Physiology international最新文献

Purpose: Contribution of the gastrocnemii muscles to ankle moment is influenced by the knee joint position because they span the knee and the ankle joint as well. However, limited information is available on the effect of knee joint position on soleus activation under dynamic plantarflexion, hence the aim of this study was to investigate if soleus have a compensatory strategy in fascicle behavior or EMG activity during knee flexed plantarflexion in order to reduce the magnitude of the decrement in ankle moment.

Equipment and methods: Isokinetic dynamometry with EMG and ultrasound measurements was used to estimate medial gastrocnemius and soleus behavior during knee flexed and extended plantarflexions using three angular velocities. Seventeen healthy males were participated in this study.

Results: Flexed knee plantarflexions resulted in lower peak ankle moments at all ankle angular velocities by 18% (P = 0.1062) at 30°∙s-1, 44% (P < 0.001) at 60°∙s-1 and by 18% (P = 0.0001) at 120°∙s-1. Soleus showed significantly higher EMG activity during knee flexed plantarflexion at 30°∙s-1 (P = 0.0094) and 60°∙s-1 (P = 0.0142). The magnitude of mean shortening of the medial gastrocnemius and soleus show statistically significant difference between knee flexed and knee extended plantarflexion at any contraction velocity.

Conclusions: Soleus may perform a compensatory EMG activity in knee flexed plantarflexions possibly to counteract the reduced contribution of gastrocnemius to ankle moment at low angular velocity contractions.

Background: Severity of chronic kidney disease (CKD) is associated with the inflammatory response, and that a decrease in glomerular filtration rate correlates positively with the concentrations of inflammatory markers. Moreover, the severity of the inflammatory response is also exacerbated by the dialysis treatment process. It is also emphasized that the introduction of appropriate dietary interventions alleviates inflammation and reduces the concentration of markers.

Objective: The aim of this pilot study was to analyze the nutritional value of daily rations and the value of the dietary inflammatory index (DII) in a group of dialysis patients.

Methods: Fifty-four patients (35 men, 19 women), with kidney replacement therapy, were enrolled in the study. The DII index was calculated according to the formula of Shivappa et al.

Results: The results showed that the vast majority of dialysis patients (83%), including almost all women (94%) and as many as 77% of men consumed a pro-inflammatory diet. The value of the DII index, in the total study group, was 2.89. Analysis of the 3-day dietary interviews showed that the pro-inflammatory nature of the diets was due in particular to low intake of: selenium, PUFA, vitamins (D, B9, C) and fiber. On the other hand, it was shown that the patients consumed saturated fatty acids and cholesterol in excess.

Conclusions: Observations made in this study, indicate the need to intensify nutrition education as an element in the routine care of dialysis patients in order to increase the effectiveness of patients' adherence to an anti-inflammatory diet.

Introduction: This study assesses the utility of photoplethysmography (PPG) as a non-invasive method to evaluate cardiac function, addressing the critical need for accessible biomarkers in various cardiovascular conditions, including heart failure management.

Methods: By conducting simultaneous echocardiography and PPG measurements on 37 healthy volunteers, we analyzed both traditional and novel composite pulse wave scores to correlate peripheral PPG data with central echocardiographic outcomes.

Results: Our results show a good correlation between PPG-based and echocardiography-derived ejection times (r = 0.648, P < 0.001), though Bland-Altmann analysis results reveal that PPG consistently overestimated ejection times by a mean difference of +95 ms. Moreover, eleven PPG parameters significantly correlated with key echocardiographic indicators of systolic and diastolic function, such as left ventricular dimensions, global longitudinal strain, aortic functionality, atrial contraction (MV-A), and ventricular filling pressure (E/e' lat) with clinical relevance indicated by correlations (r) above 0.4 (P < 0.05).

Conclusion: The findings pave the way for further studies in various patient groups to explore the potential of PPG in enhancing home monitoring and regular cardiovascular assessments. This work not only broadens our understanding of the physiological relationships between peripheral and central cardiovascular measures but also introduces innovative metrics that might bring some added value to the current standards of patient care by facilitating early detection and personalized management of heart conditions.

Introduction: Inflammatory processes play a significant role in the pathogenesis of depression. Research shows that treatment-resistant depression (TRD) may affect up to 30% of patients with depressive symptoms. Wistar-Kyoto (WKY) rats exposed to chronic mild stress (CMS) are considered to be a model of TRD.

Methods: Since inflammatory processes and disrupted signaling pathways play key roles in the pathophysiology of depression, we investigated the effect of CMS on behavior as well as on the CaMKII, JAK2/STAT3, NF-κB, and the Nrf2/HO-1 pathway in the hippocampus (HC) and medial prefrontal cortex (mPFC) of female WKY rats.

