tbuckley/cabot-search huggingface dataset:
Recurrence of Venous Thromboembolism after Unfractionated Heparin Therapy
Authors: Nic Kormas
Journal: Annals of Internal Medicine (1996)

Letters15 December 1996Recurrence of Venous Thromboembolism after Unfractionated Heparin TherapyNic Kormas, MD and Arumugam Manoharan, MDNic Kormas, MDSt. George Hospital, Kogarah, Sydney, Australia.Search for more papers by this author and Arumugam Manoharan, MDSt. George Hospital, Kogarah, Sydney, Australia.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-125-12-199612150-00028 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:The letters by Sutton [1] and Banga and colleagues [2] highlight the controversy surrounding the initiation of anticoagulant therapy in patients with thromboembolism. Although some trials have compared early with late initiation of warfarin therapy [3], we could not find any information on whether cessation of heparin therapy causes a significant decrease in the international normalized ratio (INR).During a 2-week period, all patients in a large teaching hospital who were receiving both intravenous heparin and warfarin were recruited for a prospective study. These patients were reviewed daily until 2 days after cessation of heparin therapy. We ...References1. Sutton SK. Recurrence of venous thromboembolism after treatment with unfractionated heparin [Letter]. Ann Intern Med. 1996; 124:532. Google Scholar2. Banga JD, de Valk HW, Nieuwenhuis HK. Recurrence of venous thromboembolism after treatment with unfractionated heparin [Letter]. Ann Intern Med. 1996; 124:532. Google Scholar3. Mohiuddin SM, Hilleman DE, Destache CJ, Stoysich AM, Gannon JM, Sketch MH. Efficacy and safety of early versus late initiation of warfarin during heparin therapy in acute thromboembolism. Am Heart J. 1992; 123:729-32. Google Scholar Author, Article, and Disclosure InformationAuthors: Nic Kormas, MD; Arumugam Manoharan, MDAffiliations: St. George Hospital, Kogarah, Sydney, Australia. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 December 1996Volume 125, Issue 12Page: 1012-1013KeywordsAnticoagulant therapyHeparinInternational normalized ratioMyocardial infarctionPartial thromboplastin timeProspective studiesPulmonary embolismStent implantationThrombosisVenous thromboembolism ePublished: 15 August 2000 Issue Published: 15 December 1996 Copyright & PermissionsCopyright © 1996 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
STUDIES ON INFLAMMATION
Authors: Valy Menkin
Journal: The Journal of Experimental Medicine (1931)

Trypan blue injected into the circulating blood stream of frogs accumulates rapidly in an inflamed area. When trypan blue is injected directly into the area of inflammation it is fixed in situ and fails to diffuse outward. If the dye is injected at the periphery of an inflamed area it fails to enter the site of inflammation. This failure of penetration is caused by the occlusion of lymphatic vessels and the presence of a network of fibrin in the inflamed area. These experiments furnish additional evidence that fixation of foreign substances by the inflammatory reaction is due to mechanical obstruction caused by a network of fibrin and by thrombosed lymphatics at the site of inflammation.
Genes, hormones, and gender in sociopathy
Authors: Katharine Hoyenga
Journal: Behavioral and Brain Sciences (1995)

Abstract Although serotonin, testosterone, and genes contribute to sociopathy, the relationships are probably indirect and subject to modifiers (e.g., present only under certain conditions of rearing and temperament). Age at menarche may be a marker variable as well as a causal factor. Since the genders differ in all four areas, sex differences in sociopathy represent a very complex interaction of these factors.
A direct interaction between TGFβ activated kinase 1 and the TGFβ type II receptor: Implications for TGFβ signalling and cardiac hypertrophy
Authors: S WATKINS, L JONKER, H ARTHUR
Journal: Cardiovascular Research (2005)

Objective: Transforming growth factor beta (TGFβ)-activated kinase 1 (TAK1) is a MAP kinase kinase kinase involved in numerous signalling pathways and is strongly implicated in cardiac hypertrophy and heart failure. TGFβ is also associated with hypertension and heart disease, and evidence suggests that TGFβ1 and TAK1 act together in a cardiac stress signalling pathway. Canonical TGFβ signalling is mediated through Smad transcription factors, but TGFβ can also rapidly activate TAK1. The activation of the Smad cascade is well characterised, but little is known about how TAK1 is activated in response to TGFβ, and no direct link between any MAPK kinase pathway and the TGFβ receptors has yet been established. Since TAK1 is activated by TGFβ within 1 min in cardiomyocytes, we hypothesised there might be a direct interaction between TAK1 and one of the TGFβ receptors.
Closed-circuit television in the teaching of rheumatology.
Authors: D J Holroyde, D I Haslock, V Wright
Journal: Annals of the Rheumatic Diseases (1970)

