tbuckley/cabot-search huggingface dataset:
Some metabolic and haematological effects of oesophago-jejunostomy with by-pass of the stomach
Authors: S. T. Callender, L. J. Witts, P. R. Allison, A. Gunning
Journal: Gut (1961)

Twelve subjects have been studied in whom oesophago-jejunostomy had been performed leaving the stomach in situ. All had considerable metabolic disturbance with steatorrhoea and inability to absorb vitamin B(12), and the operation has been abandoned in favour of oesophagojejuno-gastrostomy.
A meta-analysis of the effect of angiotensin receptor blockers and calcium channel blockers on blood pressure, glycemia and the HOMA-IR index in non-diabetic patients
Authors: Yue Yang, Ri-bao Wei, Yue Xing, Lu Tang, Xiao-yong Zheng, Zi-cheng Wang, Yu-wei Gao, Min-xia Li, Xiang-mei Chen
Journal: Metabolism (2013)
Correction of technical bias in clinical microarray data improves concordance with known biological information
Authors: Aron C Eklund, Zoltan Szallasi
Journal: Genome biology (2008)

The performance of gene expression microarrays has been well characterized using controlled reference samples, but the performance on clinical samples remains less clear. We identified sources of technical bias affecting many genes in concert, thus causing spurious correlations in clinical data sets and false associations between genes and clinical variables. We developed a method to correct for technical bias in clinical microarray data, which increased concordance with known biological relationships in multiple data sets.
A New Prostate Carcinoma Binding Peptide (DUP-1) for Tumor Imaging and Therapy
Authors: Sabine Zitzmann, Walter Mier, Arno Schad, Ralf Kinscherf, Vasileios Askoxylakis, Susanne Krämer, Annette Altmann, Michael Eisenhut, Uwe Haberkorn
Journal: Clinical Cancer Research (2005)

Prostate carcinomas belong to the most widespread tumors, and their number is increasing. Imaging modalities used for diagnosis, such as ultrasound, computed tomography, and positron emission tomography, often produce poor results. Radiolabeled peptides with high sensitivity and specificity for prostate cancer would be a desirable tool for tumor diagnosis and treatment.We used phage display and the prostate-specific membrane antigen-negative cell line DU-145 to identify a peptide. The isolated DUP-1 was tested in vitro for its binding specificity, kinetics, and affinity. Internalization of the peptide was evaluated with confocal microscopy. The tumor accumulation in a nude mouse model was analyzed with 131I-labeled DUP-1 in PC-3 and DU-145 prostate tumors as well as in the rat prostate tumor model AT-1.The synthesized peptide showed rapid binding kinetics peaking at 10 minutes. It shows specific binding to prostate carcinoma cells but low binding affinity to nontumor cells. Peptide binding is competed with unlabeled DUP-1, and a time-dependent internalization into DU-145 cells was shown. Biodistribution studies of DUP-1 in nude mice with s.c. transplanted DU-145 and PC-3 tumors showed a tumor accumulation of 5% and 7% injected dose per gram, and bound peptide could not be removed by perfusion. The rat prostate tumor model showed an increase of radioactivity in the prostate tumor up to 300% in comparison with normal prostate tissue.DUP-1 holds promise as a lead peptide structure applicable in the development of new diagnostic tracers or anticancer agents that specifically target prostate carcinoma.
The COXEN Principle: Translating Signatures of <i>In vitro</i> Chemosensitivity into Tools for Clinical Outcome Prediction and Drug Discovery in Cancer
Authors: Steven C. Smith, Alexander S. Baras, Jae K. Lee, Dan Theodorescu
Journal: Cancer Research (2010)

