tbuckley/cabot-search huggingface dataset:
PTU-126 Joint Hypermobility Syndrome, Rectal Hyposensitivity and Severe Constipation in young Nulliparous Females: Abstract PTU-126 Table 1
Authors: A Fikree, Q Aziz, M Ahmed, S Mohammed, C H Knowles, M Scott
Journal: Gut (2013)

<h3>Introduction</h3> The joint hypermobility syndrome (JHS) is a common non-inflammatory connective tissue disorder characterised by joint hyperflexibility and skin hyperelasticity. A validated 5 point hypermobility questionnaire screens for the presence or absence of JHS; formal diagnosis requires fulfilment of the Brighton criteria. Previous small cohorts demonstrate an association between the JHS and lower gastrointestinal symptoms (1), particularly alternating bowel habit with predominant constipation. The underlying mechanism for these symptoms is unknown. <h3>Methods</h3> Retrospective observational study of patients attending a specialist colorectal physiology unit for investigation of chronic constipation. Patients completed validated lower GI symptom and 5 point hypermobility questionnaires, then underwent lower GI physiology testing. 43 patients with an established rheumatological diagnosis of JHS were compared to 146 consecutive patients who screened negative (score = 0) for JHS (Non-JHS). Demographic features, prevalence of presenting symptoms, and physiological abnormalities were compared in JHS and Non-JHS. In view of the multiple comparisons, the significance level was set at p:0.01. <h3>Results</h3> In patients with constipation, those with JHS were younger, and females were more likely to be nulliparous. JHS patients had significantly more alternating bowel habit, infrequent bowel motions, abdominal pain, and childhood bowel problems. They were significantly more likely to require manual manoeuvres to help with rectal evacuation, but did not have an increased prevalence of other evacuatory symptoms. On physiology testing JHS patients had more rectal hyposensitivity, but were less likely to have internal (IAS) and external anal sphincter (EAS) abnormalities on ultrasound (see Table 1). There was no difference in the prevalence of pelvic dyssynergia, slow colonic transit or rectal morphological abnormalities. <h3>Conclusion</h3> JHS patients have more severe constipation which is likely to date back to childhood, and which requires digitation. These patients are more likely to have rectal hyposensitivity but less likely to have structural or transit abnormalities to account for their symptoms. The diagnosis of JHS should be considered in young nulliparous females with a longstanding history of very infrequent bowel motions. <h3>Disclosure of Interest</h3> None Declared <h3>Reference</h3> Castori, M., <i>et al.</i>, Am J Med Genet A, 2010. <b>152A</b>(3): p. 556–64.
Abstract 1900: Antioxidant studies on the Peruvian cherimoya fruit give an insight into the healthy lifestyle of the Incas
Authors: Gaytri D. Gupta Elera, John Whitaker, Jorge Chauca, Richard A. Robison, Kim L. O’ Neill
Journal: Cancer Research (2010)

Abstract Annona cherimola, known as “cherimoya” was grown as an essential crop in the Incan empire, and was believed to prevent disease. Indigenous to Peru and Ecuador, this “pearl of the Andes” is consumed mainly for its exceptional taste. American writer Mark Twain called the cherimoya “the most delicious fruit known to men.” Recent interest in this fruit stems from its high concentration of acetogenins, which are bioactive polyketides. Recent research has accredited beneficial effects to acetogenins, including the exhibition of cytotoxic and anti-tumorous activity, particularly in mammary, pancreatic and colon cancer cells (Cheng et. al 1998). This project explores the health benefits of cherimoya consumption by examining the antioxidant effect of its components, including: skin, flesh and juice. These components were analyzed for antioxidant concentrations using the Oxygen Radical Absorbance Capacity (ORAC) assay. A cellular model was also established that evaluated the antioxidant capacity of cherimoya components in the presence of Raji cells, a Burkitt lymphoma cell line, and HT-29 cells, a colon cancer cell line. After incubation with the cherimoya components, cell lysate samples were assessed for antioxidant capacity using the ORAC assay. Results for Raji cell lysate exposed to media, juice, skin and flesh were as follows: 886 Trolox Equivalents per Liter (TE/L), 1238 TE/L, 1018 TE/L, and 1045 TE/L respectively. Results for HT-29 cell lysate exposed to media, juice, skin and flesh were: 294 TE/L, 924 TE/L, 505 TE/L and 627 TE/L respectively. These data shows that cells