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@@ -1,5 +1,5 @@
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  "stage": "extract",
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  "dataset": {
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  "name": "HuggingFaceM4/FineVision",
 
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  "stage": "extract",
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  "dataset": {
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  "name": "HuggingFaceM4/FineVision",
sample_00000/document.md CHANGED
@@ -28,18 +28,18 @@ Received: 21 April 2023 Accepted: 03 June 2023 Published: 07 June 2023
28
 
29
  1. Grando SA. Pemphigus autoimmunity: hypotheses and realities. Autoimmunity. 2012 Feb;45(1):7-35. doi: 10.3109/08916934.2011.606444.
30
  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.
31
- 3. Pasricha JS, Gupta R. Pulse therapy with dexamethasonecyclophosphamide in pemphigus. Indian J Dermatol Venereol Leprol. 1984;50:199-203.
32
  4. Bystryn JC, Steinman NM. The adjuvant therapy of pemphigus. An update. Arch Dermatol. 1996 Sep;132(2):203-12.
33
 
34
- 5. Heizmann M, Itin P, Wermli 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.
35
  6. Food and Drug Administration. Rituxan label; 2012 [cited Feb 2, 2021]. Available from: http://www.accessdata.fda.gov/drugsatfda_docs/label/2012/103705s5373lbl.pdf.
36
- 7. Belgi AS, Azeze 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.xx.
37
- 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.xx.
38
  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.
39
- 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.xx.
40
  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.
41
- 12. Horváth B, Huizinga J, Pas HH, Mulder AB, 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.xx.
42
- 13. Craythorne E, Du Vivier A, Mufti GJ, Wamakulasuriya 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.xx.
43
- 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.xx.
44
  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
45
- 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.
 
28
 
29
  1. Grando SA. Pemphigus autoimmunity: hypotheses and realities. Autoimmunity. 2012 Feb;45(1):7-35. doi: 10.3109/08916934.2011.606444.
30
  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.
31
+ 3. Pasricha JS, Gupta R. Pulse therapy with dexamethasonecyclophosphamide in pemphigus. Indian J Dermatol Venereol Leprol. 1984; 50:199-203.
32
  4. Bystryn JC, Steinman NM. The adjuvant therapy of pemphigus. An update. Arch Dermatol. 1996 Sep;132(2):203-12.
33
 
34
+ 5. Heizmann M, Itin P, Wemli 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.
35
  6. Food and Drug Administration. Rituxan label; 2012 [cited Feb 2, 2021]. Available from: http://www.accessdata.fda.gov/drugsatfda_docs/label/2012/103705s5373lbl.pdf.
36
+ 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.
37
+ 8. Schmidt E, Seitz CS, Benoit S, Bröcker EB, Goebel 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.
38
  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.
39
+ 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.
40
  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.
41
+ 12. Horváth 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.
42
+ 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
43
+ 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. 2011 Sep;165(3):646-51. doi: 10.1111/j.1365- 2133.2011.10411. x
44
  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
45
+ 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.
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@@ -42,19 +42,19 @@ Received: 21 April 2023 Accepted: 03 June 2023 Published: 07 June 2023
42
  <|ref|>text<|/ref|><|det|>[[90, 607, 485, 784]]<|/det|>
43
  1. Grando SA. Pemphigus autoimmunity: hypotheses and realities. Autoimmunity. 2012 Feb;45(1):7-35. doi: 10.3109/08916934.2011.606444.
44
  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.
45
- 3. Pasricha JS, Gupta R. Pulse therapy with dexamethasonecyclophosphamide in pemphigus. Indian J Dermatol Venereol Leprol. 1984;50:199-203.
46
  4. Bystryn JC, Steinman NM. The adjuvant therapy of pemphigus. An update. Arch Dermatol. 1996 Sep;132(2):203-12.
47
 
48
- <|ref|>text<|/ref|><|det|>[[513, 75, 907, 782]]<|/det|>
49
- 5. Heizmann M, Itin P, Wermli 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.
50
  6. Food and Drug Administration. Rituxan label; 2012 [cited Feb 2, 2021]. Available from: http://www.accessdata.fda.gov/drugsatfda_docs/label/2012/103705s5373lbl.pdf.
51
- 7. Belgi AS, Azeze 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.xx.
52
- 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.xx.
53
  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.
54
- 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.xx.
55
  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.
56
- 12. Horváth B, Huizinga J, Pas HH, Mulder AB, 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.xx.
57
- 13. Craythorne E, Du Vivier A, Mufti GJ, Wamakulasuriya 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.xx.
58
- 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.xx.
59
  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
60
- 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.
 
42
  <|ref|>text<|/ref|><|det|>[[90, 607, 485, 784]]<|/det|>
43
  1. Grando SA. Pemphigus autoimmunity: hypotheses and realities. Autoimmunity. 2012 Feb;45(1):7-35. doi: 10.3109/08916934.2011.606444.
44
  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.
45
+ 3. Pasricha JS, Gupta R. Pulse therapy with dexamethasonecyclophosphamide in pemphigus. Indian J Dermatol Venereol Leprol. 1984; 50:199-203.
46
  4. Bystryn JC, Steinman NM. The adjuvant therapy of pemphigus. An update. Arch Dermatol. 1996 Sep;132(2):203-12.
47
 
48
+ <|ref|>text<|/ref|><|det|>[[514, 70, 906, 780]]<|/det|>
49
+ 5. Heizmann M, Itin P, Wemli 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.
50
  6. Food and Drug Administration. Rituxan label; 2012 [cited Feb 2, 2021]. Available from: http://www.accessdata.fda.gov/drugsatfda_docs/label/2012/103705s5373lbl.pdf.
51
+ 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.
52
+ 8. Schmidt E, Seitz CS, Benoit S, Bröcker EB, Goebel 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.
53
  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.
54
+ 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.
55
  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.
56
+ 12. Horváth 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.
57
+ 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
58
+ 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. 2011 Sep;165(3):646-51. doi: 10.1111/j.1365- 2133.2011.10411. x
59
  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
60
+ 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.
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sample_00002/document.md CHANGED
@@ -1,19 +1,19 @@
1
- 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3.
2
-
3
- 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.
4
 
5
  ## Case presentation
6
 
7
- 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- bits 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- i).
8
 
9
  ![Figure sample_00002_fig01](figures/sample_00002_fig01.png)
10
 
11
  <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>
12
 
13
- 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).
 
 
14
 
15
  ![Figure sample_00002_fig02](figures/sample_00002_fig02.png)
16
 
17
- <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>
18
 
19
  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).
 
1
+ 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3.
 
