Integrated monitoring and assessment of soil restoration treatments in the Lake Tahoe Basin.

Revegetation and soil restoration efforts, often associated with erosion control measures on disturbed soils, are rarely monitored or otherwise evaluated in terms of improved hydrologic, much less, ecologic function and longer term sustainability. As in many watersheds, sediment is a key parameter of concern in the Tahoe Basin, particularly fine sediments less than about ten microns. Numerous erosion control measures deployed in the Basin during the past several decades have under-performed, or simply failed after a few years and new soil restoration methods of erosion control are under investigation. We outline a comprehensive, integrated field-based evaluation and assessment of the hydrologic function associated with these soil restoration methods with the hypothesis that restoration of sustainable function will result in longer term erosion control benefits than that currently achieved with more commonly used surface treatment methods (e.g. straw/mulch covers and hydroseeding). The monitoring includes cover-point and ocular assessments of plant cover, species type and diversity; soil sampling for nutrient status; rainfall simulation measurement of infiltration and runoff rates; cone penetrometer measurements of soil compaction and thickness of mulch layer depths. Through multi-year hydrologic and vegetation monitoring at ten sites and 120 plots, we illustrate the results obtained from the integrated monitoring program and describe how it might guide future restoration efforts and monitoring assessments.

Application of a prototype process for developing a tube gastrostomy clinical pathway.

The development and implementation of clinical pathways as a managed care tool have been widely embraced as principal components of the healthcare industry's drive to reform costly, inconsistent, and often uncontrolled delivery of services. Clinical pathways are not new to healthcare; however, the lack of a defined and systematic process for pathway development has hindered organizational efforts to develop and implement clinical pathways. A multidisciplinary clinical pathway process prototype was identified as a means for effectively defining and linking care and outcomes for patients requiring tube gastrostomy placement at a large military medical facility. This article presents the prototype process for developing a clinical pathway with a practical application to illustrate the process and provides a process template for potential use by others interested in developing multidisciplinary clinical pathways.

Actualizing the vision of interdisciplinary team excellence.

The benefits of a case management program are effective for enhancing quality and access while reducing the cost of patient care. In this article, the authors describe a systems theory-based case management program, which represents a collaborative, interdisciplinary approach to patient care that spans the care continuum.

Vitamin D, calcium, and bone status in children with developmental delay in relation to anticonvulsant use and ambulatory status.

Reports of abnormalities in vitamin D, calcium, and bone status associated with anticonvulsant use are inconsistent and difficult to interpret because of widely varying study designs, particularly for ambulatory status. We examined the relative effects of anticonvulsant use and ambulatory status on vitamin D, calcium, and bone status in a large group (n = 338) of children who had either normal motor function (ambulatory) or were nonambulatory and either receiving anticonvulsants or not; all had developmental delays. Data included diet records, serum analyses (calcium and calcidiol), and hand-wrist radiographs evaluated for bone maturation and quality. Data were analyzed by using a general linear models (GLM) procedure. Dietary and biochemical data were compared with those of a group of 34 normal children. There were no differences in calcium or vitamin D intakes among the four study groups; however, a high percentage of intakes was below the recommended dietary allowances for calcium (56%) and vitamin D (70%). Vitamin D intakes were positively associated with serum calcium (P < 0.005) and calcidiol (P < 0.01) concentrations. Analysis of covariance indicated that ambulatory status but neither anticonvulsant use nor their interaction contributed significantly to the prediction of serum calcium (P < 0.009) and calcidiol (P < 0.0001), the Z scores for number of ossified centers (P < 0.008), bone age (P < 0.0001), and bone area (P < 0.003). A strong interaction between anticonvulsant use and ambulatory status was seen for percentage cortical area (P < 0.0008), which was entirely due to anticonvulsant use in nonambulatory children (effect size = 0.98). Results suggest that ambulatory status is more important than was recognized previously in relation to abnormalities in vitamin D, calcium, and bone statuses; that all nonambulatory children may be at risk for low serum calcidiol and osteopenia; and that routine monitoring of risk and consideration of prophylactic vitamin D supplementation are warranted.

Interspecies differences in testicular LH receptors and in vitro testosterone production among rodents.

