tbuckley/cabot-search huggingface dataset:
Diarrheal morbidity during the first 2 years of life among HIV-infected infants
Authors: K. L. Kotloff
Journal: JAMA (1994)

<h3>Objective.</h3> —To determine the incidence, cause, and patterns of diarrhea during the first 2 years of life among infants infected perinatally with the human immunodeficiency virus (HIV). <h3>Design.</h3> —A cohort study in which infants were enrolled shortly after birth and followed up longitudinally using biweekly surveillance for the occurrence of diarrhea. Stool specimens collected at the onset of diarrhea were evaluated for enteropathogens. Infants who were infected with HIV were compared with uninfected infants. <h3>Subjects.</h3> —Infants born to HIV-infected women at the University of Maryland Hospital, Baltimore, were recruited at 0 to 3 months of age. This analysis included 58 infants enrolled in the cohort and followed up at least 15 months (unless death intervened) whose HIV status was established (18 HIV-infected infants and 40 HIV-uninfected infants). <h3>Measurements and Results.</h3> —The overall incidence of diarrhea in HIV-infected infants was 3.2 episodes per 12 child-months compared with 1.5 episodes per 12 child-months among HIV-uninfected infants (incidence density ratio, 2.2;<i>P</i>&lt;.05). An enteropathogen was identified in stool specimens collected during 20% of diarrheal episodes occurring in HIV-infected infants and during 25% of diarrheal episodes occurring in HIV-uninfected infants. Episodes that persisted for 14 days or longer were significantly more common among HIV-infected infants. The peak incidence of diarrhea occurred at 0 to 5 months of age for HIV-infected infants compared with 6 to 11 months for HIV-uninfected infants. Early onset of diarrhea (&lt;6 months old) in HIV-infected infants was associated with the later development of persistent episodes of diarrhea, and those with persistent episodes had more severe HIV infection, characterized by a significantly higher frequency of opportunistic infections and lower CD4<sup>+</sup>T-lymphocyte counts by 1 year of age. <h3>Conclusions.</h3> —Both acute and persistent episodes of diarrhea are major sources of morbidity in HIV-infected infants. Moreover, persistent diarrhea is a marker for rapid progression of HIV disease. (<i>JAMA</i>. 1994;271:448-452)
THE BALLOTING.
Journal: JAMA (1896)

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
Manuscripts Approved for JNCI, February 1 to March 1, 1970
Journal: JNCI Journal of the National Cancer Institute (1970)

Manuscripts Approved for JNCI, February 1 to March 1, 1970 Get access JNCI: Journal of the National Cancer Institute, Volume 44, Issue 4, April 1970, Pages 982–983, https://doi.org/10.1093/jnci/44.4.982-c Published: 01 April 1970
National Health Service Corps and primary care training. A mutually beneficial plan affecting physician maldistribution
Authors: P. Pollner
Journal: JAMA (1974)

The National Health Service Corps (NHSC), established by passage of the Emergency Health Personnel Act of 1970, was set up to provide for the redistribution of medical personnel to communities with critical health manpower shortages. Three years later, only 4% of the 5,000 "underserved" areas have received physicians; dentists and allied personnel are still missing. Further inadequacies of the Corps are demonstrated by the substantial decline in physical applicants paralleling the end of the doctor draft and Vietnam War. To reawaken physician interest, the NHSC seeks new financial benefits to replace the defunct military fulfillment incentive. Such artificial benefits have previously proven inadequate as incentives for effecting enlistment in underserved areas. Furthermore, most physicians will no longer be available for service commitments during training because of the continuity established by the combined internship-residency. Instead we propose that establishment of a working relationship between primary care training programs and NHSC has substantive value in solving problems plaguing both groups, as well as helping to improve physician distribution nationally. (<i>JAMA</i>228:1405-1407, 1974).
Abstract 1011: SUR2 Short Form-Based Channels Confer A Glibenclamide Insensitive, ATP-Sensitive Potassium Current In Cardiac Myocytes
Authors: Jie-Li Pu, Bin Ye, Stacie Kroboth, Elizabeth M McNally, Jonathan C Makielski, Nian-Qing Shi
Journal: Circulation (2007)

