAS28) and European League Against Rheumatism response criteria based on C-reactive protein against disease progression in patients with rheumatoid arthritis, and comparison with the DAS28 based on erythrocyte sedimentation rate. Ann Rheum Dis 2009;68:954-60. 27 Felson DT, Smolen JS, Wells G, et al. American College of Rheumatology/European League Against Rheumatism provisional definition of remission in rheumatoid arthritis for clinical trials. Ann Rheum Dis 2011;70:404-13. 28 Aletaha D, Smolen J. The Simplified Disease Activity Index (SDAI) and the Clinical Disease Activity Index (CDAI): a review of their usefulness and validity in rheumatoid arthritis. Clin Exp Rheumatol 2005;23(5 suppl 39):S100-8.
\ No newline at end of file
diff --git a/stage1/sample_00011/document.md b/stage1/sample_00011/document.md
index 84ff27a900e02d43a28d4eda24254e7516f4d860..7abfc7b0bbe6d174447b793e4eb1c4a2c4735ed3 100644
--- a/stage1/sample_00011/document.md
+++ b/stage1/sample_00011/document.md
@@ -1 +1,52 @@
-2Institute of Rheumatology, Tokyo Women's Medical University, Shinjuku-ku, Tokyo, JapanDepartment of Orthopedic Surgery, Nagoya University Graduate School and School of Medicine, Showa-ku, Nagoya, JapanDepartment of Medicine and Rheumatology, Graduate School of Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, JapanDivision of Rheumatology and Hematology, Department of Medicine, Sapporo City General Hospital, Chuo-ku, Sapporo, JapanMatsubara Mayflower Hospital, Kato-ishi, Hyogo, JapanUchida Clinic of Rheumatic Diseases, Sumida-ku, Tokyo, JapanEisai Co, Ltd., Bunkyo-ku, Tokyo, JapanAbbott Lombard & Co KG, Ludwigshafen, GermanyAbbott Laboratories, Abbott Park, Illinois, USAThe First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, Yahatanishi-ku, Kitakyushu, JapanAcknowledgementsThe authors would like to thank all the patients, investigators and support staff who participated in the study, Soura Santra, PhD, formally of Abbott, who provided statistical support, and Mary Beth C. Moncrief, PhD, of MedThink SciCom, for editorial assistance in the writing of this manuscript; this assistance was funded by Abbott.ContributorsAll the authors evaluated the study results, interpreted the data and suggested additional analyses. All authors contributed to the development and critical review of manuscript and approved the final version.FundingThis study was supported by Abbott Japan Co (Tokyo, Japan) and Eisai Co (Tokyo, Japan).Competing interestsTT has received consulting fees, speaking fees, honoraria and/or research grant support from Abbott Japan Co; Astellas Pharma Inc; Astra-Zeneca K.K.; Bristol-Myers Squibb; Chugai Pharmaceutical Co; Daiichi-Sankyo Co; Eisai Co; Janssen Pharmaceutical K.K.; Mitsubishi Tanabe Pharma Corporation; Pfizer Japan Inc; and Takeda Pharmaceutical Co. HY has received research grants from Abbott Japan Co; Bristol-Myers Squibb; Chugai Pharmaceutical Co; Eisai Co; Janssen Pharmaceutical K.K.; Mitsubishi Tanabe Pharma Corporation; Otsuka Pharmaceutical Co; Pfizer Japan Inc; Takeda Industrial Pharmaceutical Co; and UCB Japan Co, and speakers honoraria/consulting fees from Abbott Japan Co; Bristol-Myers Squibb; Chugai Pharmaceutical Co; Eisai Co; Janssen Pharmaceutical K.K.; Mitsubishi Tanabe Pharma Corporation; Otsuka Pharmaceutical Co; Pfizer Japan Inc; Takeda Pharmaceutical Co; and UCB Japan Co. NH has received research grants from Astellas Pharmaceutical; Chugai Pharmaceutical Co; Eisai Co; and Mitsubishi Tanabe Pharmaceutical Co. NM has received research grants from Abbott Japan Co; Astellas Pharmaceutical; Banryu Pharmaceutical; Chugai Pharmaceutical Co; Daiichi Sankyo Pharmaceutical Co; Eisai Co; Janssen Pharmaceuticals; Mitsubishi Tanabe Pharma Corporation; Takeda Pharmaceutical Co; and Teijin Limited. MM has received research grants from Abbott Japan Co; Eli Lilly Japan K.K.; GlaxoSmithKline K.K.; Pfizer Japan Inc; Bristol-Myers Squibb; and Otsuka Pharmaceutical Co, and received compensation for work on this manuscript from Abbott Japan Co. TM has received research grants from Chugai Pharmaceutical Co; Bristol-Myers Squibb; Nippon Kayaku Co; Otsuka Pharmaceutical Co; Takeda Pharmaceutical Co; Eli Lilly Japan K.K.; Eli Lilly and Company; Astellas Pharma Inc; Pfizer Japan Inc; AstraZeneca K.K.; and Santen Pharmaceutical Co, and received compensation for work on this manuscript from Abbott Japan Co. SU has received research grants from Abbott Japan Co. HA is an employee of Eisai Co, Tokyo, Japan. HK is an employee of Abbott GmbH and Co KG, Ludwigshafen, Germany, and may hold Abbott stock or options. VA is an employee of Abbott Laboratories, Abbott Park, Illinois, USA, and may hold Abbott stock or options. YT has received consulting fees, speaking fees and/or honoraria from Mitsubishi Tanabe Pharma Corporation; Abbott Japan Co; Eisai Co; Chugai Pharmaceutical Co; Janssen Pharmaceutical K.K.; Santen Pharmaceutical Co; Pfizer Japan Inc; Astellas Pharma Inc; Daiichi-Sankyo Co; GlaxoSmithKline K.K.; Astra-Zeneca; Otsuka Pharmaceutical Co; Actelion Pharmaceuticals Japan; Eli Lilly Japan K.K.; Nippon Kayaku Co; UCB Japan Co; Quintiles Transnational Japan Co; Ono Pharmaceutical Co; and Novartis Pharma K.K. YT has received research grants from Bristol-Myers Squibb; MSD K.K.; Chugai Pharmaceutical Co; Mitsubishi Tanabe Pharma Corporation; Astellas Pharma Inc; Abbott Japan Co; Eisai Co; and Janssen Pharmaceutical K.K.Patient consent Obtained.Ethics approval An institutional review board approved the study at each site.Provenance and peer review Not commissioned; externally peer reviewed.Open Access This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 3.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially,and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/3.0/
\ No newline at end of file
+1  
+
+title[[66, 66, 485, 96]]
+# of anti-TNF-α and MTX combination therapy in patients with early RA and high disease activity.  
+
+sub_title[[66, 109, 171, 122]]
+## Author affiliations  
+
+text[[66, 123, 485, 313]]
+1'Division of Rheumatology, Department of Internal Medicine, School of Medicine, Keio University, Shinjuku- ku, Tokyo, Japan 2Institute of Rheumatology, Tokyo Women's Medical University, Shinjuku- ku, Tokyo, Japan 3Department of Orthopedic Surgery, Nagoya University Graduate School and School of Medicine, Showa- ku, Nagoya, Japan 4Department of Medicine and Rheumatology, Graduate School of Tokyo Medical and Dental University, Bunkyo- ku, Tokyo, Japan 5Division of Rheumatology and Hematology, Department of Medicine, Sapporo City General Hospital, Chuo- ku, Sapporo, Japan 6Matsubara Mayflower Hospital, Katou- shi, Hyogo, Japan 7Uchida Clinic of Rheumatic Diseases, Sumida- ku, Tokyo, Japan 8Eisai Co, Ltd., Bunkyo- ku, Tokyo, Japan  
+
+text[[66, 315, 477, 353]]
+1'The First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, Yahatanishi- ku, Kitakyushu, Japan  
+
+text[[66, 356, 477, 370]]
+Investigators and support staff who participated in the study, Soura Santra, PhD,  
+
+text[[66, 370, 475, 376]]
+formally of Abbott, who provided statistical support, and Mary Beth C. Moncrief  
+
+text[[66, 376, 477, 387]]
+PhD, of MedThink SciCom, for editorial assistance in the writing of this manuscript;  
+
+text[[66, 388, 476, 412]]
+this assistance was funded by Abbott..  
+
+text[[66, 417, 486, 432]]
+Funding This study was supported by Abbott Japan Co (Tokyo, Japan) and Eisai Co  
+
+text[[66, 434, 125, 444]]
+(Tokyo, Japan).  
+
+text[[66, 447, 484, 471]]
+Competing interests TT has received consulting fees, speaking fees, honoraria and/ or research grant support from Abbott Japan Co; Astellas Pharma Inc; Astra- Zeneca K.K.;  
+
+text[[65, 464, 485, 901]]
+Bristol- Myers Squibb; Chugai Pharmaceutical Co; Daiichi- Sankyo Co; Eisai Co; Janssen Pharmaceutical K.K.; Mitsubishi Tanabe Pharma Corporation; Pfizer Japan Inc; and Takeda Pharmaceutical Co. HY has received research grants from Abbott Japan Co; Bristol- Myers Squibb; Chugai Pharmaceutical Co; Eisai Co; Janssen Pharmaceutical K.K.; Mitsubishi Tanabe Pharma Corporation; Oracle Pharma Co; and UCB Japan Co, and speakers honoraria/ consulting fees from Abbott Japan Co; Bristol- Myers Squibb; Chugai Pharmaceutical Co; Eisai Co; Janssen Pharmaceutical K.K.; Mitsubishi Tanabe Pharma Corporation; Oracle, and UCB Japan Co. NI has received research grants from Astellas Pharmaceutical, Chugai Pharmaceutical Co; Eisai Co; and Mitsubishi Tanabe Pharmaceutical Co. NM has received research grants from Abbott Japan Co; Astellas Pharmaceutical; Banyu Pharmaceutical; Chugai Pharmaceutical Co; Daiichi Sankyo Pharmaceutical Co; Eisai Co; Janssen Pharmaceutical; Mitsubishi Tanabe Pharma Corporation; Takeda Pharmaceutical Co; and Teijin Limited. MM has received research grants from Abbott Japan Co; Eli Lilly Japan K.K.; GlaxoSmithKline K.K.; Pfizer Japan Inc; Bristol- Myers Squibb; and Otsuka Pharmaceutical Co, and received compensation for work on this manuscript from Abbott Japan Co. TM has received research grants from Chugai Pharmaceutical Co; Bristol- Myers Squibb; Nippon Kayaku Co; Otsuka Pharmaceutical Co; Takeda Pharmaceutical Co; Eli Lilly Japan K.K.; Eli Lilly and Company; Astellas Pharma Inc; Pfizer Japan Inc; AstraZeneca K.K.; and Santen Pharmaceutical Co, and received compensation for work on this manuscript from Abbott Japan Co. SU has received research grants from Abbott Japan Co, and received compensation for work on this manuscript from Abbott Japan Co. HA is an employee of Eisai Co, Tokyo, Japan. HK is an employee of Abbott GmbH and Co KG, Ludwigshafen, Germany, and may hold Abbott stock or options. VA is an employee of Abbott Laboratories, Abbott Park, Illinois, USA, and may hold Abbott stock or options. YT has received consulting fees, speaking fees and/or honoraria from Mitsubishi Tanabe Pharma Corporation; Abbott Japan Co; Eisai Co; Chugai Pharmaceutical Co; Janssen Pharmaceutical K.K.; Santen Pharmaceutical Co; Pfizer Japan Inc; Astellas Pharma Inc; Daiichi- Sankyo Co; GlaxoSmithKline K.K.; Astra- Zeneca; Otsuka Pharmaceutical Co; Action Pharmaceuticals Japan; Eli Lilly Japan K.K.; Nippon Kayaku Co; UCB Japan Co; Quintiles Transnational Japan Co; Ono Pharmaceutical Co; and Novartis Pharma K.K. YT has received research grants from Bristol- Myers Squibb; MSD K.K.; Chugai Pharmaceutical Co; Mitsubishi Tanabe Pharma Corporation; Astellas Pharma Inc; Abbott Japan Co; Eisai Co; and Janssen Pharmaceutical K.K.  
+
+text[[65, 904, 447, 916]]
+Provenance and peer review Not commissioned; externally peer reviewed.  
+
+text[[66, 920, 475, 948]]
+Open Access This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY- NC 3.0) license, which permits others to distribute, remix, adapt, build upon this work non- commercially,  
+
+text[[511, 67, 919, 101]]
+and license their derivative works on different terms, provided the original work is properly cited and the use is non- commercial. See: http://creativecommons.org/licenses/by- nc/3.0/  
+
+sub_title[[513, 136, 601, 148]]
+## REFERENCES  
+
+text[[513, 150, 920, 949]]
+1 Filipovic I, Walker D, Forster F, et al. Quantifying the economic burden of productivity loss in rheumatoid arthritis. Rheumatology (Oxford) 2011; 50:1083- 90. 2 Scott DL, Wolfe F, Huizinga TWJ. Rheumatoid arthritis. Lancet 2010;376:1094- 108. 3 Takeuchi T. Revolutionary change in rheumatoid arthritis management with biological therapy. Keio J Med 2011;60:75- 81. 4 Saag KG, Teng GG, Patkar NM, et al. American College of Rheumatology 2008 recommendations for the use of nonbiologic and biologic disease- modifying antirheumatic drugs in rheumatoid arthritis. Arthritis Rheum 2008;59:762- 84. 5 Smolen JS, Aletaha D, Bijlsma JW, et al. For the T2T Expert Committee. Treating rheumatoid arthritis to target: recommendations of an international task force. Ann Rheum Dis 2010;69:631- 7. 6 Breedveld FC, Weisman MH, Kavanaugh AF, et al. For the PREMIER Investigators. The PREMIER study: a multicenter, randomized, double- blind clinical trial of combination therapy with adalimumab plus methotrexate versus methotrexate alone or adalimumab alone in patients with early, aggressive rheumatoid arthritis who had not had previous methotrexate treatment. Arthritis Rheum 2006;54:26- 37. 7 van der Heijde D, Breedveld FC, Kavanaugh A, et al. Disease activity, physical function, and radiographic progression after longterm therapy with adalimumab plus methotrexate: 5- year results of PREMIER. J Rheumatol 2010;37:2237- 46. 8 Weinblatt ME, Keystone EC, Furst DE, et al. Adalimumab, a fully human anti- tumor necrosis factor \(\alpha\) monoclonal antibody, for the treatment of rheumatoid arthritis in patients taking concomitant methotrexate: the ARMAldalimumab trial. Arthritis Rheum 2003;48:35- 45. 9 van de Putte LBA, Atkins C, Malaisse M, et al. Efficacy and safety of adalimumab as monotherapy in patients with rheumatoid arthritis for whom previous disease modifying antirheumatic drug treatment has failed. Ann Rheum Dis 2004;63:508- 16. 10 Keystone EC, Kavanaugh AF, Sharp JT, et al. Radiographic, clinical, and functional outcomes of treatment with adalimumab (a human anti- tumor necrosis factor monoclonal antibody) in patients with active rheumatoid arthritis receiving concomitant methotrexate therapy: a randomized, placebo- controlled, 52- week trial. Arthritis Rheum 2004;50:1400- 11. 11 Furst DE, Schiff MH, Fleischmann RM, et al. Adalimumab, a fully human anti- tumor necrosis factor- alpha monoclonal antibody, and concomitant standard antirheumatic therapy for the treatment of rheumatoid arthritis: results of STAR (Safety Trial of Adalimumab in Rheumatoid Arthritis). J Rheumatol 2003;30:2563- 71. 12 Kavanaugh A, Fleischmann RM, Emery P, et al. Clinical, functional and radiographic consequences of achieving stable low disease activity and remission with adalimumab plus methotrexate or methotrexate alone in early rheumatoid arthritis: 26- week results from the randomised, controlled OPTIMA study. Ann Rheum Dis 2013;72:64- 71. 13 Takeuchi T, Kameda H. The Japanese experience with biologic therapies for rheumatoid arthritis. Nat Rev Rheumatol 2010;6:644- 52. 14 Miyasaka N, The CHANGE Study Investigators. Clinical investigation in highly disease- affected rheumatoid arthritis patients in Japan with adalimumab applying standard and general evaluation: the CHANGE study. Mod Rheumato 2008;18:252- 62. 15 Takeuchi T, Tanaka Y, Kaneko Y, et al. Effectiveness and safety of adalimumab in Japanese patients with rheumatoid arthritis: retrospective analyses of data collected during the first year of adalimumab treatment in routine clinical practice (HARMONY study). Mod Rheumato 2012;22:327- 38. 16 Koike T, Hariagi M, Ishiguro N, et al. Safety and effectiveness of adalimumab in Japanese rheumatoid arthritis patients: postmarketing surveillance report of the first 3,000 patients. Mod Rheumatol 2012;22:498- 508. 17 Arnett FC, Edworthy SM, Bloch DA, et al. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum 1988;31:315- 24. 18 Felson DT, Anderson JJ, Boers M, et al. American College of Rheumatology. Preliminary definition of improvement in rheumatoid arthritis. Arthritis Rheum 1995;38:727- 35. 19 Felson DT, Anderson JJ, Lange ML, et al. Should improvement in rheumatoid arthritis clinical trials be defined as fifty percent or seventy percent improvement in cost? see measures, rather than twenty percent? Arthritis Rheum 1998;41:1564- 70. 20 Fransen J, Creemers MCW, van Riel PLCM. Remission in rheumatoid arthritis: agreement of the disease activity score (DAS28) with the ARA preliminary remission criteria. Rheumatology (Oxford) 2004;43:1252- 5. 21 Prevoo ML, van't Hof MA, Kuper HH, et al. Modified disease activity scores that include twenty- eight- joint counts. Development and validation in a prospective
\ No newline at end of file
diff --git a/stage1/sample_00011/raw_response.md b/stage1/sample_00011/raw_response.md
index 84ff27a900e02d43a28d4eda24254e7516f4d860..7abfc7b0bbe6d174447b793e4eb1c4a2c4735ed3 100644
--- a/stage1/sample_00011/raw_response.md
+++ b/stage1/sample_00011/raw_response.md
@@ -1 +1,52 @@
-2Institute of Rheumatology, Tokyo Women's Medical University, Shinjuku-ku, Tokyo, JapanDepartment of Orthopedic Surgery, Nagoya University Graduate School and School of Medicine, Showa-ku, Nagoya, JapanDepartment of Medicine and Rheumatology, Graduate School of Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, JapanDivision of Rheumatology and Hematology, Department of Medicine, Sapporo City General Hospital, Chuo-ku, Sapporo, JapanMatsubara Mayflower Hospital, Kato-ishi, Hyogo, JapanUchida Clinic of Rheumatic Diseases, Sumida-ku, Tokyo, JapanEisai Co, Ltd., Bunkyo-ku, Tokyo, JapanAbbott Lombard & Co KG, Ludwigshafen, GermanyAbbott Laboratories, Abbott Park, Illinois, USAThe First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, Yahatanishi-ku, Kitakyushu, JapanAcknowledgementsThe authors would like to thank all the patients, investigators and support staff who participated in the study, Soura Santra, PhD, formally of Abbott, who provided statistical support, and Mary Beth C. Moncrief, PhD, of MedThink SciCom, for editorial assistance in the writing of this manuscript; this assistance was funded by Abbott.ContributorsAll the authors evaluated the study results, interpreted the data and suggested additional analyses. All authors contributed to the development and critical review of manuscript and approved the final version.FundingThis study was supported by Abbott Japan Co (Tokyo, Japan) and Eisai Co (Tokyo, Japan).Competing interestsTT has received consulting fees, speaking fees, honoraria and/or research grant support from Abbott Japan Co; Astellas Pharma Inc; Astra-Zeneca K.K.; Bristol-Myers Squibb; Chugai Pharmaceutical Co; Daiichi-Sankyo Co; Eisai Co; Janssen Pharmaceutical K.K.; Mitsubishi Tanabe Pharma Corporation; Pfizer Japan Inc; and Takeda Pharmaceutical Co. HY has received research grants from Abbott Japan Co; Bristol-Myers Squibb; Chugai Pharmaceutical Co; Eisai Co; Janssen Pharmaceutical K.K.; Mitsubishi Tanabe Pharma Corporation; Otsuka Pharmaceutical Co; Pfizer Japan Inc; Takeda Industrial Pharmaceutical Co; and UCB Japan Co, and speakers honoraria/consulting fees from Abbott Japan Co; Bristol-Myers Squibb; Chugai Pharmaceutical Co; Eisai Co; Janssen Pharmaceutical K.K.; Mitsubishi Tanabe Pharma Corporation; Otsuka Pharmaceutical Co; Pfizer Japan Inc; Takeda Pharmaceutical Co; and UCB Japan Co. NH has received research grants from Astellas Pharmaceutical; Chugai Pharmaceutical Co; Eisai Co; and Mitsubishi Tanabe Pharmaceutical Co. NM has received research grants from Abbott Japan Co; Astellas Pharmaceutical; Banryu Pharmaceutical; Chugai Pharmaceutical Co; Daiichi Sankyo Pharmaceutical Co; Eisai Co; Janssen Pharmaceuticals; Mitsubishi Tanabe Pharma Corporation; Takeda Pharmaceutical Co; and Teijin Limited. MM has received research grants from Abbott Japan Co; Eli Lilly Japan K.K.; GlaxoSmithKline K.K.; Pfizer Japan Inc; Bristol-Myers Squibb; and Otsuka Pharmaceutical Co, and received compensation for work on this manuscript from Abbott Japan Co. TM has received research grants from Chugai Pharmaceutical Co; Bristol-Myers Squibb; Nippon Kayaku Co; Otsuka Pharmaceutical Co; Takeda Pharmaceutical Co; Eli Lilly Japan K.K.; Eli Lilly and Company; Astellas Pharma Inc; Pfizer Japan Inc; AstraZeneca K.K.; and Santen Pharmaceutical Co, and received compensation for work on this manuscript from Abbott Japan Co. SU has received research grants from Abbott Japan Co. HA is an employee of Eisai Co, Tokyo, Japan. HK is an employee of Abbott GmbH and Co KG, Ludwigshafen, Germany, and may hold Abbott stock or options. VA is an employee of Abbott Laboratories, Abbott Park, Illinois, USA, and may hold Abbott stock or options. YT has received consulting fees, speaking fees and/or honoraria from Mitsubishi Tanabe Pharma Corporation; Abbott Japan Co; Eisai Co; Chugai Pharmaceutical Co; Janssen Pharmaceutical K.K.; Santen Pharmaceutical Co; Pfizer Japan Inc; Astellas Pharma Inc; Daiichi-Sankyo Co; GlaxoSmithKline K.K.; Astra-Zeneca; Otsuka Pharmaceutical Co; Actelion Pharmaceuticals Japan; Eli Lilly Japan K.K.; Nippon Kayaku Co; UCB Japan Co; Quintiles Transnational Japan Co; Ono Pharmaceutical Co; and Novartis Pharma K.K. YT has received research grants from Bristol-Myers Squibb; MSD K.K.; Chugai Pharmaceutical Co; Mitsubishi Tanabe Pharma Corporation; Astellas Pharma Inc; Abbott Japan Co; Eisai Co; and Janssen Pharmaceutical K.K.Patient consent Obtained.Ethics approval An institutional review board approved the study at each site.Provenance and peer review Not commissioned; externally peer reviewed.Open Access This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 3.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially,and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/3.0/
\ No newline at end of file
+1  
+
+title[[66, 66, 485, 96]]
+# of anti-TNF-α and MTX combination therapy in patients with early RA and high disease activity.  
+
+sub_title[[66, 109, 171, 122]]
+## Author affiliations  
+
+text[[66, 123, 485, 313]]
+1'Division of Rheumatology, Department of Internal Medicine, School of Medicine, Keio University, Shinjuku- ku, Tokyo, Japan 2Institute of Rheumatology, Tokyo Women's Medical University, Shinjuku- ku, Tokyo, Japan 3Department of Orthopedic Surgery, Nagoya University Graduate School and School of Medicine, Showa- ku, Nagoya, Japan 4Department of Medicine and Rheumatology, Graduate School of Tokyo Medical and Dental University, Bunkyo- ku, Tokyo, Japan 5Division of Rheumatology and Hematology, Department of Medicine, Sapporo City General Hospital, Chuo- ku, Sapporo, Japan 6Matsubara Mayflower Hospital, Katou- shi, Hyogo, Japan 7Uchida Clinic of Rheumatic Diseases, Sumida- ku, Tokyo, Japan 8Eisai Co, Ltd., Bunkyo- ku, Tokyo, Japan  
+
+text[[66, 315, 477, 353]]
+1'The First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, Yahatanishi- ku, Kitakyushu, Japan  
+
+text[[66, 356, 477, 370]]
+Investigators and support staff who participated in the study, Soura Santra, PhD,  
+
+text[[66, 370, 475, 376]]
+formally of Abbott, who provided statistical support, and Mary Beth C. Moncrief  
+
+text[[66, 376, 477, 387]]
+PhD, of MedThink SciCom, for editorial assistance in the writing of this manuscript;  
+
+text[[66, 388, 476, 412]]
+this assistance was funded by Abbott..  
+
+text[[66, 417, 486, 432]]
+Funding This study was supported by Abbott Japan Co (Tokyo, Japan) and Eisai Co  
+
+text[[66, 434, 125, 444]]
+(Tokyo, Japan).  
+
+text[[66, 447, 484, 471]]
+Competing interests TT has received consulting fees, speaking fees, honoraria and/ or research grant support from Abbott Japan Co; Astellas Pharma Inc; Astra- Zeneca K.K.;  
+
+text[[65, 464, 485, 901]]
+Bristol- Myers Squibb; Chugai Pharmaceutical Co; Daiichi- Sankyo Co; Eisai Co; Janssen Pharmaceutical K.K.; Mitsubishi Tanabe Pharma Corporation; Pfizer Japan Inc; and Takeda Pharmaceutical Co. HY has received research grants from Abbott Japan Co; Bristol- Myers Squibb; Chugai Pharmaceutical Co; Eisai Co; Janssen Pharmaceutical K.K.; Mitsubishi Tanabe Pharma Corporation; Oracle Pharma Co; and UCB Japan Co, and speakers honoraria/ consulting fees from Abbott Japan Co; Bristol- Myers Squibb; Chugai Pharmaceutical Co; Eisai Co; Janssen Pharmaceutical K.K.; Mitsubishi Tanabe Pharma Corporation; Oracle, and UCB Japan Co. NI has received research grants from Astellas Pharmaceutical, Chugai Pharmaceutical Co; Eisai Co; and Mitsubishi Tanabe Pharmaceutical Co. NM has received research grants from Abbott Japan Co; Astellas Pharmaceutical; Banyu Pharmaceutical; Chugai Pharmaceutical Co; Daiichi Sankyo Pharmaceutical Co; Eisai Co; Janssen Pharmaceutical; Mitsubishi Tanabe Pharma Corporation; Takeda Pharmaceutical Co; and Teijin Limited. MM has received research grants from Abbott Japan Co; Eli Lilly Japan K.K.; GlaxoSmithKline K.K.; Pfizer Japan Inc; Bristol- Myers Squibb; and Otsuka Pharmaceutical Co, and received compensation for work on this manuscript from Abbott Japan Co. TM has received research grants from Chugai Pharmaceutical Co; Bristol- Myers Squibb; Nippon Kayaku Co; Otsuka Pharmaceutical Co; Takeda Pharmaceutical Co; Eli Lilly Japan K.K.; Eli Lilly and Company; Astellas Pharma Inc; Pfizer Japan Inc; AstraZeneca K.K.; and Santen Pharmaceutical Co, and received compensation for work on this manuscript from Abbott Japan Co. SU has received research grants from Abbott Japan Co, and received compensation for work on this manuscript from Abbott Japan Co. HA is an employee of Eisai Co, Tokyo, Japan. HK is an employee of Abbott GmbH and Co KG, Ludwigshafen, Germany, and may hold Abbott stock or options. VA is an employee of Abbott Laboratories, Abbott Park, Illinois, USA, and may hold Abbott stock or options. YT has received consulting fees, speaking fees and/or honoraria from Mitsubishi Tanabe Pharma Corporation; Abbott Japan Co; Eisai Co; Chugai Pharmaceutical Co; Janssen Pharmaceutical K.K.; Santen Pharmaceutical Co; Pfizer Japan Inc; Astellas Pharma Inc; Daiichi- Sankyo Co; GlaxoSmithKline K.K.; Astra- Zeneca; Otsuka Pharmaceutical Co; Action Pharmaceuticals Japan; Eli Lilly Japan K.K.; Nippon Kayaku Co; UCB Japan Co; Quintiles Transnational Japan Co; Ono Pharmaceutical Co; and Novartis Pharma K.K. YT has received research grants from Bristol- Myers Squibb; MSD K.K.; Chugai Pharmaceutical Co; Mitsubishi Tanabe Pharma Corporation; Astellas Pharma Inc; Abbott Japan Co; Eisai Co; and Janssen Pharmaceutical K.K.  
+
+text[[65, 904, 447, 916]]
+Provenance and peer review Not commissioned; externally peer reviewed.  
+
+text[[66, 920, 475, 948]]
+Open Access This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY- NC 3.0) license, which permits others to distribute, remix, adapt, build upon this work non- commercially,  
+
+text[[511, 67, 919, 101]]
+and license their derivative works on different terms, provided the original work is properly cited and the use is non- commercial. See: http://creativecommons.org/licenses/by- nc/3.0/  
+
+sub_title[[513, 136, 601, 148]]
+## REFERENCES  
+
+text[[513, 150, 920, 949]]
+1 Filipovic I, Walker D, Forster F, et al. Quantifying the economic burden of productivity loss in rheumatoid arthritis. Rheumatology (Oxford) 2011; 50:1083- 90. 2 Scott DL, Wolfe F, Huizinga TWJ. Rheumatoid arthritis. Lancet 2010;376:1094- 108. 3 Takeuchi T. Revolutionary change in rheumatoid arthritis management with biological therapy. Keio J Med 2011;60:75- 81. 4 Saag KG, Teng GG, Patkar NM, et al. American College of Rheumatology 2008 recommendations for the use of nonbiologic and biologic disease- modifying antirheumatic drugs in rheumatoid arthritis. Arthritis Rheum 2008;59:762- 84. 5 Smolen JS, Aletaha D, Bijlsma JW, et al. For the T2T Expert Committee. Treating rheumatoid arthritis to target: recommendations of an international task force. Ann Rheum Dis 2010;69:631- 7. 6 Breedveld FC, Weisman MH, Kavanaugh AF, et al. For the PREMIER Investigators. The PREMIER study: a multicenter, randomized, double- blind clinical trial of combination therapy with adalimumab plus methotrexate versus methotrexate alone or adalimumab alone in patients with early, aggressive rheumatoid arthritis who had not had previous methotrexate treatment. Arthritis Rheum 2006;54:26- 37. 7 van der Heijde D, Breedveld FC, Kavanaugh A, et al. Disease activity, physical function, and radiographic progression after longterm therapy with adalimumab plus methotrexate: 5- year results of PREMIER. J Rheumatol 2010;37:2237- 46. 8 Weinblatt ME, Keystone EC, Furst DE, et al. Adalimumab, a fully human anti- tumor necrosis factor \(\alpha\) monoclonal antibody, for the treatment of rheumatoid arthritis in patients taking concomitant methotrexate: the ARMAldalimumab trial. Arthritis Rheum 2003;48:35- 45. 9 van de Putte LBA, Atkins C, Malaisse M, et al. Efficacy and safety of adalimumab as monotherapy in patients with rheumatoid arthritis for whom previous disease modifying antirheumatic drug treatment has failed. Ann Rheum Dis 2004;63:508- 16. 10 Keystone EC, Kavanaugh AF, Sharp JT, et al. Radiographic, clinical, and functional outcomes of treatment with adalimumab (a human anti- tumor necrosis factor monoclonal antibody) in patients with active rheumatoid arthritis receiving concomitant methotrexate therapy: a randomized, placebo- controlled, 52- week trial. Arthritis Rheum 2004;50:1400- 11. 11 Furst DE, Schiff MH, Fleischmann RM, et al. Adalimumab, a fully human anti- tumor necrosis factor- alpha monoclonal antibody, and concomitant standard antirheumatic therapy for the treatment of rheumatoid arthritis: results of STAR (Safety Trial of Adalimumab in Rheumatoid Arthritis). J Rheumatol 2003;30:2563- 71. 12 Kavanaugh A, Fleischmann RM, Emery P, et al. Clinical, functional and radiographic consequences of achieving stable low disease activity and remission with adalimumab plus methotrexate or methotrexate alone in early rheumatoid arthritis: 26- week results from the randomised, controlled OPTIMA study. Ann Rheum Dis 2013;72:64- 71. 13 Takeuchi T, Kameda H. The Japanese experience with biologic therapies for rheumatoid arthritis. Nat Rev Rheumatol 2010;6:644- 52. 14 Miyasaka N, The CHANGE Study Investigators. Clinical investigation in highly disease- affected rheumatoid arthritis patients in Japan with adalimumab applying standard and general evaluation: the CHANGE study. Mod Rheumato 2008;18:252- 62. 15 Takeuchi T, Tanaka Y, Kaneko Y, et al. Effectiveness and safety of adalimumab in Japanese patients with rheumatoid arthritis: retrospective analyses of data collected during the first year of adalimumab treatment in routine clinical practice (HARMONY study). Mod Rheumato 2012;22:327- 38. 16 Koike T, Hariagi M, Ishiguro N, et al. Safety and effectiveness of adalimumab in Japanese rheumatoid arthritis patients: postmarketing surveillance report of the first 3,000 patients. Mod Rheumatol 2012;22:498- 508. 17 Arnett FC, Edworthy SM, Bloch DA, et al. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum 1988;31:315- 24. 18 Felson DT, Anderson JJ, Boers M, et al. American College of Rheumatology. Preliminary definition of improvement in rheumatoid arthritis. Arthritis Rheum 1995;38:727- 35. 19 Felson DT, Anderson JJ, Lange ML, et al. Should improvement in rheumatoid arthritis clinical trials be defined as fifty percent or seventy percent improvement in cost? see measures, rather than twenty percent? Arthritis Rheum 1998;41:1564- 70. 20 Fransen J, Creemers MCW, van Riel PLCM. Remission in rheumatoid arthritis: agreement of the disease activity score (DAS28) with the ARA preliminary remission criteria. Rheumatology (Oxford) 2004;43:1252- 5. 21 Prevoo ML, van't Hof MA, Kuper HH, et al. Modified disease activity scores that include twenty- eight- joint counts. Development and validation in a prospective
\ No newline at end of file
diff --git a/stage1/sample_00012/document.md b/stage1/sample_00012/document.md
index e34995e98b8a92862c7a92e02e6f78c085206826..c437255812f1835d699959c0d932b45be8e6de33 100644
--- a/stage1/sample_00012/document.md
+++ b/stage1/sample_00012/document.md
@@ -1 +1,4 @@
+Local transportation for the participating teams shall be the responsibility of the participating institutions. 
+
+text[[115, 254, 790, 270]]
 Local transportation for the participating teams shall be the responsibility of the participating institutions.
\ No newline at end of file
diff --git a/stage1/sample_00012/raw_response.md b/stage1/sample_00012/raw_response.md
index e34995e98b8a92862c7a92e02e6f78c085206826..c437255812f1835d699959c0d932b45be8e6de33 100644
--- a/stage1/sample_00012/raw_response.md
+++ b/stage1/sample_00012/raw_response.md
@@ -1 +1,4 @@
+Local transportation for the participating teams shall be the responsibility of the participating institutions. 
+
+text[[115, 254, 790, 270]]
 Local transportation for the participating teams shall be the responsibility of the participating institutions.
\ No newline at end of file
diff --git a/stage1/sample_00013/document.md b/stage1/sample_00013/document.md
index b378ac66d64b535c00149635907ea020a985a939..da967826a8858d2cdd1f6bcdfb1a63a8986fb5e5 100644
--- a/stage1/sample_00013/document.md
+++ b/stage1/sample_00013/document.md
@@ -1,19 +1,27 @@
-1: 1  
+58.0
 
-title[[570, 213, 882, 231]]
-# SECTION VI: SCHEDULE OF EVENTS  
+title[[572, 213, 882, 231]]
+# SECTION VI: SCHEDULE OF EVENTS 
 
-title[[123, 251, 170, 265]]
-# Friday  
+sub_title[[123, 252, 171, 266]]
+## Friday 
 
-text[[123, 268, 463, 346]]
-Course preparation. Course walk- through with NCAA site representative. Course review and practice by participants. Packet pick- up. Mandatory coaches meeting.  
+text[[123, 269, 463, 346]]
+Course preparation.
+Course walk-through with NCAA site representative.
+Course review and practice by participants.
+Packet pick-up.
+Mandatory coaches meeting. 
 
-title[[123, 363, 188, 376]]
-# Saturday  
+sub_title[[123, 363, 189, 377]]
+## Saturday 
 
-text[[123, 379, 454, 457]]
-Course preparation. Course review and practice by participants. Women's race - race start time to be determined.\* Men's race - race start time to be determined.\* Post- competition recognition ceremony.  
+text[[123, 380, 453, 457]]
+Course preparation.
+Course review and practice by participants.
+Women's race - race start time to be determined.*
+Men's race - race start time to be determined.*
+Post-competition recognition ceremony. 
 
-text[[123, 473, 874, 504]]
-\*The men's race will go first in even years, the women's race will go first in odd years. Start times are subject to the approval of the track and field and cross country committee.
\ No newline at end of file
+text[[123, 475, 873, 506]]
+*The men's race will go first in even years, the women's race will go first in odd years. Start times are subject to the approval of the track and field and cross country committee.
\ No newline at end of file
diff --git a/stage1/sample_00013/raw_response.md b/stage1/sample_00013/raw_response.md
index b378ac66d64b535c00149635907ea020a985a939..da967826a8858d2cdd1f6bcdfb1a63a8986fb5e5 100644
--- a/stage1/sample_00013/raw_response.md
+++ b/stage1/sample_00013/raw_response.md
@@ -1,19 +1,27 @@
-1: 1  
+58.0
 
-title[[570, 213, 882, 231]]
-# SECTION VI: SCHEDULE OF EVENTS  
+title[[572, 213, 882, 231]]
+# SECTION VI: SCHEDULE OF EVENTS 
 
-title[[123, 251, 170, 265]]
-# Friday  
+sub_title[[123, 252, 171, 266]]
+## Friday 
 
-text[[123, 268, 463, 346]]
-Course preparation. Course walk- through with NCAA site representative. Course review and practice by participants. Packet pick- up. Mandatory coaches meeting.  
+text[[123, 269, 463, 346]]
+Course preparation.
+Course walk-through with NCAA site representative.
+Course review and practice by participants.
+Packet pick-up.
+Mandatory coaches meeting. 
 
-title[[123, 363, 188, 376]]
-# Saturday  
+sub_title[[123, 363, 189, 377]]
+## Saturday 
 
-text[[123, 379, 454, 457]]
-Course preparation. Course review and practice by participants. Women's race - race start time to be determined.\* Men's race - race start time to be determined.\* Post- competition recognition ceremony.  
+text[[123, 380, 453, 457]]
+Course preparation.
+Course review and practice by participants.
+Women's race - race start time to be determined.*
+Men's race - race start time to be determined.*
+Post-competition recognition ceremony. 
 
-text[[123, 473, 874, 504]]
-\*The men's race will go first in even years, the women's race will go first in odd years. Start times are subject to the approval of the track and field and cross country committee.
\ No newline at end of file
+text[[123, 475, 873, 506]]
+*The men's race will go first in even years, the women's race will go first in odd years. Start times are subject to the approval of the track and field and cross country committee.
\ No newline at end of file
diff --git a/stage1/sample_00014/document.md b/stage1/sample_00014/document.md
index 08ff64f2aab010972e36599f182f5242ab2609f0..5a594ee5b3e2c918fa4d9214cf43e197b78ca895 100644
--- a/stage1/sample_00014/document.md
+++ b/stage1/sample_00014/document.md
@@ -1,10 +1,28 @@
-75- 150 volunteers on competition day will be needed for assignments, including course safety, finish chute, concessions, parking, media and merchandise sales.  
+75-150 volunteers on competition day will be needed for assignments, including course safety, finish chute, concessions, parking, media and merchandise sales. 
 
-text[[126, 621, 882, 695]]
-The prospective host that is bidding on this championship agrees to all terms and conditions as outlined above in this Championship Bid Specifications Agreement. We agree to comply with all the requirements listed in this document and to administer the designated championship in accordance with the policies of the NCAA and the applicable NCAA sports committee. Prospective hosts that agree with all the requirements listed in this document for the designated championship shall signify agreement by selecting "Yes" below.  
+image[[116, 42, 880, 199]]
+ 
 
-text[[315, 711, 697, 728]]
-YES NO NO with Exception  
+title[[586, 212, 885, 231]]
+SECTION VIII: VOLUNTEER NEEDS 
 
-text[[128, 745, 882, 809]]
-Prospective hosts who do not agree with all requirements in this document shall select either "No" or "No with Exception" and declare any issues and/or exceptions regarding the aforementioned terms. Please note: any proposed revisions to the language in this document must be specified in the bidding portal to be considered.
\ No newline at end of file
+text[[119, 252, 884, 284]]
+Approximately 75-150 volunteers on competition day will be needed for assignments, including course safety, finish chute, concessions, parking, media and merchandise sales. 
+
+text[[130, 623, 887, 705]]
+The prospective host that is bidding on this championship agrees to all terms and conditions as outlined above in this Championship Bid Specifications Agreement. We agree to comply with all the requirements listed in this document and to administer the designated championship in accordance with the policies of the NCAA and the applicable NCAA sports committee. Prospective hosts that agree with all the requirements listed in this document for the designated championship shall signify agreement by selecting “Yes” below. 
+
+image[[314, 715, 366, 733]]
+ 
+
+image[[420, 715, 471, 733]]
+ 
+
+image[[534, 715, 587, 733]]
+ 
+
+image[[589, 715, 643, 733]]
+ 
+
+text[[128, 749, 884, 814]]
+Prospective hosts who do not agree with all requirements in this document shall select either “No” or “No with Exception” and declare any issues and/or exceptions regarding the aforementioned terms. Please note: any proposed revisions to the language in this document must be specified in the bidding portal to be considered.
\ No newline at end of file
diff --git a/stage1/sample_00014/raw_response.md b/stage1/sample_00014/raw_response.md
index 08ff64f2aab010972e36599f182f5242ab2609f0..5a594ee5b3e2c918fa4d9214cf43e197b78ca895 100644
--- a/stage1/sample_00014/raw_response.md
+++ b/stage1/sample_00014/raw_response.md
@@ -1,10 +1,28 @@
-75- 150 volunteers on competition day will be needed for assignments, including course safety, finish chute, concessions, parking, media and merchandise sales.  
+75-150 volunteers on competition day will be needed for assignments, including course safety, finish chute, concessions, parking, media and merchandise sales. 
 
-text[[126, 621, 882, 695]]
-The prospective host that is bidding on this championship agrees to all terms and conditions as outlined above in this Championship Bid Specifications Agreement. We agree to comply with all the requirements listed in this document and to administer the designated championship in accordance with the policies of the NCAA and the applicable NCAA sports committee. Prospective hosts that agree with all the requirements listed in this document for the designated championship shall signify agreement by selecting "Yes" below.  
+image[[116, 42, 880, 199]]
+ 
 
-text[[315, 711, 697, 728]]
-YES NO NO with Exception  
+title[[586, 212, 885, 231]]
+SECTION VIII: VOLUNTEER NEEDS 
 
-text[[128, 745, 882, 809]]
-Prospective hosts who do not agree with all requirements in this document shall select either "No" or "No with Exception" and declare any issues and/or exceptions regarding the aforementioned terms. Please note: any proposed revisions to the language in this document must be specified in the bidding portal to be considered.
\ No newline at end of file
+text[[119, 252, 884, 284]]
+Approximately 75-150 volunteers on competition day will be needed for assignments, including course safety, finish chute, concessions, parking, media and merchandise sales. 
+
+text[[130, 623, 887, 705]]
+The prospective host that is bidding on this championship agrees to all terms and conditions as outlined above in this Championship Bid Specifications Agreement. We agree to comply with all the requirements listed in this document and to administer the designated championship in accordance with the policies of the NCAA and the applicable NCAA sports committee. Prospective hosts that agree with all the requirements listed in this document for the designated championship shall signify agreement by selecting “Yes” below. 
+
+image[[314, 715, 366, 733]]
+ 
+
+image[[420, 715, 471, 733]]
+ 
+
+image[[534, 715, 587, 733]]
+ 
+
+image[[589, 715, 643, 733]]
+ 
+
+text[[128, 749, 884, 814]]
+Prospective hosts who do not agree with all requirements in this document shall select either “No” or “No with Exception” and declare any issues and/or exceptions regarding the aforementioned terms. Please note: any proposed revisions to the language in this document must be specified in the bidding portal to be considered.
\ No newline at end of file
diff --git a/stage1/sample_00015/document.md b/stage1/sample_00015/document.md
index 6cddf9ee05f8de608e00821abf6d3b08f5784206..612ab3958eb83e7608d1a1d882672e4342b0b5bc 100644
--- a/stage1/sample_00015/document.md
+++ b/stage1/sample_00015/document.md
@@ -1,18 +1,18 @@
 145 (Fig. 6B), which over-express EGFR (Fig. 6C). 
 
-image[[62, 97, 612, 427]]
+image[[58, 96, 610, 430]]
  
 
-image_caption[[660, 93, 914, 235]]
+image_caption[[662, 94, 901, 233]]
 <center>Figure 6. SR48692 radiosensitizes human prostate cancer cells expressing low levels of EGFR (A, PC-3M) but not prostate cancer cells overexpressing EGFR (B, DU-145). (C) Expression of EGFR in normal (RWPE-1) and PC cell lines (LNCaP, C4-2, DU-145, PC-3 and PC-3M).</center> 
 
-text[[55, 446, 940, 666]]
+text[[55, 447, 936, 668]]
 In summary, our data show that SR48692 selectively sensitizes PC cells to ionizing radiation. Our results also show that NT stimulation (a) activates a novel EGFR/Src/Stat5b signaling pathway and enhances PC cell proliferation and (b) stabilizes the androgen receptor (AR) through EGFR/Src -dependent phosphorylation; both of which can be inhibited by SR48692. Activation of the EGFR, Src and AR pathway(s) has been implicated, not only in the development of androgen-independent disease, but also in tumor metastasis, especially in bones. Future research, planned for the third and final year of this project, will concentrate on animal studies (completing Task 2 and 3), the role(s) of neuroendocrine cell secretions (Task 1c), and will finalize studies on molecular mechanisms of SR48692 radiosensitizing activity (Task 4). In addition, Cetuximab (C-225/Erbitux, ImClone), a clinically used EGFR inhibitor, will be used to study the role of EGFR in SR-induced radiosensitization. We speculate that inhibitors, such as Cetuximab or Dasatinib (Bristol-Myers-Squibb; a Src family inhibitor), will significantly improve experimental radiotherapy outcome and could establish the basis for future combined treatment therapy in humans. 
 
-sub_title[[56, 706, 424, 725]]
+sub_title[[57, 708, 423, 725]]
 ## KEY RESEARCH ACCOMPLISHMENTS 
 
-text[[84, 734, 942, 907]]
+text[[84, 735, 942, 909]]
 - We have demonstrated that radiosensitizing activity of SR48692 depends on the expression of NTR1 receptor in prostate cells. This establishes the foundation of cancer-specificity of SR48692 radiosensitizing activity.
-- We have demonstrated that radiosensitizing activity of SR48692 is not dependent on androgen receptor (AR) expression levels in prostate cells. However, SR48692 blocks neurotensin-induced AR phosphorylation/stabilization. Therefore, blocking NTR1 receptor could provide additional benefits to anti-tumor therapy.
+- We have demonstrated that radiosensitizing activity of SR48692 is not dependent on androgen receptor (AR) expression levels in prostate cells. However, SR48692 blocks neurotransmitters-induced AR phosphorylation/stabilization. Therefore, blocking NTR1 receptor could provide additional benefits to anti-tumor therapy.
 - We have demonstrated that the radiosensitizing activity of SR48692 is affected by the EGFR receptor levels in prostate cells.
\ No newline at end of file
diff --git a/stage1/sample_00015/raw_response.md b/stage1/sample_00015/raw_response.md
index 6cddf9ee05f8de608e00821abf6d3b08f5784206..612ab3958eb83e7608d1a1d882672e4342b0b5bc 100644
--- a/stage1/sample_00015/raw_response.md
+++ b/stage1/sample_00015/raw_response.md
@@ -1,18 +1,18 @@
 145 (Fig. 6B), which over-express EGFR (Fig. 6C). 
 
