Conservation of the genetic resources of Vitis

As an alternative or supplement to field collections, a repository of 35 grapevine genotypes and 15 clones of cv. Optima was set up under minimal growth conditions. To prolong the storage period between subculturing to at least 12-18 months, some factors of long-term storage were optimized and the causes responsible for early senescence of sensitive genotypes were investigated Besides indirect effects due to excision time, origin of the starting material and preculture, there is a direct influence of the light conditions on the survival rate of cultures. CCC application showed, in some cases, positive effects only after long-term storage. An increase of carbon dioxide concentration during storage is considered to be responsible for the early death of some cultures

Non-perturbative QEG Corrections to the Yang-Mills Beta Function

We discuss the non-perturbative renormalization group evolution of the gauge coupling constant by using a truncated form of the functional flow equation for the effective average action of the Yang-Mills-gravity system. Our result is consistent with the conjecture that Quantum Einstein Gravity (QEG) is asymptotically safe and has a vanishing gauge coupling constant at the non-trivial fixed point.Comment: To appear in the proceedings of CORFU 200

Associations of Observational and Genetically Determined Caffeine Intake With Coronary Artery Disease and Diabetes Mellitus

Background Caffeine is the most widely consumed psychostimulant and is associated with lower risk of coronary artery disease (CAD) and type 2 diabetes mellitus (T2DM). However, whether these associations are causal remains unknown. This study aimed to identify genetic variants associated with caffeine intake, and to investigate evidence for causal links with CAD or T2DM. In addition, we aimed to replicate previous observational findings. Methods and Results Observational associations were tested within UK Biobank using Cox regression analyses. Moderate observational caffeine intakes from coffee or tea were associated with lower risks of CAD or T2DM, with the lowest risks at intakes of 121 to 180 mg/day from coffee for CAD (hazard ratio [HR], 0.77 [95% CI, 0.73-0.82; P<1×10-16]), and 301 to 360 mg/day for T2DM (HR, 0.76 [95% CI, 0.67-0.86]; P=1.57×10-5). Next, genome-wide association studies were performed on self-reported caffeine intake from coffee, tea, or both in 407 072 UK Biobank participants. These analyses identified 51 novel genetic variants associated with caffeine intake at P<1.67×10-8. These loci were enriched for central nervous system genes. However, in contrast to the observational analyses, 2-sample Mendelian randomization analyses using the identified loci in independent disease-specific cohorts yielded no evidence for causal links between genetically determined caffeine intake and the development of CAD or T2DM. Conclusions Mendelian randomization analyses indicate genetically determined higher caffeine intake might not protect against CAD or T2DM, despite protective associations in observational analyses

Genome-wide association studies and Mendelian randomization analyses for leisure sedentary behaviours

Leisure sedentary behaviours are associated with increased risk of cardiovascular disease, but whether this relationship is causal is unknown. The aim of this study is to identify genetic determinants associated with leisure sedentary behaviours and to estimate the potential causal effect on coronary artery disease (CAD). Genome wide association analyses of leisure television watching, leisure computer use and driving behaviour in the UK Biobank identify 145, 36 and 4 genetic loci (P < 1×10−8), respectively. High genetic correlations are observed between sedentary behaviours and neurological traits, including education and body mass index (BMI). Two-sample Mendelian randomization (MR) analysis estimates a causal effect between 1.5 hour increase in television watching and CAD (OR 1.44, 95%CI 1.25–1.66, P = 5.63 × 10−07), that is partially independent of education and BMI in multivariable MR analyses. This study finds independent observational and genetic support for the hypothesis that increased sedentary behaviour by leisure television watching is a risk factor for CAD

Effects of caffeine intake prior to stress cardiac magnetic resonance perfusion imaging on regadenoson- versus adenosine-induced hyperemia as measured by T1 mapping

The antagonistic effects of caffeine on adenosine receptors are a possible cause of false-negative stress perfusion imaging. The purpose of this study was to determine the effects of coffee intake <4 h prior to stress perfusion cardiac magnetic resonance imaging (CMR) in regadenoson- versus adenosine-induced hyperemia as measured with T1-mapping. 98 consecutive patients with suspected coronary artery disease referred for either adenosine or regadenoson perfusion CMR were included in this analysis. Twenty-four patients reported coffee consumption <4 h before CMR (15 patients with adenosine, and 9 patients with regadenoson); 74 patients reported no coffee intake (50 patients with adenosine, and 24 patients with regadenoson). T1 mapping was performed using a modified look-locker inversion recovery sequence. T1 reactivity was determined by subtracting T1(rest) from T1(stress). T1(rest), T1(stress), and T1 reactivity in patients referred for regadenoson perfusion CMR were not significantly different when comparing patients with <4 h coffee intake and patients who reported no coffee intake (976 +/- 4 ms, 1019 +/- 48 ms, and 4.4 +/- 3.2% vs 971 +/- 33 ms, 1023 +/- 43 ms, and 5.4 +/- 2.4%) (p = 0.70, 0.79, and 0.40), and similar to values in patients without coffee intake undergoing adenosine CMR. In patients with <4 h coffee intake, T1(stress), and T1 reactivity were significantly lower for adenosine (898 +/- 51 ms, and -7.8 +/- 5.0%) compared to regadenoson perfusion CMR (p <0.001). Coffee intake <4 h prior to regadenoson perfusion CMR has no effect on stress-induced hyperemia as measured with T1 mapping