Heberden Society 199 DR.NUKI (Glasgow) I would challenge the statement that the synovium is probably normal after synovectomy in view of the data from xenon clearance studies.MR.TAYLOR I agree, I am probably drawing assump- tions.All I can say is that, in some cases, the arthrogram after synovectomy may revert to a more normal appear- ance.DR. NUKI (Glasgow) How long after operation was the arthrography carried out?MR.TAYLOR At varying intervals between one month and a year.
An invariant V alpha 24-J alpha Q/V beta 11 T cell receptor is expressed in all individuals by clonally expanded CD4-8- T cells.
Authors: P Dellabona, E Padovan, G Casorati, M Brockhaus, A Lanzavecchia
Journal: The Journal of Experimental Medicine (1994)

The T cell receptor (TCR)-alpha/beta CD4-8- (double negative, DN) T cell subset is characterized by an oligoclonal repertoire and a restricted V gene usage. By immunizing mice with a DN T cell clone we generated two monoclonal antibodies (mAbs) against V alpha 24 and V beta 11, which have been reported to be preferentially expressed in DN T cells. Using these antibodies, we could investigate the expression and pairing of these V alpha and V beta gene products among different T cell subsets. V alpha 24 is rarely expressed among CD4+ and especially CD8+ T cells. In these cases it is rearranged to different J alpha segments, carries N nucleotides, and pairs with different V beta. Remarkably, V alpha 24 is frequently expressed among DN T cells and is always present as an invariant rearrangement with J alpha Q, without N region diversity. This invariant V alpha 24 chain is always paired to V beta 11. This unique V alpha 24-J alpha Q/V beta 11 TCR was found in expanded DN clones from all the individuals tested. These findings suggest that the frequent occurrence of cells carrying this invariant TCR is due to peripheral expansion of rare clones after recognition of a nonpolymorphic ligand.
Elevated levels of SREBP-2 and cholesterol synthesis in livers of mice homozygous for a targeted disruption of the SREBP-1 gene.
Authors: H Shimano, I Shimomura, R E Hammer, J Herz, J L Goldstein, M S Brown, J D Horton
Journal: Journal of Clinical Investigation (1997)

The synthesis of cholesterol and its uptake from plasma LDL are regulated by two membrane-bound transcription factors, designated sterol regulatory element binding protein-1 and -2 (SREBP-1 and SREBP-2). Here, we used the technique of homologous recombination to generate mice with disruptions in the gene encoding the two isoforms of SREBP-1, termed SREBP-1a and SREBP-1c. Heterozygous gene-disrupted mice were phenotypically normal, but 50- 85% of the homozygous (-/-) mice died in utero at embryonic day 11. The surviving -/- mice appeared normal at birth and throughout life. Their livers expressed no functional SREBP-1. There was a 1.5-fold upregulation of SREBP-2 at the level of mRNA and a two- to threefold increase in the amount of mature SREBP-2 in liver nuclei. Previous studies showed that SREBP-2 is much more potent than SREBP-1c, the predominant hepatic isoform of SREBP-1, in activating transcription of genes encoding enzymes of cholesterol synthesis. Consistent with this observation, the SREBP-1 -/- animals manifested elevated levels of mRNAs for 3-hydroxy-3-methylglutaryl coenzyme A synthase and reductase, farnesyl diphosphate synthase, and squalene synthase. Cholesterol synthesis, as measured by the incorporation of [3H]water, was elevated threefold in livers of the -/- mice, and hepatic cholesterol content was increased by 50%. Fatty acid synthesis was decreased in livers of the -/- mice. The amount of white adipose tissue was not significantly decreased, and the levels of mRNAs for lipogenic enzymes, adipocyte lipid binding protein, lipoprotein lipase, and leptin were normal in the -/- mice. We conclude from these studies that SREBP-2 can replace SREBP-1 in regulating cholesterol synthesis in livers of mice and that the higher potency of SREBP-2 relative to SREBP-1c leads to excessive hepatic cholesterol synthesis in these animals.
A randomized placebo-controlled trial of repaglinide in the treatment of type 2 diabetes.
Authors: R B Goldberg, D Einhorn, C P Lucas, M S Rendell, P Damsbo, W C Huang, P Strange, R G Brodows
Journal: Diabetes Care (1998)

