tbuckley/cabot-search huggingface dataset:
An unusual lesion of the pancreas
Authors: Jérémie Albouys, Élise Deluche, Romain Legros, Aurélie Charissoux, Sophie Geyl, Denis Sautereau, Jérémie Jacques
Journal: Endoscopy (2019)

Phyllode breast tumors are rare fibroepithelial entities that may become malignant. They represent less than 1 % of all primary breast tumors [1]. Management is essentially surgical. The risk of local or metastatic recurrence varies by histological type, but most cases exhibit benign local evolution. The most common metastatic sites are the lungs and bones. No adjuvant treatment (radiotherapy or chemotherapy) is effective. Only five pancreatic metastases have been recorded in the literature, of which only one was diagnosed via endoscopy ultrasound [2] [3] [4]. We present the first video recording of endoscopic ultrasound used to diagnose a pancreatic metastasis of a phyllode tumor ([Video 1]); the diagnosis was histologically confirmed.
CRYPTOGENIC MULTIFOCAL ULCEROUS STENOSING ENTERITIS (CMUSE) IN THE ENTEROSCOPIC ERA
Authors: L Elli, GE Tontini, M Topa, M Puricelli, P Soru, R Penagini, M Soncini, M Vecchi
Journal: Endoscopy (2019)

Cryptogenic multifocal ulcerous stenosing enteritis (CMUSE) is a rare and overlooked small bowel disorder of uncertain origin. Differential diagnosis from Crohn's disease, NSAID-associated enteritis and enteric lymphoma is challenging.
The regulation of androgen receptor levels by a feedback loop in prostate cancer cells
Authors: Albert Dobi, Linda L. Xu, Vasantha Srikantan, Shiv Srivastava
Journal: Cancer Research (2005)

986  Introduction and Objectives: Modulation of androgen receptor may play an important role in normal growth and differentiation of prostate epithelial cells. AR alterations (amplification, elevated expression, mutation, co-activator/co-repressor dysfunction) leading to gain of AR functions are increasingly highlighted in prostate cancer. Materials and Methods: Our laboratory has recently contributed to comprehensive evaluation of the androgen regulated gene repertoire using SAGE and GeneChip platforms. We reported earlier the discovery of a novel prostate-abundant, androgen regulated gene, PMEPA1, which shows decreased expression in two-thirds of prostate cancer specimens analyzed thus far. Decreased PMEPA1 expression in prostatic tumors and it’s tumor cell growth in laboratory functions suggested a potential tumor suppressor gene feature of the PMEPA1. PMEPA1 protein binds to NEDD4 protein, which plays a central role in the ubiquitin-proteosome pathway. We identified the PY-motifs of the PMEPA1 protein that mediated it’s binding to NEDD4. Results: Here we report that PMEPA1 also binds to androgen receptor and that PMEPA1 may drive the degradation of AR. These findings suggested that PMEPA1 could strongly and specifically reduce the cellular levels of androgen receptor. The antagonistic function of PMEPA1 to AR is consistent with the proposed tumor suppressor role of PMEPA1. We have defined androgen responsive elements within the upstream sequences of PMEPA1 gene by using in silico regulatory model prediction strategies. Following the predictions, we validated the potential AR-binding sites by in vivo Chromatin Immunoprecipitation assays. We concluded that AR can directly bind to the PMEPA1 gene promoter and may regulate its expression. Conclusions: Taken together, we unraveled the two arms of regulatory loops in the regulation of androgen receptor by PMEPA1. This led us to propose a novel feedback loop between the potential tumor suppressor PMEPA1 and AR proteins. Thus, down-regulation of PMEPA1 in prostate cancer cells may affect increased AR levels. Further investigation of PMEPA1 in androgen receptor functions is in progress.
Glucose Variations During Driving in People With Type 1 Diabetes Using a Continuous Glucose Monitoring System
Authors: Laurent Silvan Schmied, Henryk Zulewski
Journal: Diabetes Care (2019)

