Efficient management of foot disorders requires knowledge of plausible sexual dimorphic differences in the foot structure and function. Knowledge about foot dimorphism is yet unsettled. In the present study, we mapped the multizone plantar pressure distribution in a cohort of 298 healthy subjects of both sexes using the piezoelectric pedobarographic recordings. We investigated the hypothesis that sexual foot dimorphism would entail differences in plantar pressure distribution. We delved into the issue using the k-nearest neighbors' classifier (k-NN), a supervised machine learning algorithm, to predict the correct foot phenotype classification based on the plantar pressure and anthropometric and structural features. Based on the similarity measures, the classifier assigns unknown input data to the most common class, men or women, among the closest neighbors. The major finding was the unraveling of sex-specific foot dimorphism in healthy people. The k-NN was able to recognize the person's sex based on a few discriminatory features, with an outstandingly low misclassification rate. The pressure distribution on the plantar surface of the great toe, one of the orthopedic plantar surface zones, is the most distinct feature in differentiating the foot phenotype. The results also unraveled the presence of individuals whose foot features paradoxically corresponded with those classified for the opposite sex, i.e., the female foot was classified in the men's group and vice versa. In conclusion, the study supports the presence of sexual foot dimorphism. A pedobarographic examination supplemented with the k-NN algorithm for machine learning allows one to discriminate the foot sexual phenotype with high accuracy. The foot phenotype identities exist outside the gender binary. Insights into sexual foot dimorphism may streamline the management of foot disorders. Keywords Biomechanics " Foot " K-nearest neighbors' algorithm " Pedobarography " Plantar pressure " Foot dimorphism.
{"title":"Sexual Dimorphism in Plantar Pressure Distribution Patterns.","authors":"J Lorkowski, A Jóźwik, M Pokorski","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Efficient management of foot disorders requires knowledge of plausible sexual dimorphic differences in the foot structure and function. Knowledge about foot dimorphism is yet unsettled. In the present study, we mapped the multizone plantar pressure distribution in a cohort of 298 healthy subjects of both sexes using the piezoelectric pedobarographic recordings. We investigated the hypothesis that sexual foot dimorphism would entail differences in plantar pressure distribution. We delved into the issue using the k-nearest neighbors' classifier (k-NN), a supervised machine learning algorithm, to predict the correct foot phenotype classification based on the plantar pressure and anthropometric and structural features. Based on the similarity measures, the classifier assigns unknown input data to the most common class, men or women, among the closest neighbors. The major finding was the unraveling of sex-specific foot dimorphism in healthy people. The k-NN was able to recognize the person's sex based on a few discriminatory features, with an outstandingly low misclassification rate. The pressure distribution on the plantar surface of the great toe, one of the orthopedic plantar surface zones, is the most distinct feature in differentiating the foot phenotype. The results also unraveled the presence of individuals whose foot features paradoxically corresponded with those classified for the opposite sex, i.e., the female foot was classified in the men's group and vice versa. In conclusion, the study supports the presence of sexual foot dimorphism. A pedobarographic examination supplemented with the k-NN algorithm for machine learning allows one to discriminate the foot sexual phenotype with high accuracy. The foot phenotype identities exist outside the gender binary. Insights into sexual foot dimorphism may streamline the management of foot disorders. Keywords Biomechanics \" Foot \" K-nearest neighbors' algorithm \" Pedobarography \" Plantar pressure \" Foot dimorphism.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 6","pages":"999-1005"},"PeriodicalIF":2.0,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12721814/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145775261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ling-Ling Zou, Wu Dai, Jun Ye, Yong-Hong Cao, Fa-Hui Lv
This study aimed to evaluate the predictive value of serum 25 hydroxyvitamin D (25(OH) D) levels in relation to the onset and glycemic control of gestational diabetes mellitus (GDM). This retrospective study analyzed clinical data of pregnant women who received routine prenatal care and were hospitalized at the Second People's Hospital of Hefei between January 2023 and January 2025. The study included 200 pregnant women diagnosed with GDM (study group) and 200 gestational age-matched pregnant women with normoglycemia (control group), selected through random sampling. Within the study group, 146 participants exhibited standard glycemic control (Y1 group), while 54 participants exhibited non-standard glycemic control (Y2 group) during hospitalization in the third trimester. Significant differences in serum 25(OH)D levels were observed between the control and study groups across all trimesters (53.82 ± 9.43), (56.73 ± 11.28), (49.65 ± 10.65) nmol/L, and (45.87 ± 8.45), (44.42 ± 10.04), (46.63 ± 9.87) nmol/L (p < 0.05). In the second trimester, serum 25(OH)D levels were negatively correlated with the oral glucose tolerance test (OGTT) values in the study group (p < 0.05). Comparison of the 25(OH)D levels in the third trimester between the Y1 group (48.95 ± 9.46) and the Y2 group (42.75 ± 10.23) nmol/L indicated that there was no significant statistical difference between the study group and the control group (49.65 ± 10.65 nmol/L) (p > 0.05). A receiver operating characteristic curve for first trimester 25(OH)D levels of pregnant women in the study group yielded an area under the curve of 0.84. Lower serum 25(OH)D levels were associated with an elevated risk of developing GDM and with poorer glycemic control in affected women. These findings indicate that first trimester serum 25(OH)D levels may serve as a valuable biomarker for the early prediction and management of GDM. Keywords Blood glucose " Correlation " Gestational diabetes mellitus " Pregnant women " 25-hydroxyvitamin D.