OBJECTIVE: The objective of the study was to assess the efficacy and safety of repaglinide compared with placebo in the treatment of patients with type 2 diabetes. RESEARCH DESIGN AND METHODS: This was a phase II multicenter, double-blind, placebo-controlled, randomized, dose-adjustment and maintenance trial. After screening and a 2-week washout period, 99 patients were randomized to receive either repaglinide (n = 66) or placebo (n = 33). Patients underwent 6 weeks of dose adjustment followed by 12 weeks of dose maintenance. Fasting and stimulated glycosylated hemoglobin (HbA1c), plasma glucose, insulin, and C-peptide were measured at predetermined intervals. Adverse events and hypoglycemic episodes were recorded. RESULTS: From baseline to last visit, mean HbA1c decreased from 8.5 to 7.8% in patients treated with repaglinide and increased from 8.1 to 9.3% in patients receiving placebo, with a statistically significant difference of - 1.7% (P &amp;lt; 0.0001) between treatment groups at the last visit. Mean fasting plasma glucose and postprandial glucose increased in patients receiving placebo and decreased in patients treated with repaglinide, with statistically significant (P &amp;lt; 0.01) differences between groups at the last visit. Concentrations of fasting and postprandial insulin and C-peptide were lower at the last visit compared with baseline for patients treated with placebo and higher for patients treated with repaglinide, and the differences between groups were statistically significant (P &amp;lt; 0.05). Overall, repaglinide was well tolerated. CONCLUSIONS: This study demonstrated that repaglinide was safe and efficacious in lowering blood glucose concentrations. In addition to overall improvement in glycemic control noted with repaglinide in both sulfonylurea-treated patients and oral hypoglycemic agent-naive patients, repaglinide had a potent glucose-lowering effect in the postprandial period.
QUANTIFICATION OF AMPLITUDE, SPEED AND COMPLETENESS OF ST-SEGMENT RECOVERY AFTER PRIMARY PERCUTANEOUS CORONARY INTERVENTION FOR ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION: WHAT IS THE “BEST ST” RECOVERY TO PREDICT CLINICAL OUTCOME?
Authors: Wichert J. Kuijt, Matthew T. Roe, Cindy L. Green, Niels J. Verouden, Joost D. Haeck, Dan Tzivoni, Karel T. Koch, Gregg W. Stone, Alexandra J. Lansky, Robbert J. De Winter, Mitchell W. Krucoff
Journal: Journal of the American College of Cardiology (2010)
Prediction of postoperative urinary tract infection in men undergoing cardiac surgery by preoperative measurement of urine flow.
Authors: F K Gould, R Freeman
Journal: BMJ (1984)

Etude de 61 hommes soumis a des operations a cœur ouvert. Des infections urinaires sont observees apres l'intervention dans 10% des cas environ. Le risque est nettement plus grand chez ceux presentant avant l'operation des anomalies du debit urinaire. La mesure systematique de ce debit permettrait de mettre en route une prophylaxie
Thromboxane inhibition improves renal perfusion and excretory function in severe congestive heart failure
Authors: Sergio Castellani, Rita Paniccia, Claudia Di Serio, Giuseppe La Cava, Loredana Poggesi, Stefano Fumagalli, Gian Franco Gensini, Gian Gastone Neri Serneri
Journal: Journal of the American College of Cardiology (2003)
Ultrastructure of Normal and Abnormal Skin
Authors: Samuel M. Bluefarb
Journal: JAMA (1968)

Refinement and widespread application of the electron microscope has dramatically introduced a new era to medicine, indeed, the new histology. This is especially appreciated in dermatology, where ready specimen availability has made this organ a prime target of active investigation. With the advent of the electron microscope, many previously invisible structures within and between the cells have been described. These observations have resulted in development of new theories and modification of old ones regarding functional anatomy and lay the foundations for the new horizon of ultracytochemistry and pathology. The amount of detailed information that has accumulated in the past few years is so enormous and eminently important, that usefulness demands critical summarization and accessibility in a single volume. In assuming this task, Dr. Zelickson has assembled a group of outstanding authorities whose current contributions on their given subject are presently unexcelled. Their combined talents have produced an impressive book that
Anorexogen-Related Cardiac Valvulopathy
Authors: Richard B. Rothman
Journal: Annals of Internal Medicine (2002)

