tbuckley/cabot-search huggingface dataset:
Pet Ownership and Cardiovascular Risk
Authors: Glenn N. Levine, Karen Allen, Lynne T. Braun, Hayley E. Christian, Erika Friedmann, Kathryn A. Taubert, Sue Ann Thomas, Deborah L. Wells, Richard A. Lange
Journal: Circulation (2013)

C ardiovascular disease (CVD) is the leading cause of death in the United States. 1 Despite efforts promoting primary and secondary CVD prevention, 2-8 obesity and physical inactivity remain at epidemic proportions, with >60% of Americans adults overweight or obese and >50% not performing recommended levels of physical activity. 9Similarly, hypertension, hypercholesterolemia, and other CVD risk factors remain poorly controlled in many Americans.Despite numerous pharmacological and device-based advances in the management of patients with established CVD, morbidity and mortality associated with this condition remain substantial.Hence, a critical need exists for novel strategies and interventions that can potentially reduce the risk of CVD and its attendant morbidity and mortality.Numerous studies have explored the relationship between pet (primarily dog or cat) ownership and CVD, with many reporting beneficial effects, including increased physical activity, favorable lipid profiles, lower systemic blood pressure, improved autonomic tone, diminished sympathetic responses to stress, and improved survival after an acute coronary syndrome.Accordingly, the potential cardiovascular benefits of pet ownership have received considerable lay press and medical media coverage and attention from the Centers for Disease Control and Prevention 10 and have been the focus of a meeting sponsored by the National Institutes of Health. 11The purpose of this American Heart Association Scientific Statement is to critically assess the data regarding the influence of pet ownership on the presence and reduction of CVD risk factors and CVD risk.
Controversies in thromboprophylaxis for immobile patients secondary to neurological impairment
Authors: T. A-Z K Gaber
Journal: Journal of the Royal Society of Medicine (2006)

Ezzati et al. (May 2006 JRSM 1 ) misplace their confidence by a wide margin in claiming to have reached the first 'unbiased' estimates of state and national levels and trends of obesity in the USA.To do so, they claim to have calculated rates of self-reporting biases using data from the NHANES (National Health and Nutrition Examination Survey) and Behavioral Risk Factor Surveillance System (BRFSS) surveys of the US Center for Disease Control and Prevention, which were assumed to be representative of the USA population on the basis of the original sampling design.In reality the assumption is questionable, the response rates being about 80% for NHANES and 45% for BRFSS.If nothing else, such a discrepancy sets a distance between what the two surveys may represent, also considering that the surveys represent different samples.In a crucial decision, Ezzati et al. excluded subjects who did not participate in both surveys-an exclusion that inevitably invalidates any claim that the bias estimates reached could be representative of the USA population or of individual state populations.Such elementary flaws lead to ask how scarce resources could be approved for such a wanting study design.
Anti-Invasive, Antitumoral, and Antiangiogenic Efficacy of a Pyrimidine-2,4,6-trione Derivative, an Orally Active and Selective Matrix Metalloproteinases Inhibitor
Authors: Erik Maquoi, Nor Eddine Sounni, Laetitia Devy, Fabrice Olivier, Francis Frankenne, Hans-Willi Krell, Frank Grams, Jean-Michel Foidart, Agnès Noël
Journal: Clinical Cancer Research (2004)

