tbuckley/cabot-search huggingface dataset:
Homocysteine Inhibits Arterial Endothelial Cell Growth Through Transcriptional Downregulation of Fibroblast Growth Factor-2 Involving G Protein and DNA Methylation
Authors: Po-Yuan Chang, Shao-Chun Lu, Chii-Ming Lee, Yi-Jie Chen, Tracey A. Dugan, Wen-Huei Huang, Shwu-Fen Chang, Warren S.L. Liao, Chu-Huang Chen, Yuan-Teh Lee
Journal: Circulation Research (2008)

Homocysteine (Hcy) contributes to atherogenesis and angiostasis by altering the phenotype of arterial endothelial cells (ECs). The present study was aimed at elucidating potential mechanisms by which Hcy can slow EC proliferation and induce EC apoptosis, thereby disrupting endothelial integrity. Given the strong mitogenic and antiapoptotic properties of fibroblast growth factor (FGF)2, we examined whether Hcy can modulate its expression. In cultured human coronary and bovine aortic ECs, Hcy exerted time- and concentration-dependent (0 to 500 micromol/L) reduction of the mRNA and protein levels of FGF2, whereas vascular endothelial growth factor expression was not affected until Hcy reached a proapoptotic 500 micromol/L. By testing a panel of signal transduction inhibitors, we found that the Hcy-induced downregulation of FGF2 was specifically attenuated by pertussis toxin, an inhibitor of Gi protein signaling. Hcy induced cell cycle arrest at the G(1)/S transition and increased TUNEL-positive apoptotic cells in a graded manner. These effects were effectively counteracted by exogenous FGF2. Reporter gene assays showed that Hcy downregulated FGF2 by transcriptional repression of the gene promoter encompassed in a CpG dinucleotide-rich island. This region was heavily methylated at the cytosine residues by Hcy despite decreased methylation potential (S-adenosylmethionine to S-adenosylhomocysteine ratio). Normal levels of FGF2 transcription were restored to ECs simultaneously exposed to Hcy and 5-aza-deoxycytidine. We conclude that homocysteine disrupts the growth and survival of ECs through a G protein-mediated pathway associated with altered promoter DNA methylation and the transcriptional repression of FGF2.
Hypocalcemia-Induced Pustular Psoriasis of von Zumbusch
Authors: ANDREW F. STEWART
Journal: Annals of Internal Medicine (1984)

Hypocalcemia occurs in patients with psoriasis vulgaris, pustular psoriasis of von Zumbusch, and impetigo herpetiformis. In most cases hypocalcemia is caused by accompanying hypoalbuminemia, yet reductions in ionized serum calcium concentrations due to hypoparathyroidism or malabsorption have been reported. We report the case of a patient with surgical hypoparathyroidism in whom hypocalcemia precipitated typical pustular psoriasis of von Zumbusch. The psoriasis rapidly cleared on two occasions when the patient's serum calcium was corrected by therapy with oral calcium and vitamin D or its analogues, and reappeared when treatment was discontinued. The patient's psoriasis cleared on a third occasion when her serum calcium level returned to normal with a calcium infusion. Hypocalcemia can precipitate pustular psoriasis of von Zumbusch in susceptible persons. These psoriatic flares are due not to abnormal circulating levels of parathyroid hormone or vitamin D metabolites but to hypocalcemia.
SURGERY BY DIRECT VISION IN THE OPEN HEART DURING HYPOTHERMIA
Authors: Henry Swan
Journal: JAMA (1953)

The heart for centuries was suspected of being a delicate organ; the slightest injury was said to be uniformly fatal. Both the great Billroth and Sir Stephen Paget decreed the organ to lie outside the domain of possible surgery. Yet in reality the heart is a compact muscular organ that, by virtue of highly specialized intrinsic properties, functions continuously throughout the lifetime of the individual. It has an extraordinary capacity to adjust to the changing needs of body circulation. Its inner compulsion toward perpetual function is one of the most critical aspects of the life drive of individuals and species. Only when poisoned or deprived of its flow of nutrient requirements will this persistent organ lie still or lose itself in the quivering death of disorganized activity. A great ability to withstand trauma and to adjust to the stresses imposed by intrinsic disease emphasizes its essential vitality. Given half a
Costs of Positive Tests
Authors: H. B. Weinberg
Journal: JAMA (1971)

