Protocol for The International Cohort on Lifestyle Determinants of Health Study: A Longitudinal Investigation of Complementary and Integrative Health Utilization in Postsecondary Education Students.

Objectives: The specific aims are: 1) To characterize the health, wellness, and lifestyle of graduate and undergraduate students, and how these characteristics change over time; 2) To evaluate associations between lifestyle factors and gut microbiota populations and diversity; and 3) To evaluate associations between stress and stress management practices with sleep habits, quality of life, and overall health. Design: The International Cohort on Lifestyle Determinants of Health (INCLD Health) longitudinal cohort study is designed to assess health behaviors and lifestyle practices amongst adults studying complementary and integrative health (CIH) and higher-education students more generally after at least one to six years of exposure to CIH education. INCLD Health will adhere to the Strengthening the Reporting of Observational studies in Epidemiology (STROBE) guidelines. Settings/Location: Colleges and universities with a CIH focus or interest with the flagship site being the National University of Natural Medicine. Participants: Adults currently enrolled in a college or university with a CIH focus or interest. Outcome Measures: Study visits will be conducted at baseline, 6 months, then every 12 months until the end of each participants' degree program. Measures include anthropometrics; serum and salivary biomarkers of cardiovascular risk, reproductive hormones, and cortisol; nutritional intake measured by a digital food frequency questionnaire; sequencing of fecal microbiota; plus validated questionnaires investigating mood, perceived stress, stress management practices, physical activity, sleep, and wellness. Conclusions: The INCLD Health Study, approved by the NUNM IRB in late 2018, will enroll a unique cohort of adults to characterize the use of CIH practices in relation to short- and long-term health. Our study design provides a breadth of information that could be implemented at multiple sites internationally allowing for comparisons across diverse student cohorts with relatively low cost and personnel

BOW SHOCK FRAGMENTATION DRIVEN BY A THERMAL INSTABILITY IN LABORATORY ASTROPHYSICS EXPERIMENTS

The role of radiative cooling during the evolution of a bow shock was studied in laboratory-astrophysics experiments that are scalable to bow shocks present in jets from young stellar objects. The laboratory bow shock is formed during the collision of two counter-streaming, supersonic plasma jets produced by an opposing pair of radial foil Z-pinches driven by the current pulse from the MAGPIE pulsed-power generator. The jets have different flow velocities in the laboratory frame and the experiments are driven over many times the characteristic cooling time-scale. The initially smooth bow shock rapidly develops small-scale non-uniformities over temporal and spatial scales that are consistent with a thermal instability triggered by strong radiative cooling in the shock. The growth of these perturbations eventually results in a global fragmentation of the bow shock front. The formation of a thermal instability is supported by analysis of the plasma cooling function calculated for the experimental conditions with the radiative packages ABAKO/RAPCAL.Comment: 9 pages, 5 figures, Accepted for publication in The Astrophysical Journal on 5th November 201

Autophagy modulates endothelial junctions to restrain neutrophil diapedesis during inflammation

The migration of neutrophils from the blood circulation to sites of infection or injury is a key immune response and requires the breaching of endothelial cells (ECs) that line the inner aspect of blood vessels. Unregulated neutrophil transendothelial cell migration (TEM) is pathogenic, but the molecular basis of its physiological termination remains unknown. Here, we demonstrated that ECs of venules in inflamed tissues exhibited a robust autophagic response that was aligned temporally with the peak of neutrophil trafficking and was strictly localized to EC contacts. Genetic ablation of EC autophagy led to excessive neutrophil TEM and uncontrolled leukocyte migration in murine inflammatory models, while pharmacological induction of autophagy suppressed neutrophil infiltration into tissues. Mechanistically, autophagy regulated the remodeling of EC junctions and expression of key EC adhesion molecules, facilitating their intracellular trafficking and degradation. Collectively, we have identified autophagy as a modulator of EC leukocyte trafficking machinery aimed at terminating physiological inflammation

Autophagy modulates endothelial junctions to restrain neutrophil diapedesis during inflammation

The migration of neutrophils from the blood circulation to sites of infection or injury is a key immune response and requires the breaching of endothelial cells (ECs) that line the inner aspect of blood vessels. Unregulated neutrophil transendothelial cell migration (TEM) is pathogenic, but the molecular basis of its physiological termination remains unknown. Here, we demonstrated that ECs of venules in inflamed tissues exhibited a robust autophagic response that was aligned temporally with the peak of neutrophil trafficking and was strictly localized to EC contacts. Genetic ablation of EC autophagy led to excessive neutrophil TEM and uncontrolled leukocyte migration in murine inflammatory models, while pharmacological induction of autophagy suppressed neutrophil infiltration into tissues. Mechanistically, autophagy regulated the remodeling of EC junctions and expression of key EC adhesion molecules, facilitating their intracellular trafficking and degradation. Collectively, we have identified autophagy as a modulator of EC leukocyte trafficking machinery aimed at terminating physiological inflammation

Interaction of a supersonic, radiatively cooled plasma jet with an ambient medium

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