treated with cherimoya juice exhibited a higher antioxidant uptake. An alternate cellular model was established in which Raji cells and HT-29 cells were pre-exposed to oxidant AAPH, 2,2’-azobis-(2-amidinopropane) dihydrochloride, and then treated with cherimoya juice, skin and flesh. Results for Raji cells exposed to AAPH and then treated with media, juice, skin and flesh were as follows: 1054 TE/L, 1363 TE/L, 1183 TE/L, and 1254 TE/L respectively. Results for HT-29 cells exposed to AAPH and then treated with media, juice, skin and flesh were: 1075 TE/L, 1528 TE/L, 1350 TE/L and 1374 TE/L respectively. These data indicated that when cells were pre-exposed to an oxidant, thus simulating cells under oxidative stress, antioxidant cell uptake increased for both cell lines. These results suggest that cells can sense oxidative stress in their environment and can increase their ability to uptake available antioxidants. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1900.
SAT0117 Reduction of Nsaid-Induced Small Intestinal Damage in Rheumatoid Arthritis Patients Receiving Sulfasalazine
Authors: A. Balabanceva, I. Klyaritskaya, S. Tkach, Y. Kuzenko
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Recent studies have demonstrated that nonsteroidal anti-inflammatory drugs (NSAIDs) often cause damage to the small intestine, and NSAID-induced enteropathy is mediated by different inflammatory cytokines. Sulfasalazine is being widely used in patients with rheumatoid arthritis (RA), and this drug have the potential to induce mucosal healing in patients with intestinal diseases such as inflammatory bowel diseases. <h3>Objectives</h3> To evaluate the preventive effect of sulfasalazine against small intestinal damage due to chronic NSAID use in RA patients. <h3>Methods</h3> Between March 2012 and December 2013, capsule endoscopy was performed in 51 consecutive RA patients who received NSAIDs for more than 3 months with or without sulfasalazine therapy over a period of 3 months. The findings were scored as follows according to the method described by Graham et al. (Clin Gastroenterol Hepatol. 2005): 0, normal; 1, red spots; 2, 1 to 4 erosions; 3, &gt;4 erosions; and 4, large erosions/ulcers. Scores of 3 and 4 indicated severe damage. The relationship between the use of sulfasalazine therapy and risk of severe damage (score 3 or 4) or severest damage (score 4) were assessed using multiple logistic regression. <h3>Results</h3> Comparative data were analyzed for 47 patients, and 4 patients were excluded because the entire small bowel could not be visualized in these patients. Of the 25 patients who did not receive sulfasalazine therapy, 12 (48%) had severe damage (score of 3 [n=8] or 4 [n=4]). On the other hand, of the 26 patients receiving sulfasalazine therapy, 5 (19.2%) had severe damage (score of 3 [n=3] or 4 [n=2]). On stratifying the patients by sulfasalazine therapy, we obtained a crude odds ratio (OR) of 0.26 for severe damage with a 95% confidence interval (CI) of 0.10 to 0.66, and of 0.38 for severest damage with a 95% CI of 0.17 to 0.88. This effect of sulfasalazine therapy on NSAID-induced enteropathy remained robust to adjustment for age, gender, history of peptic ulcers, disease activity score-28 (a disease activity index for RA), use of selective cyclooxygenase-2 inhibitors or steroids, blood hemoglobin concentration, and all these variables, with the adjusted ORs for severe damage ranging from 0.19 to 0.25 and those for severest damage ranging from 0.30 to 0.40. <h3>Conclusions</h3> Sulfasalazine therapy may protect against NSAID-induced small intestinal damage in RA patients and may be effective in the treatment of NSAID-induced enteropathy. <h3>References</h3> Park SCl, Chun HJ, Kang CD, Sul D. Prevention and management of non-steroidal antiinflammatory drugs-induced small intestinal injury. World J Gastroenterol 2011 November 14; 17 (42): 4647-4653. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.1671
Abstract 360: Tamoxifen treatment induces mitogen-activated protein kinase phosphatase-1 expression in T47D breast cancer cells
Authors: Kelly K. Haagenson, Dongjun Peng, Gen Sheng Wu
Journal: Cancer Research (2010)