OBJECTIVE Hypoglycemic events during driving are life-threatening complications in people with type 1 diabetes (T1D). While preliminary studies showed increased glucose demand in driving simulations, we investigated interstitial fluid (ISF) glucose when driving under real-life circumstances. RESEARCH DESIGN AND METHODS We measured ISF glucose in 10 participants with stable T1D during a 2-h driving course using a continuous glucose monitoring system. RESULTS Our data show a driving-associated rise of ISF glucose. Initially increasing glucose was followed by decreasing values. Under control conditions at the same time of the day without driving, no specific glucose changes were observed. CONCLUSIONS Real-life driving may have caused an initial glucose increase followed by decreasing glucose values in this cohort with well-controlled T1D. These findings may be limited to the selected study population.
Global, regional, and national disability-adjusted life-years (DALYs) for 359 diseases and injuries and healthy life expectancy (HALE) for 195 countries and territories, 1990–2017: a systematic analys
Authors: H Kyu, D Abate, K Abate, S Abay, C Abbafati, N Abbasi, H Abbastabar, F Abd-Allah, J Abdela, A Abdelalim
Journal: The Lancet (2018)
Genomic characteristics of deleterious BRCA1 and BRCA2 alterations and associations with baseline clinical factors in patients with metastatic castration-resistant prostate cancer (mCRPC) enrolled in TRITON2.
Authors: Wassim Abida, Alan Haruo Bryce, Nicholas J. Vogelzang, Robert J. Amato, Ivor John Percent, Jeremy David Shapiro, Raymond S. McDermott, Arif Hussain, Akash Patnaik, Daniel Peter Petrylak, Charles J. Ryan, Thomas S. Stanton, Jingsong Zhang, Andrea Loehr, Andrew Simmons, Darrin Despain, Anthony A. Golsorkhi, Simon Paul Watkins, Howard I. Scher, Simon Chowdhury
Journal: Journal of Clinical Oncology (2019)

5031 Background: The phase 2 TRITON2 study (NCT02952534) is evaluating the PARP inhibitor rucaparib in patients with mCRPC who have a deleterious germline or somatic alteration in BRCA ( BRCA1 or BRCA2) or 1 of 13 other DNA damage repair genes. Here we present analyses of tumor genomics and baseline clinical characteristics in mCRPC patients with a deleterious alteration in BRCA. Methods: Plasma (baseline) and tissue (archival or baseline) samples from patients with a deleterious alteration in BRCA were analyzed using Foundation Medicine next-generation sequencing assays. The alterations and zygosity of the alterations that were detected, as well as the somatic/germline status from Color Genomics testing, were summarized. Associations between genomic alterations, DNA yield, allele frequency, and baseline clinical characteristics were investigated. Results: Results are shown in the Table for a cohort of 40 BRCA2 and 5 BRCA1 patients enrolled in TRITON2 (Abida W et al. Presented at ESMO 2018. Abst 793PD). A biallelic alteration was observed in 21 of the 22 BRCA2 patients (95%) for whom alteration zygosity could be determined. Among the 5 BRCA1 patients, 1 alteration was monoallelic and 4 were of unknown zygosity. Co-occurring alterations in cancer-related or DNA damage repair genes were observed in many patients with BRCA alterations. At baseline, cell-free DNA (cfDNA) yield correlated positively with the sum of target lesions (STL; P= 0.04), but not with prostate-specific antigen (PSA) levels ( P= 0.86). No correlation was observed between allele frequency of the BRCA alteration baseline STL ( P= 0.68) or PSA levels ( P= 0.97). Conclusions: Patients with a BRCA mutation enrolled in TRITON2 demonstrate a profile of genomic alterations consistent with that of prior studies of patients with mCRPC. Plasma cfDNA profiling showed a correlation between baseline cfDNA yield and measurable tumor burden, but not baseline PSA. Clinical trial information: NCT02952534. [Table: see text]
Stenting for symptomatic vertebral artery stenosis: a preplanned pooled individual patient data analysis
Authors: Hugh S Markus, Eric L Harshfield, Annette Compter, Wilhelm Kuker, L Jaap Kappelle, Andrew Clifton, H Bart van der Worp, Peter Rothwell, Ale Algra, Neil Baldwin, Marcus Bradley, Stefan Brew, Robert Crossley, Anand Dixit, Hedley Emsley, Ian Ford, Peter Gaines, Anil Gholkhar, Anthony Goddard, Timothy Hampton, Ahamad Hassan, Nick Higgins, Susanna C Larsson, Ralf-Bjoern Lindert, T Hauw Lo, Jeremy Madigan, Willem P Th M Mali, Frans L Moll, Barry Moynihan, Hans Nahser, Sanjeev Nayak, Maneesh Patel, Bartlomiej Piechowski-Jozwiak, Senthil Raghunathan, Christine Roffe, Wouter J Schonewille, Ursula G Schulz, Alakendu Sekhar, Pankaj Sharma, Jan Albert Vos, David Werring, Siddhartha Wuppalapati
Journal: The Lancet Neurology (2019)
Publisher Correction: Gene expression imputation across multiple brain regions provides insights into schizophrenia risk
Authors: Laura M. Huckins, Amanda Dobbyn, Douglas M. Ruderfer, Gabriel Hoffman, Weiqing Wang, Antonio F. Pardiñas, Veera M. Rajagopal, Thomas D. Als, Hoang T. Nguyen, Kiran Girdhar, James Boocock, Panos Roussos, Menachem Fromer, Robin Kramer, Enrico Domenici, Eric R. Gamazon, Shaun Purcell, Ditte Demontis, Anders D. Børglum, James T. R. Walters, Michael C. O’Donovan, Patrick Sullivan, Michael J. Owen, Bernie Devlin, Solveig K. Sieberts, Nancy J. Cox, Hae Kyung Im, Pamela Sklar, Eli A. Stahl
Journal: Nature Genetics (2019)
BILE CAST SYNDROME- A RARE CAUSE OF BILIARY OBSTRUCTION AFTER LIVER TRANSPLANTATION SUCCESSFULLY MANAGED USING DIGITAL SINGLE-OPERATOR CHOLANGIOSCOPY
Authors: P Karagyozov, I Tishkov, I Boeva
Journal: Endoscopy (2019)

