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Aims: To evaluate the Hypoglycaemia Symptom Rating Questionnaire (HypoSRQ©) and relationships between self-reported hypoglycaemia and hypoglycaemia measured using blinded continuous glucose monitoring (CGM).Methods: Diabetes outpatients (n = 113) recruited from Ashford and St. Peter's Hospital completed the HypoSRQ (recent weeks version) and provided clinical information. Thirty participants used blinded CGM for six days and completed the HypoSRQ (24-hour version) for seven days, at the end of each week (7-day version), and after four weeks (recent weeks version).Results: The HypoSRQ had a single-factor structure and excellent internal consistency (α = 0.90). There was high correspondence in recalled symptoms, bother ratings and hypoglycaemic episodes across one week and four weeks (r = 0.84-0.98, p < 0.001). HypoSRQ-reported hypoglycaemia correlated significantly with CGM-measured hypoglycaemia (interstitial glucose ≤ 3.9 mmol/l) frequency (r = 0.72, p < 0.001) across six days. The magnitude of the correlation increased when the person's own threshold for detecting hypoglycaemia was used (r = 0.78, p < 0.001). The number of days (out of six) a person reported symptoms of hypoglycaemia was associated with the number of days CGM detected hypoglycaemia (interstitial glucose ≤ 3.9 mmol/l) (r = 0.83, p < 0.001) and remained significant after controlling for covariates.Conclusions: Psychometric properties of the HypoSRQ make it attractive for use in people with insulin-treated diabetes. The HypoSRQ may be a less-invasive and more-economical alternative to CGM. [ABSTRACT FROM AUTHOR]

Introduction A wide variety of non-genetic and genetic factors have been shown to associate with increased risk for cerebral venous thrombosis (CVT). However, there is a paucity of risk factor data and conclusions about their impact are often conflicting. Herein, we quantified the associations of non-genetic and genetic risk factors for CVT in adults. Materials and methods Electronic databases were searched up to January 2017. Meta-analyses were performed (RevMan v5.3) to determine pooled odds ratios (ORs and 95% CIs) for risk factors, interstudy heterogeneity and publication bias. Results Twenty non-genetic ( n  = 2314) and 33 genetic ( n  = 2117) studies up to January 2017 met the selection criteria. For non-genetic factors, CVT risk increased in the presence of glucocorticosteroid therapy by 18.3-fold (3.3–102.6), alcohol consumption 2.7-fold (1.8–3.9), infection 7.5-fold (2.6–21.6), surgery 9.6-fold (1.1–83.5), hypercholesterolaemia 2.4-fold (1.3–4.4), hyperhomocysteinaemia 3.1-fold (2.1–4.6), antiphospholipid antibodies 7.0-fold (2.1–23.6), autoimmune diseases 5.6-fold (2.3–13.6), anaemia 4.0-fold (2.1–7.9), malignancy 3.2-fold (1.4–7.1) and pregnancy/puerperium 11.4-fold (5.7–24.3). Smoking, hypertension and diabetes did not associate with CVT risk. For genetic factors, CVT risk increased in the presence of factor V Leiden ( G1691A ) by 2.5-fold (1.9–3.3), protein C deficiency 10.7-fold (3.1–37.7), protein S deficiency 5.7-fold (1.4–22.4), antithrombin deficiency 3.8-fold (1.0–13.8), prothrombin ( G20210A ) 5.5-fold (4.0–7.27) and TAFI gene variant ( C1040T ) 1.6-fold (1.0–2.4). Prothrombin G20210A and factor V Leiden polymorphisms tended to have higher ORs for CVT than for ischaemic stroke. Conclusions We provide quantitative data supporting a strong basis for genetic and non-genetic risk factors in CVT. Its genetic liability seems higher when compared with sporadic ischaemic stroke. [ABSTRACT FROM AUTHOR]

• Sex steroid levels are proposed to be a modifiable risk factor for cognitive ageing • We tested this hypothesis in a large-scale study of middle-aged and older men • Steroid levels did not affect cognition after adjusting for health and lifestyle • Androgen CAG repeat length did not alter hormone-cognition relationships It has been proposed that endogenous sex hormone levels may present a modifiable risk factor for cognitive decline. However, the evidence for effects of sex steroids on cognitive ageing is conflicting. We therefore investigated associations between endogenous hormone levels, androgen receptor CAG repeat length, and cognitive domains including visuoconstructional abilities, visual memory, and processing speed in a large-scale longitudinal study of middle-aged and older men. Men aged 40-79 years from the European Male Ageing Study (EMAS) underwent cognitive assessments and measurements of hormone levels at baseline and follow-up (mean = 4.4 years, SD ± 0.3 years). Hormone levels measured included total and calculated free testosterone and estradiol, dihydrotestosterone, luteinizing hormone, follicle-stimulating hormone, dehydroepiandrosterone sulphate and sex hormone-binding globulin. Cognitive function was assessed using the Rey-Osterrieth Complex Figure Copy and Recall, the Camden Topographical Recognition Memory and the Digit Symbol Substitution Test. Multivariate linear regressions were used to examine associations between baseline and change hormone levels, androgen receptor CAG repeat length, and cognitive decline. Statistical analyses included 1,827 and 1,423 participants for models investigating relationships of cognition with hormone levels and CAG repeat length, respectively. In age-adjusted models, we found a significant association of higher baseline free testosterone (β=-0.001, p =0.005) and dihydrotestosterone levels (β=-0.065, p =0.003) with greater decline on Rey-Osterrieth Complex Figure Recall over time. However, these effects were no longer significant following adjustment for centre, health, and lifestyle factors. No relationships were observed between any other baseline hormone levels, change in hormone levels, or androgen receptor CAG repeat length with cognitive decline in the measured domains. In this large-scale prospective study there was no evidence for an association between endogenous sex hormone levels or CAG repeat length and cognitive ageing in men. These data suggest that sex steroid levels do not affect visuospatial function, visual memory, or processing speed in middle-aged and older men. [ABSTRACT FROM AUTHOR]

Abstract: Few studies have directly compared the ability of the most commonly used models of frailty to predict mortality among community-dwelling individuals. Here, we used a frailty index (FI), frailty phenotype (FP), and FRAIL scale (FS) to predict mortality in the EMAS. Participants were aged 40–79 years (n =2929) at baseline and 6.6% (n =193) died over a median 4.3 years of follow-up. The FI was generated from 39 deficits, including self-reported health, morbidities, functional performance and psychological assessments. The FP and FS consisted of five phenotypic criteria and both categorized individuals as robust when they had 0 criteria, prefrail as 1–2 criteria and frail as 3+ criteria. The mean FI increased linearly with age (r 2 =0.21) and in Cox regression models adjusted for age, center, smoking and partner status the hazard ratio (HR) for death for each unit increase of the FI was 1.49. Men who were prefrail or frail by either the FP or FS definitions, had a significantly increased risk of death compared to their robust counterparts. Compared to robust men, those who were FP frail at baseline had a HR for death of 3.84, while those who were FS frail had a HR of 3.87. All three frailty models significantly predicted future mortality among community-dwelling, middle-aged and older European men after adjusting for potential confounders. Our data suggest that the choice of frailty model may not be of paramount importance when predicting future risk of death, enabling flexibility in the approach used. [Copyright &y& Elsevier]