tbuckley/cabot-search huggingface dataset:
Post-transfusion Immunologic Purpura—A Newly Recognized Disease.
Authors: N. R. Shulman
Journal: Annals of Internal Medicine (1961)

s1 May 1961Post-transfusion Immunologic Purpura—A Newly Recognized Disease.N. R. Shulman, M.D., R. H. Aster, M.D., A. Leitner, M.D., M.C. Hiller, M.D.N. R. Shulman, M.D.Search for more papers by this author, R. H. Aster, M.D.Search for more papers by this author, A. Leitner, M.D.Search for more papers by this author, M.C. Hiller, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-54-5-1064_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptA rare but serious hemorrhagic complication following blood transfusion, which heretofore had been indistinguishable from idiopathic thrombocytopenic purpura, was elucidated by finding in two patients who developed fulminant purpura one week post-transfusion, a high-titer antibody which reacted with platelets to cause complement fixation, agglutination, and inhibition of clot retraction. The antibody proved to be an iso-antibody which did not react with platelets obtained from both patients after recovery but reacted with platelets from most normal individuals. Quantitative reactions of the antibody with platelets from members of the patients' families and 300 donors selected at random showed that 74% of the... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1961Volume 54, Issue 5Page: 1064-1064KeywordsBlood transfusionIdiopathic thrombocytopenic purpuraPlatelets ePublished: 1 December 2008 Issue Published: 1 May 1961 PDF downloadLoading ...
A circulating inhibitor of fluid-phase amplification. C3 convertase formation in systemic lupus erythematosus.
Authors: F B Waldo, J Forristal, L Beischel, C D West
Journal: Journal of Clinical Investigation (1985)

C3 nephritic factor (C3NeF) was used to assess the formation of the fluid-phase amplification convertase, C3b,Bb, in 37 serum specimens from 24 patients with systemic lupus erythematosus (SLE). C3b,Bb formation was measured by the concentration of Ba, released when C3b,B is activated. Incubation of normal human serum (NHS) with C3NeF accelerates C3b amplification loop turnover with the formation of large quantities of C3b,Bb. In contrast, sera from 22 of 24 patients with SLE formed little or no convertase when incubated with C3NeF. C3 conversion to C3b was commensurately reduced. The inhibition could not be attributed to depressed serum concentrations of C3, factor B, or classical pathway components. Inhibitor present in excess could be demonstrated in 23 of 34 specimens of SLE serum by mixing experiments. The spontaneous convertase formation that occurs when a portion of the serum H is inactivated with F(ab')2 anti-H was also shown to be inhibited in SLE serum. The inhibition was found, however, to be H dependent in that convertase formation was normal in SLE serum depleted of H. It is concluded that the C3b in most SLE sera is unusually susceptible to inactivation by H, but a functional abnormality was not demonstrable in either C3 or H isolated from SLE serum. The inhibition could be simulated in NHS by addition of heparin, 100 micrograms/ml. In vivo, inhibition of convertase formation could interfere with the solubilization and disposal of immune complexes by reducing the deposition of C3b on the immune complex lattice.
Hematologic Effects of Alcohol in Man in the Absence of Nutritional Deficiency
Authors: John Lindenbaum, Charles S. Lieber
Journal: New England Journal of Medicine (1969)

When ethanol was administered to human volunteers in doses equaling 46 to 66 per cent of caloric intake, and excellent protein and vitamin intake was maintained, vacuolation of bone-marrow pronormoblasts developed. Their presence appeared to be dose-related. Vacuolation of promyelocytes was seen less consistently, and only with the larger doses. The platelet count was significantly depressed during the third to the fifth week of alcohol ingestion in four of nine subjects. Serum iron levels fell after the withdrawal of alcohol. Ferrokinetic studies yielded results within normal limits in two subjects during the periods of alcohol ingestion. The hematologic alterations occurred despite the concomitant administration of pharmacologic doses of folic acid.
Abstract 4724: Adverse prognostic significance of TNFAIP8 protein expression in non small cell lung cancer
Authors: Bhaskar V. Kallakury, Usha N. Kasid, Olga Voronel, Christopher B. Sheehan, Christine E. Sheehan, Jeffrey S. Ross
Journal: Cancer Research (2014)

