Upload extract stage outputs 2025-11-12T14:20:47.587947Z

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",

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.
+
+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.

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.
+
+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.

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).

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).

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

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

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).

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).

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.

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.

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. \(5 \times 10^6 t = 40\)
+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.

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. \(5 \times 10^6 t = 40\)
+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.

stage1/sample_00006/document.md

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stage1/sample_00006/raw_response.md

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stage1/sample_00007/raw_response.md

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stage1/sample_00008/document.md

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-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.
+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.

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.
+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.

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).
+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).

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).
+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).

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.
+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.

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.
+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.

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/
+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

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/
+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

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.

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.

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.
+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.

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.
+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.

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.
+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.

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.
+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.

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.

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.

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
+1 4 4 7 8 8

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
+1 4 4 7 8 8

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.

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.

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).

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).

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.

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.

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.
+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)

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.
+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)

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>
+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>

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>
+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>

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

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

stage1/sample_00023/document.md

@@ -1 +1 @@
-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.
+2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 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

stage1/sample_00023/raw_response.md

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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.
+2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 2004). 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stage1/sample_00024/document.md

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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
+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