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Sa1995 The Prevalence of Irritable Bowel Syndrome-Like Symptoms in Pediatric Inflammatory Bowel Disease
AGA Abstracts
Sa1993
Sa1994
Specific Inhibitor of Importin-α Mediated Nuclear Transport - Ivermectin Reduces VEGF Expression and Inhibits Colon Cancer Cell Proliferation Amrita Ahluwalia, Michael K. Jones, Andrzej S. Tarnawski
Long-Term Outcome of Children Born to IBD Mothers Preliminary Result From a Multicenter Retrospective Study in the Netherlands Shannon L. Kanis, Alison de Lima, Zuzana Zelinkova, Gerard Dijkstra, Rachel West, Rob J. Ouwendijk, Nanne K. de Boer, Andrea E. van der Meulen - de Jong, Marie J. Pierik, Liekele E. Oostenbrug, Mariëlle Romberg-Camps, Alexander Bodelier, Bas Oldenburg, Frank Hoentjen, Ruud Beukers, Jeroen M. Jansen, Christien J. van der Woude
Background & Aims: Colorectal cancer (CRC) cells (unlike normal colonic epithelial cells) secrete VEGF, which drives these cells proliferation and promotes tumor-related angiogenesis. The mechanism(s) of increased, aberrant VEGF expression in CRC cells is not known, but is likely related to transcriptional activation of VEGF gene. We hypothesized that: 1) upregulated importin-α in CRC cells (which facilitates nuclear transport of transcription factors: HIF1α and CREB, and is essential for VEGF gene promoter activation) is the underlying mechanism for increased VEGF expression in these cells and CRC cell proliferation, and, 2) inhibition and/or silencing of importin-α in CRC cells will inhibit VEGF gene activation and CRC cell proliferation. Ivermectin is a specific inhibitor of importin α nuclear transport (Biochem J. 2012: 1;443(3):851-6). We examined whether treatment of CRC cell lines with ivermectin could inhibit CRC cell growth. Methods: We used: (a) human CRC cell lines - HCT116 & HT29 and (b) normal colonic epithelial cells - NCM356 & NCM460. We treated cultured CRC cells with ivermectin (50 μM, 6 hr; specific inhibitor of importin-α nuclear transport), with importin α specific siRNA or control RNA (100nM, 48 hr). Add-back studies included treatment with exogenous VEGF (20ng/ml). Studies: 1) mRNA and protein expression of importin-α and VEGF by Real-Time RT-PCR, and/or Western blotting and immunostaining, respectively; 2) VEGF secretion into culture medium by ELISA; 3) translocation of importin to the nucleus in CRC vs. normal cells; and 4) cell proliferation by BrdU assay. Results: 1) CRC cell lines express high levels of VEGF and secrete large amounts of VEGF (up to 1530 pg/ml) into culture medium at 24 hours vs. normal epithelial cells, which only secrete minimal VEGF (<34 pg/ml); 2) Importin-α expression is significantly increased in CRC cell lines vs. normal epithelial cells by >40% (p< 0.05); 3) Selective inhibition of importin-α in CRC cells using ivermectin significantly reduced VEGF expression by ~3-fold (p<0.01) and proliferation of these cells by 2.4-fold (p<0.01). Treatment with exogenous VEGF partly reversed inhibited by ivermectin cell proliferation; 4) Importin-α silencing in CRC cells significantly reduced VEGF expression and proliferation of these cells by 2.2-fold and 2fold (both p<0.01), respectively; treatment with exogenous VEGF following importin-α silencing reversed inhibition of cell proliferation by 2-fold (p < 0.01). Conclusions: 1) VEGF gene activation in CRC cells requires functional importin-α; 2) importin-α mediates increased proliferation of CRC cells; downregulation of importin-α with specific siRNA or its inhibition with specific inhibitor - ivermectin inhibits CRC cell proliferation; 3) These studies suggest a potential therapeutic role of ivermectin in inhibiting CRC cell proliferation.