Abstract Background: Tumor necrosis factor alpha induced protein 8 (TNFAIP8) is a transcription factor NF-kB inducible antiapoptotic and oncogenic molecule. Positive correlation between TNFAIP8 expression and cancer progression/poor prognosis has been described in a few human solid cancers including pancreatic and esophageal primaries. We were the first to publish the correlation of TNFAIP8 expression with high tumor grade and its independent predictor status for disease recurrence in prostatic adenocarcinomas. In this study, we evaluated the significance of this protein in non small cell lung cancer (NSCLC). Design: A total of 144 formalin-fixed, paraffin-embedded NSCLCs were analyzed (122 primary tumor resections and 22 tissue microarray samples); including 47 squamous cell carcinomas (SCC), 59 adenocarcinomas (AC), and 38 bronchioloalveolar carcinomas (BAC), were immunostained by a manual method using a custom made anti-TNFAIP8 antibody as described earlier (Zhang et al., Int J Cancer,133: 31-42, 2013). The staining pattern was semiquantitatively assessed based on staining intensity and distribution and the results were correlated with morphologic and prognostic variables. Results: Immunoreactivity for TNFAIP8 was predominantly cytoplasmic. TNFAIP8 protein overexpression was noted in 84/144 (58%) tumors and correlated with tumor type [45/59 (76)% AC vs 29/47 (62%) SCC vs 10/38 (26%) BAC, p&amp;lt;0.0001], overall with advanced tumor stage [24/31 (77%) advanced vs 60/113 (53%) early, p=0.015] and lymph node positive status [31/41 (76%) LN+ vs 53/103 (52%) LN-, p=0.008]. Within the AC subgroup, there was a trend toward correlation with advanced tumor stage [13/14 (93%) advanced vs 32/45 (71%) early, p=0.095] and lymph node positive status [18/20 (90%) LN+ vs 27/39 (69%) LN-, p=0.076]. On multivariate analysis, LN+ status independently predicted shortened survival. Conclusion: TNFAIP8 immunohistochemical expression portends poor prognosis in NSCLC and may constitute a novel therapeutic target in the management of aggressive NSCLC, warranting further study. Citation Format: Bhaskar VS Kallakury, Usha N. Kasid, Olga Voronel, Christopher B. Sheehan, Christine E. Sheehan, Jeffrey S. Ross. Adverse prognostic significance of TNFAIP8 protein expression in non small cell lung cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4724. doi:10.1158/1538-7445.AM2014-4724
Board Certifying Examinations
Authors: HOWARD HERZENBERG
Journal: Annals of Internal Medicine (1972)

Letters, Comments, and Corrections1 December 1972Board Certifying ExaminationsHOWARD HERZENBERG, M.D.HOWARD HERZENBERG, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-77-6-1000 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Drs. Petersdorf and Beck (1) recently outlined a new procedure for evaluating the clinical competence of candidates for certification by the American Board of Internal Medicine. They stressed the need for periodic review of clinical competence by committees at the training institutions with feedback and discussion with the candidates. I endorse this new procedure and the Board's proper concern that all candidates for certification clearly demonstrate clinical competence in evaluating patients.Regretably the almost total lack of feedback in the erasure section of the Board's recent Certifying Examination made it impossible for us to "practice" medicine competently....Reference1. PETERSDORFBECK RJ: The new procedure for evaluating the clinical competence of candidates to be certified by the American Board of Internal Medicine. Ann Intern Med 76:491-496, 1972 LinkGoogle Scholar1. POSTMANWEINGARTNER NC: Teaching Us a Subversive Activity. New York, Dell Publishing Co., 1969, p. 35 Google Scholar2. ENGSTROM W: Personal communication Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byBoard ExaminationJOHN L. ROGLIERI, M.D. 1 December 1972Volume 77, Issue 6Page: 1000-1002 ePublished: 1 December 2008 Issue Published: 1 December 1972 PDF downloadLoading ...
Review of The International Textbook of Cardiology
Authors: TSUNG O. CHENG
Journal: Annals of Internal Medicine (1987)

