High mechanical load of muscles may induce muscular apoptosis on the one hand and adaptation to exercise on the other. This study aimed to explore whether changes of circulatory levels of inflammation, apoptosis and heat shock proteins (HSPs) messenger RNA (mRNA) following single bout of high-intensity interval exercise (HIIE) differs between physically active (PA) and inactive (PI) men. Nine PA and 9 PI (peak oxygen consumption: 2.6 ± 0.4 vs. 2.0 ± 0.2 L·min⁻¹) healthy men (age: 28.7 ± 6.3 vs. 30.2 ± 4.5 years and body mass index: 2.6 ± 2.1 vs. 23.3 ± 2.8 kg·m⁻²) performed HIIE, comprising 4 repeats of a Wingate test (load: 0.050 kg·kg⁻¹ body weight). Blood samples were collected before exercise, 5 min after HIIE, and 24 h after HIIE for measuring mRNA of inflammation markers interleukin-6 (IL-6) and tumor necrosis factor alpha (TNFα), apoptosis markers including Bcl-2, Bax, and HSP27, HSP60, HSP70, HSP90 using quantitative real-time PCR analysis. Post-HIIE IL-6, TNFα and HSP60 were higher in the PI than the PA group 5 min after exercise (p = 0.003, effect size (ES) = 1.59; p = 0.007, ES = 1.59 and p = 0.027, ES = 1.10 respectively). HSP70 acutely increased only in the PA group (p = 0.024, ES = 1.20). The increase in Bcl-2 (p = 0.047, ES = 1.08) and Bax (p = 0.024, ES = 1.20) levels were higher in the PI group 5 min after HIIE. The present study indicated that the response of inflammatory, apoptosis and HSP gene expressions to HIIE in blood of healthy male volunteers strongly depends on their level of regular physical activity. Novelty: Blood IL-6 and HSP60 mRNA levels following high intensity exercise may indicate metabolic stress. Increased blood HSP70 mRNA in physically active men may show an alternative apoptosis suppression pathway.

Recent community-based studies have identified sleep deprivation (SD) as an important modifiable risk factor for hypertension However, the underlying mechanisms linking SD to hypertension remain elusive. Thus, this study investigates blood pressure (BP) responses to cardiac autonomic stress tests in the presence of SD. Furthermore, we analyzed vascular inflammatory biomarkers as a possible underlying factor linking SD to increased BP. Ten healthy male volunteers (age, 21.6±1.2 years) underwent repeated autonomic stress tests for three consecutive days (baseline, SD, and recovery). The autonomic stress tests included the Valsalva maneuver, mental arithmetic, isometric handgrip, and cold pressor tests. Each day, resting BPs were measured, venous blood samples were collected for intercellular adhesion molecule 1, vascular cell adhesion molecule 1, and E-selectin measurements, and stress tests were performed between 0900 and 1100. Ambulatory BP was recorded during the entire SD period (24 h). One-night SD abolished BP reactivity to the Valsalva maneuver, isometric hand grip, and cold pressor tests, which returned after recovery sleep. Ambulatory BP monitoring showed that the mean systolic and diastolic BPs were 121.1±8.5 mm Hg and 72.8±6.3 mm Hg, respectively, between 0700 and 2300 and 120.3±9.6 mm Hg and 74.1±6.1 mm Hg, respectively, between 2300 and 0700 during the SD day (p>0.05 for both). Vascular inflammatory markers seemed unrelated to BP changes. Acute SD altered BP responses to cardiac autonomic stress tests in healthy men without affecting resting BP levels. SD led to a non-dipping pattern in BP oscillation. Collectively, these findings highlight the importance of sleep in regulating BP.

