The effectiveness of antenatal care programmes to reduce infant mortality and preterm birth in socially disadvantaged and vulnerable women in high-income countries: a systematic review

Background: Infant mortality has shown a steady decline in recent years but a marked socioeconomic gradient persists. Antenatal care is generally thought to be an effective method of improving pregnancy outcomes, but the effectiveness of specific antenatal care programmes as a means of reducing infant mortality in socioeconomically disadvantaged and vulnerable groups of women has not been rigorously evaluated.Methods: We conducted a systematic review, focusing on evidence from high income countries, to evaluate the effectiveness of alternative models of organising or delivering antenatal care to disadvantaged and vulnerable groups of women vs. standard antenatal care. We searched Medline, Embase, Cinahl, PsychINFO, HMIC, CENTRAL, DARE, MIDIRS and a number of online resources to identify relevant randomised and observational studies. We assessed effects on infant mortality and its major medical causes (preterm birth, congenital anomalies and sudden infant death syndrome (SIDS)).Results: We identified 36 distinct eligible studies covering a wide range of interventions, including group antenatal care, clinic-based augmented care, teenage clinics, prenatal substance abuse programmes, home visiting programmes, maternal care coordination and nutritional programmes. Fifteen studies had adequate internal validity: of these, only one was considered to demonstrate a beneficial effect on an outcome of interest. Six interventions were considered 'promising'.Conclusions: There was insufficient evidence of adequate quality to recommend routine implementation of any of the programmes as a means of reducing infant mortality in disadvantaged/vulnerable women. Several interventions merit further more rigorous evaluation

Cognitive effects of testosterone and finasteride administration in older hypogonadal men

Stephen E Borst,1 Joshua F Yarrow,2 Carmen Fernandez,1 Christine F Conover,2 Fan Ye,2 John R Meuleman,1 Matthew Morrow,3 Baiming Zou,4 Jonathan J Shuster5 1Geriatric Research, Education and Clinical Center, 2Research Service, 3Pharmacy Service, Malcom Randall VA Medical Center, Gainesville Florida; 4Department of Biostatistics, 5Department of Health Outcomes and Policy, University of Florida, Gainesville, FL, USA Abstract: Serum concentrations of neuroactive androgens decline in older men and, in some ­studies, low testosterone is associated with decreased cognitive function and incidence of depression. Existing studies evaluating the effect of testosterone administration on cognition in older men have been largely inconclusive, with some studies reporting minor to moderate cognitive benefit, while others indicate no cognitive effect. Our objective was to assess the cognitive effects of treating older hypogonadal men for 1 year with a supraphysiological dose of testosterone, either alone or in combination with finasteride (a type II 5α-reductase inhibitor), in order to determine whether testosterone produces cognitive benefit and whether suppressed dihydrotestosterone influences cognition. Sixty men aged ≥60 years with a serum testosterone concentration of ≤300 ng/dL or bioavailable testosterone ≤70 ng/dL and no evidence of cognitive impairment received testosterone-enanthate (125 mg/week) versus vehicle, paired with finasteride (5 mg/day) versus placebo using a 2×2 factorial design. Testosterone caused a small decrease in depressive symptoms as assessed by the Geriatric Depression Scale and a moderate increase in visuospatial memory as assessed by performance on a recall trial of the Rey-Osterrieth Complex Figure Test. Finasteride caused a small increase in performance on the Benton Judgment of Line Orientation test. In total, major improvements in cognition were not observed either with testosterone or finasteride. Further studies are warranted to determine if testosterone replacement may improve cognition in other domains. Keywords: cognition, depression, 5 alpha reductase, testosterone enanthat

Testosterone and trenbolone enanthate increase mature myostatin protein expression despite increasing skeletal muscle hypertrophy and satellite cell number in rodent muscle

Dalbo, VJ ORCiD: 0000-0002-5944-7558The androgen-induced alterations in adult rodent skeletal muscle fibre cross-sectional area (fCSA), satellite cell content and myostatin (Mstn) were examined in 10-month-old Fisher 344 rats (n = 41) assigned to Sham surgery, orchiectomy (ORX), ORX + testosterone (TEST; 7.0 mg week−1) or ORX + trenbolone (TREN; 1.0 mg week−1). After 29 days, animals were euthanised and the levator ani/bulbocavernosus (LABC) muscle complex was harvested for analyses. LABC muscle fCSA was 102% and 94% higher in ORX + TEST and ORX + TREN compared to ORX (p <.001). ORX + TEST and ORX + TREN increased satellite cell numbers by 181% and 178% compared to ORX, respectively (p <.01), with no differences between conditions for myonuclear number per muscle fibre (p =.948). Mstn protein was increased 159% and 169% in the ORX + TEST and ORX + TREN compared to ORX (p <.01). pan-SMAD2/3 protein was ~30–50% greater in ORX compared to SHAM (p =.006), ORX + TEST (p =.037) and ORX + TREN (p =.043), although there were no between-treatment effects regarding phosphorylated SMAD2/3. Mstn, ActrIIb and Mighty mRNAs were lower in ORX, ORX + TEST and ORX + TREN compared to SHAM (p <.05). Testosterone and trenbolone administration increased muscle fCSA and satellite cell number without increasing myonuclei number, and increased Mstn protein levels. Several genes and signalling proteins related to myostatin signalling were differentially regulated by ORX or androgen therapy. © 2016 Blackwell Verlag GmbHAssociated Grant:This study was also supported in part by work supported from the Office of Research and Development, Rehabilitation Research and Development (RR&D) Service, Department of Veterans Affairs Merit Award to S.E.B., Veteran’s Health Administration Advanced Geriatrics Fellowship to D.T.B., and RR&D CDA-2 to J.F.Y

Testosterone and trenbolone enanthate increase mature myostatin protein expression despite increasing skeletal muscle hypertrophy and satellite cell number in rodent muscle

The androgen-induced alterations in adult rodent skeletal muscle fibre cross-sectional area (fCSA), satellite cell content and myostatin (Mstn) were examined in 10-month-old Fisher 344 rats (n = 41) assigned to Sham surgery, orchiectomy (ORX), ORX + testosterone (TEST; 7.0 mg week−1) or ORX + trenbolone (TREN; 1.0 mg week−1). After 29 days, animals were euthanised and the levator ani/bulbocavernosus (LABC) muscle complex was harvested for analyses. LABC muscle fCSA was 102% and 94% higher in ORX + TEST and ORX + TREN compared to ORX (p <.001). ORX + TEST and ORX + TREN increased satellite cell numbers by 181% and 178% compared to ORX, respectively (p <.01), with no differences between conditions for myonuclear number per muscle fibre (p =.948). Mstn protein was increased 159% and 169% in the ORX + TEST and ORX + TREN compared to ORX (p <.01). pan-SMAD2/3 protein was ~30–50% greater in ORX compared to SHAM (p =.006), ORX + TEST (p =.037) and ORX + TREN (p =.043), although there were no between-treatment effects regarding phosphorylated SMAD2/3. Mstn, ActrIIb and Mighty mRNAs were lower in ORX, ORX + TEST and ORX + TREN compared to SHAM (p <.05). Testosterone and trenbolone administration increased muscle fCSA and satellite cell number without increasing myonuclei number, and increased Mstn protein levels. Several genes and signalling proteins related to myostatin signalling were differentially regulated by ORX or androgen therapy. © 2016 Blackwell Verlag Gmb

Avian extinctions from tropical and subtropical forests

10.1146/annurev.ecolsys.35.112202.130209Annual Review of Ecology, Evolution, and Systematics35323-34