tbuckley/cabot-search huggingface dataset:
The Harvard Way
Authors: Bradford L. Walters
Journal: JAMA (1985)

<h3>To the Editor.—</h3> I read with a great deal of sadness Dr S. Walker's<sup>1</sup>"The Harvard Way" in the March 15 issue of<i>JAMA</i>. The feelings Dr Walker expressed are a stinging indictment of what I feel to be archaic attitudes in graduate medical education. For some reason, physicians who are supposed to epitomize compassion and sensitivity tend to design training programs that are the antithesis of such desirable attributes. Residents work long hours for little pay. They are expected to withstand severe psychological and physical trials, and, instead of getting support and encouragement from their teachers, they receive stinging rebukes and are made to feel worthless and incompetent. I feel there is no reason for this. Providing residents with excellent education does not mean that they have to be subjected to such psychological battering that traditionalists seem to feel necessary in order to "toughen up" young physicians. High-quality
Intravenous salbutamol and aminophylline in asthma: a search for synergy.
Authors: P D Handslip, A M Dart, B H Davies
Journal: Thorax (1981)

The bronchodilation produced by increasing intravenous doses of aminophylline, salbutamol, and a combination of aminophylline and salbutamol given in random order was determined in 10 stable asthmatics on three consecutive days. On a fourth day, response to placebo injections was determined. Forced expiratory volume in one second (FEV1) was measured at two-minute intervals after each dose until FEV1 returned to a new baseline. At no dosage level was there synergy between the two agents in terms of either mean percentage increase in FEV1 or the integrated response. The failure to demonstrate synergy has implications both with respect to the clinical use and the underlying mechanism of action of these drugs.
The Effects of 100% Oxygen on Soccer Players-Reply
Authors: Kenneth H. Cooper
Journal: JAMA (1989)

<h3>In Reply.—</h3> When performing medical research, a classic approach is to make use of a placebo-controlled, randomized, double-blind crossover study design. In such a design, as was used in the study by Winter et al,<sup>1</sup>the potential intervention is compared against a placebo and not against no intervention at all; this approach is used to control for the possible placebo effect of potential interventions. In the event that no differences are detected between the placebo and the potential intervention, then the potential intervention is not considered to be of benefit. Dr Gabel, however, suggests in his letter that should equivalent benefits occur with the placebo and the potential intervention, then the potential intervention should be considered to be of value. This logic does not take into consideration the likelihood that once it is known that the potential intervention is of placebo value only, it will, in essence, no longer
The contraction of stunned myocardium: isovolumetric bulging and wasted ejection shortening in dog heart
Authors: G. Chen, A. D Askenase, K. Chen, L. N Horowitz, B. L Segal
Journal: Cardiovascular Research (1992)

Objective: The aim of the study was to assess the contraction of myocardium stunned by repetitive brief coronary occlusions by examining the response to alterations in loading and inotropy of systolic contraction on isovolumetric and ejection phase shortening. Methods: Fourteen open chest anaesthetised dogs were used for the studies. After destruction of the sinus node, the heart was atrially paced and atrial extrasystoles were introduced followed by a short (400 ms) or long (700 ms) postextrasystole. The left anterior descending coronary artery was occluded for 5 min and reperfused for 10 min a total of eight times to produce stunned myocardium, followed by a final 60 min of reflow. Regional function was assessed with segment length sonomicrometers. Results: With successive periods of occlusion there was an increase in the end diastolic segment length and a progressive decrease in total percent systolic shortening (baseline 22.3%, 1st reflow 14.5%, 8th reflow 7.9%) with some recovery after 60 min of reflow (12.0%). This was predominantly due to the development of bulging during isovolumetric systole (4.5%, -4.9%, and -8.3%, respectively) which diminished during 60 min recovery to -3.1%. Ejection shortening was relatively constant (17.8%, 19.4%, 16.3%, and 15.1%, respectively). Postextrasystolic potentiation resulted in an increase in total percent systolic shortening, but not to the baseline value, as slight isovolumetric bulging persisted. Similar changes were seen with the short and long postextrasystoles although the latter had a greater increase in ejection shortening. Conclusions: The decrease in function after repetitive occlusion and reflow is predominantly due to bulging during isovolumetric systole which persists after postextrasystolic potentiation in our model of stunned myocardium.
Lead Poisoning Deaths in the United States, 1979 Through 1988
Authors: Catherine Staes
Journal: JAMA (1995)