-image[[62, 97, 612, 427]]
+image[[58, 96, 610, 430]]
  
 
-image_caption[[660, 93, 914, 235]]
+image_caption[[662, 94, 901, 233]]
 <center>Figure 6. SR48692 radiosensitizes human prostate cancer cells expressing low levels of EGFR (A, PC-3M) but not prostate cancer cells overexpressing EGFR (B, DU-145). (C) Expression of EGFR in normal (RWPE-1) and PC cell lines (LNCaP, C4-2, DU-145, PC-3 and PC-3M).</center> 
 
-text[[55, 446, 940, 666]]
+text[[55, 447, 936, 668]]
 In summary, our data show that SR48692 selectively sensitizes PC cells to ionizing radiation. Our results also show that NT stimulation (a) activates a novel EGFR/Src/Stat5b signaling pathway and enhances PC cell proliferation and (b) stabilizes the androgen receptor (AR) through EGFR/Src -dependent phosphorylation; both of which can be inhibited by SR48692. Activation of the EGFR, Src and AR pathway(s) has been implicated, not only in the development of androgen-independent disease, but also in tumor metastasis, especially in bones. Future research, planned for the third and final year of this project, will concentrate on animal studies (completing Task 2 and 3), the role(s) of neuroendocrine cell secretions (Task 1c), and will finalize studies on molecular mechanisms of SR48692 radiosensitizing activity (Task 4). In addition, Cetuximab (C-225/Erbitux, ImClone), a clinically used EGFR inhibitor, will be used to study the role of EGFR in SR-induced radiosensitization. We speculate that inhibitors, such as Cetuximab or Dasatinib (Bristol-Myers-Squibb; a Src family inhibitor), will significantly improve experimental radiotherapy outcome and could establish the basis for future combined treatment therapy in humans. 
 
-sub_title[[56, 706, 424, 725]]
+sub_title[[57, 708, 423, 725]]
 ## KEY RESEARCH ACCOMPLISHMENTS 
 
-text[[84, 734, 942, 907]]
+text[[84, 735, 942, 909]]
 - We have demonstrated that radiosensitizing activity of SR48692 depends on the expression of NTR1 receptor in prostate cells. This establishes the foundation of cancer-specificity of SR48692 radiosensitizing activity.
-- We have demonstrated that radiosensitizing activity of SR48692 is not dependent on androgen receptor (AR) expression levels in prostate cells. However, SR48692 blocks neurotensin-induced AR phosphorylation/stabilization. Therefore, blocking NTR1 receptor could provide additional benefits to anti-tumor therapy.
+- We have demonstrated that radiosensitizing activity of SR48692 is not dependent on androgen receptor (AR) expression levels in prostate cells. However, SR48692 blocks neurotransmitters-induced AR phosphorylation/stabilization. Therefore, blocking NTR1 receptor could provide additional benefits to anti-tumor therapy.
 - We have demonstrated that the radiosensitizing activity of SR48692 is affected by the EGFR receptor levels in prostate cells.
\ No newline at end of file
diff --git a/stage1/sample_00016/document.md b/stage1/sample_00016/document.md
index 56967d424eb955cc3822f9503b64943f650b9e20..6e67057661b22f49c215eb038faee55e8d15dbf6 100644
--- a/stage1/sample_00016/document.md
+++ b/stage1/sample_00016/document.md
@@ -1,16 +1 @@
-............ 4  
-
-text[[114, 264, 661, 283]]
-Introduction  
-
-text[[113, 310, 660, 329]]
-Body 4  
-
-text[[113, 357, 660, 378]]
-Key Research Accomplishments 7  
-
-text[[113, 405, 660, 425]]
-Reportable Outcomes 8  
-
-text[[113, 454, 660, 473]]
-Conclusion 8
\ No newline at end of file
+1 4 4 7 8 8
\ No newline at end of file
diff --git a/stage1/sample_00016/raw_response.md b/stage1/sample_00016/raw_response.md
index 56967d424eb955cc3822f9503b64943f650b9e20..6e67057661b22f49c215eb038faee55e8d15dbf6 100644
--- a/stage1/sample_00016/raw_response.md
+++ b/stage1/sample_00016/raw_response.md
@@ -1,16 +1 @@
-............ 4  
-
-text[[114, 264, 661, 283]]
-Introduction  
-
-text[[113, 310, 660, 329]]
-Body 4  
-
-text[[113, 357, 660, 378]]
-Key Research Accomplishments 7  
-
-text[[113, 405, 660, 425]]
-Reportable Outcomes 8  
-
-text[[113, 454, 660, 473]]
-Conclusion 8
\ No newline at end of file
+1 4 4 7 8 8
\ No newline at end of file
diff --git a/stage1/sample_00017/document.md b/stage1/sample_00017/document.md
index 585766a80a03cb3f7c4521ec1cf7aca39b110de7..4142d67b9b07a3e1874fe849415154dca6f92753 100644
--- a/stage1/sample_00017/document.md
+++ b/stage1/sample_00017/document.md
@@ -1,28 +1,34 @@
 W81XWH-08-1-0114
 
-text[[115, 209, 801, 240]]
+text[[114, 208, 799, 239]]
 TITLE: Mechanisms of Radiosensitization by the Neurotensin Receptor Antagonist SR48692 in Prostate Cancer Models 
 
-text[[115, 260, 736, 274]]
-PRINCIPAL INVESTIGATOR: Jaroslaw Dziegielewski, Ph.D. 
+text[[115, 259, 737, 273]]
+PRINCIPAL INVESTIGATOR: Jarosław Dziegielewski, Ph.D. 
 
-text[[115, 293, 408, 343]]
-CONTRACTING ORGANIZATION: University of Virginia Charlottesville, VA 22904 
+text[[114, 294, 418, 305]]
+CONTRACTING ORGANIZATION: 
 
-text[[115, 415, 389, 429]]
+text[[115, 310, 379, 324]]
+University of Virginia 
+
+text[[115, 327, 411, 340]]
+Charlottesville, VA 22904 
+
+text[[114, 414, 389, 427]]
 REPORT DATE: April 2010 
 
-text[[115, 484, 376, 498]]
+text[[114, 484, 376, 497]]
 TYPE OF REPORT: Annual 
 
-text[[115, 551, 848, 584]]
+text[[115, 551, 847, 582]]
 PREPARED FOR: U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 
 
-text[[115, 622, 386, 636]]
+text[[114, 621, 386, 635]]
 DISTRIBUTION STATEMENT: 
 
-text[[175, 658, 813, 673]]
+text[[173, 658, 815, 673]]
 - Approved for public release; distribution unlimited 
 
-text[[115, 748, 881, 814]]
+text[[114, 750, 881, 814]]
 The views, opinions and/or findings contained in this report are those of the author(s) and should not be construed as an official Department of the Army position, policy or decision unless so designated by other documentation.
\ No newline at end of file
diff --git a/stage1/sample_00017/raw_response.md b/stage1/sample_00017/raw_response.md
index 585766a80a03cb3f7c4521ec1cf7aca39b110de7..4142d67b9b07a3e1874fe849415154dca6f92753 100644
--- a/stage1/sample_00017/raw_response.md
+++ b/stage1/sample_00017/raw_response.md
@@ -1,28 +1,34 @@
 W81XWH-08-1-0114
 
-text[[115, 209, 801, 240]]
+text[[114, 208, 799, 239]]
 TITLE: Mechanisms of Radiosensitization by the Neurotensin Receptor Antagonist SR48692 in Prostate Cancer Models 
 
-text[[115, 260, 736, 274]]
-PRINCIPAL INVESTIGATOR: Jaroslaw Dziegielewski, Ph.D. 
+text[[115, 259, 737, 273]]
+PRINCIPAL INVESTIGATOR: Jarosław Dziegielewski, Ph.D. 
 
-text[[115, 293, 408, 343]]
-CONTRACTING ORGANIZATION: University of Virginia Charlottesville, VA 22904 
+text[[114, 294, 418, 305]]
+CONTRACTING ORGANIZATION: 
 
-text[[115, 415, 389, 429]]
+text[[115, 310, 379, 324]]
+University of Virginia 
+
+text[[115, 327, 411, 340]]
+Charlottesville, VA 22904 
+
+text[[114, 414, 389, 427]]
 REPORT DATE: April 2010 
 
-text[[115, 484, 376, 498]]
+text[[114, 484, 376, 497]]
 TYPE OF REPORT: Annual 
 
-text[[115, 551, 848, 584]]
+text[[115, 551, 847, 582]]
 PREPARED FOR: U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 
 
-text[[115, 622, 386, 636]]
+text[[114, 621, 386, 635]]
 DISTRIBUTION STATEMENT: 
 
-text[[175, 658, 813, 673]]
+text[[173, 658, 815, 673]]
 - Approved for public release; distribution unlimited 
 
-text[[115, 748, 881, 814]]
+text[[114, 750, 881, 814]]
 The views, opinions and/or findings contained in this report are those of the author(s) and should not be construed as an official Department of the Army position, policy or decision unless so designated by other documentation.
\ No newline at end of file
diff --git a/stage1/sample_00018/document.md b/stage1/sample_00018/document.md
index 0ac045ec3b5ebf02905baba9664533a9f4a5c497..f322de76fe5d9b25da2907c51f01d42eb475e9f9 100644
--- a/stage1/sample_00018/document.md
+++ b/stage1/sample_00018/document.md
@@ -1,22 +1,22 @@
 A basic requirement of this course is that you will participate in all class meetings and conscientiously complete all required course activities and/or assignments. Keep in touch with me if you are unable to attend, participate, or complete an assignment on time. If you miss more than half of the required activities within the first 25% of the course without contacting me, you may be administratively withdrawn from this course. Administrative withdrawal may have academic, financial, and financial aid implications. Administrative withdrawal will take place after the full refund period, and if you are administratively withdrawn from the course you will not be eligible for a tuition refund. If you have questions about the administrative withdrawal policy at any point during the semester, please contact your instructor.  
 
-text[[62, 193, 935, 260]]
+text[[63, 193, 934, 258]]
 LAST WITHDRAW DATE: Last day to withdraw with automatic grade of W is Sunday, October 21, 2018. Requires advisor approval via the late drop/add classes link in One.IU. UCOL students or Engineering/Technology freshmen must see advisor by 5:00PM on the prior Friday. In person transactions must be processed by 5:00P on the prior Friday (October 19, 2018).  
 
-text[[62, 267, 935, 365]]
+text[[63, 266, 934, 364]]
 Beginning October 22, 2018, drops will be approved only in serious, extenuating circumstances and requires the approval of the student's advisor, instructor, Chair or Associate Chair in Mathematics, and the School of Science Dean's Office. If you stop attending class without officially withdrawing by the last withdraw date, your grade will be an F for the course. If you find it necessary to withdraw from the course, we encourage you to first talk to your instructor or to your advisor so that they can assist you in deciding what alternative options best fit your needs. Students should read carefully the withdraw information found on the Registrar's website (registrar.iupui.edu) under the Academic Calendar.  
 
-text[[62, 370, 935, 453]]
-INCOMPLETES: A grade of "Incomplete" (I) will only be given in accordance with the Department of Mathematical Sciences Grade of Incomplete Policy. An incomplete (grade of I) is only allowed for special circumstances: the student must have a passing grade in \(75\%\) of the course work. Specifically, students must be passing at the \(3 / 4\) mark of the session to qualify for assigning an incomplete. The instructor must agree that an incomplete is appropriate and it must be approved by the Associate Chair of the Department of Mathematical Sciences.  
+text[[62, 371, 934, 452]]
+INCOMPLETES: A grade of "Incomplete" (I) will only be given in accordance with the Department of Mathematical Sciences Grade of Incomplete Policy. An incomplete (grade of I) is only allowed for special circumstances: the student must have a passing grade in 75% of the course work. Specifically, students must be passing at the 3/4 mark of the session to qualify for assigning an incomplete. The instructor must agree that an incomplete is appropriate and it must be approved by the Associate Chair of the Department of Mathematical Sciences.  
 
-text[[62, 457, 933, 525]]
+text[[62, 458, 934, 527]]
 IUPUI POLICY ON DISABILITY ACCOMMODATIONS Students needing accommodations because of disability will need to register with Adaptive Educational Services (AES) and complete the appropriate forms issued by AES before accommodations will be given. The AES office is located in Taylor Hall, UC 100. You can also reach the office by calling 317- 274- 3241.  
 
-text[[62, 531, 934, 634]]
+text[[62, 533, 934, 633]]
 IUPUI POLICY ON RELIGIOUS HOLIDAYS IUPUI respects the right of all students to observe their religious holidays and will make reasonable accommodation, upon request, for such observances. Students seeking accommodation for religious observances MUST submit a request in writing to the course instructor by the end of the second week of the semester and should use the Request for Course Accommodation Due to Religious Observance Form. More information on the IUPUI Policy on Religious Holidays is available here: registrar.iupui.edu/religious.html. Failure to comply with the university policy will result in no accommodations given later in the semester.  
 
-text[[62, 639, 934, 786]]
-IUPUI POLICY ON ACADEMIC INTEGRITY: The IU Code of Student Rights, Responsibilities, and Conduct states that students must uphold and maintain academic and professional honesty and integrity; the code defines academic misconduct as any activity that tends to undermine the academic integrity of the institution. Students engaging in academic misconduct may therefore receive penalties from their course instructor and disciplinary action from the university. Policies against academic misconduct apply to all course-, department-, school-, and university- related activities. Academic misconduct may involve human, hard- copy, or electronic resources and includes but is not limited to the following: cheating, fabrication, plagiarism, interference, violation of course rules, and facilitating academic dishonesty. For definitions of these activities, visit studentcode.iu.edu/responsibilities/academic- misconduct.html. Additional information about the rights and responsibilities of IU students is available at studentcode.iu.edu/.  
+text[[62, 639, 934, 785]]
+IUPUI POLICY ON ACADEMIC INTEGRITY: The IU Code of Student Rights, Responsibilities, and Conduct states that students must uphold and maintain academic and professional honesty and integrity; the code defines academic misconduct as any activity that tends to undermine the academic integrity of the institution. Students engaging in academic misconduct may therefore receive penalties from their course instructor and disciplinary action from the university. Policies against academic misconduct apply to all course- , department- , school- , and university- related activities. Academic misconduct may involve human, hard- copy, or electronic resources and includes but is not limited to the following: cheating, fabrication, plagiarism, interference, violation of course rules, and facilitating academic dishonesty. For definitions of these activities, visit studentcode.i. edu/responsibilities/academic- misconduct.html. Additional information about the rights and responsibilities of IU students is available at studentcode.i. edu/.  
 
-text[[62, 791, 935, 891]]
+text[[62, 791, 934, 890]]
 STUDENT ENGAGEMENT ROSTER: This semester your instructor will be using the Student Engagement Roster (SER) to provide real- time feedback on your performance in this course. Periodically throughout the semester the instructor will be entering data on factors such as your class attendance, participation, and success with coursework, among other things. This information will provide feedback on how you are faring in the course and offer you suggestions on how you might be able to improve your performance. Students can view their submitted SER data through the One.IU tile, Student Engagement Roster (Student).
\ No newline at end of file
diff --git a/stage1/sample_00018/raw_response.md b/stage1/sample_00018/raw_response.md
index 0ac045ec3b5ebf02905baba9664533a9f4a5c497..f322de76fe5d9b25da2907c51f01d42eb475e9f9 100644
--- a/stage1/sample_00018/raw_response.md
+++ b/stage1/sample_00018/raw_response.md
@@ -1,22 +1,22 @@
 A basic requirement of this course is that you will participate in all class meetings and conscientiously complete all required course activities and/or assignments. Keep in touch with me if you are unable to attend, participate, or complete an assignment on time. If you miss more than half of the required activities within the first 25% of the course without contacting me, you may be administratively withdrawn from this course. Administrative withdrawal may have academic, financial, and financial aid implications. Administrative withdrawal will take place after the full refund period, and if you are administratively withdrawn from the course you will not be eligible for a tuition refund. If you have questions about the administrative withdrawal policy at any point during the semester, please contact your instructor.  
 
-text[[62, 193, 935, 260]]
+text[[63, 193, 934, 258]]
 LAST WITHDRAW DATE: Last day to withdraw with automatic grade of W is Sunday, October 21, 2018. Requires advisor approval via the late drop/add classes link in One.IU. UCOL students or Engineering/Technology freshmen must see advisor by 5:00PM on the prior Friday. In person transactions must be processed by 5:00P on the prior Friday (October 19, 2018).  
 
-text[[62, 267, 935, 365]]
+text[[63, 266, 934, 364]]
 Beginning October 22, 2018, drops will be approved only in serious, extenuating circumstances and requires the approval of the student's advisor, instructor, Chair or Associate Chair in Mathematics, and the School of Science Dean's Office. If you stop attending class without officially withdrawing by the last withdraw date, your grade will be an F for the course. If you find it necessary to withdraw from the course, we encourage you to first talk to your instructor or to your advisor so that they can assist you in deciding what alternative options best fit your needs. Students should read carefully the withdraw information found on the Registrar's website (registrar.iupui.edu) under the Academic Calendar.  
 
-text[[62, 370, 935, 453]]
-INCOMPLETES: A grade of "Incomplete" (I) will only be given in accordance with the Department of Mathematical Sciences Grade of Incomplete Policy. An incomplete (grade of I) is only allowed for special circumstances: the student must have a passing grade in \(75\%\) of the course work. Specifically, students must be passing at the \(3 / 4\) mark of the session to qualify for assigning an incomplete. The instructor must agree that an incomplete is appropriate and it must be approved by the Associate Chair of the Department of Mathematical Sciences.  
+text[[62, 371, 934, 452]]
+INCOMPLETES: A grade of "Incomplete" (I) will only be given in accordance with the Department of Mathematical Sciences Grade of Incomplete Policy. An incomplete (grade of I) is only allowed for special circumstances: the student must have a passing grade in 75% of the course work. Specifically, students must be passing at the 3/4 mark of the session to qualify for assigning an incomplete. The instructor must agree that an incomplete is appropriate and it must be approved by the Associate Chair of the Department of Mathematical Sciences.  
 
-text[[62, 457, 933, 525]]
+text[[62, 458, 934, 527]]
 IUPUI POLICY ON DISABILITY ACCOMMODATIONS Students needing accommodations because of disability will need to register with Adaptive Educational Services (AES) and complete the appropriate forms issued by AES before accommodations will be given. The AES office is located in Taylor Hall, UC 100. You can also reach the office by calling 317- 274- 3241.  
 
-text[[62, 531, 934, 634]]
+text[[62, 533, 934, 633]]
 IUPUI POLICY ON RELIGIOUS HOLIDAYS IUPUI respects the right of all students to observe their religious holidays and will make reasonable accommodation, upon request, for such observances. Students seeking accommodation for religious observances MUST submit a request in writing to the course instructor by the end of the second week of the semester and should use the Request for Course Accommodation Due to Religious Observance Form. More information on the IUPUI Policy on Religious Holidays is available here: registrar.iupui.edu/religious.html. Failure to comply with the university policy will result in no accommodations given later in the semester.  
 
-text[[62, 639, 934, 786]]
-IUPUI POLICY ON ACADEMIC INTEGRITY: The IU Code of Student Rights, Responsibilities, and Conduct states that students must uphold and maintain academic and professional honesty and integrity; the code defines academic misconduct as any activity that tends to undermine the academic integrity of the institution. Students engaging in academic misconduct may therefore receive penalties from their course instructor and disciplinary action from the university. Policies against academic misconduct apply to all course-, department-, school-, and university- related activities. Academic misconduct may involve human, hard- copy, or electronic resources and includes but is not limited to the following: cheating, fabrication, plagiarism, interference, violation of course rules, and facilitating academic dishonesty. For definitions of these activities, visit studentcode.iu.edu/responsibilities/academic- misconduct.html. Additional information about the rights and responsibilities of IU students is available at studentcode.iu.edu/.  
+text[[62, 639, 934, 785]]
+IUPUI POLICY ON ACADEMIC INTEGRITY: The IU Code of Student Rights, Responsibilities, and Conduct states that students must uphold and maintain academic and professional honesty and integrity; the code defines academic misconduct as any activity that tends to undermine the academic integrity of the institution. Students engaging in academic misconduct may therefore receive penalties from their course instructor and disciplinary action from the university. Policies against academic misconduct apply to all course- , department- , school- , and university- related activities. Academic misconduct may involve human, hard- copy, or electronic resources and includes but is not limited to the following: cheating, fabrication, plagiarism, interference, violation of course rules, and facilitating academic dishonesty. For definitions of these activities, visit studentcode.i. edu/responsibilities/academic- misconduct.html. Additional information about the rights and responsibilities of IU students is available at studentcode.i. edu/.  
 
-text[[62, 791, 935, 891]]
+text[[62, 791, 934, 890]]
 STUDENT ENGAGEMENT ROSTER: This semester your instructor will be using the Student Engagement Roster (SER) to provide real- time feedback on your performance in this course. Periodically throughout the semester the instructor will be entering data on factors such as your class attendance, participation, and success with coursework, among other things. This information will provide feedback on how you are faring in the course and offer you suggestions on how you might be able to improve your performance. Students can view their submitted SER data through the One.IU tile, Student Engagement Roster (Student).
\ No newline at end of file
diff --git a/stage1/sample_00019/document.md b/stage1/sample_00019/document.md
index a45d229a0df332924a9c5352deee19c73a20cc79..cff114e87068d5453d0126141fc6e94b0d761db5 100644
--- a/stage1/sample_00019/document.md
+++ b/stage1/sample_00019/document.md
@@ -1,43 +1,33 @@
-15400 Trigonometric Fall 2018 Course Policy
+5540, **See instructor for section-specific course materials**** 5540, OFFICE PHONE: 5540, OFFICE HOURS: 
 
-text[[267, 88, 729, 104]]
-**See instructor for section-specific course materials**
+text[[62, 154, 203, 168]]
+OFFICE: 
 
-text[[62, 117, 203, 133]]
-**INSTRUCTOR:**
+text[[61, 171, 145, 185]]
+E-MAIL: 
 
-text[[62, 137, 146, 154]]
-**OFFICE:**
+text[[59, 178, 939, 268]]
+A working knowledge of the concepts of college algebra and trigonometry is essential for all parts of science, engineering, and technology. Many other courses, (e.g. business, economics, health sciences, and more), will require you to apply the mathematical tools you learn in your college algebra and trigonometry courses, so keep in mind that success in future courses may depend heavily on your ability to apply the material from MATH 15400. 
 
-text[[62, 156, 146, 170]]
-**E-MAIL:**
+text[[59, 277, 934, 343]]
+OFFICIAL IUPUI COURSE DESCRIPTION: MATH 15400 Trigonometry (3 cr.) P: MATH 15300 (with a minimum grade of C). MATH 15300-15400 is a two-semester version of MATH 15900. Not open to students with credit in MATH 15900. This course covers college-level trigonometry and, together with MATH 15300, provides preparation for MATH 16500, MATH 22100, and MATH 23100. 
 
-text[[59, 183, 933, 267]]
-**A working knowledge of the concepts of college algebra and trigonometry is essential for all parts of science, engineering, and technology. Many other courses, (e.g. business, economics, health sciences, and more), will require you to apply the mathematical tools you learn in your college algebra and trigonometry courses, so keep in mind that success in future courses may depend heavily on your ability to apply the material from MATH 15400.**
+text[[59, 357, 934, 438]]
+**MORE ON PREREQUISITES:** It is assumed that you have recently mastered the material of MATH 15300 (College Algebra) with a grade of C or better within the last year. If this is not the case then you should talk to your instructor as soon as possible to decide if this is the correct class for you. The main reason people have difficulty with MATH 15400 is because of insufficient background. Again, if you are not sure if this is the right class for you, talk to your instructor early. It is not difficult to determine which class you should be in. 
 
-text[[62, 280, 933, 344]]
-**OFFICIAL** **IUPUI** **COURSE** **DESCRIPTION:** **MATH** **15400** **Trigonometry (3 cr.)** P: MATH 15300 (with a minimum grade of C). MATH 15300-15400 is a two-semester version of MATH 15900. Not open to students with credit in MATH 15900. This course covers college-level trigonometry and, together with MATH 15300, provides preparation for MATH 16500, MATH 22100, and MATH 23100.
+text[[59, 452, 934, 535]]
+**TEXTBOOK:** The correct textbook for all sections of MATH 15400 is, Algebra and Trigonometry with Analytic Geometry, Classic 12th Edition, by Swokowski and Cole, with Enhanced WebAssign Access Card, ISBN: 9781305525849, Loose-leaf 3-ring textbook, Cengage Publisher. There are over a dozen different editions and formats of this textbook so it is important that you get the correct one. The required textbook may be purchased at the IUPUI Barnes & Noble Bookstore. 
 
-text[[62, 359, 933, 438]]
-**MORE** **ON** **PREREQUISITES:** It is assumed that you have recently mastered the material of MATH 15300 (College Algebra) with a grade of C or better within the last year. If this is not the case then you should talk to your instructor as soon as possible to decide if this is the correct class for you. The main reason people have difficulty with MATH 15400 is because of insufficient background. Again, if you are not sure if this is the right class for you, talk to your instructor early. It is not difficult to determine which class you should be in.
+sub_title[[59, 550, 743, 565]]
+## IUPUI DEPARTMENT OF MATHEMATICAL SCIENCES CALCULATOR POLICY: 
 
-text[[62, 455, 933, 535]]
-**TEXTBOOK:** The correct textbook for all sections of MATH 15400 is, Algebra and Trigonometry with Analytic Geometry, Classic 12th Edition, by Swokowski and Cole, with Enhanced WebAssign Access Card, ISBN: 9781305525849, Loose-leaf 3-ring textbook, Cengage Publisher. There are over a dozen different editions and formats of this textbook so it is important that you get the correct one. The required textbook may be purchased at the IUPUI Barnes & Noble Bookstore.
+text[[28, 565, 933, 679]]
+- In all developmental and introductory courses at IUPUI numbered below MATH 16500, the only technology that can be used on in-class, closed-book assessments (quizzes, tests, final exam) is the Texas Instruments TI-30XA scientific calculator.
+- In all calculus and calculus-related courses at IUPUI with numbers MATH 16500 or above, no calculators or other forms of technology can be used on in-class, closed-book assessments (quizzes, tests, final).
+- For math/stat courses with numbers above MATH 26600, it is up to the instructor's discretion as to what forms of technology may be used on in-class, closed-book assessments. 
 
-title[[62, 552, 745, 566]]
-# IUPUI DEPARTMENT OF MATHEMATICAL SCIENCES CALCULATOR POLICY:
+text[[59, 695, 934, 762]]
+**MORE ON CALCULATOR POLICY:** The TI-30XA is the only calculator allowed on quizzes and exams. No other calculator is allowed in the classroom. It does not matter what you were allowed to use in your previous math course. Bring your TI-30XA scientific calculator with you to every class period. The calculator slide cover must be removed and put away when taking an exam or quiz. 
 
-text[[35, 568, 933, 613]]
-·In all developmental and introductory courses at IUPUI numbered below MATH 16500, the only technology that can be used on in-class, closed-book assessments (quizzes, tests, final exam) is the Texas Instruments TI-30XA scientific calculator.
-
-text[[35, 616, 892, 646]]
-·In all calculus and calculus-related courses at IUPUI with numbers MATH 16500 or above, no calculators or other forms of technology can be used on in-class, closed-books assessments (quizzes, tests, final)
-
-text[[35, 649, 887, 679]]
-·For math/stat courses with numbers above MATH 26600, it is up to the instructor's discretion as to what forms of technology may be used on in-class, closed-book assessments.
-
-text[[62, 700, 933, 763]]
-**MORE ON** **CALCULATOR** **POLICY:** The TI-30XA is the only calculator allowed on quizzes and exams. No other calculator is allowed in the classroom. It does not matter what you were allowed to use in your previous math course. Bring your TI-30XA scientific calculator with you to every class period. The calculator slide cover must be removed and put away when taking an exam or quiz.
-
-text[[62, 780, 933, 841]]
+text[[59, 777, 934, 843]]
 **ATTENDANCE:** Attendance is required of all students without exception. A student absent from class bears full responsibility for all material covered in class. Quizzes will be given at the beginning of class, so please be on time. If you anticipate having to leave class early, please let your instructor know before the beginning of class. Regular attendance is crucial for success in this course.
\ No newline at end of file
diff --git a/stage1/sample_00019/raw_response.md b/stage1/sample_00019/raw_response.md
index a45d229a0df332924a9c5352deee19c73a20cc79..cff114e87068d5453d0126141fc6e94b0d761db5 100644
--- a/stage1/sample_00019/raw_response.md
+++ b/stage1/sample_00019/raw_response.md
@@ -1,43 +1,33 @@
-15400 Trigonometric Fall 2018 Course Policy
+5540, **See instructor for section-specific course materials**** 5540, OFFICE PHONE: 5540, OFFICE HOURS: 
 
-text[[267, 88, 729, 104]]
-**See instructor for section-specific course materials**
+text[[62, 154, 203, 168]]
+OFFICE: 
 
-text[[62, 117, 203, 133]]
-**INSTRUCTOR:**
+text[[61, 171, 145, 185]]
+E-MAIL: 
 
-text[[62, 137, 146, 154]]
-**OFFICE:**
+text[[59, 178, 939, 268]]
+A working knowledge of the concepts of college algebra and trigonometry is essential for all parts of science, engineering, and technology. Many other courses, (e.g. business, economics, health sciences, and more), will require you to apply the mathematical tools you learn in your college algebra and trigonometry courses, so keep in mind that success in future courses may depend heavily on your ability to apply the material from MATH 15400. 
 
-text[[62, 156, 146, 170]]
-**E-MAIL:**
+text[[59, 277, 934, 343]]
+OFFICIAL IUPUI COURSE DESCRIPTION: MATH 15400 Trigonometry (3 cr.) P: MATH 15300 (with a minimum grade of C). MATH 15300-15400 is a two-semester version of MATH 15900. Not open to students with credit in MATH 15900. This course covers college-level trigonometry and, together with MATH 15300, provides preparation for MATH 16500, MATH 22100, and MATH 23100. 
 
-text[[59, 183, 933, 267]]
-**A working knowledge of the concepts of college algebra and trigonometry is essential for all parts of science, engineering, and technology. Many other courses, (e.g. business, economics, health sciences, and more), will require you to apply the mathematical tools you learn in your college algebra and trigonometry courses, so keep in mind that success in future courses may depend heavily on your ability to apply the material from MATH 15400.**
+text[[59, 357, 934, 438]]
+**MORE ON PREREQUISITES:** It is assumed that you have recently mastered the material of MATH 15300 (College Algebra) with a grade of C or better within the last year. If this is not the case then you should talk to your instructor as soon as possible to decide if this is the correct class for you. The main reason people have difficulty with MATH 15400 is because of insufficient background. Again, if you are not sure if this is the right class for you, talk to your instructor early. It is not difficult to determine which class you should be in. 
 
-text[[62, 280, 933, 344]]
-**OFFICIAL** **IUPUI** **COURSE** **DESCRIPTION:** **MATH** **15400** **Trigonometry (3 cr.)** P: MATH 15300 (with a minimum grade of C). MATH 15300-15400 is a two-semester version of MATH 15900. Not open to students with credit in MATH 15900. This course covers college-level trigonometry and, together with MATH 15300, provides preparation for MATH 16500, MATH 22100, and MATH 23100.
+text[[59, 452, 934, 535]]
+**TEXTBOOK:** The correct textbook for all sections of MATH 15400 is, Algebra and Trigonometry with Analytic Geometry, Classic 12th Edition, by Swokowski and Cole, with Enhanced WebAssign Access Card, ISBN: 9781305525849, Loose-leaf 3-ring textbook, Cengage Publisher. There are over a dozen different editions and formats of this textbook so it is important that you get the correct one. The required textbook may be purchased at the IUPUI Barnes & Noble Bookstore. 
 
-text[[62, 359, 933, 438]]
-**MORE** **ON** **PREREQUISITES:** It is assumed that you have recently mastered the material of MATH 15300 (College Algebra) with a grade of C or better within the last year. If this is not the case then you should talk to your instructor as soon as possible to decide if this is the correct class for you. The main reason people have difficulty with MATH 15400 is because of insufficient background. Again, if you are not sure if this is the right class for you, talk to your instructor early. It is not difficult to determine which class you should be in.
+sub_title[[59, 550, 743, 565]]
+## IUPUI DEPARTMENT OF MATHEMATICAL SCIENCES CALCULATOR POLICY: 
 
-text[[62, 455, 933, 535]]
-**TEXTBOOK:** The correct textbook for all sections of MATH 15400 is, Algebra and Trigonometry with Analytic Geometry, Classic 12th Edition, by Swokowski and Cole, with Enhanced WebAssign Access Card, ISBN: 9781305525849, Loose-leaf 3-ring textbook, Cengage Publisher. There are over a dozen different editions and formats of this textbook so it is important that you get the correct one. The required textbook may be purchased at the IUPUI Barnes & Noble Bookstore.
+text[[28, 565, 933, 679]]
+- In all developmental and introductory courses at IUPUI numbered below MATH 16500, the only technology that can be used on in-class, closed-book assessments (quizzes, tests, final exam) is the Texas Instruments TI-30XA scientific calculator.
+- In all calculus and calculus-related courses at IUPUI with numbers MATH 16500 or above, no calculators or other forms of technology can be used on in-class, closed-book assessments (quizzes, tests, final).
+- For math/stat courses with numbers above MATH 26600, it is up to the instructor's discretion as to what forms of technology may be used on in-class, closed-book assessments. 
 
-title[[62, 552, 745, 566]]
-# IUPUI DEPARTMENT OF MATHEMATICAL SCIENCES CALCULATOR POLICY:
+text[[59, 695, 934, 762]]
+**MORE ON CALCULATOR POLICY:** The TI-30XA is the only calculator allowed on quizzes and exams. No other calculator is allowed in the classroom. It does not matter what you were allowed to use in your previous math course. Bring your TI-30XA scientific calculator with you to every class period. The calculator slide cover must be removed and put away when taking an exam or quiz. 
 
-text[[35, 568, 933, 613]]
-·In all developmental and introductory courses at IUPUI numbered below MATH 16500, the only technology that can be used on in-class, closed-book assessments (quizzes, tests, final exam) is the Texas Instruments TI-30XA scientific calculator.
-
-text[[35, 616, 892, 646]]
-·In all calculus and calculus-related courses at IUPUI with numbers MATH 16500 or above, no calculators or other forms of technology can be used on in-class, closed-books assessments (quizzes, tests, final)
-
-text[[35, 649, 887, 679]]
-·For math/stat courses with numbers above MATH 26600, it is up to the instructor's discretion as to what forms of technology may be used on in-class, closed-book assessments.
-
-text[[62, 700, 933, 763]]
-**MORE ON** **CALCULATOR** **POLICY:** The TI-30XA is the only calculator allowed on quizzes and exams. No other calculator is allowed in the classroom. It does not matter what you were allowed to use in your previous math course. Bring your TI-30XA scientific calculator with you to every class period. The calculator slide cover must be removed and put away when taking an exam or quiz.
-
-text[[62, 780, 933, 841]]
+text[[59, 777, 934, 843]]
 **ATTENDANCE:** Attendance is required of all students without exception. A student absent from class bears full responsibility for all material covered in class. Quizzes will be given at the beginning of class, so please be on time. If you anticipate having to leave class early, please let your instructor know before the beginning of class. Regular attendance is crucial for success in this course.
\ No newline at end of file
diff --git a/stage1/sample_00020/document.md b/stage1/sample_00020/document.md
index df1f8f59dd1707bd125e15119514eb1e8c4550b2..1ac16653e5b3f8e839553721588dc207f925c463 100644
--- a/stage1/sample_00020/document.md
+++ b/stage1/sample_00020/document.md
@@ -1,23 +1,28 @@
-7, 2018, from 6:00P-8:00P. The location will be announced later. The final exam is a departmental comprehensive exam. It will be worth 200 points, i.e., it will be weighted the same as two in-class exams. Be sure that you do not have a conflict (work, personal, or class) with the time and date of the common departmental final exam. No make-ups will be given except for the following documented situations: 1) IUPUI sponsored event, for example athletic competition, 2) Military training or deployment, and 3) Jury duty. Documentation must be provided in advance. More information about the common departmental final exam (practice problems, practice finals, etc.) can be found on the Mathematics Department's course web pages (math.iupui.edu/math/undergraduate/courses). The IUPUI departmental final exam schedule can be found at: registrar.iupui.edu/acacl.html.  
+The common departmental final exam will be on Friday, December 7, 2018, from 6:00P-8:00P. The location will be announced later. The final exam is a departmental comprehensive exam. It will be worth 200 points, i.e., it will be weighted the same as two in-class exams. **Be sure that you do not have a conflict (work, personal, or class) with the time and date of the common departmental final exam.** No make-ups will be given except for the following documented situations: 1) IUPUI sponsored event, for example athletic competition, 2) Military training or deployment, and 3) Jury duty. Documentation must be provided in advance. More information about the common departmental final exam (practice problems, practice finals, etc.) can be found on the Mathematics Department’s course web pages (math.iupui.edu/math/undergraduate/courses). The IUPUI departmental final exam schedule can be found at: registrar.iupui.edu/accal.html.  
 
-text[[64, 217, 934, 266]]
+text[[63, 215, 933, 266]]
 REMINDER: To receive credit for quiz and exam problems you must show all your work. Check your answers carefully before submitting your quiz/exam. Problems involving units must have the units represented on the answer to receive full credit. Keep all returned graded quizzes and exams until after you receive your final course grade.  
 
-text[[63, 281, 935, 392]]
+text[[63, 280, 935, 392]]
 GRADING: To perform well in this course you must not only understand the mathematical concepts, you must be able to use them correctly in solving problems. Accurate computations go together with understanding the method. MATH 15300- 15400 is a prerequisite for MATH 16500- 16600, Analytic Geometry and Calculus I & II, MATH 17100, Multidimensional Mathematics, MATH 22100- 22200, Calculus for Technology I & II, MATH 23100- 23200, Calculus for Life Sciences I & II and all physics courses. It is important to get into the habit (the earlier the better) of checking your work before submitting it to be evaluated by someone else. You will find this habit to be very valuable in your later courses.  
 
-text[[63, 407, 933, 441]]
-GRADES: Y our letter grade for the course will be determined from your total scores which will be computed as follows. Exam scores and/or the final course grades may be adjusted.  
+text[[65, 407, 933, 440]]
+GRADES: Your letter grade for the course will be determined from your total scores which will be computed as follows. Exam scores and/or the final course grades may be adjusted.  
 
-table[[94, 455, 665, 550]]
+text[[91, 456, 339, 541]]
+TOTAL POSSIBLE POINTS Best 3 out of 4 in- class exams 300 Quizzes 100 Final exam 200 Total 600  
 
-<table><td colspan="2">TOTAL POSSIBLE POINTSGRADESBest 3 out of 4 in-class exams300540-600A&#x27;sQuizzes100480-539B&#x27;sFinal exam200420-479C&#x27;sTotal600360-419D&#x27;s0 - 359F</table>  
+text[[532, 456, 662, 556]]
+GRADES 540- 600 480- 539 420- 479 360- 419 0 - 359 F  
 
-text[[64, 553, 570, 570]]
+text[[63, 551, 570, 569]]
 Pluses and minuses will be awarded on the final grades as follows:  
 
-text[[120, 570, 406, 650]]
-90- 92% A-, 93- 96% A, 97% and above A+ 80- 82% B-, 83- 86% B, 87- 89% B+ 70- 72% C-, 73- 76% C, 77- 79% C+ 60- 62% D-, 63- 66% D, 67- 69% D+ 0- 59% F  
+text[[100, 568, 420, 647]]
+\(90–92\%\) A-, \(93 - 96\%\) A, \(97\%\) and above \(A +\) \(80 - 82\%\) B- , \(83 - 86\%\) B, \(87 - 89\%\) B+ \(70–72\%\) C-, \(73 - 76\%\) C, \(77 - 79\%\) C+ \(60 - 62\%\) D-, \(63 - 66\%\) D, \(67 - 69\%\) D+ \(0–59\%\) F  
 
-text[[63, 665, 936, 795]]
-IUPUI CAMPUS- WIDE POLICIES: Students are expected to read carefully the IUPUI policies concerning attendance, academics, and conduct. Students are expected read the university policies within the few days of classes as some policies have early deadlines. Information on university campus- wide course policies related to attendance (Aadministrative Withdrawal, Disabilities, Emergency Withdrawal, Military Service, Religious Holidays), academic policies (Auditing a class, Final Exam Scheduling, Grade Replacement, Grade Forgiveness, and Pass/Fail Option), and conduct (Academic Integrity, Academic Misconduct, and Code of Conduct) and related policies can be accessed in Canvas under the “Syllabus Supplement”, “Campus Course Policies” and “IUPUI Academic and Student Support Services” links.
\ No newline at end of file
+text[[63, 665, 934, 796]]
+IUPUI CAMPUS- WIDE POLICES: Students are expected to read carefully the IUPUI policies concerning attendance, academics, and conduct. Students are expected read the university policies within the few days of classes as some policies have early deadlines. Information on university campus- wide course policies related to attendance (Aadministrative Withdrawal, Disabilities, Emergency Withdrawal, Military Service, Religious Holidays), academic policies (Auditing a class, Final Exam Scheduling, Grade Replacement, Grade Forgiveness, and Pass/Fail Option), and conduct (Academic Integrity, Academic Misconduct, and Code of Conduct) and related policies can be accessed in Canvas under the "Syllabus Supplement", "Campus Course Policies" and "IUPUI Academic and Student Support Services" links.  
+
+text[[63, 931, 177, 960]]
+Instructor Class Number(s)
\ No newline at end of file
diff --git a/stage1/sample_00020/raw_response.md b/stage1/sample_00020/raw_response.md
index df1f8f59dd1707bd125e15119514eb1e8c4550b2..1ac16653e5b3f8e839553721588dc207f925c463 100644
--- a/stage1/sample_00020/raw_response.md
+++ b/stage1/sample_00020/raw_response.md
@@ -1,23 +1,28 @@
-7, 2018, from 6:00P-8:00P. The location will be announced later. The final exam is a departmental comprehensive exam. It will be worth 200 points, i.e., it will be weighted the same as two in-class exams. Be sure that you do not have a conflict (work, personal, or class) with the time and date of the common departmental final exam. No make-ups will be given except for the following documented situations: 1) IUPUI sponsored event, for example athletic competition, 2) Military training or deployment, and 3) Jury duty. Documentation must be provided in advance. More information about the common departmental final exam (practice problems, practice finals, etc.) can be found on the Mathematics Department's course web pages (math.iupui.edu/math/undergraduate/courses). The IUPUI departmental final exam schedule can be found at: registrar.iupui.edu/acacl.html.  
+The common departmental final exam will be on Friday, December 7, 2018, from 6:00P-8:00P. The location will be announced later. The final exam is a departmental comprehensive exam. It will be worth 200 points, i.e., it will be weighted the same as two in-class exams. **Be sure that you do not have a conflict (work, personal, or class) with the time and date of the common departmental final exam.** No make-ups will be given except for the following documented situations: 1) IUPUI sponsored event, for example athletic competition, 2) Military training or deployment, and 3) Jury duty. Documentation must be provided in advance. More information about the common departmental final exam (practice problems, practice finals, etc.) can be found on the Mathematics Department’s course web pages (math.iupui.edu/math/undergraduate/courses). The IUPUI departmental final exam schedule can be found at: registrar.iupui.edu/accal.html.  
 
-text[[64, 217, 934, 266]]
+text[[63, 215, 933, 266]]
 REMINDER: To receive credit for quiz and exam problems you must show all your work. Check your answers carefully before submitting your quiz/exam. Problems involving units must have the units represented on the answer to receive full credit. Keep all returned graded quizzes and exams until after you receive your final course grade.  
 
-text[[63, 281, 935, 392]]
+text[[63, 280, 935, 392]]
 GRADING: To perform well in this course you must not only understand the mathematical concepts, you must be able to use them correctly in solving problems. Accurate computations go together with understanding the method. MATH 15300- 15400 is a prerequisite for MATH 16500- 16600, Analytic Geometry and Calculus I & II, MATH 17100, Multidimensional Mathematics, MATH 22100- 22200, Calculus for Technology I & II, MATH 23100- 23200, Calculus for Life Sciences I & II and all physics courses. It is important to get into the habit (the earlier the better) of checking your work before submitting it to be evaluated by someone else. You will find this habit to be very valuable in your later courses.  
 
-text[[63, 407, 933, 441]]
-GRADES: Y our letter grade for the course will be determined from your total scores which will be computed as follows. Exam scores and/or the final course grades may be adjusted.  
+text[[65, 407, 933, 440]]
+GRADES: Your letter grade for the course will be determined from your total scores which will be computed as follows. Exam scores and/or the final course grades may be adjusted.  
 
-table[[94, 455, 665, 550]]
+text[[91, 456, 339, 541]]
+TOTAL POSSIBLE POINTS Best 3 out of 4 in- class exams 300 Quizzes 100 Final exam 200 Total 600  
 
-<table><td colspan="2">TOTAL POSSIBLE POINTSGRADESBest 3 out of 4 in-class exams300540-600A&#x27;sQuizzes100480-539B&#x27;sFinal exam200420-479C&#x27;sTotal600360-419D&#x27;s0 - 359F</table>  
+text[[532, 456, 662, 556]]
+GRADES 540- 600 480- 539 420- 479 360- 419 0 - 359 F  
 
-text[[64, 553, 570, 570]]
+text[[63, 551, 570, 569]]
 Pluses and minuses will be awarded on the final grades as follows:  
 
-text[[120, 570, 406, 650]]
-90- 92% A-, 93- 96% A, 97% and above A+ 80- 82% B-, 83- 86% B, 87- 89% B+ 70- 72% C-, 73- 76% C, 77- 79% C+ 60- 62% D-, 63- 66% D, 67- 69% D+ 0- 59% F  
+text[[100, 568, 420, 647]]
+\(90–92\%\) A-, \(93 - 96\%\) A, \(97\%\) and above \(A +\) \(80 - 82\%\) B- , \(83 - 86\%\) B, \(87 - 89\%\) B+ \(70–72\%\) C-, \(73 - 76\%\) C, \(77 - 79\%\) C+ \(60 - 62\%\) D-, \(63 - 66\%\) D, \(67 - 69\%\) D+ \(0–59\%\) F  
 
-text[[63, 665, 936, 795]]
-IUPUI CAMPUS- WIDE POLICIES: Students are expected to read carefully the IUPUI policies concerning attendance, academics, and conduct. Students are expected read the university policies within the few days of classes as some policies have early deadlines. Information on university campus- wide course policies related to attendance (Aadministrative Withdrawal, Disabilities, Emergency Withdrawal, Military Service, Religious Holidays), academic policies (Auditing a class, Final Exam Scheduling, Grade Replacement, Grade Forgiveness, and Pass/Fail Option), and conduct (Academic Integrity, Academic Misconduct, and Code of Conduct) and related policies can be accessed in Canvas under the “Syllabus Supplement”, “Campus Course Policies” and “IUPUI Academic and Student Support Services” links.
\ No newline at end of file
+text[[63, 665, 934, 796]]
+IUPUI CAMPUS- WIDE POLICES: Students are expected to read carefully the IUPUI policies concerning attendance, academics, and conduct. Students are expected read the university policies within the few days of classes as some policies have early deadlines. Information on university campus- wide course policies related to attendance (Aadministrative Withdrawal, Disabilities, Emergency Withdrawal, Military Service, Religious Holidays), academic policies (Auditing a class, Final Exam Scheduling, Grade Replacement, Grade Forgiveness, and Pass/Fail Option), and conduct (Academic Integrity, Academic Misconduct, and Code of Conduct) and related policies can be accessed in Canvas under the "Syllabus Supplement", "Campus Course Policies" and "IUPUI Academic and Student Support Services" links.  
+
+text[[63, 931, 177, 960]]
+Instructor Class Number(s)
\ No newline at end of file
diff --git a/stage1/sample_00021/document.md b/stage1/sample_00021/document.md
index 10ee0bb8408c139954dd8eabcccac83206fb6644..4b1b7e9810d75f7c09b05fc2603b9c23fb4c23c4 100644
--- a/stage1/sample_00021/document.md
+++ b/stage1/sample_00021/document.md
@@ -1,17 +1,16 @@
-3: Basic infiltration rate (cm/h) after the first, second and third seasons from treatments executed.  
+0-15 15-30 30-60 60-90 0-15 15-30 30-60 60-90 0-15 15-30 30-60 60-90
 
-image[[211, 88, 779, 338]]
-image_caption[[270, 321, 683, 337]]
-<center>Fig (3): Bulk denisty and total porosity as affected by different tillage practices. </center>  
+image[[211, 94, 780, 348]]
 
-sub_title[[210, 357, 362, 371]]
-## Infiltration rate (IR)  
+title[[208, 358, 363, 370]]
+# Infiltration rate (IR)
 
-text[[208, 369, 790, 589]]
-The values of basic infiltration rate (IR) of soil as affected by different treatments are presented in Table (3). Data show that, basic infiltration rate values after each season are increased in the treated soils, where as, the values of basic IR under subsoling and/or moling varied from 0.9 to 1.66 cm/h while, under open drainage they ranged from 0.39 to 0.59 cm/h. This may be due to the subsurface tillage gave the top soil layer a chance to dry and permitted for shrinkage and formation of water passage ways which allowed a rather easier movement of water into mole or subsoil line. Similar results were obtained by Abdel- Mawgoud et al., (2003 and 2006). Basic IR in all seasons is in somewhat higher with subsoll+mole than that with subsoil or mole treatment. Also, no obvious different between basic IR values under both subsoil and mole treatments. Data also clear that, mean values of basic IR are lower after rice crop than after sugar beet crop by 41.81, 35.13, 46.31 and 38.42 % for open drainage, subsoll+open drainage, mole+open drainage and subsoll+mole+open drains, respectively. Basic IR after first season is superior to after the third season from treatments installation.  
+text[[208, 371, 789, 587]]
+The values of basic infiltration rate (IR) of soil as affected by different treatments are presented in Table (3). Data show that, basic infiltration rate values after each season are increased in the treated soils, where as, the values of basic IR under subsoliling and/or moling varied from 0.9 to 1.66 cm/h while, under open drainage they ranged from 0.39 to 0.59 cm/h. This may be due to the subsurface tillage gave the top soil layer a chance to dry and permitted for shrinkage and formation of water passage ways which allowed a rather easier movement of water into mole or subsoil line. Similar results were obtained by Abdel-Mawgoud et al., (2003 and 2006). Basic IR in all seasons is in somewhat higher with subsoil+mole than that with subsoil or mole treatment. Also, no obvious different between basic IR values under both subsoil and mole treatments. Data also clear that, mean values of basic IR are lower after rice crop than after sugar beet crop by 41.81, 35.13, 46.31 and 38.42% for open drainage, subsoil+open drainage, mole+open drainage and subsoil+mole+open drains, respectively. Basic IR after first season is superior to after the third season from treatments installation.
 
