Propagation of fire generated smoke in shipboard spaces

The propagation of fire generated smoke into a shipboard space has been computationally modeled using a commercial code generated by Computational Fluid Dynamics Research Corporation (CFDRC). This study was based on space 01- 163-2-L of an Arleigh Burke Class Flight IIA Destroyer. However, with changes, the model can be reconfigured to represent other shipboard spaces. Multiple smoke scenarios are applied to the space. For all scenarios, the inlet used is forward water tight door. Smoke enters the upper half of the door, while air enters through the bottom half. The temperature of the inlet fluids is altered to observe its effect on propagation. In the last scenario, the floor temperature is isothermally held at 1200 K to simulate a fire in the space below. The results of this scenario shows that extreme temperatures of adjacent spaces has minimal effect on propagation. The overall goal of this study is to show how computational methods can be used to model propagation of smoke in shipboard spaceshttp://www.archive.org/details/propagationoffir00mehlU.S. Navy (U.S.N.) author

Assessment of total body water in paediatric patients on dialysis

Background Various anthropometric techniques are used to assess total body water in children on dialysis; however, their predictive accuracy and precision has not been validated. Methods We compared total body water measurements obtained by deuterium oxide (D2O) dilution with predictions of total body water from (1) height and weight, (2) skinfold measurements, and (3) bioelectrical impedance analysis, using previously published formulae for healthy children. Measurements were performed in 14 patients on peritoneal and in nine patients on haemodialysis, aged 4-22 years. Results In the total population of dialysed patients, weight was the strongest single predictor of total body water (R2=0.93) followed by the resistance index (RI=height2/impedance; R2=0.85) and height (R2=0.93). A prediction formula based on height and weight predicted total body water with a residual mean square error (RMSE) of 1.97 l (coefficient of variation (CV)=10.0%) and with a systematic overestimation of true total body water by 0.4%. A prediction equation based on skinfold measurements yielded a total body water estimate with an RMSE of 2.15 1 (CV=10.5%) and overpredicted true total body water by an average of 2.2%. Using three published prediction equations incorporating RI, RMSEs of 2.78 1 (CV=14.1%) with a mean under- or overestimation of true total body water by 6.9, 7.1, and 0.8% respectively, were achieved. The prediction of total body water was optimized by linear combinations of RI or the log-transformed sum of four skinfolds (logsum) with weight by the following equations: total body water (1) = 9.97−3.13×logsum +0.59×weight (kg) (1) (R2 = 0.951; RMSE=1.67 1; CV = 8.17%). total body water (1) = 1.99 + 0.144 × RI (Ohm/cm2) + 0.40 × weight (kg) (2) (R2 = 0.949; RMSE = 1.671; CV = 8.53%). The fit of these prediction formulae, which were derived from the total population, did not differ significantly between haemo- and peritoneal dialysis patients or between boys and girls. Conclusions Both skinfold measurements and bioelectrical impedance analysis can be used to improve the height- and weight- based prediction of total body water in children on dialysi

Multi-scale Habitat Use of Male Ruffed Grouse in the Black Hills National Forest

Ruffed grouse (Bonasa umbellus) are native upland game birds and a management indicator species (MIS) for aspen (Populus tremuloides) in the Black Hills National Forest (Black Hills). Our objective was to assess resource selection of male ruffed grouse to identify the most appropriate scale to manage for aspen and ruffed grouse in the Black Hills. During spring 2007 and 2008, we conducted drumming surveys throughout the central and northern Black Hills to locate used and unused sites from which we compared habitat characteristics at increasing spatial scales. Aspen with \u3e70% overstory canopy cover (OCC) was important to the occurrence of ruffed grouse across all spatial scales, but was most influential within 1600 m of drumming sites. Probability of a site being used was maximized when 20% of the 1600-m scale (~804 ha) had aspen with \u3e70% OCC. Ruffed grouse also selected for areas with many small, regular shaped patches of aspen over those with few large patches. At the smallest scale evaluated of 200 m (~12.5 ha), ruffed grouse selected drumming logs in close proximity to high stem densities of aspen with a minimal presence of roads. Ponderosa pine (Pinus ponderosa) had a negative influence on site selection at the 400-m (~50 ha), 1600-m (~804 ha), and 4800-m (~7200 ha) scales. Management for ruffed grouse in the Black Hills as the MIS for aspen should focus on increasing the extent of aspen with a goal of at least 20% occurrence on the landscape. Management efforts also should incorporate multiple age and size classes of aspen with an emphasis on enhancing early successional habitat to provide valuable cover through increased stem densities

Differential effects of insulin-like growth factor binding proteins-1, -2, -3, and -6 on cultured growth plate chondrocytes

