tbuckley/cabot-search huggingface dataset:
Drugs That May Cause or Exacerbate Heart Failure
Authors: Robert L. Page, Cindy L. O’Bryant, Davy Cheng, Tristan J. Dow, Bonnie Ky, C. Michael Stein, Anne P. Spencer, Robin J. Trupp, JoAnn Lindenfeld
Journal: Circulation (2016)

Heart failure is a common, costly, and debilitating syndrome that is associated with a highly complex drug regimen, a large number of comorbidities, and a large and often disparate number of healthcare providers. All of these factors conspire to increase the risk of heart failure exacerbation by direct myocardial toxicity, drug-drug interactions, or both. This scientific statement is designed to serve as a comprehensive and accessible source of drugs that may cause or exacerbate heart failure to assist healthcare providers in improving the quality of care for these patients.
Epigenome-Wide Meta-Analysis of Methylation in Children Related to Prenatal NO <sub>2</sub> Air Pollution Exposure
Authors: Olena Gruzieva, Cheng-Jian Xu, Carrie V. Breton, Isabella Annesi-Maesano, Josep M. Antó, Charles Auffray, Stéphane Ballereau, Tom Bellander, Jean Bousquet, Mariona Bustamante, Marie-Aline Charles, Yvonne de Kluizenaar, Herman T. den Dekker, Liesbeth Duijts, Janine F. Felix, Ulrike Gehring, Mònica Guxens, Vincent V.W. Jaddoe, Soesma A. Jankipersadsing, Simon Kebede Merid, Juha Kere, Ashish Kumar, Nathanael Lemonnier, Johanna Lepeule, Wenche Nystad, Christian Magnus Page, Sviatlana Panasevich, Dirkje Postma, Rémy Slama, Jordi Sunyer, Cilla Söderhäll, Jin Yao, Stephanie J. London, Göran Pershagen, Gerard H. Koppelman, Erik Melén
Journal: Environmental Health Perspectives (2016)

Prenatal exposure to air pollution is considered to be associated with adverse effects on child health. This may partly be mediated by mechanisms related to DNA methylation.We investigated associations between exposure to air pollution, using nitrogen dioxide (NO2) as marker, and epigenome-wide cord blood DNA methylation.We meta-analyzed the associations between NO2 exposure at residential addresses during pregnancy and cord blood DNA methylation (Illumina 450K) in four European and North American studies (n = 1,508) with subsequent look-up analyses in children ages 4 (n = 733) and 8 (n = 786) years. Additionally, we applied a literature-based candidate approach for antioxidant and anti-inflammatory genes. To assess influence of exposure at the transcriptomics level, we related mRNA expression in blood cells to NO2 exposure in 4- (n = 111) and 16-year-olds (n = 239).We found epigenome-wide significant associations [false discovery rate (FDR) p < 0.05] between maternal NO2 exposure during pregnancy and DNA methylation in newborns for 3 CpG sites in mitochondria-related genes: cg12283362 (LONP1), cg24172570 (3.8 kbp upstream of HIBADH), and cg08973675 (SLC25A28). The associations with cg08973675 methylation were also significant in the older children. Further analysis of antioxidant and anti-inflammatory genes revealed differentially methylated CpGs in CAT and TPO in newborns (FDR p < 0.05). NO2 exposure at the time of biosampling in childhood had a significant impact on CAT and TPO expression.NO2 exposure during pregnancy was associated with differential offspring DNA methylation in mitochondria-related genes. Exposure to NO2 was also linked to differential methylation as well as expression of genes involved in antioxidant defense pathways. Citation: Gruzieva O, Xu CJ, Breton CV, Annesi-Maesano I, Antó JM, Auffray C, Ballereau S, Bellander T, Bousquet J, Bustamante M, Charles MA, de Kluizenaar Y, den Dekker HT, Duijts L, Felix JF, Gehring U, Guxens M, Jaddoe VV, Jankipersadsing SA, Merid SK, Kere J, Kumar A, Lemonnier N, Lepeule J, Nystad W, Page CM, Panasevich S, Postma D, Slama R, Sunyer J, Söderhäll C, Yao J, London SJ, Pershagen G, Koppelman GH, Melén E. 2017. Epigenome-wide meta-analysis of methylation in children related to prenatal NO2 air pollution exposure. Environ Health Perspect 125:104-110; http://dx.doi.org/10.1289/EHP36.
Dyspepsia and the microbiome: time to focus on the small intestine
Authors: Laurie Zhong, Erin R Shanahan, Ashok Raj, Natasha A Koloski, Linda Fletcher, Mark Morrison, Marjorie M Walker, Nicholas J Talley, Gerald Holtmann
Journal: Gut (2016)

