Physiology international最新文献

In recent years, free fatty acid binding proteins (FABPs) are implicated in spermatogenesis and sperm morphology. FABPs are members of the intracellular lipid-binding protein family; they exhibit tissue specific expression like the FABP9/PERF15 (Perforated15) male germ cell-specific fatty acid linkage-protein.The aim of the study was to assess the levels of seminal FABP-9 in normozoospermic and oligozoospermic men, and the possible relations between seminal FABP-9 levels and semen parameters.Research was carried out on 60 male volunteers who were admitted to Selcuk University Faculty of Medicine of Andrology Laboratory. Normozoospermic individuals (n = 30) were identified as Group 1, and Oligozoospermic individuals (n = 30) were identified as Group 2. The semen samples were collected in sterile plastic containers. Sperm parameters were assessed according to Kruger's criteria. Seminal plasma FABP-9 levels were analyzed by ELISA method. Outcomes were statistically evaluated at 0.05 significance level with SPSS (22.0). The Receiver Operating Characteristic (ROC) curve was used to evaluate the performance of FABP-9 levels as compared to that of the concentration and motility data of the sperm. FABP-9 levels were significantly higher in normozoospermic individuals (3.41 ± 1.64 ng/mL) than in oligozoospermic individuals (1.99 ± 0.78 ng/mL). There were significant correlations between FABP-9 levels and sperm concentration, total sperm count, motility, progressive motility, immobility, Total Progressive Motil Sperm Count (TPMSC), head anomaly, and teratozoospermia index.We suggest that FABP-9 level is an important biomarker, and low levels of semen FABP-9 may impact the fertility status based on the ROC findings.

Objective: Parkinson's disease (PD) is a progressive neurodegenerative disorder. In order to explore a noninvasive treatment of PD, in the current study the authors evaluated the neuroprotective efficacy of caloric vestibular stimulation (CVS) using the rotenone-induced rat model of PD. The rotenone models of PD are gaining attention due to high reproducibility. It is also considered to be an improved model to exhibit the pathogenesis of PD and test the neuroprotective effect of various therapeutic interventions.

Materials and methods: Rotenone was i.p. injected (3 mg/kg body weight) to male Wistar albino rats for 21 days to induce PD. As PD is chronic and progressive in nature, the efficacy of chronic CVS intervention was evaluated for 30 days after inducing PD in rats. Motor symptoms were evaluated by assessing locomotor activity in actophotometer, whereas movement analysis was done using Ludolph test and motor coordination was evaluated using rotarod apparatus. The neurochemical and neuropathological changes were also observed in the corpus striatum of rats.

Results: Rotenone administration showed decreased locomotor activity, motor coordination and general movement associated with significant (P < 0.05) reduction in dopamine content in the corpus striatum. The immunohistochemical analysis revealed a marked decrease in tyrosine hydroxylase (TH) immunoreactivity in striatal neurons indicating the significant loss of dopaminergic neurons in substantia nigra (SN) following rotenone injection. However, chronic treatment with CVS restored the nerve terminals in the striatum from rotenone damage. CVS treatment improved the dopaminergic system function by restoring dopamine content in the striatum. CVS also improved the motor deformities clearly suggesting the neuroprotective function.

Conclusion: The results of the present study suggested CVS to be a safe and simple neuroprotective measure against neurodegenerative changes in PD and a promising noninvasive technique to overcome the motor symptoms associated with it. The findings could be useful for further investigations and clinical applications of CVS in the treatment of PD.

Reports of VO2 response differences between normoxia and hypoxia during incremental exercise do not agree. In this study VO2 and VE were obtained from 15-s averages at identical work rates during continuous incremental cycle exercise in 8 subjects under ambient pressure (633 mmHg ≈1,600 m) and during duplicate tests in acute hypobaric hypoxia (455 mmHg ≈4,350 m), ranging from 49 to 100% of VO2 peak in hypoxia and 42-87% of VO2 peak in normoxia. The average VO2 was 96 mL/min (619 mL) lower at 455 mmHg (n.s. P = 0.15) during ramp exercises. Individual response points were better described by polynomial than linear equations (mL/min/W). The VE was greater in hypoxia, with marked individual variation in the differences which correlated significantly and directly with the VO2 difference between 455 mmHg and 633 mmHg (P = 0.002), likely related to work of breathing (Wb). The greater VE at 455 mmHg resulted from a greater breathing frequency. When a subject's hypoxic ventilatory response is high, the extra work of breathing reduces mechanical efficiency (E). Mean ∆E calculated from individual linear slopes was 27.7 and 30.3% at 633 and 455 mmHg, respectively (n.s.). Gross efficiency (GE) calculated from mean VO2 and work rate and correcting for Wb from a VE-VO2 relationship reported previously, gave corresponding values of 20.6 and 21.8 (P = 0.05). Individual variation in VE among individuals overshadows average trends, as also apparent from other reports comparing hypoxia and normoxia during progressive exercise and must be considered in such studies.