<h3>To the Editor.—</h3> In your editorial (<b>214</b>:2047,1970) you properly point out two deficiencies in Collen and coworkers' report on the dollar cost per positive test for automated multiphasic screening. Actually both had been noted by the authors. They admitted omitting some overhead costs, perhaps on the premise that the screening could have been as well done without these particular costs. They also described the second, which you state to be, the failure to take into account the cost per proved "true" positive test. For example, while the cost per positive mammogram was $408, follow-up studies in the positive cases brought the cost per "true" positive test to approximately $2,000. Casual reading of your statement would suggest that the reason the cost jumps five-fold is that the expense of the follow-up studies is that great. The original report clearly indicates, however, that the "true" cost was arrived at by a
SLE Myocarditis Detection By Ga-67 Citrate Scintigraphy
Authors: PAUL R. JOLLES, JAMES L. TATUM
Journal: Clinical Nuclear Medicine (1996)

Cardiac uptake of Ga-67 in myocarditis has been described in association with a number of disease entitles. However, there are no reports in the current literature describing Ga-67 uptake in myocarditis due to systemic lupus erythematosus, a disease that often involves the heart. The authors present the case of a patient with a long history of systemic lupus erythematosus in whom new ECG changes and left ventricular wall motion abnormality developed, and who demonstrated significant global myocardial uptake on Ga-67 scintigraphy. Other etiologies including myocardial infarction, epicardial coronary disease, pericarditis, endocarditis, dilated cardiomyopathy, and viral infection were excluded during extensive work-up.
Death to Dust: What Happens to Dead Bodies?
Authors: Irving Root
Journal: JAMA (1994)

Perhaps because of our natural aversion to thinking about our own mortality, this rather comprehensive, interestingly illustrated, and well-documented treatise on what happens to the human body after death may contain substantially more information that we ever wanted to know. On the other hand, for members of the Kreepy Krawler generation who might have expected a spinechilling thriller, a goose-bump—producing experience based on the title, this book will probably prove a disappointment. <i>Death to Dust</i>is well written, informative, and readable. To the physician faced with the pressure and necessity of obtaining organs or tissue for donation purposes and with dealing with the donor and the donor's loved ones, as well as to the potential recipient and the family, the chapter "Help for the Living: Organ, Tissue and Whole Body Donation" should prove an excellent resource for information and guidance. The desperate need for organ tissue and whole-body donation is
Outcomes of Percutaneous Coronary Interventions Performed at Centers Without and With Onsite Coronary Artery Bypass Graft Surgery
Authors: David E. Wennberg
Journal: JAMA (2004)

An ongoing debate focuses on whether institutions should perform percutaneous coronary interventions (PCIs) without an onsite coronary artery bypass graft (CABG) surgery program.To compare patient outcomes following PCI at US institutions performing this procedure without and with onsite cardiac surgery.Medicare hospital (part A) data were used to identify PCIs performed on fee-for-service Medicare enrollees (n = 625,854) aged at least 65 years at acute care facilities between January 1, 1999, and December 1, 2001. Hospitals without and with onsite cardiac surgery were identified based on the presence of claims for CABG surgery. Patients were characterized as undergoing primary/rescue PCI, defined as an emergency procedure performed on the same day of admission for an acute myocardial infarction (MI), vs all other PCIs.Post-PCI CABG surgery and combined in-hospital and 30-day mortality.A total of 178 hospitals performed PCIs without onsite cardiac surgery and 943 hospitals performed PCIs with onsite cardiac surgery. Patients undergoing PCIs in hospitals without onsite cardiac surgery were similar to those with onsite cardiac surgery with respect to age, sex, race, and measurable comorbidities; however, patients undergoing PCIs in hospitals without onsite cardiac surgery were more likely to have a primary/rescue PCI (22.0% vs 5.6%, P < .001). Patients undergoing PCIs in hospitals without cardiac surgery were more likely to die (6.0% vs 3.3%; adjusted odds ratio [OR], 1.29; 95% confidence interval [CI], 1.14-1.47; P < .001). After accounting for baseline differences, mortality for patients with primary/rescue PCI was similar in institutions without and with cardiac surgery (adjusted OR, 0.93; 95% CI, 0.80-1.08; P = .34). However, for the larger non-primary/rescue PCI population, mortality was higher in hospitals without onsite cardiac surgery (adjusted OR, 1.38; 95% CI, 1.14-1.67; P=.001). This increase in mortality was primarily confined to hospitals performing 50 or less Medicare PCIs per year.Percutaneous coronary interventions in hospitals without onsite cardiac surgery are often performed for reasons other than immediate treatment of an MI and are associated with a higher risk of adverse outcomes. Policies aimed at increasing access to primary/rescue PCI through promoting PCI in hospitals without cardiac surgery may inadvertently lead to an overall increase in mortality related to PCI.
8 EARLY PREDICTION OF SUSTAINED RESPONSE TO PEGINTERFERON ALFA-2A IN HBEAG-NEGATIVE PATIENTS: THE ROLE OF ON-TREATMENT HBSAG AND HBV DNA LEVELS
Authors: V. Rijckborst, B.E. Hansen, Y. Cakaloglu, P. Ferenci, F. Tabak, M. Akdogan, K. Simon, U.S. Akarca, R. Flisiak, E. Verhey, A.J. van Vuuren, C.A.B. Boucher, M.J. ter Borg, H.L.A. Janssen
Journal: Journal of Hepatology (2010)
Do readmission reduction targets punish quality care?
Authors: E. Davies
Journal: BMJ (2013)