{"title":"Predictive Value of Serum 25-Hydroxyvitamin D Levels in the Onset and Glycemic Control of Gestational Diabetes Mellitus.","authors":"Ling-Ling Zou, Wu Dai, Jun Ye, Yong-Hong Cao, Fa-Hui Lv","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This study aimed to evaluate the predictive value of serum 25 hydroxyvitamin D (25(OH) D) levels in relation to the onset and glycemic control of gestational diabetes mellitus (GDM). This retrospective study analyzed clinical data of pregnant women who received routine prenatal care and were hospitalized at the Second People's Hospital of Hefei between January 2023 and January 2025. The study included 200 pregnant women diagnosed with GDM (study group) and 200 gestational age-matched pregnant women with normoglycemia (control group), selected through random sampling. Within the study group, 146 participants exhibited standard glycemic control (Y1 group), while 54 participants exhibited non-standard glycemic control (Y2 group) during hospitalization in the third trimester. Significant differences in serum 25(OH)D levels were observed between the control and study groups across all trimesters (53.82 ± 9.43), (56.73 ± 11.28), (49.65 ± 10.65) nmol/L, and (45.87 ± 8.45), (44.42 ± 10.04), (46.63 ± 9.87) nmol/L (p < 0.05). In the second trimester, serum 25(OH)D levels were negatively correlated with the oral glucose tolerance test (OGTT) values in the study group (p < 0.05). Comparison of the 25(OH)D levels in the third trimester between the Y1 group (48.95 ± 9.46) and the Y2 group (42.75 ± 10.23) nmol/L indicated that there was no significant statistical difference between the study group and the control group (49.65 ± 10.65 nmol/L) (p > 0.05). A receiver operating characteristic curve for first trimester 25(OH)D levels of pregnant women in the study group yielded an area under the curve of 0.84. Lower serum 25(OH)D levels were associated with an elevated risk of developing GDM and with poorer glycemic control in affected women. These findings indicate that first trimester serum 25(OH)D levels may serve as a valuable biomarker for the early prediction and management of GDM. Keywords Blood glucose \" Correlation \" Gestational diabetes mellitus \" Pregnant women \" 25-hydroxyvitamin D.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 6","pages":"981-987"},"PeriodicalIF":2.0,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12721828/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145775111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The aim of this observational, descriptive, and cross-sectional study was to analyze the relationship between phase angle (PhA), determined by bioelectrical impedance analysis (BIA), and body composition parameters in healthy adult individuals. The study included 265 participants (122 women and 143 men) aged 18-77 years, examined at a nutritional outpatient clinic in Prague between April 2022 and December 2023. Segmental multi-frequency BIA was performed using the Tanita MC-780 MA analyzer with eight electrodes and frequencies of 5 kHz, 50 kHz, and 250 kHz. The mean PhA values were significantly higher in men than in women (6.29° vs. 5.57°; p < 0.001). A strong negative correlation between the extracellular water-to-total body water ratio (ECW/TBW) and PhA was observed in men (r = 0.78; p < 0.001), whereas in women, the correlation was moderate (r = -0.33; p < 0.001). Conversely, a strong positive correlation was observed between PhA and intracellular water (ICW) volume in women (r = 0.71; p < 0.001), while in men this association was weaker (r = 0.17; p < 0.05). The data indicate that PhA is significantly correlated with body fluid distribution and body composition. The key determinants differ by sex-fat mass, particularly visceral fat, plays a predominant role in men, while in women, muscle mass appears to be the dominant factor. PhA thus emerges as a valid, non-invasive marker of body composition, sensitive to changes in internal milieu, with potential clinical applications for assessing nutritional status and the patient's physiological condition. Keywords Bioelectrical impedance analysis " Phase angle " Body composition " Sex characteristics " Body water distribution.
