tbuckley/cabot-search huggingface dataset:
Abstract 241: Intermittent Hypoxia Protects Cardiomyocytes Against Ischemia/Reperfusion-Induced Ca <sup>2+</sup> Overload and Contraction Suppression via Activation of α <sub>1b</sub> -adrenoceptors
Authors: Huangtian Yang, Hong Gao, Le Chen, Zhi-Zhen Lu, You-Yi Zhang, Zhao-Nian Zhou
Journal: Circulation (2008)

We have demonstrated that long-term training to intermittent high altitude hypoxia (IH) protects hearts against ischemia-reperfusion (I/R)-induced Ca 2+ overload and improved postischemic myocardial contractility. This cardioprotection is non-invasive and maintains much longer time compared with that induced by ischemic preconditioning, thereby, it may have great clinical potential. However, its precise signaling pathways are not fully clarified. Here we hypothesized that IH may attenuate I/R-induced cytosolic and mitochondrial Ca 2+ overload via activation of α 1 -adrenoceptor (α 1 -ARs) pathways. To test it, dynamics of cytosolic free Ca 2+ concentration ([Ca 2+ ] c ), mitochondrial [Ca 2+ ] ([Ca 2+ ] m ) and cell contraction were examined during preischemia and I/R in ventricular cardiomyocytes from normoxic and IH rats. IH significantly attenuated I/R-induced [Ca 2+ ] c and [Ca 2+ ] m overload by 63.5 ± 3.6% and 57.0 ± 4.5% at 30 min of reperfusion (R30), respectively. Consistently, I/R-induced depression on Ca 2+ transients and cell shortening was markedly attenuated by IH, with decreases in mitochondrial cytochrome c release and ATP reduction during reperfusion. Meanwhile, the α 1B -AR and α 1D -AR density obviously decreased during ischemia, while α 1A -AR density remained unchanged. IH did not change α 1A -AR density, but increased α 1B -AR density by ~50% and decreased α 1D -AR density further by 30% during I/R. Moreover, IH-induced protections were abolished by α 1B -AR antagonist chloroethylclonidine but not α 1A - or α 1D -AR antagonist. Furthermore, IH-afforded protection was lost when epsilon isoform of protein kinase C (PKCϵ) was inhibited with PKCϵ V1–2 and mitochondrial ATP sensitive potassium (mitoK ATP ) channels with 5-hydroxydecanoate, a downstream signaling pathway and effector of α 1 -ARs. Our findings indicate that α 1B -AR subtype might be one of the important mediators in IH protects myocytes against I/R injury via maintaining intracellular Ca 2+ homeostasis and protecting the ability of mitochondria through activation of the α 1B -ARs and PKCϵ pathway as well as mitoK ATP channel.. by via translocation of PKCϵ and opening of mitoK ATP channels. Mitochondrial function appears to be a determinant of cardioprotection induced by IH.
Protease Inhibitors May Reverse AIDS Dementia
Authors: A. A. Skolnick
Journal: JAMA (1998)

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
ELECTROCARDIOGRAM BASED SCORING SYSTEM FOR PREDICTING SECONDARY PULMONARY HYPERTENSION: A CROSS-SECTIONAL STUDY
Authors: Ghanshyam Palamaner Subash Shantha, Nimesh Patel, Sindhu Chandran, Sukrut Nanavaty, Pranjal Boruah, Jignesh Sheth, Samir Pancholy
Journal: Journal of the American College of Cardiology (2014)
Therapeutic Gazette.
Journal: JAMA (1885)

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
THE MEDICAL RESEARCH COMMITTEE
Journal: BMJ (1916)

Whatever be the controversial passions of the 0ur, medical practitioners generally will welcome appointment, recently announced, of a Medical esearch.Committee in connection with the adminisfration of the National Insurance Act.The com- position of the Committee, too, will, we believe, c?ttimand the confidence of the profession, and it is,In our judgment, all to the good that such a Com- mittee should include members whose point of view not.that of the mere expert.Medical research a term of which much has been heard ln recent years, and it has, we think, very requently received an unduly narrow inter- pretation.To many minds, even yet, it carries suggestion of something done or attempted in a laboratory?this and nothing else.It means ^mical, bacteriological, or microscopical investi- gations; these and these alone, it is assumed, can aim the countenance and form of a truly scientific mquiry.No one will for a moment question the }alue and indeed the necessity for such activities, laboratory methods and results do not andCannot touch at all points the complex problems are associated with the cause and prevention ?disease.Confident, clear cut, and precise in 111 as these results often appear, they deal almost
&lt;TITLE&gt;Genital Herpes&lt;/TITLE&gt;
Journal: JAMA (2001)