 
2
 
3
  ## Case presentation
4
 
5
+ 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- - 1. 1. 1. 1. 1. 1. 1. 1. 1. 1. 1 1. 1. 1. 1. 1. 1. 1. 1. 1. 1
6
 
7
  ![Figure sample_00002_fig01](figures/sample_00002_fig01.png)
8
 
9
  <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>
10
 
11
+ 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
12
+
13
+ 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).
14
 
15
  ![Figure sample_00002_fig02](figures/sample_00002_fig02.png)
16
 
17
+ <center>Figure 2: Photomicrograph showing acantholysis of the keratinocytes, tombstone appearance, epithelium exhibiting spongiosis, and superficial perivascular mixed infiltrate (H & E stain, x5). </center>
18
 
19
  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).
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sample_00002/raw_response.md CHANGED
@@ -1,24 +1,24 @@
1
- 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3.
2
 
3
- <|ref|>text<|/ref|><|det|>[[92, 75, 484, 140]]<|/det|>
4
- 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.
5
-
6
- <|ref|>sub_title<|/ref|><|det|>[[93, 157, 235, 172]]<|/det|>
7
  ## Case presentation
8
 
9
- <|ref|>text<|/ref|><|det|>[[92, 173, 483, 499]]<|/det|>
10
- 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- bits 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- i).
11
 
12
- <|ref|>image<|/ref|><|det|>[[93, 511, 483, 796]]<|/det|>
13
- <|ref|>image_caption<|/ref|><|det|>[[91, 800, 483, 865]]<|/det|>
14
  <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>
15
 
16
- <|ref|>text<|/ref|><|det|>[[91, 878, 484, 920], [513, 73, 904, 254]]<|/det|>
17
- 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).
 
 
 
18
 
19
- <|ref|>image<|/ref|><|det|>[[515, 269, 904, 507]]<|/det|>
20
- <|ref|>image_caption<|/ref|><|det|>[[512, 512, 904, 550]]<|/det|>
21
- <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>
22
 
23
- <|ref|>text<|/ref|><|det|>[[512, 567, 904, 924]]<|/det|>
24
  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).
 
1
+ 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3. 3.
2
 
3
+ <|ref|>sub_title<|/ref|><|det|>[[93, 156, 235, 171]]<|/det|>
 
 
 
4
  ## Case presentation
5
 
6
+ <|ref|>text<|/ref|><|det|>[[93, 172, 483, 499]]<|/det|>
7
+ 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- - 1. 1. 1. 1. 1. 1. 1. 1. 1. 1. 1 1. 1. 1. 1. 1. 1. 1. 1. 1. 1
8
 
9
+ <|ref|>image<|/ref|><|det|>[[93, 512, 482, 797]]<|/det|>
10
+ <|ref|>image_caption<|/ref|><|det|>[[92, 799, 483, 866]]<|/det|>
11
  <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>
12
 
13
+ <|ref|>text<|/ref|><|det|>[[92, 879, 483, 920]]<|/det|>
14
+ 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
15
+
16
+ <|ref|>text<|/ref|><|det|>[[514, 71, 904, 256]]<|/det|>
17
+ 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).
18
 
19
+ <|ref|>image<|/ref|><|det|>[[514, 269, 905, 507]]<|/det|>
20
+ <|ref|>image_caption<|/ref|><|det|>[[513, 511, 904, 552]]<|/det|>
21
+ <center>Figure 2: Photomicrograph showing acantholysis of the keratinocytes, tombstone appearance, epithelium exhibiting spongiosis, and superficial perivascular mixed infiltrate (H & E stain, x5). </center>
22
 
23
+ <|ref|>text<|/ref|><|det|>[[513, 568, 904, 924]]<|/det|>
24
  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).
sample_00003/document.md CHANGED
@@ -1,47 +1,13 @@
1
- 0
2
 
3
- To build and operate an efficient water system, you need both the right products and experts who know the application. Aquavar® IPC and Hydrovar® controllers have been designed by Xylem's engineers with these things in mind. The Aquavar® IPC or Hydrovar® variable speed controller provide built in pump protection controls and monitoring to help you optimize pump operations and increase energy savings up to 70% (vs. fixed speed) while reducing installation time.
4
 
5
- ![Figure sample_00003_fig01](figures/sample_00003_fig01.png)
6
 
7
- # SPECIFICATIONS
8
 
9
- <table><tr><td>Indoor enclosures</td><td>IP20 Open, TYPE 1, TYPE 12</td></tr><tr><td>Outdoor enclosures</td><td>TYPE 3R, TYPE 4X</td></tr><tr><td>Input supply</td><td>1.5-600 hp (frame A-D) wall or base mounted</td></tr><tr><td>Ambient<br>temperature</td><td>14°F-113°F(-10°C-45°C)</td></tr><tr><td></td><td>Higher temperatures can be achieved by derating the output amperage of the drive 10% for up to 122°F (50°C)</td></tr><tr><td>Communication</td><td>Modbus® RTU, Metasys N2, FLN, and BACnet standard<br>Others available with option cards</td></tr><tr><td></td><td>At altitudes from 0 to 1,000 meters<br>(0 to 3,300 ft)<br>Nameplate rated current is available<br>Derate for altitudes above 1,000<br>(3,300 ft) with a maximum operating<br>altitude of 3,000 m (9,900 ft)<br>Consult factory for applications above<br>3,000 m (9,900 ft)</td></tr><tr><td>Altitudes</td><td></td></tr><tr><td></td><td>Lower than 95% without condensation</td></tr><tr><td>Electrical -<br>input power</td><td>3 phase 380 V to 480 V ±10%<br>1 phase 200 V to 240 V ±10%<br>3 phase 200 V to 240 V ±10%<br>3 phase 525 V to 600 V ±10%<br>Frequency 50 or 60 Hz, ±2 Hz</td></tr><tr><td>Electrical -<br>output power</td><td>3 phase from 0 to V supply</td></tr></table>
10
 
11
- # AQUAVAR® IPC VARIABLE SPEED CONTROLLER
12
 
13
- # FEATURES
14
-
15
- ·Easier start-up and programming with Start-Up Genie
16
-
17
- ·Wide range of standard and permanent magnet motors with power up to 600 hp
18
-
19
- ·Multi-pump configuration for up to four (4) pumps - no need for programmable logic controller (PLC)
20
-
21
- ·Remote commissioning and monitoring with USB connectivity and software
22
-
23
- ·Two wire multi-pump connection for faster installation
24
-
25
- ·Hand on, off, and auto-on buttons available for easy pump operation at the keypad. No toggling between local and remote operation
26
-
27
- ·System redundancy with multi-master control in case of drive failure
28
-
29
- ·BACnet and Modbus as a standard for seamless BMS integration
30
-
31
- ·Submersible and above ground applications
32
-
33
- ·Wide range of voltage and enclosure options
34
-
35
- ·True 208 V coverage
36
-
37
- ·Dedicated single phase input
38
-
39
- ·Remote commissioning and monitoring with USB connectivity and software
40
-
41
- ·In-panel or handheld keypad with backlit display
42
-
43
- ·Alarm Log for last 5 alarms and maintenance events
44
-
45
- ·EMC/RFI filters and dual DC-link reactors to reduce drive noise emissions and interference
46
-
47
- ·I/O expansion cards, factory installed or field configured
 
