The founder of physiology studies in the Balkans and the pioneer of research on hypothermia, Ivan Djaja (Jean Giaja) was born 1884 in L’Havre. Giaja gained his PhD at the Sorbonne in 1909. In 1910 he established the first Chair of Physiology in the Balkans and organized the first Serbian In stitute for Physiology at the School of Philosophy of the University of Belgrade. He led this Institute for more than 40 subsequent years. His most notable papers were in the field of thermoregulation and bioenergetics. Djaja became member of the Serbian and Croatian academies of science and doctor honoris causa of Sorbonne. In 1952 for the seminal work on the behavior of deep cooled warm blooded animals he became associate member of the National Medical Academy in Paris. In 1955 the French Academy of Sciences elected him as associate member in place of deceased Sir Alexander Fleming. Djaja died in 1957 during a congress held in his honor. He left more than 200 scientific and other papers and the golden DaVincian credo “Nulla dies sine experimento”. His legacy was continued by several generations of researchers, the most prominent among them being Stefan Gelineo, Radoslav Andjus and Vojislav Petrović ., P. R. Andjus, S. S: Stojilkovic, G. Cvijic., and Obsahuje bibliografii a bibliografické odkazy
Regulatory volume decrease (RVD) is essential for the survival of animal cells. The aim of this study was to observe the RVD process in rat ventricular myocytes, and to determine if the KATP channels are involved in the RVD process in these cells. By using reverse transcriptase polymerase chain reaction and Western blot analysis, we demonstrated that there are two types of KATP channels expressed in rat ventricular myocytes: Kir6.1 and Kir6.2. When rat cardiac myocytes were exposed to hypotonic solution, cell volume increased significantly within 15 min and then gradually recovered. This typical RVD process could be inhibited by a Cl– channel blocker (0.5 mM 9-anthracene-carboxylic acid , 9-AC), a K+ channel blocker (5.0 mM CsCl) and a KATP channel blocker glibenclamide (10 μM). Electrophysiological results showed that hypotonic solution activated a whole-cell current, which had similar biophysical characteristics with KATP opener (pinacidil)-induced currents. This current could be blocked by glibenclamide. Our data suggested that the RVD process in rat ventricular myocytes is dependent on the activation of K+ channels, and that KATP channels are involved in this process., L. Shi ... [et al.]., and Obsahuje seznam literatury
MK-801 impaired social recognition potency of adult male rats when given immediately after the initial interaction with a juvenile rat. Administration of kynurenic acid prior to the initial interaction protected the adults against recognition deficits induced by MK-801. When re-exposed at a delay of 30 min to the familiar juvenile, social investigation in the adults was significantly reduced. Thus, the adults are able to remember olfactory stimuli emitted by juvenile con-specifics., Z. Hliňák, I. Krejčí., and Obsahuje bibliografii
Previous studies in our laboratory reported L-malate as a free radical scavenger in aged rats. To investigate the antioxidant mechanism of L-malate in the mitochondria, we analyzed the change in gene expression of two malate-aspartate shuttle (MAS)-related carried proteins (A GC, aspartate/glutamate carrier and OMC, oxoglutarate/malate carrier) in the inner mitochondrial membrane, and three antioxidant enzymes (CAT, SOD, and GSH-Px) in the mitochondria. The changes in gene expression of these proteins and enzymes were examined by real-time RT-PCR in the heart and liver of aged rats treated with L-malate. L-malate was orally administered in rats continuously for 30 days using a feeding atraumatic needle. We found that the gene expression of OMC and GSH-Px mRNA in the liver increased by 39 % and 38 %, respectively, in the 0.630 g/kg L-malate treatment group than that in the control group. The expression levels of SOD mRNA in the liver increased by 39 %, 56 %, and 78 % in the 0.105, 0.210, and 0.630 g/kg L-malate treatment groups, respectively. No diffe rence were observed in the expression levels of AGC, OMC, CAT, SOD, and GSH-Px mRNAs in the heart of rats between the L-malate treatment and control groups. These results predicted that L-malate may increase the antioxidant capacity of mitochondr ia by enhancing the expression of mRNAs involved in the MAS and the antioxidant enzymes., X: Zeng, J. Wu, Q. Wu, J. Zhang., and Obsahuje bibliografii
The intracellular levels of antioxidant and free radical scavenging enzymes are gradually altered during the aging process. An age-dependent increase of oxidative stress occurring throughout the lifetime is hypothesized to be the major cause of aging. The current study examined the effects of L-malate on oxidative stress and antioxidative defenses in the liver and heart of aged rats. Sprague-Dawley male rats were randomly divided into four groups, each group consisting of 6 animals. Group Ia and Group IIa were young and aged control rats. Group Ib and Group IIb were young and aged rats treated with L-malate (210 mg/kg body weight per day). L-malate was orally administrated via intragastric canula for 30 days, then the rats were sacrificed and the liver and heart were removed to determine the oxidant production, lipid peroxidation and antioxidative defenses of young and aged rats. Dietary L-malate reduced the accumulation of reactive oxygen species (ROS) and significantly decreased the level of lipid peroxidation in the liver and heart of the aged rats. Accordingly, L-malate was found to enhance the antioxidative defense system with an increased activity of antioxidant enzymes, such as superoxide dismutase (SOD) and glutathione peroxidase (GPx) and increased glutathione (GSH) levels in the liver of aged rats, a phenomenon not observed in the heart of aged rats. Our data indicate that oxidative stress was reversed and the antioxidative defense system was strengthened by dietary supplementation with L-malate., J.-L. Wu, Q.-P. Wu, X.-F. Yang, M.-K. Wei, J.-M. Zhang, Q. Huang, X.-Y. Zhou., and Obsahuje bibliografii a bibliografické odkazy
