Churches and poor people: the impact of covenant discipleship groups in local churches and their relation to increased face-to-face contact with the poor

https://place.asburyseminary.edu/ecommonsatsdissertations/1120/thumbnail.jp

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α4-Containing GABAA Receptors are Required for Antagonism of Ethanol-Induced Motor Incoordination and Hypnosis by the Imidazobenzodiazepine Ro15-4513

Alcohol (ethanol) is widely consumed for its desirable effects but unfortunately has strong addiction potential. Some imidazobenzodiazepines such as Ro15-4513 are able to antagonize many ethanol-induced behaviors. Controversial biochemical and pharmacological evidence suggest that the effects of these ethanol antagonists and ethanol are mediated specifically via overlapping binding sites on α4/δ-containing GABAA-Rs. To investigate the requirement of α4-containing GABAA-Rs in the mechanism of action of Ro15-4513 on behavior, wildtype (WT) and α4 knockout (KO) mice were compared for antagonism of ethanol-induced motor incoordination and hypnosis. Motor effects of ethanol were tested in two different fixed speed rotarod assays. In the first experiment, mice were injected with 2.0 g/kg ethanol followed 5 min later by 10 mg/kg Ro15-4513 (or vehicle) and tested on a rotarod at 8 rpm. In the second experiment, mice received a single injection of 1.5 g/kg ethanol ± 3 mg/kg Ro15-4513 and were tested on a rotarod at 12 rpm. In both experiments, the robust Ro15-4513 antagonism of ethanol-induced motor ataxia that was observed in WT mice was absent in KO mice. A loss of righting reflex (LORR) assay was used to test Ro15-4513 (20 mg/kg) antagonism of ethanol (3.5 g/kg)-induced hypnosis. An effect of sex was observed on the LORR assay, so males and females were analyzed separately. In male mice, Ro15-4513 markedly reduced ethanol-induced LORR in WT controls, but α4 KO mice were insensitive to this effect of Ro15-4513. In contrast, female KO mice did not differ from WT controls in the antagonistic effects of Ro15-4513 on ethanol-induced LORR. We conclude that Ro15-4513 requires α4-containing receptors for antagonism of ethanol-induced LORR (in males) and motor ataxia

The alpha1 subunit of the GABA(A) receptor modulates fear learning and plasticity in the lateral amygdala.

Synaptic plasticity in the amygdala is essential for emotional learning. Fear conditioning, for example, depends on changes in excitatory transmission that occur following NMDA receptor activation and AMPA receptor modification in this region. The role of these and other glutamatergic mechanisms have been studied extensively in this circuit while relatively little is known about the contribution of inhibitory transmission. The current experiments addressed this issue by examining the role of the GABA(A) receptor subunit alpha1 in fear learning and plasticity. We first confirmed previous findings that the alpha1 subunit is highly expressed in the lateral nucleus of the amygdala. Consistent with this observation, genetic deletion of this subunit selectively enhanced plasticity in the lateral amygdala and increased auditory fear conditioning. Mice with selective deletion of alpha1 in excitatory cells did not exhibit enhanced learning. Finally, infusion of a alpha1 receptor antagonist into the lateral amygdala selectively impaired auditory fear learning. Together, these results suggest that inhibitory transmission mediated by alpha1-containing GABA(A) receptors plays a critical role in amygdala plasticity and fear learning

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Muscle Glycogen Utilization during Exercise after Ingestion of Alcohol

Purpose Ingested ethanol (EtOH) is metabolized gastrically and hepatically, which may influence resting and exercise metabolism. Previous exercise studies have provided EtOH intravenously rather than orally, altering the metabolic effects of EtOH. No studies to date have investigated the effects of EtOH ingestion on systemic and peripheral (e.g., skeletal muscle) exercise metabolism. Methods Eight men (mean ± SD; age = 24 ± 5 yr, body mass = 76.7 ± 5.6 kg, height = 1.80 ± 0.04 m, VO2peak = 4.1 ± 0.2 L·min-1) performed two bouts of fasted cycling exercise at 55% VO2peak for 2 h, with (EtOH) and without (control) prior ingestion of EtOH 1 h and immediately before exercise (total dose = 0.1 g·kg lean body mass-1·h-1; 30.2 ± 1.1 g 40% ABV Vodka; fed in two equal boluses) in a randomized order, separated by 7-10 d. Results Muscle glycogen use during exercise was not different between conditions (mean [normalized 95% confidence interval]; EtOH, 229 [156-302] mmol·kg dm-1, vs control, 258 [185-331] mmol·kg dm-1; P = 0.67). Mean plasma glucose concentrations during exercise were similar (control, 5.26 [5.22-5.30], vs EtOH, 5.34 [5.30-5.38]; P = 0.06). EtOH ingestion resulted in similar plasma nonesterified fatty acid concentrations compared with rest (control, 0.43 [0.31-0.55] mmol·L-1, vs EtOH, 0.30 [0.21-0.40] mmol·L-1) and during exercise. Plasma lactate concentration was higher during the first 30 min of rest after EtOH consumption (mean concentration; control, 0.83 [0.77-0.90] mmol·L-1, vs EtOH, 1.00 [0.93-1.07] mmol·L-1), but the response during exercise was similar between conditions. Conclusions Muscle glycogen utilization was similar during exercise with or without prior EtOH ingestion, reflected in similar total whole-body carbohydrate oxidation rates observed.</p

