tbuckley/cabot-search huggingface dataset:
810 FREQUENCY OF RVR AND ITS UTILITY AS A PREDICTOR OF TREATMENT OUTCOME IN INDIVIDUALS TREATED WITHIN THE AUSTRALIAN TRIAL IN ACUTE HEPATITIS C (ATAHC)
Authors: G.V. Matthews, M. Hellard, P. Haber, B. Yeung, P. Marks, J. Sasadeusz, D. Baker, G. McCaughan, P. White, W. Rawlinson, A. Lloyd, J. Kaldor, G.J. Dore
Journal: Journal of Hepatology (2008)
Differential regulation of hepatic bile salt and organic anion transporters in pregnant and postpartum rats and the role of prolactin
Authors: Jingsong Cao, Liyue Huang, Yong Liu, Tim Hoffman, Bruno Stieger, Peter J. Meier, Mary Vore
Journal: Hepatology (2001)

We characterized expression and activity of the bile salt transporters Na + /taurocholate (TC) cotransporting polypeptide (Ntcp), and bile salt export pump (Bsep), and the expression of organic anion transporting polypeptides 1 and 2 (Oatp1 and 2) and multidrug resistance associated protein–2 (Mrp2) in pregnancy and throughout lactation in rats. The V max for Na + /TC cotransport in basolateral liver plasma membrane was increased 1.7–fold in 2 days postpartum relative to control and pregnant rats. This correlated well with an increase in Ntcp messenger RNA (mRNA) and a 2–fold increase in Ntcp protein. Ntcp mRNA remained significantly elevated until 14 days postpartum but had begun to decline by 21 days postpartum. The maximal secretory rate (nmol/min/g liver) for TC in the single pass isolated perfused liver was also increased by 10%, 31%, and 24% at 2, 14, and 21 days postpartum and correlated with increased expression of Ntcp and Bsep mRNA and protein. Infusion of ovine prolactin (oPRL) to ovariectomized rats increased expression of both Ntcp and Bsep mRNA and protein. These data indicate a coordinate increased expression of bile salt transporters postpartum and by PRL. Mrp2 mRNA was stable in pregnancy and postpartum, whereas Mrp2 protein expression decreased significantly in pregnancy, but returned to control levels postpartum. Organic anion transporting polypeptide 2 (Oatp2) mRNA was decreased in pregnancy and increased postpartum, but changes in Oatp2 protein were not significant. Oatp1 mRNA and protein were unchanged in pregnancy and postpartum.
Watchful Waiting in Low–Tumor Burden Follicular Lymphoma in the Rituximab Era: Results of an F2-Study Database
Authors: Philippe Solal-Céligny, Monica Bellei, Luigi Marcheselli, Emanuela Anna Pesce, Stefano Pileri, Peter McLaughlin, Stefano Luminari, Barbara Pro, Silvia Montoto, Andrés J.M. Ferreri, Eric Deconinck, Noël Milpied, Leo I. Gordon, Massimo Federico
Journal: Journal of Clinical Oncology (2012)

