Number of results to display per page
Search Results
4732. Chronic hypobaric hypoxia increases isolated rat fast-twitch and slow-twitch limb muscle force and fatigue
- Creator:
- El-Khoury, R., Bradford, A., and O´Halloran, K. D.
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, hypoxia, skeletal muscle, fatigue, 14, and 612
- Language:
- English
- Description:
- Chronic hypoxia alters respiratory muscle force and fatigue, effects that could be attributed to hypoxia and/or increased activation due to hyperventilation. We hypothesized that chronic hypoxia is associated with phenotypic change in non-respiratory muscles and therefore we tested the hypothesis that chronic hypobaric hypoxia increases limb muscle force and fatigue. Adult male Wistar rats were exposed to normoxia or hypobaric hypoxia (PB=450 mm Hg) for 6 weeks. At the end of the treatment period, soleus (SOL) and extensor digitorum longus (EDL) muscles were removed under pentobarbitone anaesthesia and strips were mounted for isometric force determination in Krebs solution in standard water-jacketed organ baths at 25 °C. Isometric twitch and tetanic force, contractile kinetics, forcefrequency relationship and fatigue characteristics were determined in response to electrical field stimulation. Chronic hypoxia increased specific force in SOL and EDL compared to age-matched normoxic controls. Furthermore, chronic hypoxia decreased endurance in both limb muscles. We conclude that hypoxia elicits functional plasticity in limb muscles perhaps due to oxidative stress. Our results may have implications for respiratory disorders that are characterized by prolonged hypoxia such as chronic obstructive pulmonary disease (COPD)., R. El-Khoury, A. Bradford, K. D. O´Halloran., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
4733. Chronic inflammation and low-dose glucocorticoid effects on glucose metabolism in premenopausal females with rheumatoid arthritis free of conventional metabolic risk factors
- Creator:
- Adela Penesová, Rádiková, Ž., Vlček, M., Kerlik, J., Jozef Lukáč, Jozef Rovenský, and Richard Imrich
- Type:
- article, články, model:article, and TEXT
- Subject:
- fyziologie člověka, human physiology, inflammation, glucose metabolism, rheumatoid arthritis, insulin sensitivity, and glucocorticoid treatment
- Language:
- English
- Description:
- Chronic systemic inflammation is associated with increased cardiovascular mortality in patients with rheumatoid arthritis (RA). The aim of our study was to investigate association of glucose metabolism and inflammatory markers in a group of patients with rheumatoid arthritis free of other metabolic risk factors. Twenty-two premenopausal RA females (11 patients on low-dose GC (<8.5 mg/day of prednisone or equivalent), 11 patients without glucocorticoid therapy) and 15 age- and BMImatched healthy females underwent the oral glucose tolerance test. The insulin sensitivity indices according Matsuda (ISIMAT) and Cederholm (ISICED) as well as HOMA2 %S were calculated. Cytokines, lipid profile, non-esterified fatty acids (NEFA) and plasminogen activator inhibitor-1 (PAI-1) were measured in baseline blood samples. Despite elevated interleukin IL-6 and TNF alpha, glucose, insulin and C-peptide responses to oral glucose load as well as ISIMAT, ISICED, PAI-1 and NEFA were comparable in both RA groups and healthy controls. HOMA 2 %S correlated with disease activity. In conclusions, low-dose glucocorticoid treatment does not lead to glucose metabolism impairment in RA patients without other metabolic risk factors. Increased cardiovascular mortality and morbidity is probably due to a direct effect of systemic inflammation on myocardium and/or blood vessels., A. Penesová, ... [et al.]., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
4734. Chronic low-dose L-NAME treatment increases nitric oxide production and vasorelaxation in normotensive rats
- Creator:
- Iveta Bernátová, Kopincová, J., Angelika Púzserová, Pavol Janega, and Pavel Babál
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, hypertenze, krevní tlak, acetylcholin, hypertension, blood pressure, acetylcholine, cardiac and vascular structure, negative feedback regulation, serotonin, 14, and 612
- Language:
- English
- Description:
- NG-nitro-L-arginine methyl ester (L-NAME) is a non-specific nitric oxide (NO) synthase inhibitor, commonly used for the induction of NO-deficient hypertension. The aim of this study was to investigate the effect of chronic low-dose administration of L-NAME on NO production, vascular function and structure of the heart and selected arteries of rats. Adult male Wistar rats were treated with L-NAME in the dose of approximately 1.5 mg/kg/day in drinking water for 8 weeks. Basal blood pressure (BP) of rats (determined by tail-cuff) was 112±3 mm Hg. The low-dose administration of L-NAME significantly elevated BP measured on the third and sixth week of treatment vs. controls by approximately 9 % and 12 %, respectively. After this period, BP of L-NAME-treated rats returned to the control values. The relative left ventricular mass, heart fibrosis and collagen III/collagen I ratio were not affected by L-NAME. Similarly, there were no alterations in the cross-sectional area and wall thickness/diameter ratio of the aorta and the femoral artery of LNAME- treated rats. NO synthase activity (determined by conversion of [3H]-L-arginine to [3H]-L-citrulline) was not altered in the hypothalamus of L-NAME-treated rats. Interestingly, chronic low-dose L-NAME treatment significantly elevated NO synthase activity in the left ventricle and aorta, increased endothelium-dependent acetylcholine-induced vasorelaxation and reduced serotonin-induced vasoconstriction of the femoral artery. The data suggest that chronic lowdose L-NAME treatment can increase NO production and vasorelaxation in normotensive rats without negative structural changes in the cardiovascular system., I. Bernátová, J. Kopincová, A. Púzserová, P. Janega, P. Babál., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
4735. Chronic obstructive pulmonary disease in iron-steel and ferrochrome industry workers
- Creator:
- Bala, Silvana
- Type:
- model:article and TEXT
- Language:
- English
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
4736. Chronic oral administraton of beta-adrenoceptor agonist clenbuterol affects myosin heavy chain (MHC) expression in adult mouse heart
- Creator:
- Patiyal, Som N. and Sharma, S.
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Biologické vědy, fyziologie, srdce, physiology, heart, clenbuterol, myosin heavy chain isoforms, left ventricle, actomyosin ATPase, cardiac muscle contraction, 2, and 57/59
- Language:
- English
- Description:
- The aim of this study was to analyze the effects of chronic administration of the β-adrenoceptor agonist clenbuterol (2 mg/kg body weight/day for a period of 30 days) on the major contractile protein (myosin) in the left ventricular muscle of the adult mouse heart. Separation of myosin heavy chain (MHC) isoforms on 7.5 % glycerol SDS-PAGE and subsequent quantification of the gels by laser densitometry showed a 6.5-fold increase in the β-isoform of MHC in the clenbuterol-treated group. The α: β ratio of these two isoforms in the control group was 98.16±0.14 %: 1.83±0.14 %, whereas in the treated group it was 88.05±1.15 %: 11.95±1.15 %. Actomyosin ATPase activity assay demonstrated a significant (20 %) decline in ATPase activity of the tissue in the β-agonist-treated group. These results suggest that chronic clenbuterol treatment is capable to induced the transformation of MHC isoforms increasing the slow β-MHC isoform, which may contribute to the altered contractile mechanics of clenbuterol-treated hearts., S. N. Patiyal, S. Sharma., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
4737. Chronic peripheral ghrelin injection exerts antifibrotic effects by increasing growth differentiation factor 15 in rat hearts with myocardial fibrosis induced by isoproterenol
- Creator:
- Ren, Qian, Lin, Ping, Wang, Qin, Zhang, Bin, and Feng, Li
- Format:
- počítač and online zdroj
- Type:
- model:article and TEXT
- Subject:
- ghrelin, myocardial fibrosis, growth differentiation factor 15, and Akt/GSK-3β pathway
- Language:
- English
- Description:
- This study aimed to investigate the anti-fibrotic effects of ghrelin in isoproterenol (ISO)-induced myocardial fibrosis and the underlying mechanism. Sprague-Dawley rats were randomized to control, ISO, and ISO + ghrelin groups. ISO (2 mg/kg per day, subcutaneous) or vehicle was administered once daily for 7 days, then ghrelin (100 µg/kg per day, subcutaneous) was administered once daily for the next 3 weeks. Ghrelin treatment greatly improved the cardiac function of ISO-treated rats. Ghrelin also decreased plasma brain natriuretic peptide level and ratios of heart weight to body weight and left ventricular weight to body weight. Ghrelin significantly reduced myocardial collagen area and hydroxyproline content, accompanied by decreased mRNA levels of collagen type I and III. Furthermore, ghrelin increased plasma level of growth differentiation factor 15 (GDF15) and GDF15 mRNA and protein levels in heart tissues, which were significantly decreased with ISO alone. The phosphorylation of Akt at Ser473 and GSK-3β at Ser9 was decreased with ISO, and ghrelin significantly reversed the downregulation of p-Akt and p-GSK-3β. Mediated by GDF15, ghrelin could attenuate ISO-induced myocardial fibrosis via Akt-GSK-3β signaling.