To the Editor.  —Deaths due to lead poisoning reportedly have dramatically decreased in the United States since the 1960s 1 ; however, recent national estimates of the number and distribution of such deaths have not been published.  We used computerized data tapes from the National Center for Health Statistics (NCHS) 2,3 to identify deaths occurring from 1979 through 1988 for which lead poisoning was listed as an underlying or contributing cause. We selected records that included International Classification of Dis-  eases, Ninth Revision (ICD-9)  4 codes specific for lead (984, 984.0, 984.1, 984.8, 984.9, E861.5, and E866.0) or heavy metals (961.2 and E931.2). To confirm a diagnosis of lead poisoning, we requested a copy of the original death certificate for the selected records from the vital records department with jurisdiction for the location where the death occurred.  The ICD-9 codes of interest appeared in 166 records in the NCHS death tapes
Temporal trends in multiple births after in vitro fertilisation in Sweden, 1982-2001: a register study
Authors: Bengt Källén, Orvar Finnström, Karl Gösta Nygren, Petra Otterblad Olausson
Journal: BMJ (2005)

further, from two to one, and a further reduction in multiple births is to be expected whereas the pregnancy rate seems to be little affected. 4 5
Association between Arsenic Exposure from Drinking Water and Plasma Levels of Soluble Cell Adhesion Molecules
Authors: Yu Chen, Regina M. Santella, Muhammad G. Kibriya, Qiao Wang, Maya Kappil, Wendy J. Verret, Joseph H. Graziano, Habibul Ahsan
Journal: Environmental Health Perspectives (2007)

Epidemiologic studies of cardiovascular disease risk factors and appropriate biomarkers in populations exposed to a wide range of arsenic levels are a public health research priority.We investigated the relationship between inorganic arsenic exposure from drinking water and plasma levels of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular adhesion molecule-1 (sVCAM-1), both markers of endothelial dysfunction and vascular inflammation, in an arsenic-exposed population in Araihazar, Bangladesh.The study participants included 115 individuals with arsenic-related skin lesions participating in a 2 x 2 randomized, placebo-controlled, double-blind trial of vitamin E and selenium supplementation. Arsenic exposure status and plasma levels of sICAM-1 and sVCAM-1 were assessed at baseline and after 6 months of follow-up.Baseline well arsenic, a long-term measure of arsenic exposure, was positively associated with baseline levels of both sICAM-1 and sVCAM-1 and with changes in the two markers over time. At baseline, for every 1-mug/L increase in well arsenic there was an increase of 0.10 ng/mL [95% confidence interval (CI), 0.00-0.20] and 0.33 ng/mL (95% CI, 0.15-0.51) in plasma sICAM-1 and sVCAM-1, respectively. Every 1-microg/L increase in well arsenic was associated with a rise of 0.11 ng/mL (95% CI, 0.01-0.22) and 0.17 ng/mL (95% CI, 0.00-0.35) in sICAM-1 and sVCAM-1 from baseline to follow-up, respectively, in spite of recent changes in urinary arsenic as well as vitamin E and selenium supplementation during the study period.The findings indicate an effect of chronic arsenic exposure from drinking water on vascular inflammation that persists over time and also suggest a potential mechanism underlying the association between arsenic exposure and cardiovascular disease.
Problems with the imprinting hypothesis of schizophrenia and autism
Authors: Matthew C. Keller
Journal: Behavioral and Brain Sciences (2008)

Abstract Crespi &amp; Badcock (C&amp;B) convincingly argue that autism and schizophrenia are diametric malfunctions of the social brain, but their core imprinting hypothesis is less persuasive. Much of the evidence they cite is unrelated to their hypothesis, is selective, or is overstated; their hypothesis lacks a clearly explained mechanism; and it is unclear how their explanation fits in with known aspects of the disorders.
Flock Worker's Lung
Authors: Lawrence W. Raymond
Journal: Annals of Internal Medicine (1999)

