A deep tensor-based approach for automatic depression recognition from speech utterances.

Depression is one of the significant mental health issues affecting all age groups globally. While it has been widely recognized to be one of the major disease burdens in populations, complexities in definitive diagnosis present a major challenge. Usually, trained psychologists utilize conventional methods including individualized interview assessment and manually administered PHQ-8 scoring. However, heterogeneity in symptomatic presentations, which span somatic to affective complaints, impart substantial subjectivity in its diagnosis. Diagnostic accuracy is further compounded by the cross-sectional nature of sporadic assessment methods during physician-office visits, especially since depressive symptoms/severity may evolve over time. With widespread acceptance of smart wearable devices and smartphones, passive monitoring of depression traits using behavioral signals such as speech presents a unique opportunity as companion diagnostics to assist the trained clinicians in objective assessment over time. Therefore, we propose a framework for automated depression classification leveraging alterations in speech patterns in the well documented and extensively studied DAIC-WOZ depression dataset. This novel tensor-based approach requires a substantially simpler implementation architecture and extracts discriminative features for depression recognition with high f1 score and accuracy. We posit that such algorithms, which use significantly less compute load would allow effective onboard deployment in wearables for improve diagnostics accuracy and real-time monitoring of depressive disorders.

Practical Review of Recognition and Management of Obesity and Lipohypertrophy in Human Immunodeficiency Virus Infection.

BACKGROUND: Obesity and lipohypertrophy are common in treated human immunodeficiency virus (HIV) infection and contribute to morbidity and mortality among HIV-infected adults on antiretroviral therapy (ART). METHODS: We present a consensus opinion on the diagnosis, clinical consequences, and treatment of excess adiposity in adults with treated HIV infection. RESULTS: Obesity and lipohypertrophy commonly occur among HIV-infected adults on ART and may have overlapping pathophysiologies and/or synergistic metabolic consequences. Traditional, HIV-specific, and ART-specific risk factors all contribute. The metabolic and inflammatory consequences of excess adiposity are critical drivers of non-AIDS events in this population. Although promising treatment strategies exist, further research is needed to better understand the pathophysiology and optimal treatment of obesity and lipohypertrophy in the modern ART era. CONCLUSIONS: Both generalized obesity and lipohypertrophy are prevalent among HIV-infected persons on ART. Aggressive diagnosis and management are key to the prevention and treatment of end-organ disease in this population and critical to the present and future health of HIV-infected persons.

Endogenous sex hormones and cardiovascular disease incidence in men.

BACKGROUND: Data suggest that endogenous sex hormones (testosterone, dehydroepiandrosterone sulfate [DHEA-S], and estradiol) influence cardiovascular disease (CVD) risk factors and vascular function. Yet, prospective studies relating sex hormones to CVD incidence in men have yielded inconsistent results. OBJECTIVE: To examine the association of circulating sex hormone levels and CVD risk in men. DESIGN: Prospective cohort study. SETTING: Community-based study in Framingham, Massachusetts. PARTICIPANTS: 2084 middle-aged white men without CVD at baseline. MEASUREMENTS: The authors used multivariable Cox regression to relate baseline levels of testosterone, DHEA-S, and estradiol to the incidence of CVD (coronary, cerebrovascular, or peripheral vascular disease or heart failure) during 10 years of follow-up. RESULTS: During follow-up, 386 men (18.5%) experienced a first CVD event. After adjustment for baseline standard CVD risk factors, higher estradiol level was associated with lower risk for CVD (hazard ratio per SD increment in log estradiol, 0.90 [95% CI, 0.82 to 0.99]; P = 0.035). The authors observed effect modification by age: Higher estradiol levels were associated with lower CVD risk in older (median age >56 years) men (hazard ratio per SD increment, 0.86 [CI, 0.78 to 0.96]; P = 0.005) but not in younger (median age < or =56 years) men (hazard ratio per SD increment, 1.11 [CI, 0.89 to 1.38]; P = 0.36). The association of higher estradiol level with lower CVD incidence remained robust in time-dependent Cox models (updating standard CVD risk factors during follow-up). Serum testosterone and DHEA-S levels were not statistically significantly associated with incident CVD. LIMITATIONS: Sex hormone levels were measured only at baseline, and the findings may not be generalizable to women and nonwhite people. CONCLUSIONS: In the community-based sample, a higher serum estradiol level was associated with lower risk for CVD events in older men. The findings are consistent with the hypothesis that endogenous estrogen has vasculoprotective influences in men.

Myostatin is a skeletal muscle target of growth hormone anabolic action.

Myostatin is a cytokine that has recently been shown to selectively and potently inhibit myogenesis. To investigate the mechanisms of anabolic actions of GH on skeletal muscle growth, we examined the in vitro and in vivo effects of GH on myostatin regulation. Twelve GH-deficient hypopituitary adult subjects were treated with recombinant GH (5 micro g/kg.d) in a double-blind, placebo-controlled fashion. Body composition and physical function were assessed and skeletal muscle biopsies from the vastus lateralis performed at 6-monthly intervals during 18 months of treatment. Myostatin mRNA expression was significantly inhibited to 31 +/- 9% (P < 0.001) of control by GH but not by placebo administration (79 +/- 11%) as determined by quantitative real-time PCR normalized for the housekeeping glyceraldehyde-3-phosphate dehydrogenase gene. The inhibitory effect of GH on myostatin was sustained after 12 and 18 months of GH treatment. These effects were associated with increases in lean body mass and translated into enhanced aerobic performance as determined by maximal oxygen uptake and ventilation threshold. Parallel in vitro studies of skeletal muscle cells demonstrated significant reduction of myostatin expression by myotubes in response to GH, compared with vehicle treatment. Conversely, GH receptor antagonism resulted in up-regulation of myostatin in myoblasts. Given the potent catabolic actions of myostatin, our data suggest that myostatin represents a potential key target for GH-induced anabolism.