Letters and Corrections1 August 1987Review of The International Textbook of CardiologyTSUNG O. CHENG, M.D.TSUNG O. CHENG, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-107-2-256_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: I appreciate the critical review of my book, The International Textbook Of Cardiology, by Dr. Franch (1). However, I take issue with his remark that ". . . clinical laboratory data are not expressed in le Systeme International d'Unités (SI units) nor are SI units given parenthetically with conventional values."I should point out that in the sixth edition ofThe Heartby Hurst, Dr. Franch did not use the SI units in his chapter on techniques of cardiac catheterization. For example, hemoglobin was still expressed in the metric unit of g% (which should be g/dL),...References1. FRANCH R. The international textbook of cardiology [Book review]. Ann Intern Med. 1987;106:787. LinkGoogle Scholar2. LUNDBERGIVERSONRADULESCU GCG: NOW read this: the SI units are here. JAMA 1986;225:2329-39. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByHerb–drug interaction studies of herbs used in treatment of cardiovascular disorders—A narrative review of preclinical and clinical studies 1 August 1987Volume 107, Issue 2Page: 256-256KeywordsCatheterizationClinical laboratoriesHeartHemoglobin Issue Published: 1 August 1987 PDF DownloadLoading ...
Computerizing Patient Records
Authors: H. Phelps Potter
Journal: Annals of Internal Medicine (1992)

Letters1 June 1992Computerizing Patient RecordsH. Phelps Potter Jr., MDH. Phelps Potter Jr., MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-116-11-959_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editors: Shortliffe and colleagues (1) cite the faults of today's medical records and suggest computerization as the solution. However, computerization would necessitate changes in record structure and volume.The traditional hospital and office record format would have to be replaced by a problem-oriented model of the type suggested by Weed (2). Problem-oriented hospital discharge summaries and updated office problem lists provide a compact database for subsequent effective management. The current dictum that "if it's not in the record, it wasn't done" swells charts with excessive documentation that is unnecessary for patient care and generally superfluous for future quality...References1. ShortliffeTangDetmer EPD. Patient records and computers. Ann Intern Med. 1991;979-81. LinkGoogle Scholar2. Weed L. Medical records that guide and teach. New Engl J Med. 1968;278:593-600, 652-7. CrossrefMedlineGoogle Scholar1. . The Computer-Based Patient Record: An Essential Technology for Health Care. Washington, DC: National Academy Press; 1991. Google Scholar2. Weed L. Medical records that guide and teach. New Engl J Med. 1968;278:593-600, 652-7. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Paoli Memorial Hospital Paoli, PA 19301 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 June 1992Volume 116, Issue 11Page: 959-959KeywordsChartsComputersDatabasesElectronic medical recordsForecastingPatients ePublished: 1 December 2008 Issue Published: 1 June 1992 PDF downloadLoading ...
Phosphatidylinositol 4-Kinases and the Role of Polyphosphoinositides in Cellular Regulation
Authors: LINDA J. PIKE
Journal: Endocrine Reviews (1992)

Phosphoinositides play a central role in the transduction of signals for a variety of hormone and growth factor receptors. Multiple derivatives of phosphatidylinositol are present within the cell including phosphatidylinositol 4,5-bisphosphate, the phosphorylated derivative that is hydrolyzed by phospholipase C to produce the two intracellular second messengers, diacylglycerol and inositol 1,4,5-trisphosphate. The synthesis, degradation, and subsequent resynthesis of the phosphoinositides form a metabolic cycle known as the phosphoinositide cycle. The phosphoinositide cycle begins with the phosphorylation of phosphatidylinositol to form phosphatidylinositol 4-phosphate, a reaction catalyzed by phosphatidylinositol 4-kinase. Phosphatidylinositol kinase activity has been reported to be present in a variety of cellular membranes, and multiple isozymes of phosphatidylinositol 4-kinase are present within the cell, suggesting that the product of this reaction may have more than one biological function. The activity of phosphatidylinositol 4-kinase is regulated by growth factors, further underscoring the importance of this enzyme in cellular regulation. Recent data suggest that in addition to serving as substrates for phospholipase C, the polyphosphoinositides may themselves function as intracellular mediators of hormone action. For example, polyphosphoinositides have marked effects on the activity of certain actin binding proteins that may allow these lipids to participate in the regulation of actin polymerization. This review focuses on the properties of the phosphatidylinositol 4-kinases and the potential role of polyphosphoinositides in the regulation of cellular processes.
The Oliver-Sharpey Lectures ON NEW FACTS IN RELATION TO THE PROCESSES OF NERVOUS DEGENERATION AND REGENERATION: Delivered before the Royal College of Physicians, London, April 29th and 30th
Authors: W. D. Halliburton
Journal: BMJ (1907)