Background The long term outcome of children born to mothers with inflammatory bowel disease(IBD) are relatively unexplored. The aim of this study is to analyze the health status of children who were born to mothers with IBD. Methods All women diagnosed with IBD prior to their pregnancy that gave birth between 1999 and 2011 were invited. After informed consent from both parents, the general practitioner (GP) was contacted for the following child outcomes: growth, number of infections for which antibiotics were needed, allergies and allergic reactions to vaccinations. Low birth weight was stated as <2500g, preterm birth as gestational age <37 weeks. The EUROCAT guideline was used to classify congenital abnormalities. Results In total 935 invitations (in 2 rounds) were sent to women with IBD from 8 Dutch hospitals. The response was 46.8%(438). Until November 2014 362 children from 239 IBD mothers (257(71.0%) CD, 93(25.7%) UC and 12(3.3%) IBDU) were included. Median child age at follow up was 6 years (IQR 4-11). In utero 118(32.6%) children were not exposed to any IBD drug, 97(26.8%) to only mesalazine, 79(21.8%) to thiopurine, 38(10.5%) to anti- TNF, 20(5.5%) to both anti- TNF and thiopurine and for 10(2.8%) children drug exposure was unknown. There was no difference in anti- TNF exposed and the non- anti TNF exposed children considering; median gestational age (39 weeks(IQR3840)), pre- term births (67(18.5%)), overall birth weight (3268 gram(IQR 2893-3638)), low birth weight (40(11 %)) and major congenital abnormalities (8(2.2 %)). Five(1.5%) children showed a primary or secondary growth deficiency. None of these children were exposed to anti- TNF. Apart from one extended rash after vaccination there were no reports of severe vaccination reactions. Overall 88 children had allergies. These allergies were more common in the non- anti TNF exposed children (36.9%)compared to the anti- TNF exposed children (15.7%)(p=0.03). Median number of infections was 1(IQR 0-3). There was no difference in infections rate between anti- TNF exposed children compared to non- anti TNF exposed children. Furthermore, there was no increased infection rate in thiopurine exposed children or children exposed to both anti-TNF and thiopurine. Conclusion In this long term followup study in children born to IBD mothers we show no major adverse events, an overall normal growth and development as compared to the Dutch population. Apart from a lower incidence of allergies no difference was observed between in utero anti-TNF exposed and non-exposed children.
Sa1993a Sa1995 Reduced Expression of Prostaglandin Transporter Promotes Angiogenesis in Gastric Cancer Shogo Takeda, Tetsuya Tanigawa, Toshio Watanabe, Hiroshi Tatsuwaki, Yuji Nadatani, Koji Otani, Fumio Tanaka, Noriko Kamata, Hirokazu Yamagami, Masatsugu Shiba, Kazunari Tominaga, Yasuhiro Fujiwara, Kazuya Muguruma, Kosei Hirakawa, Tetsuo Arakawa
The Prevalence of Irritable Bowel Syndrome-Like Symptoms in Pediatric Inflammatory Bowel Disease Kay Diederen, Daniel R. Hoekman, Bart Koot, Merit Tabbers, Angelika Kindermann, Marc A. Benninga Background: Data from studies of adult patients showed a high prevalence (35.0%) of irritable bowel syndrome (IBS) in patients with quiescent inflammatory bowel disease (IBD)[1], although it is debated whether a large proportion of these symptoms may actually reflect ongoing inflammation. To date, pediatric data are scarce. Therefore, we aimed to investigate the prevalence of symptoms of IBS in children with IBD, and the relation of these symptoms with biochemical markers of inflammation. Methods: In this prospective, observational study, all children (4-18 years) with an established diagnosis of Crohn's disease (CD), ulcerative colitis (UC) or unclassified inflammatory bowel disease (IBD-U) who visited our outpatient pediatric gastroenterology clinic between March 2014 and November 2014 were included. Clinical disease activity was scored using the abbreviated Pediatric Crohn's Disease Activity Index (aPCDAI) or Pediatric Ulcerative Colitis Activity Index (PUCAI), for CD or UC, respectively. Clinical remission was defined as an aPCDAI or PUCAI score <10. Biochemical disease activity was assessed using fecal calprotectin (FC) and serum C-reactive protein (CRP). The presence of symptoms of IBS was investigated using a physician-administered Rome III-questionnaire. Comparisons between groups was done using Mann-Whitney U tests for continuous variables and Fisher's exact tests for categorical variables. Results: A total of 135 children were included (77% CD, 21% UC, 2% IBD-U; 50.4% male; median age 14.9 years (IQR 12.5-16.8)). The majority of patients was in clinical remission (65%; CD 69.9%, UC 51.9%) The overall prevalence of IBS was 12.6% (CD 13.5%, UC 10.7%). Most patients had diarrhea-predominant IBS (IBS-Diarrhea 64.7%, IBS-Constipation 17.6%, IBS-Unsubtyped 11.8%, IBS-Mixed 5.9%). In patients in clinical remission, the prevalence of IBS was 7.5% (CD 6.2%, UC 14.3%). No difference in FC or CRP levels was found between patients with IBS (IBS+) and patients without IBS (IBS-) (FC: IBS+ median 400 mg/kg, IBS- 344 mg/kg, p=0.88; CRP: IBS+ median 2.3 mg/l, IBS-1.1 mg/l, p=0.50). Furthermore, no difference in FC or CRP levels was found between patients in clinical remission with or without IBS (FC: IBS+ median 87.5 mg/kg, IBS- 225 mg/kg, p=0.14; CRP: IBS+ median 1.1 mg/l, IBS- 0.9 mg/l, p=0.69). Conclusion: We found a much lower prevalence of IBS-like symptoms in children with IBD, compared to studies in adult IBD patients. Furthermore, no difference in biochemical markers of disease activity was found between IBD patients with and without IBS-like symptoms. 1. Halpin SJ, Ford AC. Prevalence of symptoms meeting criteria for irritable bowel syndrome in inflammatory bowel disease: systematic review and meta-analysis. Am J Gastroenterol 2012; 107: 1474-82.