这项观察性、描述性和横断面研究的目的是分析由生物电阻抗分析(BIA)确定的相位角(PhA)与健康成人身体成分参数之间的关系。该研究包括265名参与者(122名女性和143名男性),年龄在18-77岁之间,于2022年4月至2023年12月在布拉格的一家营养门诊进行了检查。使用Tanita MC-780 MA分析仪进行分段多频BIA,有8个电极,频率为5 kHz, 50 kHz和250 kHz。男性的平均PhA值显著高于女性(6.29°vs. 5.57°;p < 0.001)。在男性中观察到细胞外水与全身水比(ECW/TBW)与PhA之间存在很强的负相关(r = 0.78, p < 0.001),而在女性中,相关性为中度(r = -0.33, p < 0.001)。相反,在女性中,PhA与细胞内水(ICW)体积呈正相关(r = 0.71, p < 0.001),而在男性中,这种相关性较弱(r = 0.17, p < 0.05)。数据表明,PhA与体液分布和身体成分显著相关。关键的决定因素因性别而异——脂肪量,尤其是内脏脂肪,在男性中起主导作用,而在女性中,肌肉量似乎是主导因素。因此,PhA作为一种有效的、非侵入性的身体成分标记物,对体内环境的变化很敏感,在评估营养状况和患者生理状况方面具有潜在的临床应用价值。关键词:生物电阻抗分析;相角;人体组成;
{"title":"Phase Angle in Bioelectrical Impedance: New Perspectives in Health and Body Composition Assessment.","authors":"J Jirků, J Křížová","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The aim of this observational, descriptive, and cross-sectional study was to analyze the relationship between phase angle (PhA), determined by bioelectrical impedance analysis (BIA), and body composition parameters in healthy adult individuals. The study included 265 participants (122 women and 143 men) aged 18-77 years, examined at a nutritional outpatient clinic in Prague between April 2022 and December 2023. Segmental multi-frequency BIA was performed using the Tanita MC-780 MA analyzer with eight electrodes and frequencies of 5 kHz, 50 kHz, and 250 kHz. The mean PhA values were significantly higher in men than in women (6.29° vs. 5.57°; p < 0.001). A strong negative correlation between the extracellular water-to-total body water ratio (ECW/TBW) and PhA was observed in men (r = 0.78; p < 0.001), whereas in women, the correlation was moderate (r = -0.33; p < 0.001). Conversely, a strong positive correlation was observed between PhA and intracellular water (ICW) volume in women (r = 0.71; p < 0.001), while in men this association was weaker (r = 0.17; p < 0.05). The data indicate that PhA is significantly correlated with body fluid distribution and body composition. The key determinants differ by sex-fat mass, particularly visceral fat, plays a predominant role in men, while in women, muscle mass appears to be the dominant factor. PhA thus emerges as a valid, non-invasive marker of body composition, sensitive to changes in internal milieu, with potential clinical applications for assessing nutritional status and the patient's physiological condition. Keywords Bioelectrical impedance analysis \" Phase angle \" Body composition \" Sex characteristics \" Body water distribution.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 6","pages":"1007-1019"},"PeriodicalIF":2.0,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12721815/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145774807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
P Mlejnek, M Šimáková, J Šilhavý, T Mráček, J Houštěk, I Marková, M Hüttl, H Malínská, M Pravenec
The spontaneously hypertensive rat (SHR) is a widely used model of essential hypertension that also exhibits metabolic disturbances under specific conditions. Oxidative stress plays a central role in the pathogenesis of both hypertension and metabolic dysfunction, with the transcription factor Nrf2 regulating key antioxidant defenses. Here, we examined whether Nrf2 overexpression in the SHR improves adipose tissue metabolism. A mouse Nrf2 transgene under a universal promoter was markedly overexpressed in white adipose tissue, leading to increased insulin sensitivity, reduced saturated fatty acids, and higher n-3 polyunsaturated fatty acids in adipose membrane phospholipids. Transgenic rats also displayed reduced mitochondrial complex I levels, enhanced antioxidant enzyme activities, and decreased lipoperoxidation. Transcriptomic analysis revealed downregulation of oxidative phosphorylation genes. These findings suggest that Nrf2 overexpression confers antidiabetic and hypolipidemic effects in the SHR, potentially via redox-sensitive remodeling of adipose tissue metabolism. Key words: Nrf2 o Spontaneously hypertensive rat (SHR) o Oxidative stress o Adipose tissue o Metabolism o Mitochondrial function o Oxidative phosphorylation o Antioxidant defense o Insulin sensitivity o Fatty acids o transcriptomics o Transgenic rats o Gene expression.