Spontaneously hypertensive rats (SHR) are characterized by enhanced nifedipine-sensitive component of sympathetic vasoconstriction. Our study tried to elucidate the mechanisms responsible for long-term reduction of blood pressure (BP) in SHR subjected to early transient captopril treatment. Adult untreated SHR aged 30-34 weeks were compared with animals subjected to chronic captopril treatment for 6 weeks either in youth (between 4 and 10 weeks of age) or in adulthood (between 24 and 30 weeks of age). Antihypertensive effects of captopril were more pronounced in young than adult SHR. This was due to greater attenuation of sympathetic and nifedipine-sensitive BP components and prevention of residual BP rise in young captopril-treated SHR in which the reductions of nifedipine-sensitive BP component and residual BP persisted for 20 weeks after captopril withdrawal. The magnitude of nifedipine-sensitive component of sympathetic vasoconstriction is decisive for BP maintenance not only in untreated SHR but also in SHR during active captopril treatment by or after its withdrawal., J. Zicha, Z. Dobešová,J. Kuneš., and Obsahuje bibliografii a bibliografické odkazy
The aim of our in vitro studies was to understand the role of leptin in controlling proliferation, apoptosis, and protein kinase A (PKA) in human ovarian cells. We analyzed the in vitro effects of leptin (0, 1, 10 or 100 ng/ml) on the accumulation of proliferation-related peptides (PCNA, cyclin B1), apoptosis-associated peptide (Bax) and the intracellular signaling molecule PKA in cultured human granulosa cells using immunocytochemistry and Western immunoblotting. It was observed that leptin stimulated in a dose-dependent manner the accumulation of PCNA (at doses 1-100 ng/ml), cyclin B1 (at doses 10 or 100 ng/ml), Bax (at doses 10 or 100 ng/ml) and PKA (at doses 1-100 ng/ml) in cultured human ovarian cells. These observations suggest the ability of leptin to control directly human ovarian cell functions: proliferation, apoptosis, and intracellular messenger PKA., A. V. Sirotkin, M. Mlynček, A. V. Makarevich, I. Florkovičová, L. Hetényi., and Obsahuje bibliografii a bibliografické odkazy
a1_Leptin regulates energy homeostasis and body weight by balancing energy intake and expenditure. It was recently reported that leptin, released into the gut lumen during the cephalic phase of gastric secretion, is capable of initiating intestinal nutrient absorption. Vagal afferent neurons also express receptors for both CCK and leptin, which are believed to interact in controlling food intake. The present study was undertaken to investigate the central and peripheral effects of leptin on gastric emptying rate. Under anesthesia, male Sprague-Dawley rats (250-300 g) were fitted with gastric Gregory cannulas (n=12) and some had additional cerebroventricular cannulas inserted into their right lateral ventricles. Following recovery, the rate of gastric emptying of saline (300 mOsm/kg H2O) was determined after instillation into the gastric fistula (3 ml, 37°C, containing phenol red, 60 mg/l as a non-absorbable dilution marker). Gastric emptying rate was determined from the volume and phenol red concentrations recovered after 5 min. Leptin, injected intraperitoneally (ip; 10, 30, 60, 100 μg/kg) or intracerebroventricularly (icv; 5, 15 μg/rat) 15 min before the emptying, delayed gastric emptying rate of saline at the dose of 30 μg/kg or 15 μg/rat (p<0.001). When CCK 1 receptor blocker L-364,718 (1 mg/kg, ip), CCK 2 receptor blocker L-365,260 (1 mg/kg, ip) or adrenergic ganglion blocker bretylium tosylate (15mg/kg, ip) was administered 15 min before ip leptin (30 μg/kg) injections, leptin-induced delay in gastric emptying was abolished only by the CCK 1 receptor blocker (p<0.001)., a2_However, the inhibitory effect of central leptin on gastric emptying was reversed by adrenergic blockade, but not by either CCK antagonists. Our results demonstrated that leptin delays gastric emptying. The peripheral effect of leptin on gastric motility appears to be mediated by CCK 1 receptors, suggesting the release of CCK and the involvement of vagal afferent fibers. On the other hand, the central effect of leptin on gastric emptying is likely to be mediated by adrenergic neurons. These results indicate the existence of a functional interaction between leptin and CCK receptors leading to inhibition of gastric emptying and short-term suppression of food intake, providing an additional feedback control in producing satiety., B. Çakir, Ö. Kasimay, E. Devseren, B. Ç. Yeğen., and Obsahuje bibliografii a bibliografické odkazy