Background and Aim: Prostaglandin (PG) E2 promotes gastrointestinal carcinogenesis and tumor progression by stimulating angiogenesis and cell proliferation. The total amount of biologically active PGE2 in the tissue is determined by the balance between biosynthesis of PG and degradation system of PG, which involves PG transporter (PGT) and 15-hydroxyprostaglandin dehydrogenase (15-PGDH). In this study, we investigated the expression pattern of PGT in gastric adenocarcinoma and its association with prognostic significance and tumor angiogenesis. Methods: (1) Expression of PGT and 15-PGDH was determined by immunohistochemistry in advanced gastric adenocarcinoma obtained from 96 patients undergoing surgical resection at our hospital. The expression patterns of PGT and 15-PGDH were assessed using a scoring system based on the staining intensity and stained tumor area. Correlations between expression level of PGT and 15-PGDH and clinicopathological factors were analyzed using the Cox's proportional hazards model. Cumulative survival rates stratified by immunoreactivity of PGT and 15-PGDH in gastric cancer were calculated by the KaplanMeier method. Angiogenesis in the tumor tissue was evaluated by counting the number of microvessels determined by immunohistochemistry using antibody against CD31, a marker of endothelial cells, in 10 randomly chosen high power fields (HPF). The average number of microvessels was used to estimate the microvessel density (MVD). (2) Expression of PGT in gastric cancer cell lines (AGS, NCI-N87, MKN7, MKN45 and NUGC3) was screened. The effect of gene silencing of PGT with siRNA specific for PGT on expression of mRNA for vascular endothelial growth factor (VEGF) and production of VEGF protein in gastric cancer cells stimulated by PGE2 was examined. Results: (1) In 22.4% of well and moderately differentiated tubular gastric adenocarcinoma, PGT protein was reduced in the cytoplasm of tumor cells as compared with normal gastric-gland cells, while PGT was observed in only 42.6% of poorly differentiated gastric adenocarcinoma samples (P < 0.01, chi-square test). Based on a multivariate analysis and Kaplan-Meier analysis, PGT and 15-PGDH expression were significant prognostic factors. MVD in the tumor tissue was higher in PGT-negative cases than in PGT-positive cases (72.3 ± 4.22 vs. 55 ± 2.94 /HPF respectively, P < 0.05). (2) In AGS and MKN7 cells mRNA for PGT and PGT protein were expressed, while they were undetectable in NCI-N87, MKN45 and NUGC3 cells. Gene silencing using siRNA specific for PGT significantly increased the expression of mRNA for VEGF and production of VEGF protein in AGS and MKN7 cells accompanied by increase in PGE2 in culture media. Conclusion: These findings suggest that reduced PGT expression is an independent predictor of poor survival associated with tumor angiogenesis in gastric adenocarcinoma.
