tbuckley/cabot-search huggingface dataset:
"Who Goes There?"—A Critical Evaluation of Admissions to a Psychiatric Day Hospital
Authors: GERARD E. HOGARTY, HELEN DENNIS, WILLIAM GUY, GERTRUDE M. GROSS
Journal: American Journal of Psychiatry (1968)

Day hospitalization has been cited as a means of circumventing inpatient confinement. This would imply, however, that day hospital patients are representative of inpatient admissions. Comparing Baltimore Psychiatric Day Center patients with other patient groups, these authors found that the day hospital sample does not resemble a typical inpatient group. Both day center admission criteria and community referral sources foster selectivity along socioeconomic and symptomatologic lines, so that day hospitalization, as it is currently practiced, does not necessarily represent a true alternative to inpatient hospitalization.
Clearance of Immunoreactive Somatostatin by Perfused Rat Liver
Authors: Harold Sacks, L. Cass Terry
Journal: Journal of Clinical Investigation (1981)

Other investigators have demonstrated that concentrations of immunoreactive somatostatin (IRS) are higher in blood from the hepatic portal vein or its tributaries than in blood from the hepatic or peripheral systemic veins of man and animals. This suggests that there is hepatic extraction of IRS from the portal system in vivo. In the rat, portal vein plasma IRS is reported to be heterogeneous and to contain, in part, a 1,600 mol wt form of IRS which is immunochemically similar to synthetic somatostatin and not significantly bound to high molecular weight plasma protein. Our study was undertaken to determine directly whether unbound synthetic cyclic somatostatin was cleared by the rat liver perfused through the hepatic portal vein in vitro with a recirculating, plasma-free, erythrocyte-containing perfusate.
ELISpot as a predictor for development of TB in children with TB contact
Authors: N Sharma
Journal: Thorax (2009)

T cell interferon γ release assays such as the enzyme-linked immunospot (ELISpot) assay are widely used to diagnose latent tuberculosis (TB) infection. Currently, however, there are few data on the benefit of such tests in predicting active TB infection among exposed individuals. This study focuses on the prognostic value of such assays in children with recent household exposure to TB compared …
Hepatic effects of fenzlozic acid.
Authors: F D Hart, L S Bain, E C Huskisson, T R Littler, R T Taylor
Journal: Annals of the Rheumatic Diseases (1970)

Fenclozic acid (I.C.I. 54,450: Myalex) has recently been withdrawn from trial because of hepatotoxicity.In a published trial (Chalmers, Kellgren, and Platt, 1969), which suggests that it has some effect as an anti-inflammatory agent in rheumatoid arthritis, up to 400 mg.fenclozic acid were given daily for 10 days to 40 patients and compared with 3 6 g. aspirin daily.Two of these patients showed abnormal serum glutamic-oxaloacetic transaminase (SGOT) values after treatment with fenclozic acid.As more patients had raised SGOT values after treatment with aspirin it was concluded that further evaluation of fenclozic acid was justified. Present investigationWe have recently completed trials of fenclozic acid in rheumatoid arthritis.Eight patients developed jaundice or abnormalities of hepatic function, as City Hospital, Aberdeen, and the General Hospital, detailed in the Table .As these investigations were performed in different laboratories, the normal values for each laboratory are also given.The four patients who became jaundiced had received fen- clozic acid for 17 to 35 days.
“Cheerleaders Pep Up Drug Sales,” New York Times reports
Authors: Janice Hopkins Tanne
Journal: BMJ (2005)

US drug companies are hiring cheerleaders as sales representatives to promote drugs to doctors, the New York Times said on its front page on 28 November. The story claimed that drug companies were turning to cheerleaders as sales people because they were good looking and had enthusiastic outgoing personalities.

“Some industry critics view wholesomely sexy drug representatives as a variation on the seductive inducements, like dinners, golf outings, and speaking fees that pharmaceutical companies have dangled to sway doctors to their brands,” the story reported.

