tbuckley/cabot-search huggingface dataset:
Photocatabolism of labeled bilirubin in the congenitally jaundiced (Gunn) rat
Authors: J. Donald Ostrow
Journal: Journal of Clinical Investigation (1971)

To elucidate the mechanism by which phototherapy reduces serum bilirubin, studies were performed on the catabolism of labeled bilirubin in homozygous jaundiced Gunn rats before, during, and after a period of exposure to 1700 foot candles of daylight fluorescent light. Following equilibration with the body pool of an intravenously administered tracer dose of (3)H- or (14)C-bilirubin, radioactive and diazo reactive compounds were excreted in the bile at a slow, steady rate and plasma specific activity declined semilogarithmically. Subsequent exposure to light caused a marked increase in the biliary excretion of radioactive and diazoreactive compounds. Fecal and urinary radioactivity increased also but remained minor fractions of the total excreted radioactivity. After extinguishing the lights, these variables reverted gradually to control values. Spectral and chromotographic analysis of the excreted pigments and their azopigments demonstrated that the increased biliary radioactivity during phototherapy consisted of two roughly equal fractions: (a) unconjugated bilirubin, excreted at rates comparable to the output of conjugated bilirubin in the bile of normal nonjaundiced rats; and (b) water-soluble bilirubin derivatives, chromatographically identical with those found in Gunn rat bile under control lighting conditions but different from the products of photodecomposition of bilirubin in vitro. In some animals, phototherapy produced little decline in plasma bilirubin despite comparable acceleration of bilirubin catabolism. This was attributed tentatively to increased synthesis of early labeled bilirubin in these animals.
Prognostic Value of Health-Related Quality-of-Life Data in Predicting Survival in Patients With Anaplastic Oligodendrogliomas, From a Phase III EORTC Brain Cancer Group Study
Authors: Murielle E.L. Mauer, Martin J.B. Taphoorn, Andrew Bottomley, Corneel Coens, Fabio Efficace, Marc Sanson, Alba A. Brandes, Carin C.D. van der Rijt, Hans J.J.A. Bernsen, Marc Frénay, Cees C. Tijssen, Denis Lacombe, Martin J. van den Bent
Journal: Journal of Clinical Oncology (2007)

This is one of a few studies that have explored the value of baseline symptoms and health-related quality of life (HRQOL) in predicting survival in patients with brain cancer.Baseline HRQOL scores (from the European Organisation for Research and Treatment of Cancer [EORTC] Quality of Life Questionnaire C30 and the EORTC Brain Cancer Module) were examined in 247 patients with anaplastic oligodendrogliomas to determine the relationship with overall survival by using Cox proportional hazards regression models. Refined techniques as the bootstrap resampling procedure and the computation of C indexes and R2 coefficients were used to explore the stability of the models as well as better assess the potential benefit of using HRQOL to predict survival in clinical practice and research.Classical analysis controlled for major clinical prognostic factors selected emotional functioning (P = .0016), communication deficit (P = .0261), future uncertainty (P = .0481), and weakness of legs (P = .0001) as statistically significant prognostic factors of survival. However, several issues question the validity of these findings and no single model was found to be preferable over all others. C indexes, which estimate the probability of a model to correctly predict which patient among a randomly chosen pair of patients will survive longer, and R2 coefficients, which measure the proportion of variability explained by the model, did not exhibit major improvement when adding selected or all HRQOL scores to clinical factors.While classical techniques lead to positive results, more refined analyses suggest that baseline HRQOL scores add relatively little to clinical factors to predict survival. These results may have implications for future use of HRQOL as a prognostic factor for patients with cancer.
Chronic calcifying pancreatitis in rheumatic diseases.
Authors: C Hortas, G de Las Heras, M J Lopez-Arias, L Martin, F Pons-Romero
Journal: Annals of the Rheumatic Diseases (1995)

