The purpose of this study was to evaluate the effects of hyperglycemia on skeletal muscle recovery following disuseinduced muscle atrophy in rats. Wistar rats were grouped as streptozotocin-induced diabetic rats and non-diabetic rats. Both ankle joints of each rat were immobilized to induce atrophy of the gastrocnemius muscles. After two weeks of immobilization and an additional two weeks of recovery, tail blood and gastrocnemius muscles were isolated. Serial cross sections of muscles were stained for myosin ATPase (pH 4.5) and alkaline phosphatase activity. Serum insulin and muscle insulin-like growth factor-1 (IGF-1) levels were also measured. Serum insulin levels were significantly reduced in the diabetic rats compared to the non-diabetic controls. The diameters of type I, IIa, and IIb myofibers and capillary-to-myofiber ratio in the isolated muscle tissue were decreased after immobilization in both treatments. During the recovery period, these parameters were restored in the non-diabetic rats, but not in the diabetic rats. In addition, muscle IGF-1 levels after recovery increased significantly in the non-diabetic rats, but not in the diabetic rats. We conclude that decreased levels of insulin and IGF-1 and impairment of angiogenesis associated with diabetes might be partly responsible for the inhibition of regrowth in diabetic muscle., H. Kataoka, J. Nakano, Y. Morimoto, Y. Honda, J. Sakamoto, T. Origuchi, M. Okita, T. Yoshimura., and Obsahuje bibliografii
Hyperinflation is the consequence of a dysbalance of static forces (determining the relaxation volume) and/or of the dynamic components. The relaxation volume is determined by an equilibrium between the elastic recoil of the lungs and of the chest walls. The dynamic components include the pattern of breathing, upper airway resistance and postinspiratory activity of inspiratory muscles. The respiratory and laryngeal muscles are under control and thus both static and dynamic hyperinflation can be secured. Our knowledge of the mechanism of increased FRC is based on clinical observations and on experiments. The most frequent stimuli leading to a dynamic increase of functional residual lung capacity (FRC) include hypoxia and vagus afferentation. Regulation of FRC is still and undetermined concept. The controlled increase of FRC, hyperinflation, participates in a number of lung diseases., F. Paleček., and Obsahuje bibliografii
The aim of the study was to compare the effect of short-term hyperglycemia and short-term hyperinsulinemia on parameters of oxidative stress in Wistar rats. Twenty male rats (aged 3 months, average body weight 325 g) were tested by hyperinsulinemic clamp (100 IU/l) at two different glycemia levels (6 and 12 mmol/l). Further 20 rats were used as a control group infused with normal saline (instead of insulin) and 30 % glucose simultaneously. Measured parameters of oxidative stress were malondialdehyde (MDA), reduced glutathione (GSH) and total antioxidant capacity (AOC). AOC remained unchanged during hyperglycemia and hyperinsulinemia. Malondialdehyde (as a marker of lipid peroxidation) decreased significantly (p<0.05) during the euglycemic hyperinsulinemic clamp, and increased significantly during isolated hyperglycemia without hyperinsulinemia. Reduced glutathione decreased significantly (p<0.05) during hyperglycemia without hyperinsulinemia. These results suggest that the short-term exogenous hyperinsulinemia reduced the production of reactive oxygen species (ROS) during hyperglycemia in an animal model compared with the control group., P. Kyselová, M. Žourek, Z. Rušavý, L. Trefil, J. Racek., and Obsahuje bibliografii