Psychiatrist Thomas Carli, an associate professor at the University of Michigan, who has tried to …
p27kip1 regulates the apoptotic response of gastric epithelial cells to Helicobacter pylori
Authors: H Eguchi
Journal: Gut (2004)

<b>Background:</b><i>Helicobacter pylori</i> infection increases the risk of gastric cancer but the molecular mechanisms responsible are not well understood. Gastric cells chronically exposed to <i>H pylori</i> in vitro develop resistance to apoptosis associated with low levels of p27, a cyclin dependent kinase inhibitor and haplo insufficient tumour suppressor gene that is downregulated in gastric cancer. <b>Aim:</b> To determine whether the low level of p27 protein is responsible for the resistance to apoptosis of gastric cancer cells. <b>Methods:</b> The effects of increasing the expression of p27 protein were examined by transiently and stably transfecting a plasmid encoding full length p27 mRNA into apoptosis resistant gastric cancer cell lines with low p27 expression that were derived from AGS gastric cancer cells by chronic <i>H pylori</i> coculture followed by dilutional cloning. <b>Results:</b> Low p27 expression in the apoptosis resistant derivative cell lines was associated with an approximate 30% decrease in p27 mRNA and an 80% decrease in p27 protein that was not due to increased proteasome dependent degradation of p27 protein. Transient or stable transfection with p27 constructs partially restored the sensitivity of the apoptosis resistant cells to 5-fluorouracil and <i>H pylori</i> induced apoptosis without altering spontaneous apoptotic cell death. <b>Conclusions:</b> These results demonstrate that p27 positively regulates, at least in part, the apoptotic response of gastric epithelial cells to <i>H pylori</i>. Low gastric p27 may promote gastric carcinogenesis associated with <i>H pylori</i> infection by inhibiting apoptotic pathways.
In the RyR2 <sup>R4496C</sup> Mouse Model of CPVT, β-Adrenergic Stimulation Induces Ca Waves by Increasing SR Ca Content and Not by Decreasing the Threshold for Ca Waves
Authors: Takeshi Kashimura, Sarah J. Briston, Andrew W. Trafford, Carlo Napolitano, Silvia G. Priori, David A. Eisner, Luigi A. Venetucci
Journal: Circulation Research (2010)

mutations of the ryanodine receptor (RyR) cause catecholaminergic polymorphic ventricular tachycardia (CPVT). These mutations predispose to the generation of Ca waves and delayed afterdepolarizations during adrenergic stimulation. Ca waves occur when either sarcoplasmic reticulum (SR) Ca content is elevated above a threshold or the threshold is decreased. Which of these occurs in cardiac myocytes expressing CPVT mutations is unknown.we tested whether the threshold SR Ca content is different between control and CPVT and how it relates to SR Ca content during β-adrenergic stimulation.ventricular myocytes from the RyR2 R4496C(+/-) mouse model of CPVT and wild-type (WT) controls were voltage-clamped; diastolic SR Ca content was measured and compared with the Ca wave threshold. The results showed the following. (1) In 1 mmol/L [Ca(2+)](o), β-adrenergic stimulation with isoproterenol (1μmol/L) caused Ca waves only in R4496C. (2) SR Ca content and Ca wave threshold in R4496C were lower than those in WT. (3) β-Adrenergic stimulation increased SR Ca content by a similar amount in both R4496C and WT. (4) β-Adrenergic stimulation increased the threshold for Ca waves. (5) During β-adrenergic stimulation in R4496C, but not WT, the increase of SR Ca was sufficient to reach threshold and produce Ca waves.in the R4496C CPVT model, the RyR is leaky, and this lowers both SR Ca content and the threshold for waves. β-Adrenergic stimulation produces Ca waves by increasing SR Ca content and not by lowering threshold.
Temporal Pathogenesis of Experimental Neonatal Woodchuck Hepatitis Virus Infection: Increased Initial Viral Load and Decreased Severity of Acute Hepatitis During the Development of Chronic Viral Infection
Authors: Paul J. Cote, Ilia Toshkov, Christine Bellezza, Mary Ascenzi, Carol Roneker, Lou Ann Graham, Betty H. Baldwin, Karen Gaye, Ikuo Nakamura, Brent E. Korba, Bud C. Tennant, John L. Gerin
Journal: Hepatology (2000)