We note with interest two recent publications in Gut regarding alterations to the gut microbiome in individuals on proton pump inhibitor (PPI) therapy.1 ,2 With PPI use, both studies observed an increase in oral bacteria in the stool. These changes overlap with those described in patients with cirrhosis of the liver.3 However, very little is known about the impact of this dysbiosis over the length of the GI tract, and how it may link to gut function.

While the data from both Jackson et al 1 and Imhann et al 2 are demonstrative of a shift towards oral-associated bacteria, it is important to note that many of these bacteria have also been identified in the stomach and small intestine. Recently, we have shown that although the microbiota found in the healthy duodenum are taxonomically similar to the oral microbiota, their presence and association with the intestinal mucosa is not merely a result of luminal contamination.4 Thus, small intestinal dysbiosis and its potential impact on the gut must also be considered.

Compared with studies …
Evaluation of New-Onset Ascites
Authors: Yuval A. Patel, Andrew J. Muir
Journal: JAMA (2016)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Loss of PIKFyve Kinase Function Driven by Platelet Factor 4 Promoter Results in Platelet Lysosomal Storage Defects and Infiltration of Multiple Organs with Vacuolated Macrophages
Authors: Sang Min, Aae Suzuki, Liang Zhao, Lurong Lian, Timothy J. Stalker, John K. Choi, Charles S. Abrams
Journal: Blood (2011)
A Phase I Trial of the Histone Deacetylase (HDAC) Inhibitor, Panobinostat, in Combination with Lenalidomide in Patients with Relapsed/Refractory Hodgkin's Lymphoma (HL)
Authors: Beth Christian, Anne Kopko, Todd A. Fehniger, Nancy L. Bartlett, Kristie A. Blum
Journal: Blood (2012)
Abstract 106: Transcriptionnal profiling of upper-tumor urothelial carcinomas
Authors: Gabriel Malouf, Roger Mouawad, Xiaoping Su, Hui Yao, Eva Comperat, Morgan Roupret, Jean-Philippe Spano, David Khayat
Journal: Cancer Research (2016)