-table[[210, 618, 787, 727]]
-table_caption[[208, 592, 787, 621]]
-Table (3): Basic infiltration rate (cm/h) after the first, second and third seasons from treatments executed.   
+table_caption[[208, 593, 789, 618]]
+Table (3): Basic infiltration rate (cm/h) after the first, second and third seasons from treatments executed.
 
-<table><td rowspan="2">Treatments<td colspan="3">First season<td colspan="3">second season<td colspan="3">third season<td colspan="3">MeansRiceSugar beetRiceSugar beetRiceSugar beetRiceSugar beetRiceSugar beetRiceSugar beetOpen drainage0.390.520.390.590.410.580.3970.563Subsoil+open drains1.211.561.051.481.021.391.0931.477Mole + open drains1.111.591.081.510.91.421.0301.507Subsoil+mole+open drains1.221.661.111.551.051.471.1271.56</table>
\ No newline at end of file
+table[[211, 618, 785, 725]]
+
+<table><td rowspan="2">Treatments<td colspan="3">First season<td colspan="3">second season<td colspan="3">third season<td colspan="3">MeansRiceSugar<br>beetRiceSugar<br>beetRiceSugar<br>beetRiceSugar<br>beetRiceSugar<br>beetRiceSugar<br>beetOpen drainage0.390.520.390.590.410.580.3970.563Subsoil+open drains1.211.561.051.481.021.391.0931.477Mole + open drains1.111.591.081.510.91.421.0301.507Subsoil+mole+open<br>drains1.221.661.111.551.051.471.1271.56</table>
\ No newline at end of file
diff --git a/stage1/sample_00021/raw_response.md b/stage1/sample_00021/raw_response.md
index 10ee0bb8408c139954dd8eabcccac83206fb6644..4b1b7e9810d75f7c09b05fc2603b9c23fb4c23c4 100644
--- a/stage1/sample_00021/raw_response.md
+++ b/stage1/sample_00021/raw_response.md
@@ -1,17 +1,16 @@
-3: Basic infiltration rate (cm/h) after the first, second and third seasons from treatments executed.  
+0-15 15-30 30-60 60-90 0-15 15-30 30-60 60-90 0-15 15-30 30-60 60-90
 
-image[[211, 88, 779, 338]]
-image_caption[[270, 321, 683, 337]]
-<center>Fig (3): Bulk denisty and total porosity as affected by different tillage practices. </center>  
+image[[211, 94, 780, 348]]
 
-sub_title[[210, 357, 362, 371]]
-## Infiltration rate (IR)  
+title[[208, 358, 363, 370]]
+# Infiltration rate (IR)
 
-text[[208, 369, 790, 589]]
-The values of basic infiltration rate (IR) of soil as affected by different treatments are presented in Table (3). Data show that, basic infiltration rate values after each season are increased in the treated soils, where as, the values of basic IR under subsoling and/or moling varied from 0.9 to 1.66 cm/h while, under open drainage they ranged from 0.39 to 0.59 cm/h. This may be due to the subsurface tillage gave the top soil layer a chance to dry and permitted for shrinkage and formation of water passage ways which allowed a rather easier movement of water into mole or subsoil line. Similar results were obtained by Abdel- Mawgoud et al., (2003 and 2006). Basic IR in all seasons is in somewhat higher with subsoll+mole than that with subsoil or mole treatment. Also, no obvious different between basic IR values under both subsoil and mole treatments. Data also clear that, mean values of basic IR are lower after rice crop than after sugar beet crop by 41.81, 35.13, 46.31 and 38.42 % for open drainage, subsoll+open drainage, mole+open drainage and subsoll+mole+open drains, respectively. Basic IR after first season is superior to after the third season from treatments installation.  
+text[[208, 371, 789, 587]]
+The values of basic infiltration rate (IR) of soil as affected by different treatments are presented in Table (3). Data show that, basic infiltration rate values after each season are increased in the treated soils, where as, the values of basic IR under subsoliling and/or moling varied from 0.9 to 1.66 cm/h while, under open drainage they ranged from 0.39 to 0.59 cm/h. This may be due to the subsurface tillage gave the top soil layer a chance to dry and permitted for shrinkage and formation of water passage ways which allowed a rather easier movement of water into mole or subsoil line. Similar results were obtained by Abdel-Mawgoud et al., (2003 and 2006). Basic IR in all seasons is in somewhat higher with subsoil+mole than that with subsoil or mole treatment. Also, no obvious different between basic IR values under both subsoil and mole treatments. Data also clear that, mean values of basic IR are lower after rice crop than after sugar beet crop by 41.81, 35.13, 46.31 and 38.42% for open drainage, subsoil+open drainage, mole+open drainage and subsoil+mole+open drains, respectively. Basic IR after first season is superior to after the third season from treatments installation.
 
-table[[210, 618, 787, 727]]
-table_caption[[208, 592, 787, 621]]
-Table (3): Basic infiltration rate (cm/h) after the first, second and third seasons from treatments executed.   
+table_caption[[208, 593, 789, 618]]
+Table (3): Basic infiltration rate (cm/h) after the first, second and third seasons from treatments executed.
 
-<table><td rowspan="2">Treatments<td colspan="3">First season<td colspan="3">second season<td colspan="3">third season<td colspan="3">MeansRiceSugar beetRiceSugar beetRiceSugar beetRiceSugar beetRiceSugar beetRiceSugar beetOpen drainage0.390.520.390.590.410.580.3970.563Subsoil+open drains1.211.561.051.481.021.391.0931.477Mole + open drains1.111.591.081.510.91.421.0301.507Subsoil+mole+open drains1.221.661.111.551.051.471.1271.56</table>
\ No newline at end of file
+table[[211, 618, 785, 725]]
+
+<table><td rowspan="2">Treatments<td colspan="3">First season<td colspan="3">second season<td colspan="3">third season<td colspan="3">MeansRiceSugar<br>beetRiceSugar<br>beetRiceSugar<br>beetRiceSugar<br>beetRiceSugar<br>beetRiceSugar<br>beetOpen drainage0.390.520.390.590.410.580.3970.563Subsoil+open drains1.211.561.051.481.021.391.0931.477Mole + open drains1.111.591.081.510.91.421.0301.507Subsoil+mole+open<br>drains1.221.661.111.551.051.471.1271.56</table>
\ No newline at end of file
diff --git a/stage1/sample_00022/document.md b/stage1/sample_00022/document.md
index eeced11b42d01b9d2c27fb3bdebb7efdc65e7fdb..b3e905114636eaa86ebfe01343fdbad0fcda917d 100644
--- a/stage1/sample_00022/document.md
+++ b/stage1/sample_00022/document.md
@@ -1,37 +1,37 @@
-33 (10): 7675- 7687, 2008  
+33 (10): 7675 - 7687, 2008  
 
-title[[211, 86, 788, 134]]
-# IMPROVING SOME PROPERTIES OF HEAVY CLAY SALT AFFECTED SOIL AS A RESULT OF DIFFERENT SUBSURFACE TILLAGE.  
+sub_title[[207, 85, 785, 132]]
+## IMPROVING SOME PROPERTIES OF HEAVY CLAY SALT AFFECTED SOIL AS A RESULT OF DIFFERENT SUBSURFACE TILLAGE.  
 
-text[[210, 134, 758, 177]]
-Antar, S. A. \*; A. S. El- Henawy. \* and A. A. E. Atwa \*  \* Soils, Water and Environment Res. Inst., Agric. Res. Center, Egypt.  \* Soils dept., Fac. of Agric., Kafrelsheikh Univ., Egypt.  
+text[[207, 132, 761, 178]]
+Antar, S. A. \*; A. S. El- Henawy. \*\* and A. A. E. Atwa \* \*Soils, Water and Environment Res. Inst., Agric. Res. Center, Egypt. \*\*Soils dept., Fac. of Agric., Kafrelsheikh Univ., Egypt.  
 
-sub_title[[441, 190, 554, 205]]
+sub_title[[439, 191, 552, 205]]
 ## ABSTRACT  
 
-text[[211, 206, 788, 270]]
-A field experiment was conducted at North Nile Delta, Egypt (Islah- Perepmal Region, Motobus District, Kafer El- Shiek Governorate), to evaluate the effect of subsoiling and mole drains with open drainage on improving some soil properties and yields of rice and sugar beet crops as well as raising the efficiency of the open drainage system.  
+text[[208, 206, 788, 270]]
+A field experiment was conducted at North Nile Delta, Egypt (Islah- Perepmal Region, Motobus District, Kafer El- Shiek Governorate), to evaluate the effect of subsoliling and mole drains with open drainage on improving some soil properties and yields of rice and sugar beet crops as well as raising the efficiency of the open drainage system.  
 
-text[[211, 268, 788, 330]]
-Results indicate that, subsurface tillage operations with open surface drainage lowered the water table level, after all growing seasons. The mean values of water table levels are 59.5, 59.5 and 62.3 cm with subsoiling, mole drain and subsoiling +mole, respectively while, it is \(44.3\mathrm{cm}\) with the control (open drainage).  
+text[[208, 269, 788, 330]]
+Results indicate that, subsurface tillage operations with open surface drainage lowered the water table level, after all growing seasons. The mean values of water table levels are 59.5, 59.5 and 62.3 cm with subsoliling, mole drain and subsoliling +mole, respectively while, it is 44.3 cm with the control (open drainage). Water table level is lower after sugar beet than after rice.  
 
-text[[211, 329, 788, 400]]
-Soil salinity and sodicity in the topsoil, were reduced after subsoiling and moling installation. The reductions of salinity, after three years from experiment installation were 86.71, 96.81 and \(98.76\%\) for subsoiling, moling and subsoiling \(+\) moling, respectively over the control. The corresponding values of ESP decreases were 83.93, 83.20 and \(119.40\%\) , respectively. Ratio of \(\mathrm{Ca^{++} / TSS}\) in the topsoil (0- 60cm) was increased in the treated soils.  
+text[[208, 330, 788, 401]]
+Soil salinity and sodicity in the topsoil, were reduced after subsoliling and moling installation. The reductions of salinity, after three years from experiment installation were 86.71, 96.81 and 98.76% for subsoliling, moling and subsoliling +moling, respectively over the control. The corresponding values of ESP decreases were 83.93, 83.20 and 119.40%, respectively. Ratio of \(\mathrm{Ca^{++} / TSS}\) in the topsoil (0- 60cm) was increased in the treated soils.  
 
-text[[211, 400, 788, 475]]
-Subsoiling and/or moling seemed to be more effective on reducing soil bulk density especially in the surface layer (0- 30cm). Subsoiling and/or moling treatments were superior in enhancing soil porosity. Basic infiltration rate (BIR) was increased with subsoiling and/or moling (from 0.9 to 1.66 cm/h) while, it was ranged from 0.39 to 0.59 cm/h with the control (open drainage). Data also cleared that, BIR after rice crop season was lower than that after sugar beet crop season.  
+text[[208, 401, 788, 476]]
+Subsoliling and/or moling seemed to be more effective on reducing soil bulk density especially in the surface layer (0- 30cm). Subsoliling and/or moling treatments were superior in enhancing soil porosity. Basic infiltration rate (BIR) was increased with subsoliling and/or moling (from 0.9 to 1.66 cm/h) while, it was ranged from 0.39 to 0.59 cm/h with the control (open drainage). Data also cleared that, BIR after rice crop season was lower than that after sugar beet crop season.  
 
-text[[211, 475, 788, 571]]
-The saturation percent, field capacity and wilting point values are lower in the treated soils than untreated soils. Subsoiling and/or moling realized increases in quickly and slowly drainable pores (QDP and SDP) and higher decrease in fine capillary pores (FCP) than open drains. Mean values of QDP, SDP and \(\mathrm{FCP\%}\) in the soil depth of 0- 60cm, are 8.71, 12.93 and \(32.35\%\) , respectively with open drainage. The corresponding values are 10.66, 16.57 and \(23.80\%\) , respectively with subsoiling and 11.56, 16.35 and \(23.52\%\) , respectively with moling and 12.52, 18.84 and \(20.87\%\) , respectively with subsoiling +moling.  
+text[[208, 475, 788, 572]]
+The saturation percent, field capacity and wilting point values are lower in the treated soils than untreated soils. Subsoliling and/or moling realized increases in quickly and slowly drainable pores (QDP and SDP) and higher decrease in fine capillary pores (FCP) than open drains. Mean values of QDP, SDP and FCP% in the soil depth of 0- 60cm, are 8.71, 12.93 and \(32.35\%\) , respectively with open drainage. The corresponding values are 10.66, 16.57 and \(23.80\%\) , respectively with subsoliling and 11.56, 16.35 and \(23.52\%\) , respectively with moling and 12.52, 18.84 and \(20.87\%\) , respectively with subsoliling +moling.  
 
-text[[211, 571, 788, 659]]
-Rice and sugar beet yields are related to the salinity contents in soil. The yields increased when the EC decreased as affected by subsoiling and/or moling. Rice and sugar beet yields are higher under subsoiling and/or moling than with open drains in all growing seasons. Rice grain yield is higher under subsoiling tillage, moling and subsoiling +moling by 37.19, 38.43, and \(34.30\%\) , respectively, than the control. The corresponding values of sugar beet yield are 5.31, 4.65 and 7.65 ton/fed., respectively.  
+text[[209, 571, 788, 662]]
+Rice and sugar beet yields are related to the salinity contents in soil. The yields increased when the EC decreased as affected by subsoliling and/or moling. Rice and sugar beet yields are higher under subsoliling and/or moling than with open drains in all growing seasons. Rice grain yield is higher under subsoliling tillage, moling and subsoliling +moling by 37.19, 38.43, and \(34.30\%\) , respectively, than the control. The corresponding values of sugar beet yield are 5.31, 4.65 and 7.65 ton/fed., respectively.  
 
-text[[211, 658, 709, 672]]
-Keywords: Drainage, mole drains, Subsoiling, Clay soil, Rice, sugar beet.  
+text[[209, 661, 707, 675]]
+Keywords: Drainage, mole drains, Subsoliling, Clay soil, Rice, sugar beet.  
 
-sub_title[[421, 678, 576, 693]]
+sub_title[[421, 679, 576, 696]]
 ## INTRODUCTION  
 
-text[[210, 698, 788, 738]]
+text[[210, 700, 789, 741]]
 In Egypt, northern part of the Nile Delta represents a large area of heavy clay soils with shallow open drainage which are low permeability that might have a low productivity. These soils are always threatened by a shallow
\ No newline at end of file
diff --git a/stage1/sample_00022/raw_response.md b/stage1/sample_00022/raw_response.md
index eeced11b42d01b9d2c27fb3bdebb7efdc65e7fdb..b3e905114636eaa86ebfe01343fdbad0fcda917d 100644
--- a/stage1/sample_00022/raw_response.md
+++ b/stage1/sample_00022/raw_response.md
@@ -1,37 +1,37 @@
-33 (10): 7675- 7687, 2008  
+33 (10): 7675 - 7687, 2008  
 
-title[[211, 86, 788, 134]]
-# IMPROVING SOME PROPERTIES OF HEAVY CLAY SALT AFFECTED SOIL AS A RESULT OF DIFFERENT SUBSURFACE TILLAGE.  
+sub_title[[207, 85, 785, 132]]
+## IMPROVING SOME PROPERTIES OF HEAVY CLAY SALT AFFECTED SOIL AS A RESULT OF DIFFERENT SUBSURFACE TILLAGE.  
 
-text[[210, 134, 758, 177]]
-Antar, S. A. \*; A. S. El- Henawy. \* and A. A. E. Atwa \*  \* Soils, Water and Environment Res. Inst., Agric. Res. Center, Egypt.  \* Soils dept., Fac. of Agric., Kafrelsheikh Univ., Egypt.  
+text[[207, 132, 761, 178]]
+Antar, S. A. \*; A. S. El- Henawy. \*\* and A. A. E. Atwa \* \*Soils, Water and Environment Res. Inst., Agric. Res. Center, Egypt. \*\*Soils dept., Fac. of Agric., Kafrelsheikh Univ., Egypt.  
 
-sub_title[[441, 190, 554, 205]]
+sub_title[[439, 191, 552, 205]]
 ## ABSTRACT  
 
-text[[211, 206, 788, 270]]
-A field experiment was conducted at North Nile Delta, Egypt (Islah- Perepmal Region, Motobus District, Kafer El- Shiek Governorate), to evaluate the effect of subsoiling and mole drains with open drainage on improving some soil properties and yields of rice and sugar beet crops as well as raising the efficiency of the open drainage system.  
+text[[208, 206, 788, 270]]
+A field experiment was conducted at North Nile Delta, Egypt (Islah- Perepmal Region, Motobus District, Kafer El- Shiek Governorate), to evaluate the effect of subsoliling and mole drains with open drainage on improving some soil properties and yields of rice and sugar beet crops as well as raising the efficiency of the open drainage system.  
 
-text[[211, 268, 788, 330]]
-Results indicate that, subsurface tillage operations with open surface drainage lowered the water table level, after all growing seasons. The mean values of water table levels are 59.5, 59.5 and 62.3 cm with subsoiling, mole drain and subsoiling +mole, respectively while, it is \(44.3\mathrm{cm}\) with the control (open drainage).  
+text[[208, 269, 788, 330]]
+Results indicate that, subsurface tillage operations with open surface drainage lowered the water table level, after all growing seasons. The mean values of water table levels are 59.5, 59.5 and 62.3 cm with subsoliling, mole drain and subsoliling +mole, respectively while, it is 44.3 cm with the control (open drainage). Water table level is lower after sugar beet than after rice.  
 
-text[[211, 329, 788, 400]]
-Soil salinity and sodicity in the topsoil, were reduced after subsoiling and moling installation. The reductions of salinity, after three years from experiment installation were 86.71, 96.81 and \(98.76\%\) for subsoiling, moling and subsoiling \(+\) moling, respectively over the control. The corresponding values of ESP decreases were 83.93, 83.20 and \(119.40\%\) , respectively. Ratio of \(\mathrm{Ca^{++} / TSS}\) in the topsoil (0- 60cm) was increased in the treated soils.  
+text[[208, 330, 788, 401]]
+Soil salinity and sodicity in the topsoil, were reduced after subsoliling and moling installation. The reductions of salinity, after three years from experiment installation were 86.71, 96.81 and 98.76% for subsoliling, moling and subsoliling +moling, respectively over the control. The corresponding values of ESP decreases were 83.93, 83.20 and 119.40%, respectively. Ratio of \(\mathrm{Ca^{++} / TSS}\) in the topsoil (0- 60cm) was increased in the treated soils.  
 
-text[[211, 400, 788, 475]]
-Subsoiling and/or moling seemed to be more effective on reducing soil bulk density especially in the surface layer (0- 30cm). Subsoiling and/or moling treatments were superior in enhancing soil porosity. Basic infiltration rate (BIR) was increased with subsoiling and/or moling (from 0.9 to 1.66 cm/h) while, it was ranged from 0.39 to 0.59 cm/h with the control (open drainage). Data also cleared that, BIR after rice crop season was lower than that after sugar beet crop season.  
+text[[208, 401, 788, 476]]
+Subsoliling and/or moling seemed to be more effective on reducing soil bulk density especially in the surface layer (0- 30cm). Subsoliling and/or moling treatments were superior in enhancing soil porosity. Basic infiltration rate (BIR) was increased with subsoliling and/or moling (from 0.9 to 1.66 cm/h) while, it was ranged from 0.39 to 0.59 cm/h with the control (open drainage). Data also cleared that, BIR after rice crop season was lower than that after sugar beet crop season.  
 
-text[[211, 475, 788, 571]]
-The saturation percent, field capacity and wilting point values are lower in the treated soils than untreated soils. Subsoiling and/or moling realized increases in quickly and slowly drainable pores (QDP and SDP) and higher decrease in fine capillary pores (FCP) than open drains. Mean values of QDP, SDP and \(\mathrm{FCP\%}\) in the soil depth of 0- 60cm, are 8.71, 12.93 and \(32.35\%\) , respectively with open drainage. The corresponding values are 10.66, 16.57 and \(23.80\%\) , respectively with subsoiling and 11.56, 16.35 and \(23.52\%\) , respectively with moling and 12.52, 18.84 and \(20.87\%\) , respectively with subsoiling +moling.  
+text[[208, 475, 788, 572]]
+The saturation percent, field capacity and wilting point values are lower in the treated soils than untreated soils. Subsoliling and/or moling realized increases in quickly and slowly drainable pores (QDP and SDP) and higher decrease in fine capillary pores (FCP) than open drains. Mean values of QDP, SDP and FCP% in the soil depth of 0- 60cm, are 8.71, 12.93 and \(32.35\%\) , respectively with open drainage. The corresponding values are 10.66, 16.57 and \(23.80\%\) , respectively with subsoliling and 11.56, 16.35 and \(23.52\%\) , respectively with moling and 12.52, 18.84 and \(20.87\%\) , respectively with subsoliling +moling.  
 
-text[[211, 571, 788, 659]]
-Rice and sugar beet yields are related to the salinity contents in soil. The yields increased when the EC decreased as affected by subsoiling and/or moling. Rice and sugar beet yields are higher under subsoiling and/or moling than with open drains in all growing seasons. Rice grain yield is higher under subsoiling tillage, moling and subsoiling +moling by 37.19, 38.43, and \(34.30\%\) , respectively, than the control. The corresponding values of sugar beet yield are 5.31, 4.65 and 7.65 ton/fed., respectively.  
+text[[209, 571, 788, 662]]
+Rice and sugar beet yields are related to the salinity contents in soil. The yields increased when the EC decreased as affected by subsoliling and/or moling. Rice and sugar beet yields are higher under subsoliling and/or moling than with open drains in all growing seasons. Rice grain yield is higher under subsoliling tillage, moling and subsoliling +moling by 37.19, 38.43, and \(34.30\%\) , respectively, than the control. The corresponding values of sugar beet yield are 5.31, 4.65 and 7.65 ton/fed., respectively.  
 
-text[[211, 658, 709, 672]]
-Keywords: Drainage, mole drains, Subsoiling, Clay soil, Rice, sugar beet.  
+text[[209, 661, 707, 675]]
+Keywords: Drainage, mole drains, Subsoliling, Clay soil, Rice, sugar beet.  
 
-sub_title[[421, 678, 576, 693]]
+sub_title[[421, 679, 576, 696]]
 ## INTRODUCTION  
 
-text[[210, 698, 788, 738]]
+text[[210, 700, 789, 741]]
 In Egypt, northern part of the Nile Delta represents a large area of heavy clay soils with shallow open drainage which are low permeability that might have a low productivity. These soils are always threatened by a shallow
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-2004). sobsoiling to conserve rootzone stratum of heavy clay soil. Minufiya J. Agric. Res. Vol. 29 No. 6: 1456- 1478. Abdel-Mawgoud A.S.A., M. B. El Shewikh, A. N. Abdel-Aal and M.I.I. Abdel-Khalik (2003). Open drainage and moiling for desalinization of Salty Clay Soils of Northeastern Egypt. Presented at the 9th International Drainage Workshop, September 10 - 13, 2003, Utrecht, The Netherlands.Abdel-Mawgoud A.S.A, A.A.S. Gendy and S.A. Ramadan (2006). Improving root zone environment and production of a salty clay soil using subsoling and gypsum application. Assiut J. of Agri. Sci., 37, 2: 147-164. Amer, M. H. (1999). Effect of tillage operations on some soil physical properties and water relations of corn. Egypt. J. Appl. Sci., 14 (6):354-365. Campbell, D.J. (1994). Determination and use of bulk density in relation to soil compaction. In Soane and Ouwerk (Eds). Soil compaction in crop production. Elsevier, London and Amsterdam.David Hopkins, Colac (2002). Managing wet soils: mole drainage. WWW.dse. Vic. Gov.De Leenher, L. and M. De Boodt (1965). Soil physics. Intre. Training Center for Post Graduate Soil Scientists, Gent, pp. 126-135. Garcia, G. (1978). Soil water Engineering Laboratory Manual. Colorado State Univ. Dept. of Agric. and Chemical Engineering. Fortcollins, Colorado.J odi Dej ong, H. (2004). Can subsoling increase crop yields in Minnesota? Agric. World Wide Correspondent. Meredith Corporation.Lickacz, J. (1993). Management of solonetzic soils. Agdex 518-8. Revised, Edmonton, Alberta, Canada.Moukhtar M. M., Madiha H. El-Hakim, A, S.A. Abdel-Mawgoud, A. I. N. Abdel-Aal, M. B. El Shewikh and M.I.I. Abdel-Khalik (2003b). Drainage and role of mole drains for heavy clay soils under saline water table, Egypt. Paper No 078. Presented at the 9th International Drainage Workshop, September 10-13, 2003, Utrecht, The Netherlands.Moukhtar M. M., Aly I.N.Abdel-Aal, M.A.B.El-Sheikh and M.I.I. Abdel-Khalik (2002a). The Role of Mole Drainage in Degradation Soils Under Saline Ground water Table, Egypt The Second International Conference on Sustainable Agriculture for Food, Energy and Industry September 8-13, Beijing, China.Moukhtar, M. M., E. M. El-Hadidy, M.Y.S. El-Arquan and M.A.B. El-Shewikh (2002b). Soil Amelioration Technique of Cover Drainage Combined Subsoiling for Saline-Sodic Clay in North Egypt. XVth World Congress of the International Commission of Agricultural Engineering (CIGR) on J u ly 28-31-2002, Chicago, USA.Moukhtar, M.M., M.Y.S. El-Arquan, E.M. El-Hadidy and M.A.B. El-Shewikh (2003a). Amelioration of salt affected soils in north Dakhlia Governorate through application of tile drainage and subsoiling. J. Agric. Sci. Mansoura Univ., Special Issue, Sci. Symp. On Problems of soils and waters in Dakhlia and Damietta Governorate. March 18.
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+2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 200
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-2004). sobsoiling to conserve rootzone stratum of heavy clay soil. Minufiya J. Agric. Res. Vol. 29 No. 6: 1456- 1478. Abdel-Mawgoud A.S.A., M. B. El Shewikh, A. N. Abdel-Aal and M.I.I. Abdel-Khalik (2003). Open drainage and moiling for desalinization of Salty Clay Soils of Northeastern Egypt. Presented at the 9th International Drainage Workshop, September 10 - 13, 2003, Utrecht, The Netherlands.Abdel-Mawgoud A.S.A, A.A.S. Gendy and S.A. Ramadan (2006). Improving root zone environment and production of a salty clay soil using subsoling and gypsum application. Assiut J. of Agri. Sci., 37, 2: 147-164. Amer, M. H. (1999). Effect of tillage operations on some soil physical properties and water relations of corn. Egypt. J. Appl. Sci., 14 (6):354-365. Campbell, D.J. (1994). Determination and use of bulk density in relation to soil compaction. In Soane and Ouwerk (Eds). Soil compaction in crop production. Elsevier, London and Amsterdam.David Hopkins, Colac (2002). Managing wet soils: mole drainage. WWW.dse. Vic. Gov.De Leenher, L. and M. De Boodt (1965). Soil physics. Intre. Training Center for Post Graduate Soil Scientists, Gent, pp. 126-135. Garcia, G. (1978). Soil water Engineering Laboratory Manual. Colorado State Univ. Dept. of Agric. and Chemical Engineering. Fortcollins, Colorado.J odi Dej ong, H. (2004). Can subsoling increase crop yields in Minnesota? Agric. World Wide Correspondent. Meredith Corporation.Lickacz, J. (1993). Management of solonetzic soils. Agdex 518-8. Revised, Edmonton, Alberta, Canada.Moukhtar M. M., Madiha H. El-Hakim, A, S.A. Abdel-Mawgoud, A. I. N. Abdel-Aal, M. B. El Shewikh and M.I.I. Abdel-Khalik (2003b). Drainage and role of mole drains for heavy clay soils under saline water table, Egypt. Paper No 078. Presented at the 9th International Drainage Workshop, September 10-13, 2003, Utrecht, The Netherlands.Moukhtar M. M., Aly I.N.Abdel-Aal, M.A.B.El-Sheikh and M.I.I. Abdel-Khalik (2002a). The Role of Mole Drainage in Degradation Soils Under Saline Ground water Table, Egypt The Second International Conference on Sustainable Agriculture for Food, Energy and Industry September 8-13, Beijing, China.Moukhtar, M. M., E. M. El-Hadidy, M.Y.S. El-Arquan and M.A.B. El-Shewikh (2002b). Soil Amelioration Technique of Cover Drainage Combined Subsoiling for Saline-Sodic Clay in North Egypt. XVth World Congress of the International Commission of Agricultural Engineering (CIGR) on J u ly 28-31-2002, Chicago, USA.Moukhtar, M.M., M.Y.S. El-Arquan, E.M. El-Hadidy and M.A.B. El-Shewikh (2003a). Amelioration of salt affected soils in north Dakhlia Governorate through application of tile drainage and subsoiling. J. Agric. Sci. Mansoura Univ., Special Issue, Sci. Symp. On Problems of soils and waters in Dakhlia and Damietta Governorate. March 18.
\ No newline at end of file
+2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 200
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-The AGGLOM vector includes several variables to assess whether it is access or proximity to agglomeration economies that are driving the results. First, for nonmetropolitan counties, we include the county’s own population and the population of the nearest metropolitan area. For metropolitan counties, we include the overall metropolitan area population. Then to more accurately account for spillovers over distance, the AGGLOM also includes several spatial distance measures to reflect proximity to metropolitan areas differentiated by their status in the hierarchy. Partridge et al. (2008a, 2008b, 2009) found these distance measures to be highly associated with job and population growth as well as wages and housing values dating back to the mid-20<sup>th</sup> Century. For a county that is part of a metropolitan area, the first distance is from the population-weighted center of the county to the population-weighted center of the metropolitan area. Inside a metropolitan area, the influence of longer distances would largely reflect any offsetting effects of agglomeration or congestion effects. For a nonmetropolitan county, the variable is the distance from the county center to the center of the nearest metropolitan area.<sup>7</sup>  
+The AGGLOM vector includes several variables to assess whether it is access or proximity to agglomeration economies that are driving the results. First, for nonmetropolitan counties, we include the county's own population and the population of the nearest metropolitan area. For metropolitan counties, we include the overall metropolitan area population. Then to more accurately account for spillovers over distance, the AGGLOM also includes several spatial distance measures to reflect proximity to metropolitan areas differentiated by their status in the hierarchy. Partridge et al. (2008a, 2008b, 2009) found these distance measures to be highly associated with job and population growth as well as wages and housing values dating back to the mid-20<sup>th</sup> Century. For a county that is part of a metropolitan area, the first distance is from the population-weighted center of the county to the population-weighted center of the metropolitan area. Inside a metropolitan area, the influence of longer distances would largely reflect any offsetting effects of agglomeration or congestion effects. For a nonmetropolitan county, the variable is the distance from the county center to the center of the nearest metropolitan area.  
 
-text[[114, 491, 883, 681]]
-Beyond the nearest metropolitan area, we also include the incremental distances to larger higher- tiered metropolitan areas to reflect added spillovers from higher- ordered cities. They reflect the incremental or marginal costs to reach each higher- tiered (larger) metropolitan areas. First, are incremental (or additional) distances to reach metropolitan areas of at least 250,000, and then at least 500,000, and finally over 1.5 million population.<sup>8</sup> The largest category generally reflects national and top- tier regional cities. There may be measurement error bias when using straight- line distance ratherthan travel time, but this classic measurement error would bias the distance
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+text[[115, 491, 882, 681]]
+Beyond the nearest metropolitan area, we also include the incremental distances to larger higher- tiered metropolitan areas to reflect added spillovers from higher- ordered cities. They reflect the incremental or marginal costs to reach each higher- tiered (larger) metropolitan areas. First, are incremental (or additional) distances to reach metropolitan areas of at least 250,000, and then at least 500,000, and finally over 1.5 million population. The largest category generally reflects national and top- tier regional cities. There may be measurement error bias when using straight- line distance rather than travel time, but this classic measurement error would bias the distance
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diff --git a/stage1/sample_00024/raw_response.md b/stage1/sample_00024/raw_response.md
index ebe15efaedef13b966ec0b6324b9d9f39c16f4d9..86551c71c20dd4f63eb2bb9b437c8ddd4f6a8e0c 100644
--- a/stage1/sample_00024/raw_response.md
+++ b/stage1/sample_00024/raw_response.md
@@ -1,4 +1,4 @@
-The AGGLOM vector includes several variables to assess whether it is access or proximity to agglomeration economies that are driving the results. First, for nonmetropolitan counties, we include the county’s own population and the population of the nearest metropolitan area. For metropolitan counties, we include the overall metropolitan area population. Then to more accurately account for spillovers over distance, the AGGLOM also includes several spatial distance measures to reflect proximity to metropolitan areas differentiated by their status in the hierarchy. Partridge et al. (2008a, 2008b, 2009) found these distance measures to be highly associated with job and population growth as well as wages and housing values dating back to the mid-20<sup>th</sup> Century. For a county that is part of a metropolitan area, the first distance is from the population-weighted center of the county to the population-weighted center of the metropolitan area. Inside a metropolitan area, the influence of longer distances would largely reflect any offsetting effects of agglomeration or congestion effects. For a nonmetropolitan county, the variable is the distance from the county center to the center of the nearest metropolitan area.<sup>7</sup>  
+The AGGLOM vector includes several variables to assess whether it is access or proximity to agglomeration economies that are driving the results. First, for nonmetropolitan counties, we include the county's own population and the population of the nearest metropolitan area. For metropolitan counties, we include the overall metropolitan area population. Then to more accurately account for spillovers over distance, the AGGLOM also includes several spatial distance measures to reflect proximity to metropolitan areas differentiated by their status in the hierarchy. Partridge et al. (2008a, 2008b, 2009) found these distance measures to be highly associated with job and population growth as well as wages and housing values dating back to the mid-20<sup>th</sup> Century. For a county that is part of a metropolitan area, the first distance is from the population-weighted center of the county to the population-weighted center of the metropolitan area. Inside a metropolitan area, the influence of longer distances would largely reflect any offsetting effects of agglomeration or congestion effects. For a nonmetropolitan county, the variable is the distance from the county center to the center of the nearest metropolitan area.  
 
-text[[114, 491, 883, 681]]
-Beyond the nearest metropolitan area, we also include the incremental distances to larger higher- tiered metropolitan areas to reflect added spillovers from higher- ordered cities. They reflect the incremental or marginal costs to reach each higher- tiered (larger) metropolitan areas. First, are incremental (or additional) distances to reach metropolitan areas of at least 250,000, and then at least 500,000, and finally over 1.5 million population.<sup>8</sup> The largest category generally reflects national and top- tier regional cities. There may be measurement error bias when using straight- line distance ratherthan travel time, but this classic measurement error would bias the distance
\ No newline at end of file
+text[[115, 491, 882, 681]]
+Beyond the nearest metropolitan area, we also include the incremental distances to larger higher- tiered metropolitan areas to reflect added spillovers from higher- ordered cities. They reflect the incremental or marginal costs to reach each higher- tiered (larger) metropolitan areas. First, are incremental (or additional) distances to reach metropolitan areas of at least 250,000, and then at least 500,000, and finally over 1.5 million population. The largest category generally reflects national and top- tier regional cities. There may be measurement error bias when using straight- line distance rather than travel time, but this classic measurement error would bias the distance
\ No newline at end of file
diff --git a/stage1/sample_00025/document.md b/stage1/sample_00025/document.md
index 55bdd5867ab84e7d99fa6272a3089fdcc4b81d8e..4378e4f271eb3752bbc6289ee12b649d722faedb 100644
--- a/stage1/sample_00025/document.md
+++ b/stage1/sample_00025/document.md
@@ -1,13 +1,13 @@
 1. We also account for the average of median household incomes in nearby counties to account for nearby markets. State fixed effects account for state-specific factors including tax and expenditure policies, regulatory differences, geographic location with respect to coasts, and settlement period.  
 
-sub_title[[115, 243, 287, 260]]
+sub_title[[115, 245, 289, 261]]
 ## 4. Empirical Results  
 
-text[[113, 271, 885, 537]]
-Table 1 reports descriptive statistics for the dependent and independent variables. Tables 2 and 3 respectively report the metropolitan and nonmetropolitan regression results for overall high- tech employment growth and for corresponding non- high- tech categories: overall total employment growth, manufacturing employment growth, and private services employment growth. \(^{11}\) For each industry category, the first column of results report a parsimonious model that does not include the demographic variables including educational attainment, total population, age, and racial/ethnic population shares. These more parsimonious models help us assess whether multicollinearity is greatly affecting the results and whether there is demographic self- sorting (such as whether college- educated workers self- sort into places they expect to have better long- term employment prospects). \(^{12}\)  
+text[[114, 272, 883, 540]]
+Table 1 reports descriptive statistics for the dependent and independent variables. Tables 2 and 3 respectively report the metropolitan and nonmetropolitan regression results for overall high- tech employment growth and for corresponding non- high- tech categories: overall total employment growth, manufacturing employment growth, and private services employment growth. For each industry category, the first column of results report a parsimonious model that does not include the demographic variables including educational attainment, total population, age, and racial/ethnic population shares. These more parsimonious models help us assess whether multicollinearity is greatly affecting the results and whether there is demographic self- sorting (such as whether college- educated workers self- sort into places they expect to have better long- term employment prospects).  
 
-sub_title[[114, 547, 578, 566]]
+sub_title[[115, 548, 579, 566]]
 ### 4.1 High-Technology vs Aggregate Industry Categories  
 
-text[[114, 574, 884, 791]]
+text[[114, 575, 886, 791]]
 Comparing the parsimonious model results to the base model results in both Tables 2 and 3 suggests that the results are relatively stable. One exception is that the magnitude of the regression coefficient for the log of initial employment generally becomes much more negative in the parsimonious model. For example, the magnitude of the coefficient approximately doubled in the overall high- technology employment and overall total employment cases. Thus, there is some evidence of a correlation between the initial demographic composition and the initial industry employment. Nonetheless, given that the results did not significantly change, we focus on the more fully- specified base models.
\ No newline at end of file
diff --git a/stage1/sample_00025/raw_response.md b/stage1/sample_00025/raw_response.md
index 55bdd5867ab84e7d99fa6272a3089fdcc4b81d8e..4378e4f271eb3752bbc6289ee12b649d722faedb 100644
--- a/stage1/sample_00025/raw_response.md
+++ b/stage1/sample_00025/raw_response.md
@@ -1,13 +1,13 @@
 1. We also account for the average of median household incomes in nearby counties to account for nearby markets. State fixed effects account for state-specific factors including tax and expenditure policies, regulatory differences, geographic location with respect to coasts, and settlement period.  
 
-sub_title[[115, 243, 287, 260]]
+sub_title[[115, 245, 289, 261]]
 ## 4. Empirical Results  
 
-text[[113, 271, 885, 537]]
-Table 1 reports descriptive statistics for the dependent and independent variables. Tables 2 and 3 respectively report the metropolitan and nonmetropolitan regression results for overall high- tech employment growth and for corresponding non- high- tech categories: overall total employment growth, manufacturing employment growth, and private services employment growth. \(^{11}\) For each industry category, the first column of results report a parsimonious model that does not include the demographic variables including educational attainment, total population, age, and racial/ethnic population shares. These more parsimonious models help us assess whether multicollinearity is greatly affecting the results and whether there is demographic self- sorting (such as whether college- educated workers self- sort into places they expect to have better long- term employment prospects). \(^{12}\)  
+text[[114, 272, 883, 540]]
+Table 1 reports descriptive statistics for the dependent and independent variables. Tables 2 and 3 respectively report the metropolitan and nonmetropolitan regression results for overall high- tech employment growth and for corresponding non- high- tech categories: overall total employment growth, manufacturing employment growth, and private services employment growth. For each industry category, the first column of results report a parsimonious model that does not include the demographic variables including educational attainment, total population, age, and racial/ethnic population shares. These more parsimonious models help us assess whether multicollinearity is greatly affecting the results and whether there is demographic self- sorting (such as whether college- educated workers self- sort into places they expect to have better long- term employment prospects).  
 
-sub_title[[114, 547, 578, 566]]
+sub_title[[115, 548, 579, 566]]
 ### 4.1 High-Technology vs Aggregate Industry Categories  
 
-text[[114, 574, 884, 791]]
+text[[114, 575, 886, 791]]
 Comparing the parsimonious model results to the base model results in both Tables 2 and 3 suggests that the results are relatively stable. One exception is that the magnitude of the regression coefficient for the log of initial employment generally becomes much more negative in the parsimonious model. For example, the magnitude of the coefficient approximately doubled in the overall high- technology employment and overall total employment cases. Thus, there is some evidence of a correlation between the initial demographic composition and the initial industry employment. Nonetheless, given that the results did not significantly change, we focus on the more fully- specified base models.
\ No newline at end of file
diff --git a/stage1/sample_00026/document.md b/stage1/sample_00026/document.md
index a51e404902b06d21c8f5f2cfd2f970ed72d192db..47aa55a02a70e5e6ff29c86ca4e04333d4ca9e8e 100644
--- a/stage1/sample_00026/document.md
+++ b/stage1/sample_00026/document.md
@@ -1,13 +1,13 @@
 9  
 
-text[[113, 134, 784, 152]]
-regression coefficients toward zero, suggesting a larger distance effect than we report.9  
+text[[113, 133, 785, 153]]
+regression coefficients toward zero, suggesting a larger distance effect than we report.  
 
-text[[113, 160, 880, 427]]
-The EDUC vector controls for human capital and includes variables for the initial 1990 percent of the population 25 years or older that has (1) at least a high school degree but no further education, (2) some college/university but no degree, (3) Associates Degree but no further degree, and (4) at least a Bachelors degree. We expect that a greater share with a Bachelors degree to be positively linked to high- technology growth. But for assembly- line positions in manufacturing there may be aneed for workers with medium skill or education levels. Likewise, to account for knowledge spillovers from research- intensive universities, we include a dummy variable for being located within 100 miles of a Carnegie Classification research- intensive university including major Land Grant universities. We also tried a dummy for being located within 50 miles, but the results were virtually identical.  
+text[[114, 159, 880, 427]]
+The EDUc vector controls for human capital and includes variables for the initial 1990 percent of the population 25 years or older that has (1) at least a high school degree but no further education, (2) some college/university but no degree, (3) Associates Degree but no further degree, and (4) at least a Bachelors degree. We expect that a greater share with a Bachelors degree to be positively linked to high- technology growth. But for assembly- line positions in manufacturing there may be a need for workers with medium skill or education levels. Likewise, to account for knowledge spillovers from research- intensive universities, we include a dummy variable for being located within 100 miles of a Carnegie Classification research- intensive university including major Land Grant universities. We also tried a dummy for being located within 50 miles, but the results were virtually identical.  
 
-text[[113, 437, 884, 675]]
-Akin to the within- industry knowledge spillovers accounted for by the surrounding county industry employment, we also include the average share of the population with at least a Bachelors degree in the nearest 5 counties.1° Greater human capital in nearby regions may have spillovers or allow the focal county to be more innovative or technologically progressive through a greater ease in adopting innovation spillovers (Rodríguez- Pose and Crescenzi, 2008). Neighboring county educational attainment may also have labor market impacts because it may increase the available labor supply for local firms in the focal county through commuting. Alternatively, it may reduce local employment growth because high- technology firms would rather locate in the neighboring county due to better access to an educated workforce.  
+text[[114, 437, 883, 679]]
+Akin to the within- industry knowledge spillovers accounted for by the surrounding county industry employment, we also include the average share of the population with at least a Bachelors degree in the nearest 5 counties. Greater human capital in nearby regions may have spillovers or allow the focal county to be more innovative or technologically progressive through a greater ease in adopting innovation spillovers (Rodriguez- Pose and Crescenzi, 2008). Neighboring county educational attainment may also have labor market impacts because it may increase the available labor supply for local firms in the focal county through commuting. Alternatively, it may reduce local employment growth because high- technology firms would rather locate in the neighboring county due to better access to an educated workforce.  
 
-text[[114, 688, 884, 817]]
+text[[115, 689, 884, 819]]
 Natural AMENITIES are measured using a 1 to 7 scale developed by the U.S. Department of Agriculture (see Appendix Table 2). This variable assesses the hypothesis that high- technology workers may be more footloose than other workers and that these firms may be better able to locate in areas preferred by its workforce. The X vector controls for other factors that potentially influence growth including population- age composition shares and race and ethnic population
\ No newline at end of file
diff --git a/stage1/sample_00026/raw_response.md b/stage1/sample_00026/raw_response.md
index a51e404902b06d21c8f5f2cfd2f970ed72d192db..47aa55a02a70e5e6ff29c86ca4e04333d4ca9e8e 100644
--- a/stage1/sample_00026/raw_response.md
+++ b/stage1/sample_00026/raw_response.md
@@ -1,13 +1,13 @@
 9  
 
-text[[113, 134, 784, 152]]
-regression coefficients toward zero, suggesting a larger distance effect than we report.9  
+text[[113, 133, 785, 153]]
+regression coefficients toward zero, suggesting a larger distance effect than we report.  
 
-text[[113, 160, 880, 427]]
-The EDUC vector controls for human capital and includes variables for the initial 1990 percent of the population 25 years or older that has (1) at least a high school degree but no further education, (2) some college/university but no degree, (3) Associates Degree but no further degree, and (4) at least a Bachelors degree. We expect that a greater share with a Bachelors degree to be positively linked to high- technology growth. But for assembly- line positions in manufacturing there may be aneed for workers with medium skill or education levels. Likewise, to account for knowledge spillovers from research- intensive universities, we include a dummy variable for being located within 100 miles of a Carnegie Classification research- intensive university including major Land Grant universities. We also tried a dummy for being located within 50 miles, but the results were virtually identical.  
+text[[114, 159, 880, 427]]
+The EDUc vector controls for human capital and includes variables for the initial 1990 percent of the population 25 years or older that has (1) at least a high school degree but no further education, (2) some college/university but no degree, (3) Associates Degree but no further degree, and (4) at least a Bachelors degree. We expect that a greater share with a Bachelors degree to be positively linked to high- technology growth. But for assembly- line positions in manufacturing there may be a need for workers with medium skill or education levels. Likewise, to account for knowledge spillovers from research- intensive universities, we include a dummy variable for being located within 100 miles of a Carnegie Classification research- intensive university including major Land Grant universities. We also tried a dummy for being located within 50 miles, but the results were virtually identical.  
 