Letters21 May 2002Anorexogen-Related Cardiac ValvulopathyRichard B. Rothman, MD, PhDRichard B. Rothman, MD, PhDFairfax, VA 22030 (Rothman)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-136-10-200205210-00016 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:In addition to those described by Howlin (1), additional errors in the editorial by St John Sutton (2) require correction. St John Sutton indicated that phentermine decreases appetite by inhibiting serotonin clearance in the lung. However, it is generally well accepted that the ability of phentermine to release the neurotransmitters norepinephrine and dopamine produces its anorectic effects (3). The incorrect notion that phentermine inhibits pulmonary clearance of serotonin first arose when Connolly and coworkers (4) apparently confused chlorphentermine, which does inhibit pulmonary serotonin clearance, with phentermine, which does not. Finally, the lack of valvular heart disease cases ...References1. Howlin D. Fenfluramine and phentermine [Letter]. Ann Intern Med. 2001;135:840-1. [PMID: 11694113] LinkGoogle Scholar2. St John Sutton M. Silver lining to the cloud over anorexogen-related cardiac valvulopathy? [Editorial]. Ann Intern Med. 2001;134:335-7. [PMID: 11182845] LinkGoogle Scholar3. Rothman RB, Baumann MH. Neurochemical mechanisms of phentermine and fenfluramine: therapeutic and adverse effects. Drug Development Research. 2000;51:52-65. CrossrefGoogle Scholar4. Connolly HM, Crary JL, McGoon MD, Hensrud DD, Edwards BS, Edwards WD, et al . Valvular heart disease associated with fenfluramine-phentermine. N Engl J Med. 1997;337:581-8. [PMID: 9271479] CrossrefMedlineGoogle Scholar5. Rich S, Rubin L, Walker AM, Schneeweiss S, Abenhaim L. Anorexigens and pulmonary hypertension in the United States: results from the surveillance of North American pulmonary hypertension. Chest. 2000;117:870-4. [PMID: 10713017] CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAffiliations: Fairfax, VA 22030 (Rothman) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoSilver Lining to the Cloud over Anorexogen-Related Cardiac Valvulopathy? Martin St John Sutton Fenfluramine and Phentermine Diane Howlin Metrics Cited ByDiagnostic and Therapeutic Targets for Aortic Valve and Ascending Aorta Pathologies: Challenges and OpportunitiesSerotonin receptor 2B signaling with interstitial cell activation and leaflet remodeling in degenerative mitral regurgitationStructural Basis for Molecular Recognition at Serotonin ReceptorsCellular Mechanisms in Mitral Valve Disease 21 May 2002Volume 136, Issue 10Page: 779KeywordsCardiovascular therapyDopamineLungsNeurotransmittersNorepinephrinePulmonary hypertensionSerotonin ePublished: 21 May 2002 Issue Published: 21 May 2002 CopyrightCopyright © 2002 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Abstract 2949: The VEGF quadruplex-forming sequence inhibits cell growth of lung cancer
Authors: Shelia D. Thomas, Campbell M. Grant, Cortney R. Clarkson, Donald M. Miller, Kara C. Sedoris
Journal: Cancer Research (2010)

Abstract Vascular endothelial growth factor (VEGF), commonly overexpressed in a variety of malignancies including lung cancer, is a key regulator of angiogenesis promoting tumor survival, growth, and metastasis. The promoters of several cancer-related genes, including VEGF, contain disproportionate sequences within nuclease hypersensitivity regions capable of forming quadruplex (four-stranded) DNA. The VEGF quadruplex-forming sequence (VEGFq), a polyG/polyC tract located in the proximal promoter region upstream of the transcription initiation site, has been implicated in the regulation of both basal and inducible VEGF expression. However, the biological role of this sequence remains unclear. We hypothesize that treatment of A549 non-small lung cancer cells with VEGFq induces cell death by inhibiting gene expression. To determine the biological role of VEGF on lung cancer cell proliferation, A549 cells were treated with VEGFq or the corresponding mutant sequence (MutVEGF), which lacks runs of two or more guanines. Changes in cell proliferation were compared to levels of VEGF protein expression. Quadruplex formation was confirmed by circular dichroism spectroscopy. Our results demonstrate that VEGFq formed a stable parallel quadruplex structure, while the MutVEGF sequence did not form a quadruplex. Treatment of A549 cells with VEGFq caused a significant dose and time-dependent decrease in cell proliferation after 3 and 6 days (IC50&amp;lt;5µM) as determined by MTT assay. No change in the growth of nontransformed fibroblast cells occurred in response to VEGFq indicating the effect is specific for malignant cells. Confocal and flow cytometry analysis of cells treated with FITC-labeled VEGFq or MutVEGF showed prominent uptake and nuclear localization of VEGFq not MutVEGF after 72 h. Inhibition of cell proliferation corresponded with decreased VEGF protein expression. No specific change in the cell cycle was measured after 72 h. These results demonstrate striking growth inhibition of A549 cells in response to the VEGF quadruplex-forming sequence related to inhibition of VEGF expression and suggest significant therapeutic implications for the treatment of non-small cell lung cancer. 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 2949.
Difference in the Mechanism of Emotion in Japanese and Westerner
Authors: Tadanobu Tsunoda
Journal: Psychotherapy and Psychosomatics (1979)

