tbuckley/cabot-search huggingface dataset:
Ambulatory Surgical Centers and Infection Control—Reply
Authors: Melissa K. Schaefer, Marilyn Dahl, Joseph F. Perz
Journal: JAMA (2010)

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
Modulation of the molecular composition of large conductance, Ca2+ activated K+ channels in vascular smooth muscle during hypertension
Authors: Gregory C. Amberg, Adrian D. Bonev, Charles F. Rossow, Mark T. Nelson, Luis F. Santana
Journal: Journal of Clinical Investigation (2003)

Hypertension is a clinical syndrome characterized by increased vascular tone. However, the molecular mechanisms underlying vascular dysfunction during acquired hypertension remain unresolved. Localized intracellular Ca2+ release events through ryanodine receptors (Ca2+ sparks) in the sarcoplasmic reticulum are tightly coupled to the activation of large-conductance, Ca2+-activated K+ (BK) channels to provide a hyperpolarizing influence that opposes vasoconstriction. In this study we tested the hypothesis that a reduction in Ca2+ spark–BK channel coupling underlies vascular smooth muscle dysfunction during acquired hypertension. We found that in hypertension, expression of the β1 subunit was decreased relative to the pore-forming α subunit of the BK channel. Consequently, the BK channels were functionally uncoupled from Ca2+ sparks. Consistent with this, the contribution of BK channels to vascular tone was reduced during hypertension. We conclude that downregulation of the β1 subunit of the BK channel contributes to vascular dysfunction in hypertension. These results support the novel concept that changes in BK channel subunit composition regulate arterial smooth muscle function.
Keeping Children and Adolescents Safe From Firearms
Authors: Megan A. Moreno
Journal: JAMA Pediatrics (2015)

Firearm-related deaths continue to be one of the top 3 causes of death among US children and adolescents. Of all injury deaths of youths 15 to 19 years of age in the United States in 2009, more than 1 in 4 were related to firearms (28.7%). Firearm-related deaths are associated with unintentional shootings, suicides, and homicides. Unintentional shootings typically happen when a child or adolescent shoots a gun and kills another person, usually a friend or sibling. The risk of adolescent suicide is strongly associated with the availability of a firearm and is particularly high if the firearm is kept loaded. Laws that require the safe storage of firearms are associated with lower rates of adolescent suicide. In 2009, more than 80% of all homicides of youths 15 to 19 years of age were firearm-related homicides. Most homicides occur during interpersonal conflict, typically between relatives, friends, or acquaintances.... Language: en
CYP2E1 and oxidant stress in alcoholic and non-alcoholic fatty liver disease
Authors: Tung-Ming Leung, Natalia Nieto
Journal: Journal of Hepatology (2012)

Alcoholic (ALD) and non-alcoholic fatty liver diseases (NAFLD) are clinical conditions leading to hepatocellular injury and inflammation resulting from alcohol consumption, high fat diet, obesity and diabetes, among others. Oxidant stress is a major contributing factor to the pathogenesis of ALD and NAFLD. Multiple studies have shown that generation of reactive oxygen species (ROS) is key for the progression of fatty liver to steatohepatitis. Cytochrome P450 2E1 (CYP2E1) plays a critical role in ROS generation and CYP2E1 is also induced by alcohol itself. This review summarizes the role of CYP2E1 in ALD and NAFLD.
An Address on the Morbid Anatomy and Pathology of Chronic Alcoholism
Authors: J. F. Payne
Journal: BMJ (1888)

Since it is obviously impossible to speak of all the organs which may be altered, 1 shall confine my remarks to a few, especially the liver and the nervous system, taking the morbid changes in these parts as types of the effects produced in the organs generally.Effects of Alcoholism as seen in the Liver.-It is generally recognised that one effect of alcohol is to produce accumulationi of fat or steatosis in the liver.This change is produced especially by
Loss of Nrdp1 Enhances ErbB2/ErbB3–Dependent Breast Tumor Cell Growth
Authors: Lily Yen, Zhongwei Cao, Xiuli Wu, Ellen R.Q. Ingalla, Colin Baron, Lawrence J.T. Young, Jeffrey P. Gregg, Robert D. Cardiff, Alexander D. Borowsky, Colleen Sweeney, Kermit L. Carraway
Journal: Cancer Research (2006)