Letters6 April 1999Flock Worker's LungLawrence W. Raymond, MDLawrence W. Raymond, MDCarolinas Medical Center; Charlotte, NC 28232 (Raymond)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-130-7-199904060-00012 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:The unsavory saga of flock worker's lung and the critical analysis of secrecy in science by Schuchman combine with Dr. Davidoff's editorial (1-3) to call attention to the need for a priori damage control when physicians contract to provide occupational health services to industry. One simple step might help, at least when dealing with employers in the United States—to include in such contracts reference to the Toxic Substances Control Act (TSCA). Specifically, section 8(e) of this Act requires manufacturers to notify the Administrator of the Environmental Protection Agency when new findings of adverse effects constitute a substantial ...References1. Kern DG, Crausman RS, Durand KT, Nayer A, Kuhn C. Flock worker's lung: chronic interstitial lung disease in the nylon flocking industry. Ann Intern Med. 1998;129:261-72. LinkGoogle Scholar2. Schuchman M. Secrecy in science: the flock worker's lung investigation. Ann Intern Med. 1998;129:341-4. LinkGoogle Scholar3. Davidoff F. New disease, old story [Editorial]. Ann Intern Med. 1998;129:327-8. LinkGoogle Scholar4. Vu VT, Lai DY. Approaches to characterizing human health risks of exposure to fibers. Environ Health Perspect. 1997;105 Suppl 5 1329-36. MedlineGoogle Scholar5. Lougheed MD, Roos JO, Waddell WR, Munt PW. Desquamative interstitial pneumonitis and diffuse alveolar damage in textile workers. Potential role of mycotoxins. Chest. 1995;108:1196-200. CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAuthors: Lawrence W. Raymond, MDAffiliations: Carolinas Medical Center; Charlotte, NC 28232 (Raymond) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoFlock Worker's Lung: Chronic Interstitial Lung Disease in the Nylon Flocking Industry David G. Kern , Robert S. Crausman , Kate T.H. Durand , Ali Nayer , and Charles Kuhn III Metrics Cited byNonneoplastic Parenchymal Lung DiseaseImaging of Nonmalignant Occupational Lung Disease 6 April 1999Volume 130, Issue 7Page: 615KeywordsClinical trial reportingEnvironmental healthLungsMedical servicesResearch laboratories ePublished: 15 August 2000 Issue Published: 6 April 1999 Copyright & PermissionsCopyright © 1999 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Compensatory Vascular Changes of Remote Coronary Segments in Response to Lesion Progression as Observed by Sequential Angiography From a Controlled Clinical Trial
Authors: Anne M. Shircore, Wendy J. Mack, Robert H. Selzer, Paul L. Lee, Stanley P. Azen, Petar Alaupovic, Howard N. Hodis
Journal: Circulation (1995)

Background Local coronary artery enlargement to compensate for atherosclerotic plaques preserves the vessel lumen. The extent to which coronary segments remote from progressing lesions enlarge is unknown. This is clinically relevant since compensatory enlargement may be important in determining whether clinical complications result from progression of coronary artery disease (CAD). Additionally, compensatory change has implications for quantitative coronary angiographic (QCA) trials, since the effect of progression on diameter means may be mitigated by compensatory changes in remote coronary segments when QCA change is averaged over all lesions. Methods and Results Serial QCA data from 78 subjects in the Monitored Atherosclerosis Regression Study were used to demonstrate compensatory changes in coronary segments remote from progressing or regressing lesions. Coronary segments were first classified as progressing (regressing) if percent diameter stenosis (PS) increased or decreased by &gt;10 with a concurrent decrease or increase in minimum lumen diameter (MLD) of either &gt;0.32 mm or &gt;10% of the normal baseline reference diameter (DNORM). Segments not meeting these criteria were labeled stenosis stable. Stenosis-stable segments opposite progressing lesions showed increases in MLD ( P =.0006), DNORM ( P =.001), and average diameter ( P =.001). On-trial apolipoprotein (apo) B, apo C-III, and blood pressure levels inversely correlated with these compensatory changes. Conclusions Lesion progression in one coronary segment is associated with significant increases in segmental diameter of remote parts of the coronary tree. We hypothesize these increases to be vascular compensatory changes in response to progression of CAD. Vascular compensatory change is enhanced by LDL cholesterol and triglyceride-rich lipoprotein reduction and appears to be part of the treatment effect itself.
P617Peroxisome proliferator activated receptor(PPAR)alpha\gamma agonist aleglitazar reduces the inflammatory-mediated expression of monocyte chemoattractant protein(MCP)-1 selectively in human adipocytes
Authors: M Massaro, E Scoditti, MA Pellegrino, N Calabriso, MA Carluccio, C Storelli, R De Caterina
Journal: Cardiovascular Research (2014)

