tbuckley/cabot-search huggingface dataset:
Systemic and transcardiac platelet activity in acute myocardial infarction in man: resistance to prostacyclin.
Authors: H S Mueller, P S Rao, M A Greenberg, P M Buttrick, I I Sussman, H A Levite, R M Grose, V Perez-Davila, J E Strain, T H Spaet
Journal: Circulation (1985)

There is increasing evidence that platelets play an important role in the pathogenesis of acute ischemic heart disease. Therefore an understanding of factors that influence platelet performance is important. This study was undertaken (1) to characterize during evolving myocardial infarction platelet activity in the peripheral circulation and across the ischemic/infarcting myocardial compartment, the locus of presumed platelet hyperactivity, and (2) to evaluate the effects of prostacyclin (PGI2), a most potent antiplatelet agent and vasodilator. A total of 59 patients with evolving myocardial infarction were studied. Twenty-two patients were instrumented with arterial and coronary sinus catheters and received intravenous infusion of PGI2, 13 +/- 4.5 ng/kg/min (mean +/- SD), for 90 min. In 15 patients with anterior myocardial infarction, transcardiac platelet function and response to PGI2 were studied. Plasma levels of beta-thromboglobulin (beta-TG) and of thromboxane B2 (TxB2), in vivo measures of platelet activity, were elevated three- and 10-fold. 6-Keto-prostaglandin F 1 alpha, the stable end product of PGI2, was less than 10 pg/ml, reflecting a leftward shift of the TxB2/PGI2 ratio. Platelets circulating during evolving myocardial infarction ("ischemic platelets") were hyperaggregable in response to ADP and relatively resistant to PGI2, both in vivo and in vitro. Concentrations of platelet cyclic AMP and the cyclic AMP response to PGI2 were diminished. The platelet hyperreactivity, expressed by plasma beta-TG, platelet aggregation, and PGI2-induced inhibition of aggregation, was most intense early during infarct evolution and decreased with time. The increased platelet performance resulted in "platelet fatigue," indicated by decreased contents of beta-TG of the ischemic platelet and decreased TxA2 production in response to collagen. However, the ischemic platelet produced twice normal TxA2 in response to arachidonic acid (stimulus and substrate), demonstrating a heightened metabolic capacity. TxA2 was produced across the ischemic/infarcting compartment in 10 of 15 patients with anterior myocardial infarction. The antiplatelet effect of PGI2 was greatly diminished. In summary, the data define an abnormal pattern of platelet behavior during evolving myocardial infarction, characterized by a proaggregatory environment, heightened platelet reactivity in both the peripheral and coronary circulation, and relative resistance to PGI2. The clinical consequences of the data are that the patient in the acute phase of myocardial infarction may benefit from suppression of platelet function and requires significantly greater doses of PGI2 than normal subjects.(ABSTRACT TRUNCATED AT 400 WORDS)
Human rights group accuses US psychiatrists of unethical treatment of prisoners
Authors: J. Lenzer
Journal: BMJ (2011)

US psychiatrists are not fulfilling their duty to protect military prisoners from torture, concludes a doctors’ human rights organisation.

Physicians for Human Rights, which is based in Cambridge, Massachusetts, says that military psychiatrists are complicit in torture in the case of the imprisoned soldier Bradley Manning. Private Manning, a suspected source of numerous WikiLeaks documents revealing US disasters in Afghanistan, including the helicopter killing of civilians in Baghdad, has been held for nine months in solitary confinement in a 2 m by 4 m cell in Quantico, Virginia. Private Manning has not been tried or convicted of any crimes.

His lawyer and his father say that he has been subjected to humiliation and sleep deprivation. Because he has been placed on a “prevention of injury” watch, …
The Physiological Basis of Diuretic Therapy
Authors: Paul S. Rhoads
Journal: JAMA (1960)

Here is a book that should be of great use to those who read it carefully. The wondrous manner in which body water goes in and out of the vascular bed and is conserved and eliminated by the kidneys is still imperfectly understood. However, those things which are known or strongly suspected are set forth in terms which even the less sophisticated reader should understand. The many gaps in our knowledge are pointed out with equal clarity. If modern views of the astonishing properties of renal tubular epithelial cells are correct, they must be among the most versatile cells possessed by man. The complex activity going on in the kidney, however, is no more exciting than that occurring simultaneously in the lungs—"In the second or so required for an erythrocyte to traverse a pulmonary capillary, bicarbonate ion must diffuse into the erythrocyte in exchange for chloride ion and associate with
THE HISTOCHEMICAL LOCALIZATION OF PHOSPHORYLASES IN SKIN*
Authors: G. C. WELLS, K. V. SANDERSON, IRENA M. McCabe
Journal: British Journal of Dermatology (1961)

