tbuckley/cabot-search huggingface dataset:
Whither goes in/outpatient psychiatric care?
Authors: T. Ziporyn
Journal: JAMA (1983)

"Anyone reading newspapers in the United States knows that there are many former state mental hospital patients living and sleeping on the streets or in dilapidated hotels." With these words, Alfred M. Freedman, MD, chair of the Department of Psychiatry and Behavioral Sciences at New York Medical College in Valhalla, NY, engaged in a discourse at the recent Seventh World Congress of Psychiatry in Vienna on the pluses and minuses of the well-known shift from government (state) hospitals to general hospitals as the principal site of inpatient psychiatric care in the United States. According to Freedman, 75% of psychiatric patients received treatment in state hospitals in 1955 and occupied approximately 750,000 beds. By 1965, the number of beds had decreased to 650,000; by 1980, the number was below 200,000. Specific treatment episodes (such as a drug regimen or electroconvulsive therapy) in state hospitals represented 49% of all psychiatric treatment in
ADVANCES IN THE TREATMENT OF PELLAGRA
Authors: P. C.
Journal: Annals of Internal Medicine (1938)

Editorial1 March 1938ADVANCES IN THE TREATMENT OF PELLAGRAP. C.P. C.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-11-9-1760 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe success of Goldberger and his associates in experimentally producing pellagra in man and its counterpart, black tongue, in dogs proved that a dietary deficiency plays an essential part in the production of these diseases. His demonstration that yeast, liver, and other foods rich in vitamin B2 (G) prevents and usually cures the disease indicates that the active substance is probably to be found in some portion of the vitamin B2 complex.Certain facts, however, have led some investigators to believe that other factors are also concerned in the development of the disease. It seems probable that some individual predisposition...1 RUFFINSMITH JMDT: A clinical evaluation of the potency of various extracts of liver in the treatment of pellagra, South. Med. Jr., 1937, xxx, 4-14. CrossrefGoogle Scholar2 SYDENSTRICKERTHOMAS VPJW: Some factors in the etiology of pellagra, South. Med. Jr., 1937, xxx, 14-18. CrossrefGoogle Scholar3 SMITHRUFFIN DTJM: Effect of sunlight on clinical manifestations of pellagra, Arch. Int. Med., 1937, lix, 631-645. CrossrefGoogle Scholar4 SPIESCHINNMCLESTER TDAJB: Treatment of endemic pellagra, South. Med. Jr., 1937, xxx, 18-21. CrossrefGoogle Scholar5 JUKESLEPKOVSKY THS: Distribution of "filtrate factor" (water soluble vitamin belonging to vitamin B complex and preventing dietary dermatitis in chicks) in certain feedingstuffs, Jr. Biol. Chem., 1936, cxiv, 117-121. CrossrefGoogle Scholar6 ELVEHJEMMADDENSTRONGWOOLEY CARJFMDW: Relation of nicotinic acid and nicotinic acid amide to canine black tongue, Jr. Am. Chem. Soc., 1937, lix, 1767. CrossrefGoogle Scholar7 SPIESCOOPERBLANKENHORN TDCMA: Central Society for Clinical Research, Chicago, Nov. 5, 1937. Google Scholar8 SPIESCOOPERBLANKENHORN TDCMA: Nicotinic acid in the treatment of pellagra, Jr. Am. Med. Assoc., 1938, cx, 622-627. CrossrefGoogle Scholar9 SMITHRUFFINSMITH DTJMSG: Pellagra successfully treated with nicotinic acid: a case report, Jr. Am. Med. Assoc., 1937, cix, 2054-2055. CrossrefGoogle Scholar10 FOUTSHELMERLEPKOVSKYJUKES FJOMSTH: Treatment of human pellagra with nicotinic acid, Proc. Soc. Exper. Biol. and Med., 1937, xxxvii, 405. 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 1 March 1938Volume 11, Issue 9Page: 1760-1762KeywordsFoodLiverLiver diseasesTongue ePublished: 1 December 2008 Issue Published: 1 March 1938 PDF downloadLoading ...
PHARMACEUTICAL NOTES
Authors: HERBERT SKINNER
Journal: British Journal of Dermatology (1901)

Journal Article PHARMACEUTICAL NOTES Get access HERBERT SKINNER HERBERT SKINNER Pharmacist to the Great Northern Central Hospital Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 13, Issue 5, 1 May 1901, Pages 161–165, https://doi.org/10.1111/j.1365-2133.1901.tb16373.x Published: 01 May 1901
ECZEMA
Authors: H. G. Adamson
Journal: British Journal of Dermatology (1935)