Substantial effort has been devoted to in vitro testing of candidate chemotherapeutic agents. In particular, the United States National Cancer Institute Developmental Therapeutics Program (NCI-DTP) Human Tumor Cell Line Screen has screened hundreds of thousands of compounds and extracts, for which data on more than 40,000 compounds tested on a panel of 60 cancer cell lines (NCI-60) are publically available. In tandem, gene expression profiling has brought about a sea change in our understanding of cancer biology, allowing discovery of biomarkers or signatures able to characterize, classify, and prognosticate clinical behavior of human tumors. Recent studies have used tumor profiling matched to clinical trial outcome data to derive gene expression models predicting therapeutic outcomes, though such efforts are costly, time-consuming, tumor type-specific, and not amenable to rare diseases. Furthermore, addition of new or established drugs to multidrug combinations in which such models are already available requires the entire model to be re-derived. Can the aforementioned in vitro testing platform, coupled to the universal language of genomics, be used to develop, a priori, gene expression models predictive of clinical outcomes? Recent advances, including the CO-eXpression ExtrapolatioN (COXEN) algorithm, suggest that development of these models may be possible and raise important implications for future trial design and drug discovery.
LACTIC DEHYDROGENASE AND SUCCINIC DEHYDROGENASE IN PSORIASIS
Authors: E. NEUMANN, I. BELŠAN, BOŽENA BLAŽKOVA
Journal: British Journal of Dermatology (1967)

Journal Article LACTIC DEHYDROGENASE AND SUCCINIC DEHYDROGENASE IN PSORIASIS Get access E. NEUMANN, E. NEUMANN Dermatological Department of Faculty Polyelinies, Charles University Prague, Director: Doc. MUDr. Email Neumann Search for other works by this author on: Oxford Academic Google Scholar I. BELŠAN, I. BELŠAN 1st Dermatological Clinic, Charles University Medical School, Prague, Director: Prof. MUDr Jan Konopik Search for other works by this author on: Oxford Academic Google Scholar BOŽENA BLAŽKOVÁ BOŽENA BLAŽKOVÁ Institute for Sera and Vaccines, Prague, Director: MUDr Jiří Málek Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 79, Issue 3, 1 March 1967, Pages 160–163, https://doi.org/10.1111/j.1365-2133.1967.tb15825.x Published: 01 March 1967
Chronic Diffuse Interstitial Fibrosis of the Lungs
Authors: A. G. Heppleston
Journal: Thorax (1951)

Ca<sup>2+</sup>-dependent gene regulation controls many aspects of neuronal plasticity. Significant progress has been made toward understanding the roles of voltage- and ligand-gated Ca<sup>2+</sup> channels in triggering specific transcriptional responses. In contrast, the functional importance of Ca<sup>2+</sup> buffers and Ca<sup>2+</sup> transporters in neuronal gene regulation is less clear despite their critical contribution to the spatiotemporal control of Ca<sup>2+</sup> signals. Here we examined the role of mitochondrial Ca<sup>2+</sup> uptake and release in regulating the Ca<sup>2+</sup>-dependent transcription factor NFAT (nuclear factor of activated T-cells), which has been implicated in synaptic plasticity, axonal growth, and neuronal survival. Intense stimulation of sensory neurons by action potentials or TRPV1 agonists induced rapid activation and nuclear import of NFAT. Nuclear translocation of NFAT was associated with a characteristic prolonged [Ca<sup>2+</sup>]<sub>i</sub> elevation (plateau) that resulted from Ca<sup>2+</sup> uptake by, and its subsequent release from, mitochondria. Measurements using a mitochondrial Ca<sup>2+</sup> indicator, mtPericam, showed that this process recruited mitochondria throughout the cell body, including the perinuclear region. [Ca<sup>2+</sup>]<sub>i</sub> levels attained during the plateau phase were similar to or higher than those required for NFAT activation (200–300 nm). The elimination of the [Ca<sup>2+</sup>]<sub>i</sub> plateau by blocking either mitochondrial Ca<sup>2+</sup> uptake via the uniporter or Ca<sup>2+</sup> release via the mitochondrial Na<sup>+</sup>/Ca<sup>2+</sup> exchanger strongly reduced nuclear import of NFAT. Furthermore, preventing Ca<sup>2+</sup> mobilization via the mitochondrial Na<sup>+</sup>/Ca<sup>2+</sup> exchanger diminished NFAT-mediated transcription. Collectively, these data implicate activity-induced Ca<sup>2+</sup> uptake and prolonged release from mitochondria as a novel regulatory mechanism in neuronal excitation–transcription coupling.
Inositol trisphosphate promotes Na-Ca exchange current by releasing calcium from sarcoplasmic reticulum in cardiac myocytes.
Authors: J C Gilbert, T Shirayama, A J Pappano
Journal: Circulation Research (1991)

