2,517 research outputs found

    Grayanotoxin I Intoxication in Pet Pigs

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    Contaminated honey is a common cause of grayanotoxin intoxication in humans. Intoxication of animals, especially cattle, is usually due to ingestion of plants of the Ericaceae family, such as Rhododendron. Here, we report the ingestion of Pieris japonica as the cause of grayanotoxin I intoxication in 2 miniature pigs that were kept as pets. The pigs showed sudden onset of pale oral mucosa, tachycardia, tachypnea, hypersalivation, tremor, and ataxia that progressed to lateral recumbency. The pathological examination of one pig revealed no specific indications for intoxication except for the finding of plant material of Pieris japonica in the intestine. Grayanotoxin I was identified in the ingested plant, gastric content, blood, liver, bile, kidney, urine, lung, and skeletal muscle via HPLC-MS/MS. Grayanotoxin I should be considered as a differential etiological diagnosis in pigs with unspecific signs and discovery of ingested plant material as the only indication in the pathologic examination

    Associations of dyslipidaemia and lipid-lowering treatment with risk of postoperative cognitive dysfunction: a systematic review and meta-analysis

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    BACKGROUND: Lipid imbalance is linked to age-related cognitive impairment, but its role in postoperative cognitive dysfunction (POCD) is unknown. Here, we present a systematic review and meta-analysis on dyslipidaemia, lipid-lowering treatment and POCD risk. METHODS: PubMed, Ovid SP and Cochrane databases were searched for longitudinal studies that reported on associations of any measure of dyslipidaemia and/or lipid-lowering treatment with POCD as relative risks (RRs) or ORs. Fixed-effects inverse variance models were used to combine effects. RESULTS: Of 205 articles identified in the search, 17 studies on 2725 patients (grand mean age 67 years; mean age range 61-71 years) with follow-up periods of 1 day to 4 years (median 7 days; IQR 1-68 days) were included. Studies focused almost exclusively on hypercholesterolaemia as a measure of dyslipidaemia and on statins as lipid-lowering treatment. Across 12 studies on hypercholesterolaemia, we found no association with POCD risk (RR 0.93; 95% CI 0.80 to 1.08; P=0.34). Statin use before surgery was associated with a reduced POCD risk across eight studies (RR 0.81; 95% CI 0.67 to 0.98; P=0.03), but data on treatment duration were lacking. CONCLUSION: Statin users appear to be at reduced risk of POCD although hypercholesterolaemia per se may not be associated with POCD risk. Trial studies are needed to evaluate the usefulness of statins in POCD prevention

    Prediction of activity related energy expenditure using accelerometer derived physical activity under free-living conditions-a systematic review

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    BACKGROUND: Activity related energy expenditure (AEE) might be an important factor in the etiology of chronic diseases. However, measurement of free-living AEE is usually not feasible in large scale epidemiological studies but instead has traditionally been estimated based on self-reported physical activity. Recently, accelerometry has been proposed for objective assessment of physical activity, but it is unclear to what extent this methods explains the variance in AEE. METHODS: We conducted a systematic review searching MEDLINE database (until 2014) on studies that estimated AEE based on accelerometry-assessed physical activity in adults under free-living conditions (using doubly-labeled water method). Extracted study characteristics: sample size, accelerometer (type [uniaxial, triaxial], metrics [e.g. activity counts, steps, acceleration], recording period, body position, wear time), explained variance of AEE (R2), number of additional predictors. The relation of univariate and multivariate R2 with study characteristics was analyzed using non-parametric tests. RESULTS: Nineteen articles were identified. Examination of various accelerometers or subpopulations in one article was treated separately, resulting in 28 studies. Sample sizes ranged from 10-149. In most studies the accelerometer was triaxial, worn at the trunk, during waking hours, and reported activity counts as output metric. Recording periods ranged from 5-15 days. The variance of AEE explained by accelerometer assessed physical activity ranged from 4-80% (median crude R2=26%). Sample size was inversely related to the explained variance. Inclusion of 1 to 3 other predictors in addition to accelerometer output significantly increased the explained variance to a range of 12.5-86% (median total R2=41%). The increase did not depend on the number of added predictors. CONCLUSIONS: We conclude that there is large heterogeneity across studies in the explained variance of AEE when estimated based on accelerometry. Thus, data on predicted AEE based on accelerometry assessed physical activity need to be interpreted cautiously