INTRODUCTION: Leptin is an adipokine which has a direct relationship to obesity. Our aim was to measure this hormone in pregnant women at three months intervals throughout their pregnancies to determine the serum value of those who developed preeclampsia. MATERIAL AND METHODS: We followed 19 women (median age 24.8 +/- 5.7 years) with pre-gestational Body Mass Index (BMI) less than 25 kg/m2, 21 (median age 26.1 +/- 4.6 years) with BMI higher than 25 kg/m2 and 16 (median age 30.9 +/- 5.8 years) with Gestational Diabetes Mellitus (GDM) (median age 30.9 +/- 5.8 years), recruited in the 1st trimester of pregnancy. Serum levels of leptin were measured with radioimmunoassay (RIA) technique. RESULTS: In the first trimester of pregnancy leptin levels showed statistically significant differences between normal weight and overweight-obese women (p < 0.001), diabetic women (p < 0.05) and the subgroup of preeclamptic women (p < 0.001). For those women with PGBMI > or = 40 kg/m2 and leptin > or = 40 ng/ml in the second trimester, the Odds Ratio (OR) to develop preeclampsia was of 47.95% CI (4.1-527.2). Analyzing leptin values with ROC curves, the greatest area under the curve (AUC) was for leptin in the second trimester (0.773, CI: 0.634-0.911). CONCLUSION: Women with morbid obesity (BMI > or = 40 kg/m2) had significantly higher levels of serum leptin (p < 0.01) and a value of 40 ng/ml of this hormone seems to be predictive of developing preeclampsia in this group of patients. and H. Mendieta Zerón, VJ. García Solorio, PM. Nava Díaz, A. Garduño Alanís, JG. Santillán Benítez, V. Domínguez García, C. Escobar Briones, E. Denova Gutiérrez
Previous studies revealed altered levels of the circulating insulin-like growth factor-I (IGF-I) and of its binding protein-3 (IGFBP-3) in subjects with coronary atherosclerosis, metabolic syndrome and premature atherosclerosis. Hyperlipidemia is a powerful risk factor of atherosclerosis. We expected IGF-I and IGFBP-3 alterations in subjects with moderate/severe hyperlipidemia but without any clinical manifestation of atherosclerosis. Total IGF-I and IGFBP-3 were assessed in 56 patients with mixed hyperlipidemia (MHL; cholesterol>6.0 mmol/l, triglycerides>2.0 mmol/l), in 33 patients with isolated hypercholesterolemia (IHC; cholesterol>6.0 mmol/l, triglycerides<2.0 mmol/l), and in 29 healthy controls (cholesterol<6.0 mmol/l, triglycerides<2.0 mmol/l). The molar ratio of IGF-I/IGFBP-3 was used as a measure of free IGF-I. IHC subjects differed from controls by lower total IGF-I (164±60 vs. 209±73 ng/ml, p=0.01) and IGF-I/IGFBP-3 ratio (0.14±0.05 vs. 0.17±0.04, p=0.04). Compared to controls, MHL subjects had lower total IGF-I (153±54 ng/ml, p=0.0002) and IGFBP-3 (2.8±0.6 mg/ml, p<0.0001), but higher IGF-I/IGFBP-3 ratio (0.25±0.06, p<0.0001). Differences remained significant after the adjustment for clinical and biochemical covariates, except for triglycerides. Patients with both IHC and MHL have lower total IGF-I compared to controls. The mechanism is presumably different in IHC and MHL. Because of prominent reduction of IGFBP-3 in patients with MHL, they have reduced total IGF-I despite the actual elevation IGF-I/IGFBP-3 ratio as a surrogate of free IGF-I., J. Malík, T. Štulc, D. Wichterle, V. Melenovský, E. Chytilová, Z. Lacinová, J. Marek, R. Češka., and Obsahuje bibliografii a bibliografické odkazy
Hyperglykemický hyperosmolární stav (HHS) je závažnou akutní komplikací dekompenzace diabetu, především diabetu 2. typu (DM2T) s velmi vážnou prognózou. Základní charakteristickou HHS je extrémní hyperglykemie, těžká dehydratace (s prerenální hyperazotemií), hyperosmolarita plazmy, časté jsou poruchy vědomí, ketoacidóza není přítomná nebo jen minimální (vyšší hodnoty zjišťujeme jen u kombinovaných forem). Diabetická ketoacidóza (DKA) i HHS mají společný patogenetický mechanizmus, avšak oba stavy jsou protilehlé extrémní výchylky a hranice mezi nimi není zcela jednoznačná. U HHS je v popředí výrazná hyperglykemie, u DKA dominuje ketoacidóza. U HHS jsou probrány různé etiopatogenetické mechanizmy vzniku a rozvoje, avšak jednoznačné