Within recent years the popularity of sportive activities amongst older people, particularly competitive activities within certain age groups has increased. The purpose of this study was to assess the differences in the cardiorespiratory output at anaerobic threshold and at maximal power, output during an incremental exercise, among senior and young athletes. Ten elderly male subjects [mean (SD) age: 68.45 ± 9.32 years] and eight young male subjects [mean (SD) age: 25.87 ± 5.87 years] performed an incremental exercise test on a treadmill ergometer. No significant differences in body size were evident; however, the differences between the groups for peak power (451.62 ± 49 vs. 172.4 ± 32.2 W), aerobic capacity (57.97 ± 7.5 vs. 40.36 ± 8.6 mL kg-1 min-1), maximal heart rate (190.87 ± 9.2 vs. 158.5 ± 9.1 beats min-1), peak blood lactate (11 ± 1.7 vs. 7.3 ± 1.4 mmol L-1), and % VO2max at ventilatory thresholds (93.18 ± 4.3 vs. 79.29 ± 9.9%) were significantly lower in the senior athletes. The power output at anaerobic threshold was also higher (392 ± 48 vs. 151 ± 23 W) in the young athletes, explaining the significant difference in terms of performance between these groups. We have observed an evident deterioration in some of the cardiovascular parameters; however, the submaximal exercise economy seems to be preserved with aging. Exercise economy (i.e. metabolic cost of sustained submaximal exercise) was not different considerably with age in endurance-trained adults.

Objective: Prior research has evaluated the effects of acute exercise on episodic memory function. These studies have, on occasion, demonstrated that acute exercise may enhance both short- and long-term memory. It is uncertain as to whether the acute exercise improvements in long-term memory are a result of acute exercise attenuating declines in long-term memory, or rather, are driven by the enhancement effects of acute exercise on short-term memory. The present empirical study evaluates whether the decline from short- to long-term is influenced by acute exercise. This relationship is plausible as exercise has been shown to activate neurophysiological pathways (e.g., RAC1) that are involved in the mechanisms of forgetting.

Methods: To evaluate the effects of acute exercise on forgetting, we used data from 12 of our laboratory's prior experiments (N = 538). Across these 12 experiments, acute exercise ranged from 10 to 15 mins in duration (moderate-to-vigorous intensity). Episodic memory was assessed from word-list or paragraph-based assessments. Short-term memory was assessed immediately after encoding, with long-term memory assessed approximately 20-min later. Forgetting was calculated as the difference in short- and long-term memory performance.

Results: Acute exercise (vs. seated control) was not associated with an attenuated forgetting effect (d = 0.10; 95% CI: -0.04, 0.25, P = 0.17). We observed no evidence of a significant moderation effect (Q = 6.16, df = 17, P = 0.17, I2 = 0.00) for any of the evaluated parameters, including study design, exercise intensity and delay period.

Conclusion: Across our 12 experimental studies, acute exercise was not associated with an attenuated forgetting effect. We discuss these implications for future research that evaluates the effects of acute exercise on long-term memory function.

Purpose: Acid-base transport in renal proximal tubules (PTs) is mainly sodium-dependent and conducted in coordination by the apical Na+/H+ exchanger (NHE3), vacuolar H+-adenosine triphosphatase (V-ATPase), and the basolateral Na+/HCO3- cotransporter. V-ATPase on PTs is well-known to play an important role in proton excretion. Recently we reported a stimulatory effect of insulin on these transporters. However, it is unclear whether insulin is involved in acid-base balance in PTs. Thus, we assessed the role of insulin in acid-base balance in PTs.

Methods: V-ATPase activity was evaluated using freshly isolated PTs obtained from mice, and specific inhibitors were then used to assess the signaling pathways involved in the observed effects.

