Neuronal cell bodies in the hypothalamic paraventricular nucleus mediate stress-induced renin and corticosterone secretion

The present studies were undertaken to determine the involvement of neurons in the hypothalamic paraventricular nucleus (PVN) in stress-induced renin secretion. The stressor was a 10-min conditioned emotional response (CER) paradigm. Bilateral electrolytic lesions in the PVN prevented the stress-induced increase in plasma renin activity (PRA), and plasma renin concentration (PRC). Stress-induced corticosterone secretion was also blocked, supporting the histological verification and suggesting that the lesion included corticosterone-releasing factor neurons in the PVN. Stress-induced renin secretion appears to be restricted to the PVN, as electrolytic lesions in the nucleus reuniens, dorsal and caudal to the PVN, did not prevent the stress-induced increase in either PRA or PRC. The next step was to determine whether cell bodies in the PVN or fibers of passage through the PVN mediate the stress-induced increase of these hormones. For this purpose, bilateral stereotaxic injections of the cell-selective neurotoxin ibotenic acid (10 micrograms/microliter; 0.3 microliters per side) were performed 14 days prior to the stress procedure. Histological evaluation of the tissue revealed cell death and lysis in the PVN. Ibotenic acid injection into the PVN prevented the effect of stress on PRA, PRC and corticosterone levels. None of the lesions prevented the stress-induced rise in plasma prolactin concentration. These results suggest that neurons in the PVN play an important role in mediating stress-induced increases in renin and corticosterone but not prolactin secretion.     

Rate-sensitive glucocorticoid feedback inhibition of adrenocorticotropin and beta-endorphin/beta-lipotropin secretion in rats

In the present study, we present physiological evidence for rate-sensitive, fast feedback inhibition of secretion of ACTH and beta-endorphin (beta END)-related peptides. We used a 2 min restraint stress to physiologically increase plasma corticosterone, then examined the plasma responses of immunoreactive ACTH and beta END plus beta-lipotropin (beta END/beta LPH) to a subsequent restraint stress. After onset of this stress, plasma corticosterone increased from 2.5-10 min at a rate of 120 nM min-1, then remained at a peak from 10-15 min. A single 2 min restraint stress produced peak plasma levels of ACTH and beta END/beta LPH 2.5 min after onset of the stress, and these plasma concentrations declined after this initial stress at rates of 2.7 and 7.4 pM min-1, respectively. Application of a second restraint stress at the time of the peak corticosterone response produced plasma ACTH and beta END/beta LPH responses similar to those after the first stress. Application of a second stress during the period of significant rate-rise of corticosterone in plasma did not result in decreased incremental responses of plasma ACTH or beta END/beta LPH. However, the rates of decline of plasma ACTH and beta END/beta LPH of 7.6 and 32 pM min-1, respectively, from peak levels, were significantly greater after this second stress applied during the period of significant increase in plasma corticosterone concentration than the corresponding rates of decline observed after the initial stress or after a subsequent stress applied at the peak of plasma corticosterone. These differences in rates of decline of plasma ACTH or beta END/beta LPH appear to reflect differences in secretion rate rather than clearance, since disappearance of [125I]ACTH1-24 was not different after an initial vs. subsequent stress. In contrast to these data from intact rats, initial and subsequent stresses did not show different rates of decline of plasma ACTH or beta END/beta LPH in adrenalectomized rats. In conclusion, the stress-induced rate rise of glucocorticoid provides a negative feedback signal which serves to terminate and limit the duration, but not the peak, of the responses of POMC-derived peptides to subsequent stress.     

Iowa's High School High Tech Goes to College Program: Preparing Students with Mild Disabilities for Careers in Technology

This paper describes an innovative approach to preparing high school students with mild disabilities for challenging careers in high tech industries, called High School High Tech (HSHT). Iowa's HSHT Goes to College program has three central elements, each of which is discussed in this paper: High School Preparation—assisting students in identifying a suitable high tech career goal; Higher Education Preparation and Supports—assisting students in selecting college/training programs that match their career goal, and in successfully completing their postsecondary programs; Workforce Entry Assistance—linking students with employers and launching their high tech careers. The paper concludes with a presentation of outcomes to date and recommendations for program enhancements. The information presented here is intended to assist education and rehabilitation professionals interested in establishing similar efforts across the nation.     

Five‐Year Follow‐up After Sacral Neuromodulation: Single Center Experience

Objective. We studied long‐term clinical efficacy of sacral neuromodulation (SNM) therapy in patients with refractory urgency incontinence (UI), urgency/frequency (UF) and voiding difficulty (VD), together with urodynamic data at baseline and six   months postimplant. Materials and Methods. Twenty‐two patients were implanted with a neurostimulator after a positive response to a percutaneous nerve evaluation test defined as a greater than 50% improvement in symptoms. Results. At five‐year follow‐up, the number of incontinent episodes and pad usage per day decreased significantly in 10 out of 15 UI patients. Two of five UF patients were successfully treated with SNM; the number of daily voids for all UF patients decreased from 25 to 19 and average voided volume increased from 98 to 212 mL. One of the two VD patients was able to void to completion. Mean first sensation of filling at the six‐month urodynamic investigation for the UI and UF patients increased from 78 to 241 mL and 141 to 232 mL, respectively, and the maximum bladder capacity increased from 292 to 352 mL and 223 to 318 mL, respectively. Five of 22 patients underwent device explant and one patient still has an inactive stimulator implanted. Conclusion. SNM is an effective treatment modality that offers sustained clinical benefit in the majority of patients with refractory UI, UF, and VD that do not respond to other, more conservative therapies.     

Changes in sexual behavior during a safety and feasibility trial of a microbicide/diaphragm combination: an integrated qualitative and quantitative analysis.

If proven effective, vaginal microbicides and diaphragms will likely be part of a larger HIV prevention model that includes condoms and other prevention strategies. It is, therefore, important to understand how introducing new prevention methods may affect overall patterns of sexual risk behavior. Data presented were collected as part of a safety and feasibility study of ACIDFORM gel with a diaphragm among 120 women in South Africa. Interviews were administered at enrollment and months 1, 3, 5, and 6 of the trial. Focus groups were conducted at trial exit. Frequency of sex increased significantly after enrollment. This increase appears to be owing to perceived protection from HIV and greater sexual pleasure afforded by the gel. Male condom use was high overall but increased significantly from enrollment. Data suggest this is because of increased partner involvement, increased negotiating power afforded by study participation, and provision of free condoms perceived to be of high quality.     

Microbiological aspects of heat sterilization of drugs

International Journal of Clinical Pharmacy - In order to calculate the minimum sterilization process conditions to obtain the generally accepted sterility level (less than 1·10?6...     

Effects of intracerebral estradiol on the dorsal immobility response in the rat

The effects of intracerebral implants of 17 beta estradiol and cholesterol in five brain regions were tested on the duration of the dorsal immobility response in ovariectomized female rats. The dorsal immobility response was significantly prolonged by 4-hr implants of 17 beta estradiol in the dorsal striatum and nucleus accumbens, but not in the cortex, the globus pallidus, or the substantia nigra pars compacta. These data further support previous evidence that estradiol acts directly on the striatum to affect behavior in the rat.