Patients with follicular lymphoma (FL) registered in the F2-study and initially managed without treatment were analyzed to describe the presentation and outcome of a watch and wait (W&W) strategy in the rituximab era, to identify parameters for initiating treatment, and to evaluate whether initial W&W could have deleterious effects on treatment efficacy after progression or relapse.Between 2003 and 2005, 120 patients selected from the 1,093 treatment-naive patients with FL in the F2-study cohort were initially managed expectantly (W&W), and 107 patients were assessed. Most of these patients (80%) had disseminated disease with a low tumor burden according to Groupe d'Etudes des Lymphomes Folliculaires criteria.After a median follow-up of 64 months, treatment was initiated in 54 patients (50%), with a median delay of 55 months for the entire cohort. In a univariate analysis, involvement of more than four nodal areas (hazard ratio [HR], 2.26) and serum albumin less than 3.5 g/dL (HR, 3.51) were predictive of a shorter time to lymphoma treatment initiation. In a multivariate analysis, only involvement of more than four nodal areas remained significant (HR, 2.32). The 4-year freedom from treatment failure (FFTF) rate of W&W patients (79%; 95% CI, 69% to 85%) was not inferior to that of a subgroup of 242 patients from the F2-study cohort with good prognosis characteristics who were initially treated with a rituximab-based regimen (69%; 95% CI, 61% to 76%; P = .103).In the rituximab era, patients with FL in a selected prognostically favorable group can still be managed with W&W. W&W does not seem to have detrimental effects on FFTF and overall survival rates after treatment.
Longitudinal Course of Posttraumatic Stress Disorder and Posttraumatic Stress Disorder Symptoms in a Community Sample of Adolescents and Young Adults
Authors: Axel Perkonigg, Hildegard Pfister, Murray B Stein, Michael Höfler, Roselind Lieb, Andreas Maercker, Hans-Ulrich Wittchen
Journal: American Journal of Psychiatry (2005)

OBJECTIVE: Few studies have focused on the natural course of posttraumatic stress disorder (PTSD) and its determinants in samples of the general population. The authors examined determinants of remission and chronicity of PTSD and associations with other disorders in a prospective community sample. METHOD: The data were drawn from a prospective, longitudinal epidemiological study of adolescents and young adults (age 14–24 years) in Munich, Germany (N=2,548). The course of PTSD from baseline to follow-up 34–50 months later was studied in 125 respondents with DSM-IV PTSD or subthreshold PTSD at baseline. RESULTS: Although 52% of the PTSD cases remitted during the follow-up period, 48% showed no significant remission of PTSD symptoms. Respondents with a chronic course were more likely to experience new traumatic event(s) during follow-up (odds ratio=5.21, 95% confidence interval [CI]=1.95–13.92), to have higher rates of avoidant symptoms at baseline (odds ratio=10.16, 95% CI=1.73–59.51), and to report more help seeking (odds ratio=5.50, 95% CI=1.04–29.05), compared to respondents with remission. Rates of incident somatoform disorder (odds ratio=4.24, 95% CI=1.60–11.19) and other anxiety disorders (odds ratio=4.07, 95% CI=1.15–14.37) were also significantly associated with a chronic course. CONCLUSIONS: PTSD is often a persistent and chronic disorder. Specific symptom clusters—especially avoidant symptoms—might be associated with the course of PTSD. In addition, the occurrence of new traumatic events differentiates PTSD cases with a chronic course from those with remission.
Lack of antigen-specific tissue remodeling in mice deficient in the macrophage galactose-type calcium-type lectin 1/CD301a
Authors: Kayoko Sato, Yasuyuki Imai, Nobuaki Higashi, Yosuke Kumamoto, Thandi M. Onami, Stephen M. Hedrick, Tatsuro Irimura
Journal: Blood (2005)
Efficacy of a Chinese Herbal Medicine in Providing Adequate Relief of Constipation-predominant Irritable Bowel Syndrome: A Randomized Controlled Trial
Authors: Alan Bensoussan, John E. Kellow, Suzannah J. Bourchier, Paul Fahey, Lisa Shim, Allison Malcolm, Philip Boyce
Journal: Clinical Gastroenterology and Hepatology (2015)
Molecular aspects of adrenergic modulation of the transient outward current
Authors: M VANDERHEYDEN, T WIJNHOVEN, T OPTHOF
Journal: Cardiovascular Research (2006)

