{"title":"The relationship between aerobic capacity and cognitive/academic performance in medical students.","authors":"Zeynep Bayramlar, Seyit Ankarali, Handan Ankarali","doi":"10.4149/gpb_2022031","DOIUrl":"https://doi.org/10.4149/gpb_2022031","url":null,"abstract":"<p><p>The positive relationship between aerobic capacity and cognitive performance is well known, but there is little information regarding young adults. Therefore, we aimed to test the hypothesis that aerobic capacity (VO2max) correlates with cognitive and academic performance in medical students who have higher academic achievement with academic performance. We included 65 volunteer medical students who were in term 2/6 in this descriptive, cross-sectional study. Body composition and the International Physical Activity Questionnaire and cardiopulmonary exercise test results of all participants were analyzed. Lumosity application with 6 categories of cognitive tests was applied to evaluate cognitive performance. The university entrance exam scores of the students were taken into consideration to assess their academic performance. We observed a significant \"positive\" relationship between aerobic capacity and some domains of cognitive performance, especially problem solving (p < 0.05), but we did not find a significant relationship between aerobic capacity and academic performance. Consequently, although we confirmed the existence of a positive effect of high aerobic capacity on cognitive performance stated in the literature, we couldn't confirm this for all cognitive domains or academic performance. These results suggest that more comprehensive studies on this subject are needed.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40546038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Justyna Totoń-Żurańska, Lucia Balazova, Katarina Krskova, Beata Bujak-Giżycka, Stefan Zorad, Rafał Olszanecki, Maciej Suski
{"title":"Plasma proteome alterations in prediabetic, obese Zucker rats - possible cardiovascular risk implications.","authors":"Justyna Totoń-Żurańska, Lucia Balazova, Katarina Krskova, Beata Bujak-Giżycka, Stefan Zorad, Rafał Olszanecki, Maciej Suski","doi":"10.4149/gpb_2022043","DOIUrl":"https://doi.org/10.4149/gpb_2022043","url":null,"abstract":"<p><p>Hyperphagia and obesity, which underlie metabolic syndrome, have been linked to multiple health complications and increased mortality. Here, we investigate the differences in plasma proteome between obese and lean Zucker rats in order to identify circulating proteins involved in obesity-related conditions. Plasma samples of male Zucker fatty (obese) rats carrying fatty fa/fa mutation (-/-) and their lean controls were enriched using ProteoMiner technology and labeled with isobaric tags (iTRAQ) for mass spectrometry-based quantitation. We found elevation in levels of coagulation factors whereas levels of serine protease inhibitors were decreased. Levels of acute phase proteins were also altered, as well as complement components. We also noticed differences in the abundance of apolipoproteins. In summary, quantitative proteomic assessment of plasma protein composition in obese Zucker rats revealed a profound landscape of changes, reflecting altered hemostasis, disturbed metabolic processes involving insulin resistance and lipid metabolism and ongoing low-grade inflammation.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40568476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Stem cells and cardiac arrhythmias.","authors":"Boris G Yushkov, Alexey P Sarapultsev","doi":"10.4149/gpb_2022042","DOIUrl":"https://doi.org/10.4149/gpb_2022042","url":null,"abstract":"<p><p>Recent discoveries in the physiology and pathology of myocardial progenitor cells have allowed researchers to better understand a variety of cardiac pathologies and look at the pathophysiology of arrhythmias from a different perspective. Since the myocardium is composed of a syncytium of electrically interconnected cells, the process of incorporation of newly formed or imported cells into its structure is particularly important. Progenitor cells are stimulated by spontaneous electrical activity, a lengthy action potential, and easily induced triggering activity. All these can lead to