Journal Article THE HISTOCHEMICAL LOCALIZATION OF PHOSPHORYLASES IN SKIN Get access G. C. WELLS, G. C. WELLS Roussel Research Fellow, Institute of Dermatology Search for other works by this author on: Oxford Academic Google Scholar K. V. SANDERSON, K. V. SANDERSON Roussel Research Fellow, Institute of Dermatology Search for other works by this author on: Oxford Academic Google Scholar IRENA M. McCabe IRENA M. McCabe Research Assistant, Institute of Dermatology, St. John's Hospital for Diseases of the Skin, Lisle Street, London, W.C.2 Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 73, Issue 8-9, 1 August 1961, Pages 337–344, https://doi.org/10.1111/j.1365-2133.1961.tb14458.x Published: 01 August 1961
The beta2 subunit inhibits stimulation of the alpha1/beta1 form of soluble guanylyl cyclase by nitric oxide. Potential relevance to regulation of blood pressure.
Authors: G Gupta, M Azam, L Yang, R S Danziger
Journal: Journal of Clinical Investigation (1997)

Cytosolic guanylyl cyclases (GTP pyrophosphate-lyase [cyclizing; EC 4.6.1.2]), primary receptors for nitric oxide (NO) generated by NO synthases, are obligate heterodimers consisting of an alpha and a beta subunit. The alpha1/beta1 form of guanylyl cyclase has the greatest activity and is considered the universal form. An isomer of the beta1 subunit, i.e., beta2, has been detected in the liver and kidney, however, its role is not known. In this study, we investigated the function of beta2. Immunoprecipitation experiments showed that the beta2 subunit forms a heterodimer with the alpha1 subunit. NO-stimulated cGMP formation in COS 7 cells cotransfected with the alpha1 and beta2 subunits was approximately 1/3 of that when alpha1 and beta1 subunits were cotransfected. The beta2 subunit inhibited NO-stimulated activity of the alpha1/beta1 form of guanylyl cyclase and NO-stimulated cGMP formation in cultured smooth muscle cells. Our results provide the first evidence that the beta2 subunit can regulate NO sensitivity of the alpha1/beta1 form of guanylyl cyclase. Northern analysis for guanylyl cyclase subunits was performed on RNA from kidneys of Dahl salt-sensitive rats, which have been shown to have decreased renal sensitivity to NO. Compared to the Dahl salt-resistant rat, message for beta2 was increased, beta1 was decreased, and alpha1 was unchanged. These results suggest a molecular basis for decreased renal guanylyl cyclase activity, i.e. , an increase in the alpha1/beta2 heterodimer, and decrease in the alpha1/beta1 heterodimer.
Clinical study of uses of a small-volume twin-coil artificial kidney (Chron-a-coil) in acute renal failure.
Authors: C. T. Flynn, C. H. Bowden
Journal: BMJ (1966)

This paper describes our experiences in acute renal failure with the Chron-a-coil, a smaller version of the Kolff twin-coil artificial kidney.The Kolff twin-coil has been the most widely used artificial kidney in the treatment of acute renal failure (Merrill, 1963).The first report in this country was given by Jackson et al. ( 1960) from this unit.The twin-coil is supplied ready for use and is disposable; so that technical aspects are reduced to a minimum.It is capable of removing fluid by
Mouse Coronary Angiograph Using Synchrotron Radiation Microangiography
Authors: Tomoya Yamashita, Seinosuke Kawashima, Masanori Ozaki, Masayuki Namiki, Tetsuaki Hirase, Nobutaka Inoue, Ken-ichi Hirata, Keiji Umetani, Kazuro Sugimura, Mitsuhiro Yokoyama
Journal: Circulation (2002)
High spending intensive care doctors do not always achieve better outcomes
Authors: Claire Frauenfelder
Journal: BMJ (2006)

Wide variation in spending on intensive care patients resulting from doctors' different treatment styles does not affect patients' length of stay in the unit or mortality, a new study from one US hospital says. 