Abstract Mitogen Activated Protein Kinase Phosphatase-1 (MKP-1) is a dual specificity phosphatase known to target the Extracellular Signal Regulated Kinases (ERK), c-Jun N-terminal Kinases (JNK) and the p38 Mitogen Activated Protein Kinases (p38), which make up the Mitogen Activated Protein Kinase (MAP Kinase) family. These pathways play vital roles in determining whether cells continue to survive or undergo apoptosis. ERK mainly contributes to cell survival while JNK and p38 signaling can be involved in both cell survival and apoptosis. The function of MKP-1 is to attenuate the signals perpetuated by ERK, JNK and p38. Previous research in our lab has shown that knockdown of either MKP-1 or ERK-2 leads to increased cisplatin sensitivity in ovarian cancer. ERK activation has also been linked to tamoxifen resistance and poor prognosis in breast cancer, but the effects of MKP-1, JNK and p38 in this area are not well studied. A previous study by Cui et al has shown that overexpression of MKP-3, which mainly targets ERK, increased tamoxifen resistance in breast tumors. We chose to focus this investigation on the contribution of MKP-1 to tamoxifen resistance because of its ability to dephosphorylate all three MAP Kinase family members. In our study, MKP-1 protein expression was shown to be elevated in MDA-MB-231, T47D and MCF7 breast cancer cells as compared to non-malignant MCF10A cells. After four and six hours of treatment with 1 μM tamoxifen, MKP-1 protein expression was increased in T47D cells compared to untreated parental control cells. Very little change in phosphorylated ERK protein levels was observed at these same time points. There were, however, decreases in phosphorylated JNK protein levels after four and six hours of 1μM tamoxifen treatment when compared to untreated parental control cells. Since some chemotherapeutic agents induce apoptosis in a JNK mediated manner, a decrease in JNK expression in tamoxifen treated breast cancer cells could contribute to decreased therapeutic efficacy. In conclusion, by examining changes in protein expression levels in tamoxifen treated breast cancer cells we have identified that increased MKP-1 expression leads to a decrease in phosphorylated JNK expression. This finding could constitute a mechanism contributing to tamoxifen resistance in estrogen receptor positive breast cancer cells and suggests that modulation of MKP-1 expression could increase tamoxifen sensitivity in these cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 360.
P1-11-06: Barriers to Enrollment in Cancer Therapeutic Clinical Trials: A Comprehensive Cancer Center Experience.
Authors: L Bourdeanu, J Niland, T Stiller, S Swain-Cabriales, G Somlo
Journal: Cancer Research (2011)

Abstract PURPOSE: Well-conducted cancer therapeutic clinical trials are essential for improving patient outcomes. Unfortunately, less than 5% of new cancer patients participate in clinical trials on average nationwide. Failure to recruit eligible patients represents a major impediment to the success of clinical trials. Barriers to patient accrual in cancer clinical trials must be identified and overcome to increase patient participation. MATERIALS AND METHODS: A retrospective analysis of 418 patients with a diagnosis of breast cancer seen at City of Hope Medical Center in 2009 was performed. Along with descriptive analysis of patient demographic data, logistic regression analyses were performed to evaluate predictors of enrollment. RESULTS: Of the 418 new breast cancer patients in 2009, we determined that 138 (33%) were eligible for available therapeutic clinical trials at City of Hope. At the initial visits, physicians did not consider clinical trials in 32% (44/138) of these patients. Of the 138 eligible patients, 58% (80/138) of patients participated in clinical trials. The remainder (58/138, 42%) either declined trial participation despite meeting eligibility criteria (14/58, 24%), or were not considered for clinical trials by their respective physician (44/58, 76%). By logistic regression analysis, patients with Stages II and III disease were significantly more likely to enroll in clinical trials compared to those with stage 0 or I (OR=2.89, 95% CI, 1.17−7.12, P = .02; OR=9.17, 95% Cl, 2.65−31.76, P=0.0005;, respectively). Age, preferred language, marital status, family history of breast cancer, and race were not found to be significant predictors of enrollment in therapeutic clinical trials. CONCLUSION: While enrollment of eligible breast cancer patients onto therapeutic clinical trials at City of Hope is high (58%), overall the proportion going onto clinical trials remains low (80/418, 19%), though higher than national averages. We found that the majority of patients did not enroll due to lack of availability of a suitable trial, ineligibility, or lack of offering of trial enrollment by the treating MD. Barriers to cancer clinical trial accrual should be prospectively identified and addressed in future studies, with the hope of leading to more vigorous enrollment. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P1-11-06.
