tbuckley/cabot-search huggingface dataset:
A Genome-Wide Association Study of Susceptibility to Acute Lymphoblastic Leukemia in Adolescents and Young Adults
Authors: Virginia Perez-Andreu, Kathryn G. Roberts, Xu Heng, Colton Smith, Hui Zhang, Wenjian Yang, Richard C. Harvey, Debbie Payne-Turner, Meenakshi Devidas, I-Ming Cheng, William L. Carroll, Nyla A. Heerema, Andrew J. Carroll, Elizabeth A. Raetz, Julie M. Gastier-Foster, Guido Marcucci, Clara D. Bloomfield, Krzysztof Mrózek, Jessica Kohlschmidt, Wendy Stock, Steven M. Kornblau, Marina Konopleva, Elisabeth Paietta, Jacob M. Rowe, Selina M. Luger, Martin S. Tallman, Ching-Hon Pui, Sima Jeha, Mary V. Relling, William E. Evans, Daniela S. Gerhard, Mignon L. Loh, Cheryl L. Willman, Stephen P. Hunger, Charles G. Mullighan, Jun J. Yang
Journal: Blood (2014)
Long-term Outcomes Following Kidney and Liver Transplant in Recipients With HIV
Authors: Arya Zarinsefat, Arushi Gulati, Amy Shui, Hillary Braun, Rodney Rogers, Ryutaro Hirose, Nancy Ascher, Peter Stock
Journal: JAMA Surgery (2022)

<h3>Importance</h3> Kidney transplant (KT) and liver transplant (LT) in HIV-positive patients have become more widely adopted. Data looking at long-term outcomes of patient and graft survival are lacking. <h3>Objective</h3> To compare the long-term outcomes of KT and LT in HIV-positive recipients with matched HIV-negative recipients. <h3>Design, Setting, and Participants</h3> Retrospective, single-center, cohort, study using data from 2000 to 2019. Patients were observed until death, or graft failure requiring retransplant. All HIV-positive patients who underwent KT and/or LT between 2000 and 2019 were included. Propensity matching was performed to the corresponding HIV-negative cohort, which was obtained from the University of California, San Francisco's transplant recipient registry. The data were analyzed from 2020 to 2021. <h3>Exposures</h3> HIV infection. <h3>Main Outcomes and Measures</h3> Patient and graft survival for KT and patient survival for LT. Incidence of acute rejection and its association with KT graft survival. <h3>Results</h3> For KT, 655 HIV-negative recipients (mean [SD] age, 52.3 [13.6] years; 450 [68.7%] were men) and 119 HIV-positive recipients (mean [SD] age, 51.7 [9.4] years; 86 [72.3%] were men) were included. Patient survival was 79.6% (95% CI, 73.6%-86.1%) and 53.6% (95% CI, 38.9%-74.0%) at 15 years posttransplant, respectively. Graft survival was 57.0% (95% CI, 47.8%-68.0%) and 75.0% (95% CI, 65.3%-86.2%) at 15 years posttransplant, respectively. Diagnosis of HIV was not associated with worse graft survival (hazard ratio, 1.09; 95% CI, 0.61-1.97;<i>P</i> = .77). For LT, 80 HIV-positive recipients (mean [SD] age, 52.6 [8.2] years; 53 [66.3%] were men) and 440 HIV-negative recipients (mean [SD] age, 54.6 [12.8] years; 291 [66.1%] were men) were included. Patient survival was 75.7% (95% CI, 71.8%-79.8%) for HIV-negative LT recipients and 70.0% (95% CI, 60.6%-80.8%) for HIV-positive LT recipients at 15 years posttransplant. Diagnosis of HIV was not a statistically significant predictor of patient survival (hazard ratio, 1.36; 95% CI, 0.83-2.24;<i>P</i> = .22). In KT, HIV-positive patients with at least 1 episode of acute rejection had a graft survival of 52.8% (95% CI, 38.4%-72.5%;<i>P</i> &lt; .001) at 15 years posttransplant, compared with 91.8% in those without AR. <h3>Conclusions and Relevance</h3> In this single-center cohort study, KT and LT in HIV-positive patients had comparable long-term outcomes with those in matched HIV-negative patients. The high incidence of acute rejection was associated with reduced graft survival. The findings support providing transplant to HIV-positive patients, which may be an appropriate use of transplant resources and provides equitable access for HIV-positive patients.
Abstract P261: Associations of Left Ventricular Mass, Total Body Weight, and Fat-Free Mass With Body Mass Index: The Framingham Heart Study
Authors: Philimon N Gona, Jane J Lee, Carol J Salton, Saadia Qazi, Christopher J O'Donnell, Warren J Manning, Michael L Chuang
Journal: Circulation (2018)

