tbuckley/cabot-search huggingface dataset:
<i>Helicobacter pylori </i>in gastro-oesophageal reflux disease: causal agent, independent or protective factor?
Authors: JOACHIM LABENZ, PETER MALFERTHEINER
Journal: Gut (1997)

Helicobacter pylori causes chronic gastritis with variable activity and topographic distribution. Patient age at acquisition, expression of gastritis, strain virulence, host factors, and environmental factors determine the outcome of the infection. Well established consequences are peptic ulcer disease (PUD) and gastric neoplasia.1-4 

As duodenal ulcer is often associated with gastro-oesophageal reflux disease (GORD),5 and antral gastritis is a frequent finding in patients with reflux disease,6 H pylori infection may be a common cause of both conditions. Our aim was to explore the strength of the postulate that H pylori is a causal factor in GORD by reviewing publications on epidemiological studies, clinical observations or treatment trials, and identifying possible pathogenic mechanisms.

Currently, we have no clear data to show that patients with GORD are more frequently infected by H pylori than controls, neither in adults nor in children.7 Indeed, a recent well designed case control study from Japan showed a significantly lower incidence of H pylori infection in patients with reflux oesophagitis than in age and sex matched controls.8 This finding is supported by one of our own studies.9 The prevalence of both H pylori infection and GORD increases with age.10 11 Male sex is a risk factor for GORD,12 but the prevalence of H pylori is equally distributed between men and women.10 12 

H pylori is able to colonise Barrett’s epithelium. Many uncontrolled studies showed H pylori prevalence rates similar to those in the background population.7 Also, in a controlled study the prevalence of H pylori infection was similar in patients with Barrett’s oesophagus and controls.13 However, patients with Barrett’s oesophagus and an ulcer within the columnar metaplasia were more frequently infected by H pylori than those without ulcers.14 

The prevalence of H pylori infection is decreasing …
Albuminuria and Kidney Function Independently Predict Cardiovascular and Renal Outcomes in Diabetes
Authors: Toshiharu Ninomiya, Vlado Perkovic, Bastiaan E. de Galan, Sophia Zoungas, Avinesh Pillai, Meg Jardine, Anushka Patel, Alan Cass, Bruce Neal, Neil Poulter, Carl-Erik Mogensen, Mark Cooper, Michel Marre, Bryan Williams, Pavel Hamet, Giuseppe Mancia, Mark Woodward, Stephen MacMahon, John Chalmers
Journal: Journal of the American Society of Nephrology (2009)

There are limited data regarding whether albuminuria and reduced estimated GFR (eGFR) are separate and independent risk factors for cardiovascular and renal events among individuals with type 2 diabetes. The Action in Diabetes and Vascular disease: preterAx and diamicroN-MR Controlled Evaluation (ADVANCE) study examined the effects of routine BP lowering on adverse outcomes in type 2 diabetes. We investigated the effects of urinary albumin-to-creatinine ratio (UACR) and eGFR on the risk for cardiovascular and renal events in 10,640 patients with available data. During an average 4.3-yr follow-up, 938 (8.8%) patients experienced a cardiovascular event and 107 (1.0%) experienced a renal event. The multivariable-adjusted hazard ratio for cardiovascular events was 2.48 (95% confidence interval 1.74 to 3.52) for every 10-fold increase in baseline UACR and 2.20 (95% confidence interval 1.09 to 4.43) for every halving of baseline eGFR, after adjustment for regression dilution. There was no evidence of interaction between the effects of higher UACR and lower eGFR. Patients with both UACR >300 mg/g and eGFR <60 ml/min per 1.73 m2 at baseline had a 3.2-fold higher risk for cardiovascular events and a 22.2-fold higher risk for renal events, compared with patients with neither of these risk factors. In conclusion, high albuminuria and low eGFR are independent risk factors for cardiovascular and renal events among patients with type 2 diabetes.
Daylight robbery: Hospitals admissions for childhood asthma in English regions are inversely associated with hours of sunshine
Authors: Will Carroll, Amelia Saunders, Khaled Ismail, William Farrell, Richard Emes, Anthony Fryer
Journal: European Respiratory Journal (2014)

Background: Vitamin D is implicated in the expression of childhood asthma but it is difficult to pick apart cause and effect from observational data. If lack of vitamin D is secondary to a sedentary lifestyle then weather patterns should not effect asthma severity.

Aims: To examine long-term meteorological data for English regions, matching this with patterns of hospital use.