-text[[113, 437, 884, 675]]
-Akin to the within- industry knowledge spillovers accounted for by the surrounding county industry employment, we also include the average share of the population with at least a Bachelors degree in the nearest 5 counties.1° Greater human capital in nearby regions may have spillovers or allow the focal county to be more innovative or technologically progressive through a greater ease in adopting innovation spillovers (Rodríguez- Pose and Crescenzi, 2008). Neighboring county educational attainment may also have labor market impacts because it may increase the available labor supply for local firms in the focal county through commuting. Alternatively, it may reduce local employment growth because high- technology firms would rather locate in the neighboring county due to better access to an educated workforce.  
+text[[114, 437, 883, 679]]
+Akin to the within- industry knowledge spillovers accounted for by the surrounding county industry employment, we also include the average share of the population with at least a Bachelors degree in the nearest 5 counties. Greater human capital in nearby regions may have spillovers or allow the focal county to be more innovative or technologically progressive through a greater ease in adopting innovation spillovers (Rodriguez- Pose and Crescenzi, 2008). Neighboring county educational attainment may also have labor market impacts because it may increase the available labor supply for local firms in the focal county through commuting. Alternatively, it may reduce local employment growth because high- technology firms would rather locate in the neighboring county due to better access to an educated workforce.  
 
-text[[114, 688, 884, 817]]
+text[[115, 689, 884, 819]]
 Natural AMENITIES are measured using a 1 to 7 scale developed by the U.S. Department of Agriculture (see Appendix Table 2). This variable assesses the hypothesis that high- technology workers may be more footloose than other workers and that these firms may be better able to locate in areas preferred by its workforce. The X vector controls for other factors that potentially influence growth including population- age composition shares and race and ethnic population
\ No newline at end of file
diff --git a/stage1/sample_00027/document.md b/stage1/sample_00027/document.md
index b188883260fc487752d0b83f4166aaf5c67b7c68..6d1e5204fdf4432da8f3738aecfd434a4034d6c4 100644
--- a/stage1/sample_00027/document.md
+++ b/stage1/sample_00027/document.md
@@ -1,82 +1,82 @@
 8 These developments suggest that it may be appropriate to reassess the adverse findings of the Coronary Drug Project. To pursue this, we have investigated the cardiovascular effects of low-dose estrogen supplementation in a group of men rendered hypogonadal as a result of treatment for prostatic cancer, thereby reducing endogenous estrogen production. In a small, randomized, placebo-controlled study, we have examined the effects of 8 weeks of estrogen supplementation on a number of surrogate cardiovascular end points, including lipid levels, blood pressure, and forearm vascular reactivity.  
 
-text[[77, 82, 477, 273]]
-hanced knowledge is now available regarding the wide range of actions of estrogens on the cardiovascular system, even in male tissues. These developments suggest that it may be appropriate to reassess the adverse findings of the Coronary Drug Project. To pursue this, we have investigated the cardiovascular effects of low- dose estrogen supplementation in a group of men rendered hypogonadal as a result of treatment for prostatic cancer, thereby reducing endogenous estrogen production. In a small, randomized, placebo-controlled study, we have examined the effects of 8 weeks of estrogen supplementation on a number of surrogate cardiovascular end points, including lipid levels, blood pressure, and forearm vascular reactivity.  
-
-sub_title[[239, 287, 315, 303]]
+sub_title[[240, 286, 315, 303]]
 ## Methods  
 
-sub_title[[77, 311, 144, 325]]
+sub_title[[78, 310, 145, 324]]
 ## Subjects  
 
-text[[77, 325, 477, 394]]
-We studied 12 men rendered hypogonadal by surgical or pharmacologic treatment for prostatic cancer. We excluded patients with clinical evidence of cardiovascular disease (or on cardiovascular drugs) or severe renal, hepatic, respiratory, or hematologic conditions. The study was approved by the Alfred Hospital Human Ethics Committee. All subjects gave written fully informed consent.  
+text[[78, 325, 478, 395]]
+We studied 12 men rendered hypogonadal by surgical or pharmacological treatment for prostatic cancer. We excluded patients with clinical evidence of cardiovascular disease (or on cardiovascular drugs) or severe renal, hepatic, respiratory, or hematologic conditions. The study was approved by the Alfred Hospital Human Ethics Committee. All subjects gave written fully informed consent.  
 
-sub_title[[77, 407, 182, 422]]
+sub_title[[78, 409, 184, 424]]
 ## Study Design  
 
-text[[77, 423, 479, 558]]
-The study followed a randomized, double- blind, placebo- controlled design. Subjects were randomly assigned to 8 weeks of estrogen supplementation with estradiol valerate (Progynova, Schering) 1 mg daily \((n = 7\) ; mean age, \(68.4\pm 2.6\) years) or placebo \((n = 5\) ; mean age, \(69.2\pm 2.8\) years). Hemodynamic and forearm vascular studies were performed twice, 8 weeks apart. Subjects were unaware of treatments received. All measurements were made by investigators blinded to the treatment. On each study day, subjects underwent the following procedures: arterial cannulation, blood sampling, assessment of forearm vascular reactivity, and measurement of hormones and other variables.  
+text[[78, 424, 479, 558]]
+The study followed a randomized, double- blind, placebo- controlled design. Subjects were randomly assigned to 8 weeks of estrogen supplementation with estradiol valerate (Progynova, Schering) \(1\mathrm{mg}\) daily \((\mathrm{n} = 7\) ; mean age, \(68.4\pm 2.6\) years) or placebo \((\mathrm{n} = 5\) ; mean age, \(69.2\pm 2.8\) years). Hemodynamic and forearm vascular studies were performed twice, 8 weeks apart. Subjects were unaware of treatments received. All measurements were made by investigators blinded to the treatment. On each study day, subjects underwent the following procedures: arterial examination, blood sampling, assessment of forearm vascular reactivity, and measurement of hormones and other variables.  
 
-sub_title[[77, 570, 242, 584]]
+sub_title[[78, 570, 244, 585]]
 ## Arterial Cannulation  
 
-text[[77, 585, 477, 662]]
-Subjects rested supine throughout each study in a quiet, temperature- controlled room, \((22^{\circ}C)\) . The left brachial artery was cannulated with a 21- gauge, 5- cm catheter (Cook) for intra- arterial blood pressure measurement (Spacelabs Inc), drug infusions, and arterial blood sampling. Heart rate was monitored by electrocardiography. Subjects rested for 30 minutes before commencement of the study.  
+text[[78, 586, 479, 662]]
+Subjects rested supine throughout each study in a quiet, temperature- controlled room, \((22^{\circ}\mathrm{C})\) . The left brachial artery was cannulated with a 21- gauge, \(5\mathrm{- cm}\) catheter (Cook) for intra- arterial blood pressure measurement (Spacelabs Inc), drug infusions, and arterial blood sampling. Heart rate was monitored by electrocardiography. Subjects rested for 30 minutes before commencement of the study.  
 
-sub_title[[77, 674, 204, 689]]
+sub_title[[78, 674, 203, 690]]
 ## Blood Sampling  
 
-text[[77, 689, 477, 753]]
-Blood was taken on each occasion for measurement of urea, electrolytes, glucose, total cholesterol, triglycerides, HDL cholesterol, liver function, full blood count, estradiol, testosterone, andrenstenidine, dehydroepiandrosterone, sex hormone- binding globulin, follicle- stimulating hormone (FSH), and luteinizing hormone (LH).  
+text[[78, 690, 479, 754]]
+Blood was taken on each occasion for measurement of urea, electrolytes, glucose, total cholesterol, triglycerides, HDL cholesterol, liver function, full blood count, estradiol, testosterone, andtendecine, dehydroepiandrosterone, sex hormone- binding globulin, follicle- stimulating hormone (FSH), and luteinizing hormone (LH).  
 
-sub_title[[77, 764, 421, 778]]
-## Assessment of Forearm Vascular Reactivity  
+sub_title[[78, 762, 418, 780]]
+## A assessment of Forearm Vascular Reactivity  
 
-text[[77, 779, 479, 866]]
+text[[78, 779, 479, 863]]
 Forearm vascular responsiveness was assessed by venous occlusion plethysmography with a sealed alloy- filled gallium and indium double- stranded strain gauge (Medasonic). Hand blood flow was excluded via a wrist cuff ( \(200\mathrm{mm}\mathrm{Hg}\) ); venous occlusion pressure was \(50\mathrm{mm}\mathrm{Hg}\) . Basal blood flow was obtained as an average of 3 measurements. Drugs were infused via an infusion pump at 2 mL/min.  
 
-text[[77, 866, 479, 946]]
-A cyclothioline (BDH Chemicals) was infused at 9.25, 18.5, and 37 \(\mu \mathrm{g / min}\) : norepinephrine at 25, 50 and \(100~\mathrm{ng / min}\) ; and angiotensin (Ang) II at 8, 16, and \(32\mathrm{ng / min}\) , each dose for 2 minutes to allow blood flow to reach steady state. Basal NO release was assessed by intra- arterial infusion of \(\mathrm{N}^{6}\) - monomethyl- L- arginine (L- NMMA) (Calbiochem- Novabiochem) at 1, 2, and 4 \(\mu \mathrm{mol / min}\) , each dose for 5 minutes. Finally, sodium nitroprusside (David Bull Laboratories)  
+text[[78, 864, 479, 946]]
+A cyclicholine (BDH Chemicals) was infused at 9.25, 18.5, and 37 \(\mu \mathrm{g / min}\) ; norepinephrine at 25, 50 and \(100\mathrm{ng / min}\) ; and angiotensin (Ang) II at 8, 16, and 32 \(\mathrm{ng / min}\) , each dose for 2 minutes to allow blood flow to reach steady state. Basal NO release was assessed by intra- arterial infusion of \(\mathrm{N^G}\) - monomethyl- L- arginine (L- NMMA) (Calbiochem- Novabiochem) at 1, 2, and \(4\mu \mathrm{mol / min}\) , each dose for 5 minutes. Finally, sodium nitroprusside (David Bull Laboratories)  
 
-table[[517, 114, 918, 189]]
-table_caption[[517, 84, 910, 113]]
+table[[516, 116, 917, 190]]
+table_caption[[519, 85, 912, 115]]
 TABLE 1. Baseline Characteristics of Subjects Randomized to Estrogen \((n = 7)\) and Placebo \((n = 5)\)   
 
-<table>Treatment GroupAge, yWeight, kgBMI, kg/m²Systolic BP, mmHgDiastolic BP, mmHgEstrogen68.4 ± 2.172.4 ± 4.527.2 ± 2.0136 ± 187 ± 1Placebo69.2 ± 2.870.8 ± 4.927.6 ± 2.3134 ± 186 ± 2</table>
+<table><td rowspan="2">Treatment Group<td rowspan="2">Age, y<td colspan="2">Weight, kg<td rowspan="2">BMI, kg/m²<td rowspan="2">Systolic BP, mm Hg<td rowspan="2">Diastolic BP, mm HgEstrogen68.4±2.172.4±4.527.2±2.0136±187±1Placebo69.2±2.870.8±4.927.6±2.3134±186±2</table>
 
-table_footnote[[530, 193, 800, 205]]
+table_footnote[[528, 193, 801, 206]]
 BMI indicates body mass index; BP, blood pressure.  
 
-text[[517, 229, 918, 281]]
+text[[518, 229, 917, 281]]
 was infused at \(1.6\mu \mathrm{g / min}\) for 2 minutes. The peak response was determined as the average of 3 consecutive steady state measurements. A 15- minute rest period between interventions was sufficient for flow to return to resting levels.  
 
-sub_title[[517, 294, 893, 309]]
+sub_title[[518, 295, 896, 310]]
 ## Measurement of Hormones and Other Variables  
 
-text[[517, 310, 918, 385]]
-Estradiol and other hormones, namely, total testosterone, andrenstenidine, FSH, LH, and sex hormone- binding globulin were measured by specific radioimmunoassay. The intra- assay coefficient of variation for estradiol was \(9\%\) \((n = 32)\) and sensitivity 30 pmol/L. Total cholesterol, triglycerides, HDL cholesterol, and glucose were also measured.  
+text[[518, 311, 918, 386]]
+Estradiol and other hormones, namely, total testosterone, andtendecine, FSH, LH, and sex hormone- binding globulin were measured by specific radioimmunoassay. The intra- assay coefficient of variation for estradiol was \(9\%\) n \(n = 32\) and sensitivity 30 pmol/L. Total cholesterol, triglycerides, HDL cholesterol, and glucose were also measured.  
 
-sub_title[[517, 398, 801, 413]]
+sub_title[[518, 401, 802, 416]]
 ## Calculations and Statistical Analysis  
 
-text[[517, 415, 918, 480]]
-Results are expressed as mean \(\pm\) SEM. Vascular reactivity doseresponse curves were compared by 2- way repeated- measures ANOVA. Other data were compared by Student's t test. In cases in which multiple comparisons were made, the Bonferroni correction was applied. The null hypothesis was rejected at \(P< 0.05\)  
+text[[518, 417, 917, 480]]
+Results are expressed as mean \(\pm\) SEM. Vascular reactivity does- response curves were compared by 2- way repeated- measures ANOVA. Other data were compared by Student's t test. In cases in which multiple comparisons were made, the Bonferroni correction was applied. The null hypothesis was rejected at \(P< 0.05\)  
 
-sub_title[[684, 495, 748, 510]]
+sub_title[[685, 496, 750, 509]]
 ## Results  
 
-text[[517, 510, 918, 586]]
+text[[518, 511, 918, 582]]
 There were no significant adverse effects reported in any of the subjects. Only 1 subject experienced symptoms likely to be associated with estrogen treatment: mild, persistent breast tenderness. The other subjects were unable to tell whether they were receiving active treatment or placebo.  
 
-sub_title[[517, 601, 706, 615]]
+sub_title[[518, 600, 705, 615]]
 ## Baseline Characteristics  
 
-text[[517, 617, 918, 783]]
-Baseline characteristics are shown in Tables 1 and 2. There were no differences between the estrogen- and placebo- treated groups with respect to age, body mass index, systolic or diastolic blood pressure, or baseline plasma levels of estradiol, total testosterone, andrenstenidine, sex hormone- binding globulin, LH, total cholesterol, triglycerides, HDL cholesterol, hemoglobin, or glucose. FSH was higher in the placebo group as a result of very high levels in 1 individual. Testosterone levels were very low in both estrogen- and placebo- treated groups, consistent with their hypogonadal status.  
+text[[518, 616, 918, 780]]
+Baseline characteristics are shown in Tables 1 and 2. There were no differences between the estrogen- and placebo- treated groups with respect to age, body mass index, systolic or diastolic blood pressure, or baseline plasma levels of estradiol, total testosterone, andtendecine, sex hormone- binding globulin, LH, total cholesterol, triglycerides, HDL cholesterol, hemoglobin, or glucose. FSH was higher in the placebo group as a result of very high levels in 1 individual. Testosterone levels were very low in both estrogen- and placebo- treated groups, consistent with their hypogonadal status.  
+
+sub_title[[518, 797, 776, 810]]
+## Effect of Estradiol on Serum and  
 
-sub_title[[517, 798, 777, 828]]
-## Effect of Estradiol on Serum and Plasma Measurements  
+sub_title[[518, 813, 696, 827]]
+## Plasma Measurements  
 
-text[[517, 828, 918, 948]]
-Asexpected, estrogen levels increased with estrogen treatment, FSH levels fell, and androgen levels showed no change. HDL levels increased significantly with estrogen treatment, but total cholesterol and triglyceride levels were constant (Table 2). Glucose levels were unchanged with estrogen treatment. There were no significant differences in the placebo group. No changes were observed in renal function, liver function, or any hematologic parameters.
\ No newline at end of file
+text[[518, 828, 918, 946]]
+As expected, estrogen levels increased with estrogen treatment, FSH levels fell, and androgen levels showed no change. HDL levels increased significantly with estrogen treatment, but total cholesterol and triglyceride levels were constant (Table 2). Glucose levels were unchanged with estrogen treatment. There were no significant differences in the placebo group. No changes were observed in renal function, liver function, or any hematologic parameters.
\ No newline at end of file
diff --git a/stage1/sample_00027/raw_response.md b/stage1/sample_00027/raw_response.md
index b188883260fc487752d0b83f4166aaf5c67b7c68..6d1e5204fdf4432da8f3738aecfd434a4034d6c4 100644
--- a/stage1/sample_00027/raw_response.md
+++ b/stage1/sample_00027/raw_response.md
@@ -1,82 +1,82 @@
 8 These developments suggest that it may be appropriate to reassess the adverse findings of the Coronary Drug Project. To pursue this, we have investigated the cardiovascular effects of low-dose estrogen supplementation in a group of men rendered hypogonadal as a result of treatment for prostatic cancer, thereby reducing endogenous estrogen production. In a small, randomized, placebo-controlled study, we have examined the effects of 8 weeks of estrogen supplementation on a number of surrogate cardiovascular end points, including lipid levels, blood pressure, and forearm vascular reactivity.  
 
-text[[77, 82, 477, 273]]
-hanced knowledge is now available regarding the wide range of actions of estrogens on the cardiovascular system, even in male tissues. These developments suggest that it may be appropriate to reassess the adverse findings of the Coronary Drug Project. To pursue this, we have investigated the cardiovascular effects of low- dose estrogen supplementation in a group of men rendered hypogonadal as a result of treatment for prostatic cancer, thereby reducing endogenous estrogen production. In a small, randomized, placebo-controlled study, we have examined the effects of 8 weeks of estrogen supplementation on a number of surrogate cardiovascular end points, including lipid levels, blood pressure, and forearm vascular reactivity.  
-
-sub_title[[239, 287, 315, 303]]
+sub_title[[240, 286, 315, 303]]
 ## Methods  
 
-sub_title[[77, 311, 144, 325]]
+sub_title[[78, 310, 145, 324]]
 ## Subjects  
 
-text[[77, 325, 477, 394]]
-We studied 12 men rendered hypogonadal by surgical or pharmacologic treatment for prostatic cancer. We excluded patients with clinical evidence of cardiovascular disease (or on cardiovascular drugs) or severe renal, hepatic, respiratory, or hematologic conditions. The study was approved by the Alfred Hospital Human Ethics Committee. All subjects gave written fully informed consent.  
+text[[78, 325, 478, 395]]
+We studied 12 men rendered hypogonadal by surgical or pharmacological treatment for prostatic cancer. We excluded patients with clinical evidence of cardiovascular disease (or on cardiovascular drugs) or severe renal, hepatic, respiratory, or hematologic conditions. The study was approved by the Alfred Hospital Human Ethics Committee. All subjects gave written fully informed consent.  
 
-sub_title[[77, 407, 182, 422]]
+sub_title[[78, 409, 184, 424]]
 ## Study Design  
 
-text[[77, 423, 479, 558]]
-The study followed a randomized, double- blind, placebo- controlled design. Subjects were randomly assigned to 8 weeks of estrogen supplementation with estradiol valerate (Progynova, Schering) 1 mg daily \((n = 7\) ; mean age, \(68.4\pm 2.6\) years) or placebo \((n = 5\) ; mean age, \(69.2\pm 2.8\) years). Hemodynamic and forearm vascular studies were performed twice, 8 weeks apart. Subjects were unaware of treatments received. All measurements were made by investigators blinded to the treatment. On each study day, subjects underwent the following procedures: arterial cannulation, blood sampling, assessment of forearm vascular reactivity, and measurement of hormones and other variables.  
+text[[78, 424, 479, 558]]
+The study followed a randomized, double- blind, placebo- controlled design. Subjects were randomly assigned to 8 weeks of estrogen supplementation with estradiol valerate (Progynova, Schering) \(1\mathrm{mg}\) daily \((\mathrm{n} = 7\) ; mean age, \(68.4\pm 2.6\) years) or placebo \((\mathrm{n} = 5\) ; mean age, \(69.2\pm 2.8\) years). Hemodynamic and forearm vascular studies were performed twice, 8 weeks apart. Subjects were unaware of treatments received. All measurements were made by investigators blinded to the treatment. On each study day, subjects underwent the following procedures: arterial examination, blood sampling, assessment of forearm vascular reactivity, and measurement of hormones and other variables.  
 
-sub_title[[77, 570, 242, 584]]
+sub_title[[78, 570, 244, 585]]
 ## Arterial Cannulation  
 
-text[[77, 585, 477, 662]]
-Subjects rested supine throughout each study in a quiet, temperature- controlled room, \((22^{\circ}C)\) . The left brachial artery was cannulated with a 21- gauge, 5- cm catheter (Cook) for intra- arterial blood pressure measurement (Spacelabs Inc), drug infusions, and arterial blood sampling. Heart rate was monitored by electrocardiography. Subjects rested for 30 minutes before commencement of the study.  
+text[[78, 586, 479, 662]]
+Subjects rested supine throughout each study in a quiet, temperature- controlled room, \((22^{\circ}\mathrm{C})\) . The left brachial artery was cannulated with a 21- gauge, \(5\mathrm{- cm}\) catheter (Cook) for intra- arterial blood pressure measurement (Spacelabs Inc), drug infusions, and arterial blood sampling. Heart rate was monitored by electrocardiography. Subjects rested for 30 minutes before commencement of the study.  
 
-sub_title[[77, 674, 204, 689]]
+sub_title[[78, 674, 203, 690]]
 ## Blood Sampling  
 
-text[[77, 689, 477, 753]]
-Blood was taken on each occasion for measurement of urea, electrolytes, glucose, total cholesterol, triglycerides, HDL cholesterol, liver function, full blood count, estradiol, testosterone, andrenstenidine, dehydroepiandrosterone, sex hormone- binding globulin, follicle- stimulating hormone (FSH), and luteinizing hormone (LH).  
+text[[78, 690, 479, 754]]
+Blood was taken on each occasion for measurement of urea, electrolytes, glucose, total cholesterol, triglycerides, HDL cholesterol, liver function, full blood count, estradiol, testosterone, andtendecine, dehydroepiandrosterone, sex hormone- binding globulin, follicle- stimulating hormone (FSH), and luteinizing hormone (LH).  
 
-sub_title[[77, 764, 421, 778]]
-## Assessment of Forearm Vascular Reactivity  
+sub_title[[78, 762, 418, 780]]
+## A assessment of Forearm Vascular Reactivity  
 
-text[[77, 779, 479, 866]]
+text[[78, 779, 479, 863]]
 Forearm vascular responsiveness was assessed by venous occlusion plethysmography with a sealed alloy- filled gallium and indium double- stranded strain gauge (Medasonic). Hand blood flow was excluded via a wrist cuff ( \(200\mathrm{mm}\mathrm{Hg}\) ); venous occlusion pressure was \(50\mathrm{mm}\mathrm{Hg}\) . Basal blood flow was obtained as an average of 3 measurements. Drugs were infused via an infusion pump at 2 mL/min.  
 
-text[[77, 866, 479, 946]]
-A cyclothioline (BDH Chemicals) was infused at 9.25, 18.5, and 37 \(\mu \mathrm{g / min}\) : norepinephrine at 25, 50 and \(100~\mathrm{ng / min}\) ; and angiotensin (Ang) II at 8, 16, and \(32\mathrm{ng / min}\) , each dose for 2 minutes to allow blood flow to reach steady state. Basal NO release was assessed by intra- arterial infusion of \(\mathrm{N}^{6}\) - monomethyl- L- arginine (L- NMMA) (Calbiochem- Novabiochem) at 1, 2, and 4 \(\mu \mathrm{mol / min}\) , each dose for 5 minutes. Finally, sodium nitroprusside (David Bull Laboratories)  
+text[[78, 864, 479, 946]]
+A cyclicholine (BDH Chemicals) was infused at 9.25, 18.5, and 37 \(\mu \mathrm{g / min}\) ; norepinephrine at 25, 50 and \(100\mathrm{ng / min}\) ; and angiotensin (Ang) II at 8, 16, and 32 \(\mathrm{ng / min}\) , each dose for 2 minutes to allow blood flow to reach steady state. Basal NO release was assessed by intra- arterial infusion of \(\mathrm{N^G}\) - monomethyl- L- arginine (L- NMMA) (Calbiochem- Novabiochem) at 1, 2, and \(4\mu \mathrm{mol / min}\) , each dose for 5 minutes. Finally, sodium nitroprusside (David Bull Laboratories)  
 
-table[[517, 114, 918, 189]]
-table_caption[[517, 84, 910, 113]]
+table[[516, 116, 917, 190]]
+table_caption[[519, 85, 912, 115]]
 TABLE 1. Baseline Characteristics of Subjects Randomized to Estrogen \((n = 7)\) and Placebo \((n = 5)\)   
 
-<table>Treatment GroupAge, yWeight, kgBMI, kg/m²Systolic BP, mmHgDiastolic BP, mmHgEstrogen68.4 ± 2.172.4 ± 4.527.2 ± 2.0136 ± 187 ± 1Placebo69.2 ± 2.870.8 ± 4.927.6 ± 2.3134 ± 186 ± 2</table>
+<table><td rowspan="2">Treatment Group<td rowspan="2">Age, y<td colspan="2">Weight, kg<td rowspan="2">BMI, kg/m²<td rowspan="2">Systolic BP, mm Hg<td rowspan="2">Diastolic BP, mm HgEstrogen68.4±2.172.4±4.527.2±2.0136±187±1Placebo69.2±2.870.8±4.927.6±2.3134±186±2</table>
 
-table_footnote[[530, 193, 800, 205]]
+table_footnote[[528, 193, 801, 206]]
 BMI indicates body mass index; BP, blood pressure.  
 
-text[[517, 229, 918, 281]]
+text[[518, 229, 917, 281]]
 was infused at \(1.6\mu \mathrm{g / min}\) for 2 minutes. The peak response was determined as the average of 3 consecutive steady state measurements. A 15- minute rest period between interventions was sufficient for flow to return to resting levels.  
 
-sub_title[[517, 294, 893, 309]]
+sub_title[[518, 295, 896, 310]]
 ## Measurement of Hormones and Other Variables  
 
-text[[517, 310, 918, 385]]
-Estradiol and other hormones, namely, total testosterone, andrenstenidine, FSH, LH, and sex hormone- binding globulin were measured by specific radioimmunoassay. The intra- assay coefficient of variation for estradiol was \(9\%\) \((n = 32)\) and sensitivity 30 pmol/L. Total cholesterol, triglycerides, HDL cholesterol, and glucose were also measured.  
+text[[518, 311, 918, 386]]
+Estradiol and other hormones, namely, total testosterone, andtendecine, FSH, LH, and sex hormone- binding globulin were measured by specific radioimmunoassay. The intra- assay coefficient of variation for estradiol was \(9\%\) n \(n = 32\) and sensitivity 30 pmol/L. Total cholesterol, triglycerides, HDL cholesterol, and glucose were also measured.  
 
-sub_title[[517, 398, 801, 413]]
+sub_title[[518, 401, 802, 416]]
 ## Calculations and Statistical Analysis  
 
-text[[517, 415, 918, 480]]
-Results are expressed as mean \(\pm\) SEM. Vascular reactivity doseresponse curves were compared by 2- way repeated- measures ANOVA. Other data were compared by Student's t test. In cases in which multiple comparisons were made, the Bonferroni correction was applied. The null hypothesis was rejected at \(P< 0.05\)  
+text[[518, 417, 917, 480]]
+Results are expressed as mean \(\pm\) SEM. Vascular reactivity does- response curves were compared by 2- way repeated- measures ANOVA. Other data were compared by Student's t test. In cases in which multiple comparisons were made, the Bonferroni correction was applied. The null hypothesis was rejected at \(P< 0.05\)  
 
-sub_title[[684, 495, 748, 510]]
+sub_title[[685, 496, 750, 509]]
 ## Results  
 
-text[[517, 510, 918, 586]]
+text[[518, 511, 918, 582]]
 There were no significant adverse effects reported in any of the subjects. Only 1 subject experienced symptoms likely to be associated with estrogen treatment: mild, persistent breast tenderness. The other subjects were unable to tell whether they were receiving active treatment or placebo.  
 
-sub_title[[517, 601, 706, 615]]
+sub_title[[518, 600, 705, 615]]
 ## Baseline Characteristics  
 
-text[[517, 617, 918, 783]]
-Baseline characteristics are shown in Tables 1 and 2. There were no differences between the estrogen- and placebo- treated groups with respect to age, body mass index, systolic or diastolic blood pressure, or baseline plasma levels of estradiol, total testosterone, andrenstenidine, sex hormone- binding globulin, LH, total cholesterol, triglycerides, HDL cholesterol, hemoglobin, or glucose. FSH was higher in the placebo group as a result of very high levels in 1 individual. Testosterone levels were very low in both estrogen- and placebo- treated groups, consistent with their hypogonadal status.  
+text[[518, 616, 918, 780]]
+Baseline characteristics are shown in Tables 1 and 2. There were no differences between the estrogen- and placebo- treated groups with respect to age, body mass index, systolic or diastolic blood pressure, or baseline plasma levels of estradiol, total testosterone, andtendecine, sex hormone- binding globulin, LH, total cholesterol, triglycerides, HDL cholesterol, hemoglobin, or glucose. FSH was higher in the placebo group as a result of very high levels in 1 individual. Testosterone levels were very low in both estrogen- and placebo- treated groups, consistent with their hypogonadal status.  
+
+sub_title[[518, 797, 776, 810]]
+## Effect of Estradiol on Serum and  
 
-sub_title[[517, 798, 777, 828]]
-## Effect of Estradiol on Serum and Plasma Measurements  
+sub_title[[518, 813, 696, 827]]
+## Plasma Measurements  
 
-text[[517, 828, 918, 948]]
-Asexpected, estrogen levels increased with estrogen treatment, FSH levels fell, and androgen levels showed no change. HDL levels increased significantly with estrogen treatment, but total cholesterol and triglyceride levels were constant (Table 2). Glucose levels were unchanged with estrogen treatment. There were no significant differences in the placebo group. No changes were observed in renal function, liver function, or any hematologic parameters.
\ No newline at end of file
+text[[518, 828, 918, 946]]
+As expected, estrogen levels increased with estrogen treatment, FSH levels fell, and androgen levels showed no change. HDL levels increased significantly with estrogen treatment, but total cholesterol and triglyceride levels were constant (Table 2). Glucose levels were unchanged with estrogen treatment. There were no significant differences in the placebo group. No changes were observed in renal function, liver function, or any hematologic parameters.
\ No newline at end of file
diff --git a/stage1/sample_00028/document.md b/stage1/sample_00028/document.md
index cb692f468d38cb752cb14386837cccd476e4c9ea..ed168f83672345b5dbdae08eeacedbcefeca40b8 100644
--- a/stage1/sample_00028/document.md
+++ b/stage1/sample_00028/document.md
@@ -1,39 +1,36 @@
-21 Furthermore, studies in male-to-female transsexuals have shown that both flow-mediated and nitroglycerin-induced vasodilations in the brachial artery are enhanced compared with control men, suggesting that high-dose estrogen treatment enhances vascular reactivity in genetic males. In healthy young men, single doses of sublingual estradiol or intravenous conjugated equine estrogens, at plasma concentrations within the physiological range for premenopausal women, have been shown to induce rapid onset, rapid offset, nongenomic effects on the endothelium-mediated vasodilator response to acetylcholine, with no effect on the endothelium-independent action of sodium nitroprusside. Not all studies have yielded positive results: for example, a study of short-term estrogen supplementation failed to show an effect on acetylcholine-induced coronary artery vasoconstriction in men, and estrogens reportedly did not augment flow-mediated dilation in the brachial artery or influence serum levels of metabolites of NO in older male subjects. Of interest, in vitro studies of 17β-estradiol-induced vasodilation in human epicardial coronary arteries have shown an attenuated response in male compared with female patients, and neither NO synthase nor cyclooxygenase inhibition influenced this response. The present study considered hypogonadal men, who have low levels of endogenous estrogen production and who with low-dose estrogen supplementation show increases in plasma estradiol levels from very low to modest levels, comparable to those in found in premenopausal women. The results are broadly consistent with those found in perimenopausal and postmenopausal women. The attenuation of norepinephrine-induced vasoconstriction after estrogen supplementation is similar to our observation in perimenopausal women and, as previously suggested, may be related to an estrogen-induced decrease in α-adrenoceptor binding. As in this study, estrogen has previously been reported to decrease Ang II-induced vasoconstriction in experimental animals and in human internal mammary arteries in vitro, most likely through a direct effect on vascular smooth muscle cells. A decreased response to Ang II is likely to represent a potentially beneficial effect of estrogen with respect to cardiovascular risk. Of interest, a decrease in Ang II-induced vasoconstriction was not observed in our previous study in perimenopausal women. In the present study it is also possible that estrogen-induced increase in basal nitric oxide release (previously demonstrated in perimenopausal women) resulted in a decreased basal arterial tone and thus an attenuated vasoconstrictor responsiveness to both norepinephrine and Ang II. Androgen withdrawal has been shown to enhance endothelium-dependent vasodilation in adult men; in our study, however, testosterone levels were equally low in both the estrogen- and placebo-treated groups. In the present study, as in our previous studies in women, estrogen supplementation induced a fall in both systolic and diastolic blood pressure, but no change occurred in the group that did not receive estrogen. Previous studies in women examining the effect of estrogens on blood pressure have been conflicting, with some studies showing an increase in blood pressure, others showing no change, hypertension and yet others suggesting an antihypertensive effect. Different ences in the type of estrogen administered or in dose might help to explain some of the discrepancies observed in these earlier studies in women. Nevertheless, it would appear from our study that in hypogonadal men 17β-estradiol exerts blood pressure-lowering effects. In summary, our results show that, without producing significant adverse effects, short-term treatment with low-dose estrogen in elderly hypogonadal men leads to changes in cardiovascular reactivity of a potentially beneficial nature. Accordingly, we conclude that, at least in this group of patients, there may be a role for low-dose estrogen supplementation in the management of cardiovascular risk. We recognize that in our study estrogen induced an improvement in a number of surrogate end points, namely, enhanced endothelium-dependent vasorelaxation, attenuated responses to vasoconstrictors, and reduced blood pressure. We therefore suggest that to explore further the possible physiological roles of estrogen and to examine the potential therapeutic use of estrogenic compounds in men at high risk of cardiovascular disease, further studies that emphasize clinical end points are warranted.  
-
-text[[75, 73, 479, 413]]
-allografts. Furthermore, studies in male- to- female transsex- uals have shown that both flow-mediated and nitroglycerin- induced vasodilations in the brachial artery are enhanced compared with control men, suggesting that high- dose estro- gen treatment enhances vascular reactivity in genetic males. In healthy young men, single doses of sublingual estradiol or intravenous conjugated equine estrogens, at plasma concentrations within the physiological range for premenopausal women, have been shown to induce rapid onset, rapid offset, nongenomic effects on the endothelium- mediated vasodilator response to acetylcholine, with no effect on the endothelium- independent action of sodium nitroprus- side. Not all studies have yielded positive results: for example, a study of short- term estrogen supplementation failed to show an effect on acetylcholine- induced coronary artery vasoconstriction in men, and estrogens reportedly did not augment flow- mediated dilation in the brachial artery or influence serum levels of metabolites of NO in older male subjects. Of interest, in vitro studies of 17β- estradiol- induced vasodilation in human epicardial coronary arteries have shown an attenuated response in male compared with female patients, and neither NO synthase nor cyclooxygenase inhibition influenced this response.  
-
-text[[75, 415, 479, 841]]
-The present study considered hypogonadal men, who have low levels of endogenous estrogen production and who with low- dose estrogen supplementation show increases in plasma estradiol levels from very low to modest levels, comparable to those in found in premenopausal women. The results are broadly consistent with those found in perimenopausal and postmenopausal women. The attenuation of norepinephrine- induced vasoconstriction after estrogen supplementation is similar to our observation in perimenopausal women and, as previously suggested, may be related to an estrogen- induced decrease in α- adrenoceptor binding. As in this study, estrogen has previously been reported to decrease Ang II- induced vasoconstriction in experimental animals and in human internal mammary arteries in vitro, most likely through a direct effect on vascular smooth muscle cells. A decreased response to Ang II is likely to represent a potentially beneficial effect of estrogen with respect to cardiovascular risk. Of interest, a decrease in Ang II- induced vasoconstriction was not observed in our previous study in perimenopausal women. In the present study it is also possible that estrogen- induced increase in basal nitric oxide release (previously demonstrated in perimenopausal women) resulted in a decreased basal arterial tone and thus an attenuated vasoconstrictor responsiveness to both norepinephrine and Ang II. Androgen withdrawal has been shown to enhance endothelium- dependent vasodilation in adult men; in our study, however, testosterone levels were equally low in both the estrogen- and placebo- treated groups.  
-
-text[[77, 830, 479, 945]]
-In the present study, as in our previous studies in women, estrogen supplementation induced a fall in both systolic and diastolic blood pressure, but no change occurred in the group that did not receive estrogen. Previous studies in women examining the effect of estrogens on blood pressure have been conflicting, with some studies showing an increase in blood pressure, others showing no change, hypertension and yet others suggesting an antihypertensive effect.  
-
-text[[518, 83, 918, 156]]
-ences in the type of estrogen administered or in dose might help to explain some of the discrepancies observed in these earlier studies in women. Nevertheless, it would appear from our study that in hypogonadal men 17β- estradiol exerts blood pressure- lowering effects.  
-
-text[[519, 157, 920, 388]]
-In summary, our results show that, without producing significant adverse effects, short- term treatment with low- dose estrogen in elderly hypogonadal men leads to changes in cardiovascular reactivity of a potentially beneficial nature. Accordingly, we conclude that, at least in this group of patients, there may be a role for low- dose estrogen supplementation in the management of cardiovascular risk. We recognize that in our study estrogen induced an improvement in a number of surrogate end points, namely, enhanced endothelium- dependent vasorelaxation, attenuated responses to vasoconstrictors, and reduced blood pressure. We therefore suggest that to explore further the possible physiological roles of estrogen and to examine the potential therapeutic use of estrogenic compounds in men at high risk of cardiovascular disease, further studies that emphasize clinical end points are warranted.  
-
-sub_title[[639, 404, 795, 420]]
-## Acknowledgments  
-
-text[[520, 420, 919, 484]]
-Dr Komesaroff is supported by the Victorian Health Promotion Foundation. Dr Sudhir is a Senior Research Fellow of the National Health and Medical Research Council of Australia. We acknowledge the support and advice of Professor John Funder, Director, Baker Medical Research Institute.  
-
-sub_title[[657, 497, 764, 510]]
-## References  
-
-text[[521, 512, 919, 944]]
-1. Barnett-Connor E, Grady D. Hormone replacement therapy, heart disease, and other considerations. Annu Rev Public Health. 1998;19:55-72.  
-2. Hulley S, Grady D, Bush T, Furberg C, Herrington D, Riggs B, Vittinghoff E, for the Heart and Estrogen/Progestin Replacement Study (HERS) Research Group. Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. JAMA. 1998;280:605-613.  
-3. MacDonald PC, Madden JD, Brenner PF, Wilson JD, Siiteri PK. Origin of estrogen in normal men and in women with testicular feminization. J Clin Endocrinol Metab. 1979;49:905-916.  
-4. Kim-Schulze S, McGowan KA, Hubchak SC, Cid MC, Martin MB, Kleinman HK, Greene GL, Schnaper HW. Expression of an estrogen receptor by human coronary artery and umbilical vein endothelial cells. Circulation. 1996;94:1402-1407.  
-5. Sudhir K, Chou TM, Messina LM, Hutchison SJ, Korach KS, Chatterjee K, Rubanyi GM. Endothelial dysfunction in a man with disruptive mutation in oestrogen-receptor gene. Lancet. 1997;349:1146-1147.  
-6. Sudhir K, Chou TM, Chatterjee K, Smith EP, Williams TC, Kane JP, Malloy JM, Korach KS, Rubanyi GM. Premature coronary artery disease associated with a disruptive mutation in the estrogen receptor gene in a man. Circulation. 1997;96:3774-3777.  
-7. The Coronary Drug Project Research Group. The Coronary Drug Project: findings leading to discontinuation of the 2.5-mg day estrogen group. JAMA. 1973;226:652-657.  
-8. Sudhir K, Komesaroff PA. Clinical review 110: cardiovascular actions of estrogens in men. J Clin Endocrinol Metab. 1999;84:3411-3415.  
-9. Burtis CA, Ashwood ER. Tietz Textbook of Clinical Chemistry. 3rd ed. Philadelphia, PA: WB Saunders Co; 1999:95, 219-220.  
-10. Kwiterovich PO Jr. The antiatherogenic role of high-density lipoprotein cholesterol. Am J Cardiol. 1998;82:13Q-21Q.  
-11. Garg UC, Hassid A. Nitric oxide-generating vasodilators and 8-bromo-cyclic guanosine monophosphate inhibit mitogenesis and proliferation of cultured rat vascular smooth muscle cells. J Clin Invest. 1989;83:1774-1777.  
-12. Bath PM, Hassid DG, Gladwin AM, Palmer RM, Martin JF. Nitric oxide and prostaticin: divergence of inhibitory effects on monocyte chemotaxis and adhesion to endothelium in vitro. Arterioscler Thromb. 1991;11:254-260.
\ No newline at end of file
+21 Furthermore, studies in male-to-female transsexuals have shown that both flow-mediated and nitroglycerin-induced vasodilations in the brachial artery are enhanced compared with control men, suggesting that high-dose estrogen treatment enhances vascular reactivity in genetic males. 23 In healthy young men, single doses of sublingual estradiol or intravenous conjugated equine estrogens, at plasma concentrations within the physiological range for premenopausal women, have been shown to induce rapid onset, rapid offset, nongenomic effects on the endothelium-mediated vasodilator response to acetylcholine, with no effect on the endothelium-independent action of sodium nitroprusside. 24 Not all studies have yielded positive results: for example, a study of short-term estrogen supplementation failed to show an effect on acetylcholine-induced coronary artery vasoconstriction in men, and estrogens reportedly did not augment flow-mediated dilation in the brachial artery or influence serum levels of metabolites of NO in older male subjects. Of interest, in vitro studies of 17β-estradiol-induced vasodilation in human epicardial coronary arteries have shown an attenuated response in male compared with female patients, and neither NO synthase nor cyclooxygenase inhibition influenced this response. 27
+
+text[[77, 419, 479, 841]]
+The present study considered hypogonadal men, who have low levels of endogenous estrogen production and who with low-dose estrogen supplementation show increases in plasma estradiol levels from very low to modest levels, comparable to those in found in premenopausal women. The results are broadly consistent with those found in perimenopausal and postmenopausal women. The attenuation of norepinephrine-induced vasoconstriction after estrogen supplementation is similar to our observation in perimenopausal women, and, as previously suggested, may be related to an estrogen-induced decrease in α-adrenoceptor binding. As in this study, estrogen has previously been reported to decrease Ang II-induced vasoconstriction in experimental animals and in human internal mammary arteries in vitro, most likely through a direct effect on vascular smooth muscle cells. A decreased response to Ang II is likely to represent a potentially beneficial effect of estrogen with respect to cardiovascular risk. Of interest, a decrease in Ang II-induced vasoconstriction was not observed in our previous study in perimenopausal women. In the present study it is also possible that estrogen-induced increase in basal nitric oxide release (previously demonstrated in perimenopausal women) resulted in a decreased basal arterial tone and thus an attenuated vasoconstrictor responsiveness to both norepinephrine and Ang II. Androgen withdrawal has been shown to enhance endothelium-dependent vasodilation in adult men; in our study, however, testosterone levels were equally low in both the estrogen- and placebo-treated groups. 
+
+text[[77, 834, 479, 946]]
+In the present study, as in our previous studies in women, estrogen supplementation induced a fall in both systolic and diastolic blood pressure, but no change occurred in the group that did not receive estrogen. Previous studies in women examining the effect of estrogens on blood pressure have been conflicting, with some studies showing an increase in blood pressure, others showing no change, and yet others suggesting an antihypertensive effect. 
+
+text[[517, 86, 918, 154]]
+ences in the type of estrogen administered 39 or in dose might help to explain some of the discrepancies observed in these earlier studies in women. Nevertheless, it would appear from our study that in hypogonadal men 17β-estradiol exerts blood pressure-lowering effects. 
+
+text[[517, 156, 918, 386]]
+In summary, our results show that, without producing significant adverse effects, short-term treatment with low-dose estrogen in elderly hypogonadal men leads to changes in cardiovascular reactivity of a potentially beneficial nature. Accordingly, we conclude that, at least in this group of patients, there may be a role for low-dose estrogen supplementation in the management of cardiovascular risk. We recognize that in our study estrogen induced an improvement in a number of surrogate end points, namely, enhanced endothelium-dependent vasorelaxation, attenuated responses to vasoconstrictors, and reduced blood pressure. We therefore suggest that to explore further the possible physiological roles of estrogen and to examine the potential therapeutic use of estrogenic compounds in men at high risk of cardiovascular disease, further studies that emphasize clinical end points are warranted. 
+
+sub_title[[639, 405, 795, 420]]
+## Acknowledgments 
+
+text[[517, 422, 918, 476]]
+Dr Komesaroff is supported by the Victorian Health Promotion Foundation. Dr Sudhir is a Senior Research Fellow of the National Health and Medical Research Council of Australia. We acknowledge the support and advice of Professor John Funder, Director, Baker Medical Research Institute. 
+
+sub_title[[638, 495, 763, 509]]
+## References 
+
+text[[520, 512, 918, 944]]
+1. Barnett-Connor E, Grady D. Hormone replacement therapy, heart disease, and other considerations. Annu Rev Public Health. 1998;19:55-72.
+2. Hulley S, Grady D, Bush T, Furberg C, Herrington D, Riggs B, Vittinghoff E, for the Heart and Estrogen/Progestin Replacement Study (HERS) Research Group. Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. JAMA. 1998;280:605-613.
+3. MacDonald PC, Madden JD, Brenner PF, Wilson JD, Siiteri PK. Origin of estrogen in normal men and in women with testicular feminization. J Clin Endocrinol Metab. 1979;49:905-916.
+4. Kim-Schulze S, McGowan KA, Hubchak SC, Cid MC, Martin MB, Kleinman HK, Greene GL, Schnaper HW. Expression of an estrogen receptor by human coronary artery and umbilical vein endothelial cells. Circulation. 1996;94:1402-1407.
+5. Sudhir K, Chou TM, Messina LM, Hutchison SJ, Korach KS, Chatterjee K, Rubanyi GM. Endothelial dysfunction in a man with disruptive mutation in oestrogen-receptor gene. Lancet. 1997;349:1146-1147.
+6. Sudhir K, Chou TM, Chatterjee K, Smith EP, Williams TC, Kane JP, Malloy MJ, Korach KS, Rubanyi GM. Premature coronary artery disease associated with a disruptive mutation in the estrogen receptor gene in a man. Circulation. 1997;96:3774-3777.
+7. The Coronary Drug Project Research Group. The Coronary Drug Project: findings leading to discontinuation of the 2.5-mg day estrogen group. JAMA. 1973;226:652-657.
+8. Sudhir K, Komesaroff PA. Clinical review 110: cardiovascular actions of estrogens in men. J Clin Endocrinol Metab. 1999;84:3411-3415.
+9. Burtis CA, Ashwood ER. Tietz Textbook of Clinical Chemistry. 3rd ed. Philadelphia, Pa: WB Saunders Co; 1999:95, 219-220.
+10. Kwiterovich PO Jr. The antiatherogenic role of high-density lipoprotein cholesterol. Am J Cardiol. 1998;82:1392-1401.
+11. Garg UC, Hassid A. Nitric oxide-generating vasodilators and 8-bromo-cyclic guanosine monophosphate inhibit mitogenesis and proliferation of cultured rat vascular smooth muscle cells. J Clin Invest. 1989;83:1774-1777.
+12. Bath PM, Hassid DG, Gladwin AM, Palmer RM, Martin JF. Nitric oxide and prostacyclin: divergence of inhibitory effects on monocyte chemotaxis and adhesion to endothelium in vitro. Arterioscler Thromb. 1991;11:254-260.
\ No newline at end of file
diff --git a/stage1/sample_00028/raw_response.md b/stage1/sample_00028/raw_response.md
index cb692f468d38cb752cb14386837cccd476e4c9ea..ed168f83672345b5dbdae08eeacedbcefeca40b8 100644
--- a/stage1/sample_00028/raw_response.md
+++ b/stage1/sample_00028/raw_response.md
@@ -1,39 +1,36 @@
-21 Furthermore, studies in male-to-female transsexuals have shown that both flow-mediated and nitroglycerin-induced vasodilations in the brachial artery are enhanced compared with control men, suggesting that high-dose estrogen treatment enhances vascular reactivity in genetic males. In healthy young men, single doses of sublingual estradiol or intravenous conjugated equine estrogens, at plasma concentrations within the physiological range for premenopausal women, have been shown to induce rapid onset, rapid offset, nongenomic effects on the endothelium-mediated vasodilator response to acetylcholine, with no effect on the endothelium-independent action of sodium nitroprusside. Not all studies have yielded positive results: for example, a study of short-term estrogen supplementation failed to show an effect on acetylcholine-induced coronary artery vasoconstriction in men, and estrogens reportedly did not augment flow-mediated dilation in the brachial artery or influence serum levels of metabolites of NO in older male subjects. Of interest, in vitro studies of 17β-estradiol-induced vasodilation in human epicardial coronary arteries have shown an attenuated response in male compared with female patients, and neither NO synthase nor cyclooxygenase inhibition influenced this response. The present study considered hypogonadal men, who have low levels of endogenous estrogen production and who with low-dose estrogen supplementation show increases in plasma estradiol levels from very low to modest levels, comparable to those in found in premenopausal women. The results are broadly consistent with those found in perimenopausal and postmenopausal women. The attenuation of norepinephrine-induced vasoconstriction after estrogen supplementation is similar to our observation in perimenopausal women and, as previously suggested, may be related to an estrogen-induced decrease in α-adrenoceptor binding. As in this study, estrogen has previously been reported to decrease Ang II-induced vasoconstriction in experimental animals and in human internal mammary arteries in vitro, most likely through a direct effect on vascular smooth muscle cells. A decreased response to Ang II is likely to represent a potentially beneficial effect of estrogen with respect to cardiovascular risk. Of interest, a decrease in Ang II-induced vasoconstriction was not observed in our previous study in perimenopausal women. In the present study it is also possible that estrogen-induced increase in basal nitric oxide release (previously demonstrated in perimenopausal women) resulted in a decreased basal arterial tone and thus an attenuated vasoconstrictor responsiveness to both norepinephrine and Ang II. Androgen withdrawal has been shown to enhance endothelium-dependent vasodilation in adult men; in our study, however, testosterone levels were equally low in both the estrogen- and placebo-treated groups. In the present study, as in our previous studies in women, estrogen supplementation induced a fall in both systolic and diastolic blood pressure, but no change occurred in the group that did not receive estrogen. Previous studies in women examining the effect of estrogens on blood pressure have been conflicting, with some studies showing an increase in blood pressure, others showing no change, hypertension and yet others suggesting an antihypertensive effect. Different ences in the type of estrogen administered or in dose might help to explain some of the discrepancies observed in these earlier studies in women. Nevertheless, it would appear from our study that in hypogonadal men 17β-estradiol exerts blood pressure-lowering effects. In summary, our results show that, without producing significant adverse effects, short-term treatment with low-dose estrogen in elderly hypogonadal men leads to changes in cardiovascular reactivity of a potentially beneficial nature. Accordingly, we conclude that, at least in this group of patients, there may be a role for low-dose estrogen supplementation in the management of cardiovascular risk. We recognize that in our study estrogen induced an improvement in a number of surrogate end points, namely, enhanced endothelium-dependent vasorelaxation, attenuated responses to vasoconstrictors, and reduced blood pressure. We therefore suggest that to explore further the possible physiological roles of estrogen and to examine the potential therapeutic use of estrogenic compounds in men at high risk of cardiovascular disease, further studies that emphasize clinical end points are warranted.  
-
-text[[75, 73, 479, 413]]
-allografts. Furthermore, studies in male- to- female transsex- uals have shown that both flow-mediated and nitroglycerin- induced vasodilations in the brachial artery are enhanced compared with control men, suggesting that high- dose estro- gen treatment enhances vascular reactivity in genetic males. In healthy young men, single doses of sublingual estradiol or intravenous conjugated equine estrogens, at plasma concentrations within the physiological range for premenopausal women, have been shown to induce rapid onset, rapid offset, nongenomic effects on the endothelium- mediated vasodilator response to acetylcholine, with no effect on the endothelium- independent action of sodium nitroprus- side. Not all studies have yielded positive results: for example, a study of short- term estrogen supplementation failed to show an effect on acetylcholine- induced coronary artery vasoconstriction in men, and estrogens reportedly did not augment flow- mediated dilation in the brachial artery or influence serum levels of metabolites of NO in older male subjects. Of interest, in vitro studies of 17β- estradiol- induced vasodilation in human epicardial coronary arteries have shown an attenuated response in male compared with female patients, and neither NO synthase nor cyclooxygenase inhibition influenced this response.  
-
-text[[75, 415, 479, 841]]
-The present study considered hypogonadal men, who have low levels of endogenous estrogen production and who with low- dose estrogen supplementation show increases in plasma estradiol levels from very low to modest levels, comparable to those in found in premenopausal women. The results are broadly consistent with those found in perimenopausal and postmenopausal women. The attenuation of norepinephrine- induced vasoconstriction after estrogen supplementation is similar to our observation in perimenopausal women and, as previously suggested, may be related to an estrogen- induced decrease in α- adrenoceptor binding. As in this study, estrogen has previously been reported to decrease Ang II- induced vasoconstriction in experimental animals and in human internal mammary arteries in vitro, most likely through a direct effect on vascular smooth muscle cells. A decreased response to Ang II is likely to represent a potentially beneficial effect of estrogen with respect to cardiovascular risk. Of interest, a decrease in Ang II- induced vasoconstriction was not observed in our previous study in perimenopausal women. In the present study it is also possible that estrogen- induced increase in basal nitric oxide release (previously demonstrated in perimenopausal women) resulted in a decreased basal arterial tone and thus an attenuated vasoconstrictor responsiveness to both norepinephrine and Ang II. Androgen withdrawal has been shown to enhance endothelium- dependent vasodilation in adult men; in our study, however, testosterone levels were equally low in both the estrogen- and placebo- treated groups.  
-
-text[[77, 830, 479, 945]]
-In the present study, as in our previous studies in women, estrogen supplementation induced a fall in both systolic and diastolic blood pressure, but no change occurred in the group that did not receive estrogen. Previous studies in women examining the effect of estrogens on blood pressure have been conflicting, with some studies showing an increase in blood pressure, others showing no change, hypertension and yet others suggesting an antihypertensive effect.  
-
-text[[518, 83, 918, 156]]
-ences in the type of estrogen administered or in dose might help to explain some of the discrepancies observed in these earlier studies in women. Nevertheless, it would appear from our study that in hypogonadal men 17β- estradiol exerts blood pressure- lowering effects.  
-
-text[[519, 157, 920, 388]]
-In summary, our results show that, without producing significant adverse effects, short- term treatment with low- dose estrogen in elderly hypogonadal men leads to changes in cardiovascular reactivity of a potentially beneficial nature. Accordingly, we conclude that, at least in this group of patients, there may be a role for low- dose estrogen supplementation in the management of cardiovascular risk. We recognize that in our study estrogen induced an improvement in a number of surrogate end points, namely, enhanced endothelium- dependent vasorelaxation, attenuated responses to vasoconstrictors, and reduced blood pressure. We therefore suggest that to explore further the possible physiological roles of estrogen and to examine the potential therapeutic use of estrogenic compounds in men at high risk of cardiovascular disease, further studies that emphasize clinical end points are warranted.  
-
-sub_title[[639, 404, 795, 420]]
-## Acknowledgments  
-
-text[[520, 420, 919, 484]]
-Dr Komesaroff is supported by the Victorian Health Promotion Foundation. Dr Sudhir is a Senior Research Fellow of the National Health and Medical Research Council of Australia. We acknowledge the support and advice of Professor John Funder, Director, Baker Medical Research Institute.  
-
-sub_title[[657, 497, 764, 510]]
-## References  
-
-text[[521, 512, 919, 944]]
-1. Barnett-Connor E, Grady D. Hormone replacement therapy, heart disease, and other considerations. Annu Rev Public Health. 1998;19:55-72.  
-2. Hulley S, Grady D, Bush T, Furberg C, Herrington D, Riggs B, Vittinghoff E, for the Heart and Estrogen/Progestin Replacement Study (HERS) Research Group. Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. JAMA. 1998;280:605-613.  
-3. MacDonald PC, Madden JD, Brenner PF, Wilson JD, Siiteri PK. Origin of estrogen in normal men and in women with testicular feminization. J Clin Endocrinol Metab. 1979;49:905-916.  
-4. Kim-Schulze S, McGowan KA, Hubchak SC, Cid MC, Martin MB, Kleinman HK, Greene GL, Schnaper HW. Expression of an estrogen receptor by human coronary artery and umbilical vein endothelial cells. Circulation. 1996;94:1402-1407.  
-5. Sudhir K, Chou TM, Messina LM, Hutchison SJ, Korach KS, Chatterjee K, Rubanyi GM. Endothelial dysfunction in a man with disruptive mutation in oestrogen-receptor gene. Lancet. 1997;349:1146-1147.  
-6. Sudhir K, Chou TM, Chatterjee K, Smith EP, Williams TC, Kane JP, Malloy JM, Korach KS, Rubanyi GM. Premature coronary artery disease associated with a disruptive mutation in the estrogen receptor gene in a man. Circulation. 1997;96:3774-3777.  
-7. The Coronary Drug Project Research Group. The Coronary Drug Project: findings leading to discontinuation of the 2.5-mg day estrogen group. JAMA. 1973;226:652-657.  
-8. Sudhir K, Komesaroff PA. Clinical review 110: cardiovascular actions of estrogens in men. J Clin Endocrinol Metab. 1999;84:3411-3415.  
-9. Burtis CA, Ashwood ER. Tietz Textbook of Clinical Chemistry. 3rd ed. Philadelphia, PA: WB Saunders Co; 1999:95, 219-220.  
-10. Kwiterovich PO Jr. The antiatherogenic role of high-density lipoprotein cholesterol. Am J Cardiol. 1998;82:13Q-21Q.  
-11. Garg UC, Hassid A. Nitric oxide-generating vasodilators and 8-bromo-cyclic guanosine monophosphate inhibit mitogenesis and proliferation of cultured rat vascular smooth muscle cells. J Clin Invest. 1989;83:1774-1777.  
-12. Bath PM, Hassid DG, Gladwin AM, Palmer RM, Martin JF. Nitric oxide and prostaticin: divergence of inhibitory effects on monocyte chemotaxis and adhesion to endothelium in vitro. Arterioscler Thromb. 1991;11:254-260.
\ No newline at end of file
+21 Furthermore, studies in male-to-female transsexuals have shown that both flow-mediated and nitroglycerin-induced vasodilations in the brachial artery are enhanced compared with control men, suggesting that high-dose estrogen treatment enhances vascular reactivity in genetic males. 23 In healthy young men, single doses of sublingual estradiol or intravenous conjugated equine estrogens, at plasma concentrations within the physiological range for premenopausal women, have been shown to induce rapid onset, rapid offset, nongenomic effects on the endothelium-mediated vasodilator response to acetylcholine, with no effect on the endothelium-independent action of sodium nitroprusside. 24 Not all studies have yielded positive results: for example, a study of short-term estrogen supplementation failed to show an effect on acetylcholine-induced coronary artery vasoconstriction in men, and estrogens reportedly did not augment flow-mediated dilation in the brachial artery or influence serum levels of metabolites of NO in older male subjects. Of interest, in vitro studies of 17β-estradiol-induced vasodilation in human epicardial coronary arteries have shown an attenuated response in male compared with female patients, and neither NO synthase nor cyclooxygenase inhibition influenced this response. 27
+
+text[[77, 419, 479, 841]]
+The present study considered hypogonadal men, who have low levels of endogenous estrogen production and who with low-dose estrogen supplementation show increases in plasma estradiol levels from very low to modest levels, comparable to those in found in premenopausal women. The results are broadly consistent with those found in perimenopausal and postmenopausal women. The attenuation of norepinephrine-induced vasoconstriction after estrogen supplementation is similar to our observation in perimenopausal women, and, as previously suggested, may be related to an estrogen-induced decrease in α-adrenoceptor binding. As in this study, estrogen has previously been reported to decrease Ang II-induced vasoconstriction in experimental animals and in human internal mammary arteries in vitro, most likely through a direct effect on vascular smooth muscle cells. A decreased response to Ang II is likely to represent a potentially beneficial effect of estrogen with respect to cardiovascular risk. Of interest, a decrease in Ang II-induced vasoconstriction was not observed in our previous study in perimenopausal women. In the present study it is also possible that estrogen-induced increase in basal nitric oxide release (previously demonstrated in perimenopausal women) resulted in a decreased basal arterial tone and thus an attenuated vasoconstrictor responsiveness to both norepinephrine and Ang II. Androgen withdrawal has been shown to enhance endothelium-dependent vasodilation in adult men; in our study, however, testosterone levels were equally low in both the estrogen- and placebo-treated groups. 
+
+text[[77, 834, 479, 946]]
+In the present study, as in our previous studies in women, estrogen supplementation induced a fall in both systolic and diastolic blood pressure, but no change occurred in the group that did not receive estrogen. Previous studies in women examining the effect of estrogens on blood pressure have been conflicting, with some studies showing an increase in blood pressure, others showing no change, and yet others suggesting an antihypertensive effect. 
+
+text[[517, 86, 918, 154]]
+ences in the type of estrogen administered 39 or in dose might help to explain some of the discrepancies observed in these earlier studies in women. Nevertheless, it would appear from our study that in hypogonadal men 17β-estradiol exerts blood pressure-lowering effects. 
+
+text[[517, 156, 918, 386]]
+In summary, our results show that, without producing significant adverse effects, short-term treatment with low-dose estrogen in elderly hypogonadal men leads to changes in cardiovascular reactivity of a potentially beneficial nature. Accordingly, we conclude that, at least in this group of patients, there may be a role for low-dose estrogen supplementation in the management of cardiovascular risk. We recognize that in our study estrogen induced an improvement in a number of surrogate end points, namely, enhanced endothelium-dependent vasorelaxation, attenuated responses to vasoconstrictors, and reduced blood pressure. We therefore suggest that to explore further the possible physiological roles of estrogen and to examine the potential therapeutic use of estrogenic compounds in men at high risk of cardiovascular disease, further studies that emphasize clinical end points are warranted. 
+
+sub_title[[639, 405, 795, 420]]
+## Acknowledgments 
+
+text[[517, 422, 918, 476]]
+Dr Komesaroff is supported by the Victorian Health Promotion Foundation. Dr Sudhir is a Senior Research Fellow of the National Health and Medical Research Council of Australia. We acknowledge the support and advice of Professor John Funder, Director, Baker Medical Research Institute. 
+
+sub_title[[638, 495, 763, 509]]
+## References 
+
+text[[520, 512, 918, 944]]
+1. Barnett-Connor E, Grady D. Hormone replacement therapy, heart disease, and other considerations. Annu Rev Public Health. 1998;19:55-72.
+2. Hulley S, Grady D, Bush T, Furberg C, Herrington D, Riggs B, Vittinghoff E, for the Heart and Estrogen/Progestin Replacement Study (HERS) Research Group. Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. JAMA. 1998;280:605-613.
+3. MacDonald PC, Madden JD, Brenner PF, Wilson JD, Siiteri PK. Origin of estrogen in normal men and in women with testicular feminization. J Clin Endocrinol Metab. 1979;49:905-916.
+4. Kim-Schulze S, McGowan KA, Hubchak SC, Cid MC, Martin MB, Kleinman HK, Greene GL, Schnaper HW. Expression of an estrogen receptor by human coronary artery and umbilical vein endothelial cells. Circulation. 1996;94:1402-1407.
+5. Sudhir K, Chou TM, Messina LM, Hutchison SJ, Korach KS, Chatterjee K, Rubanyi GM. Endothelial dysfunction in a man with disruptive mutation in oestrogen-receptor gene. Lancet. 1997;349:1146-1147.
+6. Sudhir K, Chou TM, Chatterjee K, Smith EP, Williams TC, Kane JP, Malloy MJ, Korach KS, Rubanyi GM. Premature coronary artery disease associated with a disruptive mutation in the estrogen receptor gene in a man. Circulation. 1997;96:3774-3777.
+7. The Coronary Drug Project Research Group. The Coronary Drug Project: findings leading to discontinuation of the 2.5-mg day estrogen group. JAMA. 1973;226:652-657.
+8. Sudhir K, Komesaroff PA. Clinical review 110: cardiovascular actions of estrogens in men. J Clin Endocrinol Metab. 1999;84:3411-3415.
+9. Burtis CA, Ashwood ER. Tietz Textbook of Clinical Chemistry. 3rd ed. Philadelphia, Pa: WB Saunders Co; 1999:95, 219-220.
+10. Kwiterovich PO Jr. The antiatherogenic role of high-density lipoprotein cholesterol. Am J Cardiol. 1998;82:1392-1401.
+11. Garg UC, Hassid A. Nitric oxide-generating vasodilators and 8-bromo-cyclic guanosine monophosphate inhibit mitogenesis and proliferation of cultured rat vascular smooth muscle cells. J Clin Invest. 1989;83:1774-1777.
+12. Bath PM, Hassid DG, Gladwin AM, Palmer RM, Martin JF. Nitric oxide and prostacyclin: divergence of inhibitory effects on monocyte chemotaxis and adhesion to endothelium in vitro. Arterioscler Thromb. 1991;11:254-260.
\ No newline at end of file
diff --git a/stage1/sample_00029/document.md b/stage1/sample_00029/document.md
index 2d0c51258164642d5999dc4c76074f5f14e9e548..8656a529b5c3b1b8175e2a1046e64b339df0ef38 100644
--- a/stage1/sample_00029/document.md
+++ b/stage1/sample_00029/document.md
@@ -1,21 +1,22 @@
-13. Radomski MW, Palmer RM, Moncada S. Endogenous nitric oxide inhibits human platelet adhesion to vascular endothelium. Lancet. 1987; 2:1057-1058.  
+2:1057-1058.  
 