Abstract Purpose: The implication of matrix metalloproteinases (MMPs) in the major stages of cancer progression has fueled interest in the design of synthetic MMP inhibitors (MMPIs) as a novel anticancer therapy. Thus far, drugs used in clinical trials are broad-spectrum MMPIs the therapeutic index of which proved disappointingly low. The development of selective MMPIs for tumor progression-associated MMPs is, thus, likely to offer improved therapeutic possibilities. Experimental Design: The anti-invasive capacity of a series of pyrimidine-trione derivatives was tested in vitro in a chemoinvasion assay, and the most potent compound was further evaluated in vivo in different human tumor xenograft models. The activity of this novel selective MMPI was compared with BB-94, a broad-spectrum inhibitor. Results: Ro-28-2653, an inhibitor with high selectivity for MMP-2, MMP-9, and membrane type 1 (MT1)-MMP, showed the highest anti-invasive activity in vitro. In vivo, Ro-28-2653 reduced the growth of tumors induced by the inoculation of different cell lines producing MMPs and inhibited the tumor-promoting effect of fibroblasts on breast adenocarcinoma cells. Furthermore, Ro-28-2653 reduced tumor vascularization and blocked angiogenesis in a rat aortic ring assay. In contrast, BB-94 up-regulated MMP-9 expression in tumor cells and promoted angiogenesis in the aortic ring assay. Conclusion: Ro-28-2653, a selective and orally bioavailable MMPI with inhibitory activity against MMPs expressed by tumor and/or stromal cells, is a potent antitumor and antiangiogenic agent. In contrast to broad-spectrum inhibitors, the administration of Ro-28-2653 was not associated with the occurrence of adverse side effects that might hamper the therapeutic potential of these drugs.
Spanish woman becomes pregnant through ovarian tissue transplantation
Authors: A. Garcia Rada
Journal: BMJ (2012)

A team of surgeons from a hospital in Barcelona has achieved the first known pregnancy through transplanting ovarian tissue. 

The patient, now aged 31, had both ovaries removed in 2001 because of bilateral ovarian tumors, but some viable tissue was preserved by freezing and was reimplanted when the patient said she would like to become pregnant.

Worldwide, 13 live and healthy children are known to have been conceived through transplantation of ovarian tissue, but Justo Callejo, …
Glycine and uridine preventd-galactosamine hepatotoxicity in the rat: Role of kupffer cells
Authors: Robert F. Stachlewitz, Vitor Seabra, Blair Bradford, Cynthia A. Bradham, Ivan Rusyn, Dori Germolec, Ronald G. Thurman
Journal: Hepatology (1999)

Extrahepatic factors, such as increased gut permeability and bacteria from the gut, have been shown to play a role in d –galactosamine toxicity in rats. Because bacterial endotoxin activates Kupffer cells, the purpose of this study was to clarify the role of Kupffer cells in the mechanism of d –galactosamine hepatotoxicity in rats and determine whether uridine, a compound that rescues animals from d –galactosamine toxicity, affects Kupffer cells. Rats were fed control or glycine (5%) containing diets to prevent Kupffer cell activation or treated with gadolinium chloride (GdCl 3 , 20 mg/kg) to destroy Kupffer cells selectively before injection of d –galactosamine(500 mg/kg, intraperitoneally). d –galactosamine caused panlobular focal hepatocellular necrosis, polymorphonuclear cell infiltration, and increased serum transaminases significantly at 24 hours. Dietary glycine or pretreatment with GdCl 3 prevented these effects. d –galactosamine caused a transient increase in circulating endotoxin that was maximal at 1 hour and was blunted significantly by dietary glycine. Additionally, antisera to tumor necrosis factor–α (TNF–α) prevented hepatotoxicity caused by d –galactosamine. Moreover, apoptosis in hepatocytes caused by d –galactosamine occurred before necrosis (6 hours) and was prevented by glycine, GdCl 3 , TNF–α antiserum, and uridine. Thus, it was hypothesized that TNF–α from Kupffer cells causes apoptosis after d –galactosamine administration in the rat. Indeed, increases in TNF–α messenger RNA (mRNA) were detected as early as 2.5 hours after d –galactosamine treatment. Previous work proposed that uridine blocks d –galactosamine toxicity by preventing inhibition of mRNA synthesis. In view of these results, the possibility that uridine might affect Kupffer cells was investigated. Uridine significantly blunted the increase in [Ca 2+ ] i and release of TNF–α caused by endotoxin in isolated Kupffer cells and prevented apoptosis caused by d –galactosamine treatment in vivo . These data support the hypothesis that uridine prevents d –galactosamine hepatotoxicity not only by rescuing the hepatocyte in the late phases of the injury but also preventing TNF–α release from Kupffer cells thereby blocking apoptosis that occurs early after d –galactosamine treatment. Taken together, these data strongly support the role of Kupffer cell activation by endotoxin early after d –galactosamine treatment as an important event in the mechanism of hepatotoxicity in the rat.
CCL3 (MIP-1α) plasma levels and the risk for disease progression in chronic lymphocytic leukemia
Authors: Mariela Sivina, Elena Hartmann, Thomas J. Kipps, Laura Rassenti, Diana Krupnik, Susan Lerner, Ruth LaPushin, Lianchun Xiao, Xuelin Huang, Lillian Werner, Donna Neuberg, Hagop Kantarjian, Susan O'Brien, William G. Wierda, Michael J. Keating, Andreas Rosenwald, Jan A. Burger
Journal: Blood (2010)
Breast cancer metastasis suppressor 1 (BRMS1) inhibits osteopontin transcription by abrogating NF-κB activation
Authors: Rajeev S Samant, David W Clark, Rebecca A Fillmore, Muzaffer Cicek, Brandon J Metge, Kondethimmana H Chandramouli, Ann F Chambers, Graham Casey, Danny R Welch, Lalita A Shevde
Journal: Molecular Cancer (2007)