Methods: We interrogated two public databases to determine hours of sunlight (www.metoffice.gov.uk) and age and gender corrected hospital admission rates for children with asthma (www.hscic.gov.uk/hes) in English regions. The relationship between asthma hospitalisations, hours of sunshine and deprivation indices were examined using linear regression using STATA v 10.0.

Results: Data were available for 9 consecutive years between 2002 and 2011. There was a strong inverse correlation between hours of sunshine and asthma hospitalisations in children. This relationship was highly statistically significant (p<0.001) and this effect was undiminished following correction for deprivation index.

![Figure][1] 



Conclusions: The strong relationship between annual hours of sunshine and hospital admission for asthma in children adds weight to observational data that vitamin D is a determinant of asthma severity. It is likely that good diet and outdoor activities can reduce the burden of asthma for children and intervention studies are required.

 [1]: pending:yes
Activity of the renin-angiotensin system in acute severe asthma and the effect of angiotensin II on lung function.
Authors: E A Millar, R M Angus, G Hulks, J J Morton, J M Connell, N C Thomson
Journal: Thorax (1994)

The activity of the renin-angiotensin system in asthma has not been studied previously and the effect of angiotensin II (AII) on bronchomotor tone in vivo is unknown.Plasma levels of renin and AII levels were measured in 20 patients with acute severe asthma, nine with mild asthma, 10 with severe chronic asthma, and 16 normal volunteers. The effect of AII, given as an intravenous infusion, on bronchomotor tone was also investigated in eight mild asthmatic patients.In acute severe asthma plasma levels of renin [median (interquartile range)] were elevated on days 1, 2, and 5 after admission [48.7 (24-79), 44.2 (15-75), and 45.5 (21-70) microU/ml, respectively]. Plasma AII levels were significantly elevated at day 5 [56 (12-109) pg/ml]. In the second study a bronchoconstrictor response to intravenous AII was seen with a mean (SE) maximal fall in FEV1 of 0.34 (0.13) litres or 12.4 (3.3)% from baseline following the high dose infusion of AII (8 ng/kg/min) with a corresponding plasma AII concentration of 121.3 pg/ml.The renin-angiotensin system is activated in acute asthma and AII causes bronchoconstriction in vivo in man. These observations suggest that in some patients AII may contribute to bronchoconstriction during acute severe asthma.
In Vivo Inhibition of Murine Leukemia and Sarcoma Viruses by the Heteropolyanion 5-Tungsto-2-antimoniate2
Authors: Claude Jasmin, Jean-Claude Chermann, Gilbert Herve, André Teze, Pierre Souchay, Christiane Boy-Loustau, Nicole Raybaud, Françoise Sinoussi, Marcel Raynaud
Journal: JNCI Journal of the National Cancer Institute (1974)

Journal Article In Vivo Inhibition of Murine Leukemia and Sarcoma Viruses by the Heteropolyanion 5-Tungsto-2-antimoniate Get access Claude Jasmin, Claude Jasmin Search for other works by this author on: Oxford Academic PubMed Google Scholar Jean-Claude Chermann, Jean-Claude Chermann Search for other works by this author on: Oxford Academic PubMed Google Scholar Gilbert Herve, Gilbert Herve Search for other works by this author on: Oxford Academic PubMed Google Scholar André Teze, André Teze Search for other works by this author on: Oxford Academic PubMed Google Scholar Pierre Souchay, Pierre Souchay Search for other works by this author on: Oxford Academic PubMed Google Scholar Christiane Boy-Loustau, Christiane Boy-Loustau Search for other works by this author on: Oxford Academic PubMed Google Scholar Nicole Raybaud, Nicole Raybaud Search for other works by this author on: Oxford Academic PubMed Google Scholar Françoise Sinoussi, Françoise Sinoussi Search for other works by this author on: Oxford Academic PubMed Google Scholar Marcel Raynaud Marcel Raynaud Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 53, Issue 2, August 1974, Pages 469–474, https://doi.org/10.1093/jnci/53.2.469 Published: 01 August 1974 Article history Received: 11 January 1974 Accepted: 30 April 1974 Published: 01 August 1974
840 SEPTIN 9 REGULATES LIPID DROPLETS ACCUMULATION AND HEPATITIS C VIRUS REPLICATION IN A SUMO1 DEPENDENT PROCESS
Authors: A. Abdallah, C. Gondeau, M. Marin, S. Sar, J. Peng, P. Briolotti, S. Benjelloun, A. Benjouad, P. Maurel, D. Samuel, C. Brechot, A. Gassama
Journal: Journal of Hepatology (2012)
RHEUMATOID FACTOR AND THE PATHOGENESIS OF RHEUMATOID ARTHRITIS
Authors: Robert C. Mellors, Adam Nowoslawski, Leonhard Korngold, Beth L. Sengson
Journal: The Journal of Experimental Medicine (1961)