We agree with Dr Berthelot that technical details, such as storage time of samples, should be included in APF studies.It is nevertheless difficult to evaluate retros- pectively the effect of storage time or patient's age on APF positivity.For two of our patients, we assayed three serum samples collected over a period of four years and stored for one to five years.In each case, the initial APF was negative, but the following two were positive.However, it is difficult to conclude if this is a result of a shorter storage time, the patients growing older, or other variables.In our study, APF was most prevalent in the polyarticular onset, sero- positive JRA group, which typically consists of older children, mostly teenagers.However, it is not clear if this is related to the patients' ages or, most likely, to their type of JRA, which closely resembles adult RA.We did not find any difference in APF occurrence between younger and older JRA patients with pauciarticular and seronegative polyarticular onset diseases.These data underline the observation that APF testing can be influenced by many variables, especially in children, thus empha- sising the need to define APF positivity in JRA on the basis of universal criteria.
The erythemal response to ultraviolet radiation in subjects with polymorphic light eruption
Authors: B.L. DIFFEY, P.M. FARR
Journal: British Journal of Dermatology (1986)

A reflectance instrument was used to measure objectively the erythemal response to UV-B and UV-C radiation in subjects with polymorphic light eruption. The characteristics of the dose-response curves obtained for each quality of ultraviolet radiation were significantly different, but were essentially indistinguishable from the comparable dose-response curves measured previously in normal subjects. It is concluded that in this photodermatosis the chromophore(s) and mediator(s) of delayed (24 h) ultraviolet-induced erythema are identical to those in normal skin.
THE EFFICACY OF Tc-99m SESTAMIBI AND THALLIUM 201/Tc-99m PERTECHNETATE SCINTIGRAPHY IN LOCALIZING PARATHYROID ADENOMAS IN PATIENTS WITH PRIMARY HYPERPARATHYRODISM
Authors: J D Rauth, H A Ziessman, E A Akin, S C Shupe, R B Sessions
Journal: Clinical Nuclear Medicine (1996)
Endothelin-1 is an autocrine/paracrine growth factor for human cancer cell lines.
Authors: M Shichiri, Y Hirata, T Nakajima, K Ando, T Imai, M Yanagisawa, T Masaki, F Marumo
Journal: Journal of Clinical Investigation (1991)

We studied whether a novel vasoconstrictor peptide, endothelin-1 (ET-1), is synthesized by and released from human carcinoma cell lines, and whether ET-1 stimulates proliferation of these tumor cells. ET-1-like immunoreactivity was released from both HeLa and HEp-2 cells as a function of time. Reverse-phase HPLC of the conditioned media from HeLa cells revealed a major peak coeluting with standard ET-1. Northern blot analysis demonstrated the expression of mRNA for ET-1 precursor in both tumor cell lines. Both cell lines contained a single class of specific binding sites for ET-1. ET-1 dose-dependently induced increases in cytosolic free Ca2+ concentration in fura-2-loaded tumor cells, whose effect was completely abolished by chelating extracellular Ca2+ or by Ca(2+)-channel blocker. ET-1 stimulated proliferation of the quiescent cell lines in a dose-dependent manner, whose effect was inhibited by Ca(2+)-channel blocker. Polyclonal antibody for ET-1 inhibited proliferation of these cell lines, whereas nonimmune serum had no effect. These results demonstrate that ET-1 is synthesized by and released from human epithelial carcinoma cell lines, and that exogenous and endogenous ET-1 stimulates proliferation of the cells possibly through Ca2+ influx, suggesting its role as an autocrine/paracrine growth factor for certain tumor cells.
Abstract 11966: Maximal Stroke Volume and Total Blood Volume Are Not Reduced with Healthy Aging Despite a Reduction in VO2max: The Critical Nature of Allometric Scaling
Authors: Graeme C Carrick-Ranson, Jeffrey L Hastings, Naoki Fujimoto, Shigeki Shibata, Dean Palmer, Kara Boyd, Paul S Bhella, Benjamin D Levine
Journal: Circulation (2011)

Purpose: Maximal exercise capacity declines with healthy aging as evident by a reduction in maximal oxygen uptake (VO2max). Small sample cross-sectional studies have shown that total blood volume (...
Clinical Profile of Idiopathic Chronic Pancreatitis in North India
Authors: Deepak K. Bhasin, Gursewak Singh, Surinder S. Rana, Shoket M. Chowdry, Nusrat Shafiq, Samir Malhotra, Saroj K. Sinha, Birinder Nagi
Journal: Clinical Gastroenterology and Hepatology (2009)
An effective interferon-gamma-mediated inhibition of hepatitis C virus replication by natural killer cells is associated with spontaneous clearance of acute hepatitis C in human immunodeficiency virus-positive patients
Authors: Pavlos Kokordelis, Benjamin Krämer, Christian Körner, Christoph Boesecke, Esther Voigt, Patrick Ingiliz, Andreas Glässner, Marianne Eisenhardt, Franziska Wolter, Dominik Kaczmarek, Hans Dieter Nischalke, Jürgen K. Rockstroh, Ulrich Spengler, Jacob Nattermann
Journal: Hepatology (2014)

