tbuckley/cabot-search huggingface dataset:
Sixth Floor Lounge, Oncology
Authors: Lee Passarella
Journal: JAMA (1993)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Anti–platelet factor 4/heparin antibodies in orthopedic surgery patients receiving antithrombotic prophylaxis with fondaparinux or enoxaparin
Authors: Theodore E. Warkentin, Richard J. Cook, Victor J. Marder, Jo-Ann I. Sheppard, Jane C. Moore, Bengt I. Eriksson, Andreas Greinacher, John G. Kelton
Journal: Blood (2005)
Handbook of Ambulatory Medicine: A Concise, Logical Approach
Authors: Harold I. Nachimson
Journal: JAMA (1984)

This easy-to-read, practical hand-book was thoroughly enjoyed by this reviewer. I often refer to it for up-to-date, precise information involving those patients who are in an ambulatory care setting. The handbook is, of course, in soft-cover, with approximately 125 pages and is written by contributors from the Rhode Island Hospital and the Brown University School of Medicine, Providence, RI. The book has 13 major topics that are broad-based with system and problem orientation (ie, metabolic and endocrine problems, hematologic, gastrointestinal tract, and psychosocial). The concise introduction emphasizes preventive medicine and recurrent examination. For example, there is information concerning world travelers, weight loss and nutritional problems, immunizations for adults, and preoperative examination for surgical candidates. These are covered in a brief but useful format. The most important contribution of this manual in the field of ambulatory medical care, particularly useful to physicians, is the large number of flow charts or algorithms
Role of nitric oxide and peroxynitrite in the cytokine-induced sustained myocardial dysfunction in dogs in vivo.
Authors: J i Oyama, H Shimokawa, H Momii, X Cheng, N Fukuyama, Y Arai, K Egashira, H Nakazawa, A Takeshita
Journal: Journal of Clinical Investigation (1998)

Studies in vitro suggested that inflammatory cytokines could cause myocardial dysfunction. However, the detailed mechanism for the cytokine-induced myocardial dysfunction in vivo remains to be examined. We thus examined this point in our new canine model in vivo, in which microspheres with and without IL-1beta were injected into the left main coronary artery. Left ventricular ejection fraction (LVEF) was evaluated by echocardiography for 1 wk. Immediately after the microsphere injection, LVEF decreased to approximately 30% in both groups. While LVEF rapidly normalized in 2 d in the control group, it was markedly impaired in the IL-1beta group even at day 7. Pretreatment with dexamethasone or with aminoguanidine, an inhibitor of inducible nitric oxide synthase, prevented the IL-1beta-induced myocardial dysfunction. Nitrotyrosine concentration, an in vivo marker of the peroxynitrite production by nitric oxide and superoxide anion, was significantly higher in the myocardium of the IL-1beta group than in that of the control group or the group cotreated with dexamethasone or aminoguanidine. There was an inverse linear relationship between myocardial nitrotyrosine concentrations and LVEF. These results indicate that IL-1beta induces sustained myocardial dysfunction in vivo and that nitric oxide produced by inducible nitric oxide synthase and the resultant formation of peroxynitrite are substantially involved in the pathogenesis of the cytokine-induced sustained myocardial dysfunction in vivo.
Abstract 4942: The role of one-carbon metabolism in global and promoter methylation of breast cancer in a population-based study
Authors: Xinran Xu, Marilie D. Gammon, Yujing Zhang, Yoo H. Cho, James G. Wetmur, Patrick T. Bradshaw, Susan L. Teitelbaum, Alfred I. Neugut, Regina M. Santella, Jia Chen
Journal: Cancer Research (2010)