Journal Article ECZEMA Get access H. G. Adamson H. G. Adamson Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology and Syphilis, Volume 47, Issue 3, 1 March 1935, Page 142, https://doi.org/10.1111/j.1365-2133.1935.tb09845.x Published: 01 March 1935
Queries and Minor Notes
Journal: JAMA (1933)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Mixing Local Anesthetics Questioned
Journal: JAMA (1966)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Schweizerische Med Wochenschrift, Basel
Journal: JAMA (1965)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Cell proliferation and oncogene expression after bile duct ligation in the rat: Evidence of a specific growth effect on bile duct cells*1
Authors: L POLIMENO
Journal: Hepatology (1995)

The proliferative response of the rat liver was measured after temporary or permanent total biliary obstruction (BDO) and in different regions after selective ligation of the lobar ducts draining the right 60% of the hepatic mass. The results were compared with those after 70% partial hepatectomy (PH). Cell proliferation was assessed globally by measuring DNA synthesis and stratified to the separate cell populations with cytostaining techniques that allowed distinction of hepatocytes, duct cells, and nonparenchymal cells (NPCs). In selected experimental groups, gene expression was determined of transforming growth factor-β1 (TGFβ-1), prothrombin, c-erb-B2, transforming growth factor alpha (TGFα), human Cyclophilin (CyP), and 28S ribosomal RNA. The stimulation of a proliferative response to total BDO required obstruction for longer than 24 hours, but after this deligation did not switch off regeneration. In the first week after permanent BDO, there was progressive infiltration of NPCs, fibrous linkage of some portal areas, and a crescendo of DNA synthesis that was obvious at 24 hours, maximal at 48 hours, and back nearly to baseline at 6 days. At the 2-day mark, the bile duct cells had a 17-fold increase in proliferation, accompanied by a threefold to fourfold increase in hepatocyte renewal. Little or no increase in expression of TGFα or the hepatocyte-specific prothrombin gene was detectable in the first 48 hours, whereas levels of the oncogene c-erb-B2 that is associated with cholangiocarcinoma were expressed from 48 to 96 hours. Livers subjected to regional BDO with or without immunosuppressive treatment with FK 506 and cyclosporine had an inflammatory reaction only on the side with ligated ducts. DNA synthesis increased in both the obstructed and freely draining lobes to approximately half the level that occurred after total BDO. The proliferation of the obstructed side was similar to the mixed duct cell/hepatocyte response after total BDO, but this almost exclusively involved duct cells on the freely draining side. In contrast to the findings after BDO, livers after PH regenerated maximally at 24 hours rather than 48 hours, had a predominantly noninflammatory hepatocyte as opposed to duct cell response, and had marked expression of the prothrombin and TGFα genes but only weakly and late of c-erb-B2 messenger RNA. The results show that the liver responds as a whole and in a biologically intelligent way to the nature of the injury inflicted on any part of it. It further implies the presence of humoral communications and control networks that assure organ homeostasis and relate this to total body homeostasis.
Abstract 17452: Inter-atrial Conduction Time Can Predict New-onset Atrial Fibrillation After Radiofrequency Ablation of Isolated, Typical Atrial Flutter
Authors: Ryuta Henmi, Koichiro Ejima, Daigo Yagishita, Yuji Iwanami, Moria Shoda, Nobuhisa Hagiwara
Journal: Circulation (2015)

Introduction: Previous studies showed inter-atrial conduction delay (IACT) is an important electrophysiological factor predicting atrial fibrillation (AF) after successful atrial flutter (AFL) ablation. To the best of our knowledge, there has no previous study regarding the prognostic value of IACT as a predictor of new-onset AF after AFL ablation without AF history. Hypothesis: The purpose of this study was to determine the incidence and predictors of new-onset AF after Radiofrequency ablation (RFA) of isolated AFL in a retrospective cohort study. Methods: This study included consecutive patients who underwent successful RFA of isolated, typical AFL from 2004 to 2012. Patients with any history of AF prior to AFL ablation were excluded. IACT was defined as the interval from the onset of P-wave in 12-lead electrocardiogram to atrial intracardiac electrogram at the distal coronary sinus catheter. Results: Eighty patients were included in this study. During a mean follow-up 3.4±2.6 years after successful AFL ablation, 22 patients (27.5%) developed new-onset AF. A Cox regression multivariate analysis demonstrated that IACT was the independent predictor of new-onset AF after AFL ablation (odds ratio: 13.3; 95% confidence interval: 1.36-152.5; p=0.0255). IACT was accurate in predicting new-onset AF (AUC=0.70). The optimal cut-off point of IACT for predicting new-onset AF was ≧120ms, with a sensitivity of 0.476 and a specificity of 0.898. Kaplan-Meier curves showed that new-onset AF after AFL ablation was significantly higher in the patients with IACT ≧120ms compared to the patients with IACT&lt; 120ms (p=0.0016). Conclusions: IACT is an independent risk factor for new-onset AF after AFL ablation without a history of AF.
Abstract 5344: Genome-wide identification of PAX3-FKHR binding sites in rhabdomyosarcoma reveals candidate target genes important for development and cancer
Authors: Liang Cao, Yunkai Yu, Sven Bilke, Robert L. Walker, David O. Azorsa, Lee J. Helman, Paul S. Meltzer
Journal: Cancer Research (2011)