Hepatitis C virus (HCV) coinfection is an increasing health problem in human immunodeficiency virus-positive (HIV+) individuals. However, a considerable proportion of HIV+ patients manage to overcome acute hepatitis C (AHC) spontaneously. In the present study, we analyzed the role of natural killer (NK) cells in modulating the course of AHC in HIV+ patients. Twenty-seven HIV+ patients with AHC (self-limited course: n = 10; chronic course: n = 17), 12 HIV+ patients with chronic hepatitis C (CHC), 8 HIV monoinfected individuals, and 12 healthy controls were studied. NK cells were phenotypically analyzed by flow cytometry. Interferon-gamma (IFN-γ) secretion, degranulation (CD107a), and anti-HCV (= inhibition of HCV replication) activity of NK subpopulations were analyzed using the HuH7A2HCVreplicon cell system. NK cell frequency did not differ significantly between HIV+ patients with chronic and self-limited course of AHC. However, we found NK cells from patients with self-limiting infection to be significantly more effective in inhibiting HCV replication in vitro than NK cells from patients developing CHC. Of note, antiviral NK cell activity showed no significant correlation with NK cell degranulation, but was positively correlated with IFN-γ secretion, and blocking experiments confirmed an important role for IFN-γ in NK cell-mediated inhibition of HCV replication. Accordingly, NK cells from patients that spontaneously cleared the virus displayed a stronger IFN-γ secretion than those developing chronic infection. Finally, we observed high expression of NKG2D and NKp46, respectively, to be associated with self-limiting course of aHCV. Accordingly, we found that blocking of these NK cell receptors significantly impaired antiviral NK cell activity. Conclusion: Our data suggest a strong IFN-γ-mediated antiviral NK cell response to be associated with a self-limited course of AHC in HIV+ patients. (Hepatology 2014;59:814–827)
Interleukin 1 inhibits insulin secretion from isolated rat pancreatic islets by a process that requires gene transcription and mRNA translation.
Authors: J H Hughes, J R Colca, R A Easom, J Turk, M L McDaniel
Journal: Journal of Clinical Investigation (1990)

Recombinant human IL 1 beta inhibits glucose-induced insulin secretion from isolated pancreatic islets and from purified beta-cells obtained by fluorescence-activated cell sorting (FACS) of dispersed islet cells. Brief (1 h) exposure of isolated islets to IL 1 produces sustained inhibition of insulin secretion for at least 17 h after the IL 1 has been removed from the culture medium. An inhibitory effect of IL 1 on insulin secretion is not observed when islets are coincubated with an inhibitor of DNA transcription (actinomycin D). This finding indicates that the inhibitory effect of IL 1 on insulin secretion requires transcription of one or more genes during the first hour of exposure of islets to IL 1. The inhibitory effect of IL 1 on insulin secretion also requires mRNA translation, because three structurally distinct inhibitors of protein synthesis (cycloheximide, anisomycin, and puromycin) prevent IL 1-induced inhibition of insulin secretion when added to islets after the 1-h exposure to IL 1. Two-dimensional gel electrophoresis of islet proteins metabolically labeled with [35S]methionine demonstrates that IL 1 augments the expression of a 65-kD (pl approximately 6.5) protein by greater than 2.5-fold. These findings indicate that biochemical events occurring within 1 h of exposure of islets to IL 1 lead to an inhibition of insulin secretion that persists for at least 17 h after the removal of IL 1. One of the early biochemical effects of IL 1 on islets is gene transcription (0-1 h), which is followed by mRNA translation (after 1 h). Our results suggest that the inhibitory effect of IL 1 on insulin secretion is mediated by protein(s) whose synthesis is induced by IL 1.
Methane Production in the Gut
Authors: Michael D. Levitt
Journal: New England Journal of Medicine (1974)