arrhythmias development via the three classical mechanisms (reentrancy, automatism, or triggering activity). Transplanted stem cells can influence the electrophysiological properties of cardiomyocytes, thus creating a proarrhythmic substrate. The islets of unbound cells can form an anatomical block, causing unidirectional blockages and recurrent arrhythmias. Similarly, stem cells are capable of establishing heterotopic excitation foci with cardiac stimulatory activity. Finally, the paracrine factors produced by stem cells can also cause proarrhythmic effects. The review examines the factors that influence the proarrhythmic properties of administered stem cells and the mechanisms of arrhythmia development. The results indicate that further research should be carried out to establish the possible impact of stem cells on the development of arrhythmias.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40546030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lian Tang, Panfeng Feng, Yan Qi, Lei Huang, Xiuying Liang, Xia Chen
{"title":"TGFβ1 induces myofibroblast transdifferentiation via increasing Smad-mediated RhoGDI-RhoGTPase signaling.","authors":"Lian Tang, Panfeng Feng, Yan Qi, Lei Huang, Xiuying Liang, Xia Chen","doi":"10.4149/gpb_2022044","DOIUrl":"https://doi.org/10.4149/gpb_2022044","url":null,"abstract":"<p><p>This study serves to investigate the effects of the Smad pathway on TGFβ1-mediated RhoGDI expression and its binding to RhoGTPases in myofibroblast transdifferentiation. Myofibroblast transdifferentiation was induced by TGFβ1 in vitro. Cells were pretreated with different siRNAs or inhibitors. Myofibroblast transdifferentiation was detected by immunohistochemistry. Immunofluorescence was used to observe the nuclear translocation of Smad4, and PSR (Picrositius Red) staining was used to measure collagen concentration. TGFβ1 induced the phosphorylation of Smad2/3 and the nuclear translocation of Smad4 in human aortic adventitial fibroblasts (HAAFs). Furthermore, TGFβ1 increased the expression of RhoGDI and its binding to RhoGTPases. Nevertheless, inhibition of Smad2/3 phosphorylation decreased TGFβ1-induced RhoGDI1/2 expressions and RhoGDI2-RhoGTPases interactions. These data suggested that the inhibition of Smad phosphorylation attenuates myofibroblast transdifferentiation by inhibiting TGFβ1-induced RhoGDI1/2 expressions and RhoGDI-RhoGTPases signaling.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40456961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Ubiquitin specific peptidase 25 alleviates acute lung injury and suppresses the inflammatory response in lung epithelial cells.","authors":"Zhengzhen Xu, Qingrong Peng, Yanli Wang, Xiaobing Chen, Jinyan Zhang","doi":"10.4149/gpb_2022038","DOIUrl":"https://doi.org/10.4149/gpb_2022038","url":null,"abstract":"As COVID-19 spreads over the world, the treatment of acute lung injury (ALI) has attracted much attention. Considering ubiquitin-specific protease (USP) 25 has been relevant to inflammation, this article focused on its role in ALI and its regulatory mechanism. Lipopolysaccharide (LPS) was applied to separately stimulate mice and human lung epithelial cells to establish in vivo and in vitro ALI models. To discover the effects of USP25 overexpression on mouse, lung pathology, inflammatory factor levels, edema, number of inflammatory cells, and downstream protein levels were evaluated. USP25 overexpression in mice could alleviate LPS-induced lung tissue lesions and edema, and reduce inflammatory factors and inflammatory cells. It also inhibited the levels of downstream TRAF6, MAPK pathway-related proteins, and Fos Proto-Oncogene (FOS) in vivo. Furthermore, BEAS-2B cells were transfected with TNF receptor-associated factor 6 (TRAF6) plasmids to study the role of TRAF6 in the regulatory mechanism of USP25. TRAF6 overexpression was found to reverse the functions of USP25 overexpression on cells. In conclusion, USP25 reduced ALI and inhibited inflammation in lung epithelial cells via regulating TRAF6/MAPK/FOS signaling.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40456905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Dominika Hajduchova, Roman Holic, Peter Gajdos, Milan Certik, Erika Halasova, Renata Pecova, Michal Pokusa
