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1.
It has been speculated that exposure to the chronic stress of racism contributes to the high rates of hypertension among African Americans. Social support may buffer the effects of stress on cardiovascular (CV) health by attenuating stress-induced CV responses that have been linked to hypertension. In this study we investigated the effects of racism and social support on CV reactivity in African American women. Participants showed greater increases in CV and emotional responses while responding and listening to racist provocation. Augmented blood pressure (BP) persisted through recovery following racial stress. Participants receiving no support showed the greatest increases in anger during racist provocation. No significant effects were seen for support on CV reactivity. These results provide some of the first evidence that interactive confrontation with racism elicits significant increases in CV reactivity and emotional distress. Furthermore, individuals receiving less support may be at greater risk for the potentially health-damaging effects of racial stress. These findings may have significant implications for the health of African Americans.  相似文献   
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Retigabine (D-23129, N-(2-amino-4-(4-fluorobenzylamino)-phenyl) carbamic acid ethyl ester) is a potent anticonvulsant in a variety of animal models. Rats metabolized [14C]retigabine mainly through glucuronidation and acetylation reactions. Glucuronides were detected in incubates with liver microsomes or slices, in plasma, and in bile and feces but were absent in urine (0-24 h) that contained about 2% of the dose as retigabine and approximately 29% of the dose in > 20 metabolites, which are derived mainly from acetylation reactions. About 67% of the radioactivity was excreted into feces, approximately 10% of the dose as glucuronide. The metabolite pattern in the urine (0-24 h) of dogs was comparatively simple in that retigabine (13%), retigabine-N-glucuronide (5%), and retigabine-N-glucoside (1%) were present. In the same 24-h interval, about 39% of unchanged retigabine was excreted into feces. Plasma profiling and spectroscopic analysis (liquid chromatography with tandem mass spectrometry NMR) of two isolated urinary metabolites obtained after single oral dosing of 600 mg retigabine in healthy volunteers indicated that both acetylation and glucuronidation are major metabolic pathways of retigabine in humans. We found that in vitro assays with liver slices from rat and humans reveal the major circulating metabolites in vivo.  相似文献   
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A sensitive bioassay for inhibin based on the suppression of FSH release from cultured sheep anterior pituitary cells was used to determine whether inhibin is present in the preovulatory follicle in the domestic hen. Granulosa and thecal/stromal layers were separated from the five largest (F1-F5) yellow yolky follicles in the ovary and incubated in culture medium for 18 h. Inhibin was found predominantly in the media in which granulosa layers had been incubated. There was a progressive increase in the amount of inhibin produced per mg granulosa layer protein during the 5-6 days before ovulation. The ovary was observed to contain a growth factor which stimulated the proliferation of ovine pituitary cells. Thecal/stromal layer-conditioned medium (ThCM) but not granulosa layer-conditioned medium had a dose- and time-dependent mitogenic effect on cultured sheep pituitary cells. The maximal mitogenic effect achieved for ThCM was four to fivefold greater than control media and was significantly higher than the maximal mitogenic effects of epidermal growth factor (250 ng/ml; 1.5 x control) and transforming growth factor-beta (500 ng/ml; 1.2 x control). It is concluded that inhibin is produced by the granulosa layers in the large yellow yolky preovulatory ovarian follicles of the domestic hen. The thecal/stromal layers in these follicles produce a potent mitogenic factor, not produced by the granulosa layers, which stimulates the division of ovine anterior pituitary cells in vitro.  相似文献   
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There is an increasing expectation that children, young people and their parents should participate in decisions that affect them. This includes decisions about their health and social care and collective or public decisions about the way in which such services are designed, delivered and evaluated. Indeed this has become a policy priority across the United Kingdom. The participation of disabled children and young people, however, has been slow to develop in the United Kingdom and concerns have been expressed about progress in this area. Drawing on the results of an Economic and Social Research Council-funded, mixed-methods study, the aim of this article is to explore the participation of disabled children and young people through a social justice lens. Participants, recruited by purposeful sampling, included 18 disabled children and young people, 77 parents and 90 professionals from one health and social care trust in Northern Ireland. There were four phases of data collection: surveys to parents and professionals, parent interviews, interviews with children and young people using creative and participatory techniques, and a focus group with professionals. Results showed that for most disabled children and young people, decision-making was firmly grounded in a family-centred model. However, when children and young people were drawn into participatory processes by adults and recognised as partners in interactions with professionals, they wanted more say and were more confident about expressing their views. Choices, information and resources were at times limited and this had a key impact on participation and the lives of these children, young people and their parents. The article concludes by exploring implications for further research and practice. The need for a two-pronged, social justice approach is recommended as a mechanism to advance the participation agenda.  相似文献   
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The aim was to determine the pattern of inhibin A and inhibin B secretion during the ovulatory cycle of the macaque and to explore the effects of manipulating follicular phase FSH on inhibin B secretion by: 1) blocking the early follicular phase rise in FSH with GnRH antagonist treatment; 2) administering FSH in GnRH antagonist-treated animals; and 3) preventing the midfollicular phase decline in FSH by a specific antiestrogen. Treatment with GnRH antagonist, starting on day 25 of the cycle, abolished the early follicular phase rise in FSH and the associated increase in inhibin B. The same treatment, followed by exogenous FSH, restored the secretion of inhibin B. Treatment with antiestrogen, commencing during the midfollicular phase, induced a supraphysiological rise in FSH, followed by a marked stimulation of inhibin B and estradiol secretion. Despite continued antiestrogen treatment, FSH secretion declined before peak values of inhibin B and estradiol were attained, implying a potential endocrine role for inhibin B, in addition to estradiol, in the negative feedback regulation of FSH. These results show that follicular phase FSH is the major stimulus for inhibin B secretion.  相似文献   
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