Abstract Background Osteopontin (OPN), a secreted phosphoglycoprotein, has been strongly associated with tumor progression and aggressive cancers. MDA-MB-435 cells secrete very high levels of OPN. However metastasis-suppressed MDA-MB-435 cells, which were transfected with breast cancer metastasis suppressor 1 (BRMS1), expressed significantly less OPN. BRMS1 is a member of mSin3-HDAC transcription co-repressor complex and has been shown to suppress the metastasis of breast cancer and melanoma cells in animal models. Hence we hypothesized that BRMS1 regulates OPN expression. Results The search for a BRMS1-regulated site on the OPN promoter, using luciferase reporter assays of the promoter deletions, identified a novel NF-κB site (OPN/NF-κB). Electrophoretic mobility shift assays and chromatin immunoprecipitations (ChIP) confirmed this site to be an NF-κB-binding site. We also show a role of HDAC3 in suppression of OPN via OPN/NF-κB. Conclusion Our results show that BRMS1 regulates OPN transcription by abrogating NF-κB activation. Thus, we identify OPN, a tumor-metastasis activator, as a crucial downstream target of BRMS1. Suppression of OPN may be one of the possible underlying mechanisms of BRMS1-dependent suppression of tumor metastasis.
New time dependent prognostic models for Primary Sclerosing Cholangitis (PSC)
Authors: G. Rocca, K.M. Boberg, T. Egeland, A. Bergquist, U. Broomé, L. Caballeria, R. Chapman, R. Hultcrantz, S. Mitchell, A. Pares, F. Rosina, E. Schrumpf
Journal: Journal of Hepatology (2000)
Effect of protein ingestion on splanchnic and leg metabolism in normal man and in patients with diabetes mellitus.
Authors: J Wahren, P Felig, L Hagenfeldt
Journal: Journal of Clinical Investigation (1976)

The inter-organ flux of substrates after a protein-rich meal was studied in seven healthy subjects and in eight patients, with diabetes mellitus. Arterial concentrations as well as leg and splanchnic exchange of amino acids, carbohydrate substrates, free fatty acids (FFA), and ketone bodies were examined in the basal state and for 3 h after the ingestion of lean beef (3 g/kg body wt). Insulin was withheld for 24 h before the study in the diabetic patients. In the normal subjects, after protein ingestion, there was a large amino acid release from the splanchnic bed predominantly involving the branched chain amino acids. Valine, isoleucine, and leucine accounted together for more than half of total splanchnic amino acid output. Large increments were seen in the arterial concentrations of the branched chain amino acids (100-200%) and to a smaller extent for other amino acids. Leg exchange of most amino acids reverted from a basal net outut to a net uptake after protein feeding which was most marked for the branched chain amino acids. The latter accounted for more than half of total peripheral amino acid uptake...
Mens corpora e mens sano
Authors: P McCrory
Journal: British Journal of Sports Medicine (2003)

Interested in a Faustian bargain? Some recent research tells us how to improve brain performance, feel better and live for 500 years while doing some healthy exercise to boot. Mind you there is a downside—you have to give up most foods, exercise like an Olympian, take supplements, and put up with bad breath and flatulence. Oh, and you have to get neutered as well. I knew there was a catch somewhere!