Abstract Background: Upper-tumor urothelial carcinomas (UTUC) represent 5% among all urothelial tumors. The most frequent histological variant is transitional cell carcinomas (TCC). UTUC might arise within renal pelvis or ureters. Several studies suggested aggressive behavior of tumors arising within the ureter as compared to those which develop within renal pelvis. However, whether there is a biological basis of this difference remains unknown. Methods: We performed RNAsequencing on fourteen UTUC including 6 cases arising in the ureter and 8 in renal pelvis. Library prep followed by next-generation sequencing were done using Illumina Hiseq platform. Unsupervised clustering using differentially expressed genes was used to identify cancer subtypes. Identified subtypes were correlated with clinico-pathological features. Pathway analysis was performed using Gene Set Enrichment Analysis (GSEA). Results: Unsupervised clustering of gene expression revealed two clusters. Surprisingly, all tumors (n = 5/5) encompassing C1 were located in the ureters as compared to only one (n = 1/9) in C2 cluster (p = 0.003). No difference was observed between C1 and C2 clusters according to age, gender, grade, muscle-invasion status and stage. Using stringer cut-off (fold change ≥ or ≤-2 and FDR&amp;lt;0.05), 34 genes were found to be differentially expressed between the 2 clusters. GSEA revealed negative enrichment of several pathways related to B and T-cell activation in C1 relative to C2 cluster. This was the case for NAIVE_TCELL_VS_DC_UP (p = 0.01; FDR = 0.16) and NAIVE_BCELL_VS_NEUTROPHIL_UP (p = 0.002; FDR = 0.12). Among the most overexpressed genes in C1 cluster, we identified the serine/threonine-protein kinase gene SGK2 (Fold change = 17; FDR = 0.004) as a putative therapeutic target. Of note, AIM2 which is part of the inflammasome with a key role in tumorigenic reversion was one of the most down-regulated genes (fold change = -24; FDR = 0.02) in C1 cluster. Conclusion: Our report suggests that transcriptional profiling of UTUC arising in the ureters and renal pelvis might be distinct. The observed difference might be related to immune response. Validation of these data in a larger independent cohort with analysis of the immune infiltrate is required. Citation Format: Gabriel Malouf, Roger Mouawad, Xiaoping Su, Hui Yao, Eva Comperat, Morgan Roupret, Jean-Philippe Spano, David Khayat. Transcriptionnal profiling of upper-tumor urothelial carcinomas. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 106.
Case 55-1962
Authors: H. Walter Jones, Austin L. Vickery
Journal: New England Journal of Medicine (1962)

Presentation of CaseA fifty-six-year-old woman was admitted to the hospital because of shortness of breath.Six months previously increasing fatigue and weakness, accompanied by a chronic, nonproductive cough, developed. Three months before entry the patient was awakened by sudden, severe pain in the left arm extending to the elbow; the left hand was also painful. She perspired but was not dyspneic, and the pain disappeared spontaneously within an hour. Soon thereafter she began to experience exertional dyspnea, without orthopnea, paroxysmal nocturnal dyspnea, edema or chest pain. Two weeks before admission the exertional dyspnea rapidly increased in severity, and considerable . . .
Abstract 5174: Modeling mesothelioma initiation through disruption of the Hippo pathway revealed involvement of PLCB4 in YAP-driven mesothelioma cell proliferation
Authors: tatsuo kakiuchi.
Journal: Cancer Research (2016)