K ATP channels are widely distributed in various tissues and play important physiological roles in regulating insulin secretion in pancreatic beta-cells, providing ischemic protections to the heart and modulating vascular tone in smooth muscles. It is generally agreed that the sarcolemmal K ATP is a hetero-octamer consisting of a Kir6.0 pore and a sulfonylurea receptor (SUR). A SUR2 mutant mouse was generated by disrupting the first nucleotide-binding domain (NBD1), where a previously reported N-end component for the glibenclamide action site was located. In ventricular myocytes isolated from relatively young mutant mice, a novel ATP-sensitive current ( I KATPn ) was detected in 33% single-channel recordings with an average amplitude of 12.3 ± 5.4 pA per patch (n = 15), which was 1/4 of the conventional I KATP (55.4 ± 10.0 pA, n = 19). The IC 50 (ATP) for K ATPn was 10 μM compared to 39.3 μM for the conventional K ATP suggesting that K ATPn could respond faster to low-ATP conditions. Mean burst duration for K ATPn (20.6 ± 1.8 ms, n=4) was half of that for the conventional K ATP (44.2 ± 9.5 ms, n=4). K ATPn was insensitive to 10 μM glibenclamide and could not be re-activated by 0.1– 0.5 mM pinacidil in the presence of ATP. Newly designed SUR2-isoform or variant-specific antibodies identified several novel SUR2 short forms in the sizes of 28 – 68 kDa in addition to a 150-kDa long form in a purified WT cardiac membrane fraction. The 150-kDa long form was absent in the mutant as expected but the SUR2 short forms remained intact. We hypothesized that channels constituted by these short forms, presumably lacking NBD1, confer I KATPn . The SUR2 short forms co-immunoprecipitated with Kir6.0 suggesting that the short forms may function like hemi-transporters reported in other ATP-binding cassette transporter families. Our results show that different K ATP compositions based on the novel SUR2 short forms may exist in cardiac sarcolemmal membrane.
The importance of severity of illness in assessing hospital mortality
Authors: J. Green
Journal: JAMA (1990)

Each year, the Health Care Financing Administration (HCFA) releases a report comparing hospital mortality rates with predicted rates. Some argue that the HCFA's prediction model does not adequately account for patient severity. We tested this hypothesis by comparing the HCFA's model (replicated as closely as we could) to a second that added a severity measure (the Stage of Principal Diagnosis at Admission, a subscale of the Severity of Illness Index). In our simulation, the HCFA's model had very limited capacity to predict mortality (average<i>R</i><sup>2</sup>, 2.5%). Patients grouped according to admission severity had markedly different mortality rates, which the HCFA's model's predictions could not differentiate. The HCFA model also failed to predict large differences in mortality between hospitals with low- and high-severity admissions. Adding severity to the HCFA's model yielded more than an eightfold increase in the<i>R</i><sup>2</sup>, to 21.5%, and reduced instances of higher than expected hospital mortality to chance levels. These findings suggest that the HCFA's mortality release needs to be made much more sensitive to admission severity before it can be used to make valid inferences about the quality or effectiveness of hospital care. (<i>JAMA</i>. 1990;263:241-246)
Effect of inhaled fluticasone on bronchial responsiveness to neurokinin A in asthma
Authors: J. Van Schoor, G.F. Joos, R.A. Pauwels
Journal: European Respiratory Journal (1999)

Limited information is available regarding the physiological responses to different types of exercise training in patients with severe chronic obstructive pulmonary disease (COPD). The aim of this study was two fold: firstly, to investigate the physiological response to training at 60% of achieved peak load in patients with severe COPD; and secondly to study the effects of interval (I) versus continuous (C) training in these patients. Twenty-one patients with COPD (mean+/-SD forced expiratory volume in one second: 37+/-15% of predicted, normoxaemic at rest) were evaluated at baseline and after 8 weeks9 training. Patients were randomly allocated to either I or C training. The training was performed on a cycle ergometer, 5 days a week, 30 min daily. The total work load was the same for both training programmes. C training resulted in a significant increase in oxygen consumption (V9O2) (17%, p&lt;0.05) and a decrease in minute ventilation (V9E)/V9O2 (p&lt;0.01) and V9E/carbon dioxide production (V9CO2) (p&lt;0.05) at peak exercise capacity, while no changes in these measures were observed after interval training. During submaximal exercise a significant decrease was observed in lactic acid production, being most pronounced in the C-trained group (-31%, p&lt;0.01 versus -20%, p&lt;0.05). Only in the I-trained group did a significant increase in peak work load (17%, p&lt;0.05) and a decrease in leg pain (p&lt;0.05) occur. Training did not result in a significant improvement in lung function, but maximal inspiratory mouth pressure increased in both groups by 10% (C: p&lt;0.05) and 23% (I: p&lt;0.01). The present study shows a different physiological response pattern to interval or continuous training in chronic obstruction pulmonary disease, which might be a reflection of specific training effects in either oxidative or glycolytic muscle metabolic pathways. Further work is required to determine the role of the different exercise programmes and the particular category of patients for whom this might be beneficial.
Are we building too many medical schools?
Authors: K. B. Castleton
Journal: JAMA (1971)

