tbuckley/cabot-search huggingface dataset:
Spontaneous Abortion, Sex Ratio, and Paternal Occupational Exposure to 2,3,7,8-Tetrachlorodibenzo-p-Dioxin
Authors: Teresa M. Schnorr, Christina C. Lawson, Elizabeth A. Whelan, David A. Dankovic, James A. Deddens, Laurie A. Piacitelli, Jennita Reefhuis, Marie H. Sweeney, L. Barbara Connally, Marilyn A. Fingerhut
Journal: Environmental Health Perspectives (2001)

There is conflicting research regarding an association between fetal death and paternal exposure to Agent Orange, a phenoxy herbicide widely used in Vietnam that was contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Men who worked in the U.S. factories that produced Agent Orange were exposed to TCDD at levels hundreds of times higher than TCDD levels in the general population. Wives of TCDD-exposed chemical workers and wives of nonexposed neighborhood referents were interviewed to determine reproductive history. Paternal serum TCDD level at time of conception was estimated for each pregnancy using serum samples taken in 1987. Estimated TCDD levels of workers during or after exposure were high (median, 254 ppt; range, 3-16,340 ppt) compared to referent levels (median, 6 ppt; range, 2-19 ppt). No association between paternal TCDD level at the time of conception and spontaneous abortion was observed among pregnancies fathered by workers with TCDD levels of < 20 ppt [odds ratio (OR) = 0.77; 95% confidence interval (CI), 0.48-1.22], 20 to < 255 ppt (OR = 0.81; 95% CI, 0.40-1.63), 255 to < 1,120, (OR = 0.69; 95% CI, 0.30-1.58), and >or= 1,120 ppt (OR = 0.95; 95% CI, 0.42-2.17) compared to pregnancies fathered by referents. The sex ratio [males/(males + females)] of offspring also did not differ by TCDD exposure (0.53 and 0.54 among workers and referents, respectively). We did not find an association between paternal serum TCDD level and spontaneous abortion or sex ratio of offspring in this population. The estimated TCDD levels in this exposed worker population were much higher than in other studies, providing additional evidence that paternal TCDD exposure does not increase the risk of spontaneous abortion at levels above those observed in the general population. The study could not evaluate the effect of father's childhood or prenatal TCDD exposure on subsequent sex ratio.
Central amino acid neurotransmitters and the hypoxic ventilatory response.
Authors: I Soto-Arape, M D Burton, H Kazemi
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

Acute sustained hypoxia causes an early rise in ventilation, followed by a reduction in ventilation ("roll off") after several minutes to levels below the peak but above baseline. The underlying mechanism(s) of this biphasic response is unclear. Hypoxia induces changes in the release and metabolic turnover of glutamate and gamma aminobutyric acid (GABA). These endogenous neuroactive agents may play a role in mediating the biphasic hypoxic ventilatory response. Therefore, their role was studied in anesthetized (isoflurane), isocapnic, mechanically ventilated rats. Hypoxia alone (FIO2 = 0.1) produced the characteristic biphasic response in the phrenic neurogram (n = 6). When the glutamate receptor was blocked with application of two different N-methyl-D-aspartate (NMDA) antagonists, MK-801 or AP-5, to the ventrolateral medullary surface (VMS), the phrenic output fell by 90% during normoxia and demonstrated no response to hypoxia (n = 6 for each group). There was a rise of 60% in phrenic nerve output during normoxia when GABA antagonist bicuculline was applied to the VMS, and with hypoxia it rose another 15%, and no fall off was seen during hypoxia (n = 6). These findings suggest that during hypoxia the initial hyperventilation has a glutamatergic component and the subsequent fall off its mediated by GABAergic mechanisms.
Unexplained Noncardiac Chest Pain
Authors: Frank P. Castrina
Journal: Annals of Internal Medicine (1997)