Testes from rats, mice and hamsters were incubated for 4 h with 0, 3.125 or 12.5 mIU hCG/ml. The LH receptor concentration in incubated testes of rats and mice was higher than that observed in hamsters. Testosterone levels in incubation media were significantly different among species (mice greater than rats greater than hamsters). During the incubation, hCG caused an increase in testosterone levels in all three species, but produced no significant changes in LH receptor concentration. Furthermore, a correlation between LH receptor concentration and testosterone only in hamsters is observed. The efficiency of the LH receptor-steroidogenesis interaction was estimated from the ratio of testosterone levels to receptor concentration under basal conditions and was found to differ among species (mice greater than hamster greater than rats). The levels of PGE and PGF in incubation media were higher in mice than in rats or hamsters, and hCG did not alter prostaglandin levels in any of the species. The present results indicate that acute in vitro hCG stimulation of testosterone synthesis does not involve appreciable changes in testicular LH receptor levels.

Prolactin (PRL), follicle-stimulating hormone, and luteinizing hormone are regulators of testicular PRL receptors in golden hamsters.

The ability of PRL, FSH, and LH to regulate testicular PRL receptors in golden hamsters was evaluated using a variety of experimental protocols. Exposure to a photoperiod of 5 h of light and 19 h of darkness (5L:19D) for 11 weeks precipitated a 94% reduction in content (femtomoles per testes) of testicular PRL receptors and, concomitantly, a decrease (P less than 0.05) in plasma PRL, but not LH or FSH. One pituitary gland under the kidney capsule in 5L:19D-housed hamsters increased (P less than 0.05) both the concentration (femtomoles per mg protein) and content of PRL receptors, as well as those of plasma PRL and FSH. Similar treatment in 14L:10D-housed hamsters produced comparable changes in plasma PRL and FSH without affecting PRL receptors. Injections of L-dopa for 7 days into hamsters housed in 5L:19D for 11 weeks significantly elevated serum FSH concentrations, had no measurable effect on serum PRL and LH, and induced a greater than 2-fold increase in PRL receptor levels. In a separate study, hamsters housed in 5L:19D for 12 weeks were injected for 3 days with 250 microgram ovine (o) PRL, 25 microgram oLH, or 5 microgram oFSH, and results were compared with vehicle-injected, 5L:19D- and 14L:10D-housed controls. Injections of oPRL and oLH increased (P less than 0.05) PRL receptor concentration and content, with PRL being more efficacious. No anti-oPRL antibodies were produced by oPRL injections. In this study, injections of oFSH were without effect on PRL receptors. To ascertain the effects of each hormone in the absence of other trophic influences, experiments were conducted in hypophysectomized hamsters injected daily for 3 days (2-4 days posthypophysectomy) with one of the following: 5 or 25 microgram oLH; 10, 50, or 250 microgram oPRL; or 1 or 5 microgram oFSH. Hypophysectomy reduced the concentration and content of PRL receptors by 85%, and treatment with 50 or 250 microgram oPRL increased (P less than 0.05) these low levels almost 3-fold. Again, no anti-oPRL antibodies were induced. Injection of 5 microgram oLH or 25 microgram oFSH also induced increases (P less than 0.05) in PRL receptors. Hypophysectomy reduced basal and hCG-stimulated in vitro testicular testosterone production (nanograms per testes/4 h) to levels less than 20% of control values. None of the hormonal treatments affected (P less than 0.05) basal testosterone production in vitro.(ABSTRACT TRUNCATED AT 400 WORDS)

Hormonal regulation of testicular human chorionic gonadotropin binding and steroidogenesis in adult mice with different forms of hereditary diabetes and obesity.