Although many athletes seem overly keen to take creatine as an ergogenic …
Scaling patterns of interhemispheric connectivity in eutherian mammals
Authors: Emmanuel Gilissen
Journal: Behavioral and Brain Sciences (2006)

Because network scaling costs tend to limit absolute brain size, Striedter suggests that large cetacean brains must have evolved some novel ways to cope with these costs. A new analysis of available data shows that the scaling pattern of interhemispheric connectivity in cetaceans is isometric and differs from that observed in terrestrial mammals.
Effect of passive smoking in pregnancy on maternal, fetal and neonatal morbidities
Authors: Bouthayna Ben Safta, Jihene Ben Amar, Besma Dhahri, Saloua Azzabi, Mohammed Ali Baccar, Hichem Aouina, Hend Bouacha
Journal: European Respiratory Journal (2014)

Introduction:   Active maternal smoking during pregnancy is recognized as the most preventable risk factor for adverse birth outcomes. However, the effect of passive maternal smoking is less clear and has not been extensively studied.   Aim of the study: To demonstrate whether maternal passive exposure to tobacco smoke during pregnancy is associated with maternal fetal and neonatal complications.   Material and methods :  Our study compared 42 pregnant women exposed to passive smoking and 45 others non-exposed. We collected data on the course of their pregnancy and neonatal period.   Results :  The mean age of our patients was 31 years (20 to 44 years). The number of pregnancies per women was 2.2. Among exposed patients, we had one diabetic and another hypertensive and among the other group, we had 3 diabetics, 2 hypertensives and one asthmatic. During their pregnancies, gestational diabetes occurred in 11 exposed women (EW) and in 5 non-exposed women (NEW) (OR=3.8, p=0.349). Toxemia occurred in 7EW and in 5NEW (OR=1.6, p=0.453). Premature rupture of the amniotic sac happened in 3 EW and 1NEW at least at one of their pregnancies (OR=3.8, p=0.349). 16 EW and 9 NEW had at least one abortion and one fetal death in utero (OR=2.46, p=0.62). Fetal development was complicated with an intrauterine growth retardation in 4 EW and 2 NEW and with malformation in 2 EW and in 1 NEW (OR=2.2, p=0.608). Acute fetal distress happened in 4 EW (p=0.50). Neonatal respiratory complications have been recorded in 8 EW and 1 new born ( OR=10.35,p=0.13).   Conclusion   Passive smoking seems to increase the risk of maternal, fetal and even neonatal complications. An awareness program is mandatory to avoid such morbidities.
ANTIBODY RESPONSE IN PRIMARY HUMAN IMMUNODEFICIENCY VIRUS INFECTION
Authors: Hans Gaines, Anders Sönnerborg, Jan Czajkowski, Francesca Chiodi, EvaMaria Fenyö, MadeleineVon Sydow, Jan Albert, PehrOlov Pehrson, Lars Moberg, Birgitta Åsjö, Marianne Forsgren
Journal: The Lancet (1987)
Alzheimer's Disease: Molecular Understanding Predicts Amyloid-Based Therapeutics
Authors: Dennis J. Selkoe, Dale Schenk
Journal: The Annual Review of Pharmacology and Toxicology (2003)