{"title":"Correlation between α-synuclein and fatty acid composition in jejunum of rotenone-treated mice is dependent on acyl chain length.","authors":"Dominika Hajduchova, Roman Holic, Peter Gajdos, Milan Certik, Erika Halasova, Renata Pecova, Michal Pokusa","doi":"10.4149/gpb_2022046","DOIUrl":"https://doi.org/10.4149/gpb_2022046","url":null,"abstract":"<p><p>Events associated with the progression of Parkinson´s disease (PD) are closely related to biomembrane dysfunction. The specific role of membrane composition in the conformational stability of alpha synuclein (αS) has already been well documented. Administration of rotenone is one of the best strategies to initiate PD phenotype in animal models. In the present study, daily exposure (14 weeks) of orally administered rotenone (10 mg/kg) was employed in a mouse model. The mitochondrial complex I inhibition resulted in elevated level of αS in whole tissue homogenate of mouse jejunum. In addition, we identified a strong intra-individual correlation between αS level and the specific esterified fatty acids. The observed correlation depends mainly on the acyl chain length. Based on the obtained results, it is suggested that there is a high potential to manipulate fatty acid homeostasis in modulating αS based pathogenesis of PD, at least in experimental conditions.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40459362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The ubiquitin-editing enzyme TNFAIP3 exerts neuroprotective roles in epilepsy rats through repressing inflammation.","authors":"Zhihong Zhuo, Huimin Kong, Peina Jin, Youhong Ren","doi":"10.4149/gpb_2022041","DOIUrl":"https://doi.org/10.4149/gpb_2022041","url":null,"abstract":"<p><p>The ubiquitin-editing enzyme TNF alpha-induced protein 3 (TNFAIP3) emerges protective roles in neurological disorder, such as cerebral trauma. However, the molecular mechanisms of TNFAIP3 in epilepsy are not very clear. Hereon, the epileptic mouse models and BV2 microglial cellular models were established by kainic acid (KA) and lipopolysaccharide (LPS) respectively. We found that TNFAIP3 was highly expressed in the hippocampus of epileptic mice. Besides, TNFAIP3 overexpression relieved the spatial learning and memory, reduced the hot plate latency, as well as inhibited neuronal apoptosis in KA-treated mice. In vivo and in vitro experiments indicated that inflammation, a key characteristic of epilepsy, was inhibited by TNFAIP3 upregulation, as evidenced by the downregulated expression of pro-inflammatory cytokine interleukin (IL)-1β and inducible NO synthase (iNOS), along with the decreased levels of NLRP3 inflammasome, which could activate inflammation. Collectively, we infer that TNFAIP3 relieves neuronal injury in epilepsy by suppressing inflammation.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40556495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jinshuai Ma, Dianpu Zhang, Meng Lv, Qiqi Pan, Xiuxiang Liu
{"title":"Wnt7b/β-catenin signaling pathway mediated by retinoid acid involved in the transdifferentiation of primary fetal alveolar epithelial type II cells.","authors":"Jinshuai Ma, Dianpu Zhang, Meng Lv, Qiqi Pan, Xiuxiang Liu","doi":"10.4149/gpb_2022037","DOIUrl":"https://doi.org/10.4149/gpb_2022037","url":null,"abstract":"<p><p>This study was designed to investigate the roles of retinoic acid (RA) in transdifferentiation of primary fetal alveolar epithelial type II cells (AECIIs) into alveolar epithelial type I cells (AECIs). Primary fetal AECIIs isolated from rats at a gestational of 19 days were divided into: (i) DMSO group treated using 0.1% DMSO; (ii) RA group, treated with 1 μM RA; and (iii) RA+BMS493 group treated with 1 μM RA and 10<sup>-8</sup> M BMS493 (served as a pan-RA receptor antagonist). Then we determined the roles of AQP5 (a specific marker of AECIs), SP-C (a specific marker for AECIIs) and Wnt7b/β- catenin signaling pathway in the transdifferentiation of AECIIs to AECIs. SP-C mRNA and protein expression was significantly down-regulated in AECIIs exposure to RA for 24 h and 48 h, however, significant up-regulation was noticed after exposure for 72 h. AQP5 mRNA and protein expression showed significant increase in RA group, but showed significant decline in the RA+BMS493 group. Wnt7b mRNA, nucleus β-catenin and cyclin D1 were significantly up-regulated in RA group compared with DMSO group. RA may promote fetal AECIIs transdifferentiation into AECIs through activating Wnt7b/β-catenin signaling pathway. Our study contributed to the understanding on the pulmonary regeneration in cases of pulmonary injuries, together with the prevention and treatment of neonatal respiratory distress syndrome.