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Effective colony management is critical to guarantee the availability of captive NHP as subjects for biomedical research. Pigtailed macaques (Macaca nemestrina) are an important model for the study of human and nonhuman primate diseases and behavior. Johns Hopkins University hosts one of the largest captive colonies of pigtailed macaques in the United States. In this study, we used 56 single-nucleotide polymorphisms (SNP) to characterize this population of pigtailed macaques, understand their population structure, and assess the effectiveness of their colony management. The results demonstrate that the colony has maintained a high level of genetic diversity, with no loss of heterozygosity since its origin, and low levels of inbreeding and genetic subdivision.

In children with Sickle Cell Disease, the combination of risk stratification with Transcranial Doppler Ultrasound (TCD) and selective chronic red cell transfusion (CRCT-the STOP Protocol) is one of the most effective stroke prevention strategies in medicine. How fully it is being implemented is unclear. Nineteen of 26 sites that conducted the two pivotal clinical trials (STOP and STOP II) participated in Post STOP, a comprehensive medical records review assessing protocol implementation in the 10-15 years since the trials ended. Professional abstractors identified medical records in the Post STOP era in 2851 (74%) of the 3,840 children who took part in STOP and/or STOP II, and documented TCD rescreening, maintenance of CRCT in those at risk, and stroke. Among 1,896 children eligible for TCD rescreening (target group), evidence of any rescreening was found in 1,090 (57%). There was wide site variation in TCD rescreening ranging from 18% to 91% of eligible children. Both younger age and having a conditional TCD during STOP/II were associated with a higher likelihood of having a TCD in Post STOP. Sixty eight new abnormal, high risk cases were identified. Despite clear evidence of benefit the STOP protocol is not fully implemented even at experienced sites. Site variation suggests that system improvements might remove barriers to implementation and result in even greater reduction of ischemic stroke in children with SCD. Am. J. Hematol. 91:1191-1194, 2016. © 2016 Wiley Periodicals, Inc.

Sleep and mental health problems are common in athletic cohorts; however, our knowledge is limited to current, elite athletes. We attempted to compare the symptomology of sleep and mental health problems across different playing statuses and competition levels. An online survey was completed by 946 adults from 37 sports (52.3% women) in seven countries. Athletes were currently competing, retired from competition (<20 years ago), or temporarily unable to play (i.e. injury/season postponed), from all competition levels. Retired athletes were at greater risk of sleep disordered breathing than current athletes (OR=2.30, 95% CI[1.66,3.20]) and those unable to play (OR=1.83, 95% CI[1.07,3.13]. Retired athletes (OR=1.54, 95% CI[1.11,2.15]) and those unable to play (OR=2.15, 95% CI[1.36,3.39]) were at greater risk of compromised wellbeing than current athletes. Sports institute/university/college level and semi-professional athletes were at greater risk of anxiety than professional athletes (OR=2.82, 95% CI[1.29, 6.17]; OR=2.38, 95% CI[1.10, 5.16]), respectively. Current and retired athletes had comparable risk of sleep difficulty, depression, and anxiety, while retired athletes were at the greatest risk for sleep apnoea, reflecting previous literature. Foreclosure of sport may explain reduced wellbeing in retired and temporarily unable to compete athletes. Emerging athletes were at elevated risk for depression and anxiety, with distinct barriers and stressors to elite athletes. The high risk prevalence observed has significant implications for the assessment and identification of sleep and mental health issues in athletic populations, highlighting the importance of intervention and prevention strategies. Findings underscore the necessity for longitudinal research, increased transparency from sporting organisations, and enhanced support during and beyond athletic careers. [ABSTRACT FROM AUTHOR]

This paper summarizes historical asbestos exposure data collected during the handling of short-fiber chrysotile asbestos that was used as an additive to drilling fluid in oil and gas exploration. A total of 1171 industrial hygiene (IH) personal and area air samples were collected and analyzed from more than 20 drilling rigs between 1972 and 1985. The dataset consists of 1097 short-term samples (<240 min) with more than 80% having sample durations less than 30 min. Average airborne fiber concentrations measured during asbestos handling activities ranged from 0.62 f/cc to 3.39 f/cc using phase-contrast microscopy (PCM). An additional 14 samples were considered long-term samples (>240 min) and there were 60 samples with no reported sample duration. Eight-hour time-weighted average (8-h TWA) results, calculated using short-term samples, along with long-term samples greater than 240 min, did not exceed contemporaneous Occupational Safety and Health Administration (OSHA) permissible exposure limits (PELs). This analysis fills a data gap in the evaluation of asbestos exposures from the use of drilling mud additives (DMAs) that contained chrysotile asbestos. [ABSTRACT FROM AUTHOR]