1
+ 0 to 70% (vs. fixed speed) while reducing installation time.
2
 
3
+ ![Figure sample_00003_fig01](figures/sample_00003_fig01.png)
4
 
5
+ ## SPECIFICATIONS
6
 
7
+ <table><tr><td>Indoor enclosures</td><td>IP20 Open, TYPE 1, TYPE 12</td></tr><tr><td>Outdoor enclosures</td><td>TYPE 3R, TYPE 4X</td></tr><tr><td>Input supply</td><td>1.5 - 600 hp (frame A - D) wall or base mounted</td></tr><tr><td>Ambient temperature</td><td>14°F - 113°F (-10°C - 45°C)</td></tr><tr><td>Communication</td><td>Higher temperatures can be achieved by derating the output amperage of the drive 10% for up to 122°F (50°C)</td></tr><tr><td>Altitudes</td><td>Modbus® RTU, Metasys N2, FLN, and BACnet standard<br>Others available with option cards</td></tr><tr><td>Relative humidity</td><td>At altitudes from 0 to 1,000 meters (0 to 3,300 ft)<br>Nameplate rated current is available<br>Derate for altitudes above 1,000 (3,300 ft) with a maximum operating altitude of 3,000 m (9,900 ft)<br>Consult factory for applications above 3,000 m (9,900 ft)</td></tr><tr><td>Electrical input power</td><td>Lower than 95% without condensation</td></tr><tr><td>Electrical input power</td><td>3 phase 380 V to 480 V ±10%<br>1 phase 200 V to 240 V ±10%<br>3 phase 200 V to 240 V ±10%<br>3 phase 525 V to 600 V ±10%<br>Frequency 50 or 60 Hz, ±2 Hz</td></tr><tr><td>Electrical output power</td><td>3 phase from 0 to V supply</td></tr></table>
8
 
9
+ ## AQUAVAR® IPC VARIABLE SPEED CONTROLLER
10
 
11
+ ## FEATURES
12
 
13
+ - Easier start-up and programming with Start-Up Genie- Wide range of standard and permanent magnet motors with power up to 600 hp- Multi-pump configuration for up to four (4) pumps - no need for programmable logic controller (PLC)- Remote commissioning and monitoring with USB connectivity and software- Two wire multi-pump connection for faster installation- Hand on, off, and auto-on buttons available for easy pump operation at the keypad. No toggling between local and remote operation- System redundancy with multi-master control in case of drive failure- BACnet and Modbus as a standard for seamless BMS integration- Submersible and above ground applications- Wide range of voltage and enclosure options- True 208 V coverage- Dedicated single phase input- Remote commissioning and monitoring with USB connectivity and software- In-panel or handheld keypad with backlit display- Alarm Log for last 5 alarms and maintenance events- EMC/RFI filters and dual DC-link reactors to reduce drive noise emissions and interference- I/O expansion cards, factory installed or field configured
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
sample_00003/document_with_boxes.png CHANGED

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sample_00003/raw_response.md CHANGED
@@ -1,70 +1,19 @@
1
- 0
2
 
3
- <|ref|>text<|/ref|><|det|>[[52, 145, 929, 234]]<|/det|>
4
- To build and operate an efficient water system, you need both the right products and experts who know the application. Aquavar® IPC and Hydrovar® controllers have been designed by Xylem's engineers with these things in mind. The Aquavar® IPC or Hydrovar® variable speed controller provide built in pump protection controls and monitoring to help you optimize pump operations and increase energy savings up to 70% (vs. fixed speed) while reducing installation time.
5
 
6
- <|ref|>image<|/ref|><|det|>[[55, 239, 403, 515]]<|/det|>
 
7
 
8
- <|ref|>title<|/ref|><|det|>[[56, 529, 197, 541]]<|/det|>
9
- # SPECIFICATIONS
10
 
11
- <|ref|>table<|/ref|><|det|>[[56, 545, 486, 954]]<|/det|>
12
 
13
- <table><tr><td>Indoor enclosures</td><td>IP20 Open, TYPE 1, TYPE 12</td></tr><tr><td>Outdoor enclosures</td><td>TYPE 3R, TYPE 4X</td></tr><tr><td>Input supply</td><td>1.5-600 hp (frame A-D) wall or base mounted</td></tr><tr><td>Ambient<br>temperature</td><td>14°F-113°F(-10°C-45°C)</td></tr><tr><td></td><td>Higher temperatures can be achieved by derating the output amperage of the drive 10% for up to 122°F (50°C)</td></tr><tr><td>Communication</td><td>Modbus® RTU, Metasys N2, FLN, and BACnet standard<br>Others available with option cards</td></tr><tr><td></td><td>At altitudes from 0 to 1,000 meters<br>(0 to 3,300 ft)<br>Nameplate rated current is available<br>Derate for altitudes above 1,000<br>(3,300 ft) with a maximum operating<br>altitude of 3,000 m (9,900 ft)<br>Consult factory for applications above<br>3,000 m (9,900 ft)</td></tr><tr><td>Altitudes</td><td></td></tr><tr><td></td><td>Lower than 95% without condensation</td></tr><tr><td>Electrical -<br>input power</td><td>3 phase 380 V to 480 V ±10%<br>1 phase 200 V to 240 V ±10%<br>3 phase 200 V to 240 V ±10%<br>3 phase 525 V to 600 V ±10%<br>Frequency 50 or 60 Hz, ±2 Hz</td></tr><tr><td>Electrical -<br>output power</td><td>3 phase from 0 to V supply</td></tr></table>
 
14
 
15
- <|ref|>title<|/ref|><|det|>[[509, 309, 752, 384]]<|/det|>
16
- # AQUAVAR® IPC VARIABLE SPEED CONTROLLER
17
 