“How do you use the relatively blunt instruments of quality measures and financial penalties over widely disparate settings to achieve desirable outcomes?” asks Douglas Kamerow in his column this week.

With the implementation of the Affordable Care Act now roughly halfway through its four year implementation, the impact is starting to be felt and, although many headlines are given over to the goal of universal insurance, it is in some of the detail that physicians are starting to feel its impact. …
European court overturns preimplantation testing ban
Authors: F. Turone
Journal: BMJ (2012)

The European Court of Human Rights has overturned Italy’s ban on preimplantation diagnosis of embryos for couples seeking to have a baby through in vitro fertilisation.

The case was brought by a couple who wanted to ensure that their second child was born without cystic fibrosis after their first was diagnosed with the disease. Italian law currently only allows for diagnosis during pregnancy. 

The ban on preimplantation genetic testing was part of a law on assisted reproduction, introduced in 2004, which ruled that assisted reproduction was only available to infertile heterosexual couples. The same law ruled that it …
Report of the International Workshop on Screening for Breast Cancer
Authors: Suzanne W. Fletcher, William Black, Russell Harris, Barbara K. Rimer, Sam Shapiro
Journal: JNCI Journal of the National Cancer Institute (1993)

Over the past 30 years, eight major randomized controlled trials of breast cancer screening--with mammography and/or clinical breast examination--have been conducted. Results from several trials have been updated during the past year, and initial results of three other trials have been reported.The National Cancer Institute held an International Workshop on Screening for Breast Cancer in February 1993 to conduct a thorough and objective critical review of the world's most recent clinical trial data on breast cancer screening, consider the new evidence, assess the current state of knowledge, and identify issues needing further research.Investigators representing the eight randomized controlled trials of breast cancer screening in women aged 40-74 presented published and unpublished data. Evidence relating to the effectiveness of breast cancer screening in different age groups, especially women aged 40-49, was presented.For women aged 40-49, randomized controlled trials consistently demonstrated no benefit from screening in the first 5-7 years after study entry. A meta-analysis of six trials found a relative risk of 1.08 (95% confidence interval = 0.85-1.39) after 7 years' follow-up. After 10-12 years of follow-up, none of four trials have found a statistically significant benefit in mortality; a combined analysis of Swedish studies showed a statistically insignificant 13% decrease in mortality at 12 years. Only one trial (Health Insurance Plan) has data beyond 12 years of follow-up, and results show a 25% decrease in mortality at 10-18 years. Statistical significance of this result is disputed, however. In women aged 50-69, all studies show mortality reductions; three of four studies show reductions of about 30% at 10-12 years after study entry. Results from two of these trials were statistically significant. Too few women over age 70 have been included in studies for adequate analysis.For women aged 40-49, randomized controlled trials of breast cancer screening show no benefit 5-7 years after entry. At 10-12 years, benefit is uncertain and, if present, marginal; thereafter, it is unknown. For women aged 50-69, screening reduces breast cancer mortality by about a third. Currently available data for women age 70 or older are inadequate to judge the effectiveness of screening.Randomized trials have provided stronger scientific evidence regarding the effectiveness of screening for breast cancer than for any other cancer. However, much still needs to be learned. Periodic gatherings of scientists in the field should speed the process.
IMPROVED CARBOLIC FUCHSIN STAIN FOR TUBERCLE BACILLUS.
Authors: R. O. LeBARON
Journal: JAMA (1907)

