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Objectives: To assess the prevalence of vitamin D deficiency and hyperparathyroidism as well as their relationship to blood pressure and arterial stiffness in hypertensive patients with stage 3 chronic kidney disease (CKD). Methods: Cross-sectional study that included 134 treated hypertensives (76 women, 56,7%) with stage 3 CKD (eGFR 49,2 ml/min, SD±8) without previous vitamin D supplementation treatment. Standard clinical care was performed including ECG, microalbuminuria and usual laboratory parameters. Arterial stiffness was measured by brachial oscillometry with the validated Mobil-O-Graph® device. Normal values for vitamin D and PTH were set as 30 ng/ml and 65 pg/ml, respectively. Results: The mean age was 73,0 years (SD±10) with office BP of 131/75 mmHg (SD±17/11). The prevalence of vitamin D deficiency was 89% (mean: 19 ng/ml (SD±10)), secondary hyperparathytoidism was observed in 49% of patients (mean: 70,5 pg/ml (SD±10)), 84 (62,7%) patients had a pulse wave velocity (PWV) over 10 m/sec (mean 10,7 m/sec, (SD±1,8). In bivariate analysis PWV correlated best with age (r=930;p

Objectives: To measure the extent of correction of vitamin D deficiency and hyperparathyroidism after treatment with calcifediol as well as their relationship to blood pressure and arterial stiffness in hypertensive patients with stage 3 chronic kidney disease (CKD). Methods: Longitudinal study that included 74 treated hypertensives (46 women, 62,2%) with stage 3 CKD (eGFR 47,7 ml/min, SD±10) without previous vitamin D supplementation treatment. Calcifediol 266 μg/2 weeks and calcium 600 mg/d were given if baseline-vitamin D < 30 ng/ml and < 9,5 mmol/l, respectively. A second visit took place after 4 months. Results: The mean age was 72,9 years (SD±10). The prevalence of vitamin D deficiency decreased from initially 96% to 23% (mean baseline: 18, mean final: 42 ng/ml), and of secondary hyperparathytoidism from 62% to 37% (mean at baseline: 87, mean final: 63 pg/ml). There were no significant changes in eGFR, calcium or phosphor or number of antihypertensive drugs, but pulse wave velocity (measured with MOBILOGRAPH®) and BP decreased significantly form initially 133/76 to 123/72 (p