{"title":"Nrf2 Overexpression in Spontaneously Hypertensive Rats Enhances Adipose Tissue Metabolism through Redox-Mediated Suppression of Mitochondrial Oxidative Phosphorylation.","authors":"P Mlejnek, M Šimáková, J Šilhavý, T Mráček, J Houštěk, I Marková, M Hüttl, H Malínská, M Pravenec","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The spontaneously hypertensive rat (SHR) is a widely used model of essential hypertension that also exhibits metabolic disturbances under specific conditions. Oxidative stress plays a central role in the pathogenesis of both hypertension and metabolic dysfunction, with the transcription factor Nrf2 regulating key antioxidant defenses. Here, we examined whether Nrf2 overexpression in the SHR improves adipose tissue metabolism. A mouse Nrf2 transgene under a universal promoter was markedly overexpressed in white adipose tissue, leading to increased insulin sensitivity, reduced saturated fatty acids, and higher n-3 polyunsaturated fatty acids in adipose membrane phospholipids. Transgenic rats also displayed reduced mitochondrial complex I levels, enhanced antioxidant enzyme activities, and decreased lipoperoxidation. Transcriptomic analysis revealed downregulation of oxidative phosphorylation genes. These findings suggest that Nrf2 overexpression confers antidiabetic and hypolipidemic effects in the SHR, potentially via redox-sensitive remodeling of adipose tissue metabolism. Key words: Nrf2 o Spontaneously hypertensive rat (SHR) o Oxidative stress o Adipose tissue o Metabolism o Mitochondrial function o Oxidative phosphorylation o Antioxidant defense o Insulin sensitivity o Fatty acids o transcriptomics o Transgenic rats o Gene expression.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 6","pages":"923-934"},"PeriodicalIF":2.0,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12721821/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145774488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The growing popularity of microgreens is due to several health-promoting effects. Current evidence suggests a reduction in the risk of cardiovascular and neurodegenerative diseases, or anti-carcinogenic and anti-inflammatory effects. However, in vitro studies investigating cellular changes and molecular mechanisms are limited. Therefore, the use of various cell lines is required for a better understanding of microgreens' effects. In this study, the effect of Trigonella-foenum graecum L. microgreens (10 300 µg/mL) extract on morphological and functional changes in HUVEC cells were investigated. Basic cellular parameters such as mitochondrial activity (MTT assay), cell membrane integrity (CFDA-AM assay), and lysosomal activity (NR uptake) were evaluated after 24 h exposure to experimental ethanolic extract. In addition, the release of cytokine IL-6 was measured. Results revealed significant changes (p<0.05; p<0.01) in mitochondrial activity, followed by no defect in cell membrane integrity and non-significant changes in lysosomal activity of HUVEC cells. At the same time, some experimental doses of Trigonella slightly modulate IL-6 release, but showed no significant changes after 24 h exposure. Overall, our pilot study suggests the potential of Trigonella microgreens to modulate mitochondrial activity of HUVEC cells, without significant changes in cell membrane integrity, lysosomal activity, or IL-6 release. Key words Trigonella-foenum graecum L. " Microgreens " Cytokines " HUVEC cells.
{"title":"Potential Effect of Trigonella Microgreens on Functional Parameters of HUVEC Cells in vitro.","authors":"T Jambor, Z Goc, K Tokarova, N Lukac","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The growing popularity of microgreens is due to several health-promoting effects. Current evidence suggests a reduction in the risk of cardiovascular and neurodegenerative diseases, or anti-carcinogenic and anti-inflammatory effects. However, in vitro studies investigating cellular changes and molecular mechanisms are limited. Therefore, the use of various cell lines is required for a better understanding of microgreens' effects. In this study, the effect of Trigonella-foenum graecum L. microgreens (10 300 µg/mL) extract on morphological and functional changes in HUVEC cells were investigated. Basic cellular parameters such as mitochondrial activity (MTT assay), cell membrane integrity (CFDA-AM assay), and lysosomal activity (NR uptake) were evaluated after 24 h exposure to experimental ethanolic extract. In addition, the release of cytokine IL-6 was measured. Results revealed significant changes (p<0.05; p<0.01) in mitochondrial activity, followed by no defect in cell membrane integrity and non-significant changes in lysosomal activity of HUVEC cells. At the same time, some experimental doses of Trigonella slightly modulate IL-6 release, but showed no significant changes after 24 h exposure. Overall, our pilot study suggests the potential of Trigonella microgreens to modulate mitochondrial activity of HUVEC cells, without significant changes in cell membrane integrity, lysosomal activity, or IL-6 release. Key words Trigonella-foenum graecum L. \" Microgreens \" Cytokines \" HUVEC cells.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 6","pages":"1027-1031"},"PeriodicalIF":2.0,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12721813/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145774824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