Acute hepatitis B virus (HBV) infections either resolve or progress to chronicity. Identification of early deviations in host-virus responses associated with these outcomes can further differentiate cause-effect mechanisms that initiate and maintain chronicity. Neonatal woodchucks were infected experimentally with the woodchuck hepatitis virus (WHV) at 3 days of age. At 8 or 14 weeks of age (i.e. , the early- or mid-acute stage of infection), whole blood and large surgical biopsies of the liver were obtained from infected animals and uninfected controls. These were stored for later correlating histopathologic responses and viral load with the subsequently determined outcome of infection. As of 1 year postinfection, half of the surgically treated infected woodchucks had developed self-limited infections, while the other half developed chronic infections. The self-limited outcome was characterized by decreased viral load in acute-phase liver and plasma and a generally robust acute hepatic inflammatory response. Comparisons at the same early time points revealed that the chronic outcome was characterized by increasing initial viral load in liver and plasma, and a detectable, but diminished, acute hepatic inflammation. These cotemporal comparisons indicate that there is an early host-response deviation during the acute phase of a developing chronic infection. Continued analysis of the tissues banked from this study will facilitate further temporal characterization of acute-phase mechanisms that determine resolution versus chronicity in WHV infection. Understanding such mechanisms may be useful in the rational design of therapy for established chronic HBV infection.
Macrophage polarization in interstitial lung diseases
Authors: Pawel Wojtan, Michal Mierzejewski, Iwona Osinska, Joanna Domagala-Kulawik
Journal: European Respiratory Journal (2014)

The role of BALf examination in differential diagnosis of interstitial lung diseases (ILD) was established. Macrophages are most numerous cell population retrieved by BAL. Recently, functional polarization into M1 (pro-inflammatory) and M2 (anti-inflammatory) subpopulations is emphasized.  The aim of our study was to compare proportion of M1 and M2 in the BALf of patients with different ILD.  BALf samples were collected from 75 patients with ILD: sarcoidosis (SA, 36), hypersensitivity pneumonitis (HP, 10), non-specific interstitial pneumonia (NSIP, 8), idiopathic pulmonary fibrosis (IPF, 6) and other ILD (15). Phenotyping was performed by immunocytochemistry with antibodies anti-CD40 and CD163 (for M1 and M2 respectively). Initially, we confirmed the specificity of this staining on cultured macrophages.  For both, CD40 and CD163, three populations of cells have been specified: small cells with strong (+++), large cells with weak (+) and cells with no (-) reaction (Photo).  We found significantly higher proportion of M1 cells in SA when compared with other ILD (table, median values).  No differences between HP, NSIP, IPF were found. There was positive correlation between proportion of CD40+ cells with the number of lymphocytes in SA group.  Our study showed polarization of BALf macrophages towards M1 population in SA and indicated their possible role in granuloma formation.
Keeping the Fire Alive
Authors: Stacey Marie Kerr
Journal: JAMA (2004)

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
Actin from Heart Muscle: Sulfhydryl Groups
Authors: ARNOLD M. KATZ, JOYCE B. MAXWELL
Journal: Circulation Research (1964)

The number and reactivity of the sulfhy-dryl groups of cardiac and skeletal actin preparations have been examined, using material from dogs and rabbits. The number of sulfhy-dryl groups of all actins was approximately six per mole, two of which could be characterized as fast-reacting and were not essential for polymerization. The time course of the reaction of the sulfhydryl groups of heart and skeletal actins with - p mercuribenzoate were identical, and the effects of Ca ++ Mg ++ and adenosinetriphosphate upon this reaction were similar for actins from the two tissues. In accord with previous structural comparisons, no difference between cardiac and skeletal actin has been detected.
Molecular Mechanisms of Cyclosporin A Inhibition of the Cytokine-Induced Matrix Metalloproteinase-9 in Glomerular Mesangial Cells
Authors: Anke Doller, El-Sayed Akool, Roswitha Müller, Paul Gutwein, Christine Kurowski, Josef Pfeilschifter, Wolfgang Eberhardt
Journal: Journal of the American Society of Nephrology (2007)