<h3>Background</h3> Several studies have investigated the predictors of morbidity and mortality in Systemic sclerosis (SSc). However long-term follow-up data from inception cohorts of early SSc patients are limited. <h3>Objectives</h3> To identify predictors of morbidity and mortality in a single centre inception cohort of early SSc patients at long-term follow-up. <h3>Methods</h3> Our inception cohort comprised SSc patients who fulfilled the American College of Rheumatology criteria, were recruited within 12 months of disease onset and followed prospectively for at least 3 years. Clinical manifestations, laboratory and lung function tests were recorded for each patient at baseline and at 3rd and 6th years of follow up. Multivariate regression analysis and Cox proportional hazard models were used to identify predictors (clinical manifestations, laboratory and lung function tests at baseline) of morbidity and mortality in SSc, respectively. <h3>Results</h3> A total of 114 patients (96 female, mean age at diagnosis 48.1±13.5 years, 53 diffuse SSc subtype) were included in the study, from January 1997 to December 2012. All patients were followed for at least 3 years and 84 patients for at least 6 years. Twenty (17.5%) of 114 patients died during a mean follow up of 101.8±48.5 months. In multivariate regression analysis predictors for major SSc outcomes at 6 years were: diffuse subtype (OR: 6.2, p=0.015), anti-scl-70 positivity (OR: 3.9, p=0.05), esophageal involvement (OR: 6.5, p=0.017) and digital ulcers (OR: 8.6, p=0.003) at baseline for the development of pulmonary fibrosis (PF). The presence of digital ulcers at baseline was a predictor for the development of arrhythmias (OR: 3.7, p=0.05) and the presence of arrhythmias at baseline for the development of pulmonary hypertension (PH) (OR: 5.4, p=0.039). Cox proportional hazard models multivariate analysis revealed that independent predictors of mortality were: male gender (HR: 3.3, p=0.023), diffuse type (HR: 8.7, p=0.004), PF at baseline (HR: 2.7, p=0.05), PH based on echocardiography at baseline (HR: 12.7, p=0.001) FVC &lt;80% (HR: 2.74, p=0.042) and DLCO &lt;60% of predicted value at baseline (HR: 2.97, p=0.019). <h3>Conclusions</h3> Results from long-term follow-up data from a single centre inception cohort indicate that diffuse SSc subtype, anti-Scl-70 positivity, esophageal involvement and digital ulcers at baseline are independent predictors for the development of PF. Male gender, diffuse subtype, PF, PH and decreased FVC and DLCO at baseline are prognostic factors of mortality. <h3>Disclosure of Interest</h3> None declared
Impaired Hyperpolarization in Regenerated Endothelium After Balloon Catheter Injury
Authors: Ralf Köhler, Susanne Brakemeier, Meike Kühn, Claudia Behrens, Robert Real, Christiane Degenhardt, Hans-Dieter Orzechowski, Axel R. Pries, Martin Paul, Joachim Hoyer
Journal: Circulation Research (2001)