Abstract Dysregulation of ErbB receptor tyrosine kinases is thought to promote mammary tumor progression by stimulating tumor cell growth and invasion. Overexpression and aberrant activation of ErbB2/HER2 confer aggressive and malignant characteristics to breast cancer cells, and patients displaying ErbB2-amplified breast cancer face a worsened prognosis. Recent studies have established that ErbB2 and ErbB3 are commonly co-overexpressed in breast tumor cell lines and in patient samples. ErbB2 heterodimerizes with and activates the ErbB3 receptor, and the two receptors synergize in promoting growth factor–induced cell proliferation, transformation, and invasiveness. Our previous studies have shown that the neuregulin receptor degradation protein-1 (Nrdp1) E3 ubiquitin ligase specifically suppresses cellular ErbB3 levels by marking the receptor for proteolytic degradation. Here, we show that overexpression of Nrdp1 in human breast cancer cells results in the suppression of ErbB3 levels, accompanied by the inhibition of cell growth and motility and the attenuation of signal transduction pathways. In contrast, either Nrdp1 knockdown or the overexpression of a dominant-negative form enhances ErbB3 levels and cellular proliferation. Additionally, Nrdp1 expression levels inversely correlate with ErbB3 levels in primary human breast cancer tissue and in a mouse model of ErbB2 mammary tumorigenesis. Our observations suggest that Nrdp1-mediated ErbB3 degradation suppresses cellular growth and motility, and that Nrdp1 loss in breast tumors may promote tumor progression by augmenting ErbB2/ErbB3 signaling. (Cancer Res 2006; 66(23): 11279-86)
Genomic Classification of Serous Ovarian Cancer with Adjacent Borderline Differentiates RAS Pathway and <i>TP53</i>-Mutant Tumors and Identifies <i>NRAS</i> as an Oncogenic Driver
Authors: Catherine Emmanuel, Yoke-Eng Chiew, Joshy George, Dariush Etemadmoghadam, Michael S. Anglesio, Raghwa Sharma, Peter Russell, Catherine Kennedy, Sian Fereday, Jillian Hung, Laura Galletta, Russell Hogg, Gerard V. Wain, Alison Brand, Rosemary Balleine, Laura MacConaill, Emanuele Palescandolo, Sally M. Hunter, Ian Campbell, Alexander Dobrovic, Stephen Q. Wong, Hongdo Do, Christine L. Clarke, Paul R. Harnett, David D.L. Bowtell, Anna deFazio
Journal: Clinical Cancer Research (2014)

Low-grade serous ovarian carcinomas (LGSC) are Ras pathway-mutated, TP53 wild-type, and frequently associated with borderline tumors. Patients with LGSCs respond poorly to platinum-based chemotherapy and may benefit from pathway-targeted agents. High-grade serous carcinomas (HGSC) are TP53-mutated and are thought to be rarely associated with borderline tumors. We sought to determine whether borderline histology associated with grade 2 or 3 carcinoma was an indicator of Ras mutation, and we explored the molecular relationship between coexisting invasive and borderline histologies.We reviewed >1,200 patients and identified 102 serous carcinomas with adjacent borderline regions for analyses, including candidate mutation screening, copy number, and gene expression profiling.We found a similar frequency of low, moderate, and high-grade carcinomas with coexisting borderline histology. BRAF/KRAS alterations were common in LGSC; however, we also found recurrent NRAS mutations. Whereas borderline tumors harbored BRAF/KRAS mutations, NRAS mutations were restricted to carcinomas, representing the first example of a Ras oncogene with an obligatory association with invasive serous cancer. Coexisting borderline and invasive components showed nearly identical genomic profiles. Grade 2 cases with coexisting borderline included tumors with molecular features of LGSC, whereas others were typical of HGSC. However, all grade 3 carcinomas with coexisting borderline histology were molecularly indistinguishable from typical HGSC.Our findings suggest that NRAS is an oncogenic driver in serous ovarian tumors. We demonstrate that borderline histology is an unreliable predictor of Ras pathway aberration and underscore an important role for molecular classification in identifying patients that may benefit from targeted agents.
Incremental Prognostic Value of Elevated Baseline C-Reactive Protein Among Established Markers of Risk in Percutaneous Coronary Intervention
Authors: Derek P. Chew, Deepak L. Bhatt, Mark A. Robbins, Marc S. Penn, Jakob P. Schneider, Michael S. Lauer, Eric J. Topol, Stephen G. Ellis
Journal: Circulation (2001)