Transient outward channels have a different impact on action potential configuration in small mammals compared to large mammals. Small mammals depend primarily on Ito1 for repolarization, while in larger animals Ito1 only indirectly determines action potential duration by setting the level of the plateau. Transient outward channel expression and distribution also differ between animal species. Nevertheless, the primary protein sequence of the underlying Kv1.4, Kv4.2 and Kv4.3 alpha1-subunits displays remarkably high levels of amino acid identity. Transient outward channels are subject to alpha- and beta-adrenergic regulation, mainly decreasing Ito1. However, adrenergic stimulation is also an important determinant of transient outward channel downregulation in cardiac disease. Adrenergic stimulation of PKA as well as PKC leads to an inhibition of Ito1, which has been correlated with phosphorylation of the Kv1.4, Kv4.2 and Kv4.3 alpha1-subunits. Calmodulin-dependent kinase II, on the other hand, has been shown to be involved in an increase of Ito1. Comparison of Kv1.4, Kv4.2 and Kv4.3 primary amino acid sequences demonstrates a strong conservation of (potential) phosphorylation sites between different species, despite the fact that Ito1 has a different effect on action potential configuration in mammalian species.
Impact of premenopausal status at breast cancer diagnosis in women entered on the placebo-controlled NCIC CTG MA17 trial of extended adjuvant letrozole
Authors: P.E. Goss, J.N. Ingle, S. Martino, N.J. Robert, H.B. Muss, R.B. Livingston, N.E. Davidson, E.A. Perez, Y. Chavarri-Guerra, D.A. Cameron, K.I. Pritchard, T. Whelan, L.E. Shepherd, D. Tu
Journal: Annals of Oncology (2012)
Effects of colestipol-niacin therapy on human femoral atherosclerosis.
Authors: D H Blankenhorn, S P Azen, D W Crawford, S A Nessim, M E Sanmarco, R H Selzer, A M Shircore, E C Wickham
Journal: Circulation (1991)

The 2-year therapy effect on femoral atherosclerosis was evaluated in the Cholesterol Lowering Atherosclerosis Study (CLAS), a randomized, placebo-plus-diet-controlled angiographic trial of colestipol-niacin therapy plus diet in men with previous coronary bypass surgery. Different diet compositions were prescribed to enhance the differential in blood cholesterol responses between the two groups. The annual rate of change in computer-estimated atherosclerosis (CEA), a measure of lumen abnormality, was evaluated between treatment groups. A significant per-segment therapy effect was found in segments with moderately severe atherosclerosis (p less than 0.04) and in proximal segments (p less than 0.02). When segmental CEA measures were combined into a per-patient score using an adaptation of the National Heart, Lung, and Blood Institute scoring procedure, a significant therapy effect was observed (p less than 0.02). Total variance of the annual change rate in CEA was as predicted from pilot studies, but measurement variation was larger. The therapy effect observed in femoral arteries, although significant, was less marked than the strong and consistent benefit previously reported for both native coronary arteries and aortocoronary bypass grafts.
Overview of gender aspects of cardiac syndrome X
Authors: J Kaski
Journal: Cardiovascular Research (2002)