In analogy with the two categories of reactants which are used in the serological tests for the unusual category of macroglobulins called rheumatoid factor, two fluorescent reactants have been prepared for the detection of rheumatoid factor in situ in tissue sections: fluorescent antigen-rabbit antibody (immune) complex, in the present study, and fluorescent aggregated human gamma-globulin, in previous work. Plasma cells in the synovial membrane and germinal center cells and internodular plasma cells in lymph nodes are the sites of origin of rheumatoid factor in active rheumatoid arthritis, whether occurring in adults or children. Plasma cells and germinal center cells which form rheumatoid factor detectable with fluorescent immune complex are less numerous than those which contain factor demonstrable with fluorescent aggregate. In the same tissues, plasma cells and germinal center cells which contain macroglobulin (19S human gamma-globulin) detectable with fluorescent antibody-but not showing the reactivity of rheumatoid factor-are more abundant than those containing rheumatoid factor. While macroglobulin and rheumatoid factor are almost exclusively formed in the cytoplasm, these proteins are also detectable in the nucleus of an occasional plasma cell. Normal and pathological synovial and capsular tissues, lymph nodes, and connective tissues obtained from individuals without rheumatoid arthritis are not stained with fluorescent immune complex or, except for an unusual example of Waldenstrom's macroglobulinemia, with fluorescent aggregate. The cellular origin, as well as certain chemical and immunological attributes, of rheumatoid factor suggests an antibody-like nature and function. The observations cited are consistent with the behavior anticipated for cellular rheumatoid factor, were it primarily an antibody direct to an altered human gamma-globulin and cross-reacting with rabbit gamma-globulin. However, it is also possible that there are two or more cellular rheumatoid factors. Lesion-associated protein precipitates having the composition anticipated for rheumatoid factor-antigen complex are localized in the amyloid depositions in kidney and spleen of an individual who died with amyloidosis secondary to rheumatoid arthritis.
Paricalcitol Inhibits Renal Inflammation by Promoting Vitamin D Receptor–Mediated Sequestration of NF-κB Signaling
Authors: Xiaoyue Tan, Xiaoyan Wen, Youhua Liu
Journal: Journal of the American Society of Nephrology (2008)

Inflammation is a pathologic feature of a variety of chronic kidney diseases. Several lines of evidence suggest a potential anti-inflammatory role for vitamin D in chronic kidney disease, but the underlying mechanism remains unknown. Here, the effect of the synthetic vitamin D analogue paricalcitol on renal inflammation was investigated in a mouse model of obstructive nephropathy. Paricalcitol reduced infiltration of T cells and macrophages in the obstructed kidney. This inhibition of inflammatory cell infiltration was accompanied by a decreased expression of RANTES and TNF-α. Induction of RANTES was localized primarily to the tubular epithelium, underscoring a role for tubular cells in renal inflammation. In a human proximal tubular cell line (HKC-8), paricalcitol inhibited RANTES mRNA and protein expression and abolished the ability of tubular cells to recruit lymphocytes and monocytes after TNF-α stimulation. Although RANTES induction depended on NF-κB signaling, paricalcitol affected neither TNF-α–mediated IκBα phosphorylation and degradation nor p65 NF-κB activation and nuclear translocation. Instead, chromatin immunoprecipitation assay showed that paricalcitol abolished the binding of p65 to its cognate cis-acting element in the RANTES promoter. The vitamin D receptor (VDR) and p65 formed a complex in tubular cells after paricalcitol treatment, which inhibited the ability of p65 to trans-activate gene transcription. In vivo, paricalcitol did not block NF-κB nuclear translocation after obstructive injury but did increase the expression and nuclear distribution of VDR. These results suggest that paricalcitol inhibits renal inflammatory infiltration and RANTES expression by promoting VDR-mediated sequestration of NF-κB signaling.
Angiotensin-converting enzyme (CD143) marks hematopoietic stem cells in human embryonic, fetal, and adult hematopoietic tissues
Authors: Vanta J. Jokubaitis, Lidia Sinka, Rebecca Driessen, Genevieve Whitty, David N. Haylock, Ivan Bertoncello, Ian Smith, Bruno Péault, Manuela Tavian, Paul J. Simmons
Journal: Blood (2007)
Effects of a 3-month course of rosuvastatin in patients with systemic lupus erythematosus
Authors: M D de Kruif, M Limper, H R Hansen, J de Ruiter, C A Spek, E C M van Gorp, I J ten Berge, A T Rowshani, H ten Cate, E W Meesters
Journal: Annals of the Rheumatic Diseases (2009)