vysvětlení absence ketoacidózy u HHS schází. Nejčastějšími příčinami vzniku HHS jsou závažná kardiovaskulární onemocnění, náhlé cévní mozkové příhody, infekce především urogenitální, respirační, stavy znemožňující nemocnému dostatečný příjem vody při osmotické diuréze, následky nevhodné medikamentózní terapie, sociální podmínky, a v neposlední řadě je to často první manifestace zvláště diabetu 2. typu. Klinický obraz ovlivňuje především dehydratace, oběhové změny mohou vést k srdečnímu nebo oběhovému selhání a renální insuficienci. HHS je příčinou častých poruch vědomí a v diferenciální diagnostice je nutno vždy pomýšlet na cerebrovaskulární příhodu. Vzhledem k závažnosti prognózy HHS má včasná komplexní, správně vedená terapie zásadní prognostický význam. Léčba HHS (rehydratace, inzulinová léčba, substituce iontů) se řídí sice obdobnými pravidly jako léčba diabetické ketoacidózy, ale v mnoha směrech se také liší. Zvláštní pozornost je nutno věnovat především korekci dehydratace. Nemocný pacient s HHS má být vždy hospitalizován na jednotce intenzivní péče. Mezi nejzávažnější komplikace patří kardiovaskulární komplikace, akutní selhání ledvin, trombotické příhody a infekční komplikace. Vzhledem ke stále vysoké úmrtnosti pacientů s HHS je výzkum zaměřen nejen na nejasnosti etiopatogeneze, ale především na stanovení bezpečné a účinné strategie léčby., The hyperglycemic hyperosmolar state (HHS) is a serious acute complication of diabetes decompensation, especially in type 2 diabetes (T2DM), and with critical prognosis. Primary characteristics of HHS include extreme hyperglycemia, severe dehydration (with prerenal hyperazotaemia), plasma hyperosmolarity, frequent disorders of consciousness, absent or minimum ketoacidosis (with higher values, only found in combined forms). Both DKA and HHS have a common pathogenetic mechanism, but both states are opposite extreme deviations, and the boundaries between them are not entirely clear. Significant hyperglycemia is at the forefront of HHS, while ketoacidosis dominates in DKA. Various etiopathogenic mechanisms of the onset and development of HHS are discussed, but a clear explanation of the absence of ketoacidosis in HHS is lacking. The most frequent cause of HHS is serious cardiovascular disease, acute stroke, particularly genitourinary and/or respiratory infections, conditions preventing the patient from adequate water intake during osmotic diuresis, the consequences of inappropriate medication therapy, social conditions, and last but not least, it is often the first manifestation especially in type 2 diabetes. The clinical picture is influenced mainly by dehydration, while circulatory changes can lead to heart or circulatory failure and renal insufficiency. HHS is the cause of frequent disturbances of consciousness, and a cerebrovascular event should always be considered. Given the seriousness of HHS prognosis, timely comprehensive and properly guided therapy is of major prognostic significance. HHS treatment (rehydration, insulin therapy, ion substitution) is governed by similar rules as the treatment of diabetic ketoacidosis, but it also varies in many respects. Particular attention should be paid mainly to the control of dehydration. The patient with HHS should always be admitted to the intensive care unit. The most serious complications include cardiovascular complications, acute renal failure, thrombotic events and infectious complications. Given the still high mortality of patients with HHS the research focuses not only on the uncertainties concerning etiopathogenesis, but particularly on establishing safe and effective therapeutic strategies., and Jaroslav Rybka, Jerguš Mistrík
