ABSENCE OF OXIDATIVE STRESS AND SIRTUINS RECRUITMENT ON CARDIAC TISSUE POST STRESS

Stress has emerged as a factor associated with cardiovascular disease. Catecholamines released during the stress reaction by the sympathetic nerves and the adrenal medulla couple to β1-and β2-adrenoceptors in the cardiomyocytes membrane enhancing heart function in order to attend the organism demand. This might produce excessive reactive oxygen species what may culminate with oxidative stress and progression of several cardiac diseases. Sirtuins have been described as cardioprotective factors and important regulators of the cellular stress response in the heart. The aim of this work is to investigate the putative participation of oxidative stress and sirtuins in the heart of rats submitted to foot shock stress, an experimental model where there is up regulation of β2-adrenoceptors and downregulation of β1-adrenoceptors. The data have shown that in the myocardium of rats submitted to foot shock stress the H2O2 concentration, catalase and superoxide dismutase activity, NAD+/NADH ratio, as well as the protein expression of sirtuins 1 and 3 were not altered. Pharmacological blockade of the β2-adrenoceptors by ICI118,551, did not modify this scenario. It is concluded that foot shock stress does not cause disruptions in oxidative stress or redox state processes in the myocardium, and consequently, sirtuins are not recruited to stress response.

Analysis of Dynamic Response Behavior of Crack under Impact Stress Wave

The structural parts of construction machinery mostly fail due to impact load, but current research on the failure behavior of the impact load has not established a complete theoretical system. Based on wave theory and fracture mechanics, this paper analyzed the wave behavior of shock stress waves and established a model of shock stress wave propagation. Given the dynamic response behavior of the stress and strain field at the crack tip, dynamic fracture mechanics theory was used to solve the dynamic fracture strength stress factor and evaluate the dynamic fracture performance of the structure with crack damage under shock waves. Through dynamic response analysis and numerical calculation of the typical SHPB (split Hopkinson pressure bar) test standard compact tension (CT) specimens under the short-term strong shock stress wave, the stress and strain evolution law of the material under the shock wave was analyzed, and the correlation of the shock stress wave was verified. This research work can meet the requirements of engineering design and has practical engineering significance, playing an important role in material safety design.

Anxiogenic and anxiolytic effects of memantine injected into the ventral hippocampus in male stressed mice

Objectives The effects of intra-ventral hippocampal memantine administration in male NMRI stressed mice were studied. Methods Two stainless steel gauge 23 guide cannulas were placed in the middle part of the mice ventral hippocampus using stereotaxic coordination. Seven days later, the animals were undergone to the stress protocol as follows: They experience four consecutive electro-foot shock stress sessions lasting for 10 min. Five or 30 min before each stress session, the animals received intra-ventral hippocampal (0.1, 1 and, 5 µg/mouse) or intraperitoneal (1, 5, and 10 mg/kg) memantine respectively. Eight days after stress termination, the animals were tested either for the maintenance of either anxiety (elevated plus maze) or depression (forced swimming test). Results Animals show anxiety eight days after stress termination. Intra-ventral hippocampal infusion of memantine (5 µg/mouse) 5 min before stress inhibited the anxiety-like behaviors. However, other doses of the drug exacerbate the stress effect. The drug, when injected peripherally exacerbated the stress effect in all doses. The drug by itself had no effect. In addition, animals also show depression nine days after stress termination and memantine (0.1, 1, and 5 µg/mouse) reduced the stress effect. The drug (0.1 µg/mouse) by itself induced depression in the animals. However, the drug when injected peripherally reduced the stress effect in all doses. Conclusions It could be concluded that NMDA glutamate receptors in the ventral hippocampus may play a pivotal role in the mediation of maintenance of anxiety and depression induced by stress in the mice.

The CRZ-1 Transcription Factor Regulates Hsp 80 Involves in the Acquisition of Thermotolerance, and NCA-2 for Calcium Stress Tolerance in Neurospora Crassa