    Hypertension and risk of post-operative cognitive dysfunction (POCD): a systematic review and meta-analysis

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    BACKGROUND: Post-operative cognitive dysfunction (POCD) occurs frequently after major surgery. Hypertension is well-established as a risk factor for age-related cognitive impairment, but it is unclear whether or not it also increases the risk of POCD. OBJECTIVE: To evaluate the role of hypertension in POCD risk in a systematic review and meta-analysis. METHOD: PubMed, Ovid SP and the Cochrane Database of Systematic Reviews were searched for longitudinal studies of adults undergoing surgery with reporting of hypertension, blood pressure and/or anti-hypertensive treatment associations with POCD as relative risks or odds ratios. Fixed-effects meta-analyses were performed using Review Manager (version 5.3). RESULTS: Twenty-four studies on 4317 patients (mean age 63 years) were included. None of the studies had set out to assess hypertension as a risk factor for POCD. Hypertension was used as a categorical predictor throughout and only 2 studies adjusted for potential confounders. Across all 24 studies, hypertension was not significantly associated with POCD risk (RR 1.01; 95% CI 0.93, 1.09; p=0.82), though among 8 studies with >75% males, we found hypertension associations with a 27% increased risk of POCD (RR 1.27, 95% CI 1.07, 1.49; p=0.005). CONCLUSION: Our findings do not support the hypothesis that hypertension is a risk factor for POCD. However, since none of the studies included in our analysis were hypothesis-driven and most did not adjust for potential confounders, further systematic investigations are needed to evaluate the role of hypertension in the epidemiology of POCD

    Influence of obesity and related metabolic alterations on colorectal cancer risk

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    Obesity and related metabolic alterations have been implicated to play a role in colorectal cancer risk. The metabolic syndrome, as assessed according to current international definitions by the key components, abdominal obesity, dyslipidemia, elevated blood pressure, and abnormal glucose metabolism, is associated with colorectal cancer. Recent studies suggest that abdominal obesity and abnormal glucose metabolism may primarily account for this association. Visceral adipose tissue is physiologically more active than subcutaneous adipose tissue and generates hormones and cytokines with inflammatory, metabolic, and direct carcinogenic potential, which may directly or indirectly increase colorectal cancer risk. Current evidence suggests that obesity acts as a risk factor for colorectal cancer by several mechanisms, including chronic low-grade inflammation, hyperinsulinemia, as well as alterations in insulin-like growth factor and adipokine concentrations. Metabolic biomarkers reflecting these processes may not only provide clues for etiological understanding of colorectal carcinogenesis but also might be an alternative way to define an "obesity phenotype" that is relevant for colorectal cancer development

    Genetic association analysis based on a joint model of gene expression and blood pressure

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    Recent work on genetic association studies suggests that much of the heritable variation in complex traits is unexplained, which indicates a need for using more biologically meaningful modeling approaches and appropriate statistical methods. In this study, we propose a biological framework and a corresponding statistical model incorporating multilevel biological measures, and illustrate it in the analysis of the real data provided by the Genetic Analysis Workshop (GAW) 19, which contains whole genome sequence (WGS), gene expression (GE), and blood pressure (BP) data. We investigate the direct effect of single-nucleotide variants (SNVs) on BP and GE, while considering the non-directional dependence between BP and GE, by using copula functions to jointly model BP and GE conditional on SNVs. We implement the method for analysis on a genome-wide scale, and illustrate it within an association analysis of 68,727 SNVs on chromosome 19 that lie in or around genes with available GE measures. Although there is no indication for inflated type I errors under the proposed method, our results show that the association tests have smaller p values than tests under univariate models for common and rare variants using single-variant tests and gene-based multimarker tests. Hence, considering multilevel biological measures and modeling the dependence structure between these measures by using a plausible graphical approach may lead to more informative findings than standard univariate tests of common variants and well-recognized gene-based rare variant tests

    Association between dietary factors and plasma fetuin-A concentrations in the general population