Although gas production in the human intestinal tract has long been a topic of considerable interest to the lay public, this subject has received little scientific attention. Much of what is known about bacterial gas production in the gut has resulted from veterinary studies. This disproportionate attention to the "gas" of animals is motivated not by concern for their flatulent discomfort but rather for the financial implications of gas production in ruminants.Methane, the primary constituent of natural gas, is liberated in the rumen by strictly anerobic organisms via a reaction in which carbon dioxide is reduced to methane by . . .
ICE-Classification of Interatrial Septum Anatomy in Patients With R→L Shunt
Authors: Gianluca Rigatelli, Fabio Dell'Avvocata, Dobrin Vassiliev, Ramesh Daggubati, Ashesh Buch, Aravinda Nanjiundappa, Massimo Giordan, Laura Oliva, Dario Adami, Paolo Cardaioli
Journal: JACC. Cardiovascular imaging (2014)
Drug Delivery: Macromolecular Prodrugs of Ribavirin: Concerted Efforts of the Carrier and the Drug (Adv. Healthcare Mater. 9/2014)
Authors: Anton A. A. Smith, Benjamin M. Wohl, Mille B. L. Kryger, Natasha Hedemann, Carlos Guerrero‐Sanchez, Almar Postma, Alexander N. Zelikin
Journal: Advanced Healthcare Materials (2014)

Automated parallel synthesis is applied by A. Postma, A. Zelikin, and team on page 1404 to obtain libraries of macromolecular prodrugs of ribavirin. Polymers differ in their average molar mass and drug content, the two parameters independently vary in broad respective ranges. Screening the libraries for intracellular activity identifies at least 10 formulations with efficacy matching that of the drug and at the same time significantly reducing toxicity.
Abstract 3985: MicroRNA-21 regulates Sox2 expression and tumor self-renewal in PDGF-driven glioma
Authors: Pernilla Roswall, Jelena Põlajeva, Fredrik J. Swartling, Yiwen Jiang, Umashankar Singh, Lene Uhrbom, Bengt Westermark
Journal: Cancer Research (2011)

Abstract The Platelet-Derived Growth Factor (PDGF) has a known role in the progression of malignant primary brain tumors, glioma, but the mechanisms behind PDGF-driven brain tumor development are still not clarified. MicroRNAs regulate many genes in our genome at a post-transcriptional level. We recently identified microRNA-21 (miR-21) as a target in a retroviral screen for candidate brain tumor initiating genes in mice. To explore a role for miR-21 in brain tumors we used Northern blot and in situ hybridization to show that the expression levels of miR-21 in PDGF-induced mouse brain tumors and primary mouse glioma cell lines were strongly increased as compared to normal mouse brain. In normal fibroblasts, the expression of miR-21 was induced by a number of growth factors, including PDGF-B, suggesting miR-21 is downstream of PDGF signaling. By inhibiting PDGF-B with siRNA in Sox2-expressing mouse glioma initiating cells, we showed that miR-21 expression could be suppressed, followed by a decrease in tumor cell self-renewal. To understand the mechanisms of miR-21 in normal development, we identified miR-21 to be highly expressed during embryonic development and in newborn brain with its expression turned off before postnatal day 7 (P7) in the mouse brain. The expression of miR-21 overlapped with Sox2 expression in embryonic and newborn normal mouse brain, whose expression levels similarly decreased at P7. In situ hybridization of miR-21 and IHC staining of Sox2 showed consistent co-expression in mouse brain tumor specimens. Irreversible depletion of miR-21 by using an LNA-modified siRNA was shown to repress Sox2 in primary mouse brain tumor cells but also in human glioma cell lines. Our data suggest that miR-21 regulates Sox2, maintains the tumor initiating cell population and the progression of PDGF-driven brain tumors which insinuates miR-21 as a promising target for future treatment of glioma. 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 3985. doi:10.1158/1538-7445.AM2011-3985
Which method for quantifying urinary albumin excretion gives what outcome? A comparison of immunonephelometry with HPLC
Authors: Jacoline W. Brinkman, Stephan J.L. Bakker, Ron T. Gansevoort, Hans L. Hillege, Ido P. Kema, Reinold O.B. Gans, Paul E. De Jong, Dick De Zeeuw
Journal: Kidney International (2004)
The Spread of the Obesity Epidemic in the United States, 1991-1998
Authors: Ali H. Mokdad
Journal: JAMA (1999)