Introduction: Increased left ventricular mass (LVM) predicts excess cardiovascular morbidity and mortality. LVM is often indexed to height (HT) or body surface area (BSA). HT-indexation ignores weight and thus obesity. The relationship of indexed LVM with weight, obesity, and adiposity is unclear. We investigated the association of LVM with total-body mass (TBM, i.e. weight) and fat-free mass (FFM), hypothesizing that LVM scales better to FFM than TBM. Methods: From the 1794 members of Framingham Offspring cohort who underwent cardiac magnetic resonance (CMR), we identified 845 (aged 65±9y) without any history of hypertension, myocardial infarction, heart failure, or CMR wall-motion abnormality. LVM was measured from cine bSSFP images and indexed to HT, BSA, TBM and FFM (by DEXA). Participants were stratified by sex and body mass index (BMI) category (NL=BMI 18.5 - 24.9; OW=25.0 - 29.9; OB=30.0+ kg/m 2 ). We used sex-specific ANCOVA to test for linear trend across BMI categories, and determined sex-specific Pearson correlation coefficients of LVM with BMI; both sets of analyses were adjusted for age and systolic blood pressure. Data are summarized as mean ± SD. Results: The Table shows that LVM and LVM/HT increase with greater BMI-category in both sexes. LVM/BSA was similar across BMI-categories, while LVM/TBM decreased. There was no linear trend across BMI-categories for LVM/FFM in either sex. On a continuous basis, LVM and LVM/HT were positively correlated with BMI in both sexes (r=0.20 to 0.35, p&lt;0.001 for all); LVM/BSA was weakly inversely correlated with BMI in women only (r=-0.14, p=0.001) but not men (r=-0.08, p=0.18); LVM/TBM was inversely correlated with BMI (M: r=-0.39, W: r=-0.54; p&lt;0.0001 both); LVM/FFM was not correlated with BMI in either sex (M: r=-0.05, p=0.38, W: r=0.08, p=0.055). Conclusion: LVM as a proportion of TBM (weight) actually decreases with greater BMI, while LVM/FFM is not associated with BMI. Whether LVM is better scaled to FFM vs HT, BSA or TBM for risk stratification purposes remains to be determined.
Survival expressed in best-case, typical and worst-case scenarios for patients with nonmetastatic esophagogastric cancer: A population-based study.
Authors: Steven Kuijper, Marieke Pape, Pauline A.J. Vissers, Paul M. Jeene, Ewout Kouwenhoven, Nadia Haj Mohammad, Meindert Sosef, Rob Verhoeven, Hanneke W.M. Van Laarhoven
Journal: Journal of Clinical Oncology (2022)

259 Background: In recent years new treatment options and the centralization of surgery have improved survival for patients with non-metastatic esophageal and gastric cancer. However, it is currently unknown which patients have mostly benefitted from these treatment advances. The aim of this study was to use population-based data to identify best-case, typical and worst-case scenarios in terms of survival time, and to assess if the survival of these scenarios have changed over time. Methods: Patients diagnosed between 2006-2019 with non-metastatic esophageal (including gastro-esophageal junction tumors) or gastric cancer were selected from the Netherlands Cancer Registry. Best-case, typical, and worst-case scenarios were calculated from the 20 th (best-case scenario), 40 th (upper-typical), 50 th (median), 60 th (lower-typical) and 80 th (worst-case scenario) percentiles of the survival curves. Linear trend analysis was used to investigate the change in survival time for each scenario across diagnosis years. Results: We identified 23350 patients with non-metastatic esophageal cancer and 10150 patients with non-metastatic gastric cancer. Linear trend analyses across diagnosis years showed that for esophageal cancer patients, survival of all scenarios significantly increased over time: the best-case scenario increased from 55 to 112 months (p =.003); the upper typical increased from 18 to 33 months (p &lt;.001); the median increased from 13 to 23 months (p &lt;.001); the lower typical increased from 8 to 15 months (p &lt;.001) and the worst-case scenario increased from 4 to 7 months (p &lt;.001). For patients with gastric cancer, all scenarios also improved significantly: the best-case scenario increased from 73 to 99 months (p =.045); the upper-typical increased from 22 to 33 months (p &lt;.001); the median increased from 14 to 18 months (p &lt;.001); the lower-typical increased from 14 to 18 months (p &lt;.001) and the worst-case scenario increased slightly from 2.9 months to 3.0 (p =.017). Conclusions: All patients with non-metastatic esophageal and gastric cancer have improved their survival over time.The largest survival advantage was among the best-case and upper-typical scenarios. Therefore, treatment advances over the last years have improved survival for all patients with non-metastatic esophagogastric cancer.
Intravascular ultrasound characteristics of restenotic carotid stenoses following surgical endarterectomy Michael A. Peterson, Neil J. Weissman, Gary S. Mintz, Daniel A. Canos, Michael R. Jaff, Olga Rosales, John R. Laird, Jr., Lowell F. Satler. Washington Hospital Center, Washington, DC
Journal: Journal of the American College of Cardiology (2001)
Update Alert: Use of N95, Surgical, or Cloth Masks to Prevent COVID-19 in Health Care and Community Settings: Living Practice Points From the American College of Physicians (Version 1)
Authors: Amir Qaseem, Itziar Etxeandia-Ikobaltzeta, Jennifer Yost, Linda L. Humphrey
Journal: Annals of Internal Medicine (2020)

