Effects of growth hormone-releasing factor and(or) thyrotropin-releasing hormone on growth, feed efficiency, carcass characteristics, and blood hormones and metabolites in beef heifers

The objective of this study was to determine the effect of long-term administration of a growth hormone (GH)-releasing factor analog (GRFa) and(or) thyrotropin-releasing hormone (TRH) on growth, feed efficiency, carcass characteristics, and blood hormones and metabolites in beef heifers. Crossbred heifers (n = 48; 345.9 +/- 2.8 kg) were divided into four equal groups: control (vehicle), 1 microgram of GRFa (human GRF 1-29 analog).kg BW-1.d-1, 1 microgram of TRH.kg BW-1.d-1, or GRFa + TRH. Daily s.c. injections continued for 86 d. Blood samples were collected from half of the heifers after injection on d 1, 36, and 78. On d 89, all heifers were slaughtered. Treatments did not affect (P > .05) ADG but GRFa + TRH decreased (P < .05) ADFI relative to all other treatments. Feed conversion efficiency tended (P < .10) to be improved in the groups given GRFa alone or TRH alone. Treatment with GRFa and(or) TRH did not affect carcass weight, dressing percentage, conformation score, backfat thickness, or weights of liver, kidneys, pituitary, and ovaries. The GRFa + TRH treatment reduced (P < .05) fat score and increased (P < .05) longissimus muscle area relative to other treatments. The GRFa treatments reduced (P < .05) the weight and fat percentage of the mammary gland and increased (P < .05) heart weight. Treatment with TRH alone failed to stimulate GH on d 1, 36, and 78. Treatment with GRFa alone increased (P < .05) GH above controls on d 36, whereas GRFa + TRH increased (P < .05) GH on d 1, 36, and 78. Treatment with GRFa alone increased (P < .05) IGF-I only on d 1, whereas GRFa + TRH was without effect on all days. Across sampling days, treatments had little effect on blood concentrations of insulin, triiodothyronine, nonesterified fatty acids, urea nitrogen, and glucose. The GRFa alone and GRFa + TRH decreased (P < .05) and TRH alone increased (P < .05) thyroxine concentrations. In conclusion, with the dose and administration regimen used, GRFa and(or) TRH yielded small but positive improvements in animal performance.     

In vivo characterization of cytotoxic intracellular edema by multicomponent analysis of transverse magnetization decay curves

The precise measurement of low numbers of leukocyte below 0.1 WBC/microliter in filtered red cell or platelet suspensions meet both aims: to check the compliance with previously determined requirements and to evaluate the performances of novel filtering material (5 log depletion or more), justified by more and more important clinical use. The reliability of results, obtained with the chosen method, is ensured by applying of validation protocol, including training of technologist, assessment of the analytical range and the detection limit, assessment of precision and accuracy. The flow cytometry (FC) and Nageotte Chamber (NC) method are the both techniques which are currently used in routine Quality Control (QC) and validated by multicenter studies. Recent developments are made for increasing the sensibility of these counting methods, thanks to higher concentration or volume of the sample to be analysed. Among the experimental techniques, requiring more advances before implementing in QC program, quantitative PCR must become essential as reference method for evaluating the efficiency of filtration, in the future.     

Comparison of the active-site conformations of bovine alpha-thrombin and meizothrombin(desF1) by electron spin resonance

The annual time-series analysis examines the impact of changes in per capita alcohol consumption (NIAAA,AEDS) on changes in community hospital admission rates (AHA) in the United States from 1950 to 1992 (n = 43). Increases in per capita alcohol consumption were expected to increase hospital admission rates contemporaneously and several years thereafter following an exponential risk function. Distributed lag models based on differenced data controlling for changes in: (1) per capita cigarette consumption; (2) private hospital insurance coverage; (3) the drinking age population; (4) per capita disposable personal income; and (5) health care regulatory interventions show a contemporaneous effect of per capita alcohol consumption on hospital admission rates. The time-series analyses imply that between 22-26% of US community hospital admissions are alcohol related. A comparable analysis indicates that per capita alcohol and tobacco expenditures contribute to approximately 28% of US community hospital admissions. The absence of statistically significant lagged effects is inconsistent with an exponentially declining risk functions. However, the contemporaneous effects of per capita alcohol and tobacco consumption suggest that a reduction in smoking and drinking will produce quick reductions in morbidity and hospitalizations.     