Abstract Promoter-CpG island hypermethylation, accompanied by global DNA hypomethylation, are common molecular defects in cancer cells. One-carbon metabolism is involved in the DNA methylation process as it provides the universal methyl donor for methylation reactions. Thus, perturbation of one-carbon metabolism might influence DNA methylation status. Using the resource of the Long Island Breast Cancer Study Project, a population-based case-control study, we investigate the relationships of dietary and genetic factors involved in the one-carbon metabolism pathway with LINE-1 methylation level in blood cells as well as promoter methylation status of a panel of breast cancer genes in tumor tissue. LINE-1 methylation level was assessed by Pyrosequencing. Gene promoter methylation was examined by MS-PCR and MethyLight assays. Global methylation measured as LINE-1 methylation level from blood DNA was not associated with risk of developing breast cancer. Neither dietary intakes of methyl-related micronutrients nor genetic polymorphisms in one-carbon metabolism was associated with LINE-1 methylation level. LINE-1 methylation level was higher among cases with methylated APC (p=0.04). Promoter methylation of APC and p16 were correlated (p=0.0007). Higher betaine intake was associated with methylated APC promoter (p, trend=0.01). Cases with the 2R/2R genotype of TYMS are more likely to have a methylated ER promoter (p, trend=0.03). Our results indicate that one-carbon metabolism has a limited influence on DNA methylation. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4942.
Expression of cystic fibrosis transmembrane conductance regulator in liver tissue from patients with cystic fibrosis
Authors: Nils Kinnman, Anders Lindblad, Chantal Housset, Eva Buentke, Annika Scheynius, Birgitta Strandvik, Rolf Hultcrantz
Journal: Hepatology (2000)

The authors examined the expression of cystic fibrosis transmembrane conductance regulator (CFTR) and its relationship to histopathological changes in cystic fibrosis (CF) liver tissue. Immunohistochemistry was used to examine expression of CFTR, intercellular adhesion molecule-1 (ICAM-1) and liver cell-type markers in liver cryosections in 11 patients with CF-associated liver disease, and non-CF controls with (n = 17) and without (n = 3) liver disease. In CF patients prominent inflammatory infiltrates were not found, yet hepatic stellate cells were identified within fibrotic areas around bile ducts. Proliferating bile ducts displayed ICAM-1 immunoreactivity in 3 cases, but bile ducts were otherwise negative. In 2 patients homozygous for R764X and for 1112delT no CFTR immunoreactivity was detected. Bile-duct epithelial cells in patients carrying the DeltaF508 mutation displayed aberrant cytoplasmic immunolocalization of CFTR, as determined with confocal laser scanning microscopy, in contrast to the distinct CFTR expression at the luminal surface seen in controls. No clear relationship between CFTR expression and fibrosis or inflammation was evidenced in CF patients. In conclusion, these findings are consistent with an impairment of DeltaF508 CFTR processing in intrahepatic biliary epithelium. ICAM-1 expression on bile-duct epithelial cells and inflammatory infiltrates were rare findings in CF liver tissue, indicating that immunological mechanisms are unlikely to be involved in initiation of CF-associated liver disease.
Importance of Heterosexual Activity in the Transmission of Hepatitis B and Non-A, Non-B Hepatitis
Authors: Miriam J. Alter
Journal: JAMA (1989)

To identify previously unrecognized sources for acquiring acute hepatitis B and non-A, non-B (NANB) hepatitis, we interviewed patients with these types of hepatitis who were reported to two county health departments in the United States and matched control subjects for known and potential risk factors for acquiring hepatitis. Of 218 patients with hepatitis B and 140 patients with NANB hepatitis, 46% and 53%, respectively, had no commonly recognized source for infection. When these patients were compared with control subjects, significantly more patients with hepatitis B had multiple heterosexual partners, accounting for 14% of all hepatitis B infections; more patients with NANB hepatitis either had sexual or household contact with a person who had hepatitis in the past or had multiple heterosexual partners, accounting for 11% of all NANB infections. This is the first study to suggest that heterosexual transmission may play an important role in the spread of NANB hepatitis.
Increased Skeletal Uptake of Tc-99m Methylene Diphosphonate in Milk-Alkali Syndrome
Authors: S. B. CAMPBELL, D. J. MACFARLANE, S. J. FLEMING, F. A. KHAFAGI
Journal: Clinical Nuclear Medicine (1994)

A case of milk-alkali syndrome is described in a 34-year-old man taking an over-the-counter antacid preparation for gastroesophageal reflux. A Tc-99m MDP bone scan performed in the initial investigation of the hypercalcemia was markedly abnormal with a "metabolic" pattern of tracer uptake similar to that seen in hyperparathyroidism and humoral hypercalcemia. Following withdrawal of the antacid and calcium, the bone scan appearance returned to normal, as did the biochemical markers of his disease.
Routine measurement of fibrinogen concentration: Problems exaggerated
Authors: P. J Gaffney
Journal: BMJ (1993)