Sa1996 Increased Risk of Varicella- and Zoster-Related Hospitalizations Among Children With Inflammatory Bowel Disease Daniel J. Adams, Cade M. Nylund Background: The treatment of children with inflammatory bowel disease (IBD) involves long-term courses of immunosuppressive medications, including anti-tumor necrosis factoralpha agents. As a result, children with IBD are at an increased risk for the development of
AGA Abstracts
S-378
Sa1993
Sa1994
Specific Inhibitor of Importin-α Mediated Nuclear Transport - Ivermectin Reduces VEGF Expression and Inhibits Colon Cancer Cell Proliferation Amrita Ahluwalia, Michael K. Jones, Andrzej S. Tarnawski
Long-Term Outcome of Children Born to IBD Mothers Preliminary Result From a Multicenter Retrospective Study in the Netherlands Shannon L. Kanis, Alison de Lima, Zuzana Zelinkova, Gerard Dijkstra, Rachel West, Rob J. Ouwendijk, Nanne K. de Boer, Andrea E. van der Meulen - de Jong, Marie J. Pierik, Liekele E. Oostenbrug, Mariëlle Romberg-Camps, Alexander Bodelier, Bas Oldenburg, Frank Hoentjen, Ruud Beukers, Jeroen M. Jansen, Christien J. van der Woude
Background & Aims: Colorectal cancer (CRC) cells (unlike normal colonic epithelial cells) secrete VEGF, which drives these cells proliferation and promotes tumor-related angiogenesis. The mechanism(s) of increased, aberrant VEGF expression in CRC cells is not known, but is likely related to transcriptional activation of VEGF gene. We hypothesized that: 1) upregulated importin-α in CRC cells (which facilitates nuclear transport of transcription factors: HIF1α and CREB, and is essential for VEGF gene promoter activation) is the underlying mechanism for increased VEGF expression in these cells and CRC cell proliferation, and, 2) inhibition and/or silencing of importin-α in CRC cells will inhibit VEGF gene activation and CRC cell proliferation. Ivermectin is a specific inhibitor of importin α nuclear transport (Biochem J. 2012: 1;443(3):851-6). We examined whether treatment of CRC cell lines with ivermectin could inhibit CRC cell growth. Methods: We used: (a) human CRC cell lines - HCT116 & HT29 and (b) normal colonic epithelial cells - NCM356 & NCM460. We treated cultured CRC cells with ivermectin (50 μM, 6 hr; specific inhibitor of importin-α nuclear transport), with importin α specific siRNA or control RNA (100nM, 48 hr). Add-back studies included treatment with exogenous VEGF (20ng/ml). Studies: 1) mRNA and protein expression of importin-α and VEGF by Real-Time RT-PCR, and/or Western blotting and immunostaining, respectively; 2) VEGF secretion into culture medium by ELISA; 3) translocation of importin to the nucleus in CRC vs. normal cells; and 4) cell proliferation by BrdU assay. Results: 1) CRC cell lines express high levels of VEGF and secrete large amounts of VEGF (up to 1530 pg/ml) into culture medium at 24 hours vs. normal epithelial cells, which only secrete minimal VEGF (<34 pg/ml); 2) Importin-α expression is significantly increased in CRC cell lines vs. normal epithelial cells by >40% (p< 0.05); 3) Selective inhibition of importin-α in CRC cells using ivermectin significantly reduced VEGF expression by ~3-fold (p<0.01) and proliferation of these cells by 2.4-fold (p<0.01). Treatment with exogenous VEGF partly reversed inhibited by ivermectin cell proliferation; 4) Importin-α silencing in CRC cells significantly reduced VEGF expression and proliferation of these cells by 2.2-fold and 2fold (both p<0.01), respectively; treatment with exogenous VEGF following importin-α silencing reversed inhibition of cell proliferation by 2-fold (p < 0.01). Conclusions: 1) VEGF gene activation in CRC cells requires functional importin-α; 2) importin-α mediates increased proliferation of CRC cells; downregulation of importin-α with specific siRNA or its inhibition with specific inhibitor - ivermectin inhibits CRC cell proliferation; 3) These studies suggest a potential therapeutic role of ivermectin in inhibiting CRC cell proliferation.