Heat shock proteins (Hsps) are molecular chaperones and required for survival of organisms under heat stress conditions. In this study, we studied Hsp80, a member of the Hsp90 family, in Neurospora crassa. The expression of hsp80 was severely reduced in the N. crassa calcineurin B subunit RIP-mutant (cnb-1RIP) strains under the heat shock conditions. Furthermore, the expression levels of cnb-1, hsp60, hsp80, and the calcineurin-regulated transcription factor crz-1 were increased, but expression levels were reduced in the presence of the calcineurin inhibitor FK506 under the heat shock stress in the N. crassa wild type. Therefore, the calcineurin-crz-1 signaling pathway transcriptionally regulates hsp60 and hsp80 under the heat shock stress condition in N. crassa. In addition, the transcript levels of trm-9 and nca-2, a Ca2+ sensor and a Ca2+ ATPase, respectively, were increased under the heat shock stress condition. Moreover, the expression of the hsp80, but not the hsp60, was reduced in the Δtrm-9, Δnca-2, and the Δtrm-9 Δnca-2 double mutants. These results suggested that hsp80, trm-9, and nca-2 play a role in coping the heat shock stress in N. crassa. We found that CRZ-1 binds to 5ʹ-CCTTCACA-3ʹ and 5ʹ-AGCGGAGC-3ʹ 8 bp nucleotide sequences, located about 1075 bp and 679 bp upstream of the ATG start codon, respectively, of hsp80. We also found that CRZ-1 binds to an 8 bp nucleotide sequence 5ʹ-ACCGCGCC-3ʹ, located 234 bp upstream of the ATG start codon of nca-2 under Ca2+ stress condition. Thus, cnb-1, hsp60, hsp80, and crz-1 are involved in the heat shock stress response in N. crassa. Moreover, CRZ-1 upregulates the expressions of hsp80 and nca-2 under the heat shock stress and Ca2+ stress conditions, respectively, in N. crassa.

Stress-induced differential gene expression in cardiac tissue

The stress response is adaptive and aims to guarantee survival. However, the persistence of a stressor can culminate in pathology. Catecholamines released as part of the stress response over activate beta adrenoceptors (β-AR) in the heart. Whether and how stress affects the expression of components of the intracellular environment in the heart is still, however, unknown. This paper used microarray to analyze the gene expression in the left ventricle wall of rats submitted to foot shock stress, treated or not treated with the selective β2-AR antagonist ICI118,551 (ICI), compared to those of non-stressed rats also treated or not with ICI, respectively. The main findings were that stress induces changes in gene expression in the heart and that β2-AR plays a role in this process. The vast majority of genes disregulated by stress were exclusive for only one of the comparisons, indicating that, in the same stressful situation, the profile of gene expression in the heart is substantially different when the β2-AR is active or when it is blocked. Stress induced alterations in the expression of such a large number of genes seems to be part of stress-induced adaptive mechanism.

EPIGENETIC REGULATION OF ADAPTOGENESIS BY PATHOLOGY AND AGING

В обзоре с точки зрения эпигенетики рассмотрены адаптационные возможности организма при патологии и старении. Апаптация организма к внутренним и внешним факторам осуществляется единой гуморальной защитной системой организма, включающей гипоталамо-гипофизарно-эпифизарную и гипоталамогипофизарно-тимусную оси. Короткие пептиды AEDG, AEDP, EDR, KED, EW, KE являются эпигенетическими регуляторами экспрессии генов и синтеза белков, которые могут быть вовлечены в адаптацию при стрессе и активацию гипоталамо-гипофизарно-эпифизарной и гипоталамогипофизарно-тимусной осей. Указанные короткие пептиды регулируют синтез белков теплового шока, стресспротекторных белков, цитокинов, факторов фибринолиза и гемостаза. Эти пептиды могут участвовать в первичной и отсроченной эпигенетической регуляции адаптивного ответа при стрессе, патологии и старении. Ранняя функциональная диагностика нарушения сопряжения звеньев единой гуморальной защитной системы организма при возраст-ассоциированных заболеваниях позволит выявить недостаточную синхронность эпигенетических механизмов, при которой наступает истощение и снижение резервных возможностей организма. Применение пептидов может нивелировать проявления адаптационного синдрома при стрессе и возрастной патологии. The organism adaptive possibilities by pathology and aging are discussed in account of the epigenetic. The organism adaptation to inner and external factors is carried out by organism unite humoral protective system, inclusive hypothalamus-hypophysis-pineal and hypothalamus-hypophysis-thymus axises. AEDG, AEDP, EDR, KED, EW, KE short peptides are the epigenetic regulators of gene expression and protein synthesis, which can be involve to the adaptation by stress and in the activation of hypothalamus-hypophysispineal and hypothalamus-hypophysis-thymus axises. These short peptides regulate the synthesis of proteins of heat shock, stress-protective proteins, cytocines, fibrinolysis and hemostasis factors and can participate in primary and tardive epigenetic regulation of adaptive response by stress, pathology and aging. The early functional diagnostic of element disturbances of organism unite humoral protective system by age-associative pathology can be usefull for the detection of deficient synchronization of epigenetic mechanisms, by wich the depletion and decrease of organism reserve possibilities occurs. The use of peptide can grade the adaptive syndrome manifestation by the stress and age pathology.