We report a case of bile cast syndrome 6 months after orthotopic liver transplantation successfully diagnosed and treated using digital single-operator cholangioscopy.
Comment on: ‘Anti-Ro52 autoantibodies are associated with interstitial lung disease and more severe disease in patients with juvenile myositis’ by Sabbagh<i>et al</i>
Authors: Zaixing Yang, Yan Liang
Journal: Annals of the Rheumatic Diseases (2019)

Response to: 'Anti-Ro52 autoantibodies are associated with interstitial lung disease and more severe disease in patients with juvenile myositis' by Sabbagh et alWe read with great interest the article by Sabbagh et al 1 published in the Annals of the Rheumatic Diseases.We congratulate the authors for their accuracy and the exhaustive data presented, which clearly demonstrate the importance of anti-Ro52 autoantibodies in disease monitoring, management and prognosis in patients with juvenile myositis.We would like, however, to highlight some key points.First, in this study, 1 the patients with juvenile myositis including juvenile dermatomyositis (JDM), juvenile polymyositis (JPM) and juvenile connective tissue disease-myositis (JCTM) overlap are a highly heterogeneous population.In particular, JCTM added a great heterogeneity to the study population.In reality, there has been still controversy on considering CTM as a distinct entity or rather a complication related to other connective tissue disease itself. 2 3 A recent study 3 showed a distinct entity of CTM compared with PM and DM, featuring more extramuscular involvement and more severe infections.Especially, the prevalence of interstitial lung disease (ILD) in patients with CTM (48%) was significantly higher than that in those with PM (35%) and DM (30.8%).The results of the study by Sabbagh et al indicated that the positive rate of anti-Ro52 autoantibodies in patients with JCTM was higher than that in those with PM and DM.However, the positive rate is also highly heterogeneous among patients with different JCTM, varying from 0 (juvenile systemic sclerosis) to 29% (juvenile idiopathic arthritis). 1 Furthermore, in subgroup analyses of this study, there was a significant difference regarding the prevalence of ILD between patients with and without anti-Ro52 autoantibodies only in JDM group, but no difference in JPM or JCTM groups.As such, anti-Ro52 autoantibodies seemed to be only associated with JDM, but not with JPM or JCTM.In addition, we consider it necessary to validate the association between anti-Ro52 autoantibodies and ILD and other clinical features separately in DM patients by univariate and multivariate analyses, given too few numbers of patients with JCTM or PM.If so, the results will be more significant for clinical practice.Second, in this study, 1 length of follow-up, as one of confounding factors, was included in multivariate analyses using linear or logistic regression to test the independent association of anti-Ro52 autoantibodies with clinical features of juvenile myositis.Although it was not detailed enough about the time when various clinical features occurred (at illness onset or diagnosis or during follow-up), we presume that authors investigated the association between anti-Ro52 autoantibodies and clinical features at illness onset or diagnosis.In this case, length of
A CASE OF EOSINOPHILIC ESOPHAGITIS: HEARTBURN DOES NOT ALWAYS MEAN GASTROESOPHAGEAL REFLUX DISEASE
Authors: N Vidyaeva, S Kashin, V Kaybysheva, E Kraynova, R Kuvaev
Journal: Endoscopy (2019)