Use of mastectomy in rural versus urban patients: the effects of medical community factors.
Authors: LK Jacobs, ME Detrani, KA Kelley, GD Rosson, DC Chang
Journal: Cancer Research (2009)

Abstract Abstract #5089 Background: Disparity exists in surgical treatment of breast cancer patients living in rural versus urban counties. Past studies evaluating this used patient level data. We examine county-level medical community factors that potentially impact the geographic variation of mastectomy versus breast-conserving therapy.&amp;#x2028; Methods: Data from 137,303 patients and 200 counties were analyzed combining the 2006 SEER and 2004 ARF (Area Resource File) databases. Inclusion criteria identified in SEER were: stage I, II, or III disease, female, diagnosis after 1992. Patients were linked to county level data from the ARF based on their county of residence. Medical community variables analyzed with ARF are seen in Table 1.&amp;#x2028; Results: A total of 9.58% of the patients reside in a rural county, and 59.90% of these received a mastectomy, compared to 44.92% of the urban patients. Multivariate analysis of the medical community factors was calculated by both land area and population with calculation by population accounting for the disparity in mastectomy use (Table 1). Of the medical community factors in this analysis, the screening hospital density was highly significant, accounted for the difference in rural versus urban mastectomy rates, and resulted in an increased likelihood of receiving mastectomy (OR 1.009, 95% CI 1.004-1.014). Bivariate analysis also revealed a higher density of screening hospitals in rural counties (57.62) than in urban counties (18.22).&amp;#x2028; Conclusions: Analysis using land area versus population to estimate availability of services suggests that disparity in the rural community is most affected by availability of providers and not to required travel distance. Density of screening hospitals was found to be the most important factor resulting in disparity between rural versus urban mastectomy rates. Rural counties have a higher density of screening facilities, yet they also have a higher mastectomy rate. This may represent a volume/quality issue that will require further investigation.&amp;#x2028; &amp;#x2028; Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 5089.