-text[[76, 111, 480, 591]]
+text[[75, 96, 480, 591]]
+13. Radomski MW, Palmer RM, Moncada S. Endogenous nitric oxide inhibits human platelet adhesion to vascular endothelium. Lancet. 1987; 2:1057-1058.  
 14. Anderson TJ. Assessment and treatment of endothelial dysfunction in humans. J Am Coll Cardiol. 1999;34:631-638.  
 15. Esler M, Lambert G, Jennings G, Turner A, Kaye D. Central and peripheral norepinephrine kinetics in heart failure, coronary artery disease, and hypertension. Adv Pharmacol. 1998;42:650-653.  
 16. Dzau VJ. Vascular renin-angiotensin system and vascular protection. J Cardiovasc Pharmacol. 1993;22(suppl 5):S1-S9.  
 17. Chatterjee K. Inhibitors of the renin-angiotensin system in established cardiac failure. Heart. 1996;76(suppl 3):83-91.  
 18. The Writing Group for the PEPI Trial. Effects of estrogen or estrogen/progestin regimens on heart disease risk factors in postmenopausal women: the Postmenopausal Estrogen/Progestin Interventions (PEPI) Trial. JAMA. 1995;273:199-208.  
-19. Blumenthal RS, Heldman AW, Brinker JA, Resar JR, Coombs VJ, Gloth ST, Gerstenbith G, Reis SE. Acute effects of conjugated estrogens on coronary blood flow response to acetyicholine in men. Am J Cardiol. 1997;80:1021-1024.  
+19. Blumenthal RS, Heldman AW, Brinker JA, Resar JR, Coombs VJ, Gloth ST, Gerstenblith G, Reis SE. Acute effects of conjugated estrogens on coronary blood flow response to acetylcholine in men. Am J Cardiol. 1997;80:1021-1024.  
 20. Reis SE, Holubkov R, Zell KA, Smith AJ, Cohen HA, Feldman MD, Blumenthal RS. Estrogen acutely abolishes abnormal cold-induced coronary constriction in men. Chest. 1998;114:1556-1561.  
-21. Reis SE, Bhoopalam V, Zell KA, Counihan PJ, Smith AJ, Pham S, Murali S. Conjugated estrogens acutely abolish abnormal cold-induced coronary vasoconstriction in male cardiac allografts. Circulation. 1998;97:23-25.  
+21. Reis SE, Bhoopalam V, Zell KA, Counihan PJ, Smith AJ, Pham S, Murali S. Conjugated estrogens acutely abolishes abnormal cold-induced coronary vasoconstriction in male cardiac allografts. Circulation. 1998;97:23-25.  
 22. New G, Timmins KL, Duffy SJ, Tran BT, O'Brien RC, Harper RW, Meredith IT. Long-term estrogen therapy improves vascular function in male to female transsexuals. J Am Coll Cardiol. 1997;29:1437-1444.  
 23. McCrohon JA, Walters WA, Robinson JT, McCredie RJ, Turner L, Adams MR, Handelsman DJ, Celermajer DS. Arterial reactivity is enhanced in genetic males taking high dose estrogens. J Am Coll Cardiol. 1997;29:1432-1436.  
 24. Komesaroff PA, Black CV, Westerman RA. A novel, nongenomic action of estrogen on the cardiovascular system. J Clin Endocrinol Metab. 1998;83:2313-2316.  
-25. Collins P, Rosano GM, Sarrel PM, Ulrich L, Adamopoulos S, Beale CM, McNeill JG, Poole-Wilson PA. 17β-Estradiol attenuates acetylcholine-induced coronary arterial constriction in women but not men with coronary heart disease. Circulation. 1995;92:24-30.  
-26. Kawano H, Motoyama T, Kugiyama K, Hirashima O, Ohgushi M, Fujii H, Ogawa H, Yasue H. Gender difference in improvement of endothelium-dependent vasodilation after estrogen supplementation. J Am Coll Cardiol. 1997;30:914-919.  
+25. Collins P, Rosano GM, Sarrel PM, Ulrich L, Adamopoulos S, Beale CM, McNeill JG, Poole-Wilson PA. 17β-Estradiol attenuates acetylcholin- induced coronary arterial constriction in women but not men with coronary heart disease. Circulation. 1995;92:24-30.  
+26. Kawano H, Motoyama T, Kugiyama K, Hirashima O, Ohgushi M, Fujii H, Ogawa H, Yase H. Gender difference in improvement of endothelium-dependent vasodilation after estrogen supplementation. J Am Coll Cardiol. 1997;30:914-919.  
 
-text[[518, 81, 921, 583]]
+text[[516, 91, 919, 582]]
 27. Chester AH, Jiang C, Borland JA, Y acoub MH, Collins P. Oestrogen relaxes human epicardial coronary arteries through non-endothelium-dependent mechanisms. Coron Artery Dis. 1995;6:417-422.  
 28. Sudhir K, Esler MD, Jennings GL, Komesaroff PA. Estrogen supplementation decreases norepinephrine-induced vasoconstriction and total body norepinephrine spillover in perimenopausal women. Hypertension. 1997;30:1538-1543.  
 29. Ford SP, Reynolds LP, Farley DB, Bhatnagar RK, Van Orden DE. Interaction of ovarian steroids and periarterial alpha1-adrenergic receptors in altering uterine blood flow during the estrous cycle of gilts. Am J Obstet Gynecol. 1984;150:480-484.  
diff --git a/stage1/sample_00029/raw_response.md b/stage1/sample_00029/raw_response.md
index 2d0c51258164642d5999dc4c76074f5f14e9e548..8656a529b5c3b1b8175e2a1046e64b339df0ef38 100644
--- a/stage1/sample_00029/raw_response.md
+++ b/stage1/sample_00029/raw_response.md
@@ -1,21 +1,22 @@
-13. Radomski MW, Palmer RM, Moncada S. Endogenous nitric oxide inhibits human platelet adhesion to vascular endothelium. Lancet. 1987; 2:1057-1058.  
+2:1057-1058.  
 
-text[[76, 111, 480, 591]]
+text[[75, 96, 480, 591]]
+13. Radomski MW, Palmer RM, Moncada S. Endogenous nitric oxide inhibits human platelet adhesion to vascular endothelium. Lancet. 1987; 2:1057-1058.  
 14. Anderson TJ. Assessment and treatment of endothelial dysfunction in humans. J Am Coll Cardiol. 1999;34:631-638.  
 15. Esler M, Lambert G, Jennings G, Turner A, Kaye D. Central and peripheral norepinephrine kinetics in heart failure, coronary artery disease, and hypertension. Adv Pharmacol. 1998;42:650-653.  
 16. Dzau VJ. Vascular renin-angiotensin system and vascular protection. J Cardiovasc Pharmacol. 1993;22(suppl 5):S1-S9.  
 17. Chatterjee K. Inhibitors of the renin-angiotensin system in established cardiac failure. Heart. 1996;76(suppl 3):83-91.  
 18. The Writing Group for the PEPI Trial. Effects of estrogen or estrogen/progestin regimens on heart disease risk factors in postmenopausal women: the Postmenopausal Estrogen/Progestin Interventions (PEPI) Trial. JAMA. 1995;273:199-208.  
-19. Blumenthal RS, Heldman AW, Brinker JA, Resar JR, Coombs VJ, Gloth ST, Gerstenbith G, Reis SE. Acute effects of conjugated estrogens on coronary blood flow response to acetyicholine in men. Am J Cardiol. 1997;80:1021-1024.  
+19. Blumenthal RS, Heldman AW, Brinker JA, Resar JR, Coombs VJ, Gloth ST, Gerstenblith G, Reis SE. Acute effects of conjugated estrogens on coronary blood flow response to acetylcholine in men. Am J Cardiol. 1997;80:1021-1024.  
 20. Reis SE, Holubkov R, Zell KA, Smith AJ, Cohen HA, Feldman MD, Blumenthal RS. Estrogen acutely abolishes abnormal cold-induced coronary constriction in men. Chest. 1998;114:1556-1561.  
-21. Reis SE, Bhoopalam V, Zell KA, Counihan PJ, Smith AJ, Pham S, Murali S. Conjugated estrogens acutely abolish abnormal cold-induced coronary vasoconstriction in male cardiac allografts. Circulation. 1998;97:23-25.  
+21. Reis SE, Bhoopalam V, Zell KA, Counihan PJ, Smith AJ, Pham S, Murali S. Conjugated estrogens acutely abolishes abnormal cold-induced coronary vasoconstriction in male cardiac allografts. Circulation. 1998;97:23-25.  
 22. New G, Timmins KL, Duffy SJ, Tran BT, O'Brien RC, Harper RW, Meredith IT. Long-term estrogen therapy improves vascular function in male to female transsexuals. J Am Coll Cardiol. 1997;29:1437-1444.  
 23. McCrohon JA, Walters WA, Robinson JT, McCredie RJ, Turner L, Adams MR, Handelsman DJ, Celermajer DS. Arterial reactivity is enhanced in genetic males taking high dose estrogens. J Am Coll Cardiol. 1997;29:1432-1436.  
 24. Komesaroff PA, Black CV, Westerman RA. A novel, nongenomic action of estrogen on the cardiovascular system. J Clin Endocrinol Metab. 1998;83:2313-2316.  
-25. Collins P, Rosano GM, Sarrel PM, Ulrich L, Adamopoulos S, Beale CM, McNeill JG, Poole-Wilson PA. 17β-Estradiol attenuates acetylcholine-induced coronary arterial constriction in women but not men with coronary heart disease. Circulation. 1995;92:24-30.  
-26. Kawano H, Motoyama T, Kugiyama K, Hirashima O, Ohgushi M, Fujii H, Ogawa H, Yasue H. Gender difference in improvement of endothelium-dependent vasodilation after estrogen supplementation. J Am Coll Cardiol. 1997;30:914-919.  
+25. Collins P, Rosano GM, Sarrel PM, Ulrich L, Adamopoulos S, Beale CM, McNeill JG, Poole-Wilson PA. 17β-Estradiol attenuates acetylcholin- induced coronary arterial constriction in women but not men with coronary heart disease. Circulation. 1995;92:24-30.  
+26. Kawano H, Motoyama T, Kugiyama K, Hirashima O, Ohgushi M, Fujii H, Ogawa H, Yase H. Gender difference in improvement of endothelium-dependent vasodilation after estrogen supplementation. J Am Coll Cardiol. 1997;30:914-919.  
 
-text[[518, 81, 921, 583]]
+text[[516, 91, 919, 582]]
 27. Chester AH, Jiang C, Borland JA, Y acoub MH, Collins P. Oestrogen relaxes human epicardial coronary arteries through non-endothelium-dependent mechanisms. Coron Artery Dis. 1995;6:417-422.  
 28. Sudhir K, Esler MD, Jennings GL, Komesaroff PA. Estrogen supplementation decreases norepinephrine-induced vasoconstriction and total body norepinephrine spillover in perimenopausal women. Hypertension. 1997;30:1538-1543.  
 29. Ford SP, Reynolds LP, Farley DB, Bhatnagar RK, Van Orden DE. Interaction of ovarian steroids and periarterial alpha1-adrenergic receptors in altering uterine blood flow during the estrous cycle of gilts. Am J Obstet Gynecol. 1984;150:480-484.  
diff --git a/stage1/sample_00030/document.md b/stage1/sample_00030/document.md
index db6180b04e861c819669c85501610c90ecdccb60..4fb8289659ac629126cc065fbfce6faaddf8a127 100644
--- a/stage1/sample_00030/document.md
+++ b/stage1/sample_00030/document.md
@@ -1,7 +1,34 @@
-7. Unless waived, applies the service fee automatically to the student's university bill, regardless of the outcome of the petition (charge normally appears within a week or two after the processing of the petition). PeopleSoftE: 8. Processes approved fee waivers, or: Registrar: adjusts the student's tuition assessment based on Enrollment Agreement form [1]. 9. Unless waived, pays the service fee as part of the university bill. Student: Back to top 
+7. Unless waived, applies the service fee automatically to the student's university bill, regardless of the outcome of the petition (charge normally appears within a week or two after the processing of the petition).  
 
-text[[53, 332, 833, 372]]
-Source URL: https://gap.stanford.edu/handbooks/gap-handbook/chapter-5/subchapter-1/page-5-1-2 Links 
+text[[129, 111, 180, 126]]
+Either:  
 
-text[[53, 367, 457, 385]]
+text[[61, 148, 85, 163]]
+8.  
+
+text[[139, 141, 628, 195]]
+processes approved fee waivers, or adjusts the student's tuition assessment based on Enrollment Agreement form [1].  
+
+text[[714, 142, 787, 158]]
+Registrar  
+
+text[[61, 216, 84, 231]]
+9.  
+
+text[[130, 215, 617, 233]]
+Unless waived, pays the service fee as part of the university bill.  
+
+text[[714, 217, 778, 231]]
+Student  
+
+text[[52, 315, 141, 331]]
+Back to top  
+
+text[[52, 331, 833, 368]]
+Source URL: https://gap.stanford.edu/handbooks/gap-handbook/chapter-5/subchapter-1/page-5-1-2.  
+
+text[[52, 368, 456, 386]]
+Links  
+
+text[[52, 366, 454, 386]]
 [1] https://stanford.app.box.com/multiple-prog-agree
\ No newline at end of file
diff --git a/stage1/sample_00030/raw_response.md b/stage1/sample_00030/raw_response.md
index db6180b04e861c819669c85501610c90ecdccb60..4fb8289659ac629126cc065fbfce6faaddf8a127 100644
--- a/stage1/sample_00030/raw_response.md
+++ b/stage1/sample_00030/raw_response.md
@@ -1,7 +1,34 @@
-7. Unless waived, applies the service fee automatically to the student's university bill, regardless of the outcome of the petition (charge normally appears within a week or two after the processing of the petition). PeopleSoftE: 8. Processes approved fee waivers, or: Registrar: adjusts the student's tuition assessment based on Enrollment Agreement form [1]. 9. Unless waived, pays the service fee as part of the university bill. Student: Back to top 
+7. Unless waived, applies the service fee automatically to the student's university bill, regardless of the outcome of the petition (charge normally appears within a week or two after the processing of the petition).  
 
-text[[53, 332, 833, 372]]
-Source URL: https://gap.stanford.edu/handbooks/gap-handbook/chapter-5/subchapter-1/page-5-1-2 Links 
+text[[129, 111, 180, 126]]
+Either:  
 
-text[[53, 367, 457, 385]]
+text[[61, 148, 85, 163]]
+8.  
+
+text[[139, 141, 628, 195]]
+processes approved fee waivers, or adjusts the student's tuition assessment based on Enrollment Agreement form [1].  
+
+text[[714, 142, 787, 158]]
+Registrar  
+
+text[[61, 216, 84, 231]]
+9.  
+
+text[[130, 215, 617, 233]]
+Unless waived, pays the service fee as part of the university bill.  
+
+text[[714, 217, 778, 231]]
+Student  
+
+text[[52, 315, 141, 331]]
+Back to top  
+
+text[[52, 331, 833, 368]]
+Source URL: https://gap.stanford.edu/handbooks/gap-handbook/chapter-5/subchapter-1/page-5-1-2.  
+
+text[[52, 368, 456, 386]]
+Links  
+
+text[[52, 366, 454, 386]]
 [1] https://stanford.app.box.com/multiple-prog-agree
\ No newline at end of file
diff --git a/stage1/sample_00031/document.md b/stage1/sample_00031/document.md
index cf5cf300ca64c55f63c002580a740d2f80728dd0..05f73dac5c456c5afd7cf8991f2430481112cbb4 100644
--- a/stage1/sample_00031/document.md
+++ b/stage1/sample_00031/document.md
@@ -1,20 +1,22 @@
-5.1.2 Changes and Additions of Degree Programs: Implementation
+1.2 Changes and Additions of Degree Programs: Implementation 
 
-text[[52, 280, 195, 295]]
-Last updated on:
+sub_title[[53, 195, 877, 268]]
+## 5.1.2 Changes and Additions of Degree Programs: Implementation 
 
-title[[52, 312, 217, 342]]
-# Jump To:
+text[[53, 280, 195, 297]]
+Last updated on: 
 
-text[[84, 357, 443, 371]]
-1. Changes and Additions of Degree Programs
+sub_title[[53, 312, 214, 343]]
+## Jump To: 
 
-title[[52, 395, 819, 428]]
-# 1. Changes and Additions of Degree Programs
+text[[83, 356, 443, 372]]
+1. Changes and Additions of Degree Programs 
 
-text[[52, 442, 827, 457]]
-Steps for the filing and processing of the Graduate Program Authorization P etition are described here.
+sub_title[[54, 395, 820, 429]]
+## 1. Changes and Additions of Degree Programs 
 
-table[[50, 465, 947, 927]]
+text[[53, 440, 828, 457]]
+Steps for the filing and processing of the Graduate Program Authorization Petition are described here. 
 
-<table><td colspan="2">PROCESS STEPSRESPONSIBILITY1.Completes and submits the Graduate Program Authorization P etition electronically by the last day of classes for the effective quarter (from the "Academics" panel in the Axess Student Center, select "P etitions and<br>Forms" from the drop-down menu).Student2.Discusses the student's plans as appropriate, reviews and, if approved, indicates approval electronically in P eopleSoft Worklist.Current department and new departmentIf the students qualifies for a waiver of the service fee, submit a Stanford<br>Services & Support to the attention of Degree Progress, including:3.·the student's name and Stanford University ID number, and<br>·the circumstance qualifying the student for a fee waiver. For<br>dismissals, include date of dismissal or discontinuation from PhD<br>program.Student Services staff4.If an international student, confers with staff at the Bechtel International Center regarding visa status.Student5.Reviews the international student's visa status to determine if an extension or additional verification of financial support is needed. If approved, indicates this electronically in P eopleSoft Worklist.Bechtel6.Upon complete approval, activates the student in the new degree program in P eopleSoft Student Administration.PeopleSoft</table>
\ No newline at end of file
+table[[51, 465, 944, 928]]
+<table>PROCESS STEPSRESPONSIBILITY1.Completes and submits the Graduate Program Authorization Petition electronically by the last day of classes for the effective quarter (from the "Academics" panel in the Axess Student Center, select "Petitions and Forms" from the drop-down menu).Student2.Discusses the student's plans as appropriate, reviews and, if approved, indicates approval electronically in PeopleSoft Worklist.Current department and new department3.If the students qualifies for a waiver of the service fee, submit a Stanford Services & Support to the attention of Degree Progress, including:<br/>the student's name and Stanford University ID number, and<br/>the circumstance qualifying the student for a fee waiver. For dismissals, include date of dismissal or discontinuation from PhD program.Student Services staff4.If an international student, confers with staff at the Bechtel International Center regarding visa status.Student5.Reviews the international student's visa status to determine if an extension or additional verification of financial support is needed. If approved, indicates this electronically in PeopleSoft Worklist.Bechtel6.Upon complete approval, activates the student in the new degree program in PeopleSoft Student Administration.PeopleSoft</table>
\ No newline at end of file
diff --git a/stage1/sample_00031/raw_response.md b/stage1/sample_00031/raw_response.md
index cf5cf300ca64c55f63c002580a740d2f80728dd0..05f73dac5c456c5afd7cf8991f2430481112cbb4 100644
--- a/stage1/sample_00031/raw_response.md
+++ b/stage1/sample_00031/raw_response.md
@@ -1,20 +1,22 @@
-5.1.2 Changes and Additions of Degree Programs: Implementation
+1.2 Changes and Additions of Degree Programs: Implementation 
 
-text[[52, 280, 195, 295]]
-Last updated on:
+sub_title[[53, 195, 877, 268]]
+## 5.1.2 Changes and Additions of Degree Programs: Implementation 
 
-title[[52, 312, 217, 342]]
-# Jump To:
+text[[53, 280, 195, 297]]
+Last updated on: 
 
-text[[84, 357, 443, 371]]
-1. Changes and Additions of Degree Programs
+sub_title[[53, 312, 214, 343]]
+## Jump To: 
 
-title[[52, 395, 819, 428]]
-# 1. Changes and Additions of Degree Programs
+text[[83, 356, 443, 372]]
+1. Changes and Additions of Degree Programs 
 
-text[[52, 442, 827, 457]]
-Steps for the filing and processing of the Graduate Program Authorization P etition are described here.
+sub_title[[54, 395, 820, 429]]
+## 1. Changes and Additions of Degree Programs 
 
-table[[50, 465, 947, 927]]
+text[[53, 440, 828, 457]]
+Steps for the filing and processing of the Graduate Program Authorization Petition are described here. 
 
-<table><td colspan="2">PROCESS STEPSRESPONSIBILITY1.Completes and submits the Graduate Program Authorization P etition electronically by the last day of classes for the effective quarter (from the "Academics" panel in the Axess Student Center, select "P etitions and<br>Forms" from the drop-down menu).Student2.Discusses the student's plans as appropriate, reviews and, if approved, indicates approval electronically in P eopleSoft Worklist.Current department and new departmentIf the students qualifies for a waiver of the service fee, submit a Stanford<br>Services & Support to the attention of Degree Progress, including:3.·the student's name and Stanford University ID number, and<br>·the circumstance qualifying the student for a fee waiver. For<br>dismissals, include date of dismissal or discontinuation from PhD<br>program.Student Services staff4.If an international student, confers with staff at the Bechtel International Center regarding visa status.Student5.Reviews the international student's visa status to determine if an extension or additional verification of financial support is needed. If approved, indicates this electronically in P eopleSoft Worklist.Bechtel6.Upon complete approval, activates the student in the new degree program in P eopleSoft Student Administration.PeopleSoft</table>
\ No newline at end of file
+table[[51, 465, 944, 928]]
+<table>PROCESS STEPSRESPONSIBILITY1.Completes and submits the Graduate Program Authorization Petition electronically by the last day of classes for the effective quarter (from the "Academics" panel in the Axess Student Center, select "Petitions and Forms" from the drop-down menu).Student2.Discusses the student's plans as appropriate, reviews and, if approved, indicates approval electronically in PeopleSoft Worklist.Current department and new department3.If the students qualifies for a waiver of the service fee, submit a Stanford Services & Support to the attention of Degree Progress, including:<br/>the student's name and Stanford University ID number, and<br/>the circumstance qualifying the student for a fee waiver. For dismissals, include date of dismissal or discontinuation from PhD program.Student Services staff4.If an international student, confers with staff at the Bechtel International Center regarding visa status.Student5.Reviews the international student's visa status to determine if an extension or additional verification of financial support is needed. If approved, indicates this electronically in PeopleSoft Worklist.Bechtel6.Upon complete approval, activates the student in the new degree program in PeopleSoft Student Administration.PeopleSoft</table>
\ No newline at end of file
diff --git a/stage1/sample_00032/document.md b/stage1/sample_00032/document.md
index b1158d7f39897a8479c2a65fb0095e59a414ed6d..fa336afb45d1d6ca65284a201f9d341b43936a8a 100644
--- a/stage1/sample_00032/document.md
+++ b/stage1/sample_00032/document.md
@@ -1,4 +1,4 @@
-the recent past is just as unfulfilling as the present, as seen in the previous description of the young Milkman kneeling on the car seat looking out the back window ("not knowing where he was going--just where he had been--troubled him"). The distant past, his origin, on the other hand, is liberating. Struggling to exist in the confusion and dis-ease of his life, Milkman is introduced to his aunt Pilate, a "woman who had as much to do with his future as she had his past" (Song 36), at a time when he begins to feel "as though there were no future to be had" (Song 35). Pilate rearranges the chronology of Milkman's life by sending him back to his earliest origins, Shalimar.  
+1. The recent past is just as unfulfilling as the present, as seen in the previous description of the young Milkman kneeling on the car seat looking out the back window ("not knowing where he was going--just where he had been--troubled him"). The distant past, his origin, on the other hand, is liberating. Struggling to exist in the confusion and dis-ease of his life, Milkman is introduced to his aunt Pilate, a "woman who had as much to do with his future as she had his past" (Song 36), at a time when he begins to feel "as though there were no future to be had" (Song 35). Pilate rearranges the chronology of Milkman's life by sending him back to his earliest origins, Shalimar. 
 
-text[[147, 519, 913, 917]]
-Even though Milkman sets off on a treasure hunt for gold that Pilate may have buried in a cave, the spiritual liberation, the ability of flight, and the connectedness with his past overshadow the value of any gold. There is a slight comfort, a subtle relaxation that occurs when he feels himself getting closer to the past, the origin of his family. He is recognized in Danville, Pennsylvania. And there is a suggestion that this is the first time Milkman drops his defensive, self- protecting stance. "Milkman smiled and let his shoulders slump a little," Morrison writes. "It was a good feeling to come into a strange town and find a stranger who knew your people" (Song 259). Furthermore, Morrison describes Milkman as beaming.
\ No newline at end of file
+text[[146, 535, 912, 916]]
+Even though Milkman sets off on a treasure hunt for gold that Pilate may have buried in a cave, the spiritual liberation, the ability of flight, and the connectedness with his past overshadow the value of any gold. There is a slight comfort, a subtle relaxation that occurs when he feels himself getting closer to the past, the origin of his family. He is recognized in Danville, Pennsylvania. And there is a suggestion that this is the first time Milkman drops his defensive, self-protecting stance. "Milkman smiled and let his shoulders slump a little," Morrison writes. "It was a good feeling to come into a strange town and find a stranger who knew your people" (Song 259). Furthermore, Morrison describes Milkman as beaming.
\ No newline at end of file
diff --git a/stage1/sample_00032/raw_response.md b/stage1/sample_00032/raw_response.md
index b1158d7f39897a8479c2a65fb0095e59a414ed6d..fa336afb45d1d6ca65284a201f9d341b43936a8a 100644
--- a/stage1/sample_00032/raw_response.md
+++ b/stage1/sample_00032/raw_response.md
@@ -1,4 +1,4 @@
-the recent past is just as unfulfilling as the present, as seen in the previous description of the young Milkman kneeling on the car seat looking out the back window ("not knowing where he was going--just where he had been--troubled him"). The distant past, his origin, on the other hand, is liberating. Struggling to exist in the confusion and dis-ease of his life, Milkman is introduced to his aunt Pilate, a "woman who had as much to do with his future as she had his past" (Song 36), at a time when he begins to feel "as though there were no future to be had" (Song 35). Pilate rearranges the chronology of Milkman's life by sending him back to his earliest origins, Shalimar.  
+1. The recent past is just as unfulfilling as the present, as seen in the previous description of the young Milkman kneeling on the car seat looking out the back window ("not knowing where he was going--just where he had been--troubled him"). The distant past, his origin, on the other hand, is liberating. Struggling to exist in the confusion and dis-ease of his life, Milkman is introduced to his aunt Pilate, a "woman who had as much to do with his future as she had his past" (Song 36), at a time when he begins to feel "as though there were no future to be had" (Song 35). Pilate rearranges the chronology of Milkman's life by sending him back to his earliest origins, Shalimar. 
 
-text[[147, 519, 913, 917]]
-Even though Milkman sets off on a treasure hunt for gold that Pilate may have buried in a cave, the spiritual liberation, the ability of flight, and the connectedness with his past overshadow the value of any gold. There is a slight comfort, a subtle relaxation that occurs when he feels himself getting closer to the past, the origin of his family. He is recognized in Danville, Pennsylvania. And there is a suggestion that this is the first time Milkman drops his defensive, self- protecting stance. "Milkman smiled and let his shoulders slump a little," Morrison writes. "It was a good feeling to come into a strange town and find a stranger who knew your people" (Song 259). Furthermore, Morrison describes Milkman as beaming.
\ No newline at end of file
+text[[146, 535, 912, 916]]
+Even though Milkman sets off on a treasure hunt for gold that Pilate may have buried in a cave, the spiritual liberation, the ability of flight, and the connectedness with his past overshadow the value of any gold. There is a slight comfort, a subtle relaxation that occurs when he feels himself getting closer to the past, the origin of his family. He is recognized in Danville, Pennsylvania. And there is a suggestion that this is the first time Milkman drops his defensive, self-protecting stance. "Milkman smiled and let his shoulders slump a little," Morrison writes. "It was a good feeling to come into a strange town and find a stranger who knew your people" (Song 259). Furthermore, Morrison describes Milkman as beaming.
\ No newline at end of file
diff --git a/stage1/sample_00033/document.md b/stage1/sample_00033/document.md
index 32ac17b8f82b9621247c8cc2db1f6506eca838a1..8dbe5fbd42bdf7417d0b0fcd16590743419d4feb 100644
--- a/stage1/sample_00033/document.md
+++ b/stage1/sample_00033/document.md
@@ -1,7 +1,7 @@
 61
 
-text[[133, 118, 907, 444]]
-One can see how in creating the world of Sweet Home and 124, Morrison is rediscovering her own past. Morrison herself implies such a significance in the act of writing when she says in her interview with Claudia Tate that those periods of time between novels make her feel that she has "lost touch, though momentarily, with some collective memory" (Tate 131). Only through writing, then, does Toni Morrison feel in tune with the "collective memory" of her African-American heritage, and only then can she assert her will in countering the isolating, alienating effect of white, bourgeois society on African-American individuals.  
+text[[133, 116, 905, 447]]
+One can see how in creating the world of Sweet Home and 124, Morrison is rediscovering her own past. Morrison herself implies such a significance in the act of writing when she says in her interview with Claudia Tate that those periods of time between novels make her feel that she has "lost touch, though momentarily, with some collective memory" (Tate 131). Only through writing, then, does Toni Morrison feel in tune with the "collective memory" of her African-American heritage, and only then can she assert her will in countering the isolating, alienating effect of white, bourgeois society on African-American individuals. 
 
-text[[133, 459, 907, 915]]
+text[[132, 460, 907, 915]]
 Toni Morrison's effort to find her cultural heritage and to maintain her "collective memory" is her attempt at sharing grief with her African-American brothers and sisters who have in common a history of enslavement by the white-dominated society. The African-American community in Morrison's novel Beloved comes to help Sethe at the end; they are sharing her suffering and buttressing her in her attack on those forces (anger and guilt) which threaten to obliterate her, to obsess her life. Life for Toni Morrison in the 1980s must surely have been threatening, threatening because of its inverted value system. To counter the growing sense of alienation that Morrison felt in the Reagan era, 'she forced portions of the past into the present. Parallel to Morrison's looking back in order to find stability for the present is Sethe's catching the elusive past in order to lay it all down and go on with
\ No newline at end of file
diff --git a/stage1/sample_00033/raw_response.md b/stage1/sample_00033/raw_response.md
index 32ac17b8f82b9621247c8cc2db1f6506eca838a1..8dbe5fbd42bdf7417d0b0fcd16590743419d4feb 100644
--- a/stage1/sample_00033/raw_response.md
+++ b/stage1/sample_00033/raw_response.md
@@ -1,7 +1,7 @@
 61
 
-text[[133, 118, 907, 444]]
-One can see how in creating the world of Sweet Home and 124, Morrison is rediscovering her own past. Morrison herself implies such a significance in the act of writing when she says in her interview with Claudia Tate that those periods of time between novels make her feel that she has "lost touch, though momentarily, with some collective memory" (Tate 131). Only through writing, then, does Toni Morrison feel in tune with the "collective memory" of her African-American heritage, and only then can she assert her will in countering the isolating, alienating effect of white, bourgeois society on African-American individuals.  
+text[[133, 116, 905, 447]]
+One can see how in creating the world of Sweet Home and 124, Morrison is rediscovering her own past. Morrison herself implies such a significance in the act of writing when she says in her interview with Claudia Tate that those periods of time between novels make her feel that she has "lost touch, though momentarily, with some collective memory" (Tate 131). Only through writing, then, does Toni Morrison feel in tune with the "collective memory" of her African-American heritage, and only then can she assert her will in countering the isolating, alienating effect of white, bourgeois society on African-American individuals. 
 