The relationship between testosterone and related hormones and cardiovascular and mortality outcomes is debated. The authors of this study obtained individual patient–level data from 9 cohort studies and aggregate data from 11 studies in total. These data enabled them to describe the associations of testosterone, sex hormone–binding globulin (SHBG), luteinizing hormone (LH), dihydrotestosterone (DHT), and estradiol with all-cause mortality, cardiovascular death, and incident cardiovascular events while accounting for other cardiac risk factors. Background: Whether circulating sex hormones modulate mortality and cardiovascular disease (CVD) risk in aging men is controversial. Purpose: To clarify associations of sex hormones with these outcomes. Data Sources: Systematic literature review to July 2019, with bridge searches to March 2024. Study Selection: Prospective cohort studies of community-dwelling men with sex steroids measured using mass spectrometry and at least 5 years of follow-up. Data Extraction: Independent variables were testosterone, sex hormone–binding globulin (SHBG), luteinizing hormone (LH), dihydrotestosterone (DHT), and estradiol concentrations. Primary outcomes were all-cause mortality, CVD death, and incident CVD events. Covariates included age, body mass index, marital status, alcohol consumption, smoking, physical activity, hypertension, diabetes, creatinine concentration, ratio of total to high-density lipoprotein cholesterol, and lipid medication use. Data Synthesis: Nine studies provided individual participant data (IPD) (255 830 participant-years). Eleven studies provided summary estimates (n = 24 109). Two-stage random-effects IPD meta-analyses found that men with baseline testosterone concentrations below 7.4 nmol/L (<213 ng/dL), LH concentrations above 10 IU/L, or estradiol concentrations below 5.1 pmol/L had higher all-cause mortality, and those with testosterone concentrations below 5.3 nmol/L (<153 ng/dL) had higher CVD mortality risk. Lower SHBG concentration was associated with lower all-cause mortality (median for quintile 1 [Q1] vs. Q5, 20.6 vs. 68.3 nmol/L; adjusted hazard ratio [HR], 0.85 [95% CI, 0.77 to 0.95]) and lower CVD mortality (adjusted HR, 0.81 [CI, 0.65 to 1.00]). Men with lower baseline DHT concentrations had higher risk for all-cause mortality (median for Q1 vs. Q5, 0.69 vs. 2.45 nmol/L; adjusted HR, 1.19 [CI, 1.08 to 1.30]) and CVD mortality (adjusted HR, 1.29 [CI, 1.03 to 1.61]), and risk also increased with DHT concentrations above 2.45 nmol/L. Men with DHT concentrations below 0.59 nmol/L had increased risk for incident CVD events. Limitations: Observational study design, heterogeneity among studies, and imputation of missing data. Conclusion: Men with low testosterone, high LH, or very low estradiol concentrations had increased all-cause mortality. SHBG concentration was positively associated and DHT concentration was nonlinearly associated with all-cause and CVD mortality. Primary Funding Source: Medical Research Future Fund, Government of Western Australia, and Lawley Pharmaceuticals. (PROSPERO: CRD42019139668) [ABSTRACT FROM AUTHOR]

Summary: Previous prospective studies examining associations of obstructive sleep apnea and sleep macroarchitecture with future cognitive function recruited older participants, many demonstrating baseline cognitive impairment. This study examined obstructive sleep apnea and sleep macroarchitecture predictors of visual attention, processing speed, and executive function after 8 years among younger community‐dwelling men. Florey Adelaide Male Ageing Study participants (n = 477) underwent home‐based polysomnography, with 157 completing Trail‐Making Tests A and B and the Mini‐Mental State Examination. Associations of obstructive sleep apnea (apnea–hypopnea index, oxygen desaturation index, and hypoxic burden index) and sleep macroarchitecture (sleep stage percentages and total sleep time) parameters with future cognitive function were examined using regression models adjusted for baseline demographic, biomedical, and behavioural factors, and cognitive task performance. The mean (standard deviation) age of the men at baseline was 58.9 (8.9) years, with severe obstructive sleep apnea (apnea–hypopnea index ≥30 events/h) in 9.6%. The median (interquartile range) follow‐up was 8.3 (7.9–8.6) years. A minority of men (14.6%) were cognitively impaired at baseline (Mini‐Mental State Examination score <28/30). A higher percentage of light sleep was associated with better Trail‐Making Test A performance (B = −0.04, 95% confidence interval [CI] −0.06, −0.01; p = 0.003), whereas higher mean oxygen saturation was associated with worse performance (B = 0.11, 95% CI 0.02, 0.19; p = 0.012). While obstructive sleep apnea and sleep macroarchitecture might predict cognitive decline, future studies should consider arousal events and non‐routine hypoxaemia measures, which may show associations with cognitive decline. [ABSTRACT FROM AUTHOR]

Summary: Quetiapine is an antipsychotic medication indicated for schizophrenia and bipolar disorder. However, quetiapine also has hypnotic properties and as such is increasingly being prescribed at low doses 'off‐label' in people with insomnia symptoms. Pharmacologically, in addition to its dopaminergic properties, quetiapine also modulates multiple other transmitter systems involved in sleep/wake modulation and potentially breathing. However, very little is known about the impact of quetiapine on obstructive sleep apnoea (OSA), OSA endotypes including chemosensitivity, and control of breathing. Given that many people with insomnia also have undiagnosed OSA, it is important to understand the effects of quetiapine on OSA and its mechanisms. Accordingly, this concise review covers the existing knowledge on the effects of quetiapine on sleep and breathing. Further, we highlight the pharmacodynamics of quetiapine and its potential to alter key OSA endotypes to provide potential mechanistic insight. Finally, an agenda for future research priorities is proposed to fill the current key knowledge gaps. [ABSTRACT FROM AUTHOR]