a1_Chronic hypoxia causes pulmonary hypertension, the mechanism of which includes altered collagen metabolism in the pulmonary vascular wall. This chronic hypoxic pulmonary hypertension is gradually reversible upon reoxygenation. The return to air after the adjustment to chronic hypoxia resembles in some aspects a hyperoxic stimulus and we hypothesize that the changes of extracellular matrix proteins in peripheral pulmonary arteries may be similar. Therefore, we studied the exposure to moderate chronic hyperoxia (FiO2 = 0.35, 3 weeks) in rats and compared its effects on the rat pulmonary vasculature to the effects of recovery (3 weeks) from chronic hypoxia (FiO2 = 0.1, 3 weeks). Chronically hypoxic rats had pulmonary hypertension (Pap = 26±3 mm Hg, controls 16±1 mm Hg) and right ventricular hypertrophy. Pulmonary arterial blood pressure and right ventricle weight normalized after 3 weeks of recovery in air (Pap = 19±1 mm Hg). The rats exposed to moderate chronic hyperoxia also did not have pulmonary hypertension (Pap = 18±1 mm Hg, controls 17±1 mm Hg). Collagenous proteins isolated from the peripheral pulmonary arteries (100-300 mm) were studied using polyacrylamide gel electrophoresis. A dominant low molecular weight peptide (approx. 76 kD) was found in hypoxic rats. The proportion of this peptide decreases significantly in the course of recovery in air. In addition, another larger peptide doublet was found in rats recovering from chronic hypoxia. It was localized in polyacrylamide gels close to the zone of a2 chain of collagen type I. It was bound to anticollagen type I antibodies. An identically localized peptide was found in rats exposed to moderate chronic hyperoxia. The apparent molecular weight of this collagen fraction suggests that it is a product of collagen type I cleavage by a rodent-type interstitial collagenase (MMP-13)., a2_We conclude that chronic moderate hyperoxia and recovery from chronic hypoxia have a similar effect on collagenous proteins of the peripheral pulmonary arterial wall., J. Novotná, J. Bíbová, V. Hampl, Z. Deyl, J. Herget., and Obsahuje bibliografii
Experimental pneumonia induced by intratracheal application of carrageenan or paraquat increases the functional residual lung capacity (FRC) in rats. The mechanism of this increase is not clear, but a decrease in PO2 may be involved. To test this possibility, we attempted to eliminate the PO2 decrease in carrageenan-treated rats by exposing them to hyperoxia. Animals of the first group were exposed to 7 days of hyperoxia (FIO2 0.78-0.84, group Car+O2) after intratracheal application of carrageenan (0.5 ml of 0.7 % carageenan in saline), whereas animals of the second group were given the same dose of carrageenan but breathed air (group Car+A). The third group of rats was kept for seven days in hyperoxia (group O2) and the fourth group served as controls (C). The animals were then anesthetized and intubated and their ventilatory parameters and FRC were measured during air breathing. Carrageenan application induced a FRC increase (Car+A 2.0±0.2 ml, C 1.6±0.1 ml), which was not seen in carrageenan-treated rats exposed to hyperoxia (Car+O2 1.6±0.1 ml). Hyperoxia alone did not affect the value of FRC (O2 1.5±0.1 ml). These results support the hypothesis that a decrease in PO2 plays an important role in the carrageenan-induced increase of FRC in rats., B. Fišárková, M. Vízek., and Obsahuje bibliografii
The notion of a bilattice was introduced by Shulman. A bilattice is a subspace analogue for a lattice. In this work the definition of hyperreflexivity for bilattices is given and studied. We give some general results concerning this notion. To a given lattice L we can construct the bilattice \sum {_L}. Similarly, having a bilattice Σ we may consider the lattice \mathcal{L}_\Sigma . In this paper we study the relationship between hyperreflexivity of subspace lattices and of their associated bilattices. Some examples of hyperreflexive or not hyperreflexive bilattices are given., Kamila Kliś-Garlicka., and Obsahuje seznam literatury