Excessive adiposity in obese individuals is accompanied by low-level inflammation, which is regarded as the mechanistic link between obesity and related cardiovascular and diabetic complications. Improvement of the inflammatory components accompanying diabetes and metabolic syndrome is a current goal. Co-ligands of PPARα and Γ, combining the metabolic- and anti-inflammatory properties of α and Γ agonists, are one therapeutic option. Adipose tissue production of MCP-1 orchestrates monocyte-macrophage recruitment into inflamed adipose tissue. We therefore investigated whether the dual agonist ALE, in comparison to selective agonists for PPARα and Γ, fenofibrate(FENO) and rosiglitazone(RSG) respectively, regulates MCP-1 expression in fully differentiated human Simpson-Golabi-Behmel syndrome adipocytes (SGBS cells) and human umbilical vein endothelial cells (HUVEC), and explored underlying mechanisms. Methods: SGBS cells and HUVEC were treated with 0.01-1000 nmol/L ALE and RSG or 5-50 μmol/L FENO for 24 h before stimulation with 10 ng/mL TNFα. Conditioned media were then tested for MCP-1 release by ELISA, while in parallel, MCP-1 mRNA expression was investigated by q-PCR, the activation of NF-κB by transactivation assay, and the activation status of p38 mitogen-activated protein (MAP) kinase, Jun N-terminal kinase (JNK) and p44/42 extracellular-signal-regulated kinase (ERK1/2) were assessed by Western analysis using antibodies recognizing the phosphorylated (activated) forms of each kinases. Results: MCP-1 release, in both SGBS cells and HUVEC increased significantly after stimulation with TNFα for 24 h (P<0.01). In SGBS cells, but not in HUVEC, ALE, RSG and FENO reduced TNFα-induced MCP-1 release in a concentration dependent manner, with a maximal inhibitory concentration, at 10 and 125 nmol/L for ALE and RSG respectively (P<0.01) and 50 μmol/L (P<0.01) for FENO. At the same concentrations ALE also reduced MCP-1 mRNA expression by 40% (P<0.05 versus TNFα). At 10 nmol/L ALE minimally inhibited TNFα-induced activation of NF-κB, but significantly reduced the activation of p38 MAP kinase and JNK. Conclusions: ALE, at concentrations as low as 10 nmol/L, which ensure the half-maximal activation of both PPARα and PPARΓ, selectively reduces the expression of MCP-1 in mature adipocytes. Such effect seems to be mediated, at least in part, by the interference with the activation of p38 MAP kinase. Overall, these data suggest that ALE may benefit diabetic and obese patients suppressing, in a highly cellular-selective fashion, the contribution of adipose tissue to systemic and perivascular inflammation.
Rapid estimation of plasma theophylline concentrations.
Authors: F M Cuss, J B Palmer, P J Barnes
Journal: BMJ (1985)

12 year old and 19% of 18 year old Finns.'These differences may be related to the socioeconomic climate in the two countries when the studies were undertaken.The Finnish study was undertaken in Febru- ary 1983, when the percentage of unemployment was 6% (abstracts from the Finnish Embassy's annual statistical year book, 1984 (unpublished)), whereas unemployment in the United Kingdom in March 1984 was 13% and within the city of Nottingham 12%.3War was the second most cited source of anxiety in adolescents from Nottingham (133 (25%) of 538 aged 11-12; 127 (21%) of 626 1 Solantaus T, Rimpela M, Taipale V.The threat of war in the minds of 12-18 year olds in Finland.
The George Fahr Lecture
Authors: G. E. BURCH, C. T. RAY, J. A. CRONVICH
Journal: Circulation (1952)

This is a general theoretic consideration of certain mechanical peculiarities of the human heart. It includes a discussion of mechanical advantages of the average size and average pressures, the effects of various pressures and ventricular volumes on ventricular work and "load," mechanical advantages of the structural arrangement of muscular fibers and manner of contraction, as well as the time course of ventricular work and power produced during a cardiac cycle. The role of the trabeculae carneae and papillary muscles in the emptying of a normal sized ventricle is also discussed.
Pulmonary embolism in a patient taking clozapine
Authors: Vinod H Srihari, T Warren Lee
Journal: BMJ (2008)

A 45 year old man with schizophrenia began experiencing auditory hallucinations at the age of 25. These were well controlled for several years by a monthly intramuscular injection of haloperidol decanoate. One year after he switched to oral haloperidol, the intensity of the hallucinations increased and included a voice commanding him to end his life. Concerns for his safety led to a brief admission to psychiatric hospital. When he had to return to hospital within a month, the inpatient psychiatrist inferred a loss of response to haloperidol and encouraged the patient to switch to clozapine. Six months later he was brought to an emergency department in an acute confusional state after a clozapine overdose. The drug was discontinued and his mental status improved rapidly, but investigation of acute dyspnoea showed bilateral pulmonary emboli. The patient was not overweight and had no history of recent surgery, trauma to the legs, or malignancy, but he was a heavy smoker. Laboratory tests for hypercoagulable states had negative results. He was treated with intravenous heparin and then oral warfarin and was transferred to a psychiatric unit for resumption of treatment with clozapine.