Abstract Disruption of the Hippo pathway as a result of deletion and/or mutation of the involved genes (e.g., neurofibromin 2 [NF2]) is frequently observed in mesothelioma. The disruption results in reduced phosphorylation of yes-associated protein (YAP), and the non-phosphorylated YAP translocates to the nucleus and regulates gene expression. While the roles of the disrupted Hippo pathway in the maintenance of established tumors have been investigated using mesothelioma cell lines, its involvement in the initiation of mesothelioma remains unclear. We used immortalized human mesothelial cells to study the transformation process, and found that NF2 knockdown led to transformation of the cells concurrently with reduction in YAP phosphorylation. The cells exhibited enhanced growth in vitro, and formed tumors following transplantation into nude mice. Similar results to those obtained by NF2 knockdown were also obtained using enforced expression of wild-type (wt) or constitutively active (S127A) YAP. Although enforced expression of YAPwt or YAPS127A was insufficient to transform primary (unimmortalized) human mesothelial cells, our findings provide evidence for the crucial roles of activated YAP in the transformation of mesothelial cells. To identify YAP-regulated genes critical for mesothelial tumorigenesis, we conducted gene expression analysis comparing control- and YAP-transduced immortalized human mesothelial cells. Gene Set Enrichment Analysis (GSEA) using a gene set down-regulated by YAP knock-down in mesothelioma cell lines revealed phospholipase C beta 4 (PLCB4) to be among the top-ranking genes up-regulated by YAP in our experiments. PLCB4 was up-regulated by YAP in immortalized human mesothelial cells, and down-regulated by YAP knock-down in YAP-driven mesothelioma cells. shRNA-mediated silencing of PLCB4 attenuated the growth of YAP-transduced mesothelial cells and Hippo-disrupted, but not -proficient, mesothelioma cell lines. Our model system thus provides a versatile tool to investigate the mechanisms underlying mesothelioma development. We suggest that PLCB4 may be an attractive drug target for the treatment of malignant mesothelioma. Citation Format: tatsuo kakiuchi. Modeling mesothelioma initiation through disruption of the Hippo pathway revealed involvement of PLCB4 in YAP-driven mesothelioma cell proliferation. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 5174.
Peripherally Inserted Central Catheters—Improving Appropriateness With a Dedicated and Rigorous Team—Reply
Authors: Vineet Chopra, Steven J. Bernstein, Scott A. Flanders
Journal: JAMA Internal Medicine (2016)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Internal Medicine journal
Treatment of AL Amyloidosis with Tandem Cycles of High Dose Melphalan and Autologous Stem Cell Transplantation: Final Analysis of a Prospective Trial.
Authors: Vaishali Sanchorawala, Daniel G. Wright, Karen Quillen, Laura M. Dember, John L. Berk, Kathleen T. Finn, Martha Skinner, David C. Seldin
Journal: Blood (2006)
Role of Operative Complexity Variables in Risk Adjustment for Patients With Cancer
Authors: Jason B. Liu, Sharon M. Weber, Julia R. Berian, Shenglin Chen, Mark E. Cohen, Clifford Y. Ko, Karl Y. Bilimoria
Journal: JAMA Surgery (2016)

This study reports on the Oncology NSQIP National Cancer Center Collaborative collecting 3 additional case characteristics representing greater operative complexity and risk with the aim to improve patient risk prediction and case-mix adjustment.
The Bone Marrow Niche of Patients with Acute Lymphoblastic Leukemia Produces No Increased Asparagine Levels In Vivo That May Lead to Clinical Asparaginase Resistance
Authors: Wing H. Tong, Rob Pieters, Wim C.J. Hop, Claudia Lanvers-Kaminsky, Joachim Boos, Inge M. van der Sluis
Journal: Blood (2011)
Abstract 2187: Garcinone inhibits nasopharyngeal carcinoma cell growth and arrests cell cycle via modulating the expression of ATR/Stat3/4E-BP1
Authors: Yudui Xia, Xia Liu, Chunllin Zou, Hongwei Guo, Yeguo Yang, Yong Lei, Jian Zhang, Yi Lu
Journal: Cancer Research (2016)