The JAMA Patient Page is a public service of JAMA.The information and recommendations appearing on this page are appropriate in most instances, but they are not a substitute for medical diagnosis.For specific information concerning your personal medical condition, JAMA suggests that you consult your physician.This page may be reproduced noncommercially by physicians and other health care professionals to share with patients.Any other reproduction is subject to AMA approval.
Cystatin C in Patients with Coronary Artery Disease
Authors: Mohamed Mohamed
Journal: Clinical Cardiology and Cardiovascular Interventions (2020)

Background: Cystatin C, a marker for early stage chronic kidney dysfunction, mediates the pathogenesis of cardiovascular diseases.Objectives: To assess the relation between level of serum Cystatin C and severity of coronary artery disease (CAD) in patients without chronic kidney disease (CKD).Patients and Methods: In this cross-sectional study, we included 80 patients with CAD divided in two groups (group I with acute coronary artery disease and group II with chronic stable coronary artery disease) 40 patients each and acquired their demographic characteristics, medical histories, and listings of the concurrent medications they were taking.All patients with CAD underwent ECG, echocardiography, coronary angiography, serum Cystatin C level, cardiac enzymes and other routine laboratory tests.Results: As regard demographic data and comorbidities there was no significant difference between the two groups as regard gender, diabetes mellitus, hypertension or smoking.Also, As regard level of serum Cystatin C, the mean and SD in 1 vessel affection was 0.92±0.07while in 2 vessels affection was 1.07±0.13and 3 vessels affection was 1.41±0.05with (P< 0.01).Finally, there was a highly significant difference as regard Cystatin C level with mean and SD 1.21±0.18 in ST-segment elevation MI while mean and SD was 0.96±0.09 in Non ST-segment MI or unstable angina with (P< 0.01).There was a statistically significant correlation between level of Cystatin C and severity of CAD (p < 0.05). Conclusion:Serum cystatin C has a significant effect on the severity of coronary artery disease (CAD), being higher in patients with 3 vessels disease and severe CAD.
Errata
Journal: Journal of Clinical Oncology (2018)

The second sentence of the third paragraph under the section heading Efficacy reads: "PFS was longer with eribulin treatment compared with dacarbazine in patients with dedifferentiated, myxoid/round cell, or pleomorphic LPS subtypes (HR, 0.69; 95% CI, 0.36 to 1.33; HR, 0.57; 95% CI, 0.29 to 1.11; and HR, 0.34; 95% CI, 0.09 to 1.30; respectively; Fig 2B)."This should read: "The HRs for PFS favored eribulin treatment compared with dacarbazine in patients with dedifferentiated, myxoid/round cell, or pleomorphic LPS subtypes (HR, 0.69; 95% CI, 0.36 to 1.33; HR, 0.57; 95% CI, 0.29 to 1.11; and HR, 0.34; 95% CI, 0.09 to 1.30; respectively; Fig 2B)."This has been corrected as of December 20, 2017.
Secondary syphilis with unusual clinical and laboratory findings
Authors: L. Biro
Journal: JAMA (1968)

Physical examination of a patient yielded cutaneous findings suggestive of lymphoma or sarcoidosis. A roentgenogram of the chest revealed nodular infiltrates at the bases of both lungs, lending support for the diagnosis of sarcoidosis. On biopsy, skin lesions showed noncaseating granulomata. The correct diagnosis of syphilis was first suspected on the basis of a reactive Venereal Disease Research Laboratory test. Clinically, atypical forms of syphilis may be on the rise because of short-term antibiotic treatment given to patients during the incubation period of the disease.
Official Call to the Officers and Members of the American Medical Association to Attend the Interim Meeting of the House of Delegates in Dallas, Dec 4 Through 7, 1988
Authors: James E. Davis
Journal: JAMA (1988)