Degenerative diseases of the brain were long considered among the most obscure and intractable of human maladies. However, recent advances in understanding their mechanisms have brought us to the verge of potential disease-modifying agents. This progress is perhaps best exemplified by the case of Alzheimer's disease. The application of molecular pathology and genetics has led to the recognition that the four genes implicated to date in familial Alzheimer's disease all chronically elevate cerebral levels of the amyloid β-protein (Aβ). Accordingly, small molecule inhibitors of the β- and γ-secretases, the proteases that generate Aβ from its precursor, are under active development, and some have shown in vivo efficacy in mouse models. An alternative approach, active or passive immunization against Aβ, has received extensive pre-clinical validation in mice, but an effective preparation free of significant side effects in humans is still awaited. Several other potential therapies are also reviewed here. If one or more of these varied approaches is ultimately proven to slow or prevent dementia, Alzheimer's disease will become a salient example of the successful application of reductionist biology to the most complex of organs, the human cerebral cortex.
Cystic Fibrosis Pulmonary Guidelines
Authors: Patrick A. Flume, Brian P. O'Sullivan, Karen A. Robinson, Christopher H. Goss, Peter J. Mogayzel, Donna Beth Willey-Courand, Janet Bujan, Jonathan Finder, Mary Lester, Lynne Quittell, Randall Rosenblatt, Robert L. Vender, Leslie Hazle, Kathy Sabadosa, Bruce Marshall
Journal: American Journal of Respiratory and Critical Care Medicine (2007)

Section:ChooseTop of pageAbstract <<METHODSRESULTSRECOMMENDATIONSKey Unanswered QuestionsConclusionsReferencesCITING ARTICLES
Potentiation of TRPV4 signalling by histamine and serotonin: an important mechanism for visceral hypersensitivity
Authors: N. Cenac, C. Altier, J.-P. Motta, E. d'Aldebert, S. Galeano, G. W Zamponi, N. Vergnolle
Journal: Gut (2010)

<h3>Background</h3> Although evidence points to a role for histamine and serotonin in visceral hypersensitivity, activation of calcium channels such as transient receptor potential vanilloid 4 (TRPV4) also causes visceral hypersensitivity. We hypothesised that TRPV4 is important for the generation of hypersensitivity, mediating histamine- and serotonin-induced visceral hypersensitivity. <h3>Methods</h3> In response to histamine, serotonin and/or TRPV4 agonist (4αPDD), calcium signals and TRPV4 localisation studies were performed on dorsal root ganglia (DRG) neurons projecting from the colon. To evaluate visceral nociception, colorectal distension (CRD) was performed in mice treated with serotonin or histamine and with 4αPDD. Intrathecal injection of TRPV4 silencer RNA (SiRNA) or mismatch SiRNA was used to target TRPV4 expression. <h3>Results</h3> Pre-exposure of DRG neurons projecting from the colon, to histamine or serotonin, increased Ca<sup>2+</sup> responses induced by 4αPDD by a protein kinase C (PKC), phospholipase Cβ (PLCβ), mitogen-activated protein kinase kinase (MAPKK) and phospholipase A<sub>2</sub> (PLA<sub>2</sub>)-dependent mechanisms. Serotonin or histamine treatments enhanced TRPV4 expression at the plasma membrane by a MAPKK mechanism. Hypersensitivity induced by serotonin or histamine were both significantly inhibited by TRPV4 SiRNA intrathecal injection. Administration of sub-nociceptive doses of serotonin or histamine potentiated 4αPDD-induced hypersensitivity in response to CRD. <h3>Conclusions</h3> Serotonin and histamine sensitise TRPV4 response to 4αPDD both in vivo (increased visceral hypersensitivity) and in vitro, in sensory neurons, by a PKC, PLA<sub>2</sub>, PLCβ and MAPKK-dependent mechanism. Serotonin and histamine caused a MAPKK-dependent increase in TRPV4 expression in colonic sensory neurons plasma membranes. Further, histamine- or serotonin-mediated visceral hypersensitivity depend on TRPV4 expression in sensory neurons. TRPV4 appears as a common mechanism to several known mediators of visceral hypersensitivity.
Effect of a Paraprofessional Home-Visiting Intervention on American Indian Teen Mothers’ and Infants’ Behavioral Risks: A Randomized Controlled Trial
Authors: Allison Barlow, Britta Mullany, Nicole Neault, Scott Compton, Alice Carter, Ranelda Hastings, Trudy Billy, Valerie Coho-Mescal, Sherilynn Lorenzo, John T. Walkup
Journal: American Journal of Psychiatry (2013)