Introduction: Masked uncontrolled hypertension (MUCH) carries an increased risk of cardiovascular (CV) complications and can be identified through combined use of office (O) and ambulatory (A) blood pressure (BP) monitoring (M) in treated patients. However, it is still debated whether the information carried by ABPM should be considered for MUCH management. Aim of the MASked-unconTrolled hypERtension management based on OBP or on ambulatory blood pressure measurement (MASTER) Study is to assess the impact on outcome of MUCH management based on OBPM or ABPM., Methods and Analysis: MASTER is a 4-year prospective, randomised, open-label, blinded-endpoint investigation. A total of 1240 treated hypertensive patients from about 40 secondary care clinical centres worldwide will be included -upon confirming presence of MUCH (repeated on treatment OBP <140/90 mm Hg, and at least one of the following: daytime ABP ≥135/85 mm Hg; night-time ABP ≥120/70 mm Hg; 24 hour ABP ≥130/80 mm Hg), and will be randomised to a management strategy based on OBPM (group 1) or on ABPM (group 2). Patients in group 1 will have OBP measured at 0, 3, 6, 12, 18, 24, 30, 36, 42 and 48 months and taken as a guide for treatment; ABPM will be performed at randomisation and at 12, 24, 36 and 48 months but will not be used to take treatment decisions. Patients randomised to group 2 will have ABPM performed at randomisation and all scheduled visits as a guide to antihypertensive treatment. The effects of MUCH management strategy based on ABPM or on OBPM on CV and renal intermediate outcomes (changing left ventricular mass and microalbuminuria, coprimary outcomes) at 1 year and on CV events at 4 years and on changes in BP-related variables will be assessed., Ethics and Dissemination: MASTER study protocol has received approval by the ethical review board of Istituto Auxologico Italiano. The procedures set out in this protocol are in accordance with principles of Declaration of Helsinki and Good Clinical Practice guidelines. Results will be published in accordance with the CONSORT statement in a peer-reviewed scientific journal., Trial Registration Number: NCT02804074; Pre-results., Competing Interests: Competing interests: GP: honoraria as lecturer for Pfizer, Daiichi Sankyo, Menarini, Omron Healthcare. EA-R: honoraria and/or support from Menarini, Servier, Recordati,Guidotti,Malesci, Ferrer, DOC gen, Bruno farm. GLB: principal investigator (FIDElio)-Bayer, Steering committee (CREDENCE(Janssen), SONAR (AbbVie)-Consultant for Merck, Relypsa, Vascular Dynamics, Elceyx, Bayer, Janssen, AbbVie. FC: collaboration with Smart Solutions Technologies S.A.; AMICUS; Boston Scientific International S.A . ADS: honoraria as lecturer for Abbott, Daiichi-Sankyo, Lacer, Menarini, and Pfizer. MD: Honoria from Recordati and Servier. TK: Research grants Karolinska Institutet from Amgen, Medtronic, Pfizer, and Record, all outside the presented work. SL: Honoraria for lecturing from Axelife, Daichi-Sankyo, Fukuda-Denshi, Menarini, Novartis, Omron, Servier and Recordati. GM: honoraria aslecturer Actavis, Amgen, Boehringer Ingelheim, CVRx, Daiichi Sankyo, Ferrer, Medtronic, Menarini, Merck, Novartis, Recordati, Sanofi,Servier. RJM: has received BP Monitors forresearch use from Omron. JR: hasbeen paid as lecturer by Daiichi Sankyo, Menarini, BoehringerIngelheim, MSD. MYR: Lecture honoraria from Pfizer,LG Life Sciences, Bayer Korea, Hanmi Pharm. Co., Yuhan Co., Boryung Pharmaceutical Co., Research grant fromBoryung Pharmaceutical Co. and Dong-A Pharmaceutical Co., CJ HealthCare Co. GS: Conductedvalidation studies for various manufacturers; advised manufacturerson device development. JGW: lecture and consulting fees from Bayer, Daiichi-Sankyo, Novartis,Omron, Pfizer, Sanofi, and Servier. AZ: Honoraria from Menarini International., (© Author(s) (or their employer(s)) 2018. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Background and Objectives: The aim of this study was to assess the factors related to new diabetes in hypertensive., Patients and Methods: This prospective follow-up study involved 2588 non-diabetic, hypertensive patients. The total follow-up was 15053 patient-years with a median of 3.4 years (interquartile interval 1.4-6.8)., Results: During the follow-up 333 (13%) patients had new diabetes, with a conversion rate of 2.21 (95% confidence interval [CI], 1.98-2.46) 100/patients/year. In a Cox proportional hazard model including baseline characteristics and modifications during the follow up the three components of metabolic syndrome (excluding blood pressure and glucose values) HR 1.69 (95% CI, 1.36-2.09), family history of diabetes HR 1,49 (95% CI, 1,20-1,85) and baseline blood glucose ≥110 mg/dl HR 7.84 (95% CI, 5.99-10.29) were the most important factors related to new diabetes. Weight variation during the follow up, and statins, beta-bloquers or diuretic treatment did not increase the risk of new diabetes, blood pressure control at the end of study reduce the risk HR 0,74 (95% CI, 0.61-0.91)., Conclusions: In hypertensive non-diabetic patients in primary prevention the factors related to new diabetes can easily identified at the beginning of follow up. Being obese, with family history of diabetes, and glucose values ≥110 mg/dl dramatically increase the risk of developing new diabetes., (Copyright © 2016 Elsevier España, S.L.U. All rights reserved.)

The America's Cup is the oldest competing trophy in sport, yet little is known of the nature and intensity of racing or the physical characteristics of the athletes. In this study, aspects of the physical demands of America's Cup yacht racing were analysed, including the intensity of exercise and activity pattern of "grinding". Anthropometric data were collected from 92 professional male America's Cup sailors, and fitness data from a top-4 and a lower-7 ranking team during the 32nd America's Cup. Over the 135 races, mean race duration was 82 min (s = 9), with 20 tacks (s = 10) and 8 gybes (s = 3) per race. Grinding bouts were 5.5 s (s = 5.4; range: 2.2-66.3) long, with 143 exercise bouts per race and an exercise-to-rest ratio of 1:6. Mean and peak heart rate was 64% and 92% of maximum for all positions, with bowmen highest (71% and 96%). Grinders were taller, heavier, and stronger than all other positions. Body fat was similar between positions (13%, s = 4). The higher-standard team was stronger and had greater strength endurance, which probably contributed to their quicker manoeuvres. Intensity of exercise was dependent on the similarity of competing boats and the role of the athlete. The short duration and intermittent nature of grinding is indicative of predominantly anaerobic energy provision.

A monoclonal antibody to the rat liver membrane fatty acid binding protein (MFABP) was prepared by immunizing mice with purified MFABP isolated from solubilized rat liver plasma membrane proteins by oleate-agarose affinity chromatography technique. The monoclonal antibody K15/6 identified a single 40 kDa protein in rat liver plasma membranes with pI values of 8.5, 8.8 and 9.0, which is identical to the authentic MFABP, but clearly distinct from rat mitochondrial GOT. The antibody K15/6 selectively inhibited cellular influx as well as membrane binding of fatty acids, but not of cholesterol or vitamin E. The same antibody was used in immunofluorescence, ELISA and Western blot analysis to determine the subcellular and organ distribution pattern of MFABP. The protein was identified in rat liver plasma membranes and mitochondria, but in no other cell compartment. It was detectable in homogenates of rat liver but not in homogenates of other organs. Therefore, the monoclonal antibody K15/6 represents an organ specific antibody to MFABP which reveals inhibitory action on membrane binding/transport of fatty acids.