Established methods of risk assessment in percutaneous coronary intervention have focused on clinical and anatomical lesion characteristics. Emerging evidence indicates the substantial contribution of inflammatory processes to short-term and long-term outcomes in coronary artery disease.Within a single-center registry of contemporary percutaneous coronary revascularization strategies with postprocedural creatine kinase and clinical events routinely recorded, we assessed the association of baseline C-reactive protein with death or myocardial infarction within the first 30 days. Predictive usefulness of baseline C-reactive protein within the context of established clinical and angiographic predictors of risk was also examined. Among 727 consecutive patients, elevated baseline C-reactive protein before percutaneous coronary intervention was associated with progressive increase in death or myocardial infarction at 30 days (lowest quartile, 3.9%, versus highest quartile, 14.2%; P=0.002). Among clinical and procedural characteristics, baseline C-reactive protein remained independently predictive of adverse events, with the highest quartile of C-reactive protein associated with an odds ratio for excess 30-day death or myocardial infarction of 3.68 (95% CI, 1.51 to 8.99; P=0.004). A predictive model that included baseline C-reactive protein quartiles, American College of Cardiology/American Heart Association lesion score, acute coronary syndrome presentation, and coronary stenting appears strongly predictive of 30-day death or myocardial infarction within this population (C-statistic, 0.735) and among individual patients (Brier score, 0.006).Elevated baseline C-reactive protein portends heightened risk of 30-day death or myocardial infarction after coronary intervention. Coupled anatomic, clinical, and inflammatory risk stratification demonstrates strong predictive utility among patients undergoing percutaneous coronary intervention and may be useful for guiding future strategies.
O93 GENE EXPRESSION-BASED PROGNOSTIC SIGNATURE AND GENOMIC CHARACTERIZATION OF FIBROLAMELLAR HEPATOCELLULAR CARCINOMA
Authors: H. Cornella, C. Alsinet, S. Sayols, Z. Zhang, K. Hao, L. Cabellos, A. Quaglia, A. Villanueva, Y. Hoshida, D.M. Nagorney, S. Thung, S. Ward, L. Rodriguez-Carunchio, A. Lachenmayer, B. Minguez, L.R. Roberts, V. Mazzaferro, N. Heaton, M. Esteller, J.M. Llovet
Journal: Journal of Hepatology (2014)
Dutch doctors call for new approach to reporting “mercy killings”
Authors: Tony Sheldon
Journal: BMJ (2004)

in Britain and as Paxil in the United States) (12 June, p 1395).The trials, which studied the drugs in adolescents, either showed no benefit over placebo or a slight increase in self harming behaviour.On 25 August GSK settled the lawsuit, saying in a statement that although it believed the allegations were "unfounded," it wanted to avoid the expense of a protracted legal battle.
Low-molecular-weight heparin alone and with IIb/IIIa inhibitors in patients with renal failure and non-ST elevation acute coronary syndromes: Insights from the global registry of acute coronary events
Authors: Jean-Philippe Collet, Giancarlo Agnelli, Frans J. ban de Werf, David Brieger, Enrique P. Gurfinkel, Jose Lopez-Sendon, Neelam Gowda, Gilles Montalescot
Journal: Journal of the American College of Cardiology (2003)
Both IGH translocations and chromosome 13q deletions are early events in monoclonal gammopathy of undetermined significance and do not evolve during transition to multiple myeloma
Authors: H Kaufmann, J Ackermann, C Baldia, T Nösslinger, R Wieser, S Seidl, V Sagaster, H Gisslinger, U Jäger, M Pfeilstöcker, C Zielinski, J Drach
Journal: Leukemia (2004)
Transforming Growth Factor-β Signaling in Prostate Stromal Cells Supports Prostate Carcinoma Growth by Up-regulating Stromal Genes Related to Tissue Remodeling
Authors: Erik V. Verona, Abdel G. Elkahloun, Junhua Yang, Abhik Bandyopadhyay, I-Tien Yeh, Lu-Zhe Sun
Journal: Cancer Research (2007)