Cardiac syndrome X, a condition defined by the presence of angina-like chest pain, a positive response to stress testing and normal coronary arteriograms, has been shown to occur in approximately 20--30% of angina patients undergoing coronary arteriography. The prevalence of syndrome X is significantly higher in women compared to men. In the majority of patients with chest pain and normal coronary arteriograms, symptoms are likely to be non-cardiac in origin. However, myocardial ischaemia may be the pathogenic mechanism in a proportion of syndrome X patients. Indeed, the clinical characteristics, the ischaemic electrocardiographic findings and the presence of myocardial perfusion defects during stress testing are similar in syndrome X and coronary artery disease patients. Moreover, coronary sinus oxygen saturation abnormalities and pH changes, as well as myocardial lactate production and alterations of cardiac high energy phosphate are seen during stress testing in patients with syndrome X and appear to endorse an ischaemic origin of symptoms in at least a proportion of these individuals. Patients with chest pain and normal coronary arteries have abnormal vasodilatory coronary blood flow responses and an increased sensitivity of the coronary microcirculation to vasoconstrictor stimuli (microvascular angina). Microvascular endothelial dysfunction appears to be responsible for these coronary microcirculation abnormalities. Given the high prevalence of peri- and post-menopausal women in cardiac syndrome X, it has been hypothesized that oestrogen deficiency may play a major role in the pathogenesis of this condition. Oestrogen vasoactive properties involve endothelium-dependent effects and, in postmenopausal women, forearm vasodilatation induced by acetylcholine is potentiated by the acute local administration of intravenous oestradiol. This suggests that endothelium-dependent responses in the peripheral circulation may be modulated by steroid hormones. Impairment of endothelial function in post-menopausal women with syndrome X has been reported by various groups and it could be hypothesized that oestrogen deficiency may contribute to the development of microvascular angina through endothelial dysfunction and that exogenous oestrogen administration may have a beneficial effect in syndrome X patients. This article reviews current knowledge regarding the role of oestrogen deficiency in the pathogenesis of syndrome X and the potential therapeutic role of oestrogen replacement therapy in women with chest pain and normal coronary arteriograms
Urinary Excretion of Urodilatin in Patients With Cirrhosis
Authors: J Salo, W Jimenez, M Kuhn, A Gines, P Gines, G Fernandez-Esparrach, P Angeli, J Claria, R Bataller, V Arroyo, W Forssmann, J Rodes
Journal: Hepatology (1996)

Cirrhotic patients with ascites show increased plasma levels of natriuretic peptides from cardiac origin (i.e., atrial natriuretic peptide [ANP] and brain natriuretic peptide [BNP]). Urodilatin is a unique member of the natriuretic peptide family because it is exclusively synthesized in the kidney acting on a paracrine fashion in the regulation of sodium excretion. To investigate the renal production of urodilatin in cirrhosis and its relationship with other natriuretic peptides and sodium retention, urodilatin excretion and plasma levels of ANP were measured in 21 healthy subjects, 13 cirrhotic patients without ascites and 23 cirrhotic patients with ascites. Urine urodilatin was measured with a highly specific radioimmunoassay using a polyclonal antibody against human urodilatin. Patients with ascites had marked sodium retention (UNa 7 ± 2 mEq/d) as compared to patients without ascites and healthy subjects (29 ± 3 mEq/d and 34 ± 5 mEq/d, respectively, P &lt; .001). Patients with cirrhosis and ascites had urine urodilatin excretion similar to patients without ascites and healthy subjects (82 ± 8 pmol/g, 95 ± 10 pmol/g, and 89 ± 9 pmol/ g of creatinine, respectively; not significant). In addition, immunoreactive urodilatin from cirrhotic patients with ascites and healthy subjects showed a similar chromatographic pattern. By contrast, plasma ANP levels were increased significantly in patients with ascites (29 ± 3 fmol/mL) as compared with patients without ascites or healthy subjects (14 ± 3 fmol/mL and 6 ± 1 fmol/mL, respectively; P &lt; .01). In conclusion, urine urodilatin excretion is normal in patients with cirrhosis even in the presence of marked sodium retention. The coexistence of increased ANP levels and normal urodilatin excretion suggests that in cirrhosis both natriuretic peptides are regulated independently.
Goji Berries, a Novel Potent Allergenic Source with High Cross-Reactivity with Other Fruits
Authors: M.A. Lopez-Matas, J. Carnes, C.H. de Larramendi, A. Ferrer, A.J. Huertas, J.A. Pagan, L.A. Navarro, J.L. Garcia-Abujeta, M. Pena, S. Vicario
Journal: Journal of Allergy and Clinical Immunology (2012)
Non–Transferrin-Bound Iron in the Serum of Hemodialysis Patients Who Receive Ferric Saccharate
Authors: Barbara Scheiber-Mojdehkar, Barbara Lutzky, Roland Schaufler, Brigitte Sturm, Hans Goldenberg
Journal: Journal of the American Society of Nephrology (2004)