Results: Our results demonstrated that unstressed WKY females had depressive symptoms accompanied by cognitive deficits, whereas chronic stress led to further behavioral impairments. The findings indicate that the baseline levels of JAK2/STAT3 and the expression level of NF-κB protein in the HC and mPFC were upregulated in unstressed WKY rats. When WKY rats are exposed to CMS there is a further increase of JAK2/STAT3 pathway (mPFC: 12%, P < 0.05; HC: 20%, P < 0.05) and NF-κB (25%, P < 0.05) in the HC and the mPFC. Our results confirmed a positive correlation between the index of depression, pJAK2/pSTAT3, and NF-κB expression, as well as a negative correlation between recognition memory and these protein levels in both unstressed and stressed WKY rats. WKY rats showed reduced pCaMKII levels in the HC and mPFC, while CMS significantly increased pCaMKII in both brain structures (40%, P < 0.001). There is a strong association between pCAMKII overexpression in the hippocampus of stressed WKY rats and the depression index. Our results showed unchanged expressions of Nrf2 and HO-1 in the hippocampus and mPFC of unstressed WKY females. After exposure to CMS, WKY females showed decreased levels of Nrf2 and HO-1 only in the hippocampus.

Conclusion: The most significant changes in CaMKII, NF-κB and JAK2/STAT3 levels during chronic mild stress may contribute to the impairments in neural plasticity, neurogenesis, and cellular resilience observed in the brains of WKY rats as a model of TRD.

Background: The most prevalent form of lung cancer, lung adenocarcinoma (LUAD), has significant incidence and fatality rates worldwide. When treating LUAD, osimertinib resistance is a typical problem. Thus, it is imperative to address the concerns of clarifying the mechanism of osimertinib resistance in LUAD and enhancing medication sensitivity.

Methods: Using bioinformatics techniques, expression and possible biological roles of BMP8A in LUAD were examined, and predictions were made about upstream regulatory variables and binding locations. H1975 cell line, resistant to osimertinib, was created. Western blot and RT-qPCR were instrumental to determine mRNA and protein expression of FABP5, ACC1, and FASN associated to lipid metabolism. A fluorescent lipid synthesis test kit was utilized to detect amount of triglycerides present in culture medium. BMP8A and RUNX2 mRNA levels were assayed using RT-qPCR. Utilizing CCK-8 and ANNEXIN V-FITC/PI flow cytometry, cell viability was assessed. Through the use of dual luciferase assays, whether RUNX2 could regulate BMP8A was confirmed. CHIP was further employed to confirm whether the two were bound together.

Results: BMP8A and fatty acid metabolism (FAM) have a strong association, as revealed by bioinformatics investigation, and RUNX2 is its upstream transcription factor. Osimertinib-resistant H1975 cell lines were successfully created, and these cell lines showed a significant upregulation of BMP8A expression. The drug sensitivity of the resistant cell lines was decreased, and their FAM level was considerably enhanced by overexpressing BMP8A. Changes in drug sensitivity and FAM were reversed by using FAM inhibitors. An efficient binding of RUNX2 to the BMP8A promoter region was demonstrated by experimental validation, hence activating the production of the BMP8A gene. Lowering LUAD cell survival rates, lipid metabolism levels, and BMP8A expression were all caused by RUNX2 knockdown.

Conclusion: RUNX2 activated BMP8A-mediated FAM to facilitate osimertinib resistance in LUAD.

Purpose: Osteosarcoma (OS) is the most common primary bone tumor. Insulin Growth Factor-2 Binding Protein 3 (IGF2BP3) regulates mRNA stability and is a potential oncogene in many cancers, but its role in OS remains unknown.

Methods: The CCK-8 assay was used to evaluate the cell viability. Cell cycle and apoptosis were determined using flow cytometry. Real-time PCR and western blot were performed to measure gene expression.

Results: Silencing IGF2BP3 weakened cell proliferation and inhibited cell cycle progression. Mechanistically, we demonstrated the regulation of E3 ubiquitin ligase ubiquitination factor E4A (UBE4A) by IGF2BP3. The RIP, MeRIP, and RNA decay assays showed that IGF2BP3 bound to the m6A-modified UBE4A mRNA, thereby enhancing its stability and subsequently promoting the malignant proliferation of OS. Overexpression of UBE4A reversed the decrease in cell viability and induction of apoptosis caused by IGFBP3 knockdown. Furthermore, UBE4A promoted the ubiquitination modification of Natriuretic Peptide Receptor 3 (NPR3), a previously known tumor suppressor in OS. High expression of NPR3 significantly inhibited proliferation and promoted apoptosis in UBE4A-overexpressing cells.

Conclusions: IGF2BP3 is upregulated in OS and promotes the malignant phenotype of OS cells. Mechanistically, IGF2BP3 stabilizes UBE4A mRNA to increase UBE4A expression, thereby facilitating the ubiquitination and proteasomal degradation of tumor-suppressor NPR3 to exert pro-tumor functions in OS.

