Gravitational Radiation: Maxwell-Heaviside Formulation

To fully describe gravitational energy flux by using an analog to the Maxwell-Heaviside equations for electrodynamics, the Liénard–Wiechert potentials and fields are derived for gravitation along with radiation patterns and corresponding Larmor formulas for total radiated power. Due to attraction of like gravitational charges (masses) as opposed to repulsion of like electrical charges, the mass-density and current-density terms pick up a negative sign along with a factor of the universal gravitational constant, G. This results in a sign change of the Poynting vector, indicating energy is gained by the field as opposed to energy being lost by the field, such is the case for electromagnetic radiation. The gravitational and cogravitational fields, analogous to the electric and magnetic fields, respectively, behave as described by Heaviside and Lorentz. Like an electric charge, a gravitic charge (mass) in uniform motion is found to produce a spherical field which contracts along the axis of motion as its velocity approaches the limiting speed of propagation. The speed of gravitational propagation is assumed to be equivalent to that of light, though this may not necessarily be the case. For an accelerated mass, the resulting gravitational radiation mirrors the dipole pattern produced by an accelerated electric charge, similarly oriented about the axis of acceleration yet contracting in the reverse direction at relativistic speeds. These results seek to further inquire on the nature of gravitational fields

Measurement of the J/ψ\psi photoproduction cross section over the full near-threshold kinematic region

We report the total and differential cross sections for $J/\psi$ photoproduction with the large acceptance GlueX spectrometer for photon beam energies from the threshold at 8.2~GeV up to 11.44~GeV and over the full kinematic range of momentum transfer squared, $t$. Such coverage facilitates the extrapolation of the differential cross sections to the forward ($t = 0$) point beyond the physical region. The forward cross section is used by many theoretical models and plays an important role in understanding $J/\psi$ photoproduction and its relation to the $J/\psi-$proton interaction. These measurements of $J/\psi$ photoproduction near threshold are also crucial inputs to theoretical models that are used to study important aspects of the gluon structure of the proton, such as the gluon Generalized Parton Distribution (GPD) of the proton, the mass radius of the proton, and the trace anomaly contribution to the proton mass. We observe possible structures in the total cross section energy dependence and find evidence for contributions beyond gluon exchange in the differential cross section close to threshold, both of which are consistent with contributions from open-charm intermediate states.Comment: 15 pages 18 figure

Effect of sitagliptin on cardiovascular outcomes in type 2 diabetes

BACKGROUND: Data are lacking on the long-term effect on cardiovascular events of adding sitagliptin, a dipeptidyl peptidase 4 inhibitor, to usual care in patients with type 2 diabetes and cardiovascular disease. METHODS: In this randomized, double-blind study, we assigned 14,671 patients to add either sitagliptin or placebo to their existing therapy. Open-label use of antihyperglycemic therapy was encouraged as required, aimed at reaching individually appropriate glycemic targets in all patients. To determine whether sitagliptin was noninferior to placebo, we used a relative risk of 1.3 as the marginal upper boundary. The primary cardiovascular outcome was a composite of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for unstable angina. RESULTS: During a median follow-up of 3.0 years, there was a small difference in glycated hemoglobin levels (least-squares mean difference for sitagliptin vs. placebo, -0.29 percentage points; 95% confidence interval [CI], -0.32 to -0.27). Overall, the primary outcome occurred in 839 patients in the sitagliptin group (11.4%; 4.06 per 100 person-years) and 851 patients in the placebo group (11.6%; 4.17 per 100 person-years). Sitagliptin was noninferior to placebo for the primary composite cardiovascular outcome (hazard ratio, 0.98; 95% CI, 0.88 to 1.09; P<0.001). Rates of hospitalization for heart failure did not differ between the two groups (hazard ratio, 1.00; 95% CI, 0.83 to 1.20; P = 0.98). There were no significant between-group differences in rates of acute pancreatitis (P = 0.07) or pancreatic cancer (P = 0.32). CONCLUSIONS: Among patients with type 2 diabetes and established cardiovascular disease, adding sitagliptin to usual care did not appear to increase the risk of major adverse cardiovascular events, hospitalization for heart failure, or other adverse events