Both nesfatin-1 and cannabinoid systems involved in the regulation of sleep, metabolism, and food intake. The relationship between cannabinoid system and nesfatin-1 levels remains to be elucidated. This study investigated nesfatin-1 and insulin resistance in 72-h rapid eye movement (REM) sleep-deprived mice under the effects of cannabinoid, and cannabinoid receptors CB1R and CB2R blocking. Sixty mice were exposed to 72-h sleep deprivation. Groups and drug administrations were as follows: Group 1 (control) received injection of vehicle. Group 2 received WIN 55,212,2. Group 3 received AM251 (CB1R antagonist) followed by WIN 55,212,2 injection. Group 4 received SR144528 (CB2R antagonist) followed by WIN 55,212,2 injection. Group 5 received only AM251. Group 6 received only SR144528. Blood samples were collected 1 h after drug administration and prepared for biochemical measurements. Glucose levels were measured by glucometer, whereas insulin and nesfatin-1 levels were measured by ELISA. Central nesfatin-1 was also assessed using immunohistochemistry. One-way analysis of variance together with post hoc Tukey's test was used for inter-group comparisons. Serum nesfatin-1 levels were comparable in all study groups. Brain nesfatin-1 immune-positive cell count was lower in WIN group compared to controls. The administration of CB1R or CB2R antagonist prevented reduction in nesfatin-1-positive cell count. Insulin resistance was higher in WINCB2 and CB2 groups than in control and WINCB1 groups. Cannabinoid treatment reduced nesfatin-1 immunoreactivity in the central nervous system and this effect was prevented by either CB1R or CB2R antagonist pretreatment. Insulin resistance might be related to CB2 receptor activation which was independent from central nesfatin-1 immunoreactivity.

Background and Objectives: Allergic contact dermatitis is a common type IV hypersensitivity reaction characterised by redness, itching, oedema and thickening of the skin. It occurs in about 7% of the population and its incidence is increasing. It has been observed that the preconditioning of tissues by exposing them to transient ischemia increases resistance to subsequent permanent ischemia, and this phenomenon is called ischemic preconditioning. It has been shown that conditioning in one organ can also protect other organs. The protective effect of remote ischemic preconditioning is thought to be based on the induction of anti-inflammatory responses. The aim of this project was to investigate the anti-inflammatory and antipruritic effects of remote ischemic postconditioning in a mouse model of experimental allergic contact dermatitis. Methods: Experimental allergic contact dermatitis was induced with 1-fluoro-2,4-dinitrobenzene. Remote ischemic postconditioning was performed at 3 and 25 h after the challenge. Ear thickness and number of scratches 24 and 48 h after challenge, as well as cytokine levels and the infiltration of mast cells, neutrophils, CD4⁺ and CD8⁺ T lymphocytes in serum and ear tissue at 48 h were measured to determine the effect of RIPsC. Results: Remote ischemic postconditioning decreased ear thickness, one of the symptoms of allergic contact dermatitis (p < 0.0001). It had no significant effect on the number of scratches. It reduced serum IL-17 levels (p < 0.01). It alleviated local inflammation by suppressing CD8⁺ T lymphocyte and neutrophil infiltration. Conclusions: It was concluded that remote ischemic postconditioning may alleviate the symptoms of allergic contact dermatitis by suppressing CD8⁺ T lymphocyte and neutrophil infiltration and reducing IL-17 secretion.

Aim: The aim of the study was to evaluate the opinions of research assistants working in clinical departments about basic medical sciences education and their tendency in career choices. Methods: The study was conducted on 110 research assistants working in the internal and surgical medical sciences. The data were obtained by using a questionnaire developed by the researcher and based on volunteering. Results: When the study group was asked about the field of basic medical sciences they used most during their professional lives, physiology ranked first with 36.8% (n=32). 73.2% of the participants responded to the proposition that I need basic medical science knowdelge in my specialty. 43.1% of the participants agreed with the statement that I absolutely did not want to do specialty training in the field of basic medical sciences. Conclusion: It was thought that basic medical sciences curriculum should be structured according to the needs of clinical sciences. The positive opinion on basic medical education does not reflect on career choice.