Data quoted by McGavock and colleagues are sometimes misleading.They quote relapse rates for peptic ulceration of 30% after bismuth chelate treatment.However, the references they quote indicated relapse rates of 61% and 47% in patients treated with bismuth chelate alone.45To obtain the quoted improved rates of relapse with, for example, bismuth chelate and tinidazole would incur additional net NHS costs of about C69 per patient for tinidazole.Such discrepancies in quoted data further weaken the conclusions of the paper.Consideration of crude prescribing figures without regard to morbidity data, secular trends, and emerging evidence of efficacy is an insecure foundation for the criticisms which the authors make of general practitioners in Northern Ireland and, by extension, the pharmaceutical industry.Neither general practitioners nor administrators should act on the conclusions drawn from such inadequate data.
An Address ON PULMONARY OEDEMA: Delivered before the Bexhill Medical Society
Authors: F. J. Wethered
Journal: BMJ (1906)

Pulmonary oedema is a subject which receives but scant notice in the textbooks and other volumes dealing with general medicine which crowd the bookshelves of our libraries and consulting rooms at the present day.It is, however, a condition constantly met with in clinical work, and, owing to the fact that under certain circumstances it may prove most serious in itself, and at other times resemble other grave maladies, the question of diagnosis is often a source of considerable anxiety and concern to the medical attendant.I need scarcely remind you that oedema of the lungs is not a primary disease, but is secondary to some pre- existing malady.Pulmonary oedema is, as you know, very commonly seen in the post-mortem room.It does not necessarily follow that it occurred during life, as it may have developed during the lethal agony.You may, perhaps, remember Cohnheim's remark: 'The patients do not die because of the oedema, but the oedema develops because the patient is dying.For clinical purposes pulmonary oedema may bd divided into three classes-acute, subacute, and chronic (or a better term would be " persistent ").ACUTE PULMONARY OEDEMA.I do not intend to consider at length the pathology or mechanism of this condition, but would merely remark that acute oedema of the lungs may be an outcome of most of the more severe forms of both acute and passive congestion of the lungs, those being also secondary pro- cesses.Authorities differ as to the exact manner of its production; many, however, favouring the view that owing to obstruction of the pulmonary circulation due to cardiac failure or other causes, there is some interference with the proper circulation through the lymph channels, and exudation accordingly ensues.Acute oedema of the lungs is especially prominent in death by asphycia brought about by pneumonia and acute
The Hyperkinetic Child and Stimulant Drugs
Authors: Leon Eisenberg
Journal: New England Journal of Medicine (1972)

The possibility that stimulant drugs used in the treatment of the hyperkinetic syndrome suppress growth adds another strident warning to a growing literature that emphasizes medical responsibility for meticulous long-term care and follow-up study of children with this disorder. The data presented by Safer and his co-workers in this issue of the Journal challenge conventional belief that tolerance to anorectic effects develops with relative rapidity. Clinicians have long been familiar with initial weight loss followed by resumption of weight gain, but few have reported measures of long-term effects. Dr. Kenneth Zike, of Harbor General Hospital, in an unpublished study generously . . .
Role of Actin Depolymerization in the Surfactant Secretory Response of Alveolar Epithelial Type II Cells
Authors: FRANK ROSE, CRISTOPHER KÜRTH-LANDWEHR, ULF SIBELIUS, KARL H. REUNER, KLAUS AKTORIES, WERNER SEEGER, FRIEDRICH GRIMMINGER
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