Differential effects of insulin-like growth factor binding proteins-1, -2, -3, and -6 on cultured growth plate chondrocytes.BackgroundIn children with chronic renal failure (CRF), impairment of longitudinal growth is in part due to excess amounts of circulating high-affinity insulin-like growth factor binding proteins (IGFBPs) that might decrease or prevent insulin-like growth factor (IGF) binding to its signaling receptor. However, it appears from the clinical studies that various IGFBPs may have contrasting effects on longitudinal growth. Because of the potential importance of the IGFBPs as modulators of longitudinal growth in pediatric CRF, the aim of the present study was to investigate the biological effects of IGFBP-1, -2, -3, and -6 on cultured growth plate chondrocytes that express the type 1 IGF receptor.MethodsThe effects of exogenous IGFBPs on IGF-independent and IGF-dependent proliferation of rat growth plate chondrocytes in primary culture were investigated. Proliferation was assessed by colony formation of agarose-stabilized long-term suspension cultures and by the [3H]thymidine assay. The effects of IGFBPs on IGF-I binding and the binding of IGFBPs to chondrocytes were assessed by binding studies with radiolabeled proteins in monolayer culture.ResultsIntact IGFBP-1, IGFBP-2 and IGFBP-6 inhibited in equimolar concentration the IGF-I- and IGF-II-stimulated DNA synthesis and cell proliferation, whereas the biological activity of IGFBP-3 was complex. It had an IGF-independent antiproliferative effect and also inhibited IGF-dependent chondrocyte proliferation under coincubation conditions, whereas under preincubation conditions IGFBP-3 enhanced IGF-I-responsiveness. Studies on the mechanism by which IGFBP-3 potentiated IGF activity demonstrated that under preincubation conditions IGFBP-3 is capable to associate with the cell membrane and to facilitate IGF-I cell surface binding.ConclusionsIntact IGFBP-1, IGFBP-2 and IGFBP-6 act exclusively as growth inhibitors on IGF-dependent proliferation of growth plate chondrocytes. IGFBP-3, however, can either inhibit IGF-independent and IGF-dependent cell proliferation, or enhance IGF responsiveness of chondrocytes dependent on the temporal relationship to the IGF exposure

Growth promoting effects of growth hormone and IGF-I are additive in experimental uremia.

Exogenous growth hormone (GH) stimulates the endogenous production of IGF-I and improves growth in uremia. We investigated whether exogenous IGF-I is also able to improve uremic growth failure in rats and whether the growth promoting effects of GH and IGF-I are additive. In female 150 g uremic (subtotal nephrectomy, NX) Sprague-Dawley rats, both rhGH in doses from 2 X 1.25 to 2 X 10 IU/kg bid s.c. and rhIGF-I in doses from 2 X 0.5 to 2 X 4.0 mg/kg bid s.c. caused a dose-dependent increase in weight gain and length gain. However, endogenous production of GH was suppressed by both agents. Peptide hormone treatment did not affect cumulative food intake, but significantly increased food efficiency ratio (weight gain/food intake). Concomitant s.c. treatment with maximally effective doses of rhGH (12 X 5 IU/kg bid) and of rhIGF-I (2 X 2 mg/kg bid) resulted in additive growth promoting effects in NX and pair-fed control (CO) animals during the observation period of 12 days. Cumulative length gain was 3.2 +/- 0.5 cm in solvent-treated NX-animals, 4.1 +/- 0.5 cm with rhGH (+ 28% above solvent), 4.2 +/- 0.6 cm with rhIGF-I (+ 31%) and 4.9 +/- 0.5 cm with both peptides (+ 53%). The food efficiency ratio was 0.16 +/- 0.05 in solvent NX, 0.33 +/- 0.04 with rhGH (+ 106% above solvent), 0.23 +/- 0.02 with rhIGF-I (+ 44%), and 0.38 +/- 0.02 with both peptides (+ 138%). Histomorphometric analysis and measurements of length gain by fluorescence microscopy in the upper tibial metaphysis confirmed the growth promoting effects of both peptide hormones. The serum concentrations of IGF binding protein (BP)-4 (Western ligand blotting analysis) and of IGFBP-2 (immunoblot) were increased in uremic animals whereas IGFBP-3 was unchanged. Treatment with IGF-I and/or rhGH increased serum concentration of IGF-I but did not change the IGFBP pattern. rhIGF-I lowered blood glucose levels within one to two hours after injection. The effect was most pronounced during the first treatment day and declined thereafter. Concomitant treatment with rhGH attenuated the glucose lowering effect of rhIGF-I (glucose serum concentration at day one: 120 +/- 11 mg% in solvent NX, 50 +/- 21 mg% with rhIGF-I, 80 +/- 24 mg% with both peptides). It is concluded that: (i) IGF-I is able to stimulate growth in NX animals but suppresses endogenous GH production in the long run; (ii) the concomitant treatment with IGF-I and GH has additive effects on growth; and (iii) concomitant treatment with rhGH prevents hypoglycemia that is noted with rhIGF-I alone