in Health Care and Community Settings: Living Practice Points From the American College of Physicians (Version 1)This letter serves as a brief update and notification to retire the American College of Physicians' (ACP) living practice points on the use of N95, surgical, or cloth masks to prevent coronavirus disease 2019 in health care and community settings (1) from living status.The decision to retire these practice points from living status was made in light of several considerations.Since the initial publication, 2 surveillance reports for the rapid, living review have been published (2, 3) and both determined that the new evidence does not change the conclusions of the original evidence report (4).Through 2 August 2020, two new observational studies were identified: 1 on mask use and risk for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in community settings (insufficient evidence) (2) and 1 on mask use and risk for SARS-CoV-2 infection in a health care setting (insufficient evidence) (3).The ACP's Scientific Medical Policy Committee (SMPC) reviewed the surveillance reports and determined that, in the absence of any conclusive evidence, an update to the current practice points is not warranted at this time (1).Given that the past 2 updates have identified only 2 new studies of poor methodological quality, the SMPC considers this a signal that the likelihood of new evidence emerging in the near future that would lead to a change in the practice points is low.In addition, the practice points on this topic were initially developed to meet a priority need for decision making.However, with the increased alignment in guidance from key health organizations (such as the Centers for Disease Control and Prevention [5] and World Health Organization [6]), the implementation of community and statewide guidelines, and the widespread adherence to such guidelines in community and health care settings, the SMPC has determined that maintaining this topic as living is no longer a priority for decision making.
Abstract 212: Card9-mediated Signaling is Critical to Cytokine Production in Mice With PM Exposure
Authors: Xuanyou Liu, Yuqi Cui, Yichao Xiao, Qingyi Zhu, Meng Jiang, Yunyan Duan, Hong Hao, Joseph Abraham, Bimei Jiang, Rulong Shen, Qinghua Sun, Zhenguo LIU
Journal: Circulation Research (2017)

Oxidative stress and inflammation are considered an important mechanism for the development of cardiovascular diseases. Cytokines including interleukin (IL)-6 and tumor necrosis factor-α (TNF-α) play an important role in oxidative stress and inflammation. It is known that ambient fine particulate matter ( PM ) exposure is closely associated with cardiovascular diseases and oxidative stress. Caspase-recruitment domain 9 ( Card9 ) signaling is critically involvement in the function of macrophages, neutrophils and monocytes that are important for oxidative stress and inflammation. The present study was designed to evaluate the role of CARD9-mediated signaling in cytokines production in mice with PM exposure. Both male wild-type (WT) C57BL/6 mice (8-10 weeks) and age-matched CARD9 knockout (KO) mice (with C57BL/6 background) were exposed to PM2.5 for 6 weeks via intranasal approach with PBS as the control. Serum concentrations of the cytokines including IL-6, IL-1β, and TNF-α were measured with ELISA in the mice before and after PM exposure. There was no difference in the serum levels of IL-6, IL-1β, or TNF-α between WT mice and CARD9 KO mice exposed to PBS. As expected, PM exposure substantially increased the serum levels of IL-6, IL-1β, and TNF-α in the WT mice (by up to 6 times). However, no significant increase in the serum concentrations for IL-6, IL-1β, and TNF-α was observed in CARD9 KO mice exposed to PM. Increased inflammatory infiltrations in the lungs were observed in the WT mice as compared to the CARD9 KO mice with PM exposure. In conclusion, the present study demonstrated that increased cytokines were produced in WT mice, but not in CARD9 KO mice with PM exposure. The data suggested that CARD9 signaling played a critical role in the production of inflammatory cytokines in the mice in response to PM exposure, and might contribute to the development of cardiovascular diseases related to PM exposure.
Deaths
Journal: JAMA (1931)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
ADDRESSES.
Journal: JAMA (1893)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
Oxidative Stress and Metabolism: A Mechanistic Insight for Glyphosate Toxicology
Authors: Xiaojing Wang, Qirong Lu, Jingchao Guo, Irma Ares, Marta Martínez, María-Rosa Martínez-Larrañaga, Xu Wang, Arturo Anadón, María-Aránzazu Martínez
Journal: The Annual Review of Pharmacology and Toxicology (2022)