The report said that doctors' adoption of a more uniform approach would not harm patients and could save resources ( American Journal of Respiratory and Critical Care …
Homozygous Protein C Deficiency Manifested by Massive Venous Thrombosis in the Newborn
Authors: Uri Seligsohn, Anna Berger, Martha Abend, Lisa Rubin, Dina Attias, Ariela Zivelin, Samuel I. Rapaport
Journal: New England Journal of Medicine (1984)

We studied a family in which two infants had died with massive venous thrombosis shortly after birth. Protein C antigen was undetectable by immunologic assays of plasma available from one infant. (Protein C is a potent naturally occurring anticoagulant that inactivates activated coagulation factors V and VIII). The parents, who were first cousins, both had partial protein C deficiency. Reduced protein C levels were also observed in 12 of 25 additional family members. None of the partially deficient family members (age range 4 to 70 years) had thrombotic episodes. Our data support the view that hereditary protein C deficiency is an autosomal disorder in which the homozygous state may be manifested by the virtual absence of plasma protein C and by fatal thrombosis in the neonatal period.
Long-Term Effects of Change in Body Weight on All-Cause Mortality: A Review
Authors: R Andres, D C Muller, J D Sorkin
Journal: Annals of Internal Medicine (1993)

Objective: To summarize published studies analyzing the effects of long-term change in body weight on all-cause mortality and have not been reported elsewhere in these proceedings. Data Sources: Thirteen reports from 11 diverse population studies, 7 from the United States and 4 from Europe. Study Selection: All studies included a weight change period of 4 or more years, followed by a mortality assessment period of 8 or more years. All weight changes occurred in persons 17 years or older. Data Extraction: Data from individual studies are presented as number of participants, number of deaths, ages at initial and final weight measurements, duration of the mortality follow-up period, consideration of cigarette smoking and other potential confounders, exclusion criteria, temporal separation between the weight change and mortality follow-up periods, and the association between weight change and all-cause mortality. Data Synthesis: Results are summarized by weight change associated with the lowest mortality rate and by the effects of long-term weight loss on mortality rate. Conclusions: Despite the diversity of the populations studied, the degree of clinical clean-up at entry, the techniques used to assess weight change, and the differences in analytic techniques (including consideration of potentially confounding variables), certain conclusions may be drawn. Evidence suggests that the highest mortality rates occur in adults who either have lost weight or have gained excessive weight. The lowest mortality rates are generally associated with modest weight gains.
Erratum: Corrigendum: G12-G13–LARG–mediated signaling in vascular smooth muscle is required for salt-induced hypertension
Authors: Angela Wirth, Zoltán Benyó, Martina Lukasova, Barbara Leutgeb, Nina Wettschureck, Stefan Gorbey, Petra Örsy, Béla Horváth, Christiane Maser-Gluth, Erich Greiner, Björn Lemmer, Günther Schütz, Silvio Gutkind, Stefan Offermanns
Journal: Nature Medicine (2008)
BLOOD PRESSURE LEVELS MODULATE MORTALITY IN PATIENTS WITH ATRIAL FIBRILLATION AND HEART FAILURE WITH DEPRESSED BUT NOT IN PATIENTS WITH PRESERVED EJECTION FRACTION
Authors: Michel White, Maxime Tremblay-Gravel, Paul Khairy, Denis Roy, Hugues Leduc, D. George Wyse, Ali Ahmed, Julia Cadrin-Tourigny, Laurent Macle, Marc Dubuc, Jason Andrade, Lena Rivard, Peter G. Guerra, Bernard Thibault, Mario Talajic
Journal: Journal of the American College of Cardiology (2013)
Israeli soldiers shoot 23 Palestinian children in 2010, report says
Authors: T. Traubmann
Journal: BMJ (2011)

In the past year 23 boys were shot near the Israel-Gaza Strip border fence, according to a report published by the Palestine section of the human rights organisation, Defense for Children International on 29 December 2010.

The report lists 23 shooting incidents of 13-17 year olds between 26 March and 23 December 2010. Most of the boys were shot while collecting construction material to help their families.