An early inward tail current evoked by membrane depolarization (from -80 to -40 mV) sufficient to activate sodium but not calcium current was studied in single voltage-clamped ventricular myocytes isolated from guinea pig hearts. Like forward-mode Na-Ca exchange, this early inward tail current required [Na+]o and [Ca2+]i and is thought to follow earlier reverse-mode Na-Ca exchange that triggers Ca2+ release from sarcoplasmic reticulum. The dependence of the early inward tail current on [Ca2+]i was supported by the ability of small (+10 mV) and large (+80 mV) voltage jumps from -40 mV to decrease and increase, respectively, the size of early inward tail currents evoked by subsequent voltage steps from -80 to -40 mV. As expected, tetrodotoxin selectively inhibited the early inward tail current but not the late inward tail current that followed voltage jumps to +40 mV test potentials. Although tetrodotoxin also blocked the fast Na+ current, replacement of extracellular Na+ by Li+ sustained the fast Na+ current. However, Li+, which does not support Na-Ca exchange, reversibly suppressed both the early and late inward tail currents. Inhibitors (ryanodine and caffeine) and promoters (intracellularly dialyzed inositol 1,4,5-trisphosphate) of sarcoplasmic reticulum Ca2+ release decreased and increased, respectively, the magnitude of the early inward tail current. The results substantiate the hypothesis that Ca2+ release from the sarcoplasmic reticulum participates in early Na-Ca exchange current and demonstrate that inositol 1,4,5-trisphosphate, by releasing Ca2+ from the sarcoplasmic reticulum, can promote Na-Ca exchange across the plasma membrane.
Normal liver regeneration in p50/nuclear factor κB1 knockout mice
Authors: Robert A. DeAngelis, Kellen Kovalovich, Drew E. Cressman, Rebecca Taub
Journal: Hepatology (2001)

Nuclear factor κB (NF–κB) is rapidly activated during liver regeneration following partial hepatectomy or carbon tetrachloride (CCl 4 )–mediated liver injury and is felt to be important in the antiapoptotic and regenerative responses. After partial hepatectomy, livers of mice deficient in the p50 subunit of NF–κB (p50 -/- ) showed a loss of NF–κB and decreased STAT3 transcription factor DNA binding activities. However, nuclear levels of the NF–κB p65 subunit were increased and peaked earlier in p50 -/- livers. Both messenger RNA and cytoplasmic protein levels of the NF–κB inhibitor IκBα were lower in p50 -/- livers, potentially accounting for the increase in p65 protein. Small effects on gene expression posthepatectomy were observed in p50 -/- livers, but no effects were seen on hepatocyte DNA synthetic or mitotic responses, serum enzyme levels, or overall liver mass restoration. After CCl 4 treatment, hepatocyte DNA synthesis and mitosis and serum enzyme levels were similar in p50 -/- and p50 +/+ mice, and histologic analysis indicated a slight decrease in overall damage in p50 -/- livers. After injection of Fas antibody, p50 -/- livers showed an earlier onset of nuclear changes consistent with apoptosis. These data indicate that absence of p50 affects certain protein and gene activation pathways following partial hepatectomy, CCl 4 , and Fas treatment but does not impair overall liver regeneration. Interleukin 6 (IL–6) levels were reduced but still adequate to support regeneration. We hypothesize that increased levels of the NF–κB p65 subunit in p50 -/- livers may provide compensation for the absence of p50, thereby allowing normal liver regeneration and repair following liver injury.
Childhood and Adolescent Predictors of Major Depression in the Transition to Adulthood
Authors: Helen Z. Reinherz, Angela D. Paradis, Rose M. Giaconia, Cecilia K. Stashwick, Garrett Fitzmaurice
Journal: American Journal of Psychiatry (2003)