18
- <|ref|>title<|/ref|><|det|>[[510, 432, 597, 445]]<|/det|>
19
- # FEATURES
20
-
21
- <|ref|>text<|/ref|><|det|>[[510, 455, 924, 485]]<|/det|>
22
- ·Easier start-up and programming with Start-Up Genie
23
-
24
- <|ref|>text<|/ref|><|det|>[[510, 476, 888, 506]]<|/det|>
25
- ·Wide range of standard and permanent magnet motors with power up to 600 hp
26
-
27
- <|ref|>text<|/ref|><|det|>[[510, 512, 935, 542]]<|/det|>
28
- ·Multi-pump configuration for up to four (4) pumps - no need for programmable logic controller (PLC)
29
-
30
- <|ref|>text<|/ref|><|det|>[[510, 548, 888, 576]]<|/det|>
31
- ·Remote commissioning and monitoring with USB connectivity and software
32
-
33
- <|ref|>text<|/ref|><|det|>[[510, 584, 928, 613]]<|/det|>
34
- ·Two wire multi-pump connection for faster installation
35
-
36
- <|ref|>text<|/ref|><|det|>[[510, 612, 921, 643]]<|/det|>
37
- ·Hand on, off, and auto-on buttons available for easy pump operation at the keypad. No toggling between local and remote operation
38
-
39
- <|ref|>text<|/ref|><|det|>[[510, 654, 939, 682]]<|/det|>
40
- ·System redundancy with multi-master control in case of drive failure
41
-
42
- <|ref|>text<|/ref|><|det|>[[510, 691, 922, 720]]<|/det|>
43
- ·BACnet and Modbus as a standard for seamless BMS integration
44
-
45
- <|ref|>text<|/ref|><|det|>[[510, 730, 860, 743]]<|/det|>
46
- ·Submersible and above ground applications
47
-
48
- <|ref|>text<|/ref|><|det|>[[510, 751, 864, 764]]<|/det|>
49
- ·Wide range of voltage and enclosure options
50
-
51
- <|ref|>text<|/ref|><|det|>[[510, 772, 679, 784]]<|/det|>
52
- ·True 208 V coverage
53
-
54
- <|ref|>text<|/ref|><|det|>[[510, 793, 746, 806]]<|/det|>
55
- ·Dedicated single phase input
56
-
57
- <|ref|>text<|/ref|><|det|>[[510, 815, 890, 844]]<|/det|>
58
- ·Remote commissioning and monitoring with USB connectivity and software
59
-
60
- <|ref|>text<|/ref|><|det|>[[510, 852, 890, 866]]<|/det|>
61
- ·In-panel or handheld keypad with backlit display
62
-
63
- <|ref|>text<|/ref|><|det|>[[510, 873, 910, 886]]<|/det|>
64
- ·Alarm Log for last 5 alarms and maintenance events
65
-
66
- <|ref|>text<|/ref|><|det|>[[510, 893, 907, 922]]<|/det|>
67
- ·EMC/RFI filters and dual DC-link reactors to reduce drive noise emissions and interference
68
-
69
- <|ref|>text<|/ref|><|det|>[[510, 929, 861, 958]]<|/det|>
70
- ·I/O expansion cards, factory installed or field configured
 
1
+ 0 to 70% (vs. fixed speed) while reducing installation time.
2
 
3
+ <|ref|>image<|/ref|><|det|>[[55, 240, 405, 515]]<|/det|>
 
4
 
5
+ <|ref|>sub_title<|/ref|><|det|>[[55, 525, 199, 540]]<|/det|>
6
+ ## SPECIFICATIONS
7
 
8
+ <|ref|>table<|/ref|><|det|>[[55, 546, 487, 954]]<|/det|>
 
9
 
10
+ <table><tr><td>Indoor enclosures</td><td>IP20 Open, TYPE 1, TYPE 12</td></tr><tr><td>Outdoor enclosures</td><td>TYPE 3R, TYPE 4X</td></tr><tr><td>Input supply</td><td>1.5 - 600 hp (frame A - D) wall or base mounted</td></tr><tr><td>Ambient temperature</td><td>14°F - 113°F (-10°C - 45°C)</td></tr><tr><td>Communication</td><td>Higher temperatures can be achieved by derating the output amperage of the drive 10% for up to 122°F (50°C)</td></tr><tr><td>Altitudes</td><td>Modbus® RTU, Metasys N2, FLN, and BACnet standard<br>Others available with option cards</td></tr><tr><td>Relative humidity</td><td>At altitudes from 0 to 1,000 meters (0 to 3,300 ft)<br>Nameplate rated current is available<br>Derate for altitudes above 1,000 (3,300 ft) with a maximum operating altitude of 3,000 m (9,900 ft)<br>Consult factory for applications above 3,000 m (9,900 ft)</td></tr><tr><td>Electrical input power</td><td>Lower than 95% without condensation</td></tr><tr><td>Electrical input power</td><td>3 phase 380 V to 480 V ±10%<br>1 phase 200 V to 240 V ±10%<br>3 phase 200 V to 240 V ±10%<br>3 phase 525 V to 600 V ±10%<br>Frequency 50 or 60 Hz, ±2 Hz</td></tr><tr><td>Electrical output power</td><td>3 phase from 0 to V supply</td></tr></table>
11
 
12
+ <|ref|>sub_title<|/ref|><|det|>[[511, 307, 751, 385]]<|/det|>
13
+ ## AQUAVAR® IPC VARIABLE SPEED CONTROLLER
14
 
15
+ <|ref|>sub_title<|/ref|><|det|>[[512, 431, 597, 446]]<|/det|>
16
+ ## FEATURES
17
 
18
+ <|ref|>text<|/ref|><|det|>[[511, 451, 934, 955]]<|/det|>
19
+ - Easier start-up and programming with Start-Up Genie- Wide range of standard and permanent magnet motors with power up to 600 hp- Multi-pump configuration for up to four (4) pumps - no need for programmable logic controller (PLC)- Remote commissioning and monitoring with USB connectivity and software- Two wire multi-pump connection for faster installation- Hand on, off, and auto-on buttons available for easy pump operation at the keypad. No toggling between local and remote operation- System redundancy with multi-master control in case of drive failure- BACnet and Modbus as a standard for seamless BMS integration- Submersible and above ground applications- Wide range of voltage and enclosure options- True 208 V coverage- Dedicated single phase input- Remote commissioning and monitoring with USB connectivity and software- In-panel or handheld keypad with backlit display- Alarm Log for last 5 alarms and maintenance events- EMC/RFI filters and dual DC-link reactors to reduce drive noise emissions and interference- I/O expansion cards, factory installed or field configured
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
sample_00004/document.md CHANGED
@@ -1,25 +1,21 @@
1
- 2645-9248 Journal homepage: www.jidhealth.com Open A ccess
2
 
3
- Original Article
4
 
5
- # A case report on generalized pemphigus vulgaris treated with rituximaba
6
 
7
- J agdish J adavbhai Sakhiya1*, Dhruv J agdish Sakhiya1, J ashmine Mukeshbhai Gandhi1, Feral Ravi Daruwala2
8
 
9
- ## Abstract
10
 
11
- **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.
12
 
13
- **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.
14
 
15
- **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.
16
 
17
- **Keywords:** Autoantibodies; Pemphigus, Rituximab, Oral Hygiene, Ulceration, Tobacco Smoking, Alcohol
18
 
19
- consumption, India
20
 
21
- ## Background
22
-
23
- 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 life-threatening 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
24
-
25
- 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
 
1
+ 2645-9248 Journal homepage: www.jidhealth.com 0pen A ccess
2
 
3
+ # A case report on generalized pemphigus vulgaris treated with rituximaba
4
 
5
+ J agdish J adavbhai Sakhiya \(^{1\ast}\) , Dhruv J agdish Sakhiya \(^{1}\) , J ashmine Mukeshbhai Gandhi \(^{1}\) , Feral Ravi Daruwala \(^{2}\)
6
 
