FEELING SAFE: INTERGENERATIONAL CONNECTIONS AND NEIGHBORHOOD DISORGANIZATION AMONG URBAN AND RURAL AFRICAN AMERICAN YOUTH

Neighborhood disorganization and the perception of neighborhood disorganization are linked to several adverse outcomes for youth. Disorganized communities often lack the social structures to promote well‐being, maintain social control, and provide an environment in which youth feel safe. Intergenerational connections, similar to cultural attributes of collectiveness and extended family found among people of African ancestry, was expected to be linked to less perceived neighborhood disorganization. Neighborhood type, rural versus urban, was also investigated as a moderator of the relationship between intergenerational connections and perceived neighborhood disorganization. Participants were 564 elementary, middle, and high school students who were recruited from urban and rural schools in a mid‐Atlantic region of the United States. Students completed measures of Intergenerational Connections and Neighborhood Disorganization along with demographic items. The findings indicated that higher levels of intergenerational connections were associated with perceptions of less disorganized neighborhoods. A significant interaction was found between neighborhood type and intergenerational connections. Intergenerational connections lowered perceptions of disorganization in urban neighborhoods such that youth in neighborhoods with high intergenerational connections reported lower disorganization than those in areas of low intergenerational connections. This effect was not found for youth in rural neighborhoods. Benefits and methods for increasing intergenerational connections among African American youth are discussed.     

Adolescent Mothers,Stress, and Prevention

Abstract

Adolescent mothers face problems that can lead to psychological stress. Based on prospective data from the present study, these problems point toward the need for a coping skills prevention approach to help adolescent mothers manage stress. This paper reports data from outcome research on such an approach with adolescent mothers. Subjects were 79 adolescent mothers who were tested before, immediately after, and three months following the provision of coping skills intervention in an experimental condition. Subjects in a test-only control condition received no special intervention. At posttest, experimental condition subjects showed more positive outcomes on measures of social support, cognitive performance, conflict management, and interpersonal competence. At three-month follow-up, experimental condition subjects had more positive outcomes on social support, cognitive performance, parenting ability, child care self-efficacy, and measures of psychological well-being.     

Partial heat acclimation of athletes with spinal cord lesion

Heat acclimation (HA) can improve thermoregulatory stability in able-bodied athletes in part by an enhanced sweat response. Athletes with spinal cord lesion are unable to sweat below the lesion and it is unknown if they can HA. Five paralympic shooting athletes with spinal cord lesion completed seven consecutive days HA in hot conditions (33.4 ± 0.6 °C, 64.8 ± 3.7 %rh). Each HA session consisted of 20 min arm crank exercise at 50 % $ \dot{V}{\text{O}}_{{ 2 {\text{peak}}}} $ followed by 40 min rest, or simulated shooting. Aural temperature (T _aur) was recorded throughout. Body mass was assessed before and after each session and a sweat collection swab was fixed to T12 of the spine. Fingertip whole blood was sampled at rest on days 1 and 7 for estimation of the change in plasma volume. Resting T _aur declined from 36.3 ± 0.2 °C on day 1 to 36.0 ± 0.2 °C by day 6 (P < 0.05). During the HA sessions mean, T _aur declined from 37.2 ± 0.2 °C on day 1, to 36.7 ± 0.3 °C on day 7 (P < 0.05). Plasma volume increased from day 1 by 1.5 ± 0.6 % on day 7 (P < 0.05). No sweat secretion was detected or changes in body mass observed from any participant. Repeated hyperthermia combined with limited evaporative heat loss was sufficient to increase plasma volume, probably by alterations in fluid regulatory hormones. In conclusion, we found that although no sweat response was observed, athletes with spinal cord lesion could partially HA.     

Transcranial Direct Current Stimulation of the Dorsolateral Prefrontal Cortex Alters Emotional Modulation of Spinal Nociception

Emotion has a strong modulatory effect on pain perception and spinal nociception. Pleasure inhibits pain and nociception, whereas displeasure facilitates pain and nociception. Dysregulation of this system has been implicated in development and maintenance of chronic pain. The current study sought to examine whether emotional modulation of pain could be altered through the use of transcranial direct current stimulation (tDCS) to enhance (via anodal stimulation) or depress (via cathodal stimulation) cortical excitability in the dorsolateral prefrontal cortex. Thirty-two participants (15 female, 17 male) received anodal, cathodal, and sham tDCS on three separate occasions, followed immediately by testing to examine the impact of pleasant and unpleasant images on pain and nociceptive flexion reflex (NFR) responses to electrocutaneous stimulation. Results indicated that tDCS modulated the effect of image content on NFR, F(2, 2175.06) = 3.20, P= .04, with the expected linear slope following anodal stimulation (ie, pleasant < neutral < unpleasant) but not cathodal stimulation. These findings provide novel evidence that the dorsolateral prefrontal cortex is critical to emotional modulation of spinal nociception. Moreover, the results suggest a physiological basis for a previously identified phenotype associated with risk for chronic pain and thus a potentially new target for chronic pain prevention efforts.PerspectiveThis study demonstrated that reduction of dorsolateral prefrontal cortical excitability by transcranial direct current stimulation attenuates the impact of emotional image viewing on nociceptive reflex activity during painful electrocutaneous stimulation. This result confirms there is cortical involvement in emotional modulation of spinal nociception and opens avenues for future clinical research.     