R Tanimura, H Watanabe, T Shirai, K Uemichi, T Iwata, T Takemasa
Combining diet and physical activity is known to be more effective for health than either intervention alone. Recent research has shown that skeletal muscle secretes myokines in response to exercise, which contribute to the adaptation of other organs to exercise. Therefore, we hypothesized that muscle adaptation by calorie restriction (CR) might enhance myokine responses to exercise. It is known that the myokine fibroblast growth factor-21 (FGF-21) secreted by skeletal muscle during exercise activates adipose tissue browning. We have already reported that irisin, a myokine that contributes to the metabolic activation of adipose tissue and weight loss, is secreted in response to muscle contraction by electrical stimulation (ES). Thus, we investigated the secretion of FGF21 and irisin upon the combination of ES with CR in this study. Mice were divided into four groups: control mice (Con), calorie restriction mice (CR), acute muscle contraction mice (ES), and acute muscle contraction after calorie restriction mice (CRES). After 1 week of acclimation, we subjected the mice to 60 % calorie restriction. After 2 weeks of CR, we performed ES. The results showed that the irisin expression level in serum was significantly increased by the combination of ES and CR, and an interaction between CR and ES was confirmed. FGF21 expression in serum was significantly decreased by CR. In conclusion, we confirm that irisin is a myokine whose secretion is increased synergistically by CR and muscle contraction. Keywords Muscle " Calorie restriction " Myokine " Irisin " FGF21.
{"title":"Effect of Muscle Contraction Under Caloric Restriction on Irisin and FGF21 Secretion in Mice.","authors":"R Tanimura, H Watanabe, T Shirai, K Uemichi, T Iwata, T Takemasa","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Combining diet and physical activity is known to be more effective for health than either intervention alone. Recent research has shown that skeletal muscle secretes myokines in response to exercise, which contribute to the adaptation of other organs to exercise. Therefore, we hypothesized that muscle adaptation by calorie restriction (CR) might enhance myokine responses to exercise. It is known that the myokine fibroblast growth factor-21 (FGF-21) secreted by skeletal muscle during exercise activates adipose tissue browning. We have already reported that irisin, a myokine that contributes to the metabolic activation of adipose tissue and weight loss, is secreted in response to muscle contraction by electrical stimulation (ES). Thus, we investigated the secretion of FGF21 and irisin upon the combination of ES with CR in this study. Mice were divided into four groups: control mice (Con), calorie restriction mice (CR), acute muscle contraction mice (ES), and acute muscle contraction after calorie restriction mice (CRES). After 1 week of acclimation, we subjected the mice to 60 % calorie restriction. After 2 weeks of CR, we performed ES. The results showed that the irisin expression level in serum was significantly increased by the combination of ES and CR, and an interaction between CR and ES was confirmed. FGF21 expression in serum was significantly decreased by CR. In conclusion, we confirm that irisin is a myokine whose secretion is increased synergistically by CR and muscle contraction. Keywords Muscle \" Calorie restriction \" Myokine \" Irisin \" FGF21.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 6","pages":"969-980"},"PeriodicalIF":2.0,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12721820/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145775536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
P Škrha, A Hořínek, J Hajer, J Potočková, P Frič, J Bureš, M Anděl, J Škrha
Sustained poor survival rate in pancreatic ductal adenocarcinoma (PDAC) calls for an earlier diagnosis to assure curative treatment. New powerful biomarkers are necessary because the currently used CA19-9 is not sensitive enough to distinguish PDAC, especially from chronic pancreatitis (CP). Expressions of miRNA-21, -30 -192, -196, -200, and -423 were measured in 77 patients with PDAC, 26 patients with CP and 64 non-cancer/non-CP subjects (39 patients with type 2 diabetes mellitus and 25 control healthy persons). Eleven patients with PDAC had CP at the background. The expressions of all microRNAs were significantly 1.4-3.7 times higher in the PDAC group compared to non-cancer/non-CP subjects and 2.2-6.1 times higher compared to CP patients. No difference in miRNA expressions was found between diabetic and non-diabetic patients. CA19-9 did not distinguish CP from PDAC patients with the history of CP, whereas all six miRNAs were able to do it. Adding miR-196, -200 and -423 to current marker CA19-9 improved sensitivity by 7 % (to 93 %) and specificity by 8 % (to 89 %). MicroRNA-423 could significantly distinguish PDAC from CP with both sensitivity and specificity 96 %. Panel of six miRNAs could be used as reliable marker in differentiating PDAC from chronic pancreatitis with the most impressive difference in miR-196 and miR-423. Key words microRNA " Pancreatic ductal adenocarcinoma " Chronic pancreatitis " Biomarker " CA19-9.