-text[[133, 459, 907, 915]]
+text[[132, 460, 907, 915]]
 Toni Morrison's effort to find her cultural heritage and to maintain her "collective memory" is her attempt at sharing grief with her African-American brothers and sisters who have in common a history of enslavement by the white-dominated society. The African-American community in Morrison's novel Beloved comes to help Sethe at the end; they are sharing her suffering and buttressing her in her attack on those forces (anger and guilt) which threaten to obliterate her, to obsess her life. Life for Toni Morrison in the 1980s must surely have been threatening, threatening because of its inverted value system. To counter the growing sense of alienation that Morrison felt in the Reagan era, 'she forced portions of the past into the present. Parallel to Morrison's looking back in order to find stability for the present is Sethe's catching the elusive past in order to lay it all down and go on with
\ No newline at end of file
diff --git a/stage1/sample_00034/document.md b/stage1/sample_00034/document.md
index 3eb005b6b5d5293d92b01af160053be1213c0da9..7d2765494c14e70b3e71256caa19bbc06f77ae6d 100644
--- a/stage1/sample_00034/document.md
+++ b/stage1/sample_00034/document.md
@@ -1,4 +1,4 @@
 60 animal, therefore, exemplifies her ties to her cultural heritage, and this heritage is the tool she must use to counter the alienating influence of the white-dominated society--the society practicing enslavement--in which she lives. 
 
-text[[133, 273, 903, 917]]
+text[[133, 272, 904, 922]]
 Just as Sethe depends on her cultural heritage to counter the effects of her maddening present, Morrison looks back to that same heritage. Sethe found within her the memory of a language and images of animals that have no representative in America. Going deeper within herself to grasp her culture--while Denver goes outside 124 to enlist the help of the African-American community--Sethe's home is exorcised of its anger and guilt. In this same way Morrison goes deep within herself and reaches out to the African-American community. In Claudia Tate's collection of interviews with African-American female writers, Morrison claims that "Writing is discovery; it's talking deep within myself, 'deep talking' as you say" (Tate 130). This "deep talking," Morrison goes on to say, helps her to grapple with seemingly unresolvable things, one of which might be an African-American cultural identity which includes enslavement by a white-dominated society. The Publisher's Weekly quotation by Morrison in this paper's introduction comes to mind once again. To reiterate, Morrison says, "I didn't want my head and my life to be enslaved by slavery" (PW 51). She must come to terms with this aspect of her past in order to move beyond it, further back as it were.
\ No newline at end of file
diff --git a/stage1/sample_00034/raw_response.md b/stage1/sample_00034/raw_response.md
index 3eb005b6b5d5293d92b01af160053be1213c0da9..7d2765494c14e70b3e71256caa19bbc06f77ae6d 100644
--- a/stage1/sample_00034/raw_response.md
+++ b/stage1/sample_00034/raw_response.md
@@ -1,4 +1,4 @@
 60 animal, therefore, exemplifies her ties to her cultural heritage, and this heritage is the tool she must use to counter the alienating influence of the white-dominated society--the society practicing enslavement--in which she lives. 
 
-text[[133, 273, 903, 917]]
+text[[133, 272, 904, 922]]
 Just as Sethe depends on her cultural heritage to counter the effects of her maddening present, Morrison looks back to that same heritage. Sethe found within her the memory of a language and images of animals that have no representative in America. Going deeper within herself to grasp her culture--while Denver goes outside 124 to enlist the help of the African-American community--Sethe's home is exorcised of its anger and guilt. In this same way Morrison goes deep within herself and reaches out to the African-American community. In Claudia Tate's collection of interviews with African-American female writers, Morrison claims that "Writing is discovery; it's talking deep within myself, 'deep talking' as you say" (Tate 130). This "deep talking," Morrison goes on to say, helps her to grapple with seemingly unresolvable things, one of which might be an African-American cultural identity which includes enslavement by a white-dominated society. The Publisher's Weekly quotation by Morrison in this paper's introduction comes to mind once again. To reiterate, Morrison says, "I didn't want my head and my life to be enslaved by slavery" (PW 51). She must come to terms with this aspect of her past in order to move beyond it, further back as it were.
\ No newline at end of file
diff --git a/stage1/sample_00035/document.md b/stage1/sample_00035/document.md
index a4531e7b1020806e21264dc91f2261b3178c7128..43207919cbba357be90952118683b146fdfc010c 100644
--- a/stage1/sample_00035/document.md
+++ b/stage1/sample_00035/document.md
@@ -1 +1 @@
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\ No newline at end of file
diff --git a/stage1/sample_00036/document.md b/stage1/sample_00036/document.md
index f907a0b60c04f7a6c288c45fb00bdfa7762af20f..6fda4260fc160f63d50e22fc0b60235a4811b675 100644
--- a/stage1/sample_00036/document.md
+++ b/stage1/sample_00036/document.md
@@ -1,19 +1,19 @@
-Summer or Winter Construction Costs - It is anticipated that some agency stipulations will require that at least portions of the construction will be required to be completed in the winter when ground conditions reduce impacts.  
+Summer or Winter Construction Costs – It is anticipated that some agency stipulations will require that at least portions of the construction will be required to be completed in the winter when ground conditions reduce impacts.  
 
-sub_title[[128, 213, 366, 229]]
+sub_title[[129, 213, 365, 230]]
 ### 3.4 Routing Alternatives  
 
-text[[128, 233, 834, 266]]
-Table 1 is a tabulation of Route Miles (length of the corridor) and Circuit Miles (total miles of circuits within the corridor).  
+text[[128, 233, 832, 267]]
+3.4 Routing AlternativesTable 1 is a tabulation of Route Miles (length of the corridor) and Circuit Miles (total miles of circuits within the corridor).  
 
-table[[118, 292, 859, 766]]
+table[[117, 292, 858, 767]]
 table_caption[[347, 277, 639, 291]]
 TABLE 1-ALTERNATIVE SUMMARIES   
 
 <table>CorridorDescriptionRoute MilesCircuit MilesSusitna North3 Circuits Watana to Chultina<br>Substation via Susitna North Corridor37111Susitna South3 Circuits Watana to Gold Creek<br>Substation via Susitna South Corridor35105Denali3 Circuits Watana to Cantwell<br>Substation via Denali Corridor62186Susitna North and Denali2 Circuits Watana to Chultina<br>Substation via Susitna North Corridor;<br>1 Circuit Watana to Cantwell<br>Substation via Denali Corridor99136Susitna South and Denali2 Circuits Watana to Gold Creek<br>Substation via Susitna South Corridor;<br>1 Circuit Watana to Cantwell<br>Substation via Denali Corridor97132</table>  
 
-sub_title[[125, 815, 276, 833]]
+sub_title[[124, 815, 276, 833]]
 ### 3.5 Permitting  
 
-text[[122, 836, 858, 871]]
-Agency permits can be a significant part of acquiring permission to construct a new transmission line. Table 2 presents a list of potential permits for this transmission line.
\ No newline at end of file
+text[[123, 836, 858, 871]]
+3.5 PermittingAgency permits can be a significant part of acquiring permission to construct a new transmission line. Table 2 presents a list of potential permits for this transmission line.
\ No newline at end of file
diff --git a/stage1/sample_00036/raw_response.md b/stage1/sample_00036/raw_response.md
index f907a0b60c04f7a6c288c45fb00bdfa7762af20f..6fda4260fc160f63d50e22fc0b60235a4811b675 100644
--- a/stage1/sample_00036/raw_response.md
+++ b/stage1/sample_00036/raw_response.md
@@ -1,19 +1,19 @@
-Summer or Winter Construction Costs - It is anticipated that some agency stipulations will require that at least portions of the construction will be required to be completed in the winter when ground conditions reduce impacts.  
+Summer or Winter Construction Costs – It is anticipated that some agency stipulations will require that at least portions of the construction will be required to be completed in the winter when ground conditions reduce impacts.  
 
-sub_title[[128, 213, 366, 229]]
+sub_title[[129, 213, 365, 230]]
 ### 3.4 Routing Alternatives  
 
-text[[128, 233, 834, 266]]
-Table 1 is a tabulation of Route Miles (length of the corridor) and Circuit Miles (total miles of circuits within the corridor).  
+text[[128, 233, 832, 267]]
+3.4 Routing AlternativesTable 1 is a tabulation of Route Miles (length of the corridor) and Circuit Miles (total miles of circuits within the corridor).  
 
-table[[118, 292, 859, 766]]
+table[[117, 292, 858, 767]]
 table_caption[[347, 277, 639, 291]]
 TABLE 1-ALTERNATIVE SUMMARIES   
 
 <table>CorridorDescriptionRoute MilesCircuit MilesSusitna North3 Circuits Watana to Chultina<br>Substation via Susitna North Corridor37111Susitna South3 Circuits Watana to Gold Creek<br>Substation via Susitna South Corridor35105Denali3 Circuits Watana to Cantwell<br>Substation via Denali Corridor62186Susitna North and Denali2 Circuits Watana to Chultina<br>Substation via Susitna North Corridor;<br>1 Circuit Watana to Cantwell<br>Substation via Denali Corridor99136Susitna South and Denali2 Circuits Watana to Gold Creek<br>Substation via Susitna South Corridor;<br>1 Circuit Watana to Cantwell<br>Substation via Denali Corridor97132</table>  
 
-sub_title[[125, 815, 276, 833]]
+sub_title[[124, 815, 276, 833]]
 ### 3.5 Permitting  
 
-text[[122, 836, 858, 871]]
-Agency permits can be a significant part of acquiring permission to construct a new transmission line. Table 2 presents a list of potential permits for this transmission line.
\ No newline at end of file
+text[[123, 836, 858, 871]]
+3.5 PermittingAgency permits can be a significant part of acquiring permission to construct a new transmission line. Table 2 presents a list of potential permits for this transmission line.
\ No newline at end of file
diff --git a/stage1/sample_00037/document.md b/stage1/sample_00037/document.md
index 8ef59eb4ce38df04cf71b438e04a22a19a4b776e..2bac4d0156030fc7b928b45051e5970e63c0da7f 100644
--- a/stage1/sample_00037/document.md
+++ b/stage1/sample_00037/document.md
@@ -1,25 +1 @@
-1. COE - The Army Corps of Engineers (COE) regulates impacts to wetlands. The COE enforces Section 404 of the Clean Water Act by issuing individual or nationwide permits for wetlands impacts.  
-
-text[[160, 178, 854, 251]]
-ADEC - The Alaska Department of Environmental Conservation (ADEC), in conjunction with the COE 404 permitting, will analyze projects for impacts to water quality and recommend mitigation measures to prevent water pollution. ADEC will issue a Certificate of Assurance in accordance with Section 401 of the Clean Water Act.  
-
-text[[160, 259, 846, 310]]
-ADNR - The Alaska Department of Natural Resources (ADNR) regulates temporary withdrawals of water from state-owned sources and issues a water use permit. ADNR coordinates this permit application with all state agencies.  
-
-text[[187, 318, 864, 388]]
-The ADNR Division of Mining, Land and Water also issues right- of- way permits for crossing state lands. The exception is when a project crosses a state highway. If a state highway is crossed, the Department of Transportation & Public Facilities (DOT&PF) regulates the crossing.  
-
-text[[187, 396, 864, 466]]
-The State Historic Preservation Office (SHPO) is a division of ADNR and it regulates impacts to historic, cultural, and archeological resources. According to the 1966 Historic Preservation Act, all projects must be submitted to the SHPO for their analysis and approval.  
-
-text[[186, 473, 865, 545]]
-ADNR regulates specific rivers, lakes, and streams or parts of them that are important for the spawning, rearing, or migration of anadromous fish. According to Alaska Statute 16.05.870, ADF&G must issue a permit for any activity occurring in habitat important to anadromous fish.  
-
-text[[158, 552, 849, 589]]
-ADOT&PF - The ADOT&PF regulates state- owned roads. A new transmission line along or crossing a state- owned road would require a utility permit from ADOT&PF.  
-
-text[[159, 597, 832, 634]]
-ARRC - If a route uses the Alaska Railroad Corporation (ARRC) corridor or crosses the Alaska Railroad, a Right of Way Permit will be required.  
-
-text[[127, 691, 456, 709]]
-3.6 Land Classification/Ownership
\ No newline at end of file
+1- 3. 4- 5. 6- 7. 8- 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 47. 48. 49. 50. 51. 52. 53. 54. 55. 56. 57. 58. 59. 60. 61. 62. 63. 64. 65. 66. 67. 68. 69. 70. 71. 72. 73. 74. 75. 76. 77. 78. 79. 80. 81. 82. 83. 84. 85. 86. 87. 88. 89. 90. 91. 92. 93. 94. 95. 96. 97. 98. 99. 100. 101. 102. 103. 104. 105. 106. 107. 108. 109. 110. 111. 112. 113. 114. 115. 116. 117. 118. 119. 120. 121. 122. 123. 124. 125. 126. 127. 128. 129. 130. 131. 132. 133. 134. 135. 136. 137. 138. 139. 140. 141. 142. 143. 144. 145. 146. 147. 148. 149. 150. 151. 152. 153. 154. 155. 156. 157. 158. 159. 160. 161. 162. 163. 164. 165. 166. 167. 168. 169. 170. 171. 172. 173. 174. 175. 176. 177. 178. 179. 180. 181. 182. 183. 184. 185. 186. 187. 188. 189. 190. 191. 192. 193. 194. 195. 196. 197. 198. 199. 200. 201. 202. 203. 204. 205. 206. 207. 208. 209. 210. 211. 212. 213. 214. 215. 216. 217. 218. 219. 220. 221. 222. 223. 224. 225. 226. 227. 228. 229. 230. 231. 232. 233. 234. 235. 236. 237. 238. 239. 240. 241. 242. 243. 244. 245. 246. 247. 248. 249. 250. 251. 252. 253. 254. 255. 256. 257. 258. 259. 260. 261. 262. 263. 264. 265. 266. 267. 268. 269. 270. 271. 272. 273. 274. 275. 276. 277. 278. 279. 280. 281. 282. 283. 284. 285. 286. 287. 288. 289. 290. 291. 292. 293. 294. 295. 296. 297. 298. 299. 300. 301. 302. 303. 304. 305. 306. 307. 308. 309. 310. 311. 312. 313. 314. 315. 316. 317. 318. 319. 320. 321. 322. 323. 324. 325. 326. 327. 328. 329. 330. 331. 332. 333. 334. 335. 336. 337. 338. 339. 340. 341. 342. 343. 344. 345. 346. 347. 348. 349. 350. 351. 352. 353. 354. 355. 356. 357. 358. 359. 360. 361. 362. 363. 364. 365. 366. 367. 368. 369. 370. 371. 372. 373. 374. 375. 376. 377. 378. 379. 380. 381. 382. 383. 384. 385. 386. 387. 388. 389. 390. 391. 392. 393. 394. 395. 396. 397. 398. 399. 400. 401. 402. 403. 404. 405. 406. 407. 408. 409. 410. 411. 412. 413. 414. 415. 416. 417. 418. 419. 420. 421. 422. 423. 424. 425. 426. 427. 428. 429. 430. 431. 432. 433. 434. 435. 436. 437. 438. 439. 440. 441. 442. 443. 444. 445. 446. 447. 448. 449. 450. 451. 452. 453. 454. 455. 456. 457. 458. 459. 460. 461. 462. 463. 464. 465. 466. 467. 468. 469. 470. 471. 472. 473. 474. 475. 476. 477. 478. 479. 480. 481. 482. 483. 484. 485. 486. 487. 488. 489. 490. 491. 492. 493. 494. 495. 496. 497. 498. 499. 500. 501. 502. 503. 504. 505. 506. 507. 508. 509. 510. 511. 512. 513. 514. 515. 516. 517. 518. 519. 520. 521. 522. 523. 524. 525. 526. 527. 528. 529. 530. 531. 532. 533. 534. 535. 536. 537. 538. 539. 540. 541. 542. 543. 544. 545. 546. 547. 548. 549. 550. 551. 552. 553. 554. 555. 556. 557. 558. 559. 560. 561. 562. 563. 564. 565. 566. 567. 568. 569. 570. 571. 572. 573. 574. 575. 576. 577. 578. 579. 580. 581. 582. 583. 584. 585. 586. 587. 588. 589. 590. 591. 592. 593. 594. 595. 596. 597. 598. 599. 600. 601. 602. 603. 604. 605. 606. 607. 608. 609. 610. 611. 612. 613. 614. 615. 616. 617. 618. 619. 620. 621. 622. 623. 624. 625. 626. 627. 628. 629. 630. 631. 632. 633. 634. 635. 636. 637. 638. 639. 640. 641. 642. 643. 644. 645. 646. 647. 648. 649. 650. 651. 652. 653. 654. 655. 656. 657. 658. 659. 660. 661. 662. 663. 664. 665. 666. 667. 668. 669. 670. 671. 672. 673. 674. 675. 676. 677. 678. 679. 680. 681. 682. 683. 684. 685. 686. 687. 688. 689. 690. 691. 692. 693. 694. 695. 696. 697. 698. 699. 700. 701. 702. 703. 704. 705. 706. 707. 708. 709. 710. 711. 712. 713. 714. 715. 716. 717. 718. 719. 720. 721. 722. 723. 724. 725. 726. 727. 728. 729. 730. 731. 732. 733. 734. 735. 736. 737. 738. 739. 740. 741. 742. 743. 744. 745. 746. 747. 748. 749. 750. 751. 752. 753. 754. 755. 756. 757. 758. 759. 760. 761. 762. 763. 764. 765. 766. 767. 768. 769. 770. 771. 772. 773. 774. 775. 776. 777. 778. 779. 780. 781. 782. 783. 784. 785. 786. 787. 788. 789. 790. 791. 792. 793. 794. 795. 796. 797. 798. 799. 800. 801. 802. 803. 804. 805. 806. 807. 808. 809. 810. 811. 812. 813. 814. 815. 816. 817. 818. 819. 820. 821. 822. 823. 824. 825. 826. 827. 828. 829. 830. 831. 832. 833. 834. 835. 836. 837. 838. 839. 840. 841. 842. 843. 844. 845. 846. 847. 848. 849. 850. 851. 852. 853. 854. 855. 856. 857. 858. 859. 860. 861. 862. 863. 864. 865. 866. 867. 868. 869. 870. 871. 872. 873. 874. 875. 876. 877. 878. 879. 880. 881. 882. 883. 884. 885. 886. 887. 888. 889. 890. 891. 892. 893. 894. 895. 896. 897. 898. 899. 900. 901. 902. 903. 904. 905. 906. 907. 908. 909. 910. 911. 912. 913. 914. 915. 916. 917. 918. 919. 920. 921. 922. 923. 924. 925. 926. 927. 928. 929. 930. 931. 932. 933. 934. 935. 936. 937. 938. 939. 940. 941. 942. 943. 944. 945. 946. 947. 948. 949. 950. 951. 952. 953. 954. 955. 956. 957. 958. 959. 960. 961. 962. 963. 964. 965. 966. 967. 968. 969. 970. 971. 972. 973. 974. 975. 976. 977. 978. 979. 980. 981. 982. 983. 984. 985. 986. 987. 988. 989. 990. 991. 992. 993. 994. 995. 996. 997. 998. 999. 1000. 1001. 1002. 1003. 1004. 1005. 1006. 1007. 1008. 1009. 1010. 1011. 1012. 1013. 1014. 1015. 1016. 1017. 1018. 1019. 1020. 1021. 1022. 1023. 1024. 1025. 1026. 1027. 1028. 1029. 1030. 1031. 1032. 1033. 1034. 1035. 1036. 1037. 1038. 1039. 1040. 1041. 1042. 1043. 1044. 1045.
\ No newline at end of file
diff --git a/stage1/sample_00037/raw_response.md b/stage1/sample_00037/raw_response.md
index 8ef59eb4ce38df04cf71b438e04a22a19a4b776e..2bac4d0156030fc7b928b45051e5970e63c0da7f 100644
--- a/stage1/sample_00037/raw_response.md
+++ b/stage1/sample_00037/raw_response.md
@@ -1,25 +1 @@
-1. COE - The Army Corps of Engineers (COE) regulates impacts to wetlands. The COE enforces Section 404 of the Clean Water Act by issuing individual or nationwide permits for wetlands impacts.  
-
-text[[160, 178, 854, 251]]
-ADEC - The Alaska Department of Environmental Conservation (ADEC), in conjunction with the COE 404 permitting, will analyze projects for impacts to water quality and recommend mitigation measures to prevent water pollution. ADEC will issue a Certificate of Assurance in accordance with Section 401 of the Clean Water Act.  
-
-text[[160, 259, 846, 310]]
-ADNR - The Alaska Department of Natural Resources (ADNR) regulates temporary withdrawals of water from state-owned sources and issues a water use permit. ADNR coordinates this permit application with all state agencies.  
-
-text[[187, 318, 864, 388]]
-The ADNR Division of Mining, Land and Water also issues right- of- way permits for crossing state lands. The exception is when a project crosses a state highway. If a state highway is crossed, the Department of Transportation & Public Facilities (DOT&PF) regulates the crossing.  
-
-text[[187, 396, 864, 466]]
-The State Historic Preservation Office (SHPO) is a division of ADNR and it regulates impacts to historic, cultural, and archeological resources. According to the 1966 Historic Preservation Act, all projects must be submitted to the SHPO for their analysis and approval.  
-
-text[[186, 473, 865, 545]]
-ADNR regulates specific rivers, lakes, and streams or parts of them that are important for the spawning, rearing, or migration of anadromous fish. According to Alaska Statute 16.05.870, ADF&G must issue a permit for any activity occurring in habitat important to anadromous fish.  
-
-text[[158, 552, 849, 589]]
-ADOT&PF - The ADOT&PF regulates state- owned roads. A new transmission line along or crossing a state- owned road would require a utility permit from ADOT&PF.  
-
-text[[159, 597, 832, 634]]
-ARRC - If a route uses the Alaska Railroad Corporation (ARRC) corridor or crosses the Alaska Railroad, a Right of Way Permit will be required.  
-
-text[[127, 691, 456, 709]]
-3.6 Land Classification/Ownership
\ No newline at end of file
+1- 3. 4- 5. 6- 7. 8- 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 47. 48. 49. 50. 51. 52. 53. 54. 55. 56. 57. 58. 59. 60. 61. 62. 63. 64. 65. 66. 67. 68. 69. 70. 71. 72. 73. 74. 75. 76. 77. 78. 79. 80. 81. 82. 83. 84. 85. 86. 87. 88. 89. 90. 91. 92. 93. 94. 95. 96. 97. 98. 99. 100. 101. 102. 103. 104. 105. 106. 107. 108. 109. 110. 111. 112. 113. 114. 115. 116. 117. 118. 119. 120. 121. 122. 123. 124. 125. 126. 127. 128. 129. 130. 131. 132. 133. 134. 135. 136. 137. 138. 139. 140. 141. 142. 143. 144. 145. 146. 147. 148. 149. 150. 151. 152. 153. 154. 155. 156. 157. 158. 159. 160. 161. 162. 163. 164. 165. 166. 167. 168. 169. 170. 171. 172. 173. 174. 175. 176. 177. 178. 179. 180. 181. 182. 183. 184. 185. 186. 187. 188. 189. 190. 191. 192. 193. 194. 195. 196. 197. 198. 199. 200. 201. 202. 203. 204. 205. 206. 207. 208. 209. 210. 211. 212. 213. 214. 215. 216. 217. 218. 219. 220. 221. 222. 223. 224. 225. 226. 227. 228. 229. 230. 231. 232. 233. 234. 235. 236. 237. 238. 239. 240. 241. 242. 243. 244. 245. 246. 247. 248. 249. 250. 251. 252. 253. 254. 255. 256. 257. 258. 259. 260. 261. 262. 263. 264. 265. 266. 267. 268. 269. 270. 271. 272. 273. 274. 275. 276. 277. 278. 279. 280. 281. 282. 283. 284. 285. 286. 287. 288. 289. 290. 291. 292. 293. 294. 295. 296. 297. 298. 299. 300. 301. 302. 303. 304. 305. 306. 307. 308. 309. 310. 311. 312. 313. 314. 315. 316. 317. 318. 319. 320. 321. 322. 323. 324. 325. 326. 327. 328. 329. 330. 331. 332. 333. 334. 335. 336. 337. 338. 339. 340. 341. 342. 343. 344. 345. 346. 347. 348. 349. 350. 351. 352. 353. 354. 355. 356. 357. 358. 359. 360. 361. 362. 363. 364. 365. 366. 367. 368. 369. 370. 371. 372. 373. 374. 375. 376. 377. 378. 379. 380. 381. 382. 383. 384. 385. 386. 387. 388. 389. 390. 391. 392. 393. 394. 395. 396. 397. 398. 399. 400. 401. 402. 403. 404. 405. 406. 407. 408. 409. 410. 411. 412. 413. 414. 415. 416. 417. 418. 419. 420. 421. 422. 423. 424. 425. 426. 427. 428. 429. 430. 431. 432. 433. 434. 435. 436. 437. 438. 439. 440. 441. 442. 443. 444. 445. 446. 447. 448. 449. 450. 451. 452. 453. 454. 455. 456. 457. 458. 459. 460. 461. 462. 463. 464. 465. 466. 467. 468. 469. 470. 471. 472. 473. 474. 475. 476. 477. 478. 479. 480. 481. 482. 483. 484. 485. 486. 487. 488. 489. 490. 491. 492. 493. 494. 495. 496. 497. 498. 499. 500. 501. 502. 503. 504. 505. 506. 507. 508. 509. 510. 511. 512. 513. 514. 515. 516. 517. 518. 519. 520. 521. 522. 523. 524. 525. 526. 527. 528. 529. 530. 531. 532. 533. 534. 535. 536. 537. 538. 539. 540. 541. 542. 543. 544. 545. 546. 547. 548. 549. 550. 551. 552. 553. 554. 555. 556. 557. 558. 559. 560. 561. 562. 563. 564. 565. 566. 567. 568. 569. 570. 571. 572. 573. 574. 575. 576. 577. 578. 579. 580. 581. 582. 583. 584. 585. 586. 587. 588. 589. 590. 591. 592. 593. 594. 595. 596. 597. 598. 599. 600. 601. 602. 603. 604. 605. 606. 607. 608. 609. 610. 611. 612. 613. 614. 615. 616. 617. 618. 619. 620. 621. 622. 623. 624. 625. 626. 627. 628. 629. 630. 631. 632. 633. 634. 635. 636. 637. 638. 639. 640. 641. 642. 643. 644. 645. 646. 647. 648. 649. 650. 651. 652. 653. 654. 655. 656. 657. 658. 659. 660. 661. 662. 663. 664. 665. 666. 667. 668. 669. 670. 671. 672. 673. 674. 675. 676. 677. 678. 679. 680. 681. 682. 683. 684. 685. 686. 687. 688. 689. 690. 691. 692. 693. 694. 695. 696. 697. 698. 699. 700. 701. 702. 703. 704. 705. 706. 707. 708. 709. 710. 711. 712. 713. 714. 715. 716. 717. 718. 719. 720. 721. 722. 723. 724. 725. 726. 727. 728. 729. 730. 731. 732. 733. 734. 735. 736. 737. 738. 739. 740. 741. 742. 743. 744. 745. 746. 747. 748. 749. 750. 751. 752. 753. 754. 755. 756. 757. 758. 759. 760. 761. 762. 763. 764. 765. 766. 767. 768. 769. 770. 771. 772. 773. 774. 775. 776. 777. 778. 779. 780. 781. 782. 783. 784. 785. 786. 787. 788. 789. 790. 791. 792. 793. 794. 795. 796. 797. 798. 799. 800. 801. 802. 803. 804. 805. 806. 807. 808. 809. 810. 811. 812. 813. 814. 815. 816. 817. 818. 819. 820. 821. 822. 823. 824. 825. 826. 827. 828. 829. 830. 831. 832. 833. 834. 835. 836. 837. 838. 839. 840. 841. 842. 843. 844. 845. 846. 847. 848. 849. 850. 851. 852. 853. 854. 855. 856. 857. 858. 859. 860. 861. 862. 863. 864. 865. 866. 867. 868. 869. 870. 871. 872. 873. 874. 875. 876. 877. 878. 879. 880. 881. 882. 883. 884. 885. 886. 887. 888. 889. 890. 891. 892. 893. 894. 895. 896. 897. 898. 899. 900. 901. 902. 903. 904. 905. 906. 907. 908. 909. 910. 911. 912. 913. 914. 915. 916. 917. 918. 919. 920. 921. 922. 923. 924. 925. 926. 927. 928. 929. 930. 931. 932. 933. 934. 935. 936. 937. 938. 939. 940. 941. 942. 943. 944. 945. 946. 947. 948. 949. 950. 951. 952. 953. 954. 955. 956. 957. 958. 959. 960. 961. 962. 963. 964. 965. 966. 967. 968. 969. 970. 971. 972. 973. 974. 975. 976. 977. 978. 979. 980. 981. 982. 983. 984. 985. 986. 987. 988. 989. 990. 991. 992. 993. 994. 995. 996. 997. 998. 999. 1000. 1001. 1002. 1003. 1004. 1005. 1006. 1007. 1008. 1009. 1010. 1011. 1012. 1013. 1014. 1015. 1016. 1017. 1018. 1019. 1020. 1021. 1022. 1023. 1024. 1025. 1026. 1027. 1028. 1029. 1030. 1031. 1032. 1033. 1034. 1035. 1036. 1037. 1038. 1039. 1040. 1041. 1042. 1043. 1044. 1045.
\ No newline at end of file
diff --git a/stage1/sample_00038/document.md b/stage1/sample_00038/document.md
index d0e6965bc264d8f52db001339212db214d981fce..977c63986f9e567218553ec0d33a7f16aff436c4 100644
--- a/stage1/sample_00038/document.md
+++ b/stage1/sample_00038/document.md
@@ -1 +1,13 @@
-0.37 0.73 0.93 0.2 0.1 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0
\ No newline at end of file
+and sufficiently large in magnitude, the mixed phase is stable in a triangular region of the phase diagram, exhibiting continuous phase transitions, with increasing normalized light-atom coupling \(\hat{\Omega}\) , to the \(\downarrow^{\prime}\) superfluid (for large \(|c_{2}| / c_{0}\) , to the left in the phase diagram) and to the \(\uparrow^{\prime}\) superfluid (for small \(|c_{2}| / c_{0}\) , to the right in the phase diagram). The same structure of the phase diagram holds for any ratio \(\mu_{\downarrow^{\prime}} / \mu_{\uparrow^{\prime}}\) , with the three curves that separate the phases moving as a function of the chemical potential ratio \(\mu_{\downarrow^{\prime}} / \mu_{\uparrow^{\prime}}\) ; the two sets of dashed lines in Fig. 6-8 indicate the locations of these boundaries for \(\mu_{\downarrow^{\prime}} / \mu_{\uparrow^{\prime}} = 0.37\) and \(\mu_{\downarrow^{\prime}} / \mu_{\uparrow^{\prime}} = 0.93\) . 
+
+image[[267, 332, 729, 564]]
+ 
+
+image_caption[[143, 583, 853, 746]]
+<center>Figure 6-8: This diagram shows the phases for the experimentally relevant regime. The solid lines show the phase diagram, at fixed \(\mu_{\downarrow^{\prime}} / \mu_{\uparrow^{\prime}} = 0.73\) , separating regions of BEC \(\downarrow^{\prime}\) (upper left, green), BEC \(\uparrow^{\prime}\) (upper right, blue), and a mixed BEC of both species (lower triangle, red). The two sets of dashed lines show the phase diagram at two additional values of \(\mu_{\downarrow^{\prime}} / \mu_{\uparrow^{\prime}}\) , showing the evolution of the phase diagram at fixed chemical potential. For experiments at fixed particle number, the relevant phase boundary is the dotted line: Below this dotted line, the mixed BEC is stable, while above this dotted line the system will phase separate into regions of uniform \(\uparrow^{\prime}\) superfluid and uniform \(\downarrow^{\prime}\) superfluid.</center> 
+
+sub_title[[143, 798, 626, 815]]
+## PHASE DIAGRAM: TRANSITION INTO THE UNSTABLE REGION 
+
+text[[143, 836, 853, 911]]
+Previous discussions are all based on the assumption that both \(\mu_{\sigma^{\prime}}\) are positive. But this is not absolutely necessary. Positive chemical potentials are indeed required for the case \(\mu_{\uparrow^{\prime}} = \mu_{\downarrow^{\prime}}\) for fixed chemical potential, following from that the
\ No newline at end of file
diff --git a/stage1/sample_00038/raw_response.md b/stage1/sample_00038/raw_response.md
index d0e6965bc264d8f52db001339212db214d981fce..977c63986f9e567218553ec0d33a7f16aff436c4 100644
--- a/stage1/sample_00038/raw_response.md
+++ b/stage1/sample_00038/raw_response.md
@@ -1 +1,13 @@
-0.37 0.73 0.93 0.2 0.1 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0.2 C2/C0 0.2 0.8 0.6 0.4 0
\ No newline at end of file
+and sufficiently large in magnitude, the mixed phase is stable in a triangular region of the phase diagram, exhibiting continuous phase transitions, with increasing normalized light-atom coupling \(\hat{\Omega}\) , to the \(\downarrow^{\prime}\) superfluid (for large \(|c_{2}| / c_{0}\) , to the left in the phase diagram) and to the \(\uparrow^{\prime}\) superfluid (for small \(|c_{2}| / c_{0}\) , to the right in the phase diagram). The same structure of the phase diagram holds for any ratio \(\mu_{\downarrow^{\prime}} / \mu_{\uparrow^{\prime}}\) , with the three curves that separate the phases moving as a function of the chemical potential ratio \(\mu_{\downarrow^{\prime}} / \mu_{\uparrow^{\prime}}\) ; the two sets of dashed lines in Fig. 6-8 indicate the locations of these boundaries for \(\mu_{\downarrow^{\prime}} / \mu_{\uparrow^{\prime}} = 0.37\) and \(\mu_{\downarrow^{\prime}} / \mu_{\uparrow^{\prime}} = 0.93\) . 
+
+image[[267, 332, 729, 564]]
+ 
+
+image_caption[[143, 583, 853, 746]]
+<center>Figure 6-8: This diagram shows the phases for the experimentally relevant regime. The solid lines show the phase diagram, at fixed \(\mu_{\downarrow^{\prime}} / \mu_{\uparrow^{\prime}} = 0.73\) , separating regions of BEC \(\downarrow^{\prime}\) (upper left, green), BEC \(\uparrow^{\prime}\) (upper right, blue), and a mixed BEC of both species (lower triangle, red). The two sets of dashed lines show the phase diagram at two additional values of \(\mu_{\downarrow^{\prime}} / \mu_{\uparrow^{\prime}}\) , showing the evolution of the phase diagram at fixed chemical potential. For experiments at fixed particle number, the relevant phase boundary is the dotted line: Below this dotted line, the mixed BEC is stable, while above this dotted line the system will phase separate into regions of uniform \(\uparrow^{\prime}\) superfluid and uniform \(\downarrow^{\prime}\) superfluid.</center> 
+
+sub_title[[143, 798, 626, 815]]
+## PHASE DIAGRAM: TRANSITION INTO THE UNSTABLE REGION 
+
+text[[143, 836, 853, 911]]
+Previous discussions are all based on the assumption that both \(\mu_{\sigma^{\prime}}\) are positive. But this is not absolutely necessary. Positive chemical potentials are indeed required for the case \(\mu_{\uparrow^{\prime}} = \mu_{\downarrow^{\prime}}\) for fixed chemical potential, following from that the
\ No newline at end of file
diff --git a/stage1/sample_00039/document.md b/stage1/sample_00039/document.md
index 0173a822ceaca02d88b51c9b32c5bc3d19fd603b..e1ed5df02cd68ddd9c489342b1c324f8a471f796 100644
--- a/stage1/sample_00039/document.md
+++ b/stage1/sample_00039/document.md
@@ -1,19 +1,19 @@
-6.7 and 6.10), we have the time-dependent Gross-Pitaevskii equations (recall \(\hbar = 1\) ):  
+6.10), we have the time-dependent Gross-Pitaevskii equations (recall \(\hbar = 1\) ):  
 
-equation[[273, 170, 852, 230]]
-\[\begin{array}{r l} & {i\partial_{t} - \epsilon (\mathbf{p}) + \mu_{\uparrow^{\prime}})\psi_{\uparrow^{\prime}} = c_{0}|\psi_{\uparrow^{\prime}}|^{2}\psi_{\uparrow^{\prime}} + \bar{\epsilon} |\psi_{\downarrow^{\prime}}|^{2}\psi_{\downarrow^{\prime}},}\\ & {(i\partial_{t} - \epsilon (\mathbf{p}) + \mu_{\downarrow^{\prime}})\psi_{\downarrow^{\prime}} = (c_{0} + c_{2})|\psi_{\downarrow^{\prime}}|^{2}\psi_{\downarrow^{\prime}} + \bar{\epsilon} |\psi_{\uparrow^{\prime}}|^{2}\psi_{\uparrow^{\prime}},} \end{array} \quad (6.64)\]  
+equation[[272, 169, 851, 232]]
+\[\begin{array}{r l} & {(i\partial_{t} - \epsilon (\mathbf{p}) + \mu_{\uparrow \uparrow})\psi_{\uparrow \uparrow} = c_{0}\vert \psi_{\uparrow \uparrow}\vert^{2}\psi_{\uparrow \uparrow} + \bar{\epsilon}\vert \psi_{\downarrow \downarrow}\vert^{2}\psi_{\downarrow \downarrow},}\\ & {(i\partial_{t} - \epsilon (\mathbf{p}) + \mu_{\downarrow \uparrow})\psi_{\downarrow \downarrow} = (c_{0} + c_{2})\vert \psi_{\downarrow \downarrow}\vert^{2}\psi_{\downarrow \downarrow} + \bar{\epsilon}\vert \psi_{\uparrow \uparrow}\vert^{2}\psi_{\uparrow \uparrow},} \end{array} \quad (6.64)\]  
 
-text[[142, 259, 853, 313]]
-where we defined \(\bar{\epsilon} \equiv c_{0}(1 + \hat{\Omega}^{2}) + c_{2}\) . Here, \(\epsilon (\mathbf{p})\) is the effective dispersion Eq. 6.8), and \(\mathbf{p} = - i\nabla\) is the momentum operator.  
+text[[143, 260, 853, 314]]
+where we defined \(\bar{c} \equiv c_{0}(1 + \hat{\Omega}^{2}) + c_{2}\) . Here, \(\epsilon (\mathbf{p})\) is the effective dispersion Eq. 6.8), and \(\mathbf{p} = - i\nabla\) is the momentum operator.  
 
-text[[142, 324, 854, 433]]
-The next step is to consider small time- dependent fluctuations \(\phi_{\sigma}(\mathbf{r}, t)\) around the equilibrium mixed phase solution, writing \(\psi_{\sigma}(\mathbf{r}, t) = \psi_{\sigma} + \phi_{\sigma}(\mathbf{r}, t)\) , where \(\psi_{\sigma}\) is the homogeneous mixed- phase solution satisfying Eq. 6.24, that we'll take to be real below. We can further express the fluctuation part as  
+text[[143, 323, 855, 434]]
+The next step is to consider small time- dependent fluctuations \(\phi_{\sigma}(\mathbf{r},t)\) around the equilibrium mixed phase solution, writing \(\psi_{\sigma}(\mathbf{r},t) = \psi_{\sigma} + \phi_{\sigma}(\mathbf{r},t)\) , where \(\psi_{\sigma}\) is the homogeneous mixed- phase solution satisfying Eq. 6.24, that we'll take to be real below. We can further express the fluctuation part as  
 
-equation[[375, 466, 852, 489]]
+equation[[375, 466, 852, 491]]
 \[\phi_{\sigma} = u_{\sigma}(\mathbf{r})e^{-i\omega t} + v_{\sigma}^{*}(\mathbf{r})e^{i\omega t}. \quad (6.65)\]  
 
-text[[143, 522, 853, 575]]
+text[[143, 521, 853, 574]]
 Plugging this into the time- dependent GP equations, keeping only linear terms in the fluctuations, and eliminating the chemical potentials using Eq. 6.24, we obtain  
 
-equation[[389, 597, 852, 723]]
-\[\begin{array}{r}P\left( \begin{array}{c}u_{\uparrow^{\prime}}(\mathbf{r})\\ v_{\uparrow^{\prime}}(\mathbf{r})\\ u_{\downarrow^{\prime}}(\mathbf{r})\\ v_{\downarrow^{\prime}}(\mathbf{r}) \end{array} \right) = \omega \left( \begin{array}{c}u_{\uparrow^{\prime}}(\mathbf{r})\\ v_{\uparrow^{\prime}}(\mathbf{r})\\ u_{\downarrow^{\prime}}(\mathbf{r})\\ v_{\downarrow^{\prime}}(\mathbf{r}) \end{array} \right), \end{array} \quad (6.66)\]
\ No newline at end of file
+equation[[377, 597, 852, 722]]
+\[\begin{array}{r}P\left( \begin{array}{c}u_{\uparrow \uparrow}(\mathbf{r})\\ v_{\uparrow \uparrow}(\mathbf{r})\\ u_{\downarrow \uparrow}(\mathbf{r})\\ v_{\downarrow \uparrow}(\mathbf{r}) \end{array} \right) = \omega \left( \begin{array}{c}u_{\uparrow \uparrow}(\mathbf{r})\\ v_{\uparrow \uparrow}(\mathbf{r})\\ u_{\downarrow \uparrow}(\mathbf{r})\\ v_{\downarrow \uparrow}(\mathbf{r}) \end{array} \right), \end{array} \quad (6.66)\]
\ No newline at end of file
diff --git a/stage1/sample_00039/raw_response.md b/stage1/sample_00039/raw_response.md
index 0173a822ceaca02d88b51c9b32c5bc3d19fd603b..e1ed5df02cd68ddd9c489342b1c324f8a471f796 100644
--- a/stage1/sample_00039/raw_response.md
+++ b/stage1/sample_00039/raw_response.md
@@ -1,19 +1,19 @@
-6.7 and 6.10), we have the time-dependent Gross-Pitaevskii equations (recall \(\hbar = 1\) ):  
+6.10), we have the time-dependent Gross-Pitaevskii equations (recall \(\hbar = 1\) ):  
 
-equation[[273, 170, 852, 230]]
-\[\begin{array}{r l} & {i\partial_{t} - \epsilon (\mathbf{p}) + \mu_{\uparrow^{\prime}})\psi_{\uparrow^{\prime}} = c_{0}|\psi_{\uparrow^{\prime}}|^{2}\psi_{\uparrow^{\prime}} + \bar{\epsilon} |\psi_{\downarrow^{\prime}}|^{2}\psi_{\downarrow^{\prime}},}\\ & {(i\partial_{t} - \epsilon (\mathbf{p}) + \mu_{\downarrow^{\prime}})\psi_{\downarrow^{\prime}} = (c_{0} + c_{2})|\psi_{\downarrow^{\prime}}|^{2}\psi_{\downarrow^{\prime}} + \bar{\epsilon} |\psi_{\uparrow^{\prime}}|^{2}\psi_{\uparrow^{\prime}},} \end{array} \quad (6.64)\]  
+equation[[272, 169, 851, 232]]
+\[\begin{array}{r l} & {(i\partial_{t} - \epsilon (\mathbf{p}) + \mu_{\uparrow \uparrow})\psi_{\uparrow \uparrow} = c_{0}\vert \psi_{\uparrow \uparrow}\vert^{2}\psi_{\uparrow \uparrow} + \bar{\epsilon}\vert \psi_{\downarrow \downarrow}\vert^{2}\psi_{\downarrow \downarrow},}\\ & {(i\partial_{t} - \epsilon (\mathbf{p}) + \mu_{\downarrow \uparrow})\psi_{\downarrow \downarrow} = (c_{0} + c_{2})\vert \psi_{\downarrow \downarrow}\vert^{2}\psi_{\downarrow \downarrow} + \bar{\epsilon}\vert \psi_{\uparrow \uparrow}\vert^{2}\psi_{\uparrow \uparrow},} \end{array} \quad (6.64)\]  
 
-text[[142, 259, 853, 313]]
-where we defined \(\bar{\epsilon} \equiv c_{0}(1 + \hat{\Omega}^{2}) + c_{2}\) . Here, \(\epsilon (\mathbf{p})\) is the effective dispersion Eq. 6.8), and \(\mathbf{p} = - i\nabla\) is the momentum operator.  
+text[[143, 260, 853, 314]]
+where we defined \(\bar{c} \equiv c_{0}(1 + \hat{\Omega}^{2}) + c_{2}\) . Here, \(\epsilon (\mathbf{p})\) is the effective dispersion Eq. 6.8), and \(\mathbf{p} = - i\nabla\) is the momentum operator.  
 