Association of Recognized and Unrecognized Myocardial Infarction With Depressive and Anxiety Disorders in 125,988 Individuals:A Report of the Lifelines Cohort Study

Objective No previous study has focused on recognition of myocardial infarction (MI) and the presence of both depressive and anxiety disorders in a large population-based sample. The aim of this study was to investigate the association of recognized MI (RMI) and unrecognized MI (UMI) with depressive and anxiety disorders. Methods Analyses included 125,988 individuals enrolled in the Lifelines study. Current mental disorders according to the Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition) were assessed with the Mini-International Neuropsychiatric Interview. UMI was detected using electrocardiogram in participants who did not report a history of MI. The classification of RMI was based on self-reported MI history together with the use of either antithrombotic medications or electrocardiogram signs of MI. Analyses were adjusted for age, sex, smoking, somatic comorbidities, and physical health-related quality of life as measured by the RAND 36-Item Health Survey in different models. Results Participants with RMI had significantly higher odds of having any depressive and any anxiety disorder as compared with participants without MI (depressive disorder: Odds ratio [OR] = 1.86, 95% confidence interval [CI] = 1.38-2.52; anxiety disorder: OR = 1.60, 95% CI = 1.32-1.94) after adjustment for age and sex. Participants with UMI did not differ from participants without MI (depressive disorder: OR = 1.60, 95% CI = 0.96-2.64; anxiety disorder: OR = 0.73, 95% CI = 0.48-1.11). After additional adjustment for somatic comorbidities and low physical health-related quality of life, the association between RMI with any depressive disorder was no longer statistically significant (OR = 1.18; 95% CI =0.84-1.65), but the association with any anxiety disorder remained (OR = 1.27, 95% CI = 1.03-1.57). Conclusions Recognition of MI seems to play a major role in the occurrence of anxiety, but not depressive, disorders

Transcatheter interatrial shunt device for the treatment of heart failure with preserved ejection fraction (REDUCE LAP-HF I [Reduce Elevated Left Atrial Pressure in Patients With Heart Failure]): A phase 2, randomized, sham-controlled trial

Background -In non-randomized, open-label studies, a transcatheter interatrial shunt device (IASD, Corvia Medical) was associated with lower pulmonary capillary wedge pressure (PCWP), less symptoms, and greater quality of life and exercise capacity in patients with heart failure (HF) and mid-range or preserved ejection fraction (EF ≥ 40%). We conducted the first randomized, sham-controlled trial to evaluate the IASD in HF with EF ≥ 40%. Methods -REDUCE LAP-HF I was a phase 2, randomized, parallel-group, blinded multicenter trial in patients with New York Heart Association (NYHA) class III or ambulatory class IV HF, EF ≥ 40%, exercise PCWP ≥ 25 mmHg, and PCWP-right atrial pressure gradient ≥ 5 mmHg. Participants were randomized (1:1) to the IASD vs. a sham procedure (femoral venous access with intracardiac echocardiography but no IASD placement). The participants and investigators assessing the participants during follow-up were blinded to treatment assignment. The primary effectiveness endpoint was exercise PCWP at 1 month. The primary safety endpoint was major adverse cardiac, cerebrovascular, and renal events (MACCRE) at 1 month. PCWP during exercise was compared between treatment groups using a mixed effects repeated measures model analysis of covariance that included data from all available stages of exercise. Results -A total of 94 patients were enrolled, of which n=44 met inclusion/exclusion criteria and were randomized to the IASD (n=22) and control (n=22) groups. Mean age was 70±9 years and 50% were female. At 1 month, the IASD resulted in a greater reduction in PCWP compared to sham-control (P=0.028 accounting for all stages of exercise). Peak PCWP decreased by 3.5±6.4 mmHg in the treatment group vs. 0.5±5.0 mmHg in the control group (P=0.14). There were no peri-procedural or 1-month MACCRE in the IASD group and 1 event (worsening renal function) in the control group (P=1.0). Conclusions -In patients with HF and EF ≥ 40%, IASD treatment reduces PCWP during exercise. Whether this mechanistic effect will translate into sustained improvements in symptoms and outcomes requires further evaluation. Clinical Trial Registration -URL: http://clinicaltrials.gov. Unique identifier: NCT02600234