The effects of the immunosuppressants cyclosporin A (CsA) and tacrolimus (FK506) on the IL-1beta-induced matrix metalloproteinase-9 (MMP-9) were investigated. Impairment of the protease-antiprotease balance contributes to renal fibrosis, which is observed collectively under long-term treatment with either immunosuppressant. It is demonstrated that CsA, in contrast to FK506, reduced the IL-1beta-induced MMP-9 content in conditioned media of mesangial cells, which coincides with a reduction in the cytokine-induced MMP-9 mRNA level. Similar to FK506, the VIVIT peptide, a specific inhibitor of the nuclear factor of activated T cells, did not affect the cytokine-induced MMP-9 level. Moreover, CsA caused a dose-dependent inhibition on the IL-1beta-induced luciferase activity of a 1.3-kb MMP-9 promoter fragment. Concomitant, electrophoretic mobility shift assay revealed that CsA selectively inhibits the cytokine-induced DNA binding of activator protein-1 and NF-kappaB. The effects on NF-kappaB binding were accompanied by a marked reduction in the nuclear content of the p65 subunit of NF-kappaB. Accordingly, CsA specifically impaired the IL-1beta-triggered degradation of inhibitory NF-kappaB. The suppressive effects by CsA on MMP-9 expression were accompanied by a reduction in the cytokine-induced phosphorylation of p42/p44 and c-Jun N-terminal Kinase (JNK). It is interesting that only the JNK inhibitor SP600125 impaired the cytokine-triggered MMP-9 level, suggesting that CsA, via inhibition of the JNK pathway, negatively interferes with the NF-kappaB-dependent transcriptional control of MMP-9. Interference with MMP-9 transcription may account for the accumulation of extracellular matrix underlying the high fibrotic potential of CsA during anti-inflammatory therapies with calcineurin inhibitors.
Langerhans cells in lichen planus
Authors: M. Piepkorn
Journal: British Journal of Dermatology (1983)

Journal Article Langerhans cells in lichen planus Get access M. Piepkorn M. Piepkorn Division of Dermatology, Medical Center, 50 North Medical Drive, Salt Lake City, Utah 84132, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 108, Issue 6, 1 June 1983, Page 736, https://doi.org/10.1111/j.1365-2133.1983.tb01091.x Published: 01 June 1983
Proposals and rationale for revision of the World Health Organization diagnostic criteria for polycythemia vera, essential thrombocythemia, and primary myelofibrosis: recommendations from an ad hoc international expert panel
Authors: Ayalew Tefferi, Juergen Thiele, Attilio Orazi, Hans Michael Kvasnicka, Tiziano Barbui, Curtis A. Hanson, Giovanni Barosi, Srdan Verstovsek, Gunnar Birgegard, Ruben Mesa, John T. Reilly, Heinz Gisslinger, Alessandro M. Vannucchi, Francisco Cervantes, Guido Finazzi, Ronald Hoffman, D. Gary Gilliland, Clara D. Bloomfield, James W. Vardiman
Journal: Blood (2007)
A case of hepatopulmonary syndrome solved by mycophenolate mofetil (an inhibitor of angiogenesis and nitric oxide production)
Authors: Helena Moreira Silva, Guilhermina Reis, Margarida Guedes, Esmeralda Cleto, José Ramón Vizcaíno, Deirdre Kelly, Andrew R. Gennery, Ermelinda Santos Silva
Journal: Journal of Hepatology (2012)

The autoimmune lymphoproliferative syndrome (ALPS) is a rare, multisystemic disease, caused by an inherited defect in the Fas apoptotic pathway, characterized by a chronic non-malignant lymphoid accumulation and autoimmune manifestations. Lung, kidney, liver, and gut infiltration is described in severe, multisystemic cases; so far there has been no description of hepatopulmonary syndrome (HPS), for which orthotopic liver transplantation (OLT) is currently the only known effective treatment. A teenage boy, diagnosed with ALPS at 4years of age (lymph nodes enlargement, splenomegaly, immune cytopenias), was stable until 13years of age, when he developed insidious hypoxemia (PaO<sub>2</sub>=46.7mmHg). He was diagnosed with HPS on the basis of hypoxemia, non-cirrhotic liver disease with portal hypertension, and pulmonary vascular dilatation (intrapulmonary shunt=45%). He was treated with oxygen (maximum 6L/min), prednisolone and sirolimus. There was significant regression of all manifestations of ALPS, except for the pulmonary symptoms, therefore, after evaluation in referral centers in England, OLT was proposed. Since he was to undergo major surgery, sirolimus, which has wound-healing problems, was switched to mycophenolate mofetil (MMF). Following this change, we observed a huge improvement in pulmonary symptoms and reduction of oxygen needs. The intrapulmonary shunt decreased from 45% to 0% in less than a year, and it has not changed since (18months after complete normalization), on continued treatment with MMF. Indication for OLT was suspended. In the last year, lymphoid proliferation increased again, with huge splenomegaly, but no recurrence of HPS. The addition of sirolimus to MMF produced again a rapid resolution of lymphoid proliferation. The dramatic and unexpected regression of HPS may have been due to inhibition of angiogenesis and nitric oxide (NO) production by MMF (both important pathways/mediators in HPS pathogenesis). Therefore, we propose to perform clinical trials with MMF, and/or other angiogenesis and NO inhibitors, on a long-term treatment basis, to confirm their potential as a valid alternative to medical treatment of HPS.
DNA repair gene polymorphisms and risk of adult meningioma, glioma, and acoustic neuroma
Authors: P. Rajaraman, A. Hutchinson, S. Wichner, P. M. Black, H. A. Fine, J. S. Loeffler, R. G. Selker, W. R. Shapiro, N. Rothman, M. S. Linet, P. D. Inskip
Journal: Neuro-Oncology (2009)