The health care delivery system is in trouble. An alleged shortage of physicians is only one facet of the problem and may not even be the most important. We don't know exactly how many doctors we need. First we must solve some of the other facets of the problem. We must make the system more efficient and make health care more readily available to all citizens at a reasonable cost. We must make better use of the physicians' time by better utilization of "middle medical personnel" and automation. We must provide and place greater emphasis on health services and not just medical care, and we must do something to improve distribution of available physicians. Establishment of new medical schools is probably the most expensive and surely the slowest approach to solving the problem. We will never solve our problem merely by increasing the number of doctors.
Reply
Authors: P J Guillou
Journal: Gut (1988)

with disseminated carcinoma to respond to the LAK process, and indicates the requirement for tech- niques to increase lymphocyte cellular renewal in such patients.Lymphokine activated killer source cannot simply be explained on the basis of cell type, but surely represents a functional disruption of a down regulated networks when performed outside the body.This results in large numbers of effector lymphocytes derived from those cell types, both T-cell and NK cell, in which anti-tumour activity can be augmented.
A PROOFREADER'S BLUNDER.
Journal: JAMA (2001)

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
Transactions of the Michigan State Medical Society for the Year 1894.
Journal: JAMA (1894)

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
A phase I study of TRC105 (anti-CD105 [endoglin] antibody) in metastatic castration-resistant prostate cancer (mCRPC).
Authors: Fatima H Karzai, Andrea Borghese Apolo, David E. Adelberg, Ravi Amrit Madan, James L. Gulley, Philip M. Arlen, Howard L. Parnes, Ann Pierpoint, David R. Kohler, Douglas K. Price, Seth M Steinberg, Jane B. Trepel, William Douglas Figg, William L. Dahut
Journal: Journal of Clinical Oncology (2012)

117 Background: Preclinical and clinical evidence demonstrates an important role for angiogenesis in mCRPC biology. CD105 (endoglin) is a transmembrane protein expressed on the surface of proliferating vascular endothelial cells. The expression of CD105 is required for the formation of new blood vessels. TRC105 is a human/murine chimeric IgG1 kappa monoclonal antibody that binds to human CD105 (endoglin). It inhibits angiogenesis and tumor growth through inhibition of endothelial cell proliferation, antibody-dependent cellular cytotoxicity, and induction of apoptosis. The primary objective is to evaluate safety and identify the maximum tolerable dose (MTD) of TRC105. Secondary objectives include the assessment of TRC105 pharmacokinetics, PSA response rate, evaluation of progression free survival (PFS), overall response rate (ORR) and overall survival (OS). Methods: Patients with an ECOG performance status (PS) ≤ 2, progressive mCRPC and either chemotherapy-naïve or post-docetaxel treatment were eligible. Five cohorts of patients, on escalating dose levels, receive TRC105 intravenously at doses of 1, 3, 10 or 15 mg/kg IV every 2 weeks (cohorts 1, 2, 3, and 5) or 10 mg/kg IV weekly (cohort 4) on a 4 week cycle. Response is assessed with imaging studies every 2 months for the first four months and then every 3 months thereafter. Results: Seventeen patients are enrolled in cohorts 1-5. Median age is 65 (range 48-87), median ECOG PS is 1 (range 0−2), median Gleason score is 8 (range 6−10), median on−study PSA is 147.5 (range 0.1-3373), and median number of prior (non-hormonal) therapies is 3 (range 0−6). Median time on study is 16 weeks (range 8-28 weeks). One patient experienced a dose limiting toxicity (grade 4 vasovagal episode) in cohort 5. PSA declines were seen in 6 patients ranging from 20% to 57% from baseline. Ten out of 12 patients with measurable soft tissue disease achieved stable disease for at least two cycles. Two patients remain on study (in cohort 5). Conclusions: TRC105 is tolerated up to 15 mg/kg every two weeks with early evidence of clinical activity in mCRPC. Accrual is ongoing to evaluate ORR, PFS, and OS in the phase II portion of this study.
PHYSIOLOGIC LEUKOCYTOSIS
Journal: JAMA (1929)