7
+ ## Abstract
8
 
9
+ 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.
10
 
11
+ 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.
12
 
13
+ 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.
14
 
15
+ Keywords: Autoantibodies; Pemphigus, Rituximab, Oral Hygiene, Ulceration, Tobacco Smoking, Alcohol consumption, India
16
 
17
+ ## Background
18
 
19
+ 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 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
20
 
21
+ 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
 
 
 
 
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sample_00004/raw_response.md CHANGED
@@ -1,37 +1,31 @@
1
- 2645-9248 Journal homepage: www.jidhealth.com Open A ccess
2
 
3
- <|ref|>text<|/ref|><|det|>[[90, 181, 204, 193]]<|/det|>
4
- Original Article
5
 
6
- <|ref|>title<|/ref|><|det|>[[88, 217, 793, 265]]<|/det|>
7
- # A case report on generalized pemphigus vulgaris treated with rituximaba
8
 
9
- <|ref|>text<|/ref|><|det|>[[88, 293, 893, 326]]<|/det|>
10
- J agdish J adavbhai Sakhiya1*, Dhruv J agdish Sakhiya1, J ashmine Mukeshbhai Gandhi1, Feral Ravi Daruwala2
11
 
12
- <|ref|>sub_title<|/ref|><|det|>[[101, 351, 176, 364]]<|/det|>
13
- ## Abstract
14
 
15
- <|ref|>text<|/ref|><|det|>[[101, 368, 876, 406]]<|/det|>
16
- **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.
17
 
18
- <|ref|>text<|/ref|><|det|>[[101, 415, 887, 478]]<|/det|>
19
- **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.
20
 
21
- <|ref|>text<|/ref|><|det|>[[101, 488, 894, 515]]<|/det|>
22
- **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.
23
 
24
- <|ref|>text<|/ref|><|det|>[[101, 526, 812, 539]]<|/det|>
25
- **Keywords:** Autoantibodies; Pemphigus, Rituximab, Oral Hygiene, Ulceration, Tobacco Smoking, Alcohol
26
 
27
- <|ref|>text<|/ref|><|det|>[[101, 545, 231, 557]]<|/det|>
28
- consumption, India
29
 
30
- <|ref|>sub_title<|/ref|><|det|>[[90, 597, 192, 611]]<|/det|>
31
- ## Background
32
-
33
- <|ref|>text<|/ref|><|det|>[[90, 612, 484, 835]]<|/det|>
34
- 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 life-threatening 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
35
-
36
- <|ref|>text<|/ref|><|det|>[[512, 597, 905, 904]]<|/det|>
37
- 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
 
1
+ 2645-9248 Journal homepage: www.jidhealth.com 0pen A ccess
2
 
3
+ <|ref|>title<|/ref|><|det|>[[87, 216, 794, 265]]<|/det|>
4
+ # A case report on generalized pemphigus vulgaris treated with rituximaba
5
 
6
+ <|ref|>text<|/ref|><|det|>[[87, 291, 894, 327]]<|/det|>
7
+ J agdish J adavbhai Sakhiya \(^{1\ast}\) , Dhruv J agdish Sakhiya \(^{1}\) , J ashmine Mukeshbhai Gandhi \(^{1}\) , Feral Ravi Daruwala \(^{2}\)
8
 
9
+ <|ref|>sub_title<|/ref|><|det|>[[102, 350, 175, 363]]<|/det|>
10
+ ## Abstract
11
 
12
+ <|ref|>text<|/ref|><|det|>[[101, 366, 876, 404]]<|/det|>
13
+ 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.
14
 
15
+ <|ref|>text<|/ref|><|det|>[[101, 413, 888, 476]]<|/det|>
16
+ 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.
17
 
18
+ <|ref|>text<|/ref|><|det|>[[100, 486, 893, 514]]<|/det|>
19
+ 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.
20
 
21
+ <|ref|>text<|/ref|><|det|>[[100, 523, 815, 557]]<|/det|>
22
+ Keywords: Autoantibodies; Pemphigus, Rituximab, Oral Hygiene, Ulceration, Tobacco Smoking, Alcohol consumption, India
23
 
24
+ <|ref|>sub_title<|/ref|><|det|>[[92, 594, 192, 609]]<|/det|>
25
+ ## Background
26
 
27
+ <|ref|>text<|/ref|><|det|>[[92, 610, 484, 835]]<|/det|>
28
+ 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 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
29
 
30
+ <|ref|>text<|/ref|><|det|>[[512, 594, 904, 902]]<|/det|>
31
+ 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
 
 
 
 
 
 
sample_00005/document.md CHANGED
@@ -29,4 +29,4 @@ The administered dose may increase using 2D- mode and vary for other systems acc
29
 
30
  ## Radiation Dosimetry of Brain Transmission Scans
31
 
32
- Based on transmission scans of 10 min and CT- based scans of 5- 10 s, the effective doses per scan are: 20- 30 μSv for Germanium- based transmission, \(\sim 20\) μSv for low- dose high- speed CT, and between 220 and 450 μSv for high- quality CT.
 
29
 
30
  ## Radiation Dosimetry of Brain Transmission Scans
31
 
32
+ Based on transmission scans of 10 min and CT- based scans of 5- 10 s, the effective doses per scan are: 20- 30 \(\mu \mathrm{Sv}\) for Germanium- based transmission, \(\sim 20 \mu \mathrm{Sv}\) for low- dose high- speed CT, and between 220 and \(450 \mu \mathrm{Sv}\) for high- quality CT.
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@@ -39,8 +39,8 @@ The administered dose may increase using 2D- mode and vary for other systems acc
39
  <|ref|>sub_title<|/ref|><|det|>[[511, 722, 775, 739]]<|/det|>
40
  ## Radiation Dosimetry (Table 2.1)
41
 
42
- <|ref|>sub_title<|/ref|><|det|>[[511, 749, 866, 784]]<|/det|>
43
  ## Radiation Dosimetry of Brain Transmission Scans
44
 
45
- <|ref|>text<|/ref|><|det|>[[510, 794, 886, 903]]<|/det|>
46
- Based on transmission scans of 10 min and CT- based scans of 5- 10 s, the effective doses per scan are: 20- 30 μSv for Germanium- based transmission, \(\sim 20\) μSv for low- dose high- speed CT, and between 220 and 450 μSv for high- quality CT.
 