I (VHS) received a call from a physician in training who had admitted the patient to the psychiatric unit. She wondered about a possible association between clozapine and thromboembolism. I consulted with a colleague (TWL) who, like me, had not heard of this risk. The patient was expected to be in hospital for two more weeks, which gave us some time to consider alternative drugs.

The most pressing area of uncertainty was determining whether clozapine had anything to do with this patient’s pulmonary emboli and if so, whether alternative drugs posed less of a risk.1 We formulated a structured question: in a patient with schizophrenia who does not have any risk …
Making Sense of General Practice
Authors: P. Fitton
Journal: BMJ (1995)

Ed Norman Ellis, Radcliffe, pounds sterling13.50, pp 220, ISBN 1 85775 091 8

Making Sense of General Practice is one of a series. So behind the contributors is an editorial board for the book, and behind it are eight members of an editorial board for the series. Five sevenths of the editorial board for the book are on the editorial board for the series, as is one other contributor. One contributor is on neither. So how many contributors are there? Who is on everything?

A detailed …
Alcohol relapse after liver transplantation for alcoholic liver disease: does it matter?
Authors: Georges-Philippe Pageaux, Michael Bismuth, Pascal Perney, Valérie Costes, Samir Jaber, Pascal Possoz, Jean-Michel Fabre, Francis Navarro, Pierre Blanc, Jacques Domergue, Jean-Jacques Eledjam, Dominique Larrey
Journal: Journal of Hepatology (2003)
Continued Evolution of a System of Medical Care Appraisal
Authors: Beverly C. Payne
Journal: JAMA (1967)

The quality of personal medical care is compounded of two elements: that level of excellence produced and documented by a process of diagnosis and therapy, both preventive and curative, based on the best knowledge derived from science and the humanities; and that which eventuates in the least morbidity and mortality in a population.  Urging comes from Charles L. Hudson, MD, past President of the American Medical Association and John Porterfield, MD, director of the Joint Commission for Hospital Accreditation, and many thoughtful physicians in positions of leadership for evidence of the professional exercise of responsibility in critical appraisal of the quality of medical care. Others, including the President of the United States, express concern and suggest that rising costs of medical care can be arrested without sacrificing the quality of medical care.  Many thoughtful essayists and investigators, such as Avedis Donabedian, MD, 1 C. W. Eisele, MD, and Virgil Slee,
Plasma ghrelin following cure of Helicobacter pylori
Authors: C U Nwokolo
Journal: Gut (2003)

<b>Background:</b> In the Western world, the incidence of oesophageal adenocarcinoma has increased over the last 30 years coinciding with a decrease in the prevalence of <i>Helicobacter pylori</i>. Trends of increasing oesophageal adenocarcinoma can be linked causally to increasing gastro-oesophageal reflux disease (GORD) which can be linked to an increasingly obese population. However, there is no plausible biological mechanism of association between <i>H pylori</i>, obesity, and GORD. Ghrelin, a peptide produced in the stomach, which regulates appetite, food intake, and body composition, was studied in <i>H pylori</i> positive asymptomatic subjects. <b>Methods:</b> Plasma ghrelin, leptin, and gastrin were measured for six hours after an overnight fast, before and after cure of <i>H pylori</i> in 10 subjects. Twenty four hour intragastric acidity was also assessed. <b>Results:</b> After cure, median (95% confidence intervals) integrated plasma ghrelin increased from 1160.5 (765.5–1451) pg/ml×h to 1910.4 (1675.6–2395.6) pg/ml×h (p=0.002, Wilcoxon's rank sum test), a 75% increase. This was associated with a 14% increase in 24 hour intragastric acidity (p=0.006) and non-significant changes in leptin and gastrin. There was a significant positive correlation between plasma ghrelin and intragastric acidity (<i>r</i><sub>s</sub> 0.44, p=0.05, Spearman's rank correlation) <b>Conclusions:</b> After <i>H pylori</i> cure, plasma ghrelin increased profoundly in asymptomatic subjects. This could lead to increased appetite and weight gain, and contribute to the increasing obesity seen in Western populations where <i>H pylori</i> prevalence is low. This plausible biological mechanism links <i>H pylori</i>, through increasing obesity and GORD, to the increase in oesophageal adenocarcinoma observed in the West.