The increasing prevalence of obesity is a major public health concern, since obesity is associated with several chronic diseases.To monitor trends in state-specific data and to examine changes in the prevalence of obesity among adults.Cross-sectional random-digit telephone survey (Behavioral Risk Factor Surveillance System) of noninstitutionalized adults aged 18 years or older conducted by the Centers for Disease Control and Prevention and state health departments from 1991 to 1998.States that participated in the Behavioral Risk Factor Surveillance System.Body mass index calculated from self-reported weight and height.The prevalence of obesity (defined as a body mass index > or =30 kg/m2) increased from 12.0% in 1991 to 17.9% in 1998. A steady increase was observed in all states; in both sexes; across age groups, races, educational levels; and occurred regardless of smoking status. The greatest magnitude of increase was found in the following groups: 18- to 29-year-olds (7.1% to 12.1%), those with some college education (10.6% to 17.8%), and those of Hispanic ethnicity (11.6% to 20.8%). The magnitude of the increased prevalence varied by region (ranging from 31.9% for mid Atlantic to 67.2% for South Atlantic, the area with the greatest increases) and by state (ranging from 11.3% for Delaware to 101.8% for Georgia, the state with the greatest increases).Obesity continues to increase rapidly in the United States. To alter this trend, strategies and programs for weight maintenance as well as weight reduction must become a higher public health priority.
Regulation of Axon Degeneration after Injury and in Development by the Endogenous Calpain Inhibitor Calpastatin
Authors: Jing Yang, Robby M. Weimer, Dara Kallop, Olav Olsen, Zhuhao Wu, Nicolas Renier, Kunihiro Uryu, Marc Tessier-Lavigne
Journal: Neuron (2013)
Immunological Tolerance to a Pancreatic Antigen as a Result of Local Expression of TNFα by Islet β Cells
Authors: Stephen J McSorley, Sylvelie Soldera, Laurent Malherbe, Claude Carnaud, Richard M Locksley, Richard A Flavell, Nicolas Glaichenhaus
Journal: Immunity (1997)

Recent experiments have suggested that tumor necrosis factor α (TNFα) can down-regulate islet-specific T cells and prevent the development of autoimmune diabetes. Here we demonstrate that transgenic mice expressing both TNFα and the Leishmania major LACK antigen in the pancreas (RIP-TNFα/RIP-LACK) exhibit an impaired ability to mount a CD4+ T cell response against LACK. In addition, peripheral CD4+ T cells from TCR transgenic mice (TCR-LACK/RIP-TNFα/RIP-LACK) produced reduced interleukin-2 but elevated levels of T helper 2 cytokines in response to LACK peptide in vitro. Taken together, our data suggest that TNFα may act in vivo to modulate a potentially damaging self-reactive T cell response by inducing tolerance to pancreatic antigens.
Implementing Colorectal Cancer Screening: Group 2 Report
Authors: P. Rozen, J. Blanchard, D. Campbell, E. Carlsen, R. Lambert, U. Marbet, K. Peterson, J. Regula, N. Segnan, S. Suchanek, A. Van Gossum
Journal: Endoscopy (2004)

Colorectal cancer is an important cause of morbidity and mortality throughout the developed and the industrializing and westernizing countries of Europe [1]. It is now the most common cancer afflicting both sexes combined and the incidence is apparently rising in eastern European countries as lifestyle changes and reporting improves [2]. The high mortality in some of these countries reflects not only this rising incidence, but also the availability of diagnostic and treatment facilities. The causes include the ”Western” or industrialized lifestyle, innate genetic susceptibility, and the interaction between them.
Virologic Assistance in the Management of German Measles in Pregnancy
Authors: S. A. Plotkin
Journal: JAMA (1964)

During the current epidemic of rubella, it has been possible to make use of the newly discovered methods for isolation of the virus and for the serologic diagnosis of rubella in testing of specimens from pregnant women who had suffered rubella-like illness or who had been exposed to the disease. Nasopharyngeal swabs obtained during the first week after onset of the rash and especially during the first few days were often positive. Serologic diagnosis was quite feasible using acute and convalescent specimens and on occasion it was still possible to show a rising titer when the first serum had been obtained two weeks after the rash.
Psychosocial Support for Far-flung Astronauts
Authors: Mike Mitka
Journal: JAMA (2002)

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