-text[[142, 324, 854, 433]]
-The next step is to consider small time- dependent fluctuations \(\phi_{\sigma}(\mathbf{r}, t)\) around the equilibrium mixed phase solution, writing \(\psi_{\sigma}(\mathbf{r}, t) = \psi_{\sigma} + \phi_{\sigma}(\mathbf{r}, t)\) , where \(\psi_{\sigma}\) is the homogeneous mixed- phase solution satisfying Eq. 6.24, that we'll take to be real below. We can further express the fluctuation part as  
+text[[143, 323, 855, 434]]
+The next step is to consider small time- dependent fluctuations \(\phi_{\sigma}(\mathbf{r},t)\) around the equilibrium mixed phase solution, writing \(\psi_{\sigma}(\mathbf{r},t) = \psi_{\sigma} + \phi_{\sigma}(\mathbf{r},t)\) , where \(\psi_{\sigma}\) is the homogeneous mixed- phase solution satisfying Eq. 6.24, that we'll take to be real below. We can further express the fluctuation part as  
 
-equation[[375, 466, 852, 489]]
+equation[[375, 466, 852, 491]]
 \[\phi_{\sigma} = u_{\sigma}(\mathbf{r})e^{-i\omega t} + v_{\sigma}^{*}(\mathbf{r})e^{i\omega t}. \quad (6.65)\]  
 
-text[[143, 522, 853, 575]]
+text[[143, 521, 853, 574]]
 Plugging this into the time- dependent GP equations, keeping only linear terms in the fluctuations, and eliminating the chemical potentials using Eq. 6.24, we obtain  
 
-equation[[389, 597, 852, 723]]
-\[\begin{array}{r}P\left( \begin{array}{c}u_{\uparrow^{\prime}}(\mathbf{r})\\ v_{\uparrow^{\prime}}(\mathbf{r})\\ u_{\downarrow^{\prime}}(\mathbf{r})\\ v_{\downarrow^{\prime}}(\mathbf{r}) \end{array} \right) = \omega \left( \begin{array}{c}u_{\uparrow^{\prime}}(\mathbf{r})\\ v_{\uparrow^{\prime}}(\mathbf{r})\\ u_{\downarrow^{\prime}}(\mathbf{r})\\ v_{\downarrow^{\prime}}(\mathbf{r}) \end{array} \right), \end{array} \quad (6.66)\]
\ No newline at end of file
+equation[[377, 597, 852, 722]]
+\[\begin{array}{r}P\left( \begin{array}{c}u_{\uparrow \uparrow}(\mathbf{r})\\ v_{\uparrow \uparrow}(\mathbf{r})\\ u_{\downarrow \uparrow}(\mathbf{r})\\ v_{\downarrow \uparrow}(\mathbf{r}) \end{array} \right) = \omega \left( \begin{array}{c}u_{\uparrow \uparrow}(\mathbf{r})\\ v_{\uparrow \uparrow}(\mathbf{r})\\ u_{\downarrow \uparrow}(\mathbf{r})\\ v_{\downarrow \uparrow}(\mathbf{r}) \end{array} \right), \end{array} \quad (6.66)\]
\ No newline at end of file
diff --git a/stage1/sample_00040/document.md b/stage1/sample_00040/document.md
index 14794f4a3149bfc9b2830a7834b3e20fefaba0bb..5accff743da068836de6248ac07cc8bc4ef38325 100644
--- a/stage1/sample_00040/document.md
+++ b/stage1/sample_00040/document.md
@@ -1 +1 @@
-为自己的日子 在自己的脸上留下伤口 因为没有别的一切为我们作证  ——海子《我，以及其他的证人》
\ No newline at end of file
+为自己的日子在自己的脸上留下伤口因为没有别的一切为我们作证——海子《我，以及其他的证人》
\ No newline at end of file
diff --git a/stage1/sample_00040/raw_response.md b/stage1/sample_00040/raw_response.md
index 14794f4a3149bfc9b2830a7834b3e20fefaba0bb..5accff743da068836de6248ac07cc8bc4ef38325 100644
--- a/stage1/sample_00040/raw_response.md
+++ b/stage1/sample_00040/raw_response.md
@@ -1 +1 @@
-为自己的日子 在自己的脸上留下伤口 因为没有别的一切为我们作证  ——海子《我，以及其他的证人》
\ No newline at end of file
+为自己的日子在自己的脸上留下伤口因为没有别的一切为我们作证——海子《我，以及其他的证人》
\ No newline at end of file
diff --git a/stage1/sample_00041/document.md b/stage1/sample_00041/document.md
index 6890a2d30da99262fcc0be590610141402adde9d..44503f0562b8626906ab4ba18be2ff6219102461 100644
--- a/stage1/sample_00041/document.md
+++ b/stage1/sample_00041/document.md
@@ -1 +1,5 @@
-1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 196
\ No newline at end of file
+1961
+
+table[[28, 20, 968, 927]]
+
+<table>TitleDateCall NumberDescriptionPortable extinguishers. [motion picture]19678-5549Discusses the different classes of portable fire<br>extinguishers, how they work, and what types of fires<br>they work on. Also shows how to put out electrical,<br>chemical and combustible fires. Production staff, D.<br>Frederick Cook, Don VerPloeg, John Bousek, Jack<br>Gutmann, Don Buchanan; advisory staff, Keith Royer,<br>Floyd W. Nelson.Portrait of modern egg-layer research. [19616-0153Poultry breeding and leghorn chicken.Potato farmNDPoultry raising. [motion picture]19454-1011Vocational guidance film.Power and pride. [motion picture]19596-1235no descriptionPower and pride. [motion picture]19598-7896Student film.Praire pioneers. [motion picture]19776-1021no descriptionPreparation of less tender beef cuts. [mo19724-4606Cookery (beef). Meat cuts - Identification.Preparing a crystalline candy-fondant. [19694-7359Preparing fondant frosting.Preparing an amorphous candy - butters19694-7358Preparing butterscotch candy.Preparing Pork SausagePreservation technology of the<br>1980's.[motion picture] / clibrary of1983Arc Vid 030In depth presentation on new preservation technologies<br>at the Library of Congress.Preserving the past, insuring the<br>future.[motion picture] / clowa State<br>University, Media Resources Center;<br>lowa State University Parks Library.undatedArc Vid 004Discusses factors the destroy books such as insects and<br>mildew and visits the lowa State University Conservation Laboratory where books are cleaned, fumigated,<br>repaired, and custom boxes are prepared. Script,<br>narration, Warren Kuhn ; photography, Ivan Hanthorn,<br>Tom Freelove, Warren Kuhn ; music, montage, Cynthia<br>Holden, Tom Freelove. Iowa State University Parks<br>Library.President Eaton inauguration.[motion picture] / clowa State University;<br>producer, Michelle Warnke ; director,<br>Steven Kurtenbach.1987Arc Vid 016Part 1 - A brief history of Iowa State University, the<br>inaugural committee, and Gordon Eaton. Also an<br>explanation of gown colors, the procession of academic dignitaries, and speeches by representatives of the State Board of Regents, lowa State University Department of Philosophy, Faculty Council, Professional and Scientific<br>Council, and the Government of the Student Body. Part<br>2 - Speeches by representatives of the lowa State<br>University Alumni Association, State Board of Regents,<br>the Chancellor of the University of Illinois - Chicago, and<br>the Governor of lowa. Also a performance bu the ISU<br>Singers, the investiture of President eaten, and the start<br>of his speech, "A new vision". Part 3 - The conclusion of<br>President Eaton's speech, the ISU Symphony and the ISU<br>Singers.Preventing fires - in minuteNDPrice of victory. [motion picture]19426-0126Highlights of Vice President Henry A. Wallace's May 8th,<br>1942 address to the Free World Asociation in New York<br>City. In it he describes the reasons for fighting and the<br>sacrifices that must be madePrinting4-0393Vocational guidance film.Probability & StatisticsDVD 002 767 disc 1</table>
\ No newline at end of file
diff --git a/stage1/sample_00041/raw_response.md b/stage1/sample_00041/raw_response.md
index 6890a2d30da99262fcc0be590610141402adde9d..44503f0562b8626906ab4ba18be2ff6219102461 100644
--- a/stage1/sample_00041/raw_response.md
+++ b/stage1/sample_00041/raw_response.md
@@ -1 +1,5 @@
-1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 1961 6-0153 196
\ No newline at end of file
+1961
+
+table[[28, 20, 968, 927]]
+
+<table>TitleDateCall NumberDescriptionPortable extinguishers. [motion picture]19678-5549Discusses the different classes of portable fire<br>extinguishers, how they work, and what types of fires<br>they work on. Also shows how to put out electrical,<br>chemical and combustible fires. Production staff, D.<br>Frederick Cook, Don VerPloeg, John Bousek, Jack<br>Gutmann, Don Buchanan; advisory staff, Keith Royer,<br>Floyd W. Nelson.Portrait of modern egg-layer research. [19616-0153Poultry breeding and leghorn chicken.Potato farmNDPoultry raising. [motion picture]19454-1011Vocational guidance film.Power and pride. [motion picture]19596-1235no descriptionPower and pride. [motion picture]19598-7896Student film.Praire pioneers. [motion picture]19776-1021no descriptionPreparation of less tender beef cuts. [mo19724-4606Cookery (beef). Meat cuts - Identification.Preparing a crystalline candy-fondant. [19694-7359Preparing fondant frosting.Preparing an amorphous candy - butters19694-7358Preparing butterscotch candy.Preparing Pork SausagePreservation technology of the<br>1980's.[motion picture] / clibrary of1983Arc Vid 030In depth presentation on new preservation technologies<br>at the Library of Congress.Preserving the past, insuring the<br>future.[motion picture] / clowa State<br>University, Media Resources Center;<br>lowa State University Parks Library.undatedArc Vid 004Discusses factors the destroy books such as insects and<br>mildew and visits the lowa State University Conservation Laboratory where books are cleaned, fumigated,<br>repaired, and custom boxes are prepared. Script,<br>narration, Warren Kuhn ; photography, Ivan Hanthorn,<br>Tom Freelove, Warren Kuhn ; music, montage, Cynthia<br>Holden, Tom Freelove. Iowa State University Parks<br>Library.President Eaton inauguration.[motion picture] / clowa State University;<br>producer, Michelle Warnke ; director,<br>Steven Kurtenbach.1987Arc Vid 016Part 1 - A brief history of Iowa State University, the<br>inaugural committee, and Gordon Eaton. Also an<br>explanation of gown colors, the procession of academic dignitaries, and speeches by representatives of the State Board of Regents, lowa State University Department of Philosophy, Faculty Council, Professional and Scientific<br>Council, and the Government of the Student Body. Part<br>2 - Speeches by representatives of the lowa State<br>University Alumni Association, State Board of Regents,<br>the Chancellor of the University of Illinois - Chicago, and<br>the Governor of lowa. Also a performance bu the ISU<br>Singers, the investiture of President eaten, and the start<br>of his speech, "A new vision". Part 3 - The conclusion of<br>President Eaton's speech, the ISU Symphony and the ISU<br>Singers.Preventing fires - in minuteNDPrice of victory. [motion picture]19426-0126Highlights of Vice President Henry A. Wallace's May 8th,<br>1942 address to the Free World Asociation in New York<br>City. In it he describes the reasons for fighting and the<br>sacrifices that must be madePrinting4-0393Vocational guidance film.Probability & StatisticsDVD 002 767 disc 1</table>
\ No newline at end of file
diff --git a/stage1/sample_00042/document.md b/stage1/sample_00042/document.md
index 86ce0789b444d98350614233ee8707d67238d19b..ec72d99eeb57dfc5b7652a5ca163c0b0ec287be4 100644
--- a/stage1/sample_00042/document.md
+++ b/stage1/sample_00042/document.md
@@ -1,61 +1,52 @@
-0.3.0.0
+1987 Arc Vid 020k Speakers discuss the importance of the land grant institution in biotechnology and its economic aspects, the application of BGH hormones and the speed of adoption, and the results of a survey on what are proper roles in conductive guidelines for university research and current expectations of universities in results. The panel also answers questions from the floor. November 4, 1987, 3pm.
 
-text[[58, 62, 329, 76]]
-Snapping stand & Hitzhuser beefmaker, ND
-
-text[[58, 75, 514, 105]]
-Social impacts of technology.[motion picture] / clowa State University. 1987
-
-text[[571, 73, 957, 193]]
-Speakers discuss the importance of the land grant institution in biotechnology and its economic aspects,the application of BGH hormones and the speed of adoption, and the results of a survey on what are proper roles in conductive guidelines for university research and current expectations of universities in results. The panel also answers questions from the floor. November 4, 1987,3pm.
-
-text[[58, 206, 330, 218]]
+text[[60, 206, 381, 220]]
 Sodium 1080 1955
 
-text[[58, 230, 694, 241]]
-Soil conservation districts and lowa peop 1953 16-0127 Soil conservation.
+text[[60, 228, 691, 243]]
+Soil conservation districts and Iowa peop 1953 16-0127 Soil conservation.
 
-text[[58, 252, 307, 263]]
+text[[60, 251, 309, 265]]
 Soil conservation Service (CP) spots
 
-text[[58, 275, 946, 307]]
-Soil conservation with regular farm 1960 8-3592 Suggests simple methods farmers can utilize to protect soil from water run-off. Examples include contour
+text[[60, 273, 946, 302]]
+Soil conservation with regular farm 1960 8-3592 Suggests simple methods farmers can utilize to protect seed from water run-off. Examples include contour
 
-text[[572, 310, 937, 362]]
-farming, strip farming and terracing. Shows how farmers can fill gullies and construct terraces using a simple field plow. Also instructs on how to best maintain terraces and grass waterways.
+text[[60, 302, 933, 361]]
+equipment. [motion picture] farming, strip farming and terracing. Shows how farmers can fill gullies and construct terraces using a simple field plow. Also instructs on how to best maintain terraces and grass waterways.
 
-text[[58, 372, 946, 403]]
-Soil conservation with regular farm 1960 8-3594 Suggests simple methods farmers can utilize to protect equipment. [motion picture] soil from water run-off. Examples include contour farming, strip farming and terracing. Shows how
+text[[60, 370, 945, 400]]
+Soil conservation with regular farm 1960 8-3594 Suggests simple methods farmers can utilize to protect equipment. [motion picture] soil from water run-off. Examples include contour
 
-text[[572, 408, 931, 460]]
-farmers can fill gullies and construct terraces using a simple field plow. Also instructs on how to best maintain terraces and grass waterways.
+text[[572, 403, 931, 461]]
+farming, strip farming and terracing. Shows how farmers can fill gullies and construct terraces using a simple field plow. Also instructs on how to best maintain terraces and grass waterways.
 
-text[[58, 471, 330, 499]]
-Soil erosion work in Kansas. [motion picture] 1942 4-7683
+text[[60, 469, 381, 500]]
+Soil erosion work in Kansas. [motion 1942 4-7683 pictures]
 
-text[[572, 469, 931, 527]]
+text[[572, 469, 931, 526]]
 Shows conditions along roads in Kansas and what is being done to control the erosion of the banks and runoff into ditches. Shows men inspecting damaged areas, planting and spreading ground cover.
 
-text[[58, 539, 671, 551]]
+text[[60, 540, 673, 552]]
 Soil Machine 6-1522 no description
 
-text[[58, 562, 904, 590]]
-Soil model tillage studies. [motion 1959 4-0827 Researchers in a laboratory study soil tillage and picture] compaction.
+text[[60, 562, 903, 591]]
+Soil model tillage studies. [motion 1959 4-0827 Researchers in a laboratory study soil tillage and pictures] compaction.
 
-text[[58, 601, 366, 612]]
+text[[60, 600, 367, 612]]
 Soil physical changes related to tillage to ND
 
-text[[58, 625, 778, 638]]
+text[[60, 624, 778, 637]]
 Soil test. [motion picture] 1955 8-1206 Soils analysis and soils testing.
 
-text[[58, 650, 173, 660]]
+text[[60, 647, 176, 659]]
 Solar grail drying
 
-text[[58, 672, 335, 682]]
-Solar grain drying-water pollution resea
+text[[60, 670, 338, 682]]
+Solar grain drying - water pollution resea
 
-text[[58, 694, 928, 741]]
+text[[60, 693, 930, 740]]
 Solution process. [motion picture] 1961 4-7743 Water and benzene are used as solvents for solids to demonstrate how the solids are affected after being introduced to liquids.
 
-text[[58, 753, 366, 764]]
+text[[60, 750, 365, 762]]
 Songs of the wild wood ND
\ No newline at end of file
diff --git a/stage1/sample_00042/raw_response.md b/stage1/sample_00042/raw_response.md
index 86ce0789b444d98350614233ee8707d67238d19b..ec72d99eeb57dfc5b7652a5ca163c0b0ec287be4 100644
--- a/stage1/sample_00042/raw_response.md
+++ b/stage1/sample_00042/raw_response.md
@@ -1,61 +1,52 @@
-0.3.0.0
+1987 Arc Vid 020k Speakers discuss the importance of the land grant institution in biotechnology and its economic aspects, the application of BGH hormones and the speed of adoption, and the results of a survey on what are proper roles in conductive guidelines for university research and current expectations of universities in results. The panel also answers questions from the floor. November 4, 1987, 3pm.
 
-text[[58, 62, 329, 76]]
-Snapping stand & Hitzhuser beefmaker, ND
-
-text[[58, 75, 514, 105]]
-Social impacts of technology.[motion picture] / clowa State University. 1987
-
-text[[571, 73, 957, 193]]
-Speakers discuss the importance of the land grant institution in biotechnology and its economic aspects,the application of BGH hormones and the speed of adoption, and the results of a survey on what are proper roles in conductive guidelines for university research and current expectations of universities in results. The panel also answers questions from the floor. November 4, 1987,3pm.
-
-text[[58, 206, 330, 218]]
+text[[60, 206, 381, 220]]
 Sodium 1080 1955
 
-text[[58, 230, 694, 241]]
-Soil conservation districts and lowa peop 1953 16-0127 Soil conservation.
+text[[60, 228, 691, 243]]
+Soil conservation districts and Iowa peop 1953 16-0127 Soil conservation.
 
-text[[58, 252, 307, 263]]
+text[[60, 251, 309, 265]]
 Soil conservation Service (CP) spots
 
-text[[58, 275, 946, 307]]
-Soil conservation with regular farm 1960 8-3592 Suggests simple methods farmers can utilize to protect soil from water run-off. Examples include contour
+text[[60, 273, 946, 302]]
+Soil conservation with regular farm 1960 8-3592 Suggests simple methods farmers can utilize to protect seed from water run-off. Examples include contour
 
-text[[572, 310, 937, 362]]
-farming, strip farming and terracing. Shows how farmers can fill gullies and construct terraces using a simple field plow. Also instructs on how to best maintain terraces and grass waterways.
+text[[60, 302, 933, 361]]
+equipment. [motion picture] farming, strip farming and terracing. Shows how farmers can fill gullies and construct terraces using a simple field plow. Also instructs on how to best maintain terraces and grass waterways.
 
-text[[58, 372, 946, 403]]
-Soil conservation with regular farm 1960 8-3594 Suggests simple methods farmers can utilize to protect equipment. [motion picture] soil from water run-off. Examples include contour farming, strip farming and terracing. Shows how
+text[[60, 370, 945, 400]]
+Soil conservation with regular farm 1960 8-3594 Suggests simple methods farmers can utilize to protect equipment. [motion picture] soil from water run-off. Examples include contour
 
-text[[572, 408, 931, 460]]
-farmers can fill gullies and construct terraces using a simple field plow. Also instructs on how to best maintain terraces and grass waterways.
+text[[572, 403, 931, 461]]
+farming, strip farming and terracing. Shows how farmers can fill gullies and construct terraces using a simple field plow. Also instructs on how to best maintain terraces and grass waterways.
 
-text[[58, 471, 330, 499]]
-Soil erosion work in Kansas. [motion picture] 1942 4-7683
+text[[60, 469, 381, 500]]
+Soil erosion work in Kansas. [motion 1942 4-7683 pictures]
 
-text[[572, 469, 931, 527]]
+text[[572, 469, 931, 526]]
 Shows conditions along roads in Kansas and what is being done to control the erosion of the banks and runoff into ditches. Shows men inspecting damaged areas, planting and spreading ground cover.
 
-text[[58, 539, 671, 551]]
+text[[60, 540, 673, 552]]
 Soil Machine 6-1522 no description
 
-text[[58, 562, 904, 590]]
-Soil model tillage studies. [motion 1959 4-0827 Researchers in a laboratory study soil tillage and picture] compaction.
+text[[60, 562, 903, 591]]
+Soil model tillage studies. [motion 1959 4-0827 Researchers in a laboratory study soil tillage and pictures] compaction.
 
-text[[58, 601, 366, 612]]
+text[[60, 600, 367, 612]]
 Soil physical changes related to tillage to ND
 
-text[[58, 625, 778, 638]]
+text[[60, 624, 778, 637]]
 Soil test. [motion picture] 1955 8-1206 Soils analysis and soils testing.
 
-text[[58, 650, 173, 660]]
+text[[60, 647, 176, 659]]
 Solar grail drying
 
-text[[58, 672, 335, 682]]
-Solar grain drying-water pollution resea
+text[[60, 670, 338, 682]]
+Solar grain drying - water pollution resea
 
-text[[58, 694, 928, 741]]
+text[[60, 693, 930, 740]]
 Solution process. [motion picture] 1961 4-7743 Water and benzene are used as solvents for solids to demonstrate how the solids are affected after being introduced to liquids.
 
-text[[58, 753, 366, 764]]
+text[[60, 750, 365, 762]]
 Songs of the wild wood ND
\ No newline at end of file
diff --git a/stage1/sample_00043/document.md b/stage1/sample_00043/document.md
index 7be02739faa71f54919720cbb83d7d8e44b51ab0..52f4f4bf32d2c50611e6de1212158c651aa255c4 100644
--- a/stage1/sample_00043/document.md
+++ b/stage1/sample_00043/document.md
@@ -1,28 +1,19 @@
-25th Annual Meeting of the Society for Industrial and Applied Mathematics SouthEastern A tantic Section (SIAM-SEAS) on March 17, 2001, 13 undergraduate students majoring in mathematics, computer science, or electrical and computer engineering competed in the first SIAM-SEAS JeopardyTM competition. This event was held in the Wall College of Business Building on the campus of Coastal Carolina University (Conway, SC). Representing Clemson University, Coastal Carolina University, The Citadel, and The University of Tennessee, each team was required to provide questions to answers (in the spirit of the popular TV game show) from topics in Calculus, Differential Equations, Linear Algebra, and Computer Science. This action-packed event involved two preliminary rounds of competition with the winners of the these rounds meeting in a final round to decide first and second place. All rounds included "Daily Doubles" and a "Final Jeopardy" question. The preliminary round between The University of Tennessee and The Citadel was especially exciting as UT built a commanding lead in questions from Computer Science and Linear Algebra. The 5-member team from The Citadel, however, made an impressive comeback in questions from Integral Calculus. As with the popular gameshow, incorrect questions to answers forced point deductions and solutions to several computational problems were submitted to a judge for verification. A buzzer system loaned by the Department of Mathematics at the University of Tennessee was used by the teams to signal responses and to determine control of the game. Special thanks to Profs. Mei-Qin Chen (The Citadel), Martha Abell (Georgia Southern), and Chris Cox (Clemson) for their help with game organization, judging, and time keeping. A slideshow of this event follows the final standings of the competition and roster of each team. Thanks to SIAM for their financial support of this unique (and perhaps soon to become an annual) event! The gameshow "Jeopardy" is a trademark (TM) of Columbia/Tri-star. 
+25th Annual Meeting of the Society for Industrial and A plied Mathematics SouthEastern A tantic Section (SIAM-SEAS) on March 17, 2001, 13 undergraduate students majoring in mathematics, computer science, or electrical and computer engineering competed in the first SIAM-SEAS JeopardyTM competition. This event was held in the Wall College of Business Building on the campus of Coastal Carolina University (Conway, SC). Representing Clemson University, Coastal Carolina University, The Citadel, and The University of Tennessee, each team was required to provide questions to answers (in the spirit of the popular TV game show) from topics in Calculus, Differential Equations, Linear Algebra, and Computer Science.  
 
-image[[293, 30, 695, 122]]
+text[[130, 333, 852, 461]]
+This action- packed event involved two preliminary rounds of competition with the winners of the these rounds meeting in a final round to decide first and second place. All rounds included "Daily Doubles" and a "Final Jeopardy" question. The preliminary round between The University of Tennessee and The Citadel was especially exciting as UT built a commanding lead in questions from Computer Science and Linear Algebra. The 5- member team from The Citadel, however, made an impressive comeback in questions from Integral Calculus.  
 
-title[[220, 123, 773, 149]]
-# SIAM-SEAS JeopardyTM Competition 2001 
+text[[130, 479, 863, 583]]
+As with the popular gameshow, incorrect questions to answers forced point deductions and solutions to several computational problems were submitted to a judge for verification. A buzzer system loaned by the Department of Mathematics at the University of Tennessee was used by the teams to signal responses and to determine control of the game. Special thanks to Profs. Mei- Qin Chen (The Citadel), Martha Abell (Georgia Southern), and Chris Cox (Clemson) for their help with game organization, judging, and time keeping.  
 
-text[[129, 170, 864, 325]]
-As part of the 25th Annual Meeting of the Society for Industrial and Applied Mathematics SouthEastern A tantic Section (SIAM-SEAS) on March 17, 2001, 13 undergraduate students majoring in mathematics, computer science, or electrical and computer engineering competed in the first SIAM-SEAS JeopardyTM competition. This event was held in the Wall College of Business Building on the campus of Coastal Carolina University (Conway, SC). Representing Clemson University, Coastal Carolina University, The Citadel, and The University of Tennessee, each team was required to provide questions to answers (in the spirit of the popular TV game show) from topics in Calculus, Differential Equations, Linear Algebra, and Computer Science. 
+text[[130, 598, 865, 653]]
+A slideshow of this event follows the final standings of the competition and roster of each team. Thanks to SIAM for their financial support of this unique (and perhaps soon to become an annual) event! The gameshow "Jeopardy" is a trademark (TM) of Columbia/Tri- star.  
 
-text[[129, 345, 851, 462]]
-This action-packed event involved two preliminary rounds of competition with the winners of the these rounds meeting in a final round to decide first and second place. All rounds included "Daily Doubles" and a "Final Jeopardy" question. The preliminary round between The University of Tennessee and The Citadel was especially exciting as UT built a commanding lead in questions from Computer Science and Linear Algebra. The 5-member team from The Citadel, however, made an impressive comeback in questions from Integral Calculus. 
+text[[194, 686, 806, 829]]
+Place Team Roster1st Clemson Clay Jenkins, Charles Swannack2nd The Citadel Ryan Graham, Robert Harig, Chih- Kuo Lee, Y ow- Chyun Lin, Ying- Jiun Wang3rd Tennessee Nehal Parikh, James Perkins, Yiheng Yang4th Coastal Carolina Jimmy Bailey, Margaret Leonard, Brian Richardson  
 
-text[[129, 482, 863, 583]]
-As with the popular gameshow, incorrect questions to answers forced point deductions and solutions to several computational problems were submitted to a judge for verification. A buzzer system loaned by the Department of Mathematics at the University of Tennessee was used by the teams to signal responses and to determine control of the game. Special thanks to Profs. Mei-Qin Chen (The Citadel), Martha Abell (Georgia Southern), and Chris Cox (Clemson) for their help with game organization, judging, and time keeping. 
+text[[245, 866, 499, 901]]
+- Michael W. Berry (Organizer) University of Tennessee  
 
-text[[129, 599, 864, 652]]
-A slideshow of this event follows the final standings of the competition and roster of each team. Thanks to SIAM for their financial support of this unique (and perhaps soon to become an annual) event! The gameshow "Jeopardy" is a trademark (TM) of Columbia/Tri-star. 
-
-table[[190, 686, 803, 831]]
-<table>Place TeamRoster1st ClemsonClay Jenkins, Charles Swannack2nd The CitadelRyan Graham, Robert Harig, Chih-Kuo Lee, Yow-Chyun Lin, Ying-Jiun Wang3rd TennesseeNehal Parikh, James Perkins, Yiheng Yang4th Coastal CarolinaJimmy Bailey, Margaret Leonard, Brian Richardson</table>
-
-text[[248, 869, 501, 902]]
-- Michael W. Berry (Organizer)
-University of Tennessee 
-
-text[[129, 919, 802, 943]]
-SIAM-SEAS JeopardyTM 2001 Photos (click on small triangular buttons to
\ No newline at end of file
+text[[133, 919, 801, 942]]
+SIAM- SEAS JeopardyTM 2001 Photos (click on small triangular buttons to
\ No newline at end of file
diff --git a/stage1/sample_00043/raw_response.md b/stage1/sample_00043/raw_response.md
index 7be02739faa71f54919720cbb83d7d8e44b51ab0..52f4f4bf32d2c50611e6de1212158c651aa255c4 100644
--- a/stage1/sample_00043/raw_response.md
+++ b/stage1/sample_00043/raw_response.md
@@ -1,28 +1,19 @@
-25th Annual Meeting of the Society for Industrial and Applied Mathematics SouthEastern A tantic Section (SIAM-SEAS) on March 17, 2001, 13 undergraduate students majoring in mathematics, computer science, or electrical and computer engineering competed in the first SIAM-SEAS JeopardyTM competition. This event was held in the Wall College of Business Building on the campus of Coastal Carolina University (Conway, SC). Representing Clemson University, Coastal Carolina University, The Citadel, and The University of Tennessee, each team was required to provide questions to answers (in the spirit of the popular TV game show) from topics in Calculus, Differential Equations, Linear Algebra, and Computer Science. This action-packed event involved two preliminary rounds of competition with the winners of the these rounds meeting in a final round to decide first and second place. All rounds included "Daily Doubles" and a "Final Jeopardy" question. The preliminary round between The University of Tennessee and The Citadel was especially exciting as UT built a commanding lead in questions from Computer Science and Linear Algebra. The 5-member team from The Citadel, however, made an impressive comeback in questions from Integral Calculus. As with the popular gameshow, incorrect questions to answers forced point deductions and solutions to several computational problems were submitted to a judge for verification. A buzzer system loaned by the Department of Mathematics at the University of Tennessee was used by the teams to signal responses and to determine control of the game. Special thanks to Profs. Mei-Qin Chen (The Citadel), Martha Abell (Georgia Southern), and Chris Cox (Clemson) for their help with game organization, judging, and time keeping. A slideshow of this event follows the final standings of the competition and roster of each team. Thanks to SIAM for their financial support of this unique (and perhaps soon to become an annual) event! The gameshow "Jeopardy" is a trademark (TM) of Columbia/Tri-star. 
+25th Annual Meeting of the Society for Industrial and A plied Mathematics SouthEastern A tantic Section (SIAM-SEAS) on March 17, 2001, 13 undergraduate students majoring in mathematics, computer science, or electrical and computer engineering competed in the first SIAM-SEAS JeopardyTM competition. This event was held in the Wall College of Business Building on the campus of Coastal Carolina University (Conway, SC). Representing Clemson University, Coastal Carolina University, The Citadel, and The University of Tennessee, each team was required to provide questions to answers (in the spirit of the popular TV game show) from topics in Calculus, Differential Equations, Linear Algebra, and Computer Science.  
 
-image[[293, 30, 695, 122]]
+text[[130, 333, 852, 461]]
+This action- packed event involved two preliminary rounds of competition with the winners of the these rounds meeting in a final round to decide first and second place. All rounds included "Daily Doubles" and a "Final Jeopardy" question. The preliminary round between The University of Tennessee and The Citadel was especially exciting as UT built a commanding lead in questions from Computer Science and Linear Algebra. The 5- member team from The Citadel, however, made an impressive comeback in questions from Integral Calculus.  
 
-title[[220, 123, 773, 149]]
-# SIAM-SEAS JeopardyTM Competition 2001 
+text[[130, 479, 863, 583]]
+As with the popular gameshow, incorrect questions to answers forced point deductions and solutions to several computational problems were submitted to a judge for verification. A buzzer system loaned by the Department of Mathematics at the University of Tennessee was used by the teams to signal responses and to determine control of the game. Special thanks to Profs. Mei- Qin Chen (The Citadel), Martha Abell (Georgia Southern), and Chris Cox (Clemson) for their help with game organization, judging, and time keeping.  
 
-text[[129, 170, 864, 325]]
-As part of the 25th Annual Meeting of the Society for Industrial and Applied Mathematics SouthEastern A tantic Section (SIAM-SEAS) on March 17, 2001, 13 undergraduate students majoring in mathematics, computer science, or electrical and computer engineering competed in the first SIAM-SEAS JeopardyTM competition. This event was held in the Wall College of Business Building on the campus of Coastal Carolina University (Conway, SC). Representing Clemson University, Coastal Carolina University, The Citadel, and The University of Tennessee, each team was required to provide questions to answers (in the spirit of the popular TV game show) from topics in Calculus, Differential Equations, Linear Algebra, and Computer Science. 
+text[[130, 598, 865, 653]]
+A slideshow of this event follows the final standings of the competition and roster of each team. Thanks to SIAM for their financial support of this unique (and perhaps soon to become an annual) event! The gameshow "Jeopardy" is a trademark (TM) of Columbia/Tri- star.  
 
-text[[129, 345, 851, 462]]
-This action-packed event involved two preliminary rounds of competition with the winners of the these rounds meeting in a final round to decide first and second place. All rounds included "Daily Doubles" and a "Final Jeopardy" question. The preliminary round between The University of Tennessee and The Citadel was especially exciting as UT built a commanding lead in questions from Computer Science and Linear Algebra. The 5-member team from The Citadel, however, made an impressive comeback in questions from Integral Calculus. 
+text[[194, 686, 806, 829]]
+Place Team Roster1st Clemson Clay Jenkins, Charles Swannack2nd The Citadel Ryan Graham, Robert Harig, Chih- Kuo Lee, Y ow- Chyun Lin, Ying- Jiun Wang3rd Tennessee Nehal Parikh, James Perkins, Yiheng Yang4th Coastal Carolina Jimmy Bailey, Margaret Leonard, Brian Richardson  
 
-text[[129, 482, 863, 583]]
-As with the popular gameshow, incorrect questions to answers forced point deductions and solutions to several computational problems were submitted to a judge for verification. A buzzer system loaned by the Department of Mathematics at the University of Tennessee was used by the teams to signal responses and to determine control of the game. Special thanks to Profs. Mei-Qin Chen (The Citadel), Martha Abell (Georgia Southern), and Chris Cox (Clemson) for their help with game organization, judging, and time keeping. 
+text[[245, 866, 499, 901]]
+- Michael W. Berry (Organizer) University of Tennessee  
 
-text[[129, 599, 864, 652]]
-A slideshow of this event follows the final standings of the competition and roster of each team. Thanks to SIAM for their financial support of this unique (and perhaps soon to become an annual) event! The gameshow "Jeopardy" is a trademark (TM) of Columbia/Tri-star. 
-
-table[[190, 686, 803, 831]]
-<table>Place TeamRoster1st ClemsonClay Jenkins, Charles Swannack2nd The CitadelRyan Graham, Robert Harig, Chih-Kuo Lee, Yow-Chyun Lin, Ying-Jiun Wang3rd TennesseeNehal Parikh, James Perkins, Yiheng Yang4th Coastal CarolinaJimmy Bailey, Margaret Leonard, Brian Richardson</table>
-
-text[[248, 869, 501, 902]]
-- Michael W. Berry (Organizer)
-University of Tennessee 
-
-text[[129, 919, 802, 943]]
-SIAM-SEAS JeopardyTM 2001 Photos (click on small triangular buttons to
\ No newline at end of file
+text[[133, 919, 801, 942]]
+SIAM- SEAS JeopardyTM 2001 Photos (click on small triangular buttons to
\ No newline at end of file
diff --git a/stage1/sample_00044/document.md b/stage1/sample_00044/document.md
index 251a89759deeff1e2ec5cff9058876f3da2eda0c..c227083464fb9af8955c90d2924774ee50abb547 100644
--- a/stage1/sample_00044/document.md
+++ b/stage1/sample_00044/document.md
@@ -1 +1 @@
-image[[132, 44, 865, 499]]
\ No newline at end of file
+0
\ No newline at end of file
diff --git a/stage1/sample_00044/raw_response.md b/stage1/sample_00044/raw_response.md
index 251a89759deeff1e2ec5cff9058876f3da2eda0c..c227083464fb9af8955c90d2924774ee50abb547 100644
--- a/stage1/sample_00044/raw_response.md
+++ b/stage1/sample_00044/raw_response.md
@@ -1 +1 @@
-image[[132, 44, 865, 499]]
\ No newline at end of file
+0
\ No newline at end of file
diff --git a/stage1/sample_00045/document.md b/stage1/sample_00045/document.md
index 875eb7d64de7e878d5eabb23d5e15466fdf02480..44316ede5c4667a2710a12dcb463cda1597dee0c 100644
--- a/stage1/sample_00045/document.md
+++ b/stage1/sample_00045/document.md
@@ -1 +1 @@
-10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10"
\ No newline at end of file
+image[[90, 41, 836, 657]]
\ No newline at end of file
diff --git a/stage1/sample_00045/raw_response.md b/stage1/sample_00045/raw_response.md
index 875eb7d64de7e878d5eabb23d5e15466fdf02480..44316ede5c4667a2710a12dcb463cda1597dee0c 100644
--- a/stage1/sample_00045/raw_response.md
+++ b/stage1/sample_00045/raw_response.md
@@ -1 +1 @@
-10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10" 10° 20' 10" 10° 20' 20" 10° 20' 10"
\ No newline at end of file
+image[[90, 41, 836, 657]]
\ No newline at end of file
diff --git a/stage1/sample_00046/document.md b/stage1/sample_00046/document.md
index 28b1b26cdd690c4fe728e5e562bb1b35b4393611..cadf0a0a7a5318909405ae1adee3f93a2b9a7d6e 100644
--- a/stage1/sample_00046/document.md
+++ b/stage1/sample_00046/document.md
@@ -1,41 +1,41 @@
-81. American Academy of Oral and Maxillofacial Pathology. Submission policy on excised tissue. Available at: "http:// www.aaomp.org/wp-content/uploads/2016/12/Policy_on_ Excised_Tissue-Final-11-9-2013.pdf". Accessed July 25, 2020.  
+81. American Academy of Oral and Maxillofacial Pathology. Submission policy on excised tissue. Available at: “http://www.aaomp.org/wp-content/uploads/2016/12/Policy_on_Excised_Tissue-Final-11-9-2013.pdf”. Accessed July 25, 2020.  
 
-text[[86, 72, 509, 904]]
-65. Webb AN, Hao W, Hong P. The effect of tongue-tie division on breastfeeding and speech articulation: A systematic review. Int J Pediatr Otorhinolaryngol 2013; 77(5):635-46.  
-66. Delli K, Livas C, Sculean A, Katsaros C, Bornstein MM. Facts and myths regarding the maxillary midline frenum and its treatment: A systematic review of the literature. Quintessence Int 2013;44(2):177-87.  
-67. Devishree G, Gujjari SK, Shubhashini PV. Frenectomy: A review with the reports of surgical techniques. J Clin Dent Res 2012;6(9):1587-92.  
-68. Kaban L, Troulis M. Intraoral soft tissue abnormalities. In: Pediatric Oral and Maxillofacial Surgery. Philadelphia, Pa.: Saunders; 2004:147-53.  
-69. Shetty K, Traitenberg C, Patel C, Streckfus C. Maxillary frenectomy using a carbon dioxide laser in a pediatric patient: A case report. Gen Dent 2008;56(1):60-3.  
-70. Olivi G, Chaumanet G, Genovese MD, Beneduce C, Andreana S. ErCr:YSGG laser labial frenectomy: A clinical retrospective evaluation of 156 consecutive cases. Gen Dent 2010;58(3):e126-33.  
-71. Kupietzky A, Botzer E. Ankyloglossia in the infant and young child: Clinical suggestions for diagnosis and management. Pediatr Dent 2005;27(1):40-6.  
-72. Hogan M, Wescott C, Griffiths M. Randomized, controlled trial of division of tongue-tie in infants with feeding problems. J Paediatr Child Health 2005;41(5-6):246-50.  
-73. Díaz-Pizán M, Lagrave M, Villena R. Midline diastema and frenum morphology in the primary dentition. J Dent 2006;26(1):11-14.  
-74. Gontijo I, Navarro R, Haypek P, Ciamponi A, Hadda A. The applications of diode and Er:YAG lasers in labial frenectomy in infant patients. J Dent Child 2005;72(1):10-5.  
-75. Kara C. Evaluation of patient perceptions of frenectomy: A comparison of Nd:YAG laser and conventional techniques. Photomed Laser Surg 2008;26(2):147-52.  
-76. Kleinman DV, Swango PA, Pindborg JJ. Epidemiology of oral mucosal lesions in United States school children: 1986-87. Community Dent Oral Epidemiol 1994;22(4): 243-53.  
-77. Shulman JD. Prevalence of oral mucosal lesions in children and youths in USA. Int J Pediatr Dent 2005;15 (2):89-97.  
-78. Melrose RJ, Handlers JP, Kerpel S, Summerlin DJ, Tomich CJ. The use of biopsy in dental practice. The position of the American Academy of Oral and Maxillofacial Pathology. Gen Dent 2007;55(5):457-61.  
-79. Rethman M, Carpenter W, Cohen E, et al. Evidence-based clinical recommendations on screening for oral squamous cell carcinomas. J Am Dent Assoc 2010;141(5):509-20.  
-80. Kazanowska K, Halon A, Radwan-Oczko M. The role and application of exfoliative cytology in the diagnosis of oral mucosa pathology - Contemporary knowledge with review of the literature. Adv Clin Exp Med 2014;23(2): 299-305.  
+text[[87, 80, 512, 905]]
+65. Webb AN, Hao W, Hong P. The effect of tongue-tie division on breastfeeding and speech articulation: A systematic review. Int J Pediatr Otorhinolaryngol 2013; 77(5):635-46. 
+66. Delli K, Livas C, Sculean A, Katsaros C, Bornstein MM. Facts and myths regarding the maxillary midline frenum and its treatment: A systematic review of the literature. Quintessence Int 2013;44(2):177-87. 
+67. Devishree G, Gujjari SK, Shubhashini PV. Frenectomy: A review with the reports of surgical techniques. J Clin Dent Res 2012;6(9):1587-92. 
+68. Kaban L, Troulis M. Intraoral soft tissue abnormalities. In: Pediatric Oral and Maxillofacial Surgery. Philadelphia, Pa.: Saunders; 2004:147-53. 
+69. Shetty K, Trajtenberg C, Patel C, Streckfus C. Maxillary frenectomy using a carbon dioxide laser in a pediatric patient: A case report. Gen Dent 2008;56(1):60-3. 
+70. Olivi G, Chaumane G, Genovese MD, Beneduce C, Andreana S. Er,Cr:YSGG laser labial frenectomy: A clinical retrospective evaluation of 156 consecutive cases. Gen Dent 2010;58(3):e126-33. 
+71. Kupietzky A, Botzer E. Ankyloglossia in the infant and young child: Clinical suggestions for diagnosis and management. Pediatr Dent 2005;27(1):40-6. 
+72. Hogan M, Wescott C, Griffiths M. Randomized, controlled trial of division of tongue-tie in infants with feeding problems. J Paediatr Child Health 2005;41(5-6):246-50. 
+73. Díaz-Pizán M, Lagravère M, Villena R. Midline diastema and frenum morphology in the primary dentition. J Dent 2006;26(1):11-14. 
+74. Gontijo I, Navarro R, Haypek P, Ciamponi A, Hadda A. The applications of diode and Er:YAG lasers in labial frenectomy in infant patients. J Dent Child 2005;72(1):10-5. 
+75. Kara C. Evaluation of patient perceptions of frenectomy: A comparison of Nd:YAG laser and conventional techniques. Photomed Laser Surg 2008;26(2):147-52. 
+76. Kleinman DV, Swango PA, Pindborg JJ. Epidemiology of oral mucosal lesions in United States school children: 1986-87. Community Dent Oral Epidemiol 1994;22(4): 243-53. 
+77. Shulman JD. Prevalence of oral mucosal lesions in children and youths in USA. Int J Pediatr Dent 2005;15 (2):89-97. 
+78. Melrose RJ, Handlers JP, Kerpel S, Summerlin DJ, Tomich CJ. The use of biopsy in dental practice. The position of the American Academy of Oral and Maxillofacial Pathology. Gen Dent 2007;55(5):457-61. 
+79. Rethman M, Carpenter W, Cohen E, et al. Evidence-based clinical recommendations on screening for oral squamous cell carcinomas. J Am Dent Assoc 2010;141(5):509-20. 
+80. Kazanowska K, Halon A, Radwan-Oczko M. The role and application of exfoliative cytology in the diagnosis of oral mucosa pathology – Contemporary knowledge with review of the literature. Adv Clin Exp Med 2014;23(2): 299-305.  
 
-text[[526, 73, 939, 904]]
-81. American Academy of Oral and Maxillofacial Pathology. Submission policy on excised tissue. Available at: "http:// www.aaomp.org/wp-content/uploads/2016/12/Policy_on_ Excised_Tissue-Final-11-9-2013.pdf". Accessed July 25, 2020.  
-82. Hong C, Dean D, Hull K, et al. World workshop on oral medicine: VII: Relative frequency of oral mucosal lesions in children, a scoping review. Oral Diseases 2019; 25(Suppl.1):193-203.  
-83. Fliatz CM. Differential diagnosis of oral lesions and developmental anomalies. In: Nowak AJ, Christensen JR, Mabry TR, Townsend JA, Wells MH eds. Pediatric Dentistry: Infancy through Adolescence. 6th ed. Philadelphia, Pa.: Elsevier; 2019:8-49.  
-84. Hays P. Hamartomas, eruption cysts, natal tooth, and Epstein pearls in a newborn. ASDC J Dent Child 2000; 67(5):365-8.  
-85. Aldred MJ, Cameron AC, Georgiou A. Pediatric oral medicine and pathology and radiology. In: Cameron AC, Widmer RP. eds. Handbook of Pediatric Dentistry. 4th ed. Philadelphia, Pa.: Mosby Elsevier; 2013:209-68.  
-86. Lapid O, Shaco-Levey R, Krieger Y, Kachko L, Sagi A. Congenital epulis. Pediatrics 2001;107(2):E22.  
-87. Marakoglu I, Gursoy U, Marakoglu K. Congenital epulis: Report of a case. ASDC J Dent Child 2002;69(2):191-2.  
-88. Neville BW, Damm DD, Allen CM, Chi AC. Soft tissue tumors. In: Oral and Maxillofacial Pathology. 4th ed. St. Louis, Mo.: Elsevier; 2016:473-515.  
-89. Neville BW, Damm DD, Allen CM, Chi AC. Odontogenic cysts and tumors. In: Oral and Maxillofacial Pathology. 4th ed. St. Louis, Mo.: Elsevier; 2016:632-89.  
-90. Regezi JA, Sciubba JJ, Jordan RC. Cysts of the jaws and neck. In: Oral Pathology: Clinical-Pathologic Correlations. 7th ed. St. Louis, Mo.: Elsevier; 2017:245-68.  
-91. McDonald JS. Tumors of the oral soft tissues and cysts and tumors of bone. In: Dean JA ed. McDonald and Avery's Dentistry for the Child and Adolescent. 10th ed. St. Louis, Mo.: Elsevier; 2016:603-26.  
-92. Cunha RF, Boer FA, Torriani DD, Frossard WT. Natal and neonatal teeth: Review of the literature. Pediatr Dent 2001;23(2):158-62.  
-93. Leung A, Robson W. Natal teeth: A review. J Natl Med Assoc 2006;98(2):226-8.  
-94. Galassi MS, Santos-Pinto L, Ramalho T. Natal maxillary primary molars: Case report. J Clin Pediatr Dent 2004; 29(1):41-44.  
-95. Stein S, Paller A, Haut P, Mancini A. Langerhans cell histiocytosis presenting in the neonatal period: A retrospective case series. Arch Pediatr Adolesc Med 2001;155 (7):778-83.  
-96. Slayton RL. Treatment alternatives for sublingual traumatic ulceration (Riga-Fede disease). Pediatr Dent 2000; 22(5):413-4.  
+text[[527, 84, 937, 901]]
+81. American Academy of Oral and Maxillofacial Pathology. Submission policy on excised tissue. Available at: “http://www.aaomp.org/wp-content/uploads/2016/12/Policy_on_Excised_Tissue-Final-11-9-2013.pdf”. Accessed July 25, 2020. 
+82. Hong C, Dean D, Hull K, et al. World workshop on oral medicine: VII: Relative frequency of oral mucosal lesions in children, a scoping review. Oral Diseases 2019; 25(Suppl.1):193-203. 
+83. Flaitz CM. Differential diagnosis of oral lesions and developmental anomalies. In: Nowak AJ, Christensen JR, Mabry TR, Townsend JA, Wells MH eds. Pediatric Dentistry: Infancy through Adolescence. 6th ed. Philadelphia, Pa.: Elsevier; 2019:8-49. 
+84. Hays P. Hamartomas, eruption cysts, natal tooth, and Epstein pearls in a newborn. ASDC J Dent Child 2000; 67(5):365-8. 
+85. Aldred MJ, Cameron AC, Georgiou A. Pediatric oral medicine and pathology and radiology. In: Cameron AC, Widmer RP. eds. Handbook of Pediatric Dentistry. 4th ed. Philadelphia, Pa.: Mosby Elsevier; 2013:209-68. 
+86. Lapid O, Shaco-Levey R, Krieger Y, Kachko L, Sagi A. Congenital epulis. Pediatrics 2001;107(2):E22. 
+87. Marakoglu I, Gursoy U, Marakoglu K. Congenital epulis: Report of a case. ASDC J Dent Child 2002;69(2):191-2. 
+88. Neville BW, Damm DD, Allen CM, Chi AC. Soft tissue tumors. In: Oral and Maxillofacial Pathology. 4th ed. St. Louis, Mo.: Elsevier; 2016:473-515. 
+89. Neville BW, Damm DD, Allen CM, Chi AC. Odontogenic cysts and tumors. In: Oral and Maxillofacial Pathology. 4th ed. St. Louis, Mo.: Elsevier; 2016:632-89. 
+90. Regezi JA, Sciubba JJ, Jordan RC. Cysts of the jaws and neck. In: Oral Pathology: Clinical-Pathologic Correlations. 7th ed. St. Louis, Mo.: Elsevier; 2017:245-68. 
+91. McDonald JS. Tumors of the oral soft tissues and cysts and tumors of bone. In: Dean JA ed. McDonald and Avery's Dentistry for the Child and Adolescent. 10th ed. St. Louis, Mo.: Elsiver; 2016:603-26. 
+92. Cunha RF, Boer FA, Torriani DD, Frossard WT. Natal and neonatal teeth: Review of the literature. Pediatr Dent 2001;23(2):158-62. 
+93. Leung A, Robson W. Natal teeth: A review. J Natl Med Assoc 2006;98(2):226-8. 
+94. Galassi MS, Santos-Pinto L, Ramalho T. Natal maxillary primary molars: Case report. J Clin Pediatr Dent 2004; 29(1):41-44. 
+95. Stein S, Paller A, Haut P, Mancini A. Langerhans cell histiocytosis presenting in the neonatal period: A retrospective case series. Arch Pediatr Adolesc Med 2001;155 (7):778-83. 
+96. Slayton RL. Treatment alternatives for sublingual traumatic ulceration (Riga-Fede disease). Pediatr Dent 2000; 22(5):413-4. 
 97. Rushmah M. Natal and neonatal teeth: A clinical and histological study. J Clin Pediatr Dent 1991;15(4):251-3.  
 
-title[[750, 914, 939, 926]]
-# References continued on the next page.
\ No newline at end of file
+text[[748, 914, 937, 927]]
+References continued on the next page.
\ No newline at end of file
diff --git a/stage1/sample_00046/raw_response.md b/stage1/sample_00046/raw_response.md
index 28b1b26cdd690c4fe728e5e562bb1b35b4393611..cadf0a0a7a5318909405ae1adee3f93a2b9a7d6e 100644
--- a/stage1/sample_00046/raw_response.md
+++ b/stage1/sample_00046/raw_response.md
@@ -1,41 +1,41 @@
-81. American Academy of Oral and Maxillofacial Pathology. Submission policy on excised tissue. Available at: "http:// www.aaomp.org/wp-content/uploads/2016/12/Policy_on_ Excised_Tissue-Final-11-9-2013.pdf". Accessed July 25, 2020.  
+81. American Academy of Oral and Maxillofacial Pathology. Submission policy on excised tissue. Available at: “http://www.aaomp.org/wp-content/uploads/2016/12/Policy_on_Excised_Tissue-Final-11-9-2013.pdf”. Accessed July 25, 2020.  
 