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
In vitro culture and differentiation of murine embryonic liver stem cells Leslie E. Rogler* Department of Medicine and marion Bessin Liver Research Center Albert Einstein College of Medicine, Bronx, NY 10461
Journal: Hepatology (1995)

BACKGROUND:Acute liver failure has no medically recognized effective therapy other than orthotopic liver transplantation. Development of bioartificial livers for support of patients with acute liver failure requires meaningful preclinical evaluation before clinical trials.STUDY DESIGN:Complete results from preclinical safety and efficacy evaluation of the Excorp Medical Bioartificial Liver Support System (BLSS) using a D-galactosamine (D-gal) canine liver failure model are presented. From a total cohort of 23 purpose-bred male hounds, 18 animals were administered a lethal dose (1.5 g/kg) of D-gal. The 18 animals were divided into four treatment groups: no BLSS treatment (n = 6), BLSS treatment starting at 24 to 26 hours post D-gal (n = 5), BLSS treatment starting at 16 to 18 hours post D-gal (n = 4), and “mock support” treatment with a BLSS system containing no hepatocytes (n = 3). The animals were treated until death or death equivalent, or euthanized at 60 hours. Physiologic parameters were continuously monitored. Blood chemistries were obtained every 8 hours.RESULTS:Although survival times for BLSS-supported animals were significantly greater than for the unsupported group, the greatest impact on delaying progression of liver disease was time of intervention. Intervention at 16 to 18 hours post D-gal administration showed significant delay in increasing blood ammonia, lactate, and prothrombin time as compared with untreated animals. Elevated intracranial pressure was found in two of six untreated animals, but in none of the treated animals (zero of nine). Healthy animals supported by the BLSS system evidenced no significant safety problems.CONCLUSIONS:Results suggest the BLSS impacts the course of liver failure in the animal model. Phase I clinical safety evaluation is underway.
Posterior Pericardial Ascending-to-Descending Aortic Bypass
Authors: Heidi M. Connolly, Hartzell V. Schaff, Uzi Izhar, Joseph A. Dearani, Carole A. Warnes, Thomas A. Orszulak
Journal: Circulation (2001)

Background Coarctation of the aorta is commonly associated with recoarctation or additional cardiovascular disorders that require intervention. The best surgical approach in such patients is uncertain. Ascending-to-descending aortic bypass graft via the posterior pericardium (CoA bypass) allows simultaneous intracardiac repair or an alternative approach for the patient with complex coarctation. Methods and Results Between 1985 and 2000, 18 patients (13 males and 5 females, mean age 43±13 years) with coarctation of the aorta underwent CoA bypass through median sternotomy. Before operation, average New York Heart Association class was II (range I to IV), and 15 patients (83%) had systemic hypertension. One or more previous cardiovascular operations had been performed in 12 patients (67%); 10 patients had ≥1 prior coarctation repair. Two patients had prior noncoarctation cardiovascular surgery. Concomitant procedures performed in 14 patients (78%) included the following: aortic valve replacement in 9; coronary artery bypass surgery in 3; mitral valve repair in 2; and septal myectomy, mitral valve replacement, aortoplasty, subaortic stenosis resection, ventricular septal defect closure, and ascending aorta replacement in 1 patient each. All patients survived the operation and were alive with patent CoA bypass at a mean follow-up of 45 months. No graft-related complications occurred, and there were no instances of stroke or paraplegia. Systolic blood pressure fell from 159 mm Hg before surgery to 125 mm Hg after surgery. Conclusions CoA bypass via median sternotomy can be performed with low morbidity and mortality. Although management must be individualized, extra-anatomic CoA bypass via the posterior pericardium is an excellent single-stage approach for patients with complex coarctation or recoarctation and concomitant cardiovascular disorders.
CORRECTION
Journal: JAMA (1921)

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
The Cell
Authors: Alice Jones
Journal: Annals of Internal Medicine (1993)