Ca(2+)-activated K(+) (K(Ca)) channels control endothelial Ca(2+) homeostasis and the formation of vasodilators. After angioplasty, dysfunction of the regenerated endothelium leads to abnormal vasoregulation. In this study, we tested the expression and function of K(Ca) channels in regenerated endothelium at 6 weeks after balloon catheter injury of rat carotid arteries (CAs) by using single-cell reverse transcription-polymerase chain reaction, patch-clamp techniques, and analysis of vasoreactivity. In single regenerated endothelial cells (ECs), the percentage of ECs expressing the K(Ca) genes, rSK3 (12+/-8%) and rIK1 (22+/-9%), was significantly lower compared with the percentage of native ECs expressing these genes (rSK3 58+/-8%, rIK1 64+/-10%). In patch-clamp experiments, K(Ca) currents and acetylcholine-induced hyperpolarization were markedly reduced in regenerated ECs (shift of membrane potential -6+/-3 mV) compared with those in native ECs (shift of membrane potential -21+/-5 mV). In pressure myograph experiments, acetylcholine-induced dilation was impaired in reendothelialized CAs compared with normal CAs. Intraluminal application of the K(Ca) blocker apamin and charybdotoxin inhibited dilation by 30% in normal CAs but was without effect in reendothelialized CAs. Intraluminal application of 1-ethyl-2-benzimidazolinone (100 micromol/L), an opener of K(Ca) channels, evoked dilation by 29% in normal CAs but had no effect in reendothelialized CAs. In conclusion, the impaired expression of K(Ca) channels in regenerated endothelium results in defective hyperpolarization and impaired dilation. Thus, the impaired K(Ca) channel function contributes to functional alterations of regenerated endothelium after angioplasty.
Evidence for liver cell proliferation during fatal acute liver failure.
Authors: M Milandri, J Gaub, L Ranek
Journal: Gut (1980)

Liver cell regeneration was assessed by determining the mitotic index and the frequency of liver cells with interploid DNA values in livers from patients dying from fulminant hepatitis. For comparison, the same parameters were determined in patients with uncomplicated hepatitis. We found comparable levels of regeneration in the two groups, indicating that the rate of liver cell destruction is a major determinant in the prognosis of acute liver failure. Accordingly, measures to prevent liver cell necrosis seem at least as important as stimulation of regeneration. Judged from available experimental evidence, substances with documented hepatotrophic effect in animals, such as insulin and glucagon, may therefore not be effective in acute liver failure unless the patient has impaired secretion of these substances.
Cell Growth Inhibition by Okadaic Acid Involves Gut-Enriched Kruppel-like Factor–Mediated Enhanced Expression of c-Myc
Authors: Liyue Zhang, Anil Wali, Chilakamarti V. Ramana, Arun K. Rishi
Journal: Cancer Research (2007)

Abstract Human breast cancer (HBC) cell growth suppression by okadaic acid (OA) was previously found to involve elevated expression of oncogenes c-myc and c-fos and apoptosis. Since, c-Myc influences diverse pathways of cell growth, we hypothesized that elevated levels of c-Myc are involved in HBC growth suppression. Here, we investigated whether induction of c-Myc by OA or protein synthesis inhibitor cycloheximide contributed to HBC growth inhibition and the mechanisms involved. OA, cycloheximide, or the chemotherapeutic drug Taxol suppressed HBC cell growth. However, OA or cycloheximide treatments over 6 or 10 h, respectively, induced c-Myc expression. Depletion of c-Myc, on the other hand, resulted in enhanced HBC cell viabilities when exposed to OA or cycloheximide, but not by Taxol. OA induced c-myc transcription by targeting an 80-bp region from positions −11 to +70, relative to the P1 transcription start of mouse c-myc promoter. Gel mobility shift assays revealed binding of HBC cell nuclear proteins to the OA-responsive c-myc promoter fragment, whereas binding of one complex was elevated in the case of the OA-treated or cycloheximide-treated HBC cell nuclear extracts. Database search revealed presence of a consensus sequence for zinc finger protein gut-enriched Kruppel-like factor (GKLF) in OA-responsive region of the c-myc promoter. Mutation of GKLF consensus sequences abrogated OA responsiveness of the c-myc promoter, and OA treatments caused enhanced expression of GKLF in HBC cells. Thus, OA-dependent attenuation of HBC growth is accomplished, in part, by zinc finger transcription factor GKLF-mediated enhanced transcription of c-myc. [Cancer Res 2007;67(21):10198–206]