39
  <|ref|>sub_title<|/ref|><|det|>[[511, 722, 775, 739]]<|/det|>
40
  ## Radiation Dosimetry (Table 2.1)
41
 
42
+ <|ref|>sub_title<|/ref|><|det|>[[510, 749, 865, 784]]<|/det|>
43
  ## Radiation Dosimetry of Brain Transmission Scans
44
 
45
+ <|ref|>text<|/ref|><|det|>[[510, 793, 885, 903]]<|/det|>
46
+ Based on transmission scans of 10 min and CT- based scans of 5- 10 s, the effective doses per scan are: 20- 30 \(\mu \mathrm{Sv}\) for Germanium- based transmission, \(\sim 20 \mu \mathrm{Sv}\) for low- dose high- speed CT, and between 220 and \(450 \mu \mathrm{Sv}\) for high- quality CT.
sample_00006/document.md CHANGED
@@ -62,7 +62,7 @@ Future work aims to fully identify load induced tissue changes in healthy and di
62
  REFERENCES
63
 
64
  [1] Creane et al., Biomech Model Mechanobiol., 10: 831-843, 2011
65
- [2] Billiar, K., and Sacks, M., J. Biomech. 30: 7537 56, 1997
66
 
67
  ACKNOWLEDGEMENTS
68
 
 
62
  REFERENCES
63
 
64
  [1] Creane et al., Biomech Model Mechanobiol., 10: 831-843, 2011
65
+ [2] Billiar, K., and Sacks, M., J. Biomech. 30: 753-7 56, 1997
66
 
67
  ACKNOWLEDGEMENTS
68
 
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sample_00006/raw_response.md CHANGED
@@ -59,42 +59,42 @@ An in-house SALS system has been developed making use of an unpolarised 5mW HeNe
59
  <|ref|>text<|/ref|><|det|>[[144, 684, 472, 788]]<|/det|>
60
  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.
61
 
62
- <|ref|>sub_title<|/ref|><|det|>[[144, 802, 225, 815]]<|/det|>
63
  RESULTS
64
 
65
- <|ref|>text<|/ref|><|det|>[[144, 824, 472, 903]]<|/det|>
66
  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 (\(\lambda = 1.25\)).
67
 
68
- <|ref|>text<|/ref|><|det|>[[527, 239, 850, 277]]<|/det|>
69
  Collagen fibre patterns in the artery were also obtained through the thickness of the artery wall using SALS, for both strained and unstrained configurations.
70
 
71
- <|ref|>image<|/ref|><|det|>[[527, 289, 838, 415]]<|/det|>
72
 
73
 
74
- <|ref|>image_caption<|/ref|><|det|>[[527, 417, 850, 453]]<|/det|>
75
  <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>
76
 
77
- <|ref|>sub_title<|/ref|><|det|>[[527, 466, 633, 480]]<|/det|>
78
  DISCUSSION
79
 
80
- <|ref|>text<|/ref|><|det|>[[527, 489, 850, 579]]<|/det|>
81
  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.
82
 
83
- <|ref|>text<|/ref|><|det|>[[527, 584, 850, 651]]<|/det|>
84
  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.
85
 
86
- <|ref|>text<|/ref|><|det|>[[527, 655, 850, 695]]<|/det|>
87
  Future work aims to fully identify load induced tissue changes in healthy and diseased arterial tissue using SALS.
88
 
89
- <|ref|>sub_title<|/ref|><|det|>[[527, 708, 642, 722]]<|/det|>
90
  REFERENCES
91
 
92
- <|ref|>text<|/ref|><|det|>[[527, 731, 850, 782]]<|/det|>
93
  [1] Creane et al., Biomech Model Mechanobiol., 10: 831-843, 2011
94
- [2] Billiar, K., and Sacks, M., J. Biomech. 30: 7537 56, 1997
95
 
96
- <|ref|>sub_title<|/ref|><|det|>[[527, 797, 719, 811]]<|/det|>
97
  ACKNOWLEDGEMENTS
98
 
99
- <|ref|>text<|/ref|><|det|>[[527, 819, 850, 856]]<|/det|>
100
  This research was part funded by Science Foundation Ireland (SFI/13/ERC/B2775) and the Irish Research Council (GOIPG/2014/515).
 
59
  <|ref|>text<|/ref|><|det|>[[144, 684, 472, 788]]<|/det|>
60
  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.
61
 
62
+ <|ref|>sub_title<|/ref|><|det|>[[144, 802, 223, 816]]<|/det|>
63
  RESULTS
64
 
65
+ <|ref|>text<|/ref|><|det|>[[144, 825, 472, 903]]<|/det|>
66
  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 (\(\lambda = 1.25\)).
67
 
68
+ <|ref|>text<|/ref|><|det|>[[526, 238, 852, 277]]<|/det|>
69
  Collagen fibre patterns in the artery were also obtained through the thickness of the artery wall using SALS, for both strained and unstrained configurations.
70
 
71
+ <|ref|>image<|/ref|><|det|>[[526, 290, 837, 412]]<|/det|>
72
 
73
 
74
+ <|ref|>image_caption<|/ref|><|det|>[[526, 413, 852, 450]]<|/det|>
75
  <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>
76
 
77
+ <|ref|>sub_title<|/ref|><|det|>[[526, 464, 630, 479]]<|/det|>
78
  DISCUSSION
79
 
80
+ <|ref|>text<|/ref|><|det|>[[526, 487, 852, 579]]<|/det|>
81
  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.
82
 
83
+ <|ref|>text<|/ref|><|det|>[[526, 583, 852, 650]]<|/det|>
84
  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.
85
 
86
+ <|ref|>text<|/ref|><|det|>[[526, 653, 852, 693]]<|/det|>
87
  Future work aims to fully identify load induced tissue changes in healthy and diseased arterial tissue using SALS.
88
 
89
+ <|ref|>sub_title<|/ref|><|det|>[[526, 707, 641, 722]]<|/det|>
90
  REFERENCES
91
 
92
+ <|ref|>text<|/ref|><|det|>[[526, 730, 852, 781]]<|/det|>
93
  [1] Creane et al., Biomech Model Mechanobiol., 10: 831-843, 2011
94
+ [2] Billiar, K., and Sacks, M., J. Biomech. 30: 753-7 56, 1997
95
 
96
+ <|ref|>sub_title<|/ref|><|det|>[[526, 796, 716, 810]]<|/det|>
97
  ACKNOWLEDGEMENTS
98
 
99
+ <|ref|>text<|/ref|><|det|>[[526, 817, 852, 856]]<|/det|>
100
  This research was part funded by Science Foundation Ireland (SFI/13/ERC/B2775) and the Irish Research Council (GOIPG/2014/515).
sample_00007/document.md CHANGED
@@ -1 +1 @@
1
- 2011, XLVl, 394 p., Hardcover ISBN: 978-90-481-8664-8
 
1
+ 2011, XLVI, 394 p., HardcoverISBN: 978-90-481-8664-8
sample_00007/raw_response.md CHANGED
@@ -1 +1 @@
1
- 2011, XLVl, 394 p., Hardcover ISBN: 978-90-481-8664-8
 