A 27-year-old Caucasian man visited a gastrointestinal clinic because of intermittent heartburn and substernal chest discomfort for 6 months. He did not have any allergic histories and family histories of an atopic disease, but he had obesity grade 2 and essential hypertension. Physical examination was unremarkable, and there were no abnormalities in laboratory test results. The primary care doctor diagnosed gastroesophageal reflux disease (GERD) and referred to eophagogastroduodenoscopy (EGD). EGD showed: edema, decreased vascularity, longitudinal furrows, and white exudate on the lower and mid esophagus. Biopsies were obtained: 3 specimens at the proximal and distal esophagus, and also at stomach and duodenum. Whereas histology from stomach and duodenum was normal, eosinophilic infiltration (> 80 eos/hpf) was observed on the esophageal mucosa. Moreover esophageal impedance-pH monitoring did not reveal pathological gastroesophageal reflux (acid exposure time = 0.4%). High-resolution manometry detected normal esophageal motility. Based on the clinical, endoscopic and histological findings, the patient was diagnosed with eosinophilic esophagitis (EoE). Proton pump inhibitors (PPIs) and an empiric six-food elimination diet were prescribed. The patient noted the resolution of symptoms during that therapy. After a 12-week initial therapy course the follow-up endoscopy revealed edema, decreased vascularity, longitudinal furrows, white exudate in the distal esophagus despite of treatment. Magnifying endoscopy with narrow spectrum (i-scan OE) demonstrated dot-shaped intrapapillary capillary loops (IPCL) and absent cyan vessels, which were described in literature for EoE [Tanaka K, et al., 2013] and also multiple white plaques on the mucosal surface. Mucosal biopsies showed maintenance epithelial eosinophil infiltration (> 30 eos/hpf), eosinophil microabscesses and basal zone hyperplasia. Topical corticosteroids were added to therapy. Our case report demonstrates that the proper examination of patients with heartburn provides the correct diagnosis of EoE and helps to distinguish EoE from GERD, which is the most common esophageal disorder with heartburn and sometimes esophageal eosinophilia.
Targeted invalidation of SR-B1 in macrophages reduces macrophage apoptosis and accelerates atherosclerosis
Authors: Lauriane Galle-Treger, Martine Moreau, Raphaëlle Ballaire, Lucie Poupel, Thomas Huby, Emanuele Sasso, Fulvia Troise, Francesco Poti, Philippe Lesnik, Wilfried Le Goff, Emmanuel L Gautier, Thierry Huby
Journal: Cardiovascular Research (2019)

Abstract Aims SR-B1 is a cholesterol transporter that exerts anti-atherogenic properties in liver and peripheral tissues in mice. Bone marrow (BM) transfer studies suggested an atheroprotective role in cells of haematopoietic origin. Here, we addressed the specific contribution of SR-B1 in the monocyte/macrophage. Methods and results We generated mice deficient for SR-B1 in monocytes/macrophages (Lysm-Cre × SR-B1f/f) and transplanted their BM into Ldlr−/− mice. Fed a cholesterol-rich diet, these mice displayed accelerated aortic atherosclerosis characterized by larger macrophage-rich areas and decreased macrophage apoptosis compared with SR-B1f/f transplanted controls. These findings were reproduced in BM transfer studies using another atherogenic mouse recipient (SR-B1 KOliver × Cholesteryl Ester Transfer Protein). Haematopoietic reconstitution with SR-B1−/− BM conducted in parallel generated similar results to those obtained with Lysm-Cre × SR-B1f/f BM; thus suggesting that among haematopoietic-derived cells, SR-B1 exerts its atheroprotective role primarily in monocytes/macrophages. Consistent with our in vivo data, free cholesterol (FC)-induced apoptosis of macrophages was diminished in the absence of SR-B1. This effect could not be attributed to differential cellular cholesterol loading. However, we observed that expression of apoptosis inhibitor of macrophage (AIM) was induced in SR-B1-deficient macrophages, and notably upon FC-loading. Furthermore, we demonstrated that macrophages were protected from FC-induced apoptosis by AIM. Finally, AIM protein was found more present within the macrophage-rich area of the atherosclerotic lesions of SR-B1-deficient macrophages than controls. Conclusion Our findings suggest that macrophage SR-B1 plays a role in plaque growth by controlling macrophage apoptosis in an AIM-dependent manner.
Est-il nécessaire de réaliser une coloscopie chez les patients âgés de 45 ans ou plus suivis pour des rectorragies sur pathologie hémorroïdaire?
Authors: F Bellouhou, F Belabbes, FE Haddar, S Oubaha, Z Samlani, K Krati
Journal: Endoscopy (2019)

