Occupational Sitting and Physical Activity Among University Employees

International Journal of Exercise Science 7(4) : 295-301, 2014. The prevalence of overweight and obese in the U.S. has been thoroughly documented. With the advent of inactivity physiology research and the subsequent interest in sedentary behavior, the work environment has come under closer scrutiny as a potential opportunity to reverse inactivity. Therefore, the purpose of this study was to determine the sitting and physical activity (PA) habits among different classifications of university employees. University employees (n=625) completed an online survey based on the Occupational Sitting and Physical Activity Questionnaire (OSPAQ). Participants were instructed to describe time spent sitting, standing, walking, and in heavy physical labor during the last seven days, along with the number of breaks from sitting taken per hour. To establish habitual patterns of PA outside of work, employees recalled their participation in structured PA in the past seven days. Prior to data analysis, employees were categorized as Administration, Faculty, Staff, or Facilities Management. Statistically significant differences were found among employee classifications for min sit/d, p\u3c.001; min stand/d, p\u3c.001; min walk/d, p\u3c.001; and min heavy labor/d, p\u3c.001. No significant differences were found for breaks/h from sitting, p=.259 or participation in structured PA, p=. 33. With the exception of facilities management workers, university employees spent 75% of their workday seated. In conjunction with low levels of leisure time PA, university employees appear to be prime candidates for workplace interventions to reduce physical inactivity

The Effect Of High Intensity Interval Run Training On Cross Sectional Area Of The Vastus Lateralis In Untrained College Students

International Journal of Exercise Science 10(1): 137-145, 2017 Aerobic cycling has been repeatedly shown to induce hypertrophy in skeletal muscle across a variety of populations, while there has been a lack of investigation into the impact of running upon hypertrophy. An increasingly popular model of aerobic exercise is high-intensity interval training (HIIT); in addition to its positive impact upon cardiovascular health, HIIT may be sufficient for inducing significant muscular hypertrophy. Therefore, the purpose of this investigation was to examine the influence of a high-intensity interval running protocol upon hypertrophy of the vastus lateralis in an untrained, young population. Twelve recreationally active university students (Male: 2; Female: 10; 19.9±0.5 yr.; 169.8±1.9 cm; 63.8±2.3 kg; VO2max: 42.1±1.6 ml.kg-1min-1) completed 24.5±0.6 sessionsof high-intensity interval run training over 10 weeks. The protocol consisted of four sets of 4 minutes running at 90-95% HRmax followed by 3 minutes active rest at 70% HRmax. Relative and absolute aerobic capacity increased 5.2±2.2% and 6.0±2.3% respectively as a result of the intervention (p\u3c 0.05). Cross-sectional area (CSA) of the vastus lateralis was measured via panoramic ultrasound imaging pre- and post-intervention. Following the protocol, CSA of the intervention group was 10.6±2.7% greater (p\u3c 0.05), while that of the control group did not change. This is the first data to demonstrate hypertrophy of the vastus lateralis in a young population following a running protocol. These data support the existing body of evidence suggesting aerobic exercise to be an effective mode of improving cardiorespiratory fitness as well as increasing whole muscle size of the quadriceps

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Sleep and chronotype in adults with persistent tic disorders

ObjectiveThis study examined sleep disorders and sleep medication use rates, nighttime tics, and sleep and chronotype in relation to tic and co-occurring symptoms in adults with persistent tic disorders (PTDs), including Tourette's disorder (TD).MethodsOne hundred twenty-five adult internet survey respondents rated sleep history, sleep, chronotype, tic severity, impairment, attention deficit hyperactivity disorder, obsessive-compulsive symptoms, anxiety, depression, and emotional and behavioral dyscontrol.ResultsBruxism, insomnia, tic-related difficulty falling asleep, and melatonin use were commonly endorsed. Sleep disturbance correlated with impairment, obsessive-compulsive symptoms, and emotional and behavioral dyscontrol. Eveningness correlated with vocal and total tic severity only in TD. Controlling for age and sex, age, impairment, and obsessive-compulsive symptoms predicted sleep disturbance, and age and tic severity predicted chronotype.ConclusionsImpairment and obsessive-compulsive symptoms play a role in sleep disturbance in adults with PTDs, and may be intervention targets. Eveningness relates to tic severity, which may suggest the utility of interventions to advance chronotype

Morning light therapy in adults with Tourette’s disorder

BackgroundSleep disturbance is common among individuals with Tourette's Disorder (TD). Given that sleep is influenced by the circadian system, this study examined circadian rhythms and sleep in adults with TD, and explored the possible benefit of short-wavelength wearable morning light therapy.MethodsParticipants were 34 adults with TD (n = 14) and age- and sex-matched healthy controls (HC; n = 20). Participants were screened using clinician-rated diagnostic and tic severity interviews, and procedures lasted 3 consecutive weeks. Participants completed a baseline week of actigraphy. Adults with TD completed 2 weeks of Re-Timer™ morning light therapy and continued actigraphy monitoring. Dim light melatonin-onset (DLMO) phase assessment, tic severity interview, and measures of chronotype, sleep disturbance, daytime sleepiness, disability, depression, anxiety, and stress were completed at baseline and post-intervention.ResultsAdults with TD reported significantly greater eveningness and sleep disturbance relative to controls. Per wrist actigraphy, adults with TD exhibited significantly longer sleep-onset latency, lower sleep efficiency, and greater sleep fragmentation than HC. Following morning light therapy, there was a significant advance in DLMO phase, but not self-report or actigraphy sleep variables. There were small, statistically significant decreases in tic severity and impairment. There were also significant reductions in daytime sleepiness, and self-reported anxiety, but not depression, stress, or disability. Participants reported minimal side effects and rated light therapy as acceptable and comfortable.ConclusionsFindings showed some benefits following brief light therapy in TD; further exploration of the impact of spectral tuning the photic environment as part of treatment for TD subjects is warranted

Role of tissue transglutaminase in GTP depletion-induced apoptosis of insulin-secreting (HIT-T15) cells

10.1016/S0006-2952(03)00262-4Biochemical Pharmacology662213-223BCPC