Growth hormone prevents steroid-induced growth depression in health and uremia

Growth hormone prevents steroid-induced growth depression in health and uremia. Treatment with supraphysiological doses of corticosteroids results in protein wasting and impairment of growth, whereas exogenous growth hormone (GH) causes anabolism and improvement of growth. We wanted to know whether the growth depressing effects of methylprednisolone (MP) are more expressed in an organism which is chronically diseased and whether these effects can be counterbalanced by concomitant treatment with recombinant human growth hormone (rhGH). MP in doses from 1 to 9 mg/kg/day caused a dose dependent reduction of length gain, weight gain and weight gain/food intake ratio in 140 g healthy female Sprague-Dawley rats. Food intake was not affected by MP. This points to a change in food metabolism as a mechanism for growth impairment. In addition, treatment with MP inhibited endogenous GH secretion, documented by serum GH concentration profiles over seven hours, decreased IGF-1 serum concentration and disturbed growth cartilage plate architecture. Concomitant treatment with 2.5 to 20 IU/rhGH/kg/day prevented the negative effects of MP on growth in a dose dependent manner and normallized growth plate architecture. In uremic rats in which food efficiency and growth was already reduced, 6 mg MP/kg/day further decreased length gain and prevented weight gain completely by bringing the weight gain/food conversion ratio to the nadir. All effects of MP including reduction of muscle mass could be prevented by concomitant treatment with 10 IU rhGH/kg/day. The effects of MP and rhGH on food efficiency and growth in uremic animals were numerically nearly identical to those in pair fed and ad libitum fed controls, but this may be more relevant in the diseased organism in which basal growth is already suppressed

Demographics of paediatric renal replacement therapy in Europe: 2007 annual report of the ESPN/ERA-EDTA registry

Item does not contain fulltext1 juli 201

Effects of rhGH and rhIGF-1 on renal growth and morphology.

It is known that in rodents recombinant human growth hormone (rhGH) and recombinant human insulin-like growth factor (rhIGF-1) increase renal mass. It is uncertain, however, whether renal mass increases in proportion to body growth, or whether renal growth is stimulated selectively. In 120 to 150 g female Sprague-Dawley rats, we measured the effects of rhGH and rhIGF-1 and their combination by the following parameters: kidney weight/body weight ratio, DNA/protein ratio, mRNA of GH receptor and of IGF-1, mitosis index and PCNA (by immunohistology), zonal architecture and glomerular diameter by micromorphometry. Both rhGH and rhIGF-1 dose-dependently increased renal weight and body weight over vehicle treated controls. With rhGH, liver dry weight/body weight ratio increased, but kidney dry weight/body weight ratio remained unchanged (0.99 +/- 0.06 x 10(-3) vs. 1.02 +/- 0.07 in vehicle controls). In contrast, a significant increase of kidney dry weight/body weight ratio was seen in rats treated with rhIGF-1 (1.3 +/- 0.21 x 10(-3). Addition of high doses of rhGH to high doses of rhIGF-1 caused no further increase of the ratio despite a significant further increase of body weight. rhGH increased the abundance of renal GH receptor mRNA (0.46 +/- 0.32 amol/microgram DNA vs. 0.08 +/- 0.07 in controls) and of IGF-1 mRNA (1.35 +/- 0.5 pg/micrograms DNA vs. 0.35 +/- 0.17), whereas no change was seen with IGF-1 treatment. rhGH and rhIGF-1 increased kidney DNA/protein ratio, mitoses and PCNA expression in various renal structures.(ABSTRACT TRUNCATED AT 250 WORDS

Prevention and treatment of renal osteodystrophy in children on chronic renal failure: European guidelines

Childhood renal osteodystrophy (ROD) is the consequence of disturbances of the calcium-regulating hormones vitamin D and parathyroid hormone (PTH) as well as of the somatotroph hormone axis associated with local modulation of bone and growth cartilage function. The resulting growth retardation and the potentially rapid onset of ROD in children are different from ROD in adults. The biochemical changes of ROD as well as its prevention and treatment affect calcium and phosphorus homeostasis and are directly associated with the development of cardiovascular disease in pediatric renal patients. The aims of the clinical and biochemical surveillance of pediatric patients with CRF or on dialysis are prevention of hyperphosphatemia, avoidance of hypercalcemia and keeping the calcium phosphorus product below 5 mmol(2)/l(2). The PTH levels should be within the normal range in chronic renal failure (CRF) and up to 2–3 times the upper limit of normal levels in dialysed children. Prevention of ROD is expected to result in improved growth and less vascular calcification