Defects in Mitochondrial Efficiency and H2O2 Emissions in Obese Women Are Restored to a Lean Phenotype With Aerobic Exercise Training

The notion that mitochondria contribute to obesity-induced insulin resistance is highly debated. Therefore, we determined whether obese (BMI 33 kg/m²), insulin-resistant women with polycystic ovary syndrome had aberrant skeletal muscle mitochondrial physiology compared with lean, insulin-sensitive women (BMI 23 kg/m²). Maximal whole-body and mitochondrial oxygen consumption were not different between obese and lean women. However, obese women exhibited lower mitochondrial coupling and phosphorylation efficiency and elevated mitochondrial H₂O₂ (mtH₂O₂) emissions compared with lean women. We further evaluated the impact of 12 weeks of aerobic exercise on obesity-related impairments in insulin sensitivity and mitochondrial energetics in the fasted state and after a high-fat mixed meal. Exercise training reversed obesity-related mitochondrial derangements as evidenced by enhanced mitochondrial bioenergetics efficiency and decreased mtH₂O₂ production. A concomitant increase in catalase antioxidant activity and decreased DNA oxidative damage indicate improved cellular redox status and a potential mechanism contributing to improved insulin sensitivity. mtH₂O₂ emissions were refractory to a high-fat meal at baseline, but after exercise, mtH₂O₂ emissions increased after the meal, which resembles previous findings in lean individuals. We demonstrate that obese women exhibit impaired mitochondrial bioenergetics in the form of decreased efficiency and impaired mtH₂O₂ emissions, while exercise effectively restores mitochondrial physiology toward that of lean, insulin-sensitive individuals.     

A potent small molecule inhibits polyglutamine aggregation in Huntington's disease neurons and suppresses neurodegeneration in vivo

Polyglutamine (polyQ) disorders, including Huntington's disease (HD), are caused by expansion of polyQ-encoding repeats within otherwise unrelated gene products. In polyQ diseases, the pathology and death of affected neurons are associated with the accumulation of mutant proteins in insoluble aggregates. Several studies implicate polyQ-dependent aggregation as a cause of neurodegeneration in HD, suggesting that inhibition of neuronal polyQ aggregation may be therapeutic in HD patients. We have used a yeast-based high-throughput screening assay to identify small-molecule inhibitors of polyQ aggregation. We validated the effects of four hit compounds in mammalian cell-based models of HD, optimized compound structures for potency, and then tested them in vitro in cultured brain slices from HD transgenic mice. These efforts identified a potent compound (IC50=10 nM) with long-term inhibitory effects on polyQ aggregation in HD neurons. Testing of this compound in a Drosophila HD model showed that it suppresses neurodegeneration in vivo, strongly suggesting an essential role for polyQ aggregation in HD pathology. The aggregation inhibitors identified in this screen represent four primary chemical scaffolds and are strong lead compounds for the development of therapeutics for human polyQ diseases.     

Gastric acidification inhibits meal-stimulated gastric acid secretion after prostaglandin synthesis inhibition by indomethacin in humans

The effects of cyclooxygenase inhibition by indomethacin on gastric acid secretion were studied in 8 healthy men. Oral doses of indomethacin (200 mg), administered 15 and 2 h before testing, were known to inhibit prostaglandin synthesis by 90% in 3 of the subjects as determined by prostaglandin E2 generation assay on endoscopically obtained gastric mucosal biopsy specimens. Acid-induced inhibition of gastric acid secretion was evaluated in a randomized and blinded study in which acid output was measured for 2 h during basal conditions by aspiration, for the next 2 h by intragastric titration during distention with isotonic glucose, and for the following 2 h by intragastric titration during meal stimulation with peptone. The studies were done on separate days, and intragastric pH was maintained at either 2.5 or 5.5 after administration of indomethacin or placebo. Basal acid output was not altered by indomethacin treatment. Distention of the stomach stimulated acid output significantly to a similar degree in all groups, without affecting plasma gastrin. Meal stimulation increased plasma gastrin and acid output significantly more at pH 5.5 (47 +/- 12 pM, 13 +/- 2 mmol/30 min) than at pH 2.5 (30 +/- 8 pM, 6 +/- 2 mmol/30 min). No effect of indomethacin treatment was observed. It is concluded that the participation of cyclooxygenase products in the mechanisms by which acid inhibits the gastric phase of acid secretion in humans is likely to be minor. These results also cast doubt on an important physiologic role for cyclooxygenase products in the regulation of basal acid secretion or of acid secretion stimulated by distention or a peptone meal.     

Almitrine increases the steady-state hypoxic ventilatory response in hypoxic chronic air-flow obstruction

Almitrine, a peripheral chemoreceptor agonist, exerts beneficial effects on blood gases in patients with hypoxic chronic air-flow obstruction, but as these patients exhibit poor ventilatory responses to hypoxia, the mechanism for this improvement is not clear. The effect of a 100-mg dose of almitrine given orally on ventilation and the steady-state hypoxic ventilatory response (HVR) were measured in a randomized, double-blind, placebo-controlled manner in 7 patients with severe hypoxic chronic air-flow obstruction. The isocapnic HVR (delta VE/delta SaO2) was calculated from the changes in ventilation and SaO2 from breathing 60% O2 to breathing air with the addition of CO2 to maintain isocapnia (as estimated from a transcutaneous CO2 electrode). Resting ventilation while breathing air and isocapnic HVR were measured before and 3 h after almitrine or placebo. Almitrine caused no significant change in resting ventilation. There was, however, a large increase in HVR after almitrine (almitrine: -1.5 L/min/%SaO2; range, -0.5 to -3.1; control: -0.4; range, -0.3 to -1.3), but no change after placebo. Almitrine is a powerful stimulant of chemosensitivity and of the hypoxic ventilatory response in chronic hypoxemia, with potential benefit to patients with chronic air-flow obstruction in respiratory failure.