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Mild Degree (mild + degree)
Selected AbstractsThe adaptive responses in several mediators linked with hypertrophy and atrophy of skeletal muscle after lower limb unloading in humansACTA PHYSIOLOGICA, Issue 2 2009K. Sakuma Abstract Aim:, To determine the adaptive changes in several molecules regulating muscle hypertrophy and atrophy after unloading, we examined whether unilateral lower limb suspension changes the mRNA and protein levels of SRF-linked (RhoA, RhoGDI, STARS and SRF), myostatin-linked (myostatin, Smad2, Smad3 and FLRG) and Foxo-linked (P-Akt, Foxo1, Foxo3a and Atrogin-1) mediators. Methods:, A single lower limb of each of eight healthy men was suspended for 20 days. Biopsy specimens were obtained from the vastus lateralis muscle pre- and post-suspension. Results:, The volume of the vastus lateralis muscle was significantly decreased after unloading. The amount of RhoA, RhoGDI or SRF protein in the muscle was not significantly changed post-suspension. An RT-PCR semiquantitative analysis showed increased levels of myostatin mRNA but not Smad2, Smad3 or FLRG mRNA. Unloading did not elicit significant changes in the amount of p-Smad3 or myostatin protein in the muscle. The amount of p-Akt protein was markedly reduced in the unloaded muscle. Lower limb suspension did not influence the expression pattern of Foxo1, Foxo3a or Atrogin-1. Conclusion:, Unloading inducing a mild degree of muscle atrophy may decrease p-Akt and increase myostatin but not SRF-linked mediators. [source] Subchronic toxicity of chloral hydrate on rats: a drinking water studyJOURNAL OF APPLIED TOXICOLOGY, Issue 4 2002R. Poon Abstract The subchronic toxicity of chloral hydrate, a disinfection byproduct, was studied in rats following 13 weeks of drinking water exposure. Male (262 ± 10 g) and female (190 ± 8 g) Sprague-Dawley rats, ten animals per group, were administered chloral hydrate via drinking water at 0.2, 2, 20 and 200 ppm. Control animals received distilled water only. Gross and microscopic examinations, serum chemistry, hematology, biochemical analysis, neurogenic amine analysis and serum trichloroacetic acid (TCA) analysis were performed at the end of the treatment period. Bronchoalveolar fluids were collected at necropsy and urine specimens were collected at weeks 2, 6 and 12 for biochemical analysis. No treatment-related changes in food and water intakes or body weight gains were observed. There were no significant changes in the weights of major organs. Except for a mild degree of vacuolation within the myelin sheath of the optic nerves in the highest dose males, there were no notable histological changes in the tissues examined. Statistically significant treatment-related effects were biochemical in nature, with the most pronounced being increased liver catalase activity in male rats starting at 2 ppm. Liver aldehyde dehydrogenase (ALDH) was significantly depressed, whereas liver aniline hydroxylase activity was significantly elevated in both males and females receiving the highest dose. A dose-related increase in serum TCA was detected in both males and females starting at 2 ppm. An in vitro study of liver ALDH confirmed that chloral hydrate was a potent inhibitor, with an IC50 of 8 µM, whereas TCA was weakly inhibitory and trichloroethanol was without effect. Analysis of brain biogenic amines was conducted on a limited number (n = 5) of male rats in the control and high dose groups, and no significant treatment-related changes were detected. Taking into account the effect on the myelin sheath of male rats and the effects on liver ALDH and aniline hydroxylase of both males and females at the highest dose level, the no-observed-effect level (NOEL) was determined to be 20 ppm or 1.89 mg kg,1 day,1 in males and 2.53 mg kg,1 day,1 in females. This NOEL is ca. 1000-fold higher than the highest concentration of chloral hydrate reported in the municipal water supply. Copyright © 2002 Crown in the right of Canada. Published by John Wiley & Sons, Ltd. [source] Isocitrate dehydrogenase as a marker of centrilobular hepatic necrosis in the experimental model of rats,JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 3 2001Young-Hwa Chung Abstract Background and Aims: Serum alanine aminotransferase (ALT) and aspartate aminotransferase may not detect centrilobular hepatic necrosis (CLN) of a mild degree because these enzymes are known to be located predominantly in the periportal area. The aim of this study was to evaluate the usefulness of plasma isocitrate dehydrogenase (ICDH), which is located predominantly in the centrilobular zone, as a marker of CLN. Methods: In 56 adult male rats, centrilobular (n = 21) and periportal hepatic necrosis (PPN; n = 21) were induced experimentally by the intraperitoneal injection of bromobenzene and allylalcohol, respectively. Seven rats were used as solvent controls in both groups. Isocitrate dehydrogenase and ALT activities were measured in the plasma of rats with mild to moderate hepatic necrosis (17 CLN and 19 PPN). Isocitrate dehydrogenase and ALT were compared according to the sampling time (12, 24 and 48 h) and the location of hepatic necrosis. Ratios of ICDH/ALT were also calculated and compared between CLN and PPN groups at any time points. Results: Plasma ICDH activities were higher in rats with CLN than in those with PPN. In contrast, plasma ALT levels were higher in rats with PPN than in those with CLN at 12 h and were similar in both groups after 12 h. The ICDH/ALT ratios were much higher in rats with CLN compared to those with PPN (P < 0.001). The ratios were above 1.0 in 13 of 17 rats (77%) with CLN in contrast to none of the 19 rats with PPN. Conclusions: Our data suggested that the plasma ICDH/ALT ratio might be useful to differentiate between mild to moderate degrees of CLN from PPN, at least in the experimental model of rats. [source] Specific immunoglobulin E and immunoglobulin G antibodies to toluene diisocyanate-human serum albumin conjugate: useful markers for predicting long-term prognosis in toluene diisocyanate-induced asthmaCLINICAL & EXPERIMENTAL ALLERGY, Issue 4 2002H.