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
4738. Chronic poverty in Kazakhstan
- Creator:
- Kudebayeva, Alma
- Publisher:
- CERGE-EI
- Format:
- electronic, bez média, svazek, and 37 stran : tabulky, grafy.
- Type:
- model:monograph and TEXT
- Subject:
- Sociální problémy vyžadující podporu a pomoc. Sociální zabezpečení, chudoba, poverty, Kazachstán, Kazakhstan, 364.662, (574), (048.8), 18, and 364
- Language:
- English and Czech
- Description:
- Alma Kudebayeva., Obsahuje bibliografii a bibliografické odkazy, and České a anglické resumé
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
4739. Chronic stress differentially affects antioxidant enzymes and modifies the acute stress response in liver of wistar rats
- Creator:
- Djordjevic, J., Djordjevic, A., Adzic, M., Niciforovic, A., and Marija B. Radojčić
- Format:
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, stres (fyziologie), játra, glukokortikoidy, stress (physiology), liver, glucocorticoids, antioxidant enzymes, nuclear factor kappa B, glucocorticoid receptor, 14, and 612
- Language:
- English
- Description:
- Clinical reports suggest close interactions between stressors, particularly those of long duration, and liver diseases, such as hepatic inflammation, that is proposed to occur via reactive oxygen species. In the present study we have used 21-day social isolation of male Wistar rats as a model of chronic stress to investigate protein expression/activity of liver antioxidant enzymes: superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR), and protein expression of their upstream regulators: glucocorticoid receptor (GR) and nuclear factor kappa B (NFkB). We have also characterized these parameters in either naive or chronically stressed animals that were challenged by 30-min acute immobilization. We found that chronic isolation caused decrease in serum corticosterone (CORT) and blood glucose (GLU), increase in NFkB signaling, and disproportion between CuZnSOD, peroxidases (CAT, GPx) and GLR, thus promoting H2O2 accumulation and prooxidative state in liver. The overall results suggested that chronic stress exaggerated responsiveness to subsequent stressor at the level of CORT and GLU, and potentiated GLR response, but compromised the restoration of oxido-reductive balance due to irreversible alterations in MnSOD and GPx., J. Djordjevic ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
4740. Chronic stress impairs male spermatogenesis function and nectin-3 protein expression in the testis
- Creator:
- Li, Tong , Yao, Jiwei , Zhang, Quanchao , Li, Qianwei , Li, Jingcheng , Wang, Xiujuan , Li, Weibing , Chen, Antao , and Yan, Junan
- Format:
- počítač and online zdroj
- Type:
- model:article and TEXT
- Subject:
- chronic social stress, Nectin-3, spermatogenesis dysfunction, and CRH and CRHR1
- Language:
- English
- Description:
- Chronic stress is a crucial public issue that occurs when a person is repetitively stimulated by various stressors. Previous researches have reported that chronic stress induces spermatogenesis dysfunction in the reproductive system, but its molecular mechanisms remain unclear. The nectin protein family, including nectin-1 to nectin-4, is Ca2+-independent immunoglobulin-like cell adhesion molecules, that are widely expressed in the hippocampus, testicular tissue, epithelial cells and other sites. Nectin-3 contributes to the sperm development at the late stage, and the abnormal expression of nectin-3 impairs spermatogenesis. Some recent studies have demonstrated that stress induces a decrease in nectin-3 expression in the hippocampus via corticotropin-releasing hormone (CRH) to corticotropin-releasing hormone receptor 1 (CRHR1) pathway. Here, we tested whether chronic stress also caused a reduction in nectin-3 expression in the testis. We established a chronic social defeat stress paradigm, which provides naturalistic and complex chronic stress in male C57BL/6 mice. After 25 days of chronic social defeat stress, the mice showed weight loss, thymic atrophy and some other typical symptoms of chronic stress (e.g. anxiety-like behavior and social avoidance behavior). We found gonad atrophy, testicular histological structure changes and semen quality reductions in the stressed mice. The stressed male mice significantly spent more time to impregnate the female mice than the control male mice. Moreover, nectin-3 protein levels in stressed mice were significantly decreased in the testes compared with those in control mice. In addition, we found that the CRHR1 expression level was increased in the testes of stressed mice. Therefore, we demonstrated a decreased level of nectin-3 expression and an increase in CRHR1 expression in the testis after exposure to chronic stress, which may provide a potential therapeutic target for the spermatogenesis dysfunction induced by chronic stress.
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public