Background The long term outcome of children born to mothers with inflammatory bowel disease(IBD) are relatively unexplored. The aim of this study is to analyze the health status of children who were born to mothers with IBD. Methods All women diagnosed with IBD prior to their pregnancy that gave birth between 1999 and 2011 were invited. After informed consent from both parents, the general practitioner (GP) was contacted for the following child outcomes: growth, number of infections for which antibiotics were needed, allergies and allergic reactions to vaccinations. Low birth weight was stated as <2500g, preterm birth as gestational age <37 weeks. The EUROCAT guideline was used to classify congenital abnormalities. Results In total 935 invitations (in 2 rounds) were sent to women with IBD from 8 Dutch hospitals. The response was 46.8%(438). Until November 2014 362 children from 239 IBD mothers (257(71.0%) CD, 93(25.7%) UC and 12(3.3%) IBDU) were included. Median child age at follow up was 6 years (IQR 4-11). In utero 118(32.6%) children were not exposed to any IBD drug, 97(26.8%) to only mesalazine, 79(21.8%) to thiopurine, 38(10.5%) to anti- TNF, 20(5.5%) to both anti- TNF and thiopurine and for 10(2.8%) children drug exposure was unknown. There was no difference in anti- TNF exposed and the non- anti TNF exposed children considering; median gestational age (39 weeks(IQR3840)), pre- term births (67(18.5%)), overall birth weight (3268 gram(IQR 2893-3638)), low birth weight (40(11 %)) and major congenital abnormalities (8(2.2 %)). Five(1.5%) children showed a primary or secondary growth deficiency. None of these children were exposed to anti- TNF. Apart from one extended rash after vaccination there were no reports of severe vaccination reactions. Overall 88 children had allergies. These allergies were more common in the non- anti TNF exposed children (36.9%)compared to the anti- TNF exposed children (15.7%)(p=0.03). Median number of infections was 1(IQR 0-3). There was no difference in infections rate between anti- TNF exposed children compared to non- anti TNF exposed children. Furthermore, there was no increased infection rate in thiopurine exposed children or children exposed to both anti-TNF and thiopurine. Conclusion In this long term followup study in children born to IBD mothers we show no major adverse events, an overall normal growth and development as compared to the Dutch population. Apart from a lower incidence of allergies no difference was observed between in utero anti-TNF exposed and non-exposed children.
Sa1993a Sa1995 Reduced Expression of Prostaglandin Transporter Promotes Angiogenesis in Gastric Cancer Shogo Takeda, Tetsuya Tanigawa, Toshio Watanabe, Hiroshi Tatsuwaki, Yuji Nadatani, Koji Otani, Fumio Tanaka, Noriko Kamata, Hirokazu Yamagami, Masatsugu Shiba, Kazunari Tominaga, Yasuhiro Fujiwara, Kazuya Muguruma, Kosei Hirakawa, Tetsuo Arakawa
The Prevalence of Irritable Bowel Syndrome-Like Symptoms in Pediatric Inflammatory Bowel Disease Kay Diederen, Daniel R. Hoekman, Bart Koot, Merit Tabbers, Angelika Kindermann, Marc A. Benninga Background: Data from studies of adult patients showed a high prevalence (35.0%) of irritable bowel syndrome (IBS) in patients with quiescent inflammatory bowel disease (IBD)[1], although it is debated whether a large proportion of these symptoms may actually reflect ongoing inflammation. To date, pediatric data are scarce. Therefore, we aimed to investigate the prevalence of symptoms of IBS in children with IBD, and the relation of these symptoms with biochemical markers of inflammation. Methods: In this prospective, observational study, all children (4-18 years) with an established diagnosis of Crohn's disease (CD), ulcerative colitis (UC) or unclassified inflammatory bowel disease (IBD-U) who visited our outpatient pediatric gastroenterology clinic between March 2014 and November 2014 were included. Clinical disease activity was scored using the abbreviated Pediatric Crohn's Disease Activity Index (aPCDAI) or Pediatric Ulcerative Colitis Activity Index (PUCAI), for CD or UC, respectively. Clinical remission was defined as an aPCDAI or PUCAI score <10. Biochemical disease activity was assessed using fecal calprotectin (FC) and serum C-reactive protein (CRP). The presence of symptoms of IBS was investigated using a physician-administered Rome III-questionnaire. Comparisons between groups was done using Mann-Whitney U tests for continuous variables and Fisher's exact tests for categorical variables. Results: A total of 135 children were included (77% CD, 21% UC, 2% IBD-U; 50.4% male; median age 14.9 years (IQR 12.5-16.8)). The majority of patients was in clinical remission (65%; CD 69.9%, UC 51.9%) The overall prevalence of IBS was 12.6% (CD 13.5%, UC 10.7%). Most patients had diarrhea-predominant IBS (IBS-Diarrhea 64.7%, IBS-Constipation 17.6%, IBS-Unsubtyped 11.8%, IBS-Mixed 5.9%). In patients in clinical remission, the prevalence of IBS was 7.5% (CD 6.2%, UC 14.3%). No difference in FC or CRP levels was found between patients with IBS (IBS+) and patients without IBS (IBS-) (FC: IBS+ median 400 mg/kg, IBS- 344 mg/kg, p=0.88; CRP: IBS+ median 2.3 mg/l, IBS-1.1 mg/l, p=0.50). Furthermore, no difference in FC or CRP levels was found between patients in clinical remission with or without IBS (FC: IBS+ median 87.5 mg/kg, IBS- 225 mg/kg, p=0.14; CRP: IBS+ median 1.1 mg/l, IBS- 0.9 mg/l, p=0.69). Conclusion: We found a much lower prevalence of IBS-like symptoms in children with IBD, compared to studies in adult IBD patients. Furthermore, no difference in biochemical markers of disease activity was found between IBD patients with and without IBS-like symptoms. 1. Halpin SJ, Ford AC. Prevalence of symptoms meeting criteria for irritable bowel syndrome in inflammatory bowel disease: systematic review and meta-analysis. Am J Gastroenterol 2012; 107: 1474-82.