The regulation of testicular hCG binding and steroidogenesis in adult mutant mice with hereditary diabetes and obesity was studied. Low doses of hCG caused no change in hCG binding in obese (ob/ob) mice, whereas, in diabetic (db/db) mice, the increase in binding measured 24 h after hCG administration was not as great as in normal males. Intermediate doses of hCG caused a decrease in hCG binding in obese and normal mice, but not in diabetic animals. However, 72 h after injection of intermediate doses of hCG, a decrease in hCG binding also was observed in diabetic mice. Plasma testosterone was elevated 24 h after hCG injection in all types of mice studied, but the increase in diabetic mice was smaller than in normal animals. However, 72 h after treatment with hCG, plasma testosterone was still elevated in diabetic mice, but not in normal males. In vitro, hCG stimulated testicular testosterone synthesis in all groups of mice, but the observed increase was smaller in diabetic and obese than in normal animals. Plasma LH levels were higher in diabetic than in normal mice, whereas plasma FSH and prolactin levels were lower in obese mice than in normal animals. All parameters (i.e., LH receptors and circulating hormone levels) measured in yellow (Ay/a) mice were similar to those in normal (a/a) mice. The present study indicates that in these models for noninsulin-dependent diabetes, the testicular metabolism of LH receptors and capacity to secrete steroids is altered.

Effects of inhibitory and stimulatory photoperiods and sexual maturation on the ability of hamster testes to respond to hCG in vitro.

The decrease in gonadal weight produced in adult golden hamsters by exposure to short photoperiods was accompanied by a marked reduction in the ability of the testes to produce testosterone from endogenous precursors in vitro, both without and with hCG stimulation. These changes were significant after 4-7 weeks in short photoperiod (5L: 19D) and were even more pronounced after 17-20 weeks. Production of testosterone in vitro by testes of immature hamsters was comparable to values obtained in adult animals with short photoperiod-induced gonadal atrophy. Delay of sexual maturation induced by daily injections of bromocriptine was accompanied by a further decrease in testicular testosterone production in vitro. Exposure of gonadally-regressed adult hamsters to a long, stimulatory photoperiod (14L: 10D) produced a rapid and marked increase in testicular testosterone production, which was coincident with the previously demonstrated increase in serum gonadotrophin levels after 1-5 days of photostimulation. Furthermore, testosterone production in vitro by regressed testes of animals exposed to short photoperiod was increased significantly by one large dose of hCG administered 26 h before killing the animals. It is concluded that the suppressive effects of short photoperiods on the ability of the hamster testis to produce testosterone and to respond to hCG stimulation are due to reductions in endogenous LH, FSH and prolactin release, with a consequent loss of testicular LH/hCG receptors and decreased activity of enzymes involved in the biosynthesis of testosterone.

Prolonged suppression of plasma LH levels in male rats after a single injection of an LH-RH agonist in poly(DL-lactide-co-glycolide) microcapsules.

The authors have examined the effects of a subcutaneous injection of the LH-RH agonist D-Trp6-LH-RH formulated in biodegradable poly(DL-lactide-co-glycolide) microcapsules on plasma levels of D-Trp6LH-RH, LH, and PRL in adult, gonadectomized male rats. Immunoreactive D-Trp6-LH-RH was detectable in the plasma of these animals at 1, 2, 3, and 4 weeks after injection. LH concentrations were greatly reduced 1 week after administering the D-Trp6-LH-RH microcapsule, continued to decrease during the following week, and remained suppressed until the end of the study, 6 weeks after the injection. Plasma PRL levels appeared elevated 1 to 2 weeks after the injection and suppressed thereafter, but these effects were significant only in animals rendered hyperprolactinemic by transplantation of an isologous pituitary under the renal capsule. These results demonstrate that an LH-RH agonist formulated in biodegradable microcapsules and administered as a subcutaneous injection can exert marked biologic effects in rats for at least 6 weeks. These findings also suggest that prolonged exposure to an LH-RH agonist may first produce stimulation, followed by an inhibition of PRL release from both in situ and ectopic pituitaries.

Does prolactin modify testosterone feedback in the hamster? Suppression of plasma prolactin inhibits photoperiod-induced decreases in testosterone feedback sensitivity.