Background: Among genetic variants associated with physical performance, ACTN3 R577X and ACE I/D are among the most studied. However, their prevalence and functional significance in combat sports like Taekwondo remain underexplored.

Objective: To evaluate the prevalence of ACTN3 R577X and ACE I/D polymorphisms in Taekwondo athletes and controls, and to investigate their association with competitive level and belt ranking.

Methods: A total of 204 individuals (119 athletes and 85 controls) were genotyped via PCR using DNA from buccal cells. Genotype distributions were analyzed for Hardy-Weinberg equilibrium (HWE). Associations with performance level and belt ranking were tested. A "two loci profile" variable was created by combining genotypes into power-, endurance-, or mixed-oriented categories.

Results: ACE I/D genotypes in athletes deviated from HWE due to a higher prevalence of the DD genotype (32.2%, P = 0.017). In contrast, controls were in HWE for ACE but not for ACTN3. The DD genotype was more common among national-level competitors and black belts. The ACTN3 RR genotype also showed higher frequency among black belts but without statistical significance. When combining ACE DD and/or ACTN3 RR genotypes, black belts showed significantly greater prevalence than other ranks (37.5% vs. 14.3%, P = 0.038).

Conclusion: Genotypes related to strength and power appear more frequent among higher-performing Taekwondo athletes. These results contribute to the understanding of a synergetic action of two loci in combat sports and may support future applications in personalized training and talent identification.

Purpose: To investigate the effects of exercise-induced metabolites on the perceptions of pain and fatigue.

Method: Fifty-three adults completed six visits. The first visit involved multiple baseline tests, including a blood-flow-restricted exercise performance test (i.e., 2 sets of knee extension to task-failure at 30% 1RM with 80% arterial occlusion pressure [AOP]). In subsequent visits, participants performed five experimental conditions in a randomized order: 1) time-matched, non-exercise control (Control) and four low-load exercise conditions with either 2) 80%AOP (LL+80%), 3) 40%AOP (LL+40%), 4) intermittent 80%AOP (LL+80%Int), or 5) no blood flow restriction (0 mmHg; LL). Three-minute post-exercise circulatory occlusion (PECO) was employed to assess the effect of pooled muscle metabolites on perceived pain and fatigue and pain sensitivity (via pressure pain threshold). The results from liner mixed model are presented as mean [95% confidence interval].

Results: Condition-by-time interactions were found for perceived pain (P < 0.001) and fatigue (P < 0.001). LL+80% elicited higher increase in thigh pain (2.7 [2.2, 3.1] AU) and fatigue (2.1 [1.7, 2.5] AU) compared to LL+40%, LL+80%Int, and LL. Pain and fatigue did not change differently during PECO but declined three minutes post-PECO in exercise conditions (except fatigue in LL+80%Int). There was evidence of an interaction for pressure pain threshold of the tibialis anterior but not the forearm.

Conclusion: Continuous blood flow restriction with higher pressure (80%AOP) augmented the pain and fatigue perceptions from submaximal unilateral knee extension exercise, arguably through muscle metabolite accumulation (estimated by PECO). Conflicting evidence existed for blood flow restricted exercise-induced hypoalgesia, possibly confounded by PECO.

Purpose: Epilepsy is a widespread, long-term neurological condition triggered by an overabundance of electrical activity from the neurons in the brain. Genistein, a natural isoflavone found in soybeans, can prevent chronic diseases such as cardiovascular disease and osteoporosis. We aimed to investigate the potential protective effects of genistein on epilepsy using rat models through behavior analysis and investigation of key pathways, including antioxidant activity (Nrf2 and HO-1), promoting mitochondrial biogenesis (TFAM), and reducing brain tissue apoptosis (BCL2, BAX, and caspases).

Main methods: PTZ was used to induce epilepsy in rats, and then they were treated with genistein. The hippocampus sections were stained with Nissl stain, and others were stained with anti-TFAM antibodies. Furthermore, TFAM, Nrf2, HO-1, BCL2, BAX, and caspases-3/8/9 gene expression and protein levels were quantified using quantitative real-time polymerase chain reaction (qRT-PCR) and complementary biochemical/functional assays.

Results: Rats treated with genistein displayed notable progress in their behavior during behavioral tests. Sections stained with Nissl revealed that genistein increased the staining intensity of Nissl granules in the cerebral cortex. Additionally, genistein increased the expression of TFAM, Nrf2, HO-1, and BCL2, which reduced levels of BAX and caspase-3/8/9.

Conclusions: Genistein safeguards against epilepsy in rats by enhancing their behavior and reinstating normal neuron structure. Its protective benefits may stem from its potential to boost antioxidant activity and promote mitochondrial biogenesis, which in turn decreases cell apoptosis.