Systemic lupus erythematosus (SLE) is associated with a highly increased cardiovascular risk. Statins can reduce this risk, but may possess additional anti-inflammatory effects that are relevant for the treatment of SLE. In a preliminary study, we investigated the effects of a 3-month course of rosuvastatin on lipids and markers of inflammation using a randomised cross-over design.

The study was approved by the institutional medical and ethical committee and written informed consent was obtained from all subjects. Based upon a previous, representative study,1 a sample size of 14 patients would be necessary to demonstrate a 25% reduction in C-reactive protein (CRP) levels (power = 80%). A dropout level of 35% (n = 5) was estimated.2 Patients with stable …
Dietary Supplement 4-Methylumbelliferone: An Effective Chemopreventive and Therapeutic Agent for Prostate Cancer
Authors: Travis J. Yates, Luis E. Lopez, Soum D. Lokeshwar, Nicolas Ortiz, Georgios Kallifatidis, Andre Jordan, Kelly Hoye, Norman Altman, Vinata B. Lokeshwar
Journal: JNCI Journal of the National Cancer Institute (2015)

Background:Prevention and treatment of advanced prostate cancer (PCa) by a nontoxic agent can improve outcome, while maintaining quality of life. 4-methylumbelliferone (4-MU) is a dietary supplement that inhibits hyaluronic acid (HA) synthesis. We evaluated the chemopreventive and therapeutic efficacy and mechanism of action of 4-MU.
Neuroligin-1–dependent competition regulates cortical synaptogenesis and synapse number
Authors: Hyung-Bae Kwon, Yevgenia Kozorovitskiy, Won-Jong Oh, Rui T Peixoto, Nazia Akhtar, Jessica L Saulnier, Chenghua Gu, Bernardo L Sabatini
Journal: Nature Neuroscience (2012)
Impact and Process Evaluation of Integrated Community and Clinic-Based HIV-1 Control: A Cluster-Randomised Trial in Eastern Zimbabwe
Authors: Simon Gregson, Saina Adamson, Spiwe Papaya, Jephias Mundondo, Constance A Nyamukapa, Peter R Mason, Geoffrey P Garnett, Stephen K Chandiwana, Geoff Foster, Roy M Anderson
Journal: PLoS Medicine (2007)

Background HIV-1 control in sub-Saharan Africa requires cost-effective and sustainable programmes that promote behaviour change and reduce cofactor sexually transmitted infections (STIs) at the population and individual levels. Methods and Findings We measured the feasibility of community-based peer education, free condom distribution, income-generating projects, and clinic-based STI treatment and counselling services and evaluated their impact on the incidence of HIV-1 measured over a 3-y period in a cluster-randomised controlled trial in eastern Zimbabwe. Analysis of primary outcomes was on an intention-to-treat basis. The income-generating projects proved impossible to implement in the prevailing economic climate. Despite greater programme activity and knowledge in the intervention communities, the incidence rate ratio of HIV-1 was 1.27 (95% confidence interval [CI] 0.92–1.75) compared to the control communities. No evidence was found for reduced incidence of self-reported STI symptoms or high-risk sexual behaviour in the intervention communities. Males who attended programme meetings had lower HIV-1 incidence (incidence rate ratio 0.48, 95% CI 0.24–0.98), and fewer men who attended programme meetings reported unprotected sex with casual partners (odds ratio 0.45, 95% CI 0.28–0.75). More male STI patients in the intervention communities reported cessation of symptoms (odds ratio 2.49, 95% CI 1.21–5.12). Conclusions Integrated peer education, condom distribution, and syndromic STI management did not reduce population-level HIV-1 incidence in a declining epidemic, despite reducing HIV-1 incidence in the immediate male target group. Our results highlight the need to assess the community-level impact of interventions that are effective amongst targeted population sub-groups.
Cured meat consumption increases risk of readmission in COPD patients
Authors: Jordi de Batlle, Michelle Mendez, Isabelle Romieu, Eva Balcells, Marta Benet, David Donaire-Gonzalez, Jaume J. Ferrer, Mauricio Orozco-Levi, Josep M. Antó, Judith Garcia-Aymerich
Journal: European Respiratory Journal (2012)