Intravenous iron (iv.Fe) is used to optimize response to recombinant human erythropoietin (r-HuEPO) in ESRD, but no consensus exists with respect to the best regimen to avoid transferrin "oversaturation," oxidative stress, and the occurrence of non-transferrin-bound iron (NTBI). Iv.Fe was stopped for 1 wk in 35 hemodialysis (HD) patients who were routinely receiving iv.Fe and r-HuEPO. The iv.Fe group received 100 mg of ferric saccharate (Venofer) at the end of the first HD session, whereas the time-control group was treated under the same conditions but received no iv.Fe. Serum samples were taken before the first HD session, immediately and 60 min after iv.Fe administration, and before the next HD session. Sera were analyzed for NTBI and peroxides; transferrin saturation was analyzed by urea-PAGE and Western blot. In an in vitro model system with HepG2 cells, the effects of ESRD serum on the labile iron pool (LIP) were assayed using the fluorescence calcein assay. NTBI significantly increased after iv.Fe-administration and returned to baseline values before the next HD-session. There was a shift from apo- to monoferric transferrin, but no "oversaturation" of transferrin after iv.Fe-treatment. Peroxides increased in both groups after HD. Hemodialysis decreased bioavailable iron for the LIP in HepG2-cells, whereas serum of iv.Fe-treated HD patients highly increased the LIP in these cells. A total of 100 mg of iv.Fe led to NTBI generation but not to an oversaturation of transferrin. Peroxide concentrations significantly increased during HD but were not correlated to iv.Fe administration and seemed to result from other sources of oxidative stress related to HD. NTBI can enter liver cells and increase the potentially harmful LIP.
Apoptosis and Cellular Activation in the Pathogenesis of Acute Vascular Rejection
Authors: Zoie E. Holzknecht, Karisha L. Kuypers, Timothy B. Plummer, Josie Williams, Matilda Bustos, Gregory J. Gores, Gregory J. Brunn, Jeffrey L. Platt
Journal: Circulation Research (2002)

Acute vascular or humoral rejection, a vexing outcome of organ transplantation, has been attributed by some to activation and by others to apoptosis of endothelial cells in the graft. We asked which of these processes causes acute vascular rejection by tracing the processes during the development of acute vascular rejection in porcine cardiac xenografts performed in baboons. Apoptosis, assayed by terminal deoxynucleotidyl transferase–mediated dUTP nick end-labeling (TUNEL), expression of activated caspase-3, and proapoptotic genes Bax and Bcl-x L , was not detected until acute vascular rejection was well advanced, and even then, apoptosis was largely confined to myocytes. Activation of the endothelium, as evidenced by expansion of rough endoplasmic reticulum and increased ribosomal antigen and phospho-p70 S6 kinase, occurred early in the course of acute vascular rejection and progressed through the disease process. These findings suggest that acute vascular rejection is caused by an active metabolic process and not by apoptosis in the endothelium.
New immunological assays for the diagnosis of Helicobacter pylori infection
Authors: D Vaira, J Holton, M Menegatti, C Ricci, F Landi, A Ali', L Gatta, C Acciardi, S Farinelli, M Crosatti, S Berardi, M Miglioli
Journal: Gut (1999)