Ad Libitum15 September 1993The CellAlice Jones, MDAlice Jones, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-119-6-199309150-00018 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Like every reception, there's foodand dancing and bumpinginto all those quirkyrelatives: blood, Great-aunt Henriettedeclares, is thicker thananything. Familyis in the genes, she says, as if shejust discovered the cell,the body's time capsule,recording history for the clumsy, nakedbipeds who hover atthe edge of fire,evolving into creatures who learnthe cell's workings:how it sucks upwater from the surrounding matrixthrough sticky-lippedpores; how each tinyapparatus for food or sex floatsin this one drop of opaquesalinethe primal jelly;how it composes proteins frominborn templates forgenerations of identical daughters;pull ... Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 September 1993Volume 119, Issue 6Page: 533KeywordsBirthBlood cellsChromosomesFoodProteins ePublished: 15 August 2000 Issue Published: 15 September 1993 Copyright & PermissionsCopyright © 1993 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Postvagotomy dysphagia
Authors: J. R. Sharp
Journal: JAMA (1979)

<h3>To the Editor.—</h3> I read the article by Stephen Carter, MD, on vagotomy dysphagia inThe Journal(240:2656, 1978). I, too, have been impressed with the occurrence of this clinical syndrome, its spontaneous resolution, and its probable relationship to the completeness of vagotomy. In my experience this entity seems to occur in the hands of those surgeons who are more "compulsive" about a complete vagotomy. Those surgeons who divide the anterior vagal trunk and the posterior vagal trunk, and then quit, essentially never encounter this problem. Those of us who meticulously divide each vagal fiber on the distal esophagus in a circumferential manner see it not uncommonly. I believe the problem is related to the completeness of the vagotomy and represents denervation of the sphincter. The dysphagia is obviously also related to the exact level at which the vagotomy is done. Most of us attempt to circumscribe the esophagus not
Laboratory Capacity to Detect Antimicrobial Resistance, 1998
Journal: JAMA (2000)

Emerging mechanisms of antimicrobial resistance have clinical, microbiologic, and infection-control implications for health-care providers. Antimicrobial resistant organisms include Staphylococcus aureus with reduced susceptibility to vancomycin (minimum inhibitory concentration [MIC] > or = 4 microg/mL), including vancomycin intermediate S. aureus (VISA; vancomycin MIC = 8-16 microg/mL) and Enterobacteriaceae that produce extended spectrum beta-lactamases (ESBLS), which result in resistance to a broad range of beta-lactam antibiotics. Detecting VISA and ESBLs-producing gram-negative pathogens can be difficult for clinical microbiology laboratories. Although CDC and the National Committee for Clinical Laboratory Standards (NCCLS) have published screening and confirmatory methods for these pathogens (Tables 1 and 2), the extent of use of these methods is unknown. This report summarizes results from a survey of microbiology laboratories that participate in the Active Bacterial Core Surveillance (ABCs)/Emerging Infections Program (EIP) Network to assess the capacity of clinical microbiology laboratories to detect VISA and ESBL-producing pathogens; findings indicate that despite adequate capacity for proper testing, many laboratories do not have appropriate methodology to detect these resistant pathogens.
The University and Public Health Statesmanship
Journal: JAMA (1941)

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
Isosorbide dinitrate. Effect on the vasodilator response to nitroglycerin
Authors: R. Zelis
Journal: JAMA (1975)

To evaluate whether there is cross-tolerance to the circulatory effects of isosorbide dinitrate and nitroglycerin, six subjects were given 120 mg/day of sustained-action isosorbide dinitrate in three divided doses for six to eight weeks. Prior to and during the last week of long-term isosorbide dinitrate administration, the effects of sublingually given nitroglycerin (0.9 mg) on plethysmographically measured calf blood flow and venous volume at 30 mm Hg (VV[30]) were measured on three occasions and averaged. Although the arteriolar dilation produced by nitroglycerin was unaltered by isosorbide dinitrate, the venodilation was significantly attenuated. The VV[30] increased from 3.00 to 3.28 ml/100 ml (<i>P</i>&lt;.02) with nitroglycerin prior to isosorbide dinitrate administration, but failed to increase with nitroglycerin during the long-term administration of isosorbide dinitrate (2.95 to 2.95 ml/100 ml,<i>P</i>&gt;.5). (<i>JAMA</i>234:166-170, 1975)