1
+ 2011, XLVI, 394 p., HardcoverISBN: 978-90-481-8664-8
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1
- 14 kV, which permits the conversion of the Hounsfield units into attenuation coefficients at 511 keV. The CT scan can be performed after the injection of FDG and has the advantage to significantly reduce the total scan time (usual duration is <10 s). However, the dose of the CT scan to the patient can be reduced by lowering the tube current (see radiation dosimetry above) if anatomical information is not needed. When performing PET-CT of the brain it is recommended to check for movements between the CT and the PET sessions, which might produce artefacts in the attenuation correction.
2
 
3
- Emission scan. As semiquantitative estimates of tumor- to- background uptake ratios are typically used, it is recommended to use a standardized acquisition protocol with a fixed time for start of acquisition to make the data of different patients or repeated scans comparable. If data are acquired in 3- D mode, appropriate scatter correction is mandatory. The duration of emission image acquisition should be related to the minimum required number of counts. For FDG, typically data are acquired over 15- 30 min aiming to collect 50- 200 million counts. Even though shorter acquisition times can still be used for diagnostic pattern evaluation (Chen et al. 2005), a minimum of 15 min in 3D mode is advocated. For MET and FET typically data are acquired for 20 min (20- 40 min p.i.), often supplemented by dynamic data starting directly with tracer injection.
4
 
5
- ## IMT Single Photon Emission Tomography
6
 
7
- - Multiple detectors (triple or dual head) or other dedicated SPECT cameras for brain imaging should be used for acquisition. Single detector units cannot generally be recommended. They may only be used if scan time is prolonged appropriately, a dose in the upper suggested range is applied, and meticulous care is taken to produce high-quality images.
8
 
9
- - LEHR or LEUHR parallel-hole collimators are the mostly available collimator sets for brain imaging. All purpose collimators are not suitable. The use of medium energy collimators could be advantageous; however, usually they are hampered by a low sensitivity. They may only be used if acceptable count rates are obtained. If available, collimator sets specifically adapted to the characteristics of \(^{123}\mathrm{I}\) may be used. Fanbeam collimators may be generally preferred over parallel-hole collimators due to the advantageous trade-off between resolution and count rate capability. The acquisition parameters are summarized in Table 2.2.
10
 
11
- ## TABLE 2.2. Acquisition parameters for IMT-SPECT
12
 
13
- - Rotational radius: smallest possible with appropriate patient safeguard- Matrix: \(128 \times 128\) - Angular sampling: \(\leq 3^{\circ}\) (360° rotation)- Zoom: acquisition pixel size should be \(1 / 3 - 1 / 2\) of the expected resolution; therefore it may be necessary to use a hardware zoom to achieve an appropriate pixel size- Acquisition mode: Step and shoot mode is predominantly used. Continuous mode acquisition may provide shorter total scan time, reduce mechanical wear to the system and improve patient comfort- Total scan time: depending on the imaging device, typical scan time for a triple head camera is about 30-50 min (e.g., 120 projections; 40 projections per head; 60 s/projection)
 
 
 
 
 
 
1
+ purpose of attenuation correction. The scanning parameters may vary according to the type of CT scanner. Usually the tube voltage is set at \(140 \text{kV}\) , which permits the conversion of the Hounsfield units into attenuation coefficients at 511 keV. The CT scan can be performed after the injection of FDG and has the advantage to significantly reduce the total scan time (usual duration is \(<10 \text{s}\) ). However, the dose of the CT scan to the patient can be reduced by lowering the tube current (see radiation dosimetry above) if anatomical information is not needed. When performing PET-CT of the brain it is recommended to check for movements between the CT and the PET sessions, which might produce artefacts in the attenuation correction.
2
 
3
+ - Emission scan. As semiquantitative estimates of tumor-to-background uptake ratios are typically used, it is recommended to use a standardized acquisition protocol with a fixed time for start of acquisition to make the data of different patients or repeated scans comparable. If data are acquired in 3-D mode, appropriate scatter correction is mandatory. The duration of emission image acquisition should be related to the minimum required number of counts. For FDG, typically data are acquired over \(15-30 \text{min}\) aiming to collect \(50-200 \text{million counts}\). Even though shorter acquisition times can still be used for diagnostic pattern evaluation (Chen et al. 2005), a minimum of 15 min in 3D mode is advocated. For MET and FET typically data are acquired for 20 min (20-40 min p.i.), often supplemented by dynamic data starting directly with tracer injection.
4
 
5
+ ## IMT Single Photon Emission Tomography
6
 
7
+ - Multiple detectors (triple or dual head) or other dedicated SPECT cameras for brain imaging should be used for acquisition. Single detector units cannot generally be recommended. They may only be used if scan time is prolonged appropriately, a dose in the upper suggested range is applied, and meticulous care is taken to produce high-quality images.
8
 
9
+ - LEHR or LEUHR parallel-hole collimators are the mostly available collimator sets for brain imaging. All purpose collimators are not suitable. The use of medium energy collimators could be advantageous; however, usually they are hampered by a low sensitivity. They may only be used if acceptable count rates are obtained. If available, collimator sets specifically adapted to the characteristics of \(^{123}\text{I}\) may be used. Fanbeam collimators may be generally preferred over parallel-hole collimators due to the advantageous trade-off between resolution and count rate capability. The acquisition parameters are summarized in Table 2.2.
10
 
11
+ TABLE 2.2. Acquisition parameters for IMT-SPECT
12
 
13
+ - Rotational radius: smallest possible with appropriate patient safeguard
14
+ - Matrix: \(128 \times 128\)
15
+ - Angular sampling: \(\leq 3^\circ\) (360° rotation)
16
+ - Zoom: acquisition pixel size should be \(1/3-1/2\) of the expected resolution; therefore it may be necessary to use a hardware zoom to achieve an appropriate pixel size
17
+ - Acquisition mode: Step and shoot mode is predominantly used. Continuous mode acquisition may provide shorter total scan time, reduce mechanical wear to the system and improve patient comfort
18
+ - Total scan time: depending on the imaging device, typical scan time for a triple head camera is about 30-50 min (e.g., 120 projections; 40 projections per head; 60 s/projection)
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sample_00009/raw_response.md CHANGED
@@ -1,19 +1,25 @@
1
- 14 kV, which permits the conversion of the Hounsfield units into attenuation coefficients at 511 keV. The CT scan can be performed after the injection of FDG and has the advantage to significantly reduce the total scan time (usual duration is <10 s). However, the dose of the CT scan to the patient can be reduced by lowering the tube current (see radiation dosimetry above) if anatomical information is not needed. When performing PET-CT of the brain it is recommended to check for movements between the CT and the PET sessions, which might produce artefacts in the attenuation correction.
 