Letters15 April 1997Unexplained Noncardiac Chest PainFrank P. Castrina, MDFrank P. Castrina, MDPHICO, Mechanicsburg, PA 17055-0085Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-126-8-199704150-00024 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Recent articles by Rao and colleagues [1] and Frobert and colleagues [2] add to the extensive literature about the esophagus as a cause of chest pain in patients who do not have coronary artery disease. An equally important issue is the misdiagnosis of esophageal disease in patients with acute coronary syndromes.A report based on 10 years of data from the PHICO insurance company (a medical malpractice carrier) involving myocardial infarction that was not diagnosed in the emergency department showed that a gastrointestinal diagnosis was made in 35% (24 of 64) of the claims [3]. A finding ...References1. Rao SS, Gregersen H, Hayek B, Summers RW, Christensen J. Unexplained chest pain: the hypersensitive, hyperreactive, and poorly compliant esophagus. Ann Intern Med. 1996; 124:950-8. Google Scholar2. Frobert O, Funch-Jensen P, Bagger JP. Diagnostic value of esophageal studies in patients with angina-like chest pain and normal coronary angiograms. Ann Intern Med. 1996; 124:959-69. Google Scholar3. Pelberg AL. Missed myocardial infarction in the emergency room. Quality Assurance and Utilization Review. 1989; 4:39-42. Google Scholar4. Acute myocardial infarction study. Washington, DC: Physician Insurers Association of America; 1996. Google Scholar5. Singh S, Richter JE, Hewson EG, Sinclair JW, Hackshaw BT. The contribution of gastroesophageal reflux to chest pain in patients with coronary artery disease. Ann Intern Med. 1992; 117:824-30. Google Scholar Author, Article, and Disclosure InformationAffiliations: PHICO, Mechanicsburg, PA 17055-0085 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByProtocolo diagn?stico del dolor tor?cico recurrenteIdentifying Chest Pain Emergencies in the Primary Care Setting 15 April 1997Volume 126, Issue 8Page: 663KeywordsAcute coronary syndromeAcute myocardial infarctionCardiovascular therapyCoronary arteriesCoronary heart diseaseEmergency departmentEsophagusIschemiaMyocardial infarctionStable coronary artery disease Issue Published: 15 April 1997 CopyrightCopyright © 1997 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
MONONUCLEOSIS
Journal: JAMA (1962)

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
Still Life
Authors: Woods Nash
Journal: JAMA (2014)

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
Chronic postmyelographic headache. A result of persistent epidural cerebrospinal fluid fistula
Authors: M. C. Levine
Journal: JAMA (1974)

THERE is abundant clinical as well as theoretical evidence that headaches after lumbar puncture and myelography are due to traction on pain-sensitive intracranial tissues, such as meninges and cerebral blood vessels, because of lowered intracranial pressure caused by leakage of spinal fluid through the dural puncture site. The evidence for this mechanism rests on the relief of pain by release of traction through recumbency, the demonstration of an extra-arachnoid pool of spinal fluid when air encephalography or myelography are attempted after a previous lumbar puncture, cerebrospinal fluid leaks from the site of a previous lumbar puncture (observed at subsequent laminectomy) and data provided by scintigrams of the circulation of radioactive isotopes injected into the cerebrospinal subarachnoid space. Postlumbar puncture headache might be expected to occur more frequently following myelography, when the relatively large spinal needle (18-gauge) is left in situ for the duration of the study. Autologous blood patches have
Corrigendum
Journal: British Journal of Dermatology (2010)

British Journal of DermatologyVolume 163, Issue 2 p. 437-437 Free Access Corrigendum This article corrects the following: Double-blind, randomized, placebo-controlled study of a lotion containing triethyl citrate and ethyl linoleate in the treatment of acne vulgaris A. Charakida, M. Charakida, A.C. Chu, Volume 157Issue 3British Journal of Dermatology pages: 569-574 First Published online: July 16, 2007 First published: 21 July 2010 https://doi.org/10.1111/j.1365-2133.2010.09933.xAboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat In the article by Charakida et al.1 the paper was published without author conflict of interest disclosures. The Conflict of Interest statement should have read: The trial was funded by General Topics, owners of SkinMed and manufacturers of the Aknicare product range, under a research contract arrangement between the company and The Imperial College Healthcare NHS Trust. The authors apologise for omitting this disclosure statement. Reference 1 Charakida A, Charakida M, Chu AC. Double-blind, randomized, placebo-controlled study of a lotion containing triethyl citrate and ethyl linoleate in the treatment of acne vulgaris. Br J Dermatol 2007; 157: 569– 74. Wiley Online LibraryCASPubMedWeb of Science®Google Scholar Volume163, Issue2August 2010Pages 437-437 ReferencesRelatedInformation
National Health Insurance: What Kind and How Much
Authors: Robert D. Eilers
Journal: New England Journal of Medicine (1971)

