A Double Blind, Placebo-Controlled, Randomized Crossover Study of the Acute Metabolic Effects of Olanzapine in Healthy Volunteers

Atypical antipsychotics exhibit metabolic side effects including diabetes mellitus and obesity. The adverse events are preceded by acute worsening of oral glucose tolerance (oGTT) along with reduced plasma free fatty acids (FFA) and leptin in animal models. It is unclear whether the same acute effects occur in humans.A double blind, randomized, placebo-controlled crossover trial was conducted to examine the potential metabolic effects of olanzapine in healthy volunteers. Participants included male (8) and female (7) subjects [18-30 years old, BMI 18.5-25]. Subjects received placebo or olanzapine (10 mg/day) for three days prior to oGTT testing. Primary endpoints included measurement of plasma leptin, oral glucose tolerance, and plasma free fatty acids (FFA). Secondary metabolic endpoints included: triglycerides, total cholesterol, high- and low-density lipoprotein cholesterol, heart rate, blood pressure, body weight and BMI. Olanzapine increased glucose Area Under the Curve (AUC) by 42% (2808±474 vs. 3984±444 mg/dl·min; P = 0.0105) during an oGTT. Fasting plasma leptin and triglycerides were elevated 24% (Leptin: 6.8±1.3 vs. 8.4±1.7 ng/ml; P = 0.0203) and 22% (Triglycerides: 88.9±10.1 vs. 108.2±11.6 mg/dl; P = 0.0170), whereas FFA and HDL declined by 32% (FFA: 0.38±0.06 vs. 0.26±0.04 mM; P = 0.0166) and 11% (54.2±4.7 vs. 48.9±4.3 mg/dl; P = 0.0184), respectively after olanzapine. Other measures were unchanged.Olanzapine exerts some but not all of the early endocrine/metabolic changes observed in rodent models of the metabolic side effects, and this suggest that antipsychotic effects are not limited to perturbations in glucose metabolism alone. Future prospective clinical studies should focus on identifying which reliable metabolic alterations might be useful as potential screening tools in assessing patient susceptibility to weight gain and diabetes caused by atypical antipsychotics.ClinicalTrials.gov NCT00741026

Identification of Novel QTLs for BPH Tolerance in Rice Using Resistant Donor BM 71

Rice is the most widely grown crop in the world, feeding half of the world’s population. Brown plant hopper (BPH) is a considerable risk to rice fields carrying 20-90% yield losses. Hopper burn can be effectively managed by the recognition and use of BPH genes. Marker based genetic analysis of 136 RILcollected from a high yielding susceptible variety, MTU 3626 and BM 71, a BPH donor developed at RARS, identified 3 minor novel QTLs viz; qmbph2.1,qmbph4.1 and qmbph12.1 on chromosomes 2, 4 and 12 and two other QTLson chromosome 5 and 7, namelyqmbph5.1 and qmbph7.1. The phenotyping of RIL’s revealed that ten RIL’s (2711 – 31, 2711 – 37, 2711 – 50, 2711 – 69, 2711 – 84, 2711 – 88, 2711 – 94, 2711 – 100, 2711 – 168 and 2711 – 191) recorded yields comparable to checks, Swarna and Pushyami along with BPH score similar to donor. The BPH resistance lines recognised will be further evaluated, and the confirmed lines can be employed in rice breeding programs

Clinical and polysomnographic predictors of the Natural History of poor sleep in the general population

Study Objectives: Approximately 8-10% of the general population suffers from chronic insomnia, whereas another 20-30% of the population has insomnia symptoms at any given time (i.e., poor sleep). However, few longitudinal studies have examined risk factors of the natural history of poor sleep, and none have examined the role of polysomnographic (PSG) variables. Design: Representative longitudinal study. Setting: Sleep laboratory. Participants: From a random, general population sample of 1,741 individuals of the adult Penn State Cohort, 1,395 were followed up after 7.5 yr. Measurements: Full medical evaluation and 1-night PSG at baseline and telephone interview at follow-up. Results: The rate of incident poor sleep was 18.4%. Physical (e.g., obesity, sleep apnea, and ulcer) and mental (e.g., depression) health conditions and behavioral factors (e.g., smoking and alcohol consumption) increased the odds of incident poor sleep as compared to normal sleep. The rates of persistent, remitted, and poor sleepers who developed chronic insomnia were 39%, 44%, and 17%, respectively. Risk factors for persistent poor sleep were physical health conditions combined with psychologic distress. Shorter objective sleep duration and a family history of sleep problems were risk factors for poor sleep evolving into chronic insomnia. Conclusions: Poor sleep appears to be primarily a symptom of physical and mental health conditions, whereas the persistence of poor sleep is associated with psychologic distress. Importantly, sleep apnea appears to be associated with incident poor sleep but not with chronic insomnia. Finally, this study suggests that objective short sleep duration in poor sleepers is a biologic marker of genetic predisposition to chronic insomniaThis research was funded in part by the National Institutes of Health grants RO1 51931, RO1 40916 (to Dr. Bixler), and RO1 64415 (to Dr. Vgontzas)