Abstract Nasopharyngeal carcinoma (NPC) is one of the common head and neck malignancies. Radiotherapy and chemotherapy are the standard treatments for NPC. Garcinone, a natural compound isolated from Garcinia oblongifolia Champ., is a xanthone derivative and has been shown to have potential cytotoxic effects on certain cancer types. However, there have been limited studies performed on its effects on NPC cells and the mechanisms of these effects remain unknown. In this study, we firstly found that garcinone significantly inhibited cell viability of human NPC cell lines CNE1, CNE2, HK1, and HONE1. This inhibition was in a time- and dose-dependent manner. Then, flow cytometry analysis was performed on cell cycle analysis. We observed that garcinone arrested cell cycle at S phase. With 10μM of high-dose garcinone treatment, the cells exhibited necrotic morphology changes including cell swelling, rough endoplasmic reticulum (ER) degranulation, ER dilatation, mitochondria swelling, and vacuolar degeneration. Finally, we found that garcinone stimulated the expression levels of ATR and 4E-BP1, while efficiently inhibited the expression levels of Cyclin B1, Cyclin D1, Cyclin E2, cdc2, CDK7, and Stat3. Collectively, the ability of garcinone to inhibit NPC in vitro suggested that garcinone might be a novel agent for the management of NPC. Supported by NSFC Key Project 81130046; NSFC Project 81171993 and NSFC81272415; Guangxi Key Projects 2013GXNSFEA053004 and 2012GXNSFCB053004; Guangxi Ministry of Education 201202ZD022 and 201201ZD004. Citation Format: Yudui Xia, Xia Liu, Chunllin Zou, Hongwei Guo, Yeguo Yang, Yong Lei, Jian Zhang, Yi Lu. Garcinone inhibits nasopharyngeal carcinoma cell growth and arrests cell cycle via modulating the expression of ATR/Stat3/4E-BP1. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2187.
Reply to Patrick O. Richard, Micheal A.S. Jewett and Antonio Finelli's Letter to the Editor re: Alexander Kutikov, Marc C. Smaldone, Robert G. Uzzo, Miki Haifler, Gennady Bratslavsky, Bradley C. Leibovich. Renal Mass Biopsy: Always, Sometimes, or Never? Eur Urol 2016;70:403–6
Authors: Alexander Kutikov, Robert G. Uzzo, Marc C. Smaldone, Miki Haifler, Gennady Bratslavsky, Bradley C. Leibovich
Journal: European Urology (2016)
Mucosectomie ou résection à l’anse diathermique des volumineux polypes colo-rectaux sessiles: un essai randomisé
Authors: N. Musquer
Journal: Endoscopy (2016)

Cette étude prospective randomisée monocentrique japonaise avait pour objectif principal de comparer deux techniques de résection des polypes sessiles: l’exérèse à l’anse diathermique (“anse chaude”) sans injection sous-muqueuse et la mucosectomie classique. Cent-trente polypes (109 patients) supra-centimétriques ont été inclus sur une année et ont été randomisés à part égale entre les 2 techniques.
Abstract 4557: Tip110-mediated regulation of NF-κB activity is key to tumorigenesis
Authors: Khalid Amine Timani, Amanda Whitmill, Ying Liu, Johnny J. He
Journal: Cancer Research (2016)

Abstract HIV-1 Tat-interacting protein (Tip110), also known as squamous cell carcinoma antigen recognized by T cells 3 (SART3), is a multifaceted nuclear protein and has been shown to function in tumor antigenicity. Tip110 protein expression is very low in normal tissues and non-proliferating cells but becomes highly elevated in a number of malignant tumor cell lines and cancerous tissues, pointing to its possible role in tumorigenesis. Our previous studies have shown that Tip110 specifically interacted with oncogenic deubiquitinating enzyme, USP15, and that ectopic expression of the Tip110 protein led to re-distribution of USP15 from the cytoplasm to the nucleus. USP15 is known to inhibit TNF-α-induced NF-κB activity by modulation of IκB-α ubiquitination. In the current study, we demonstrated that Tip110 augmented TNF-α-induced transcription activity of NF-κB, and that deletion of the nuclear localization domain in Tip110 obliterated the observed enhancement of TNF-α-induced NF-κB activity, providing the very first evidence to support the specific role of Tip110 in NF-κB activation. In addition, we found that Tip110 expression modulated IκB-α phosphorylation and that activation of NF-κB by Tip110 was mediated through the p38/MAPK pathway. Moreover, we showed that ectopic expression of Tip110 induced translocation of NF-κB p65 from the cytoplasm to the nucleus, reminiscent of the aforementioned translocation of USP15, in the absence of direct interaction of Tip110 with either p65 or IκB-α. Taken together, these results indicate that opposing regulation of TNFα-induced NF-κB activity by Tip110 and USP15 could be pivotal for modulation of tumorigenesis. Further delineation of the underlying signaling cascades will likely provide new insights into development of anti-tumor agents. Citation Format: Khalid Amine Timani, Amanda Whitmill, Ying Liu, Johnny J. He. Tip110-mediated regulation of NF-κB activity is key to tumorigenesis. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 4557.