-S. Park Summary Background Our previous study reported that more than 50% of toluene diisocyanate (TDI)-induced asthma patients had persistent asthmatic symptoms even after complete avoidance. Although specific IgE (sIgE) has been detected in a portion of patients with TDI-asthma, a recent investigation suggests that the presence of serum specific IgG (sIgG), not sIgE, is more closely associated with positive bronchoprovocation test (BPT) results. Objective To evaluate the possible role of sIgE and sIgG in predicting long-term prognosis of TDI-asthma. Materials and methods Forty-one TDI-asthma patients whose diagnosis was confirmed by TDI-BPT, and 20 unexposed healthy controls were enrolled. Both sIgE and sIgG to TDI-human serum albumin (HSA) conjugate were detected by ELISA. All patients with persistent asthmatic symptoms took anti-asthmatic medications during the follow-up period (mean: 67.5 months) and were instructed to avoid exposure to TDI. Airway hyper-responsiveness to methacholine (AHM) was monitored every year during the study period. The patients were classified into three groups according to changing patterns of AHM and asthmatic symptoms as follows: group I, no improvement with persistent asthmatic symptoms (n = 12); group II, partial improvement with persistent asthmatic symptoms (n = 13); group III, in remission (n = 16). Results Favourable prognosis was associated with a mild degree of AHM at initial diagnosis (P < 0.05). Although there were no significant differences in the prevalence of sIgE antibody to TDI-HSA conjugate among the three groups (P > 0.05), prevalence of sIgG in group I tended to be higher than in group II (0.05 < P < 0.1). However, the levels of sIgG were significantly higher in group I than in group II (P = 0.05), whereas levels of sIgE were significantly higher in group II than in group I (P = 0.014). No significant differences were noted in exposure duration, sex, age, atopic status, and total IgE level among the three groups (P > 0.05). Conclusion This study confirmed that a favourable outcome is related to a mild degree of AHM and to low levels of sIgG to predict persistent asthmatic symptoms, it also suggested that the presence of high serum-specific IgE at initial diagnosis may represent a better prognosis. [source] Glucocorticoid regulation of the inflammatory response to injuryACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 7 2004M. P. Yeager During the first half of the 20th century, physiologists were interested in the adrenal glands primarily because adrenalectomized animals failed to survive even mild degrees of systemic stress. It eventually became clear that hormones secreted by the adrenal cortex were critical for survival and, in this context, adrenal cortical hormones were widely considered to support or stimulate important responses to stress or injury. With the purification and manufacture of adrenal cortical hormones in the 1930s and 1940s, clinicians suddenly discovered the potent anti-inflammatory actions of glucocorticoids (GCs). This dramatic, and unexpected, discovery has dominated clinical and laboratory research into GC actions throughout the second half of the 20th century. More recent research is again reporting GC-induced stimulatory effects on a variety of inflammatory response components. These effects are usually observed at low GC concentrations, close to concentrations that are observed in vivo during basal, unstimulated states. For example, GC-mediated stimulation has been reported for the hepatic acute-phase response, for cytokine secretion, expression of cytokine/chemokine receptors, and for the pro-inflammatory mediator, macrophage migration inhibition factor. It seems clear that the long-held clinical view that GCs act solely as anti-inflammatory agents needs to be re-assessed. Varying doses of GCs do not lead simply to varying degrees of inflammation suppression, but rather GCs can exert a full range of effects from permissive to stimulatory to suppressive. [source] High prevalence of HFE gene mutations in patients with porphyria cutanea tarda in the Czech RepublicBRITISH JOURNAL OF DERMATOLOGY, Issue 3 2008K. Kratka Summary Background, Iron overload and hepatitis C virus (HCV) infection are independent factors which are thought to play a role in the pathogenesis of porphyria cutanea tarda (PCT). Objectives, To determine the prevalence of the HFE gene mutations p.Cys282Tyr (C282Y), p.His63Asp (H63D) and p.Ser65Cys (S65C), the p.Tyr250X (Y250X) mutation of the TFR2 gene, and HCV infection in patients with PCT in the Czech population, and to make comparison of the iron status among the respective genotypes. Methods, Iron metabolism indices, results of mutational analysis and serological markers of HCV infection were examined in 63 patients with PCT. Results, The HFE gene mutations were detected in 70% of patients with PCT compared with 35% in the control group (P < 0·001). Mean serum ferritin levels were increased in all genotypes, the highest being in homozygotes for the p.Cys282Tyr mutation. HCV infection was detected in only 8% of patients with PCT. Conclusions, There was a very high prevalence of the p.Cys282Tyr and p.His63Asp mutations observed in patients with PCT accompanied by mild degrees of iron overload, which was genotype dependent. [source] | ||||||||||