Results: V-ATPase activity in PTs was markedly enhanced by insulin, and its activation was completely inhibited by bafilomycin (a V-ATPase-specific inhibitor), Akt inhibitor VIII, and PP242 (an mTORC1/2 inhibitor), but not by rapamycin (an mTORC1 inhibitor). V-ATPase activity was stimulated by 1 nm insulin by approximately 20% above baseline, which was completely suppressed by Akt1/2 inhibitor VIII. PP242 completely suppressed the insulin-mediated V-ATPase stimulation in mouse PTs, whereas rapamycin failed to influence the effect of insulin. Insulin-induced Akt phosphorylation in the mouse renal cortex was completely suppressed by Akt1/2 inhibitor VIII and PP242, but not by rapamycin.

Conclusion: Our results indicate that stimulation of V-ATPase activity by insulin in PTs is mediated via the Akt2/mTORC2 pathway. These results reveal the mechanism underlying the complex signaling in PT acid-base balance, providing treatment targets for renal disease.

Purpose: Knee osteoarthritis (OA) is a common type of degenerative joint disease which decreases the quality of life. Sex-determining region Y box 9 (SOX9) and hypoxia-inducible factor-1 (HIF1) are considered as the key regulators of OA. We investigated the effect of combined therapies with mesenchymal stem cells (MSCs), ozone (O3) and exercise training on SOX9 and HIF1 expression in the cartilage of rats with knee OA.

Methods: Knee OA was induced by surgical method. OA rats were divided into model, MSCs, ozone, exercise, MSCs + ozone, MSCs + exercise, ozone + exercise and MSCs + ozone + exercise groups. Rats in the MSCs group received intraarticular injection of 1 × 106 cells/kg. Rats in the ozone group received O3 at the concentration of 20 μg/mL, once weekly for 3 weeks. Rats in the exercise group were trained on rodent treadmill three times per week. 48 hours after the programs, cartilage tissues were isolated and the expression of SOX9 and HIF1 was determined using Real-Time PCR.

Results: Significant differences were found in the expression of SOX9 and HIF1 between groups (P < 0.0001). Although combined therapies with exercise, MSCs and O3 significantly increased the expression of SOX9 and HIF1 in the cartilage tissue of rats with knee OA, combination of exercise with O3 was significantly more effective compared to the other combined therapies (P < 0.001).

Conclusions: Combined therapy with exercise, MSCs and O3 significantly increased the expression of SOX9 and HIF1 genes in the cartilage of rats with knee OA; however, exercise + O3 was significantly more effective.

A considerable number of patients arriving in dental offices are being treated with ongoing medication for a variety of chronic diseases. As a result, dentists must be familiar with the potential side effects these therapeutic agents may have on the tissues of the oral cavity, and in particular on the salivary gland. Salivary gland function may be altered by a wide range of medications, leading to effects such as xerostomia, hyposalivation, hypersalivation or even swelling of the glands. These disorders can cause a variety of other health complications. This review will focus on the most common groups of drugs responsible for salivary gland dysfunction, including psychoactive drugs, antidepressants, antipsychotics, antihypertensives, and antihistamines.

Although the use of aspirin has substantially reduced the risks of cardiovascular events and death, its potential mechanisms have not been fully elucidated. In a previous study, we found that aspirin triggers cellular autophagy. In the present study, we aimed to determine the protective effects of aspirin on human coronary artery endothelial cells (HCAECs) and explore its underlying mechanisms. HCAECs were treated with oxidized low-density lipoprotein (ox-LDL), angiotensin II (Ang-II), or high glucose (HG) with or without aspirin stimulation. The expression levels of endothelial nitric oxide (NO) synthase (eNOS), p-eNOS, LC3, p62, phosphor-nuclear factor kappa B (p-NF-κB), p-p38 mitogen-activated protein kinase (p-p38 MAPK), and Beclin-1 were detected via immunoblotting analysis. Concentrations of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were measured via ELISA. NO levels were determined using the Griess reagent. Autophagic flux was tracked by tandem mRFP-GFP-tagged LC3. Results showed that aspirin increased eNOS level and reduced injury to the endothelial cells (ECs) caused by ox-LDL, Ang-II, and HG treatment in a dose-dependent manner. Aspirin also increased the LC3II/LC3I ratio, decreased p62 expression, and enhanced autophagic flux (autophagosome and autolysosome puncta) in the HCAECs. p-NF-κB and p-p38 mitogen-activated protein kinase inhibition, sVCAM-1 and sICAM-1 secretion, and eNOS activity promotion by aspirin treatment were found to be dependent on Beclin-1. These results suggested that aspirin can protect ECs from ox-LDL-, Ang-II-, and HG-induced injury by activating autophagy in a Beclin-1-dependent manner.