Abstract Increasing evidence points to an active stromal involvement in cancer initiation and progression. Cytokines derived from tumor cells are believed to modulate stromal cells to produce growth and angiogenic factors, which in turn provide the tumor with the necessary microenvironment for expansion and invasion. Transforming growth factor β (TGFβ) has been implicated as a candidate cytokine to mediate this communication. However, how its signaling in stromal cells regulates tumorigenesis and tumor progression remains unresolved. We show that normal, presenescent fibroblasts or prostate stromal cells cotransplanted with prostate carcinoma cells s.c. into nude mice reduced tumor latency and accelerated tumor growth. When their TGFβ signaling was blocked, the fibroblasts and stromal cells still stimulated tumor initiation but no longer supported tumor growth as control cells did. The loss of the tumor growth–promoting activity of the stromal cells with attenuated TGFβ signaling was not associated with altered cellular senescence or tumor angiogenicity. TGFβ and the medium conditioned by the prostate carcinoma cells stimulated myofibroblast differentiation of the intact stromal cells, but not the stromal cells with attenuated TGFβ signaling. Gene microarray and quantitative reverse transcription-PCR analyses showed that TGFβ up-regulated a host of genes in stromal cells that are involved in tissue remodeling and wound healing. Thus, our study provides evidence for TGFβ as a supporting agent in tumor progression through the induction of a perpetual wound healing process in the tumor microenvironment. [Cancer Res 2007;67(12):5737–46]
Abstract 3547: In vitro and ex vivo anti-leukemia activity of AR-67, a novel lipophilic camptothecin
Authors: Eleftheria Tsakalozou, Dianna Howard, Markos Leggas
Journal: Cancer Research (2011)

Abstract BACKGROUND: The overall survival and disease-free rates for Acute Myelogenous Leukemia (AML) patients treated with the gold-standard therapy comprised of Cytarabine (Ara-C) and Daunorubicin (DNR) remain significantly low. Camptothecins are potent anticancer drugs that confer their cytotoxic effect by interfering with Topoisomerase-I (Top1). Semi-synthetic camptothecin analogues have been used in the past to treat AML patients with relatively low response rates. Here, we examined the anti-leukemia activity of AR-67, a novel camptothecin analogue, alone or in combination with standard agents for the treatment of AML. METHODS: The anti-leukemia activity of AR-67, TPT, Ara-C and DNR was studied in HL60, KG1 and K562 cells and in primary leukemia cell cultures after exposure to increasing drug concentrations for 48 hours. Cell proliferation was determined using a colorimetric assay (MTT) assay and IC50s were obtained using nonlinear-regression analysis. Drug combination treatments were assessed for synergy. The expression of Top1, phosphohistone (γ-H2AX), Bcl-2 and c-PARP were evaluated using biochemical assays. RESULTS: The potency of AR-67 was in the nM range in the leukemic cell lines. Consistent with the lower proliferation rates of primary cells grown in culture, their IC50 values were variable and in the µM range. IC50s estimated for TPT were higher than the respective ones for AR-67. The IC50 values for Ara-C and DNR were in the μM range for the HL60, K562 and primary cells, and higher than the ones for AR-67. However, the KG-1 cell line appeared to be more sensitive to the AML gold standard therapy, but not as sensitive as to AR-67. AR-67 treatment decreased Top1 expression, increased γ-H2AX expression in a concentration-dependent manner suggesting removal of DNA-Top1 complexes and formation of double strand DNA breaks. Induction of apoptosis was manifested by decreased Bcl-2 and increased c-PARP expression suggesting a caspace-3 mediated effect. AR-67 combination treatments that included DNR and Ara-C showed synergy in HL60 cells. Additionally, pretreatment with Ara-C revealed synergy between AR-67 and DNR in both the KG1 and K562 cells, accompanied by increased γ-H2AX and c-PARP expression. CONCLUSIONS: Our results indicate AR-67 as a potent anticancer agent that induces DNA damage and apoptosis. Using in vitro leukemia models we have shown that AR-67 is a potentially efficacious agent when combined with standard agents for the treatment of AML and may benefit AML patients resistant to Ara-C. 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 3547. doi:10.1158/1538-7445.AM2011-3547
Virus-induced dysfunction of CD4+CD25+ T cells in patients with HTLV-I–associated neuroimmunological disease
Authors: Yoshihisa Yamano, Norihiro Takenouchi, Hong-Chuan Li, Utano Tomaru, Karen Yao, Christian W. Grant, Dragan A. Maric, Steven Jacobson
Journal: Journal of Clinical Investigation (2005)