OBJECTIVE: The identification of predictors of major depression in the transition to adulthood has direct application to prevention and intervention efforts designed to forestall depression in this high-risk period. The current study identified childhood and adolescent familial and behavioral-emotional factors predicting depression during this critical developmental stage. METHOD: The 354 participants were part of a single-age cohort from a predominately Caucasian working-class community whose psychosocial development has been traced prospectively since age 5. In these analyses, data collected during childhood and adolescence were related to diagnoses of major depression at ages 18–26. RESULTS: During the transition to adulthood, 82 participants (23.2%) experienced major depression. Bivariate indicators of later depression included a family history of depression or substance use disorders, family composition, and childhood family environments perceived as violent and lacking cohesiveness. Also significant were self- and mother-reported internalizing behaviors, as well as self-rated anxiety and depressive symptoms. Multivariable analyses showed family violence, family composition, internalizing problems during adolescence, and low family cohesion to be the most salient factors. CONCLUSIONS: These results highlight familial and behavioral-emotional predictors of depression that can serve as foci for identifying youth in need of intervention.
Effect of Estrogen Replacement Therapy on Sympathetic Activity in Postmenopausal Women
Authors: Christoph Dodt, Horst L. Fehm, Gunther Weitz
Journal: Circulation (2001)

To the Editor:Two recent articles in Circulation described modulations of sympathetic nerve activity to the muscle vascular bed in postmenopausal women on long-term estrogen replacement therapy (ERT).Vongpatanasin et al 1 reported a decrease in resting muscle sympathetic nerve activity (MSNA) after transdermal but not oral estrogen administration.Furthermore, the diastolic blood pressure was significantly decreased after transdermal ERT.The authors concluded that the decrease in blood pressure was induced by a fall in MSNA to the muscle vascular bed.These data confirm and extend the results of a recent study that administered 2-day transdermal ERT to postmenopausal women and measured MSNA to the muscle vascular bed in the superficial peroneal nerve using a placebo-controlled, within-subject crossover design. 2In this study, resting MSNA decreased from 37.1Ϯ3.1 to 30.1Ϯ3.1 bursts/min by the second day of estrogen treatment.Vongpatanasin and colleagues 1 show that this effect is sustained for a treatment period of 8 weeks.In the short-term study by Weitz et al, 2 however, the identical decrease in MSNA was not accompanied by a fall in blood pressure.This finding casts doubt on the hypothesis that the decrease in blood pressure is the consequence of reduced sympathetic tone to the muscle vascular bed.Rather, other mechanisms, such as direct vascular effects, could account for the blood pressure-lowering effects of transdermal ERT after prolonged treatment.This effect, however, must be combined with an influence on baroreflex function in postmenopausal women, because otherwise a decrease in blood pressure would have resulted in an increase in MSNA.In fact, the effects of estrogens on baroreflex regulation have been repeatedly demonstrated, most recently in the study by Hunt et al 3 in postmenopausal women in the same issue of Circulation.However, in premenopausal women, an increased suppression of MSNA in response to an elevation of blood pressure has also been observed during phases of high estrogen levels during the menstrual cycle, 4 although neither study showed any change in blood pressure.Thus, these studies indicate that estrogens lower the centrally regulated baroreflex set point in normotensive postmenopausal women.This effect might explain the adaptive changes in MSNA in relation to the prevailing blood pressure, but they do not seem to explain the blood pressure decrease in the study of Vongpatanasin et al.
Control of airway inflammation maintained at a lower steroid dose with 100/50 μg of fluticasone propionate/salmeterol
Authors: Nizar N. Jarjour, Susan J. Wilson, Steven M. Koenig, Michel Laviolette, Wendy C. Moore, W. Bruce Davis, Dennis E. Doherty, Qutayba Hamid, Elliott Israel, Mani S. Kavuru, Joe W. Ramsdell, Donald P. Tashkin, Donna S. Reilly, Steven W. Yancey, Lisa D. Edwards, John L. Stauffer, Paul M. Dorinsky, Ratko Djukanovic
Journal: Journal of Allergy and Clinical Immunology (2006)
Hypoxia induced downregulation of hepcidin is mediated by platelet derived growth factor BB
Authors: Thomas Sonnweber, David Nachbaur, Andrea Schroll, Manfred Nairz, Markus Seifert, Egon Demetz, David Haschka, Anna-Maria Mitterstiller, Axel Kleinsasser, Martin Burtscher, Susanne Trübsbach, Anthony T Murphy, Victor Wroblewski, Derrick R Witcher, Katarzyna Mleczko-Sanecka, Chiara Vecchi, Martina U Muckenthaler, Antonello Pietrangelo, Igor Theurl, Günter Weiss
Journal: Gut (2014)