Abstract Although most proposals for national health insurance meet the criteria of financial accessibility and consumer participation in cost, few measure up to criteria for delivery acceptability, cost efficiency and minimization of governmental regulation. Tax-credit and catastrophic-coverage proposals are deficient in their failure to stimulate strongly changes in the health-delivery system; proposals incorporating a comprehensive health system are deficient for the opposite reason — namely, control over health delivery would probably be centralized to an extent that would preclude consumer choice. Capitation payment for a combination of hospital and physicians' services financed through national health insurance should be achieved for the bulk of the population within a 10-year period, and, in addition, every citizen should be given the freedom to choose from among competing delivery arrangements.
Brief Review
Journal: JAMA (1990)

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 Alleged Health-Protective Effects of Coffee—Reply
Authors: Erikka Loftfield, Barry I. Graubard, Neal D. Freedman
Journal: JAMA Internal Medicine (2018)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Internal Medicine journal
A randomized, double-blind, placebo-controlled, phase IIIb trial (ATLAS) comparing bevacizumab (B) therapy with or without erlotinib (E) after completion of chemotherapy with B for first-line treatment of locally advanced, recurrent, or metastatic non-small cell lung cancer (NSCLC)
Authors: V. A. Miller, P. O'Connor, C. Soh, F. Kabbinavar
Journal: Journal of Clinical Oncology (2009)

LBA8002 Background: B when added to chemotherapy, and E alone, each lead to improved survival in the treatment of patients (pts) with NSCLC (Sandler et al, NEJM 2006, 355:2542–2550; Shepherd et al, NEJM 2005, 353:123–132). Pre-clinical and clinical data (Herbst, J Clin Oncol 2007, 25: 4743–4750) suggest that the combination of B and E may improve the efficacy of NSCLC treatment. This potential was demonstrated in the BETA (B in combination with E compared with E alone for treatment of advanced NSCLC after failure of standard first-line chemotherapy) trial, a phase III trial in which progression free survival (PFS) was improved for patients treated with B + E (Hainsworth, Thoracic Oncol 2008, 3(11) Supp. 4:S302). Methods: The ATLAS study was designed to evaluate B + E (150 mg daily) versus B alone, following B + platin-containing doublet chemotherapy, in pts with stage IIIb/IV NSCLC. Enrolled pts were B-eligible, including pts with treated brain metastases, and pts anticoagulated with low molecular weight heparin(s). Pts with peripheral and/or extra-thoracic squamous tumors were also eligible. Pts received 4 cycles of B (15 mg/kg every 3 weeks) with chemotherapy. Pts who had not experienced disease progression (DP) or significant toxicity were then randomized to receive B + E or B + placebo (P). The primary objective of ATLAS was to compare PFS in pts receiving B + E versus B + placebo. Secondary objectives included the assessment of safety, and overall survival. A data safety monitoring committee (DSMC) monitored safety and efficacy. Results: 1,160 patients were enrolled and 768 randomized from May 2005 to May 2008. The DSMC recommended stopping the trial at the second planned interim efficacy analysis, because it met the primary endpoint. The median PFS after randomization was 4.8 mos for (B + E) vs. 3.7 mos for (B + P), HR= 0.722 (95% CI: 0.592–0.881), p = 0.0012. The safety profile for B + E was consistent with known profiles for B and E. Conclusions: E added to B treatment after chemotherapy with B significantly improves the PFS of patients treated in the first-line setting for locally advanced, recurrent, or metastatic NSCLC. Author Disclosure Employment or Leadership Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Genentech, Inc. Genentech, Inc. Genentech, Inc. Genentech, Inc.
Left ventricular wall stress and sarcoplasmic reticulum Ca2+-ATPase gene expression in renal hypertensive rats: dose-dependent effects of ACE inhibition and AT1-receptor blockade
Authors: W. Zierhut, R. Studer, D. Laurent, S. Kastner, P. Allegrini, S. Whitebread, F. Cumin, H.-P. Baum, M. de Gasparo, H. Drexler
Journal: Cardiovascular Research (1996)