2
 
3
- <|ref|>text<|/ref|><|det|>[[117, 441, 491, 896]]<|/det|>
4
- Emission scan. As semiquantitative estimates of tumor- to- background uptake ratios are typically used, it is recommended to use a standardized acquisition protocol with a fixed time for start of acquisition to make the data of different patients or repeated scans comparable. If data are acquired in 3- D mode, appropriate scatter correction is mandatory. The duration of emission image acquisition should be related to the minimum required number of counts. For FDG, typically data are acquired over 15- 30 min aiming to collect 50- 200 million counts. Even though shorter acquisition times can still be used for diagnostic pattern evaluation (Chen et al. 2005), a minimum of 15 min in 3D mode is advocated. For MET and FET typically data are acquired for 20 min (20- 40 min p.i.), often supplemented by dynamic data starting directly with tracer injection.
5
 
6
- <|ref|>sub_title<|/ref|><|det|>[[511, 81, 826, 97]]<|/det|>
7
- ## IMT Single Photon Emission Tomography
8
 
9
- <|ref|>text<|/ref|><|det|>[[510, 108, 886, 298]]<|/det|>
10
- - Multiple detectors (triple or dual head) or other dedicated SPECT cameras for brain imaging should be used for acquisition. Single detector units cannot generally be recommended. They may only be used if scan time is prolonged appropriately, a dose in the upper suggested range is applied, and meticulous care is taken to produce high-quality images.
11
 
12
- <|ref|>text<|/ref|><|det|>[[510, 301, 886, 619]]<|/det|>
13
- - LEHR or LEUHR parallel-hole collimators are the mostly available collimator sets for brain imaging. All purpose collimators are not suitable. The use of medium energy collimators could be advantageous; however, usually they are hampered by a low sensitivity. They may only be used if acceptable count rates are obtained. If available, collimator sets specifically adapted to the characteristics of \(^{123}\mathrm{I}\) may be used. Fanbeam collimators may be generally preferred over parallel-hole collimators due to the advantageous trade-off between resolution and count rate capability. The acquisition parameters are summarized in Table 2.2.
14
 
15
- <|ref|>sub_title<|/ref|><|det|>[[511, 684, 858, 699]]<|/det|>
16
- ## TABLE 2.2. Acquisition parameters for IMT-SPECT
17
 
18
- <|ref|>text<|/ref|><|det|>[[510, 705, 881, 892]]<|/det|>
19
- - Rotational radius: smallest possible with appropriate patient safeguard- Matrix: \(128 \times 128\) - Angular sampling: \(\leq 3^{\circ}\) (360° rotation)- Zoom: acquisition pixel size should be \(1 / 3 - 1 / 2\) of the expected resolution; therefore it may be necessary to use a hardware zoom to achieve an appropriate pixel size- Acquisition mode: Step and shoot mode is predominantly used. Continuous mode acquisition may provide shorter total scan time, reduce mechanical wear to the system and improve patient comfort- Total scan time: depending on the imaging device, typical scan time for a triple head camera is about 30-50 min (e.g., 120 projections; 40 projections per head; 60 s/projection)
 
 
 
 
 
 
1
+ <|ref|>text<|/ref|><|det|>[[137, 87, 492, 440]]<|/det|>
2
+ purpose of attenuation correction. The scanning parameters may vary according to the type of CT scanner. Usually the tube voltage is set at \(140 \text{kV}\) , which permits the conversion of the Hounsfield units into attenuation coefficients at 511 keV. The CT scan can be performed after the injection of FDG and has the advantage to significantly reduce the total scan time (usual duration is \(<10 \text{s}\) ). However, the dose of the CT scan to the patient can be reduced by lowering the tube current (see radiation dosimetry above) if anatomical information is not needed. When performing PET-CT of the brain it is recommended to check for movements between the CT and the PET sessions, which might produce artefacts in the attenuation correction.
3
 
4
+ <|ref|>text<|/ref|><|det|>[[115, 444, 492, 897]]<|/det|>
5
+ - Emission scan. As semiquantitative estimates of tumor-to-background uptake ratios are typically used, it is recommended to use a standardized acquisition protocol with a fixed time for start of acquisition to make the data of different patients or repeated scans comparable. If data are acquired in 3-D mode, appropriate scatter correction is mandatory. The duration of emission image acquisition should be related to the minimum required number of counts. For FDG, typically data are acquired over \(15-30 \text{min}\) aiming to collect \(50-200 \text{million counts}\). Even though shorter acquisition times can still be used for diagnostic pattern evaluation (Chen et al. 2005), a minimum of 15 min in 3D mode is advocated. For MET and FET typically data are acquired for 20 min (20-40 min p.i.), often supplemented by dynamic data starting directly with tracer injection.
6
 
7
+ <|ref|>sub_title<|/ref|><|det|>[[511, 83, 826, 99]]<|/det|>
8
+ ## IMT Single Photon Emission Tomography
9
 
10
+ <|ref|>text<|/ref|><|det|>[[511, 108, 886, 299]]<|/det|>
11
+ - Multiple detectors (triple or dual head) or other dedicated SPECT cameras for brain imaging should be used for acquisition. Single detector units cannot generally be recommended. They may only be used if scan time is prolonged appropriately, a dose in the upper suggested range is applied, and meticulous care is taken to produce high-quality images.
12
 
13
+ <|ref|>text<|/ref|><|det|>[[511, 302, 886, 618]]<|/det|>
14
+ - LEHR or LEUHR parallel-hole collimators are the mostly available collimator sets for brain imaging. All purpose collimators are not suitable. The use of medium energy collimators could be advantageous; however, usually they are hampered by a low sensitivity. They may only be used if acceptable count rates are obtained. If available, collimator sets specifically adapted to the characteristics of \(^{123}\text{I}\) may be used. Fanbeam collimators may be generally preferred over parallel-hole collimators due to the advantageous trade-off between resolution and count rate capability. The acquisition parameters are summarized in Table 2.2.
15
 
16
+ <|ref|>table_caption<|/ref|><|det|>[[511, 686, 855, 701]]<|/det|>
17
+ TABLE 2.2. Acquisition parameters for IMT-SPECT
18
 
19
+ <|ref|>text<|/ref|><|det|>[[511, 707, 880, 893]]<|/det|>
20
+ - Rotational radius: smallest possible with appropriate patient safeguard
21
+ - Matrix: \(128 \times 128\)
22
+ - Angular sampling: \(\leq 3^\circ\) (360° rotation)
23
+ - Zoom: acquisition pixel size should be \(1/3-1/2\) of the expected resolution; therefore it may be necessary to use a hardware zoom to achieve an appropriate pixel size
24
+ - Acquisition mode: Step and shoot mode is predominantly used. Continuous mode acquisition may provide shorter total scan time, reduce mechanical wear to the system and improve patient comfort
25
+ - Total scan time: depending on the imaging device, typical scan time for a triple head camera is about 30-50 min (e.g., 120 projections; 40 projections per head; 60 s/projection)