CD4+CD25+ Tregs are important in the maintenance of immunological self tolerance and in the prevention of autoimmune diseases. As the CD4+CD25+ T cell population in patients with human T cell lymphotropic virus type I–associated (HTLV-I–associated) myelopathy/tropical spastic paraparesis (HAM/TSP) has been shown to be a major reservoir for this virus, it was of interest to determine whether the frequency and function of CD4+CD25+ Tregs in HAM/TSP patients might be affected. In these cells, both mRNA and protein expression of the forkhead transcription factor Foxp3, a specific marker of Tregs, were lower than those in CD4+CD25+ T cells from healthy individuals. The virus-encoded transactivating HTLV-I tax gene was demonstrated to have a direct inhibitory effect on Foxp3 expression and function of CD4+CD25+ T cells. This is the first report to our knowledge demonstrating the role of a specific viral gene product (HTLV-I Tax) on the expression of genes associated with Tregs (in particular, foxp3) resulting in inhibition of Treg function. These results suggest that direct human retroviral infection of CD4+CD25+ T cells may be associated with the pathogenesis of HTLV-I–associated neurologic disease.
Pleiotropic effects of angiotensin II receptor blocker in hypertensive patients
Authors: Kwang Kon Koh, Jeong Yeal Ahn, Seung Hwan Han, Dae Sung Kim, Dong Kyu Jin, Hyung Sik Kim, Mi-Seung Shin, Tae Hoon Ahn, In Suck Choi, Eak Kyun Shin
Journal: Journal of the American College of Cardiology (2003)
Winifred Cornwell (née Drew)
Authors: Alistair Marshall
Journal: BMJ (2006)

​FormerFormer consultant anaesthetist London Chest Hospital (b 1925; q St Mary's Hospital, London, 1948; DA, FRCA), died from complications following radiotherapy for endometrial carcinoma on 6 January 2006.




Figure 1




Winifred Betty Drew (“Elizabeth”) was one of the first two women to go to St Mary's Medical School. She took resident posts in anaesthetics, passing the diploma in 1954. In 1969, after a spell abroad with her husband, she obtained her FRCA. In 1971 she was the first full time woman consultant appointed to the London Chest Hospital, where her charm and impeccable dress sense earned her the affectionate title of “the duchess.” She built a reputation for her work and for the hospital, her ideas and rules giving many a firm foundation for safe practice.
Physical Training Improves Endothelial Function in Patients With Chronic Heart Failure
Authors: Burkhard Hornig, Volker Maier, Helmut Drexler
Journal: Circulation (1996)

Chronic heart failure is associated with endothelial dysfunction including impaired endothelium-mediated, flow-dependent dilation (FDD). Since endothelial function is thought to play an important role in coordinating tissue perfusion and modulating arterial compliance, interventions to improve endothelial dysfunction are imperative.To assess the potential of physical training to restore FDD, 12 patients with chronic heart failure were studied and compared with FDD of 7 age-matched normal subjects. With a recently developed high-resolution ultrasound system, diameters of radial artery were measured at rest, during reactive hyperemia (with increased flow causing endothelium-mediated dilation), and during sodium nitroprusside, causing endothelium-independent dilation. Determination of FDD was repeated after intra-arterial infusion of NG-monomethyl-L-arginine (L-NMMA, 7 mumol/min) to inhibit endothelial synthesis and release of nitric oxide. The protocol was performed at baseline, after 4 weeks of daily handgrip training, and 6 weeks after cessation of the training program. FDD was impaired in heart failure patients compared with normal subjects. L-NMMA attenuated FDD, indicating that the endothelial release of nitric oxide is involved in FDD. Physical training restored FDD in patients with heart failure. In particular, the portion of FDD inhibited by L-NMMA (representing FDD mediated by nitric oxide) was significantly higher after physical training (8-minute occlusion: 8.0 +/- 1% versus 5.4 +/- 0.9%; P < .05; normal subjects: 9.2 +/- 1%).These results indicate that physical training restores FDD in patients with chronic heart failure, possibly by enhanced endothelial release of nitric oxide.
Mechanical restitution and post-extracontraction potentiation in guinea pig and rat atria
Authors: M. JOHANNSSON, H. ASGRIMSSON
Journal: Cardiovascular Research (1988)

Journal Article Mechanical restitution and post-extracontraction potentiation in guinea pig and rat atria Get access MAGNÚS JÓHANNSSON, MAGNÚS JÓHANNSSON From the Department of Pharmacology, PO Box 1532, IS-121 Reykjavik, Iceland Search for other works by this author on: Oxford Academic PubMed Google Scholar HAFLIDI ASGRIMSSON HAFLIDI ASGRIMSSON From the Department of Pharmacology, PO Box 1532, IS-121 Reykjavik, Iceland Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 22, Issue 8, August 1988, Page 589, https://doi.org/10.1093/cvr/22.8.589 Published: 01 August 1988