Driven by poverty and unemployment rates of over 50%, hundreds of Gaza Strip residents, including numerous young people, go to the …
A STUDY OF DIAPHRAGMATIC MOVEMENTS IN ACUTE ABDOMINAL INFLAMMATION
Authors: LLEWELLYN SALE
Journal: JAMA (1918)

Limitation of diaphragm movement in the presence of certain intra-abdominal lesions is well known. About twenty years ago Czerny<sup>1</sup>cited postoperative limitation, with its resulting pulmonary congestion, as one of the causes of postoperative pneumonia. The diagnostic importance of the position of the diaphragm and of its motility in differentiating between supraphrenic and subphrenic disease is often referred to in the literature.<sup>2</sup>The lesions to which this effect on the diaphragm is attributed are those that involve contiguous organs. Thus, Hubeny<sup>3</sup>cites gastric ulcer located at the esophageal opening. Hughes<sup>4</sup>says: The diaphragm, if its peritoneal surface be inflamed or irritated from any cause whatever, e. g., a perforating gastric ulcer, will be thrown out of action in the same way as the abdominal muscles. If only one half is affected, that half will not move so freely as normally, and it is probably on this
BMJ's impact factor increases by 24%
Authors: A. Horgan
Journal: BMJ (2002)

The BMJ 's impact factor, a measure of the average number of citations to a journal's articles, increased by almost a quarter between 2000 and 2001, from 5.331 to 6.629. Three other big general medical titles also increased their impact factor over the same period: the Lancet from 10.232 to 13.251 (a rise of 30%), JAMA from 15.402 …
ATRIAL FIBRILLATION AS AN INDEPENDENT PREDICTOR OF HEART FAILURE READMISSIONS: ANALYSIS OF “GET-WITH-THE-GUIDELINES” HEART FAILURE
Authors: Nayan K. Desai, Maryann Powell, Jad Skaf, Krystal Hunter, John Andriulli, Matthew Ortman, Lawrence Gessman, Andrea Russo
Journal: Journal of the American College of Cardiology (2014)
Expression of basic fibroblast growth factor in intact and ulcerated human gastric mucosa
Authors: M A Hull, J L Brough, D G Powe, G I Carter, D Jenkins, C J Hawkey
Journal: Gut (1998)

Background —Basic fibroblast growth factor (bFGF) promotes angiogenesis and healing of gastric ulcers in rats, and bFGF expression is up regulated in such ulcers. However, little is known about expression of bFGF in human gastric mucosa. Aims —To investigate bFGF expression in intact human gastric mucosa and gastric ulcers and to determine whether low bFGF content or altered binding by mucosa is associated with ulceration. Subjects —Endoscopy outpatients, gastrectomy patients, and organ donors. Methods —bFGF was isolated by heparin affinity chromatography and characterised by western blotting and endothelial cell bioassay. bFGF was measured by immunoassay and its distribution defined by immunohistochemistry and in situ hybridisation. Binding of bFGF by heparan sulphate proteoglycans was investigated by sodium chloride and heparin extraction. Results —Bioactive bFGF (19 kDa) was detected in normal mucosa but bFGF mRNA was not found. bFGF expression was up regulated in granulation tissue endothelial cells, mononuclear cells, and epithelial cells at the ulcer rim. Gastric ulcer patients had constitutively low bFGF concentrations in intact antral mucosa which were not explained by changes in binding to heparan sulphate proteoglycans. Conclusions —bFGF expression is up regulated in human gastric ulcers. Low intact mucosal bFGF content is associated with gastric ulceration.
Abstract 1868: Evaluation of the nucleotide excision repair polymorphisms for association with lung cancer risk
Authors: Shama C. Buch, Tomoko Nukui, Joel Weissfeld, Marjorie Romkes
Journal: Cancer Research (2010)

Abstract There is increasing evidence that decreased nucleotide excision repair (NER) capacity may be associated with increased risk of cancer, including non-small cell lung cancer (NSCLC). We have studied the relationship of the NER pathway gene single nucleotide polymorphisms and haplotypes with NSCLC risk. Using a custom-designed Illumina GoldenGate assay 384 single nucleotide polymorphism (SNP) panel, we have screened for polymorphisms in nucleotide excision repair genes, cell cycle control genes, GSTP1 and ABCB1 and a set of ancestry informative markers in 797 Caucasian incident cases and 992 controls frequency matched for age (range 50-79) and gender. All subjects were ever smokers with a minimum 10 packyear smoking history. Our SNP selection strategy incorporates six SNP classes, i.e. haplotype tagSNPs defined by predicted LD scores; functional SNPs characterized by amino acid substitutions, SNPs that alter protein stability; evolutionary conservation across species; entromics and published epidemiological data. For the estimation of individual SNP and haplotype-specific associations with risk, unconditional logistic regression was used to estimate odds ratios and 95% confidence intervals in a dominant model adjusting for age, gender and packyear. A total of 26 unique SNPs in 14 genes were significantly associated with lung cancer risk. Haplotypes were reconstructed for each gene using HPlus and associations with risk were evaluated using the Cox proportional hazards model. The most frequent haplotype was used as the referent group for the estimation of hazard ratios (HR). Hazard ratios were calculated for common haplotypes i.e. those that were present at a frequency greater than 2% and were adjusted for age, gender and packyears. Among these 14 genes, 7 haplotypes were significant. These data suggest that NER pathway genotypes may serve to define an elevated risk subgroup. Supported in part by NIH 5P50 CA090440. 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 1868.
Analgesics, Hemolysis, and Splenomegaly
Authors: ANTHONY V. PISCIOTTA
Journal: Annals of Internal Medicine (1971)