{"title":"Serum MicroRNA-196, -200 and -423 Improve Diagnostics and Differentiate Pancreatic Ductal Adenocarcinoma From Chronic Pancreatitis.","authors":"P Škrha, A Hořínek, J Hajer, J Potočková, P Frič, J Bureš, M Anděl, J Škrha","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Sustained poor survival rate in pancreatic ductal adenocarcinoma (PDAC) calls for an earlier diagnosis to assure curative treatment. New powerful biomarkers are necessary because the currently used CA19-9 is not sensitive enough to distinguish PDAC, especially from chronic pancreatitis (CP). Expressions of miRNA-21, -30 -192, -196, -200, and -423 were measured in 77 patients with PDAC, 26 patients with CP and 64 non-cancer/non-CP subjects (39 patients with type 2 diabetes mellitus and 25 control healthy persons). Eleven patients with PDAC had CP at the background. The expressions of all microRNAs were significantly 1.4-3.7 times higher in the PDAC group compared to non-cancer/non-CP subjects and 2.2-6.1 times higher compared to CP patients. No difference in miRNA expressions was found between diabetic and non-diabetic patients. CA19-9 did not distinguish CP from PDAC patients with the history of CP, whereas all six miRNAs were able to do it. Adding miR-196, -200 and -423 to current marker CA19-9 improved sensitivity by 7 % (to 93 %) and specificity by 8 % (to 89 %). MicroRNA-423 could significantly distinguish PDAC from CP with both sensitivity and specificity 96 %. Panel of six miRNAs could be used as reliable marker in differentiating PDAC from chronic pancreatitis with the most impressive difference in miR-196 and miR-423. Key words microRNA \" Pancreatic ductal adenocarcinoma \" Chronic pancreatitis \" Biomarker \" CA19-9.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 5","pages":"837-847"},"PeriodicalIF":2.0,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12746859/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145661834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
D Rajdl, M Šolcová, J Racek, D Suchý, H Vimmerová, P Broz, P Prokop
Cardiac troponins are indispensable biomarkers for the diagnosis of acute myocardial infarction, but false-positive elevations that contradict the clinical picture remain a significant challenge in laboratory medicine. Analytical interferences may arise from macrotroponins, heterophile or anti-troponin antibodies, and the limited cardiac specificity of high-sensitivity troponin T (hs-cTnT) in skeletal muscle disease. Recent studies show that hs-cTnT is elevated in up to two-thirds of patients with myopathies, while high-sensitivity troponin I (hs-cTnI) is largely unaffected, underscoring the diagnostic advantage of hs-cTnI in this setting. A pragmatic diagnostic approach should combine clinical plausibility with stepwise laboratory testing. First, preanalytical factors such as sample mislabeling, fibrin clots, or hemolysis must be excluded and the measurement repeated. If the results remain incongruent, an alternative assay - ideally hs-cTnI - should be performed. Further evaluation may include heterophile-blocking reagents, polyethylene glycol precipitation to screen for macro-analytes, and, where available, confirmatory techniques such as gel filtration chromatography or immunoglobulin depletion (protein A/G). Although these strategies can help identify assay interference, there is no universally accepted gold standard. Awareness of false-positive elevations, careful interpretation of discordant troponin results, and effective collaboration between laboratories and clinicians are essential to prevent misdiagnosis and unnecessary interventions. Clear documentation of confirmed interferences further ensures safe patient management and provides guidance on which assays are reliable for future tests. Key words Cardiac troponin " Skeletal muscle disease " False-positive results " Analytical interference " Macrotroponin " Laboratory diagnostics.