Muscle Glycogen Utilization during Exercise after Ingestion of Alcohol

Purpose Ingested ethanol (EtOH) is metabolized gastrically and hepatically, which may influence resting and exercise metabolism. Previous exercise studies have provided EtOH intravenously rather than orally, altering the metabolic effects of EtOH. No studies to date have investigated the effects of EtOH ingestion on systemic and peripheral (e.g., skeletal muscle) exercise metabolism. Methods Eight men (mean ± SD; age = 24 ± 5 yr, body mass = 76.7 ± 5.6 kg, height = 1.80 ± 0.04 m, VO2peak = 4.1 ± 0.2 L·min-1) performed two bouts of fasted cycling exercise at 55% VO2peak for 2 h, with (EtOH) and without (control) prior ingestion of EtOH 1 h and immediately before exercise (total dose = 0.1 g·kg lean body mass-1·h-1; 30.2 ± 1.1 g 40% ABV Vodka; fed in two equal boluses) in a randomized order, separated by 7-10 d. Results Muscle glycogen use during exercise was not different between conditions (mean [normalized 95% confidence interval]; EtOH, 229 [156-302] mmol·kg dm-1, vs control, 258 [185-331] mmol·kg dm-1; P = 0.67). Mean plasma glucose concentrations during exercise were similar (control, 5.26 [5.22-5.30], vs EtOH, 5.34 [5.30-5.38]; P = 0.06). EtOH ingestion resulted in similar plasma nonesterified fatty acid concentrations compared with rest (control, 0.43 [0.31-0.55] mmol·L-1, vs EtOH, 0.30 [0.21-0.40] mmol·L-1) and during exercise. Plasma lactate concentration was higher during the first 30 min of rest after EtOH consumption (mean concentration; control, 0.83 [0.77-0.90] mmol·L-1, vs EtOH, 1.00 [0.93-1.07] mmol·L-1), but the response during exercise was similar between conditions. Conclusions Muscle glycogen utilization was similar during exercise with or without prior EtOH ingestion, reflected in similar total whole-body carbohydrate oxidation rates observed.</p

The Energy Cost of Sitting versus Standing Naturally in Man

Purpose Prolonged sitting is a major health concern, targeted via government policy and the proliferation of height-adjustable workstations and wearable technologies to encourage standing. Such interventions have the potential to influence energy balance and thus facilitate effective management of body/fat mass. It is therefore remarkable that the energy cost of sitting versus standing naturally remains unknown. Methods Metabolic requirements were quantified via indirect calorimetry from expired gases in 46 healthy men and women (age, 27 ± 12 yr; mass, 79.3 ± 14.7 kg; body mass index, 24.7 ± 3.1 kg·m -2, waist/hip, 0.81 ± 0.06) under basal conditions (i.e., resting metabolic rate) and then, in a randomized and counterbalanced sequence, during lying, sitting and standing. Critically, no restrictions were placed on natural/spontaneous bodily movements (i.e., fidgeting) to reveal the fundamental contrast between sitting and standing in situ while maintaining a comfortable posture. Results The mean (95% confidence interval [CI]) increment in energy expenditure was 0.18 (95% CI, 0.06-0.31 kJ·min -1) from resting metabolic rate to lying was 0.15 (95% CI, 0.03-0.27 kJ·min -1) from lying to sitting and 0.65 (95% CI, 0.53-0.77 kJ·min -1) from sitting to standing. An ancillary observation was that the energy cost of each posture above basal metabolic requirements exhibited marked interindividual variance, which was inversely correlated with resting heart rate for all postures (r = -0.5; -0.7 to -0.1) and positively correlated with self-reported physical activity levels for lying (r = 0.4; 0.1 to 0.7) and standing (r = 0.6; 0.3-0.8). Conclusions Interventions designed to reduce sitting typically encourage 30 to 120 min·d -1 more standing in situ (rather than perambulation), so the 12% difference from sitting to standing reported here does not represent an effective strategy for the treatment of obesity (i.e., weight loss) but could potentially attenuate any continued escalation of the ongoing obesity epidemic at a population level. </p

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Silica suspension and coating developments for Advanced LIGO

The proposed upgrade to the LIGO detectors to form the Advanced LIGO detector system is intended to incorporate a low thermal noise monolithic fused silica final stage test mass suspension based on developments of the GEO 600 suspension design. This will include fused silica suspension elements jointed to fused silica test mass substrates, to which dielectric mirror coatings are applied. The silica fibres used for GEO 600 were pulled using a Hydrogen-Oxygen flame system. This successful system has some limitations, however, that needed to be overcome for the more demanding suspensions required for Advanced LIGO. To this end a fibre pulling machine based on a CO2 laser as the heating element is being developed in Glasgow with funding from EGO and PPARC. At the moment a significant limitation for proposed detectors like Advanced LIGO is expected to come from the thermal noise of the mirror coatings. An investigation on mechanical losses of silica/tantala coatings was carried out by several labs involved with Advanced LIGO R&D. Doping the tantala coating layer with titania was found to reduce the coating mechanical dissipation. A review of the results is given here