<h3>Objective</h3> Hypoxia affects body iron homeostasis; however, the underlying mechanisms are incompletely understood. <h3>Design</h3> Using a standardised hypoxia chamber, 23 healthy volunteers were subjected to hypoxic conditions, equivalent to an altitude of 5600 m, for 6 h. Subsequent experiments were performed in C57BL/6 mice, CREB-H knockout mice, primary hepatocytes and HepG2 cells. <h3>Results</h3> Exposure of subjects to hypoxia resulted in a significant decrease of serum levels of the master regulator of iron homeostasis hepcidin and elevated concentrations of platelet derived growth factor (PDGF)-BB. Using correlation analysis, we identified PDGF-BB to be associated with hypoxia mediated hepcidin repression in humans. We then exposed mice to hypoxia using a standardised chamber and observed downregulation of hepatic hepcidin mRNA expression that was paralleled by elevated serum PDGF-BB protein concentrations and higher serum iron levels as compared with mice housed under normoxic conditions. PDGF-BB treatment in vitro and in vivo resulted in suppression of both steady state and BMP6 inducible hepcidin expression. Mechanistically, PDGF-BB inhibits hepcidin transcription by downregulating the protein expression of the transcription factors CREB and CREB-H, and pharmacological blockade or genetic ablation of these pathways abrogated the effects of PDGF-BB toward hepcidin expression. <h3>Conclusions</h3> Hypoxia decreases hepatic hepcidin expression by a novel regulatory pathway exerted via PDGF-BB, leading to increased availability of circulating iron that can be used for erythropoiesis.
Corrigendum to ‘Brain natriuretic peptide‐guided treatment does not improve morbidity and mortality in extensively treated patients with chronic heart failure: responders to treatment have a significantly better outcome’ [Eur J Heart Fail 2011;13:1096–1103]
Authors: Patric Karlström, Urban Alehagen, Kurt Boman, Ulf Dahlström
Journal: European Journal of Heart Failure (2012)
Anthropometric characteristics, body composition and somatotype of elite junior tennis players
Authors: Cristóbal Sánchez-Muñoz, David Sanz, Mikel Zabala
Journal: British Journal of Sports Medicine (2007)