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40456903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Junhu Wang, Qian Wen, Xinwen Wang, Cheng Liu, Kai Zhao, Yi Li, Jie Yang, Xiaojun Liang
{"title":"Nomogram for predicting cancer-specific survival of patients with clear-cell renal cell carcinoma: a SEER-based population study.","authors":"Junhu Wang, Qian Wen, Xinwen Wang, Cheng Liu, Kai Zhao, Yi Li, Jie Yang, Xiaojun Liang","doi":"10.4149/gpb_2022040","DOIUrl":"https://doi.org/10.4149/gpb_2022040","url":null,"abstract":"<p><p>This study was aimed to develop a nomogram for predicting the cancer-specific survival (CSS) of patients with clear-cell renal cell carcinoma (ccRCC). Based on the Surveillance, Epidemiology, and End Results (SEER) database, 24,477 patients diagnosed with ccRCC between 2010 and 2015 were collected. They were randomly divided into a training cohort (n = 17,133) and a validation cohort (n = 7,344). Univariate and multivariate Cox regression analyses were performed in the training cohort to identify independent prognostic factors for construction of nomogram. Then, the nomogram was used to predict the 3- and 5-year CSS. The performance of nomogram was evaluated by using concordance index (C-index), net reclassification improvement (NRI), integrated discrimination improvement (IDI), calibration curve, and decision curve analysis (DCA). Moreover, the nomogram and tumor node metastasis (TNM) staging system (AJCC 7th edition) were compared. Eleven variables were screened to develop the nomogram. The area under the receiver operating characteristic (ROC) curve (AUC) and the calibration plots indicated satisfactory ability of the nomogram. Compared with the AJCC 7th edition of TNM stage, C-index, NRI, and IDI showed that the nomogram had improved performance. Furthermore, the 3- and 5-year DCA curves of nomogram yielded more net benefits than the AJCC 7th edition of TNM stage in both the training and validation sets. We developed and validated a nomogram for predicting the CSS of patients with ccRCC, which was more precise than the AJCC 7th edition of TNM staging system.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10718881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Homocysteine promotes migration of adventitial fibroblasts via angiotensin II type 1 receptor activation to aggravate atherosclerosis.","authors":"Zhibo Zhu, Sujuan Li, Yuchen Jia, Jianqiang Guo","doi":"10.4149/gpb_2022039","DOIUrl":"https://doi.org/10.4149/gpb_2022039","url":null,"abstract":"<p><p>This study clarified the effect of homocysteine on adventitial fibroblasts (AFs) and its relationship with angiotensin II type 1 receptor (AT1R). Hyperhomocysteinemia aggravated the plaque area and increased the expression of IL-6, MCP-1, and macrophage infiltration in the plaque and adventitia of the aorta, whereas telmisartan improved this effect. Hyperhomocysteinemia induced the occurrence of the AFs marker protein ER-TR7 in the plaque and entire layer of the aorta, whereas telmisartan improved these effects, indicating that homocysteine induced AFs migration and that AT1R mediated this process. The migration experiments of AFs also reached the same conclusion. Homocysteine increased the phosphorylation levels of PKC and ERK1/2 in the AFs and HEK293A cells transfected with the AT1R plasmid, whereas telmisartan inhibited this effect, indicating that homocysteine activated AT1R intracellular signaling pathway. Homocysteine also increased the AFs At1R expression. Conclusion, homocysteine promoted adventitial inflammation, induced AFs migration, and aggravated atherosclerosis by activating AT1R.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40456962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}