Glyphosate (GLYP) is a widely used pesticide; it is considered to be a safe herbicide for animals and humans because it targets 5-enolpyruvylshikimate-3-phosphate synthase. However, there has been increasing evidence that GLYP causes varying degrees of toxicity. Moreover, oxidative stress and metabolism are highly correlated with toxicity. This review provides a comprehensive introduction to the toxicity of GLYP and, for the first time, systematically summarizes the toxicity mechanism of GLYP from the perspective of oxidative stress, including GLYP-mediated oxidative damage, changes in antioxidant status, altered signaling pathways, and the regulation of oxidative stress by exogenous substances. In addition, the metabolism of GLYP is discussed, including metabolites,metabolic pathways, metabolic enzymes, and the toxicity of metabolites. This review provides new ideas for the toxicity mechanism of GLYP and proposes effective strategies for reducing its toxicity.
LEAP-012 trial in progress: Transarterial chemoembolization (TACE) with or without lenvatinib plus pembrolizumab for intermediate-stage hepatocellular carcinoma (HCC)
Authors: Anthony B. El-Khoueiry, Josep M Llovet, Arndt Vogel, David C. Madoff, Richard S. Finn, Sadahisa Ogasawara, Zhenggang Ren, Kalgi Mody, Jerry J. Li, Abby B. Siegel, Leonid Dubrovsky, Masatoshi Kudo
Journal: Journal of Clinical Oncology (2022)

TPS494 Background: Limited treatment options are available for patients with intermediate HCC. Lenvatinib, a potent multikinase inhibitor, and pembrolizumab, a PD-1 inhibitor, are approved first- and second-line therapies for advanced HCC, respectively. The LEAP-012 study (NCT04246177) is investigating lenvatinib plus pembrolizumab in combination with TACE versus placebo plus TACE in patients with intermediate-stage HCC. Methods: LEAP-012 is a randomized, double-blind, phase 3 study. Adults with confirmed HCC localized to the liver without portal vein thrombosis and not amenable to curative treatment, ≥1 measurable lesion per RECIST v1.1, Eastern Cooperative Oncology Group performance status of 0 or 1, and no previous systemic treatment for HCC are eligible. Patients will be randomly assigned to receive lenvatinib 8 mg (body weight &lt; 60 kg) or 12 mg (body weight ≥60 kg) orally once daily plus pembrolizumab 400 mg intravenously (IV) every 6 weeks (Q6W) plus TACE or placebo orally once daily plus placebo IV Q6W plus TACE. Response will be assessed by imaging every 9 weeks; safety will be assessed throughout the study and up to 90 days after the end of treatment. Dual primary end points are overall survival and progression-free survival (PFS) per RECIST v1.1 by blinded independent central review (BICR). Secondary end points are PFS, objective response rate (ORR), disease control rate (DCR), duration of response (DOR), and time to progression (TTP) per modified RECIST by BICR; ORR, DCR, DOR, and TTP per RECIST v1.1 by BICR; and safety. Exploratory end points are PFS, ORR, DCR, DOR, TTP, and time from randomization to second/subsequent disease progression after initiation of new anticancer therapy or death from any cause, whichever occurs first, per RECIST v1.1 by investigator review, identification of molecular biomarkers, and health-related quality of life. Recruitment began in April 2020, and the planned sample size is 950 patients. The results of the LEAP-012 study will show the clinical benefit of adding lenvatinib plus pembrolizumab to the current standard of care TACE for patients with intermediate-stage HCC not amenable to curative treatment. Clinical trial information: NCT04246177.
False-Positive Results in Rapid Antigen Tests for SARS-CoV-2
Authors: Joshua S. Gans, Avi Goldfarb, Ajay K. Agrawal, Sonia Sennik, Janice Stein, Laura Rosella
Journal: JAMA (2022)