Abstract The paired box transcription factor (PAX) family consists of 9 highly related members with critical roles in organogenesis and tissue specification during development, including skeletal muscle, pancreas, central nervous system, kidney, and immune system. In various cell model systems, PAX genes have been implicated in the maintenance of the multipotent state, the initiation of differentiation programs, cell migration, proliferation and survival. Mutations and gene rearrangement of PAX genes are frequently associated with human diseases and cancers. In particular, PAX3 and PAX7 are required during early embryogenesis for the development of the neural-crest and skeletal muscle, and gene rearrangements with FKHR are frequently implicated with rhabdomyosarcoma (RMS). The PAX3-FKHR fusion protein is present in the majority of alveolar rhabdomyosarcoma (ARMS) associated with increased aggressiveness and poor prognosis. To better understand the molecular pathogenesis of PAX3-FKHR, we carried out the first and unbiased genome-wide identification of PAX3-FKHR binding sites and associated target genes in ARMS, with a novel monoclonal antibody specific for the fusion protein. The data shows that PAX3-FKHR binds to the same sites as PAX3 at both MYF5 and MYOD enhancers. The genome-wide analysis reveals that the PAX3-FKHR sites are: 1) mostly distal to transcription start sites; 2) conserved; 3) enriched for PAX3 motifs; and 4) strongly associated with genes over-expressed in PAX3-FKHR positive RMS cells and tumors. There is little evidence in our dataset for PAX3-FKHR binding at the promoters. The genome-wide analysis further illustrates a strong association between PAX3 and E-box motifs in these binding sites, suggestive of a common co-regulation for many target genes. We further provide the first direct evidence that FGFR4 and IGF1R are the targets for PAX3-FKHR. The study is the first genome-wide analysis of direct targets for a PAX protein. The map of PAX3-FKHR binding sites provides the frame work for the understanding of PAX3-FKHR pathogenic roles and molecular targets to allow a systematic evaluation of agents against this aggressive RMS. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5344. doi:10.1158/1538-7445.AM2011-5344
Rapid Screening of Environmental Chemicals for Estrogen Receptor Binding Capacity
Authors: Randall Bolger, Thomas E. Wiese, Kerry Ervin, Scott Nestich, William Checovich
Journal: Environmental Health Perspectives (1998)

Over the last few years, an increased awareness of endocrine disrupting chemicals (EDCs) and their potential to affect wildlife and humans has produced a demand for practical screening methods to identify endocrine activity in a wide range of environmental and industrial chemicals. While it is clear that in vivo methods will be required to identify adverse effects produced by these chemicals, in vitro assays can define particular mechanisms of action and have the potential to be employed as rapid and low-cost screens for use in large scale EDC screening programs. Traditional estrogen receptor (ER) binding assays are useful for characterizing a chemical's potential to be an estrogen-acting EDC, but they involve displacement of a radioactive ligand from crude receptor preparations at low temperatures. The usefulness of these assays for realistically determining the ER binding interactions of weakly estrogenic environmental and industrial compounds that have low aqueous solubility is unclear. In this report, we present a novel fluorescence polarization (FP) method that measures the capacity of a competitor chemical to displace a high affinity fluorescent ligand from purified, recombinant human ER-[alpha] at room temperature. The ER-[alpha] binding interactions generated for 15 natural and synthetic compounds were found to be similar to those determined with traditional receptor binding assays. We also discuss the potential to employ this FP technology to binding studies involving ER-ss and other receptors. Thus, the assay introduced in this study is a nonradioactive receptor binding method that shows promise as a high throughput screening method for large-scale testing of environmental and industrial chemicals for ER binding interactions.
There are no Classes in the Association—All are Equal and Pay Annually.
Authors: None L. K. W. S.
Journal: JAMA (1893)