Cardiac hypertrophy is associated with altered Ca2+ handling and may predispose to the development of LV dysfunction and cardiac failure. At the cellular level, the re-expression of ANF represents a well-established marker of myocyte hypertrophy while the decreased expression of the sarcoplasmatic reticulum (SR) Ca2+-ATPase is thought to play a crucial role in the alterations of Ca2+ handling and LV function. We assessed the dose-dependent effect of chronic ACE inhibition or AT1 receptor blockade on cardiac function in relation to the cardiac expression of the SR Ca2+-ATPase and ANF. Renal hypertensive rats (2K-1C) were treated for 12 weeks with three different doses of the ACE inhibitor benazepril, the AT1-receptor antagonist valsartan (each drug 0.3, 3, and 10 mg/kg per day i.p.) or placebo. LV dimensions, hypertrophy and wall stress were determined in vivo by magnetic resonance imaging and the gene expressions of ANF and SR Ca2+-ATPase were quantified by Northern blot. Low doses of both drugs did not affect blood pressure, hypertrophy, systolic wall stress and the ANF and SR Ca2+-ATPase gene expression. High doses of each drug reduced systolic blood pressure, wall stress, and LV hypertrophy to a similar extent and to values comparable to normotensive, age-matched rats. In addition, high dose treatment reduced LV end-systolic and end-diastolic volume as compared to untreated 2K-1C animals and normalized the mRNA levels of both ANF and SR Ca2+-ATPase (as compared to normotensive animals). We conclude that in this model, high doses of ACE inhibition and AT1-receptor blockade are necessary to normalize systolic blood pressure, LV hypertrophy and systolic LV wall stress which, in turn, is associated with restoration of a normal cardiac phenotype with respect to SR Ca2+-ATPase and ANF and normalization of cardiac function.
Effect of chronic HCV infection on intrahepatic expression of HBV antigens . Dept. of Pathology ULSS 15-Cittadella Hospital and Padova University, Internal Medicine Padova and Verona University, Dept. of Infectious Disease Padova Hospital, Italy and* Stratton-Popper Dept. of Pathology, Mount Sinai Medical School, New York
Journal: Hepatology (1995)

Photothrombotic infarcts of the neocortex result in structural and functional alterations of cortical networks, including decreased GABAergic inhibition, and can generate epileptic seizures within 1 month of lesioning. In our study, we assessed the involvement and potential changes of cortical GABAA receptor (GABAAR) α1 subunits at 1, 3, 7, and 30 days after photothrombosis. Quantitative competitive reverse transcription-polymerase chain reaction (cRT-PCR) and semi-quantitative Western blot analysis were used to investigate GABAAR α1 subunit mRNA and protein levels in proximal and distal regions of perilesional cortex and in homotopic areas of young adult Sprague-Dawley rats. GABAAR α1 subunit mRNA levels were decreased ipsilateral and contralateral to the infarct at 7 days, but were increased bilaterally at 30 days. GABAAR α1 subunit protein levels revealed no significant change in neocortical areas of both hemispheres of lesioned animals compared with protein levels of sham-operated controls at 1, 3, 7, and 30 days. At 30 days, GABAAR α1 subunit protein expression was significantly increased in lesioned animals within proximal and distal regions of perilesional cortex compared with distal neocortical areas contralaterally (Student's t-test, p < 0.05). Short- and long-term alterations of mRNA and protein levels of the GABAAR α1 subunit ipsilateral and contralateral to the lesion may influence alterations in cell surface receptor subtype expression and GABAAR function following ischemic infarction and may be associated with formative mechanisms of poststroke epileptogenesis.
Musicogenic Epilepsy
Authors: Robert J. Joynt
Journal: JAMA (1962)

A woman aged 62 gave a history of convulsions since the age of 49. Her associates reported peculiar patterns of behavior induced in her by music, and she was aware of periods of unconsciousness induced by organ music. The electroencephalogram showed various abnormalities including basic generalized fast activity, right temporal sharp activity, and slow activity spreading over the temporal areas. In addition to the resting EEG, records were obtained during hyperventilation and during photic and acoustic stimulation. Her physical condition was normal excepting an underlying severe adrenocortical insufficiency (with brownish pigmentation of the skin) and some clumsiness of the left lower extremity.