Background and Aim: Prostaglandin (PG) E2 promotes gastrointestinal carcinogenesis and tumor progression by stimulating angiogenesis and cell proliferation. The total amount of biologically active PGE2 in the tissue is determined by the balance between biosynthesis of PG and degradation system of PG, which involves PG transporter (PGT) and 15-hydroxyprostaglandin dehydrogenase (15-PGDH). In this study, we investigated the expression pattern of PGT in gastric adenocarcinoma and its association with prognostic significance and tumor angiogenesis. Methods: (1) Expression of PGT and 15-PGDH was determined by immunohistochemistry in advanced gastric adenocarcinoma obtained from 96 patients undergoing surgical resection at our hospital. The expression patterns of PGT and 15-PGDH were assessed using a scoring system based on the staining intensity and stained tumor area. Correlations between expression level of PGT and 15-PGDH and clinicopathological factors were analyzed using the Cox's proportional hazards model. Cumulative survival rates stratified by immunoreactivity of PGT and 15-PGDH in gastric cancer were calculated by the KaplanMeier method. Angiogenesis in the tumor tissue was evaluated by counting the number of microvessels determined by immunohistochemistry using antibody against CD31, a marker of endothelial cells, in 10 randomly chosen high power fields (HPF). The average number of microvessels was used to estimate the microvessel density (MVD). (2) Expression of PGT in gastric cancer cell lines (AGS, NCI-N87, MKN7, MKN45 and NUGC3) was screened. The effect of gene silencing of PGT with siRNA specific for PGT on expression of mRNA for vascular endothelial growth factor (VEGF) and production of VEGF protein in gastric cancer cells stimulated by PGE2 was examined. Results: (1) In 22.4% of well and moderately differentiated tubular gastric adenocarcinoma, PGT protein was reduced in the cytoplasm of tumor cells as compared with normal gastric-gland cells, while PGT was observed in only 42.6% of poorly differentiated gastric adenocarcinoma samples (P < 0.01, chi-square test). Based on a multivariate analysis and Kaplan-Meier analysis, PGT and 15-PGDH expression were significant prognostic factors. MVD in the tumor tissue was higher in PGT-negative cases than in PGT-positive cases (72.3 ± 4.22 vs. 55 ± 2.94 /HPF respectively, P < 0.05). (2) In AGS and MKN7 cells mRNA for PGT and PGT protein were expressed, while they were undetectable in NCI-N87, MKN45 and NUGC3 cells. Gene silencing using siRNA specific for PGT significantly increased the expression of mRNA for VEGF and production of VEGF protein in AGS and MKN7 cells accompanied by increase in PGE2 in culture media. Conclusion: These findings suggest that reduced PGT expression is an independent predictor of poor survival associated with tumor angiogenesis in gastric adenocarcinoma.
Sa1996 Increased Risk of Varicella- and Zoster-Related Hospitalizations Among Children With Inflammatory Bowel Disease Daniel J. Adams, Cade M. Nylund Background: The treatment of children with inflammatory bowel disease (IBD) involves long-term courses of immunosuppressive medications, including anti-tumor necrosis factoralpha agents. As a result, children with IBD are at an increased risk for the development of
AGA Abstracts
S-378