Why Sleep Is Important for Health: A Psychoneuroimmunology Perspective

Sleep has a critical role in promoting health. Research over the past decade has documented that sleep disturbance has a powerful influence on the risk of infectious disease, the occurrence and progression of several major medical illnesses including cardiovascular disease and cancer, and the incidence of depression. Increasingly, the field has focused on identifying the biological mechanisms underlying these effects. This review highlights the impact of sleep on adaptive and innate immunity, with consideration of the dynamics of sleep disturbance, sleep restriction, and insomnia on antiviral immune responses with consequences for vaccine responses and infectious disease risk, and on proinflammatory immune responses with implications for cardiovascular disease, cancer, and depression. This review also discusses the neuroendocrine and autonomic neural underpinnings linking sleep disturbance and immunity, and the reciprocal links between sleep and inflammatory biology. Lastly interventions are discussed as effective strategies to improve sleep, and potential opportunities are identified to promote sleep health for therapeutic control of chronic infectious, inflammatory, and neuropsychiatric diseases

Maternal distress and child neuroendocrine and immune regulation

RATIONALE: Neuroendocrine-immune regulation is essential for maintaining health. Early-life adversity may cause dysregulation in the neuroendocrine-immune network through repeated activation of the stress response, thereby increasing disease risk. OBJECTIVE: This paper examined the extent to which maternal psychological well-being moderates neuroendocrine-immune relations in children. METHODS: We used data from a laboratory-based study of mothers and their five-year old children (n=125 mother-child pairs) conducted from 2011–2013 in Baltimore, Maryland. Child saliva was assayed for markers of immune function (i.e., cytokines: interleukin [IL]-1β, IL-6, IL-8, tumor necrosis factor alpha [TNF-α]) and hypothalamic-pituitary-adrenal activity (i.e., cortisol). A composite score for depressive symptoms, anxiety, and parenting stress characterized maternal psychological distress. Multilevel mixed models examined the relationship between maternal psychological well-being and child neuroendocrine-immune relations. RESULTS: Significant cytokine × maternal distress interactions indicated that as maternal distress increased, expected inverse cytokine-cortisol relations within children became weaker for IL-1β, IL-6, and TNF-α. Sex-stratified models revealed that these interactions were only significant among girls. Among boys, there were inverse cytokine-cortisol relations for all cytokines, and, while in the same direction as observed among girls, the cytokine × maternal distress interactions were non-significant. CONCLUSION: The findings suggest that maternal distress is associated with child neuroendocrine-immune relations in saliva and may alter the sensitivity of inflammatory immune processes to cortisol's inhibitory effects. This desensitization may place the child at risk for inflammatory diseases. The findings support efforts for the early detection and treatment of at-risk mothers to protect maternal and child health and well-being

Anger Is Associated with Increased IL-6 Stress Reactivity in Women, But Only Among Those Low in Social Support

BACKGROUND: Social connections moderate the effects of high negative affect on health. Affective states (anger, fear, and anxiety) predict interleukin-6 (IL-6) reactivity to acute stress; in turn, this reactivity predicts risk of cardiovascular disease progression. PURPOSE: Here, we examined whether perceived social support mitigates the relationship between negative affect and IL-6 stress reactivity. METHOD: Forty-eight postmenopausal women completed a standardized mental lab stressor with four blood draws at baseline and 30, 50, and 90 min after the onset of the stressor and anger, anxiety, and fear were assessed 10 min after task completion. Participants self-rated levels of social support within a week prior to the stressor. RESULTS: Only anger was related to IL-6 stress reactivity—those experiencing high anger after the stressor had significant increases in IL-6. IL-6 reactivity was marginally associated with perceived support, but more strikingly, perceived support mitigated anger associations with IL-6 stress reactivity. CONCLUSION: Supportive ties can dampen the relationship of anger to pro-inflammatory reactivity to acute stress. Implications to cardiovascular disease are discussed