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
化脓性汗腺炎在唐氏综合症患者中的普遍性:以人群为基础的横断分析
Authors: A. Garg, A. Strunk, M. Midura, V. Papagermanos, H. Pomerantz
Journal: British Journal of Dermatology (2018)

化脓性汗腺炎(HS)是一种使人衰弱且痛苦的慢性炎性疾病。科学家先前表明,唐氏综合症患者存在容易因淀粉样前体蛋白的形成增多而患上HS的潜在基因联系。但是,此项基于实验室的发现之前并未在人群中得到验证。在本研究中,我们评估了化脓性汗腺炎在一大群唐氏综合症患者中的普遍性,并利用另一组未患有唐氏综合症的患者对发现进行了比较。我们观察到,在过去的五年中,有2.1%的唐氏综合症患者被诊断出患有化脓性汗腺炎。在研究期间,与未患有唐氏综合症的患者相比,唐氏综合症患者患上化脓性汗腺炎的可能性是前者的五倍。化脓性汗腺炎最常见于18~29岁的唐氏综合症患者。在唐氏综合症患者中,无论男性还是女性,也无论白人还是非白人,都会受到化脓性汗腺炎的影响。与未患有唐氏综合症的患者相比,唐氏综合症患者会在较年轻时被诊断出化脓性汗腺炎。这表明,汗腺炎可能会发生在唐氏综合症患者的较年轻时期,或者说汗腺炎的症状可能较为严重,因此促使患者尽早就医。唐氏综合症患者较早被诊断出化脓性汗腺炎的另一个原因可能是,医生普遍会更加频繁的对唐氏综合症患者进行检查。
BERLIN
Journal: JAMA (1920)

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 Journals 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
Therapeutic effect of neutralizing endogenous IL-18 activity in the collagen-induced model of arthritis
Authors: Christine Plater-Zyberk, Leo A.B. Joosten, Monique M.A. Helsen, Pascale Sattonnet-Roche, Christiane Siegfried, Sami Alouani, Fons A.J. van de Loo, Pierre Graber, Shuki Aloni, Rocco Cirillo, Erik Lubberts, Charles A. Dinarello, Wim B. van den Berg, Yolande Chvatchko
Journal: Journal of Clinical Investigation (2001)

Two distinct IL-18 neutralizing strategies, i.e. a rabbit polyclonal anti-mouse IL-18 IgG and a recombinant human IL-18 binding protein (rhIL-18BP), were used to treat collagen-induced–arthritic DBA/1 mice after clinical onset of disease. The therapeutic efficacy of neutralizing endogenous IL-18 was assessed using different pathological parameters of disease progression. The clinical severity in mice undergoing collagen-induced arthritis was significantly reduced after treatment with both IL-18 neutralizing agents compared to placebo treated mice. Attenuation of the disease was associated with reduced cartilage erosion evident on histology. The decreased cartilage degradation was further documented by a significant reduction in the levels of circulating cartilage oligomeric matrix protein (an indicator of cartilage turnover). Both strategies efficiently slowed disease progression, but only anti–IL-18 IgG treatment significantly decreased an established synovitis. Serum levels of IL-6 were significantly reduced with both neutralizing strategies. In vitro, neutralizing IL-18 resulted in a significant inhibition of TNF-α, IL-6, and IFN-γ secretion by macrophages. These results demonstrate that neutralizing endogenous IL-18 is therapeutically efficacious in the murine model of collagen-induced arthritis. IL-18 neutralizing antibody or rhIL-18BP could therefore represent new disease-modifying anti-rheumatic drugs that warrant testing in clinical trials in patients with rheumatoid arthritis.
Missing Information About Plan for Analyses of Other Outcomes
Journal: JAMA Neurology (2019)

Anneleen Malfliet, MSc; Jeroen Kregel, PhD; Iris Coppieters, PhD; Robby De Pauw, MSc; Mira Meeus, PhD; Nathalie Roussel, PhD; Barbara Cagnie, PhD; Lieven Danneels, PhD; Jo Nijs, PhD