Alveolar epithelial type II cells (AET2) respond with exocytosis of surfactant containing lamellar bodies to stimulation with mechanical stretch and secretagogues, a process that is fundamental for maintaining alveolar stability and lung gas exchange. In the present study in cultured rat AET2, we employed botulinum C2 toxin, a binary toxin which ADP ribosylates nonmuscle G-actin, as a specific tool to probe the role of the actin microfilament system in the surfactant secretory process. Incubation of AET2 with C2 toxin caused a dose-dependent decay of the cellular F-actin content to a minimum of 20% of baseline, concomitant with an increase in monomeric actin. In parallel, a significant augmentation of baseline surfactant secretion up to twofold elevated levels above control was noted, as assessed by the release of prelabeled phosphatidylcholine. Pretreatment with phalloidin, which stabilized F-actin and reduced the level of G-actin, prevented the C2 toxin-elicited enhancement of baseline surfactant secretion. Even low C2 toxin concentrations, resulting in a reduction of total cellular F-actin content of ≈ 10%, sufficed to augment secretagogue (ATP) and, more impressively, mechanical stress elicited an increase in surfactant secretion; the response to the biophysical challenge more than doubled. When investigated in the absence of toxin, different secretagogues (ATP, phorbol ester, betamimetics) caused a rapid-onset, transient reduction of F-actin in the range between 15 and 25% as a consistent part of their secretory response pattern. These data suggest that the state of actin polymerization is intimately linked to the exocytosis process underlying surfactant secretion in AET2. Microfilament system-related compartmentalization effects and/or or the impact of the state of actin assembly on signaling events may be considered as underlying events.
Inhibition of Riboflavin Metabolism in Rat Tissues by Chlorpromazine, Imipramine, and Amitriptyline
Authors: John Pinto, Yee Ping Huang, Richard S. Rivlin
Journal: Journal of Clinical Investigation (1981)

Prompted by recognition of the similar structures of riboflavin (vitamin B(2)), phenothiazine drugs, and tricyclic antidepressants, our studies sought to determine effects of drugs of these two types upon the conversion of riboflavin into its active coenzyme derivative, flavin adenine dinucleotide (FAD) in rat tissues. Chlorpromazine, a phenothiazine derivative, and imipramine and amitriptyline, both tricyclic antidepressants, each inhibited the incorporation of [(14)C]riboflavin into [(14)C]FAD in liver, cerebrum, cerebellum, and heart. A variety of psychoactive drugs structurally unrelated to riboflavin were ineffective. Chlorpromazine, imipramine, and amitriptyline in vitro inhibited hepatic flavokinase, the first of two enzymes in the conversion of riboflavin to FAD. Evidence was obtained that chlorpromazine administration for a 3- or 7-wk period at doses comparable on a weight basis to those used clinically has significant effects upon riboflavin metabolism in the animal as a whole: (a) the activity coefficient of erythrocyte glutathione reductase, an FAD-containing enzyme used as an index of riboflavin status physiologically, was elevated, a finding compatible with a deficiency state, (b) the urinary excretion of riboflavin was more than twice that of age- and sex-matched pair-fed control rats, and (c) after administration of chlorpromazine for a 7-wk period, tissue levels of flavin mononucleotide and FAD were significantly lower than those of pair-fed littermates, despite consumption of a diet estimated to contain 30 times the recommended dietary allowance. The present study suggests that certain psychotropic drugs interfere with riboflavin metabolism at least in part by inhibiting the conversion of riboflavin to its coenzyme derivatives, and that as a consequence of such inhibition, the overall utilization of the vitamin is impaired.
Analysis of sporadic neuroendocrine tumours of the enteropancreatic system by comparative genomic hybridisation
Authors: H Tonnies
Journal: Gut (2001)

<h3>BACKGROUND</h3> Chromosomal instability is observed in a wide spectrum of human cancer syndromes. However, to date, little is known of the characteristic genetic changes in sporadic neuroendocrine tumours of the gastroenteropancreatic system. <h3>AIMS AND METHOD</h3> We have studied copy number aberrations (CNAs) in 26 sporadic neuroendocrine tumours of the enteropancreatic system (12 foregut and 14 midgut tumours) by comparative genomic hybridisation (CGH), allowing simultaneous evaluation of the entire tumour genome. <h3>RESULTS</h3> Nearly all tumours (25/26; that is, 96%) showed chromosomal imbalances, including full chromosomal aneuploidies, losses and gains of chromosome arms, interstitial deletions, and amplifications. Whereas gains of chromosomes 4, 5, and 19 were found in both foregut and midgut tumours, gains of chromosomes 20q (58%), 19 (50%), as well as 17p (50%), and partial losses of chromosomes 1p (42%), 2q (42%), 3p, 4q, and 6q (25% each) were frequently observed only in foregut tumours. In contrast, midgut tumours displayed less CNAs. Gains were detected for chromosomes 17q and 19p (57%). Most frequent losses affected chromosomes 18 (43%) and 9p (21%). <h3>CONCLUSIONS</h3> The results of our CGH analyses revealed new distinct candidate regions in the human genome associated with sporadic neuroendocrine tumours. Some of the genetic alterations were shared by foregut and midgut tumours while others discriminated between the two groups. Thus our results allude to the involvement of identical as well as discriminative genetic loci in tumorigenesis and progression of neuroendocrine neoplasms of the foregut and midgut. Based on these findings potential new candidate genes will be discussed.
Genetic and early environmental components in sociodemographic influences on adult body fatness.
Authors: T W Teasdale, T I Sorensen, A J Stunkard
Journal: BMJ (1990)