The author found that cerebral hemisphere dominance of steady-state vowels as well as human emotional and natural sounds are different between the Japanese and the Westerner; the Japanese shows a verbal hemisphere dominance, while the Westerner shows a non-verbal hemisphere dominance. He brought forward the theory of mental structure and vowels stating that such a difference in the brain related to emotional activities forms the starting point of mental structure and culture. In this study the author confirmed the above hypothesis by emotional stimulation of human olfaction.
Utility of testing for monoclonal bands in serum of patients with suspected osteoporosis: retrospective, cross sectional study
Authors: Bo Abrahamsen, Ivan Andersen, Susanne S Christensen, Jonna Skov Madsen, Kim Brixen
Journal: BMJ (2005)

To determine whether measuring monoclonal bands (M component) in serum should be part of the investigation of patients referred to osteoporosis clinics.
Relationship of protoporphyrin IX synthesis to photodynamic effects by 5-aminolaevulinic acid and its esters on various cell lines derived from the skin
Authors: J.B. Lee, J.Y. Choi, J.S. Chun, S.J. Yun, S.C. Lee, J. Oh, H.R. Park
Journal: British Journal of Dermatology (2008)

5-Aminolaevulinic acid (ALA) and its esters act as precursors to the fluorescent photosensitizer protoporphyrin IX (PpIX) in photodynamic therapy (PDT). There is little information about how ALA and its esters induce PpIX synthesis and photodynamic effects in cell lines derived from the skin.We compared the amount of PpIX synthesis induced by ALA and its esters in skin cell lines, and evaluated the relationship of PpIX synthesis to photodynamic effects by ALA and its esters in vitro.Four cell lines, including human epidermal keratinocytes (HEK), human dermal fibroblast (hF), A431, and TXM13 were used. Cell survival was evaluated by the MTT assay. Fluorescence spectroscopy was used to measure the amount of PpIX synthesis induced by ALA and its esters. Flow cytometry measured cell death induced by ALA- and its esters-mediated PDT.ALA and its esters were not toxic at concentrations lower than 2 mmol L(-1) in all cell lines. PpIX synthesis was dose-dependent at low doses (0.01-0.1 mmol L(-1)), and ALA esters were more effective than ALA. Cell death occurred from necrosis rather than apoptosis just after light irradiation illumination on both ALA and its esters-treated cells. Cell death related more to PpIX synthesis than the irradiation light dose.PpIX production by ALA and its esters was induced on both normal and malignant cell lines derived from the skin, and cell death of PDT responses is closely related to the amount of PpIX synthesis rather than to the irradiation dose.
Increased Uptake of Technetium-99m Pertechnetate in a Salivary Gland Cancer
Authors: CLARA DOSORETZ, LIONEL M. LIEBERMAN
Journal: Clinical Nuclear Medicine (1987)

A patient with acinic cell carcinoma of the parotid gland that showed increased uptake of Tc-99m pertechnetate is reported. Since increased concentration of pertechnetate in salivary gland tumors is almost always associated with benign disease, the findings suggest that caution be used in reporting a hot lesion in the parotid gland being associated with benign disease.
A Fetal Fatty-Acid Oxidation Disorder as a Cause of Liver Disease in Pregnant Women
Authors: Jamal A. Ibdah, Michael J. Bennett, Piero Rinaldo, Yiwen Zhao, Beverly Gibson, Harold F. Sims, Arnold W. Strauss
Journal: New England Journal of Medicine (1999)

Acute fatty liver of pregnancy and the HELLP syndrome (hemolysis, elevated liver-enzyme levels, and a low platelet count) are serious hepatic disorders that may occur during pregnancy in women whose fetuses are later found to have a deficiency of long-chain 3-hydroxyacyl-coenzyme A (CoA) dehydrogenase. This enzyme resides in the mitochondrial trifunctional protein, which also contains the active site of long-chain 2,3-enoyl-CoA hydratase and long-chain 3-ketoacyl-CoA thiolase. We undertook this study to determine the relation between mutations in the trifunctional protein in infants with defects in fatty-acid oxidation and acute liver disease during pregnancy in their mothers.