The staining solution is made by saturating methyl alcohol (97 per cent.) with fuchsin and adding 5 per cent. of carbolic acid. This fluid will stain the tubercle bacilli in sputum in four minutes without employing heat. As the stain is dissolved in methyl alcohol, preliminary fixation is really unnecessary, but I have found that, at least with some sputums, a smoother field is obtained by a light fixation in the flame. (The sputums were all incubated for from twelve to twenty-four hours.) The specimen is then covered with the stain, which is allowed to remain at least four, but not more that five, minutes, timed by the watch; washed thoroughly in water; decolorized (dilute nitric acid and 60 per cent. alcohol used separately), and counterstained as ordinarily. The counterstain should be rather light. The tubercle bacilli are stained deeply and the field is unusually clear.
Esophageal Lesions in Intestinal Behçet's Disease
Authors: K. Yashiro, K. Nagasako, K. Hasegawa, M. Maruyama, S. Suzuki, H. Obata
Journal: Endoscopy (1986)

Esophageal lesions are rarely seen in patients with intestinal Behçet's disease. Three patients with esophageal lesions (dissection of esophageal mucosa, esophageal ulcer, esophageal varices) were observed among 15 patients with intestinal Behçet's disease or non-specific simple ulcer (1974-1984). Two-thirds of these fifteen patients had fully developed or suspected Behçet's disease, and one-third had no symptoms typical of Behçet's disease. They are classified as non-specific simple ulcer. The average age of the 15 patients was 43 years, all patients but one were male. The recurrence rate after surgical treatment was 70%, that of medical treatment was 90%.
Diagnostic classification of the aetiology of mental retardation in children.
Authors: S J Newell, S H Green
Journal: BMJ (1987)

Children with mental retardation are often subjected to a routine battery of tests, a practice that has been criticised.1 Investigations often include a blood count, a biochemical profile, urinary screening for metabolites including amino acids, and radiography of the skull and wrist for bone age and may be more extensive. Such routine testing of all children with mental retardation is done in the hope of classifying cases in which there are no specific clinical clues to aetiology. Several series have been published, however, in which no unsuspected diagnoses were made in this way.M Our aim is to provide a basis of rational investigation planned individually for each patient. Smith and Simons have suggested primary categorisation according to the time of onset of evident mental retardation.4 This, however, leaves 41% of patients unclassified. Our method is based on clinical history and examination and takes the form of a diagnostic sieve.
Elevated fibrinogen fragment levels in uremic plasma inhibit platelet function and expression of glycoprotein IIb‐IIIa
Authors: Usha R. Thekkedath, Thanit Chirananthavat, John K. Leypoldt, Alfred K. Cheung, Syed F. Mohammad
Journal: American Journal of Hematology (2006)