{"title":"False-Positive Cardiac Troponin Elevations in Skeletal Muscle Disease: Clinical Relevance, Mechanisms, and Laboratory Approaches.","authors":"D Rajdl, M Šolcová, J Racek, D Suchý, H Vimmerová, P Broz, P Prokop","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Cardiac troponins are indispensable biomarkers for the diagnosis of acute myocardial infarction, but false-positive elevations that contradict the clinical picture remain a significant challenge in laboratory medicine. Analytical interferences may arise from macrotroponins, heterophile or anti-troponin antibodies, and the limited cardiac specificity of high-sensitivity troponin T (hs-cTnT) in skeletal muscle disease. Recent studies show that hs-cTnT is elevated in up to two-thirds of patients with myopathies, while high-sensitivity troponin I (hs-cTnI) is largely unaffected, underscoring the diagnostic advantage of hs-cTnI in this setting. A pragmatic diagnostic approach should combine clinical plausibility with stepwise laboratory testing. First, preanalytical factors such as sample mislabeling, fibrin clots, or hemolysis must be excluded and the measurement repeated. If the results remain incongruent, an alternative assay - ideally hs-cTnI - should be performed. Further evaluation may include heterophile-blocking reagents, polyethylene glycol precipitation to screen for macro-analytes, and, where available, confirmatory techniques such as gel filtration chromatography or immunoglobulin depletion (protein A/G). Although these strategies can help identify assay interference, there is no universally accepted gold standard. Awareness of false-positive elevations, careful interpretation of discordant troponin results, and effective collaboration between laboratories and clinicians are essential to prevent misdiagnosis and unnecessary interventions. Clear documentation of confirmed interferences further ensures safe patient management and provides guidance on which assays are reliable for future tests. Key words Cardiac troponin \" Skeletal muscle disease \" False-positive results \" Analytical interference \" Macrotroponin \" Laboratory diagnostics.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 5","pages":"885-889"},"PeriodicalIF":2.0,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12746863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145661807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
High mortality rates among patients with acute respiratory distress syndrome (ARDS) have been linked to pulmonary fibrosis. MicroRNAs exhibit significant potential in modulating pulmonary fibrosis. However, the specific role and underlying mechanisms of miR-93-5p in the context of ARDS-associated pulmonary fibrosis remain largely unexplored. Mitofusin 2 (Mfn2) is a highly conserved transmembrane GTPase. Our previous study demonstrated that the upregulation of Mfn2 can inhibit pulmonary fibrosis in ARDS mice. In this investigation, we identified upstream miRNAs regulating Mfn2 using bioinformatics tools such as TargetScan, miRDB, and microT-CDS. Based on the expression levels of these miRNAs in lung tissue from rats with LPS-induced ARDS, miR-93-5p was selected as the focus of our research. We modulated miR-93-5p expression in ARDS rats via tail vein injection of a miR-93-5p antagomir. Thereafter, we conducted pathological staining and molecular assays to examine the impact of miR-93-5p on pulmonary fibrosis in ARDS rats and to elucidate its potential mechanisms. The results demonstrated that the expression of miR-93-5p was significantly upregulated in the lung tissue of ARDS rats. LPS-induced ARDS rats exhibited severe pulmonary fibrosis, inflammation, and strong endoplasmic reticulum (ER) stress. Furthermore, Mfn2 expression exhibited a negative correlation with miR-93-5p expression. Inhibition of miR-93-5p markedly upregulated Mfn2 expression, attenuated ER stress and lung inflammation, and decreased collagen deposition. In conclusion, the inhibition of miR-93-5p upregulated Mfn2 expression and attenuated ER stress, consequently ameliorating pulmonary fibrosis in ARDS rats. Key words Acute respiratory distress syndrome " miR-93-5p " Pulmonary fibrosis " Endoplasmic reticulum stress " Mitofusin 2.
{"title":"Targeting of miR-93-5p/Mfn2 Axis Attenuates Lung Fibrosis in Rats With Acute Respiratory Distress Syndrome by Regulating Endoplasmic Reticulum Stress.","authors":"X Zhang, T Liu, Z Dai, Q Zhao, N An","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>High mortality rates among patients with acute respiratory distress syndrome (ARDS) have been linked to pulmonary fibrosis. MicroRNAs exhibit significant potential in modulating pulmonary fibrosis. However, the specific role and underlying mechanisms of miR-93-5p in the context of ARDS-associated pulmonary fibrosis remain largely unexplored. Mitofusin 2 (Mfn2) is a highly conserved transmembrane GTPase. Our previous study demonstrated that the upregulation of Mfn2 can inhibit pulmonary fibrosis in ARDS mice. In this investigation, we identified upstream miRNAs regulating Mfn2 using bioinformatics tools such as TargetScan, miRDB, and microT-CDS. Based on the expression levels of these miRNAs in lung tissue from rats with LPS-induced ARDS, miR-93-5p was selected as the focus of our research. We modulated miR-93-5p expression in ARDS rats via tail vein injection of a miR-93-5p antagomir. Thereafter, we