-text[[86, 72, 509, 904]]
-65. Webb AN, Hao W, Hong P. The effect of tongue-tie division on breastfeeding and speech articulation: A systematic review. Int J Pediatr Otorhinolaryngol 2013; 77(5):635-46.  
-66. Delli K, Livas C, Sculean A, Katsaros C, Bornstein MM. Facts and myths regarding the maxillary midline frenum and its treatment: A systematic review of the literature. Quintessence Int 2013;44(2):177-87.  
-67. Devishree G, Gujjari SK, Shubhashini PV. Frenectomy: A review with the reports of surgical techniques. J Clin Dent Res 2012;6(9):1587-92.  
-68. Kaban L, Troulis M. Intraoral soft tissue abnormalities. In: Pediatric Oral and Maxillofacial Surgery. Philadelphia, Pa.: Saunders; 2004:147-53.  
-69. Shetty K, Traitenberg C, Patel C, Streckfus C. Maxillary frenectomy using a carbon dioxide laser in a pediatric patient: A case report. Gen Dent 2008;56(1):60-3.  
-70. Olivi G, Chaumanet G, Genovese MD, Beneduce C, Andreana S. ErCr:YSGG laser labial frenectomy: A clinical retrospective evaluation of 156 consecutive cases. Gen Dent 2010;58(3):e126-33.  
-71. Kupietzky A, Botzer E. Ankyloglossia in the infant and young child: Clinical suggestions for diagnosis and management. Pediatr Dent 2005;27(1):40-6.  
-72. Hogan M, Wescott C, Griffiths M. Randomized, controlled trial of division of tongue-tie in infants with feeding problems. J Paediatr Child Health 2005;41(5-6):246-50.  
-73. Díaz-Pizán M, Lagrave M, Villena R. Midline diastema and frenum morphology in the primary dentition. J Dent 2006;26(1):11-14.  
-74. Gontijo I, Navarro R, Haypek P, Ciamponi A, Hadda A. The applications of diode and Er:YAG lasers in labial frenectomy in infant patients. J Dent Child 2005;72(1):10-5.  
-75. Kara C. Evaluation of patient perceptions of frenectomy: A comparison of Nd:YAG laser and conventional techniques. Photomed Laser Surg 2008;26(2):147-52.  
-76. Kleinman DV, Swango PA, Pindborg JJ. Epidemiology of oral mucosal lesions in United States school children: 1986-87. Community Dent Oral Epidemiol 1994;22(4): 243-53.  
-77. Shulman JD. Prevalence of oral mucosal lesions in children and youths in USA. Int J Pediatr Dent 2005;15 (2):89-97.  
-78. Melrose RJ, Handlers JP, Kerpel S, Summerlin DJ, Tomich CJ. The use of biopsy in dental practice. The position of the American Academy of Oral and Maxillofacial Pathology. Gen Dent 2007;55(5):457-61.  
-79. Rethman M, Carpenter W, Cohen E, et al. Evidence-based clinical recommendations on screening for oral squamous cell carcinomas. J Am Dent Assoc 2010;141(5):509-20.  
-80. Kazanowska K, Halon A, Radwan-Oczko M. The role and application of exfoliative cytology in the diagnosis of oral mucosa pathology - Contemporary knowledge with review of the literature. Adv Clin Exp Med 2014;23(2): 299-305.  
+text[[87, 80, 512, 905]]
+65. Webb AN, Hao W, Hong P. The effect of tongue-tie division on breastfeeding and speech articulation: A systematic review. Int J Pediatr Otorhinolaryngol 2013; 77(5):635-46. 
+66. Delli K, Livas C, Sculean A, Katsaros C, Bornstein MM. Facts and myths regarding the maxillary midline frenum and its treatment: A systematic review of the literature. Quintessence Int 2013;44(2):177-87. 
+67. Devishree G, Gujjari SK, Shubhashini PV. Frenectomy: A review with the reports of surgical techniques. J Clin Dent Res 2012;6(9):1587-92. 
+68. Kaban L, Troulis M. Intraoral soft tissue abnormalities. In: Pediatric Oral and Maxillofacial Surgery. Philadelphia, Pa.: Saunders; 2004:147-53. 
+69. Shetty K, Trajtenberg C, Patel C, Streckfus C. Maxillary frenectomy using a carbon dioxide laser in a pediatric patient: A case report. Gen Dent 2008;56(1):60-3. 
+70. Olivi G, Chaumane G, Genovese MD, Beneduce C, Andreana S. Er,Cr:YSGG laser labial frenectomy: A clinical retrospective evaluation of 156 consecutive cases. Gen Dent 2010;58(3):e126-33. 
+71. Kupietzky A, Botzer E. Ankyloglossia in the infant and young child: Clinical suggestions for diagnosis and management. Pediatr Dent 2005;27(1):40-6. 
+72. Hogan M, Wescott C, Griffiths M. Randomized, controlled trial of division of tongue-tie in infants with feeding problems. J Paediatr Child Health 2005;41(5-6):246-50. 
+73. Díaz-Pizán M, Lagravère M, Villena R. Midline diastema and frenum morphology in the primary dentition. J Dent 2006;26(1):11-14. 
+74. Gontijo I, Navarro R, Haypek P, Ciamponi A, Hadda A. The applications of diode and Er:YAG lasers in labial frenectomy in infant patients. J Dent Child 2005;72(1):10-5. 
+75. Kara C. Evaluation of patient perceptions of frenectomy: A comparison of Nd:YAG laser and conventional techniques. Photomed Laser Surg 2008;26(2):147-52. 
+76. Kleinman DV, Swango PA, Pindborg JJ. Epidemiology of oral mucosal lesions in United States school children: 1986-87. Community Dent Oral Epidemiol 1994;22(4): 243-53. 
+77. Shulman JD. Prevalence of oral mucosal lesions in children and youths in USA. Int J Pediatr Dent 2005;15 (2):89-97. 
+78. Melrose RJ, Handlers JP, Kerpel S, Summerlin DJ, Tomich CJ. The use of biopsy in dental practice. The position of the American Academy of Oral and Maxillofacial Pathology. Gen Dent 2007;55(5):457-61. 
+79. Rethman M, Carpenter W, Cohen E, et al. Evidence-based clinical recommendations on screening for oral squamous cell carcinomas. J Am Dent Assoc 2010;141(5):509-20. 
+80. Kazanowska K, Halon A, Radwan-Oczko M. The role and application of exfoliative cytology in the diagnosis of oral mucosa pathology – Contemporary knowledge with review of the literature. Adv Clin Exp Med 2014;23(2): 299-305.  
 
-text[[526, 73, 939, 904]]
-81. American Academy of Oral and Maxillofacial Pathology. Submission policy on excised tissue. Available at: "http:// www.aaomp.org/wp-content/uploads/2016/12/Policy_on_ Excised_Tissue-Final-11-9-2013.pdf". Accessed July 25, 2020.  
-82. Hong C, Dean D, Hull K, et al. World workshop on oral medicine: VII: Relative frequency of oral mucosal lesions in children, a scoping review. Oral Diseases 2019; 25(Suppl.1):193-203.  
-83. Fliatz CM. Differential diagnosis of oral lesions and developmental anomalies. In: Nowak AJ, Christensen JR, Mabry TR, Townsend JA, Wells MH eds. Pediatric Dentistry: Infancy through Adolescence. 6th ed. Philadelphia, Pa.: Elsevier; 2019:8-49.  
-84. Hays P. Hamartomas, eruption cysts, natal tooth, and Epstein pearls in a newborn. ASDC J Dent Child 2000; 67(5):365-8.  
-85. Aldred MJ, Cameron AC, Georgiou A. Pediatric oral medicine and pathology and radiology. In: Cameron AC, Widmer RP. eds. Handbook of Pediatric Dentistry. 4th ed. Philadelphia, Pa.: Mosby Elsevier; 2013:209-68.  
-86. Lapid O, Shaco-Levey R, Krieger Y, Kachko L, Sagi A. Congenital epulis. Pediatrics 2001;107(2):E22.  
-87. Marakoglu I, Gursoy U, Marakoglu K. Congenital epulis: Report of a case. ASDC J Dent Child 2002;69(2):191-2.  
-88. Neville BW, Damm DD, Allen CM, Chi AC. Soft tissue tumors. In: Oral and Maxillofacial Pathology. 4th ed. St. Louis, Mo.: Elsevier; 2016:473-515.  
-89. Neville BW, Damm DD, Allen CM, Chi AC. Odontogenic cysts and tumors. In: Oral and Maxillofacial Pathology. 4th ed. St. Louis, Mo.: Elsevier; 2016:632-89.  
-90. Regezi JA, Sciubba JJ, Jordan RC. Cysts of the jaws and neck. In: Oral Pathology: Clinical-Pathologic Correlations. 7th ed. St. Louis, Mo.: Elsevier; 2017:245-68.  
-91. McDonald JS. Tumors of the oral soft tissues and cysts and tumors of bone. In: Dean JA ed. McDonald and Avery's Dentistry for the Child and Adolescent. 10th ed. St. Louis, Mo.: Elsevier; 2016:603-26.  
-92. Cunha RF, Boer FA, Torriani DD, Frossard WT. Natal and neonatal teeth: Review of the literature. Pediatr Dent 2001;23(2):158-62.  
-93. Leung A, Robson W. Natal teeth: A review. J Natl Med Assoc 2006;98(2):226-8.  
-94. Galassi MS, Santos-Pinto L, Ramalho T. Natal maxillary primary molars: Case report. J Clin Pediatr Dent 2004; 29(1):41-44.  
-95. Stein S, Paller A, Haut P, Mancini A. Langerhans cell histiocytosis presenting in the neonatal period: A retrospective case series. Arch Pediatr Adolesc Med 2001;155 (7):778-83.  
-96. Slayton RL. Treatment alternatives for sublingual traumatic ulceration (Riga-Fede disease). Pediatr Dent 2000; 22(5):413-4.  
+text[[527, 84, 937, 901]]
+81. American Academy of Oral and Maxillofacial Pathology. Submission policy on excised tissue. Available at: “http://www.aaomp.org/wp-content/uploads/2016/12/Policy_on_Excised_Tissue-Final-11-9-2013.pdf”. Accessed July 25, 2020. 
+82. Hong C, Dean D, Hull K, et al. World workshop on oral medicine: VII: Relative frequency of oral mucosal lesions in children, a scoping review. Oral Diseases 2019; 25(Suppl.1):193-203. 
+83. Flaitz CM. Differential diagnosis of oral lesions and developmental anomalies. In: Nowak AJ, Christensen JR, Mabry TR, Townsend JA, Wells MH eds. Pediatric Dentistry: Infancy through Adolescence. 6th ed. Philadelphia, Pa.: Elsevier; 2019:8-49. 
+84. Hays P. Hamartomas, eruption cysts, natal tooth, and Epstein pearls in a newborn. ASDC J Dent Child 2000; 67(5):365-8. 
+85. Aldred MJ, Cameron AC, Georgiou A. Pediatric oral medicine and pathology and radiology. In: Cameron AC, Widmer RP. eds. Handbook of Pediatric Dentistry. 4th ed. Philadelphia, Pa.: Mosby Elsevier; 2013:209-68. 
+86. Lapid O, Shaco-Levey R, Krieger Y, Kachko L, Sagi A. Congenital epulis. Pediatrics 2001;107(2):E22. 
+87. Marakoglu I, Gursoy U, Marakoglu K. Congenital epulis: Report of a case. ASDC J Dent Child 2002;69(2):191-2. 
+88. Neville BW, Damm DD, Allen CM, Chi AC. Soft tissue tumors. In: Oral and Maxillofacial Pathology. 4th ed. St. Louis, Mo.: Elsevier; 2016:473-515. 
+89. Neville BW, Damm DD, Allen CM, Chi AC. Odontogenic cysts and tumors. In: Oral and Maxillofacial Pathology. 4th ed. St. Louis, Mo.: Elsevier; 2016:632-89. 
+90. Regezi JA, Sciubba JJ, Jordan RC. Cysts of the jaws and neck. In: Oral Pathology: Clinical-Pathologic Correlations. 7th ed. St. Louis, Mo.: Elsevier; 2017:245-68. 
+91. McDonald JS. Tumors of the oral soft tissues and cysts and tumors of bone. In: Dean JA ed. McDonald and Avery's Dentistry for the Child and Adolescent. 10th ed. St. Louis, Mo.: Elsiver; 2016:603-26. 
+92. Cunha RF, Boer FA, Torriani DD, Frossard WT. Natal and neonatal teeth: Review of the literature. Pediatr Dent 2001;23(2):158-62. 
+93. Leung A, Robson W. Natal teeth: A review. J Natl Med Assoc 2006;98(2):226-8. 
+94. Galassi MS, Santos-Pinto L, Ramalho T. Natal maxillary primary molars: Case report. J Clin Pediatr Dent 2004; 29(1):41-44. 
+95. Stein S, Paller A, Haut P, Mancini A. Langerhans cell histiocytosis presenting in the neonatal period: A retrospective case series. Arch Pediatr Adolesc Med 2001;155 (7):778-83. 
+96. Slayton RL. Treatment alternatives for sublingual traumatic ulceration (Riga-Fede disease). Pediatr Dent 2000; 22(5):413-4. 
 97. Rushmah M. Natal and neonatal teeth: A clinical and histological study. J Clin Pediatr Dent 1991;15(4):251-3.  
 
-title[[750, 914, 939, 926]]
-# References continued on the next page.
\ No newline at end of file
+text[[748, 914, 937, 927]]
+References continued on the next page.
\ No newline at end of file
diff --git a/stage1/sample_00047/document.md b/stage1/sample_00047/document.md
index addf2ce8664f77497cf2ede17796b536cf482c5f..7f01f8b98a2a9d0bcc9c4b4e1a9625fadbc9e065 100644
--- a/stage1/sample_00047/document.md
+++ b/stage1/sample_00047/document.md
@@ -1,37 +1,31 @@
-21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21  
+21 "Although some supernumerary teeth may be syndrome-associated (e.g., cleidocranial dysplasia or of familial inheritance pattern, most supernumerary teeth occur as isolated events.  
 
-sub_title[[88, 76, 234, 90]]
-## Supernumerary teeth  
+text[[88, 198, 505, 317]]
+Supernumerary teeth can occur in either the primary or permanent dentition.21,42,43 In 33 percent of the cases, a supernumerary tooth in the primary dentition is followed by the supernumerary tooth complement in the permanent dentition.44 Reports in incidence of supernumerary teeth can be as high as three percent, with the permanent dentition being affected five times more frequently than the primary dentition and males being affected twice as frequently as females.21  
 
-text[[87, 88, 503, 194]]
-Supernumerary teeth and hyperdontia are terms to describe an excess in tooth number. Supernumerary teeth are thought to be related to disturbances in the initiation and proliferation stages of dental development. Although some supernumerary teeth may be syndrome- associated (e.g., cleidocranial dysplasia) or of familial inheritance pattern, most supernumerary teeth occur as isolated events.  
+text[[88, 318, 505, 625]]
+Supernumerary teeth will occur 10 times more often in the maxillary arch versus the mandibular arch.21 Approximately 90 percent of all single tooth supernumerary teeth are found in the maxillary arch, with a strong predilection to the anterior region.21,42 The maxillary anterior midline is the most common site, in which case the supernumerary tooth is known as a mesiodens; the second most common site is the maxillary molar area, with the tooth known as a paramolar.21,42 A mesiodens can be suspected if there is an asymmetric eruption pattern of the maxillary incisors, delayed eruption of the maxillary incisors with or without any over- retained primary incisors, or ectopic eruption of a maxillary incisor.45 The diagnosis of a mesiodens can be confirmed with radiographs, including occlusal, periapical, or panoramic films,46 or computed tomography.9,10 Three- dimensional information needed to determine the location of the mesiodens or impacted tooth can be obtained by taking two periapical radiographs using either two projections taken at right angles to one another or the tube shift technique (buccal object rule or Clark's rule)47 or by cone beam computed tomography.10,12,13  
 
-text[[88, 194, 503, 319]]
-Supernumerary teeth can occur in either the primary or permanent dentition. In 33 percent of the cases, a supernumerary tooth in the primary dentition is followed by the supernumerary tooth complement in the permanent dentition. Reports in incidence of supernumerary teeth can be as high as three percent, with the permanent dentition being affected five times more frequently than the primary dentition and males being affected twice as frequently as females.  
+text[[88, 627, 505, 912]]
+Complications of supernumerary teeth can include delayed and/or lack of eruption of the permanent tooth, crowding, resorption of adjacent teeth, dentigerous cyst formation, periorconal space ossification, and crown resorption.42,48 Early diagnosis and appropriately timed treatment are important in the prevention and avoidance of these complications. Because only 25 percent of all mesiodens erupt spontaneously, surgical management often is necessary.44,49 A mesiodens that is conical in shape and is not inverted has a better chance for eruption than a mesiodens that is tubular in shape and is inverted.48 The treatment objective for a non- erupting permanent mesiodens is to minimize eruption problems for the permanent incisors.48 Surgical management will vary depending on the size, shape, and number of supernumeraries and the patient's dental development.48 The treatment objective for a non- erupting primary mesiodens differs in that the removal of these teeth usually is not recommended, as the surgical intervention may disrupt or damage the underlying developing permanent teeth.50 Erupted primary tooth mesiodens typically are left  
 
-text[[88, 320, 505, 625]]
-Supernumerary teeth will occur 10 times more often in the maxillary arch versus the mandibular arch. Approximately 90 percent of all single tooth supernumerary teeth are found in the maxillary arch, with a strong predilection to the anterior region. The maxillary anterior midline is the most common site, in which case the supernumerary tooth is known as a mesiodens; the second most common site is the maxillary molar area, with the tooth known as a paramolar. A mesiodens can be suspected if there is an asymmetric eruption pattern of the maxillary incisors, delayed eruption of the maxillary incisors with or without any over- retained primary incisors, or ectopic eruption of a maxillary incisor. The diagnosis of a mesiodens can be confirmed with radiographs, including occlusal, periapical, or panoramic films, or computed tomography. Three- dimensional information needed to determine the location of the mesiodens or impacted tooth can be obtained by taking two periapical radiographs using either two projections taken at right angles to one another or the tube shift technique (buccal object rule or Clark's rule) or by cone beam computed tomography.  
+text[[525, 75, 938, 105]]
+to shed normally upon the eruption of the permanent dentition.50  
 
-text[[88, 626, 505, 913]]
-Complications of supernumerary teeth can include delayed and/or lack of eruption of the permanent tooth, crowding, resorption of adjacent teeth, dentigerous cyst formation, pericoronal space ossification, and crown resorption. Early diagnosis and appropriately timed treatment are important in the prevention and avoidance of these complications. Because only 25 percent of all mesiodens erupt spontaneously, surgical management often is necessary. A mesiodens that is conical in shape and is not inverted has a better chance for eruption than a mesiodens that is tubular in shape and is inverted. The treatment objective for a non- erupting permanent mesiodens is to minimize eruption problems for the permanent incisors. Surgical management will vary depending on the size, shape, and number of supernumeraries and the patient's dental development. The treatment objective for a non- erupting primary mesiodens differs in that the removal of these teeth usually is not recommended, as the surgical intervention may disrupt or damage the underlying developing permanent teeth. Erupted primary tooth mesiodens typically are left  
+text[[525, 105, 940, 286]]
+Extraction of an unerupted primary or permanent mesiodens is recommended during the mixed dentition to allow the normal eruptive force of the permanent incisor to bring itself into the oral cavity.43 Waiting until the adjacent incisors have at least two- thirds root development will present less risk to the developing teeth but still allow spontaneous eruption of the incisors.3 In 75 percent of the cases, extraction of the mesiodens during the mixed dentition results in spontaneous eruption and alignment of the adjacent teeth.50,51 If the adjacent teeth do not erupt within six to 12 months, surgical exposure and orthodontic treatment may be necessary to aid their eruption.45,47  
 
-text[[523, 75, 937, 106]]
-to shed normally upon the eruption of the permanent dentition.  
-
-text[[524, 106, 939, 285]]
-Extraction of an unerupted primary or permanent mesiodens is recommended during the mixed dentition to allow the normal eruptive force of the permanent incisor to bring itself into the oral cavity. Waiting until the adjacent incisors have at least two- thirds root development will present less risk to the developing teeth but still allow spontaneous eruption of the incisors. In 75 percent of the cases, extraction of the mesiodens during the mixed dentition results in spontaneous eruption and alignment of the adjacent teeth. If the adjacent teeth do not erupt within six to 12 months, surgical exposure and orthodontic treatment may be necessary to aid their eruption.  
-
-sub_title[[524, 304, 680, 317]]
+sub_title[[526, 305, 680, 318]]
 ## Frenulum attachments  
 
-text[[524, 319, 939, 515]]
-Frenulum attachments Frenulum attachments and their role in oral function increasingly have become topics of interest among a variety of health care specialists. Ankyloglossia (tongue- tie) and hypertrophic/restrictive maxillary frenula have been implicated in difficulties breastfeeding, incorrect speech articulation, caries formation, gingival recession, and aberrant skeletal growth. Studies have shown differences in treatment recommendations among pediatricians, otolaryngologists, lactation consultants, speech pathologists, surgeons, and dental specialists. Clear indications and timing of surgical treatment remain controversial due to lack of consensus regarding accepted anatomical and diagnostic criteria for degree of restriction and relative impact on growth, development, feeding, or oral motor function.  
+text[[525, 320, 940, 515]]
+Frenulum attachmentsFrenulum attachments and their role in oral function increasingly have become topics of interest among a variety of health care specialists. Ankyloglossia (tongue- tie) and hypertrophic/ restrictive maxillary frenula have been implicated in difficulties breastfeeding, incorrect speech articulation and, carries formation, gingival recession and aberrant skeletal growth. Studies have shown differences in treatment recommendations among pediatrists, otolaryngologists, lactation consultants, speech pathologists, surgeons, and dental specialists.56,60- 66 Clear indications and timing of surgical treatment remain controversial due to lack of consensus regarding accepted anatomical and diagnostic criteria for degree of restriction and relative impact on growth, development, feeding, or oral motor function.54,60- 66  
 
-text[[524, 516, 939, 760]]
-When indicated, frenuloplasty/frenotomy (various methods to release the frenulum and correct the anatomic situation) or frenectomy (simple cutting of the frenulum) may be a successful approach to alleviate the problem. Each of these procedures involves surgical incision, establishing hemostasis, and wound management. Dressing placement or the use of antibiotics is not necessary. Recommendations include maintaining a soft diet, regular oral hygiene, and analgesics as needed. The use of electrosurgery or laser technology for frenectomies has demonstrated a shorter operative working time, a better ability to control bleeding, reduced intra- and post- operative pain and discomfort, fewer post- operative complications (e.g., swelling, infection), no need for suture removal, and increased patient acceptance. These procedures require extensive training as well as skillful technique and patient management.  
+text[[525, 517, 940, 760]]
+When indicated, frenuloplasty/frenotomy (various methods to release the frenulum and correct the anatomic situation) or frenectomy (simple cutting of the frenulum) may be a successful approach to alleviate the problem.54,60,65,67 Each of these procedures involves surgical incision, establishing hemostasis, and wound management.68 Dressing placement or the use of antibiotics is not necessary.68 Recommendations include maintaining a soft diet, regular oral hygiene, and analgesics as needed.69 The use of electrosurgery or laser technology for frenectomies has demonstrated a shorter operative working time, a better ability to control bleeding, reduced intra- and post- operative pain and discomfort, fewer post- operative complications (e.g., swelling, infection), no need for suture removal, and increased patient acceptance.62,69,70 These procedures require extensive training as well as skillful technique and patient management.54,60,65,67,71- 75  
 
-sub_title[[525, 778, 688, 792]]
+sub_title[[525, 779, 690, 792]]
 ## Pediatric oral pathology  
 
-text[[524, 792, 939, 913]]
-A wide spectrum of oral lesions occurs in children and adolescents, including soft and hard tissue lesions of the oral maxillofacial region. There is limited information on the prevalence of oral lesions in the pediatric population. The largest epidemiologic studies in the U.S. place the prevalence rate in children at four to 10 percent with the exclusion of infants. Although the vast majority of these lesions represent mucosal conditions, developmental anomalies, and reactive
\ No newline at end of file
+text[[525, 794, 940, 912]]
+A wide spectrum of oral lesions occurs in children and adolescents, including soft and hard tissue lesions of the oral maxillofacial region. There is limited information on the prevalence of oral lesions in the pediatric population. The largest epidemiologic studies in the U.S. place the prevalence rate in children at four to 10 percent with the exclusion of infants.76,77 Although the vast majority of these lesions represent mucosal conditions, developmental anomalies, and reactive
\ No newline at end of file
diff --git a/stage1/sample_00047/raw_response.md b/stage1/sample_00047/raw_response.md
index addf2ce8664f77497cf2ede17796b536cf482c5f..7f01f8b98a2a9d0bcc9c4b4e1a9625fadbc9e065 100644
--- a/stage1/sample_00047/raw_response.md
+++ b/stage1/sample_00047/raw_response.md
@@ -1,37 +1,31 @@
-21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21 1. 21 2 1. 21  
+21 "Although some supernumerary teeth may be syndrome-associated (e.g., cleidocranial dysplasia or of familial inheritance pattern, most supernumerary teeth occur as isolated events.  
 
-sub_title[[88, 76, 234, 90]]
-## Supernumerary teeth  
+text[[88, 198, 505, 317]]
+Supernumerary teeth can occur in either the primary or permanent dentition.21,42,43 In 33 percent of the cases, a supernumerary tooth in the primary dentition is followed by the supernumerary tooth complement in the permanent dentition.44 Reports in incidence of supernumerary teeth can be as high as three percent, with the permanent dentition being affected five times more frequently than the primary dentition and males being affected twice as frequently as females.21  
 
-text[[87, 88, 503, 194]]
-Supernumerary teeth and hyperdontia are terms to describe an excess in tooth number. Supernumerary teeth are thought to be related to disturbances in the initiation and proliferation stages of dental development. Although some supernumerary teeth may be syndrome- associated (e.g., cleidocranial dysplasia) or of familial inheritance pattern, most supernumerary teeth occur as isolated events.  
+text[[88, 318, 505, 625]]
+Supernumerary teeth will occur 10 times more often in the maxillary arch versus the mandibular arch.21 Approximately 90 percent of all single tooth supernumerary teeth are found in the maxillary arch, with a strong predilection to the anterior region.21,42 The maxillary anterior midline is the most common site, in which case the supernumerary tooth is known as a mesiodens; the second most common site is the maxillary molar area, with the tooth known as a paramolar.21,42 A mesiodens can be suspected if there is an asymmetric eruption pattern of the maxillary incisors, delayed eruption of the maxillary incisors with or without any over- retained primary incisors, or ectopic eruption of a maxillary incisor.45 The diagnosis of a mesiodens can be confirmed with radiographs, including occlusal, periapical, or panoramic films,46 or computed tomography.9,10 Three- dimensional information needed to determine the location of the mesiodens or impacted tooth can be obtained by taking two periapical radiographs using either two projections taken at right angles to one another or the tube shift technique (buccal object rule or Clark's rule)47 or by cone beam computed tomography.10,12,13  
 
-text[[88, 194, 503, 319]]
-Supernumerary teeth can occur in either the primary or permanent dentition. In 33 percent of the cases, a supernumerary tooth in the primary dentition is followed by the supernumerary tooth complement in the permanent dentition. Reports in incidence of supernumerary teeth can be as high as three percent, with the permanent dentition being affected five times more frequently than the primary dentition and males being affected twice as frequently as females.  
+text[[88, 627, 505, 912]]
+Complications of supernumerary teeth can include delayed and/or lack of eruption of the permanent tooth, crowding, resorption of adjacent teeth, dentigerous cyst formation, periorconal space ossification, and crown resorption.42,48 Early diagnosis and appropriately timed treatment are important in the prevention and avoidance of these complications. Because only 25 percent of all mesiodens erupt spontaneously, surgical management often is necessary.44,49 A mesiodens that is conical in shape and is not inverted has a better chance for eruption than a mesiodens that is tubular in shape and is inverted.48 The treatment objective for a non- erupting permanent mesiodens is to minimize eruption problems for the permanent incisors.48 Surgical management will vary depending on the size, shape, and number of supernumeraries and the patient's dental development.48 The treatment objective for a non- erupting primary mesiodens differs in that the removal of these teeth usually is not recommended, as the surgical intervention may disrupt or damage the underlying developing permanent teeth.50 Erupted primary tooth mesiodens typically are left  
 
-text[[88, 320, 505, 625]]
-Supernumerary teeth will occur 10 times more often in the maxillary arch versus the mandibular arch. Approximately 90 percent of all single tooth supernumerary teeth are found in the maxillary arch, with a strong predilection to the anterior region. The maxillary anterior midline is the most common site, in which case the supernumerary tooth is known as a mesiodens; the second most common site is the maxillary molar area, with the tooth known as a paramolar. A mesiodens can be suspected if there is an asymmetric eruption pattern of the maxillary incisors, delayed eruption of the maxillary incisors with or without any over- retained primary incisors, or ectopic eruption of a maxillary incisor. The diagnosis of a mesiodens can be confirmed with radiographs, including occlusal, periapical, or panoramic films, or computed tomography. Three- dimensional information needed to determine the location of the mesiodens or impacted tooth can be obtained by taking two periapical radiographs using either two projections taken at right angles to one another or the tube shift technique (buccal object rule or Clark's rule) or by cone beam computed tomography.  
+text[[525, 75, 938, 105]]
+to shed normally upon the eruption of the permanent dentition.50  
 
-text[[88, 626, 505, 913]]
-Complications of supernumerary teeth can include delayed and/or lack of eruption of the permanent tooth, crowding, resorption of adjacent teeth, dentigerous cyst formation, pericoronal space ossification, and crown resorption. Early diagnosis and appropriately timed treatment are important in the prevention and avoidance of these complications. Because only 25 percent of all mesiodens erupt spontaneously, surgical management often is necessary. A mesiodens that is conical in shape and is not inverted has a better chance for eruption than a mesiodens that is tubular in shape and is inverted. The treatment objective for a non- erupting permanent mesiodens is to minimize eruption problems for the permanent incisors. Surgical management will vary depending on the size, shape, and number of supernumeraries and the patient's dental development. The treatment objective for a non- erupting primary mesiodens differs in that the removal of these teeth usually is not recommended, as the surgical intervention may disrupt or damage the underlying developing permanent teeth. Erupted primary tooth mesiodens typically are left  
+text[[525, 105, 940, 286]]
+Extraction of an unerupted primary or permanent mesiodens is recommended during the mixed dentition to allow the normal eruptive force of the permanent incisor to bring itself into the oral cavity.43 Waiting until the adjacent incisors have at least two- thirds root development will present less risk to the developing teeth but still allow spontaneous eruption of the incisors.3 In 75 percent of the cases, extraction of the mesiodens during the mixed dentition results in spontaneous eruption and alignment of the adjacent teeth.50,51 If the adjacent teeth do not erupt within six to 12 months, surgical exposure and orthodontic treatment may be necessary to aid their eruption.45,47  
 
-text[[523, 75, 937, 106]]
-to shed normally upon the eruption of the permanent dentition.  
-
-text[[524, 106, 939, 285]]
-Extraction of an unerupted primary or permanent mesiodens is recommended during the mixed dentition to allow the normal eruptive force of the permanent incisor to bring itself into the oral cavity. Waiting until the adjacent incisors have at least two- thirds root development will present less risk to the developing teeth but still allow spontaneous eruption of the incisors. In 75 percent of the cases, extraction of the mesiodens during the mixed dentition results in spontaneous eruption and alignment of the adjacent teeth. If the adjacent teeth do not erupt within six to 12 months, surgical exposure and orthodontic treatment may be necessary to aid their eruption.  
-
-sub_title[[524, 304, 680, 317]]
+sub_title[[526, 305, 680, 318]]
 ## Frenulum attachments  
 
-text[[524, 319, 939, 515]]
-Frenulum attachments Frenulum attachments and their role in oral function increasingly have become topics of interest among a variety of health care specialists. Ankyloglossia (tongue- tie) and hypertrophic/restrictive maxillary frenula have been implicated in difficulties breastfeeding, incorrect speech articulation, caries formation, gingival recession, and aberrant skeletal growth. Studies have shown differences in treatment recommendations among pediatricians, otolaryngologists, lactation consultants, speech pathologists, surgeons, and dental specialists. Clear indications and timing of surgical treatment remain controversial due to lack of consensus regarding accepted anatomical and diagnostic criteria for degree of restriction and relative impact on growth, development, feeding, or oral motor function.  
+text[[525, 320, 940, 515]]
+Frenulum attachmentsFrenulum attachments and their role in oral function increasingly have become topics of interest among a variety of health care specialists. Ankyloglossia (tongue- tie) and hypertrophic/ restrictive maxillary frenula have been implicated in difficulties breastfeeding, incorrect speech articulation and, carries formation, gingival recession and aberrant skeletal growth. Studies have shown differences in treatment recommendations among pediatrists, otolaryngologists, lactation consultants, speech pathologists, surgeons, and dental specialists.56,60- 66 Clear indications and timing of surgical treatment remain controversial due to lack of consensus regarding accepted anatomical and diagnostic criteria for degree of restriction and relative impact on growth, development, feeding, or oral motor function.54,60- 66  
 
-text[[524, 516, 939, 760]]
-When indicated, frenuloplasty/frenotomy (various methods to release the frenulum and correct the anatomic situation) or frenectomy (simple cutting of the frenulum) may be a successful approach to alleviate the problem. Each of these procedures involves surgical incision, establishing hemostasis, and wound management. Dressing placement or the use of antibiotics is not necessary. Recommendations include maintaining a soft diet, regular oral hygiene, and analgesics as needed. The use of electrosurgery or laser technology for frenectomies has demonstrated a shorter operative working time, a better ability to control bleeding, reduced intra- and post- operative pain and discomfort, fewer post- operative complications (e.g., swelling, infection), no need for suture removal, and increased patient acceptance. These procedures require extensive training as well as skillful technique and patient management.  
+text[[525, 517, 940, 760]]
+When indicated, frenuloplasty/frenotomy (various methods to release the frenulum and correct the anatomic situation) or frenectomy (simple cutting of the frenulum) may be a successful approach to alleviate the problem.54,60,65,67 Each of these procedures involves surgical incision, establishing hemostasis, and wound management.68 Dressing placement or the use of antibiotics is not necessary.68 Recommendations include maintaining a soft diet, regular oral hygiene, and analgesics as needed.69 The use of electrosurgery or laser technology for frenectomies has demonstrated a shorter operative working time, a better ability to control bleeding, reduced intra- and post- operative pain and discomfort, fewer post- operative complications (e.g., swelling, infection), no need for suture removal, and increased patient acceptance.62,69,70 These procedures require extensive training as well as skillful technique and patient management.54,60,65,67,71- 75  
 
-sub_title[[525, 778, 688, 792]]
+sub_title[[525, 779, 690, 792]]
 ## Pediatric oral pathology  
 
-text[[524, 792, 939, 913]]
-A wide spectrum of oral lesions occurs in children and adolescents, including soft and hard tissue lesions of the oral maxillofacial region. There is limited information on the prevalence of oral lesions in the pediatric population. The largest epidemiologic studies in the U.S. place the prevalence rate in children at four to 10 percent with the exclusion of infants. Although the vast majority of these lesions represent mucosal conditions, developmental anomalies, and reactive
\ No newline at end of file
+text[[525, 794, 940, 912]]
+A wide spectrum of oral lesions occurs in children and adolescents, including soft and hard tissue lesions of the oral maxillofacial region. There is limited information on the prevalence of oral lesions in the pediatric population. The largest epidemiologic studies in the U.S. place the prevalence rate in children at four to 10 percent with the exclusion of infants.76,77 Although the vast majority of these lesions represent mucosal conditions, developmental anomalies, and reactive
\ No newline at end of file
diff --git a/stage1/sample_00048/document.md b/stage1/sample_00048/document.md
index ac52ac5a73c9f5b20d7d9848b8ee0b226261cd86..065bcf3009eb06e60a601a3ded30a734e1b96a18 100644
--- a/stage1/sample_00048/document.md
+++ b/stage1/sample_00048/document.md
@@ -1,42 +1 @@
-0.5cm
-
-text[[57, 74, 474, 103]]
-or inflammatory lesions, it is imperative to be vigilant for neoplastic diseases.  
-
-text[[59, 104, 474, 239]]
-Regardless of the age of the child, it is important to establish a working diagnosis for every lesion. This is based on obtaining a thorough history, assessing the risk factors and documenting the clinical signs and symptoms of the lesion. Based on these facts, a list of lesions with similar characteristics is rank ordered from most likely to least likely diagnosis. The entity that is judged to be the most likely disease becomes the working diagnosis and determines the initial management approach.  
-
-text[[58, 240, 475, 484]]
-For most oral lesions, a definitive diagnosis is best made by performing a biopsy. By definition, a biopsy is the removal of a piece of tissue from a living body for diagnostic study and is considered the gold standard of diagnostic tests. The two most common biopsies are the incisional and excisional types. Excisional biopsies usually are performed on small lesions, less than one centimeter in size, for the total removal of the affected tissue. An incisional biopsy is performed when a malignancy is suspected, the lesion is large in size or diffuse in nature, or a multifocal distribution is present. Multiple incisional biopsies may be indicated for diffuse lesions, in order to obtain a representative tissue sample. Fine needle aspiration, the cytobrush technique, and exfoliative cytology may assist in making a diagnosis, but they are considered adjunctive tests because they do not establish a definitive diagnosis.  
-
-text[[59, 486, 474, 807]]
-It is considered the standard of care that any tissue removed from the oral and maxillofacial region be submitted for histopathologic examination. Exceptions to this rule include carious teeth that do not have soft tissue attached, extirpated pulpal tissue, and clinically normal tissue, such as tissue from gingival recontouring. Gross description of all tissue that is removed should be entered into the patient record. In general, a soft tissue biopsy should be performed when a lesion persists for greater than two weeks despite removal of the suspected causative factor or empirical drug treatment. It is also imperative to submit hard or soft tissue for evaluation to a pathologist if the differential diagnosis includes at least one significant disease or neoplasm. Histopathologic examination not only furnishes a definitive diagnosis, but it provides information about the clinical behavior and prognosis and determines the need for additional treatment or follow- up. Another valuable outcome is that it allows the clinician to deliver evidence- based medical/dental care, increasing the likelihood for a positive result. Furthermore, it presents important documentation about the lesion for the patient record, including the procedures taken for establishing a diagnosis.  
-
-text[[59, 809, 475, 855]]
-Many oral biopsies are within the scope of practice for a pediatric dentist to perform. However, if the tissue is excised, the following steps should be taken for optimum results:  
-
-text[[71, 855, 474, 915]]
-1. select the most representative lesion site and not the area that is the most accessible. 
-2. remove an adequate amount of tissue. If the biopsy is too small or too superficial, a diagnosis may be compromised.  
-
-text[[509, 76, 910, 147]]
-3. avoid crushing or distorting the tissue. Damage is most often observed from the forces of the tissue forces, tearing the tissues or overheating the tissue from the use of electrosurgery or laser removal.  
-
-text[[508, 129, 910, 338]]
-4. immediately place the tissue in a fixative, which for most samples is 10 percent formalin. It is critical not to dilute the fixative with water or other liquids because tissue autolysis will render the sample nondiagnostic.  
-5. proper identification of the specimen is essential. The formalin container should be labelled with the name of the patient and the location. Multiple tissue samples from different locations should not be placed in the same container, unless they are uniquely identified, such as tagged with a suture.  
-
-text[[509, 340, 910, 379]]
-6. complete the surgical pathology form including patient demographics, the submitting dentist's name and address, and a brief but accurate history. It is important to have legible records so that the diagnosis is not delayed. Clinical photographs and radiographs often are very useful for correlating the microscopic findings.  
-
-text[[498, 394, 908, 424]]
-Worldwide, the most frequently oral biopsied lesions in children include:  
-
-text[[515, 426, 791, 736]]
-- mucocele;- fibrous lesions;- pyogenic granuloma;- dental follicle;- human papillomavirus (HPV) lesion;- chronic inflammation;- giant cell lesions (soft tissue);- hyperkeratosis;- peripheral ossifying fibroma;- gingivitis;- gingival hyperplasia;- hemangioma;- ulcer;- lymphangioma;- sialadentis;- Burkitt's lymphoma;- melanotic macule;- pleomorphic adenoma;- nevus; and-neurofibroma.  
-
-sub_title[[495, 752, 634, 765]]
-## Lesions of the newborn  
-
-text[[495, 767, 910, 915]]
-Palatal cysts of the newborn include Epstein pearls and Bohn nodules. These cysts are found in up to 85 percent of newborns. Epstein pearls occur in the median palatal raphe area as a result of trapped epithelial remnants along the line of fusion of the palatal halves. Bohn nodules are remnants of salivary gland epithelium and usually are found on the buccal and lingual aspects of the ridge, away from the midline. Gingival cysts of the newborn, or dental lamina cysts, are found on the crests of the dental ridges, and are most commonly are seen bilaterally in the region of the first primary
\ No newline at end of file
+0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0.9 0
\ No newline at end of file
diff --git a/stage1/sample_00048/raw_response.md b/stage1/sample_00048/raw_response.md
index ac52ac5a73c9f5b20d7d9848b8ee0b226261cd86..065bcf3009eb06e60a601a3ded30a734e1b96a18 100644
--- a/stage1/sample_00048/raw_response.md
+++ b/stage1/sample_00048/raw_response.md
@@ -1,42 +1 @@
-0.5cm
-
-text[[57, 74, 474, 103]]
-or inflammatory lesions, it is imperative to be vigilant for neoplastic diseases.  
-
-text[[59, 104, 474, 239]]
-Regardless of the age of the child, it is important to establish a working diagnosis for every lesion. This is based on obtaining a thorough history, assessing the risk factors and documenting the clinical signs and symptoms of the lesion. Based on these facts, a list of lesions with similar characteristics is rank ordered from most likely to least likely diagnosis. The entity that is judged to be the most likely disease becomes the working diagnosis and determines the initial management approach.  
-
-text[[58, 240, 475, 484]]
-For most oral lesions, a definitive diagnosis is best made by performing a biopsy. By definition, a biopsy is the removal of a piece of tissue from a living body for diagnostic study and is considered the gold standard of diagnostic tests. The two most common biopsies are the incisional and excisional types. Excisional biopsies usually are performed on small lesions, less than one centimeter in size, for the total removal of the affected tissue. An incisional biopsy is performed when a malignancy is suspected, the lesion is large in size or diffuse in nature, or a multifocal distribution is present. Multiple incisional biopsies may be indicated for diffuse lesions, in order to obtain a representative tissue sample. Fine needle aspiration, the cytobrush technique, and exfoliative cytology may assist in making a diagnosis, but they are considered adjunctive tests because they do not establish a definitive diagnosis.  
-
-text[[59, 486, 474, 807]]
-It is considered the standard of care that any tissue removed from the oral and maxillofacial region be submitted for histopathologic examination. Exceptions to this rule include carious teeth that do not have soft tissue attached, extirpated pulpal tissue, and clinically normal tissue, such as tissue from gingival recontouring. Gross description of all tissue that is removed should be entered into the patient record. In general, a soft tissue biopsy should be performed when a lesion persists for greater than two weeks despite removal of the suspected causative factor or empirical drug treatment. It is also imperative to submit hard or soft tissue for evaluation to a pathologist if the differential diagnosis includes at least one significant disease or neoplasm. Histopathologic examination not only furnishes a definitive diagnosis, but it provides information about the clinical behavior and prognosis and determines the need for additional treatment or follow- up. Another valuable outcome is that it allows the clinician to deliver evidence- based medical/dental care, increasing the likelihood for a positive result. Furthermore, it presents important documentation about the lesion for the patient record, including the procedures taken for establishing a diagnosis.  
-
-text[[59, 809, 475, 855]]
-Many oral biopsies are within the scope of practice for a pediatric dentist to perform. However, if the tissue is excised, the following steps should be taken for optimum results:  
-
-text[[71, 855, 474, 915]]
-1. select the most representative lesion site and not the area that is the most accessible. 
-2. remove an adequate amount of tissue. If the biopsy is too small or too superficial, a diagnosis may be compromised.  
-
-text[[509, 76, 910, 147]]
-3. avoid crushing or distorting the tissue. Damage is most often observed from the forces of the tissue forces, tearing the tissues or overheating the tissue from the use of electrosurgery or laser removal.  
-
-text[[508, 129, 910, 338]]
-4. immediately place the tissue in a fixative, which for most samples is 10 percent formalin. It is critical not to dilute the fixative with water or other liquids because tissue autolysis will render the sample nondiagnostic.  
-5. proper identification of the specimen is essential. The formalin container should be labelled with the name of the patient and the location. Multiple tissue samples from different locations should not be placed in the same container, unless they are uniquely identified, such as tagged with a suture.  
-
-text[[509, 340, 910, 379]]
-6. complete the surgical pathology form including patient demographics, the submitting dentist's name and address, and a brief but accurate history. It is important to have legible records so that the diagnosis is not delayed. Clinical photographs and radiographs often are very useful for correlating the microscopic findings.  
-
-text[[498, 394, 908, 424]]
-Worldwide, the most frequently oral biopsied lesions in children include:  
-
-text[[515, 426, 791, 736]]
-- mucocele;- fibrous lesions;- pyogenic granuloma;- dental follicle;- human papillomavirus (HPV) lesion;- chronic inflammation;- giant cell lesions (soft tissue);- hyperkeratosis;- peripheral ossifying fibroma;- gingivitis;- gingival hyperplasia;- hemangioma;- ulcer;- lymphangioma;- sialadentis;- Burkitt's lymphoma;- melanotic macule;- pleomorphic adenoma;- nevus; and-neurofibroma.  
-
-sub_title[[495, 752, 634, 765]]
-## Lesions of the newborn  
-
-text[[495, 767, 910, 915]]
-Palatal cysts of the newborn include Epstein pearls and Bohn nodules. These cysts are found in up to 85 percent of newborns. Epstein pearls occur in the median palatal raphe area as a result of trapped epithelial remnants along the line of fusion of the palatal halves. Bohn nodules are remnants of salivary gland epithelium and usually are found on the buccal and lingual aspects of the ridge, away from the midline. Gingival cysts of the newborn, or dental lamina cysts, are found on the crests of the dental ridges, and are most commonly are seen bilaterally in the region of the first primary
\ No newline at end of file
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diff --git a/stage1/sample_00049/document.md b/stage1/sample_00049/document.md
index b514fe261ffb465d83c8022df3ea965f1e820a0d..6ec9f7af58582219ea5cceccaa67ec89f85d2b46 100644
--- a/stage1/sample_00049/document.md
+++ b/stage1/sample_00049/document.md
@@ -1,31 +1 @@
-10
-
-text[[115, 46, 960, 842]]
-faith, and found repentance: here I have
-fet down the principal points of Christian
-religion in fixe plane and, asfer rules: even
-fuch is the simplest may easily learn: and
-hereunto is adjoined an exposition of them,
-word by word. If ye do want other good di-
-rectiones, then ye this my labour for your
-infurrection. In reading of it, first learne
-the fixe Principles: and when you have
-them without booke, and the meaning of
-them withal, then learne the expofition alfo.
-V.ich beeing well conceived, ant in fome
-measure felt in the heart; ye shall be able
-to profit by Sermons , whereas now ye
-cannot: and the ordinarie parts of the Cai-
-techisme, namely, te ten Commandements,
-the Creede, the Loords prayer, and the in-
-fittuition of the two Sacraments, shall more
-easily be underftood. 
-
-text[[370, 840, 701, 870]]
-Thine in Christ, Jerus. 
-
-text[[443, 872, 938, 910]]
-VILLIAM PERKINS. 
-
-text[[840, 917, 937, 954]]
-The
\ No newline at end of file
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diff --git a/stage1/sample_00049/raw_response.md b/stage1/sample_00049/raw_response.md
index b514fe261ffb465d83c8022df3ea965f1e820a0d..6ec9f7af58582219ea5cceccaa67ec89f85d2b46 100644
--- a/stage1/sample_00049/raw_response.md
+++ b/stage1/sample_00049/raw_response.md
@@ -1,31 +1 @@
-10
-
-text[[115, 46, 960, 842]]
-faith, and found repentance: here I have
-fet down the principal points of Christian
-religion in fixe plane and, asfer rules: even
-fuch is the simplest may easily learn: and
-hereunto is adjoined an exposition of them,
-word by word. If ye do want other good di-
-rectiones, then ye this my labour for your
-infurrection. In reading of it, first learne
-the fixe Principles: and when you have
-them without booke, and the meaning of
-them withal, then learne the expofition alfo.
-V.ich beeing well conceived, ant in fome
-measure felt in the heart; ye shall be able
-to profit by Sermons , whereas now ye
-cannot: and the ordinarie parts of the Cai-
-techisme, namely, te ten Commandements,
-the Creede, the Loords prayer, and the in-
-fittuition of the two Sacraments, shall more
-easily be underftood. 
-
-text[[370, 840, 701, 870]]
-Thine in Christ, Jerus. 
-
-text[[443, 872, 938, 910]]
-VILLIAM PERKINS. 
-
-text[[840, 917, 937, 954]]
-The
\ No newline at end of file
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