Although the etiology of primary brain tumors is largely unknown, prior studies suggest that DNA repair polymorphisms may influence risk of glioma. Altered DNA repair is also likely to affect the risk of meningioma and acoustic neuroma, but these tumors have not been well studied. We estimated the risk of glioma (n = 362), meningioma (n = 134), and acoustic neuroma (n = 69) in non-Hispanic whites with respect to 36 single nucleotide polymorphisms from 26 genes involved in DNA repair in a hospital-based, case–control study conducted by the National Cancer Institute. We observed significantly increased risk of meningioma with the T variant of GLTSCR1 rs1035938 (ORCT/TT = 3.5; 95% confidence interval: 1.8–6.9; Ptrend .0006), which persisted after controlling for multiple comparisons (P = .019). Significantly increased meningioma risk was also observed for the minor allele variants of ERCC4 rs1800067 (Ptrend .01); MUTYH rs3219466 (Ptrend .02), and PCNA rs25406 (Ptrend .03). The NBN rs1805794 minor allele variant was associated with decreased meningioma risk (Ptrend .006). Risk of acoustic neuroma was increased for the ERCC2 rs1799793 (Ptrend .03) and ERCC5 rs17655 (Ptrend .05) variants and decreased for the PARP1 rs1136410 (Ptrend .03). Decreased glioma risk was observed with the XRCC1 rs1799782 variant (Ptrend .04). Our results suggest that common DNA repair variants may affect the risk of adult brain tumors, especially meningioma.
Survival and Late Mortality in Long-Term Survivors of Pediatric CNS Tumors
Authors: E. Brannon Morris, Amar Gajjar, James O. Okuma, Yutaka Yasui, Dana Wallace, Larry E. Kun, Thomas E. Merchant, Maryam Fouladi, Alberto Broniscer, Leslie L. Robison, Melissa M. Hudson
Journal: Journal of Clinical Oncology (2007)

To describe the pattern of survival and late mortality among contemporary long-term survivors of pediatric CNS tumor.The study population comprised 643 pediatric patients with primary CNS tumor treated at St Jude Children's Research Hospital (Memphis, TN) from 1985 to 2000 who survived > or = 5 years from diagnosis. Patients were classified according to primary tumor type, location of tumor, and survival. Cause of death was obtained from the medical record and categorized as progression, malignant transformation, second malignancy, medical complication, or external cause.Overall survival estimates for patients who survived at least 5 years postdiagnosis was 91.3% +/- 2% and 86% +/- 3% at 10 and 15 years postdiagnosis, respectively. A significant difference in the survival rates according to original tumor type (P = .001) was seen. Sixty-six (10%) of 643 patients experienced late mortality: 38 patients (58%) died of progressive disease while 14 patients (21%) died of second malignant tumor. Twelve patients (18%), predominantly with diencephalic tumor location, died of a specific medical cause: cardiovascular disease (n = 2), cerebrovascular accident (n = 1), metabolic collapse and/or sepsis (n = 7), respiratory failure (n = 1), or shunt malfunction (n = 1).Late mortality occurs in a substantial number of long-term survivors of pediatric CNS tumors and is most influenced by the initial tumor histopathology. Progressive disease remains the most common cause of death within the first decade of diagnosis. Teenage patients requiring treatment for panhypopituitarism may be especially vulnerable and deserve significant medical surveillance.