Objective The authors sought to examine the effectiveness of Family Spirit, a paraprofessional-delivered, home-visiting pregnancy and early childhood intervention, in improving American Indian teen mothers' parenting outcomes and mothers' and children's emotional and behavioral functioning 12 months postpartum. Method Pregnant American Indian teens (N=322) from four southwestern tribal reservation communities were randomly assigned in equal numbers to the Family Spirit intervention plus optimized standard care or to optimized standard care alone. Parent and child emotional and behavioral outcome data were collected at baseline and at 2, 6, and 12 months postpartum using self-reports, interviews, and observational measures. Results At 12 months postpartum, mothers in the intervention group had significantly greater parenting knowledge, parenting self-efficacy, and home safety attitudes and fewer externalizing behaviors, and their children had fewer externalizing problems. In a subsample of mothers with any lifetime substance use at baseline (N=285; 88.5%), children in the intervention group had fewer externalizing and dysregulation problems than those in the standard care group, and fewer scored in the clinically "at risk" range (≥10th percentile) for externalizing and internalizing problems. No between-group differences were observed for outcomes measured by the Home Observation for Measurement of the Environment scale. Conclusions Outcomes 12 months postpartum suggest that the Family Spirit intervention improves parenting and infant outcomes that predict lower lifetime behavioral and drug use risk for participating teen mothers and children.
Local Intramural Delivery of <scp>l</scp> -Arginine Enhances Nitric Oxide Generation and Inhibits Lesion Formation After Balloon Angioplasty
Authors: Severin P. Schwarzacher, Tai T. Lim, Bingyin Wang, Robert S. Kernoff, Josef Niebauer, John P. Cooke, Alan C. Yeung
Journal: Circulation (1997)

Background Long-term oral administration of l -arginine has been shown to enhance production of nitric oxide (NO) and to reduce lesion formation. The goal of this study was to determine whether local intramural administration of l -arginine could enhance NO generation and reduce intimal thickening. Methods and Results New Zealand White rabbits (n=27) received a 1% cholesterol diet. For the short-term study, after 1 week of diet, both iliac arteries were balloon injured. Four weeks later, vasoreactivity was assessed angiographically during infusion of acetylcholine (Ach) before and after delivery of l -arginine or saline into the right or left iliac artery (800 mg/5 mL; 0.2 mL/min, 15 minutes) by use of a local drug-delivery balloon. Vessels were then harvested for measurements of NO. For the long-term study, after balloon injury, drugs were delivered as above into the iliac arteries. Two and 4 weeks after l -arginine delivery, vasoreactivity was determined. Subsequently, the iliac arteries were harvested for histomorphometric analysis and measurements of NO. In the short-term study, local delivery of l -arginine restored endothelium-dependent vasodilatation (Ach 10 −5 mol/L; l -arginine +35±10%; saline −14±5%; P &lt;.001) and enhanced local production of nitrogen oxides ( l -arginine 152±28; saline 78±12 nmol/L per milligram of tissue per hour; P &lt;.04). In the long-term study, local administration of l -arginine enhanced vascular NO production as long as 1 week after the injury ( l -arginine 394.4±141.6; saline 86.3±34.3 nmol/L per milligram of tissue per hour; P &lt;.01) and reduced intimal thickening 4 weeks later (intima/media ratio: l -arginine 0.56±0.1; saline 1.40±0.2; P &lt;.001), largely due to suppression of macrophage accumulation. Conclusions A single intramural administration of l -arginine enhances vascular NO generation and inhibits lesion formation. Local augmentation of NO production at the site of balloon angioplasty may be a novel strategy to prevent restenosis.