Alexander Harmon, BS; Celina Chang, BS; Nol Salcedo, MS; Brena Sena, MPH; Bobby Brooke Herrera, PhD; Irene Bosch, PhD; Laura E. Holberger, PhD
Nimodipine, a dihydropyridine-type calcium channel blocker, prevents alcoholic hepatitis caused by chronic intragastric ethanol exposure in the rat
Authors: Y Iimuro
Journal: Hepatology (1996)

It has been shown recently that inactivation of Kupffer cells prevents free radical formation and early alcohol-induced liver injury, and that hypoxia subsequent to a hypermetabolic state caused by activated Kupffer cells is likely involved in the mechanism. Calcium is essential for the activation of Kupffer cells, which contain L-type voltage-dependent Ca2+ channels. Therefore, the purpose of this study was to determine whether a Ca2+ channel blocker, nimodipine, prevents early alcohol-induced liver injury in vivo and to evaluate its effect on intracellular calcium ([Ca2+]i) in Kupffer cells in vitro. Male Wistar rats were exposed to ethanol (10-12 g/kg/d) continuously for up to 4 weeks via intragastric feeding using an enteral model developed by Tsukamoto and French. In this model, ethanol causes steatosis, necrosis, and inflammation in only a few weeks. In the experimental group, nimodipine (10 mg/kg/d) was added to the diet and was shielded from direct light. Nimodipine had no effect on body weight over a 4-week treatment period, nor were mean ethanol concentrations or their cyclic pattern in urine affected. The mean urine ethanol values were 154 ± 11 mg/dL in ethanol-fed and 144 ± 38 mg/dL in ethanol + nimodipine-fed rats. After 4 weeks, serum aspartate transaminase (AST) levels were elevated in ethanol-treated rats to 183 ± 78 U/L. In contrast, values only reached 101 ± 9 U/L in rats given nimodipine + ethanol-values which were significantly lower. Steatosis and necrosis assessed histologically were also reduced significantly by nimodipine. Nimodipine (10 micrograms/kg) also blocked the swift increase in alcohol metabolism and elevated oxygen consumption in perfused livers from rats treated with alcohol in vivo. Further, in cultured Kupffer cells, nimodipine (1 mumol/L) largely prevented the elevation in [Ca2+]i caused by lipopolysaccharide (LPS) (LPS, 200 ± 11 nmol/L; LPS + nimodipine, 94 ± 31 nmol/L; P < .05). These results indicate that nimodipine prevents alcoholic hepatitis, possibly by inhibition of endotoxin-mediated Kupffer cell activation.
Book Review Rose and Carless Manual of Surgery . Sixteenth American edition. Edited by William T. Coughlin, M.D. From the sixteenth English edition by Cecil P. G. Wakeley, D.Sc., F.R.C.S., F.R.S.E., F.R.S.A., F.R.A.C.S.; and John B. Hunter, M.C., M.Chir. (Cantab.), F.R.C.S. 8°, cloth, 1656 pp., with 1034 illustrations and 30 colored plates. Baltimore: Williams and Wilkins Company, 1940. $9.00.
Journal: New England Journal of Medicine (1941)
Management approach is changed most frequently after Electron Beam Computed Tomography (EBCT) coronary calcium scanning in patients with intermediate conventional risk profiles Thomas Knickelbine, Timothy A. Dirks, Lise Lunde, Thomas E. Gohman, Geoffrey R. Bodeau, Scott W. Sharkey, Fredarick L. Gobel. Minneapolis Heart Institute, Minneapolis, MN
Journal: Journal of the American College of Cardiology (2001)
Disrupted BRCA1‐PALB2 interaction induces tumor immunosuppression and T‐lymphocyte infiltration in HCC through cGAS‐STING pathway
Authors: Hui Ma, Zhihua Kang, Tzeh Keong Foo, Zhiyuan Shen, Bing Xia
Journal: Hepatology (2022)

BRCA1 (BRCA1 DNA repair associated) and PALB2 (partner and localizer of BRCA2) interact with each other to promote homologous recombination and DNA double-strand breaks repair. The disruption of this interaction has been reported to play a role in tumorigenesis. However, its precise function in HCC remains poorly understood.