Minoxidil — An Alternative to Nephrectomy for Refractory Hypertension
Authors: William A. Pettinger, Helen C. Mitchell
Journal: New England Journal of Medicine (1973)

Eleven patients with malignant or accelerated hypertension refractory to conventional drugs were treated with minoxidil as the primary antihypertensive agent. Seven had advanced renal disease and all were candidates, by conventional criteria for nephrectomy to control blood pressure. The blood pressure was reduced to or near normal levels in all patients, with remarkably few side effects and was well controlled in supine and standing positions. Initiation and maintenance of therapy with minoxidil required meticulous adjustment of diuretic agents to control fluid retention and of propranolol to control reflex cardiac stimulation. The cardiac status improved in all patients treated for more than two months, with reversal of myocardial ischemia and hypertrophy in some. Because of few drug-related symptoms patient acceptance was excellent. Seven patients remain on minoxidil therapy at present. The use of minoxidil in managing hypertensive patients should be carefully weighed against the more heroic alternative nephrectomy and its consequences. (N Engl J Med 289:167–173, 1973)
Abstract LB-424: A genome-wide association study identifies a locus on chromosome 14q21 as a predictor of leukocyte telomere length and as a marker of susceptibility to bladder cancer
Authors: Jian Gu, Meng Chen, Sanjay Shete, Christopher I. Amos, Ashish Kamat, Yuanqing Ye, Jie Lin, Colin P. Dinney, Xifeng Wu
Journal: Cancer Research (2011)

Abstract Telomeres play a critical role in maintaining genome integrity. Telomere shortening is associated with the risk of many aging-related diseases. Classic twin studies have shown that genetic components may contribute up to 80% of the heritability of telomere length. In the study we report here, we used a multi-stage genome-wide association study (GWAS) to identify genetic determinants of telomere length. The mean telomere length in peripheral blood leukocytes was measured by quantitative real-time polymerase chain reaction. We first analyzed 300,000 single-nucleotide polymorphisms (SNPs) in 459 healthy controls, finding 15,120 SNPs associated with telomere length at P &amp;lt; 0.05. We then validated these SNPs in two independent populations comprising 890 and 270 healthy controls, respectively. Four SNPs, including rs398652 on 14q21, were associated with telomere length across all three populations (pooled P-values of &amp;lt; 10−5). The variant alleles of these SNPs were associated with longer telomere length. We then analyzed the association of these SNPs with the risk of bladder cancer in a large case-control study. The variant allele of rs398652 was associated with a significantly reduced risk of bladder cancer (odds ratio = 0.81; 95% confidence interval, 0.67–0.97; P = 0.025), consistent with the correlation of this variant allele with longer telomeres. We then conducted a mediation analysis to examine whether the association between rs398652 and reduced bladder cancer risk is mediated by telomere length, finding that telomere length was a significant mediator of the relationship between rs398652 and bladder cancer (P = 0.013) but that it explains only 14% of the effect. In conclusion, we found that the SNP rs398652 on 14q21 was associated with longer telomere length and a reduced risk of bladder cancer and that a small portion of the effect of this SNP on bladder cancer risk was mediated by telomere length. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-424. doi:10.1158/1538-7445.AM2011-LB-424
1221 URSODEOXYCHOLYL LYSOPHOSPHATIDYLETHANOLAMIDE GENERATES HEPATOPROTECTIVE CONJUGATED UDCA, PHOSPHATIDYLCHOLINE, MEDIUM-CHAIN FATTY ACIDS AND PLASMALOGEN 16:1
Authors: W. Chamulitrat, W. Xu, A. Pathil-Warth, G. Liebisch, G. Schmitz, W. Zhang, K. Setchell, W. Stremmel
Journal: Journal of Hepatology (2012)
Prevalence of Sickle-Cell Trait and Glucose-6-Phosphate Dehydrogenase Deficiency
Authors: Nicholas L. Petrakis, Stephen L. Wiesenfeld, Bruce J. Sams, Morris F. Collen, John L. Cutler, A. B. Siegelaub
Journal: New England Journal of Medicine (1970)

The frequency of G-6-PD deficiency and sickle trait was determined in 4028 Negroes living in the San Francisco Bay Area. The frequency of G-6-PD deficiency was significantly higher among younger than older Negro males. No significant alteration by age was found for sickle-trait frequency. G-6-PD deficiency appears to define a group with higher risk of mortality than the general population. Future studies should be directed toward defining the specific clinical effects of the trait on increased mortality.
PHARMACOINVASIVE STRATEGY VERSUS PRIMARY PERCUTANEOUS CORONARY INTERVENTION IN PATIENTS WITH ST-ELEVATION MYOCARDIAL INFARCTION: A PROPENSITY SCORE MATCHED ANALYSIS
Authors: Doo Sun Sim, Woo Jin Kim, Myung Ho Jeong, Youngkeun Ahn, Young Jo Kim, Shung Chull Chae, Taek Jong Hong, In Whan Seong, Jei Keon Chae, Chong Jin Kim, Myeong Chan Cho, Seung-Woon Rha, Jang Ho Bae, Ki Bae Seung, Seung Jung Park
Journal: Journal of the American College of Cardiology (2016)