Objectives: The aims of this study were to describe the anthropometric characteristics, body composition and somatotype of elite male and female junior tennis players, to compare the anthropometric data, body composition and somatotype of the first 12 elite junior tennis players on the ranking with the lower ranked players, and to establish an anthropometric profile chart for elite junior tennis players. Methods: A total of 123 (57 males and 66 females) elite junior tennis players participated in this study. The athletes were divided into two groups, the first 12 and the lower ranked players, according to gender. A total of 17 anthropometric variables were recorded of each subject. Results: There were no significant differences in height and weight between the first 12 and the lower ranked boys, while the first 12 girls were significantly taller than the lower ranked girls (p = 0.009). Significant differences were found for humeral and femoral breadths between the first 12 and the lower ranked girls (p = 0.000; p = 0.004, respectively). The mean (SD) somatotype of elite male junior tennis players could be defined as ectomesomorphic (2.4 (0.7), 5.2 (0.8), 2.9 (0.7)) and the mean (SD) somatotype of elite female junior tennis players evaluated could be defined as endomesomorphic (3.8 (0.9), 4.6 (1.0), 2.4 (1.0)). No significant differences were found in somatotype components between the first 12 and the lower ranked players of both genders. Conclusions: When comparing the first 12 and the lower ranked elite junior tennis players of both genders, no significant differences were observed in any measured item for the boys. By contrast, significant differences were observed in height and humeral and femoral breadths between the first 12 and the lower ranked girls, whereby the first 12 were taller and had wider humeral and femoral breadths than the lower ranked players. These differences could influence the playing style of junior female players.
IgG2a restriction of murine antibodies elicited by viral infections.
Authors: J P Coutelier, J T van der Logt, F W Heessen, G Warnier, J Van Snick
Journal: The Journal of Experimental Medicine (1987)

The isotypic distribution of IgG antibodies was determined in the serum of mice after infection with a panel of RNA and DNA viruses representative of 11 different genera. The antiviral response induced by all these viruses showed a striking preponderance of the IgG2a subclass whatever the strain of mice tested or the time elapsed after infection. Together with the predominance of IgG1 in antiprotein and of IgG3 in anticarbohydrate response, this IgG2a restriction of antiviral antibodies strongly suggests the existence of highly specific mechanisms for the regulation of individual subclasses in the mouse.
Malignant B Cells Skew the Balance of Regulatory T Cells and TH17 Cells in B-Cell Non-Hodgkin's Lymphoma
Authors: Zhi-Zhang Yang, Anne J. Novak, Steven C. Ziesmer, Thomas E. Witzig, Stephen M. Ansell
Journal: Cancer Research (2009)

Using biopsy specimens from patients with B-cell non-Hodgkin's lymphoma, we observed a significantly low frequency of T(H)17 cells, including several samples with no detectable amount of interleukin (IL)-17-producing cells present in the tumor microenvironment. We found that, in the absence of lymphoma B cells, treatment with IL-1beta/IL-6 or lipopolysaccharide (LPS) enhanced IL-17 expression in CD4(+) T cells and this enhancement was attenuated when CD4(+) T cells were cocultured with lymphoma B cells. Blockade of CD27-CD70 or CD28-CD80/86 interactions by anti-CD70 or anti-CD80/86 antibodies restored LPS-mediated induction of IL-17 expression in CD4(+) T cells cocultured with lymphoma B cells. Because a subset of lymphoma B cells express IL-2 and given that IL-2 signaling is critically important in the development of regulatory T (T(reg)) cells, we tested the role of IL-2 signaling in T(H)17 cell development. We found that treatment with anti-IL-2 antibody to interrupt IL-2 signaling significantly inhibited Foxp3 expression in CD4(+) T cells. In contrast, interruption of IL-2 signaling up-regulated IL-17 expression in CD4(+) T cells and restored lymphoma-mediated down-regulation of IL-17-producing cells. Furthermore, the reversal of T(reg) cell activity by LPS or CpG-A resulted in an enhancement of IL-17-producing cells. Taken together, our study indicated that lymphoma B cells play an important role in skewing the balance between T(reg) and T(H)17 cells resulting in the establishment of a profoundly inhibitory tumor microenvironment.