great relief and cure the patient before his bladder is dis¬ eased.The dangers are almost nil because the great source of sepsis, the fetid urine, can not touch the wound if it is well packed with iodoform gauze until it heals from the bottom.Open the perineum by the bilateral section, pro¬ ceed as though you intended to enucleate the prostate, but don't.Dress as above described, and the results will prove satisiactory in most instances.
AB0056 Emerging role of IL-33/ST2 axis in endothelial cell injury of lupus nephritis
Authors: S Yu, Y Tao
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> "Alarmins" are prototypic endogenous pro-inflammatory factors as they are released from necotic cells and provoke local damage or systemic inflammation. Evidences are accumulating to support the inclusion of "Alarmins" as targets of autoreactivity as well as inducers in the pathogenesis of Systemic Lupus Erythematosus (SLE). Interleukin (IL)-33 is a novel member of the family of "Alarmins" because of its characteristics and functions in mediating host immune responses. On this background, we sought to determine the role of IL-33/ST2 axis in lupus pathogenesis. The role of IL-33/ST2 axis has not previously been described in lupus nephritis. <h3>Objectives</h3> This project will study the followings: (1) To determine whether IL-33 was present in renal glomerular endothelial cells; (2) To assess the functional and intracellular signal transuction mechanisms regulating the link between IL-33/ST2-mediated innate immunity and inflammation in CD4<sup>+</sup> T cells-endothelial cells co-culture system of lupus patients. <h3>Results</h3> Immunofluorescence (IF) for IL-33 in the kidney were performed in both MRL<sup>lpr</sup> lupus mice and C57BL/6J mice. On double staining for IL-33 and lectin, IL-33 was clearly seen in glomeruli and also in peritubular areas. To determine whether the IL-33 staining in glomeruli and peritubular areas was in endothelium, double IF staining for IL-33 and von Willebrand factor (vWF) was performed. IL-33 co-localized with vWF in glomeruli and in peritubular areas. The increased levels of IL-33 mRNA transcripts were detected in kidney of MRL<sup>lpr</sup> lupus mice compared with C57BL/6J mice. Expression of cell-surface ST2 was increased on the CD4<sup>+</sup> T cells of lupus patients when compared with healthy controls. Serum sST2 level was significantly higher in SLE patients with <i>flare</i> than those without <i>flare</i> (p&lt;0.05). <h3>Conclusions</h3> As a result of external stimuli or infection, renal glomerular endothelial cells undergo cellular death and release the "Alarmin", IL-33, to alert the lupus immune system. Released IL-33 interact with their target cells, CD4<sup>+</sup> T cells via their specific receptor ST2 to subsequently induce innate and adaptive responses, activate inflammatory pathways in the pathogenesis of lupus nephritis. <h3>Disclosure of Interest</h3> None declared
Platelet factor V New York: A defect in factor V distinct from that in factor V Quebec resulting in impaired prothrombinase generation
Authors: Harvey J. Weiss, Bruce Lages, Shilun Zheng, Catherine P.M. Hayward
Journal: American Journal of Hematology (2001)

Studies were performed on a patient with a longstanding bleeding disorder whose major defects were impaired platelet prothrombinase activity in the absence of added factor Va, and a platelet factor V value that was either decreased or at the lower limit of normal when assayed on multiple occasions.In contrast, plasma factor V values were consistently normal.Unlike Scott Syndrome, in which platelet prothrombinase activity is decreased in both the presence and absence of added factor V, her platelets appeared to utilize added factor Va normally in supporting the generation of prothrombinase activity.These findings suggest an intrinsic defect in platelet factor V as the basis of her platelet prothrombinase defect.This defect appears to be different than that described in the Quebec platelet disorder (factor V Quebec).Immunoblot analyses of washed platelet lysates demonstrated a pattern of variably sized factor V molecules that was entirely similar to that observed in normal platelets, and both the heavy and light chains of her factor V after thrombin cleavage were of the same size as that observed in normal platelets.In addition, her platelet multimerin was normal and immunoblot analysis excluded the type of generalized granular protein defect and pathological proteolysis that has been suggested to explain the factor V defect in the Quebec platelet disorder.The findings in this patient thus suggest a new type of platelet factor V defect as the basis for the impaired capacity of her activated platelets to support prothrombinase generation.The findings further support an important role for platelet factor V in hemostasis.