conducted pathological staining and molecular assays to examine the impact of miR-93-5p on pulmonary fibrosis in ARDS rats and to elucidate its potential mechanisms. The results demonstrated that the expression of miR-93-5p was significantly upregulated in the lung tissue of ARDS rats. LPS-induced ARDS rats exhibited severe pulmonary fibrosis, inflammation, and strong endoplasmic reticulum (ER) stress. Furthermore, Mfn2 expression exhibited a negative correlation with miR-93-5p expression. Inhibition of miR-93-5p markedly upregulated Mfn2 expression, attenuated ER stress and lung inflammation, and decreased collagen deposition. In conclusion, the inhibition of miR-93-5p upregulated Mfn2 expression and attenuated ER stress, consequently ameliorating pulmonary fibrosis in ARDS rats. Key words Acute respiratory distress syndrome \" miR-93-5p \" Pulmonary fibrosis \" Endoplasmic reticulum stress \" Mitofusin 2.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 5","pages":"823-835"},"PeriodicalIF":2.0,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12746852/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145661850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
C Zhao, J Liu, S Zhao, P Liu, Z Li, Y Li, R Dong, X-L Wang
Postoperative cognitive dysfunction (POCD) substantially influences patient outcomes, with its pathophysiology potentially linked to neuroinflammation induced by surgical procedures and anesthesia. Previous research has indicated that esketamine may alleviate neuroinflammation. Therefore, elucidating the mechanisms through which esketamine modulates neuroinflammation to ameliorating POCD is crucial for advancing its clinical management. An in vivo model of POCD was established using C57BL/6J mice subjected to exploratory laparotomy. Cognitive performance was evaluated through the Morris water maze. Subsequently, hippocampal tissue samples were collected to measure changes in the levels of IL-1beta, IL-6, TNF-alpha, PARP1, SIRT1, LC3, and P62. In vitro experiments were performed using BV2 microglial cells treated with lipopolysaccharides (LPS) to induce inflammation and a PARP1 plasmid to create PARP1 overexpression (OvPARP1) models. These models were treated with esketamine, followed by assessment of changes in the previously mentioned indicators. Immunofluorescence microscopy was used to examine PARP1 expression, while transmission electron microscopy was used to analyze cellular autophagy. Exploratory laparotomy induced POCD and triggered neuroinflammation within the hippocampus of the mice. Treatment with esketamine alleviated POCD by inhibiting OvPARP1 expression and increasing SIRT1 levels, which promoted cellular autophagy and reduced neuroinflammation. Esketamine regulates the PARP1-SIRT1 pathway, thereby activating autophagy, reducing neuro-inflammation, and improving POCD. These findings provide novel insights into potential therapeutic strategies for the management of POCD. Key words Autophagy " Esketamine " Neuroinflammation " PARP1 " Postoperative cognitive dysfunction.
{"title":"Role of Esketamine in Attenuating Neuroinflammation and Improving Postoperative Cognitive Function via Autophagy Activation Through PARP1 Targeting.","authors":"C Zhao, J Liu, S Zhao, P Liu, Z Li, Y Li, R Dong, X-L Wang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Postoperative cognitive dysfunction (POCD) substantially influences patient outcomes, with its pathophysiology potentially linked to neuroinflammation induced by surgical procedures and anesthesia. Previous research has indicated that esketamine may alleviate neuroinflammation. Therefore, elucidating the mechanisms through which esketamine modulates neuroinflammation to ameliorating POCD is crucial for advancing its clinical management. An in vivo model of POCD was established using C57BL/6J mice subjected to exploratory laparotomy. Cognitive performance was evaluated through the Morris water maze. Subsequently, hippocampal tissue samples were collected to measure changes in the levels of IL-1beta, IL-6, TNF-alpha, PARP1, SIRT1, LC3, and P62. In vitro experiments were performed using BV2 microglial cells treated with lipopolysaccharides (LPS) to induce inflammation and a PARP1 plasmid to create PARP1 overexpression (OvPARP1) models. These models were treated with esketamine, followed by assessment of changes in the previously mentioned indicators. Immunofluorescence microscopy was used to examine PARP1 expression, while transmission electron microscopy was used to analyze cellular autophagy. Exploratory laparotomy induced POCD and triggered neuroinflammation within the hippocampus of the mice. Treatment with esketamine alleviated POCD by inhibiting OvPARP1 expression and increasing SIRT1 levels, which promoted cellular autophagy and reduced neuroinflammation. Esketamine regulates the PARP1-SIRT1 pathway, thereby activating autophagy, reducing neuro-inflammation, and improving POCD. These findings provide novel insights into potential therapeutic strategies for the management of POCD. Key words Autophagy \" Esketamine \" Neuroinflammation \" PARP1 \" Postoperative cognitive dysfunction.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 5","pages":"871-884"},"PeriodicalIF":2.0,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12746861/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145661842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}