Recent studies have shown that a high dietary intake of cured meat increases the risk of chronic obstructive pulmonary disease (COPD) development. However, its potential effects on COPD evolution have not been tested. We aimed to assess the association between dietary intake of cured meat and risk of COPD readmission in COPD patients. 274 COPD patients were recruited during their first COPD admission between 2004 and 2006, provided information on dietary intake of cured meat during the previous 2 yrs, and were followed until December 31, 2007 (median follow-up 2.6 yrs). Associations between cured meat intake and COPD admissions were assessed using parametric regression survival–time models. Mean±sd age was 68±8 yrs, 93% of patients were male, 42% were current smokers, mean post-bronchodilator forced expiratory volume in 1 s (FEV<sub>1)</sub> was 53±16% predicted, and median cured meat intake was 23 g·day<sup>−1</sup>. After adjusting for age, FEV<sub>1</sub>, and total caloric intake, high cured meat intake (more than median value) increased the risk of COPD readmission (adjusted HR 2.02, 95% CI 1.31–3.12; p=0.001). High cured meat consumption increases the risk of COPD readmission in COPD patients. The assessment of the effectiveness of healthy diet advice should be considered in the future.
Immunological findings in blood and bronchoalveolar lavage fluid in chronic bronchitis patients with recurrent infectious exacerbations
Authors: I Qvarfordt, GC Riise, S Larsson, G Almqvist, J Rollof, T Bengtsson, BA Andersson
Journal: European Respiratory Journal (1998)

Bronchial infections are common in smokers and seem to be related to the presence of chronic bronchitis (CB). Why only some smokers develop repeated bronchial infections is not known. The aim of this study was to screen for immunological changes associated with disease in patients with CB and recurrent infectious exacerbations compared to asymptomatic smokers. Sixteen smokers with stable CB and recurrent infectious exacerbations, and 18 asymptomatic smokers, all without any immunomodulating treatment, underwent bronchoscopy and bronchoalveolar lavage (BAL). Smoking history and current smoking status were comparable. Serum levels of immunoglobulin (Ig)A, IgM, IgG and IgG subclasses were measured. Blood and BAL lymphocyte phenotypes and proliferative responses of peripheral blood mononuclear cells (PBMCs) to various stimulators were analysed. Unstimulated and tetanus toxoid-stimulated production of cytokines in PBMC cultures was measured. Natural killer (NK-) cell activity was analysed. A significantly (p&lt;0.05) lower level of IgG3 was found in the CB group, and a significantly (p&lt;0.01) higher proliferative response of PBMCs was found in the CB group after stimulation with diphtheria toxoid. Detectable levels of interleukin (IL)-6, tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma, but not of IL-2, IL-4 or transforming growth factor-beta2, were found in supernatants from cultured cells in both study groups. Stimulated TNF-alpha production was significantly (p&lt;0.05) higher in the CB group. NK-cell activity did not differ significantly between the study groups. There were no major differences between the groups in lymphocyte subpopulations in blood or BAL. In conclusion, no major alterations in the analysed indices of cell-mediated and humoral immunity were found in patients with chronic bronchitis prone to recurrent infectious exacerbations when compared with asymptomatic smoking controls.
Mechanical function of the heart and its alteration during myocardial ischemia and infarction. Specific reference to coronary atherosclerosis.
Authors: H J Swan
Journal: Circulation (1979)

Altered regional mechanical myocardial performance is an early, sensitive marker of myocardial ischemia, and can be estimated in man with reasonable accuracy. Identification, localization and quantification of abnormalities in mechanical performance can be used to predict the presence of coronary artery disease. Testing techniques that have little or no effect on diagnostic efficiency must be replaced with more sensitive indicators of ischemia. If experimental data are validated by findings in human subjects, accurate identification of regional wall motion changes during test conditions should prove to be a powerful marker of ischemia. To be of value, a diagnostic test must strongly increase the frequency of identification of subjects with a high probabilty for the presence of coronary artery disease in an otherwise low-prevalence population, and of those with known disease who are at the highest risk for complications including myocardial infarction or death.