Abstract Hemostatic dysfunction is frequently noted in uremia, but the mechanisms responsible for it are poorly understood and are assumed to be multifactorial. Preliminary findings from our laboratory suggest that elevated levels of circulating fibrinogen fragments (FF) might contribute to the hemostatic defect in uremic patients. Defibrinated plasma obtained from chronic hemodialysis (HD) patients as well as normal subjects were examined by SDS‐PAGE and immunoblotting and quantified by an immunoassay. In addition, endogenous FF isolated from normal and uremic plasma using affinity chromatography were examined by flow cytometry for their effect on glycoprotein (GP) IIb‐IIIa receptor expression and tested for their ability to inhibit platelet aggregation. The mean FF concentration in uremic plasma (1.14 ± 0.85 mg/ml) was noted to be eight times greater than in normal plasma (0.15 ± 0.01 mg/ml) ( P &lt; 0.05). Moreover, the mean FF level decreased by 48.25% following HD (from 1.14 ± 0.85 mg/ml to 0.59 ± 0.33 mg/ml; P &lt; 0.05). SDS‐PAGE and immunoblotting experiments showed that the decrease was observed in both medium‐sized (20–60 kDa) as well as large (&gt;100 kDa) FF. Further, FF isolated from uremic plasma inhibited platelet aggregation by (46.8 ± 18.1)% ( P &lt; 0.05) and the GP IIb‐IIIa receptor expression by (28.0 ± 7.6)% ( P &lt; 0.05 vs. control). The results show that (1) FF levels are elevated in uremic plasma, (2) HD results in significant decrease in FF and (3) endogenous FF inhibit platelet function, presumably via competitive binding to the fibrinogen receptor GP IIb‐IIIa. The decrease in plasma levels of FF &gt; 100 kDa following HD suggests that adsorption to the dialysis membrane contributes to their removal. Am. J. Hematol., 2006. © 2006 Wiley‐Liss, Inc.
Influences of protein films on antibacterial or bacteria-repellent surface coatings in a model system using silicon wafers
Authors: Rainer Müller, Andreas Eidt, Karl-Anton Hiller, Verena Katzur, Michael Subat, Helmut Schweikl, Satoshi Imazato, Stefan Ruhl, Gottfried Schmalz
Journal: Biomaterials (2009)
901-107 Fetal Model of Single Ventricle Physiology: Hemodynamic Effects of Epinephrine, Sodium Bicarbonate, and Calcium Chloride
Authors: V. Mohan Reddy, John R. Liddicoat, Jeffrey R. Fineman, Roger Chang, Judith R. Klein, Frank L. Hanley
Journal: Journal of the American College of Cardiology (1995)
THE ASTHMA RESEARCH COUNCIL : AN APPEAL FOR FINANCIAL SUPPORT.
Authors: ArthurF. Hurst, R.J.S. Mcdowall, H.W. Barber, L.S.T. Burrell, E.C. Dodds, J. Freeman, R.D. Gillespie, V.E. Negus, S. Gilbert Scott, T.T. Jeans
Journal: The Lancet (1928)
A granulocyte-macrophage colony–stimulating factor and interleukin-15 fusokine induces a regulatory B cell population with immune suppressive properties
Authors: Moutih Rafei, Jeremy Hsieh, Simone Zehntner, MengYang Li, Kathy Forner, Elena Birman, Marie-Noëlle Boivin, Yoon Kow Young, Claude Perreault, Jacques Galipeau
Journal: Nature Medicine (2009)
Restriction Isotyping of Apolipoprotein E
Authors: Salvatore Benvenga
Journal: Annals of Internal Medicine (1995)

Letters1 January 1995Restriction Isotyping of Apolipoprotein ESalvatore Benvenga, MDSalvatore Benvenga, MDNational Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-122-1-199501010-00014 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:I read with interest the review by Walden and Hegele [1]. The authors state that “apolipoprotein (apo) E is divided into two independently folded domains with different functions.” The boundary between these two domains is the random-coil region spanning amino acids 165 to 201, which is subject to enzymatic cleavage [2]. Thus, the region encompassing approximately the first 160 to 210 amino acids contains the apo B-E receptor-binding domain (which is located approximately between amino acids 130 and 160), whereas the C-terminal region mediates the binding to lipids.Evidence now suggests that apolipoproteins do specifically bind thyroid ...References1. Walden CC, Hegele RA. Apolipoprotein E in hyperlipidemia. Ann Intern Med. 1994; 120:1026-36. Google Scholar2. Wetterau JR, Aggerbeck LP, Rall SC Jr, Weisgraber KH. Human apolipoprotein E3 in aqueous solution. I. Evidence for two structural domains. J Biol Chem. 1988; 263:6240-8. Google Scholar3. Benvenga S, Cahnmann HJ, Robbins J. Characterization of thyroid hormone binding to apolipoprotein E: localization of the binding site in the exon 3-coded domain. Endocrinology. 1993; 133:1300-5. Google Scholar4. Benvenga S, Robbins J. Lipoprotein-thyroid hormone interactions. Trends Endocrinol Metab. 1993; 4:194-8. Google Scholar5. Benvenga S, Cahnmann HJ, Rader D, Kindt M, Facchiano A, Robbins J. Thyroid hormone binding to isolated human apolipoproteins A-II, C-I, C-II and C-III: homology in thyroxine binding sites. Thyroid. 1994; 4:261-7. Google Scholar Author, Article, and Disclosure InformationAffiliations: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byApolipoprotein E is a genetic risk factor for fetal iodine deficiency disorder in ChinaA Thyroid Hormone Binding Motif Is Evolutionarily Conserved in ApolipoproteinsBibliography NIA/AlzA Conference on Apolipoprotein E Genotyping in Alzheimer's Disease 1 January 1995Volume 122, Issue 1Page: 68-69KeywordsAmino acidsApolipoproteinsGlobulinsHigh density lipoproteinHormonesLipidsMutationPlasma proteinsThyroidThyroid hormones Issue Published: 1 January 1995 Copyright & PermissionsCopyright © 1995 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...