OBJECTIVE--To explore genetic and environmental contributions to the influence of parental social class and region of upbringing on adult human fatness. DESIGN--Survey of sample of adults who had been adopted in childhood to relate their body mass index to sociodemographic variables in a series of multiple linear regression analyses. SUBJECTS--4643 Subjects traced from a register of 5455 non-familial adoptees registered in 1924-47, of whom 3651 gave details of current height, weight, and occupation. The final sample totalled 2015 adoptees for whom there was also information on their region of upbringing and on the social class of their adoptive and biological fathers. MAIN OUTCOME MEASURES--Age, sex, body mass index, social class (of adoptee and adoptive and biological father), and geographical region. RESULTS--There was a significant inverse relation of adoptees9 body mass index with their own social class and that of both their biological and adoptive fathers. Adoptees raised in provincial areas had a significantly greater body mass index than did those raised in Copenhagen. A multivariate regression model, including age, sex, and social class of the adoptee, confirmed the significant independent influence of the social class of both adoptive and biological fathers and of region of rearing on adoptees9 body mass index. CONCLUSION--Both familial environmental and genetic factors contribute to the relation of parental social class to adult fatness, and they are partly independent of the effect of an individual9s own social class. The influence of region of upbringing on adult fatness is of environmental origin and is independent of social class characteristics.
933-99 Chronic Hydralazine or Enalapril Normalize Myosin Isoforms in the Spontaneously Hypertensive Rat, but Only Enalapril Normalizes Left Ventricular Mass
Authors: Garrie J. Haas, Margaret Ginn Pease, Melinda Hunnicutt, Mary E. Allon, A. John Merola, Robert J. Cody
Journal: Journal of the American College of Cardiology (1995)
702-1 Long-term (28-Year) Follow-up of Mustard Repair for Transposition of the Great Arteries with Intact Ventricular Septum: Freedom from Right Ventricular (Systemic) Heart Failure
Authors: Nigel J. Wilson, Patricia M. Clarkson, Brian G. Barratt-Boyes, A. Louise Calder, John M. Neutze
Journal: Journal of the American College of Cardiology (1995)
Granules live and let die
Authors: Hema Bashyam
Journal: The Journal of Experimental Medicine (2008)

Clotting linked to a memory makerA chemical that boosts our ability to learn and remember also boosts blood clotting, say Morrell et al. (page 575).The learning chemical, glutamate, is released at neuronal synapses, where it activates neurons by binding to ion channel receptors.Glutamate is also abundant in the blood-particularly in clot-forming platelets-but its function outside the brain was unknown.Morrell et al. now find that glutamate increases platelet activation and clumping.Glutamate treatment increased the expression of clot-inducing adhesion molecules on platelets that were activated with thrombin-a blood enzyme that becomes activated during infection or injury.The platelets carried glutamate receptors, which flood the cell with sodium ions when stimulated.Sodium triggers a structural change in thrombin receptors, which might enhance their affinity for thrombin.Mice lacking glutamate receptors and those treated with drugs that block them were slow to form clots.The authors speculate that, like neurons, activated platelets form synapses with neighboring platelets into which they spew glutamate.The high glutamate concentration within these spaces might keep the cells stuck together and further enlarge the clot by snaring more platelets, which then add to the glutamate pool.Drugs that block glutamate receptors might be potentially useful in preventing stroke, heart attacks, and other diseases that can be triggered by clots.