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    Circulating fetuin-A, a novel marker for hepatic fat accumulation, has been related to a higher risk of type 2 diabetes and cardiovascular diseases in a growing number of prospective studies. However, little is known about dietary determinants of fetuin-A concentrations in the general population. Therefore, we aimed to investigate the association between dietary intake of energy, energy-providing nutrients, alcohol and major food groups and plasma fetuin-A concentrations in the Bavarian Food Consumption Survey II. Dietary intake was assessed by three 24-h dietary recalls, and plasma concentrations of fetuin-A were measured in 558 adults (18-81 years). After multivariable adjustment for lifestyle factors and body fatness, higher energy intake was nonsignificantly associated with higher fetuin-A concentrations (per 2092 kJ/d (500 kcal/d) 3·7 µg/ml, 95 % CI -0·5, 7·8 µg/ml). There was no clear association between energy-providing nutrients and fetuin-A concentrations. Higher alcohol intake was associated with lower fetuin-A concentrations (P trend 0·003): mean fetuin-A concentrations were 324 (95 % CI 313, 335) µg/ml in non-drinkers, and with 293 (95 % CI 281, 306) µg/ml significantly lower in participants who drank ≥30 g alcohol per d. Mean fetuin-A concentrations decreased across quintiles of milk and dairy product intake (lowest quintile 319 (95 % CI 309, 330) µg/ml; highest quintile 304 (95 % CI 293, 314) µg/ml; P trend 0·03), and each 150-g increment in milk/dairy products per d was associated with 5·6 (95 % CI -9·6, -1·5) µg/ml lower fetuin-A. Dietary intakes of vegetables, meat or fish were not associated with fetuin-A concentrations. Because of the preventive potential of our findings, further exploration is warranted

    Increased periodontal attachment loss in patients with systemic sclerosis

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    Background: Patients with inflammatory rheumatic diseases and periodontitis share common pathogenetic characteristics, such as pro-inflammatory traits causative for tissue degradation and loss of function. Aim of the present case control study was to investigate the association between systemic sclerosis (SSc) and periodontitis. Methods: The association between SSc and periodontitis was examined in 58 SSc patients and 52 control patients, matched for age and gender. Periodontal examination included periodontal attachment loss, probing pocket depth, bleeding on probing, plaque index and gingival index. Potential risk factors of periodontitis were assessed through patients' questionnaires. Results: In unadjusted analyses, patients with SSc had a significant 0.61 mm higher periodontal attachment loss (95 % confidence interval (CI), 0.24 - 0.97; p = 0.002) when compared to controls. In a stepwise logistic regression, including SSc status, age, gender, education, smoking, alcohol consumption and BMI, only SSc status, age, and gender remained significantly associated with periodontitis. Adjusted for age and gender, patients with SSc had 0.52 mm higher periodontal attachment loss compared to controls (95 % CI, 0.16 - 0.88; p = 0.005). The strength of the association of SSc with periodontal attachment loss remained statistically significant after further adjustment for plaque index (0.44 mm; 95 % CI 0.02 - 0.86; p = 0.038) or gingival index (0.61 mm; 95 % CI, 0.24 - 0.97 p = 0.001). Conclusions: The study demonstrates higher periodontal clinical attachment loss in SSc patients, which remained significant following adjustment. The study indicates a possible relationship between SSc and periodontitis

    A Cohort Study Followed for 13 Years

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    Background There is growing evidence of an association between oral health, specifically dental status, and chronic systemic diseases. However, varying measures of dental status across different populations and low study sample has made comparison of studies and conclusion of findings unclear. Our aim is to examine whether the number of teeth as a measure of dental status is associated with incident chronic diseases in a cohort setting. Methods We conducted a cohort study among 24,313 middle-aged Germans followed up for 13 years. Data on number of teeth as a measure of dental status were obtained through self-reports. Outcomes were clinically–verified incident non–fatal myocardial infarction, stroke, type 2 diabetes mellitus, and cancer. Hazard ratio (HR) and 95% confidence intervals (CI) were obtained from Cox regression models. Results Increasing number of teeth is inversely related to risk of myocardial infarction (HR: 0.97; 95% CI: 0.96, 0.99). The full multivariate model of teeth groups showed a strong linear trend for myocardial infarction, a less strong trend for stroke, and no relation with type 2 diabetes mellitus and cancer in a competing risk model. Participants with 18–23 teeth and those without teeth were at 76% (95%CI: 1.04, 3) and 2.93 times (95%CI: 1.61, 5.18) higher risk of myocardial infarction compared to those with nearly all teeth (28–32 teeth). Conclusions Number of teeth is specifically associated with myocardial infarction and not with other chronic disease indicating that dental status further strengthens the link between oral health and cardiovascular diseases
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