Editorial Notes1 April 1971Analgesics, Hemolysis, and SplenomegalyANTHONY V. PISCIOTTA, M.D., F.A.C.P.ANTHONY V. PISCIOTTA, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-74-4-634 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptModern chemistry has not been entirely kind to man. With accumulating experience, it becomes more and more evident that some of our most widely used and apparently innocuous drugs have toxic properties. Even the analgesics aspirin and phenacetin, found in everyone's medicine cabinet, have been implicated in producing serious disease states.The most frequently implicated component of analgesic mixtures has been phenacetin. Its most obvious toxic effect, and therefore the first to be discovered, is cyanosis, which may follow ingestion of over 1 g of phenacetin daily for months. The cyanosis is a consequence of the accumulation of nonfunctioning sulf-hemoglobin...References1. GAULT M, RUDWAL T, and ENGLES W: Syndrome associated with the abuse of analgesics. Ann Intern Med 68:906-925, 1968 LinkGoogle Scholar2. MACGIBBON B, LOUGHRIDGE L, and HOURIHANE D: Autoimmune haemolytic anaemia with acute renal failure due to phenacetin and p-aminosalicylic acid. Lancet 2:7-10, 1960 CrossrefGoogle Scholar3. LORENZED I and SCHWARTZ M: Phenacetin-induced haemolysis in patients with chronic nephritis and phenacetin abuse. Acta Med Scand 168:461-466, 1970 CrossrefGoogle Scholar4. FORDHAM C and HUFFINES W: Splenomegaly, analgesic ingestion and renal disease. New Eng J Med 14:749-751, 1967 CrossrefGoogle Scholar5. SCHNITZER B and SMITH E: Observations of phagocytized red cells containing Heinz bodies. A light and electron microscopic study. Amer J Clin Path 46:538-545, 1966 CrossrefMedlineGoogle Scholar6. DUGGAN J: Splenomegaly in analgesic takers. Med J Aust Sept. 26, 580-583, 1970 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: ANTHONY V. PISCIOTTA, M.D., F.A.C.P.Affiliations: Milwaukee County General Hospital Milwaukee, Wis. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 April 1971Volume 74, Issue 4 Page: 634-635 Keywords Analgesics Aspirin Drugs Ingestion Splenomegaly ePublished: 1 December 2008 Issue Published: 1 April 1971 PDF downloadLoading ...
Enalapril in the treatment of hypertension with renal artery stenosis.
Authors: G P Hodsman, J J Brown, A M Cumming, D L Davies, B W East, A F Lever, J J Morton, G D Murray, I Robertson, J I Robertson
Journal: BMJ (1983)

The converting enzyme inhibitor enalapril, in single daily doses of 10-40 mg, was given to 20 hypertensive patients with renal artery stenosis. The blood pressure fall six hours after the first dose of enalapril was significantly related to the pretreatment plasma concentrations of active renin and angiotensin II and to the concurrent fall in angiotensin II. Blood pressure fell further with continued treatment; the long term fall was not significantly related to pretreatment plasma renin or angiotensin II concentrations. At three months, 24 hours after the last dose of enalapril, blood pressure, plasma angiotensin II, and converting enzyme activity remained low and active renin and angiotensin I high; six hours after dosing, angiotensin II had, however, fallen further. The rise in active renin during long term treatment was proportionally greater than the rise in angiotensin I; this probably reflects the fall in renin substrate that occurs with converting enzyme inhibition. Enalapril alone caused reduction in exchangeable sodium, with distinct increases in serum potassium, creatinine, and urea. Enalapril was well tolerated and controlled hypertension effectively long term; only two of the 20 patients required concomitant diuretic treatment.