The differential regulation and secretion of proteinases from fetal and neonatal fibroblasts by growth factors

Until recently, research on the pathogenesis of glomerulonephritis has been mainly focused on the characterization of humoral immune responses in the initiation of glomerular injury. However, there is a growing recognition that both cellular and humoral immune responses, in varying proportions, are involved in the pathogenesis of immunologically-mediated glomerulonephritis. T lymphocytes are essential cellular elements of cell-mediated immunity. Both in experimental models of immune-mediated renal disease and in histopathological analyses of human nephropathies, the involvement of T cells has been demonstrated in the immunoregulation of nephritogenic immune responses and in the immune injury in the kidney. T cell activation resulting in either delayed-type hypersensitivity, cytolytic reactions, abnormal expression of major histocompatibility complex (MHC) molecules, or B cell activation can result in glomerulonephritis. These different types of responses are exerted by distinct T cell subsets defined by cell surface markers and cytokine profiles. CD4+ T cells in vivo are functionally heterogeneous with respect to cytokine production and the CD45 isoforms that are found on their surface. Like CD4+ T cells, CD8+ T cells may also be heterogeneous at the level of cytokine production. The roles of CD4+ and CD8+ cells and their cytokine profiles in glomerulonephritis have not been extensively investigated yet, but such studies might improve the understanding of the pathogenesis and possibly lead to new therapeutic approaches of human glomerulonephritis. In this review the role of distinct T lymphocyte subsets in experimental and human glomerulonephritis will be discussed.     

Contact areas in the thumb carpometacarpal joint

The thumb carpometacarpal joint is a common site of osteoarthritis. It has been hypothesized that peaks of localized stress on the dorsoradial or volar-ulnar regions, or both, of the articular surfaces of the trapezium and metacarpal lead to erosion of cartilage and may be responsible for the progression of the disease. The objective of this study was to determine the contact areas in this joint under the functional position of lateral (key) pinch and in the extremes of range of motion of the joint. These contact areas were assessed relative to the observed sites of cartilage thinning. Eight hands from cadavers of women and five from cadavers of men were tested in vitro with the thumb under a 25 N load in the lateral pinch position, and under small muscle loads (0-5 N) with the thumb in flexion, extension, abduction, adduction, and neutral positions. Contact areas of articular surfaces of the thumb carpometacarpal joint were determined for these positions using a stereophotogrammetric technique. The lateral pinch position produced contact areas predominantly on the central, volar, and volar-ulnar regions of the trapezium and the metacarpal. In three specimens, contact areas were distinctly separated between the dorsoradial and volar-ulnar regions, and in one specimen, from a man, contact occurred exclusively on the dorsoradial region of the trapezium. Using stereophotogrammetry, maps of cartilage thickness also were determined for a subset of nine specimens. The volar-ulnar, ulnar, and dorsoradial regions of the trapezium were the most common sites of thin cartilage, and these may be sites of cartilage wear.(ABSTRACT TRUNCATED AT 250 WORDS)     

Association between cigarette smoking and lipid peroxidation in a controlled feeding study

BACKGROUND: Cigarette smoke may promote atherogenesis by producing oxygen-derived free radicals that damage lipids. However, evidence in support of this hypothesis is inconsistent because most studies did not control for aspects of diet (antioxidants and lipid substrate) that may confound the association between smoking and measures of lipid peroxidation. METHODS AND RESULTS: The relationships between cigarette smoking and two measures of lipid peroxidation, breath ethane (an in vivo assay) and thiobarbituric acid-reactive substances (TBARS, an in vitro assay), were examined in 123 adults (11% of whom were smokers) participating in a controlled feeding study. After 3 weeks of controlled feeding on a common diet (36% total fat, 14% saturated fats, 6% polyunsaturated fats, and 12% monounsaturated fats), breath and fasting serum samples were collected for measurement of ethane and TBARS, respectively. Baseline characteristics of smokers and nonsmokers were similar, including several indices related to diet and nutritional status (albumin, cholesterol, body mass index, and oxygen radical-absorbing capacity). Cigarette smokers had significantly higher breath ethane (8.88 versus 1.71 pmol/L; P<.0001) and TBARS (24.0 versus 20.7 micromol/mL; P=.008) than nonsmokers. The interval between breath collection and the time the last cigarette was smoked was significantly and inversely correlated with breath ethane. Neither measure of lipid peroxidation was associated with measures of serum cholesterol or albumin, body mass index, or serum oxygen radical-absorbing capacity. CONCLUSIONS: Cigarette smokers have higher rates of in vivo and in vitro lipid peroxidation. These results support the hypothesis that the atherogenic effects of smoking are mediated in part by free radical damage to lipids.