The hormonal changes during the photoperiodically driven annual reproductive cycle of the male golden hamster can be explained partially by a change in the sensitivity of the hypothalamo-pituitary axis to negative feedback by testosterone (T). The present studies test the hypothesis that the increases in plasma levels of LH and FSH that follow photo-stimulation are due to decreasing feedback sensitivity and examine if this change in sensitivity is dependent upon increasing PRL levels. Adult males were exposed to a lighting schedule of 5 h of light, 19 h of darkness (5:19) for 12 weeks to induce gonadal regression. The animals were castrated; treated with an inhibitor of PRL release, bromocriptine (CB-154), or oil; and received a Silastic capsule that was empty or filled with T. Subsequently, the animals were transferred to 14:10 and killed 9 or 31 days later. There were no significant changes in FSH and LH in animals receiving oil injections and empty implants between days 9 and 31, suggesting no steroid-independent changes in gonadotropin secretion during this time period. However, 4-mm T implants were more effective in suppressing LH and FSH levels on day 9 than on day 31. This suggests that there is a gradual decrease in feedback sensitivity to T following photostimulation. T was more effective in inhibiting LH and FSH levels in CB-154-treated than in oil-treated animals on both day 9 and day 31. Thus, increases in PRL release are instrumental in causing decreases in feedback sensitivity following photostimulation.

Does prolactin modify testosterone feedback in the hamster? Pituitary grafts alter the ability of testosterone to suppress luteinizing hormone and follicle-stimulating hormone release in castrated male hamsters.

Adult male golden hamsters maintained in a long photoperiod (14 h of light and 10 h of darkness) or in a short photoperiod (5 h of light and 19 h of darkness for 7 weeks) were castrated and either given one anterior pituitary transplant under the kidney capsule or sham-operated. Additional animals were castrated and grafted or sham-grafted at the time of transfer to the short photoperiod. Starting 2 weeks after castration, all animals were injected three times a week with 20 micrograms testosterone propionate (TP). After 3 weeks, the dose of TP was increased to 80 micrograms and, after an additional 2 weeks, to 320 micrograms per injection. Blood samples were collected 2 weeks after castration and 1 day after the last injection of 20, 80, and 320 micrograms TP. Short photoperiod reduced and pituitary grafts increased plasma PRL levels. Plasma testosterone levels were related to the dose of injected TP, but were not influenced by photoperiod or pituitary transplants. Before the onset of TP injections, plasma LH and FSH levels in grafted and sham-grafted hamsters did not differ. In each of the three photoperiod conditions, injections of TP were consistently less effective in suppressing plasma gonadotropin levels in pituitary-grafted animals than in sham-grafted controls. These results indicate that PRL modulates the effects of exogenous testosterone on LH and FSH release in adult castrated male golden hamsters, this effect of PRL is due to reducing the sensitivity of the hypothalamic-pituitary system to feedback inhibition by testosterone, and suppression of pituitary PRL release in short photoperiod may be partially responsible for the concomitant increase in the sensitivity of LH and FSH release to inhibition by testosterone.

Ectopic pituitary transplants stimulate synthesis and release of follicle-stimulating hormone in golden hamsters.

It was previously reported that PRL can stimulate FSH release in immature female rats and PRL-deficient male dwarf mice. We have examined the effects of PRL-producing ectopic pituitary grafts on plasma FSH and LH levels in adult male golden hamsters during exposure to both long (14 h of light, 10 h of darkness) and short (5 h of flight, 19 h of darkness) photoperiods. In both groups, the presence of one pituitary graft resulted in a significant elevation of pituitary and plasma FSH levels. Although there were no statistically significant changes in the concentration of LH in the pituitary or plasma of either group. LH values were more variable than FSH values, and these findings do not rule out an effect on LH. To determine whether the ability of ectopic pituitary grafts to stimulate FSH release depends on changes in testicular or adrenal function, additional experiments were done in castrated male hamsters, in castrated males given testosterone propionate, and in castrated adrenalectomized hamsters maintained with injections of cortisol. The results indicate that the increase in FSH release in engrafted animals does not depend on the testes or the adrenals, but can be prevented by exogenous cortisol. In adult female hamsters, pituitary grafts increased plasma LH levels above the concentrations observed in diestrous, proestrous, or pregnant controls, but did not alter plasma FSH levels. In contrast, in ovariectomized and ovariectomized-estradiol benzoate-treated animals, pituitary grafts increased plasma FSH levels without significantly affecting plasma LH. It is concluded that PRL-producing ectopic pituitary homografts significantly stimulate FSH synthesis and release in male golden hamsters, and that this effect is probably not mediated through the changes in gonadal or adrenal function.