<h3>Abstract</h3> Self-organized criticality is a hallmark of complex dynamic systems at phase transitions. Systems that operate at or near criticality have large-scale fluctuations or “avalanches”, the frequency and duration power of which are best fit with a power law revealing them to be scale-free and fractal, and such power laws are ubiquitous. It is an attractive concept in neuroscience since spiking avalanches are exhibited by neural tissue, and may underpin how minuscule events could scale up to circuits and provide adaptive psychobiological function. Much is yet to be understood about criticality <i>in vivo</i> in the healthy brain and in disorders such as addiction, as drugs may alter the critical state’s “tuning” to generate drug seeking and dysphoria. Thus, here a novel toolset was developed to use neural avalanches and their self-similarity, rather than power law fit slope exponents as is canonically done, to quantify criticality in a previously collected high-density electrophysiological <i>in vivo</i> corticostriatal dataset from a mouse model of early cocaine abstinence. During behavioral quiescence, in the prefrontal cortex but not ventral striatum of cocaine-dosed mice, it was found that critical tuning is enhanced compared to drug-free controls. Additionally, an empirical biological demonstration of complexity’s theoretical correlation to criticality was shown in drug-free mice, was exponentially enhanced in drug-treated cortex, but was absent in the drug-treated striatum. As shown, quantifying criticality grants experimental support for the “critical brain hypothesis” and allows for statistical interpretation of inter-subject variability and development of further testable hypotheses in systems neuroscience. <h3>Significance Statement</h3> The “critical brain hypothesis” asserts neural networks are comparable to material in phase transitions at a critical point, their “avalanches” of system-wide spike bursts best seen in log-log plots of probability vs. avalanche size or duration, with slope following a scale-free or fractal power law. In discussing criticality, “critical tuning” is mentioned but quantification thereof left for later experimentation, despite being necessary for a scientific hypothesis. Presented are methods to quantify critical tuning through assessing similarity or fractalness among corticostriatal avalanches collected using high-density electrophysiology in cocaine-conditioned mice, along with an empirical <i>in vivo</i> confirmation of the mathematical concept that data complexity correlates with criticality. Interestingly, cocaine enhances critical tuning in cortex and aberrantly modifies complexity in a region-specific manner.
Cytosolic-free calcium increases to greater than 100 micromolar in ATP-depleted proximal tubules.
Authors: J M Weinberg, J A Davis, M A Venkatachalam
Journal: Journal of Clinical Investigation (1997)

Previous studies have shown that cytosolic-free Ca2+ (Caf) increases to at least low micromolar concentrations during ATP depletion of isolated kidney proximal tubules. However, peak levels could not be determined precisely with the Ca2+-sensitive fluorophore, fura-2, because of its high affinity for Ca2+. Now, we have used two low affinity Ca2+ fluorophores, mag-fura-2 (furaptra) and fura-2FF, to quantitate the full magnitude of Caf increase. Between 30 and 60 min after treatment with antimycin to deplete ATP in the presence of glycine to prevent lytic plasma membrane damage, Caf measured with mag-fura-2 exceeded 10 microM in 91% of tubules studied and 68% had increases to greater than 100 microM. Caf increases of similar magnitude that were dependent on influx of medium Ca2+ were also seen using the new low Ca2+ affinity, Mg2+-insensitive, fluorophore fura-2FF in tubules depleted of ATP by hypoxia, and these increases were reversed by reoxygenation. Total cell Ca2+ levels in antimycin-treated or hypoxic tubules did not change, suggesting that mitochondria were not buffering the increased Caf during ATP depletion. Considered in the context of the high degree of structural preservation of glycine-treated tubule cells during ATP depletion and the commonly assumed Ca2+ requirements for phospholipid hydrolysis, actin disassembly, and Ca2+-mediated structural damage, the remarkable elevations of Caf demonstrated here suggest an unexpected resistance to the deleterious effects of increased Caf during energy deprivation in the presence of glycine.
The hippocampal system: Dissociating its functional components and recombining them in the service of declarative memory
Authors: Howard Eichenbaum, Tim Otto, Neal J. Cohen
Journal: Behavioral and Brain Sciences (1996)

Abstract Continuing commentary raised several issues concerning our proposal that the hippocampus, parahippocampal region, and cortical association areas mediate different aspects of memory function. Recent relevant findings strengthen our argument that neocortical areas and the parahippocampal region maintain persistent encodings of specific single items and that the hippocampus mediates representations of the relations among these items. The reciprocally and closely interconnected structures that compose the hippocampal memory system work interactively to support flexible memory expression that is relevant to the natural behavior of animals and to conscious recollection in humans.