Les rectorragies se définit comme la présence de sang rouge vif dans les selles ou en dehors des selles. Elle constitue un motif fréquent de consultationLa pathologie colique chez le sujet âgé est très fréquente, et la coloscopie est l'examen de référence dans l'exploration du côlon. Son rendement diagnostique dépend cependant de plusieurs facteurs notamment les indications. Est-il nécessaire de réaliser une coloscopie totale chez les patients suivie pour des rectorragies sur pathologie hémorroïdaire?
Quantifying the ki-67 heterogeneity profile in prostate cancer.
Authors: Mitchell Kamrava, Shane Mesko, Robyn Banerjee, Jiaoti Huang, D. Jeffrey Demanes, Leonard S. Marks
Journal: Journal of Clinical Oncology (2013)

73 Background: Ki-67 is a robust predictive/prognostic marker in prostate cancer however tumor heterogeneity may compromise its clinical utility when Ki-67 is determined off of prostate biopsy samples. We examined the variation of Ki-67 in prostate biopsy samples by NCCN risk groups and the location of the highest Ki-67 relative to the most dominant lesion on multiparametric (MP) MRI. Methods: An IRB approved retrospective analysis was done on 77 consecutive men whose prostate biopsies revealed cancer. Using a MRI/US fusion device (Artemis), biopsy cores were obtained systematically and when MRI indicated a lesion, by targeting. Ki-67 staining was determined by a manual semi-quantitative method and reported as % of positive cells. The highest Ki-67 per patient was used to determine inter-prostatic variation. Ki-67 range (highest Ki-67 minus lowest Ki-67 value) was used to determine intra-prostatic variation on a subset of 47 patients with ≥2 positive biopsy cores. Ki-67 range was also used to evaluate intra-lesion variation on 31 MP MRI defined lesions with &gt; 1 targeted positive biopsy core. The relationship of the dominant lesion (lesion with the largest tumor diameter) to the highest Ki-67 in the entire prostate was examined for 10 patients with ≥2 distinct lesions on MP MRI. Analysis of variance (ANOVA) was used to evaluate differences between the means of NCCN-defined risk groups. Results: Inter-prostatic Ki-67 mean±standard deviation (SD) values for low, intermediate and high risk patients were 5.1% ± 3.8%, 7.4% ± 6.8%, and 12.0% ± 12.4% (ANOVA p=0.01). Intra-prostatic mean±SD Ki-67 ranges in low, intermediate, and high risk patients were 2.6% ± 3.4%, 4.6% ± 6.4%, 9.5% ± 10.6% (ANOVA p = 0.0246). Intra-lesion mean±SD Ki-67 ranges in low, intermediate and high risk patients were 1.0%±1.0%, 4.0%±4.29%, and 6.7%±11.51% (ANOVA p=0.39). The dominant lesion harbored the highest Ki-67 30% of the time. Conclusions: High risk patients have significantly higher inter- and intra-prostatic Ki-67 heterogeneity profiles than men with low/intermediate risk disease. The highest Ki-67 is often not located in the dominant MRI defined lesion. This data can inform future biopsy strategies when integrating Ki-67 into clinical practice.
Concussions and Dementia—Are Statins the Salve in the Wound?
Authors: Rachel A. Whitmer
Journal: JAMA Neurology (2019)

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