This study aimed to investigate the expression and clinical significance of syncytin-1 in the serum exosomes of hepatocellular carcinoma (HCC) patients. Serum samples were collected from 61 patients with newly diagnosed HCC and 61 healthy individuals. Exosomes were extracted from serum samples and identified using transmission electron microscopy and Western blot. The relative expression levels of syncytin-1 in exosomes were determined by real-time quantitative PCR. The protein expression levels of alpha-fetoprotein and syncytin-1 in HCC patients were detected using enzyme-linked immunosorbent assay (ELISA). Statistical analysis was performed to evaluate the sensitivity and specificity of serum exosomal syncytin-1 in diagnosing HCC. The relationships between syncytin-1 expression and clinical pathological features were analyzed using receiver operating characteristic curve analysis. The results showed that the expression level of syncytin-1 in the serum of patients with newly diagnosed HCC was significantly higher than that in the normal control group (P < 0.0001). Using pathological diagnosis as the gold standard, the sensitivity and specificity of syncytin-1 for the auxiliary diagnosis of HCC were 91.3% and 75.5%, respectively, which were significantly higher than those of alpha-fetoprotein (P < 0.0001). The relative expression level of serum exosomal syncytin-1 was significantly associated with lymph node metastasis, degree of differentiation, and CNLC staging of HCC patients (P < 0.05). In conclusion, syncytin-1 in serum exosomes has high sensitivity and specificity for diagnosing HCC and can serve as a novel tumor marker for early screening, detection, and staging of HCC.
{"title":"The expression and clinical significance of syncytin-1 in serum exosomes of hepatocellular carcinoma patients.","authors":"Xuewei Zhuang, Xiao Shi, Hui Zhao, Shuai Shang, Xinyu Xu, Xiaomin Wang, Xin Zheng, Jing He","doi":"10.1515/biol-2022-0930","DOIUrl":"10.1515/biol-2022-0930","url":null,"abstract":"<p><p>This study aimed to investigate the expression and clinical significance of syncytin-1 in the serum exosomes of hepatocellular carcinoma (HCC) patients. Serum samples were collected from 61 patients with newly diagnosed HCC and 61 healthy individuals. Exosomes were extracted from serum samples and identified using transmission electron microscopy and Western blot. The relative expression levels of syncytin-1 in exosomes were determined by real-time quantitative PCR. The protein expression levels of alpha-fetoprotein and syncytin-1 in HCC patients were detected using enzyme-linked immunosorbent assay (ELISA). Statistical analysis was performed to evaluate the sensitivity and specificity of serum exosomal syncytin-1 in diagnosing HCC. The relationships between syncytin-1 expression and clinical pathological features were analyzed using receiver operating characteristic curve analysis. The results showed that the expression level of syncytin-1 in the serum of patients with newly diagnosed HCC was significantly higher than that in the normal control group (<i>P</i> < 0.0001). Using pathological diagnosis as the gold standard, the sensitivity and specificity of syncytin-1 for the auxiliary diagnosis of HCC were 91.3% and 75.5%, respectively, which were significantly higher than those of alpha-fetoprotein <i>(P</i> < 0.0001). The relative expression level of serum exosomal syncytin-1 was significantly associated with lymph node metastasis, degree of differentiation, and CNLC staging of HCC patients <i>(P</i> < 0.05). In conclusion, syncytin-1 in serum exosomes has high sensitivity and specificity for diagnosing HCC and can serve as a novel tumor marker for early screening, detection, and staging of HCC.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11416070/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-19eCollection Date: 2024-01-01DOI: 10.1515/biol-2022-0929
Yu Zhang, Yanchun Zhang
Atherosclerosis (AS) is a chronic vascular disease associated with lipid accumulation. Understanding the molecular mechanisms of AS is essential. Ubiquitin-specific protease 7 (USP7) is a deubiquitination enzyme involved in various cellular processes, including lipid metabolism. In this study, we aimed to elucidate the role of USP7 in AS progression and its underlying mechanism using ApoE-deficient mice. We found that USP7 ablation improved the morphological characteristics of AS in these mice. USP7 knockdown reduced inflammation, evidenced by decreases in inflammatory markers IL-6, TNF-α, and IL-1β by 35, 40, and 38%, respectively (p < 0.01). Additionally, USP7 depletion reduced oxidative stress, indicated by a 30% reduction in malondialdehyde levels and increases in superoxide dismutase and glutathione peroxidase levels by 25 and 28%, respectively (p < 0.01). Moreover, USP7 knockdown blocked lipid accumulation in aortic tissue cells. Mechanistically, USP7 knockdown inhibited enhancer of Zeste Homolog 2 (EZH2) expression, thereby suppressing AS progression. In conclusion, USP7 depletion alleviated AS progression in ApoE-deficient mice by targeting EZH2 expression. USP7 may serve as a therapeutic target for AS.
{"title":"Knockdown of USP7 alleviates atherosclerosis in ApoE-deficient mice by regulating EZH2 expression.","authors":"Yu Zhang, Yanchun Zhang","doi":"10.1515/biol-2022-0929","DOIUrl":"10.1515/biol-2022-0929","url":null,"abstract":"<p><p>Atherosclerosis (AS) is a chronic vascular disease associated with lipid accumulation. Understanding the molecular mechanisms of AS is essential. Ubiquitin-specific protease 7 (USP7) is a deubiquitination enzyme involved in various cellular processes, including lipid metabolism. In this study, we aimed to elucidate the role of USP7 in AS progression and its underlying mechanism using ApoE-deficient mice. We found that USP7 ablation improved the morphological characteristics of AS in these mice. USP7 knockdown reduced inflammation, evidenced by decreases in inflammatory markers IL-6, TNF-α, and IL-1β by 35, 40, and 38%, respectively (<i>p</i> < 0.01). Additionally, USP7 depletion reduced oxidative stress, indicated by a 30% reduction in malondialdehyde levels and increases in superoxide dismutase and glutathione peroxidase levels by 25 and 28%, respectively (<i>p</i> < 0.01). Moreover, USP7 knockdown blocked lipid accumulation in aortic tissue cells. Mechanistically, USP7 knockdown inhibited enhancer of Zeste Homolog 2 (EZH2) expression, thereby suppressing AS progression. In conclusion, USP7 depletion alleviated AS progression in ApoE-deficient mice by targeting EZH2 expression. USP7 may serve as a therapeutic target for AS.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11416069/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mohammed Bassouya, Mohamed Chedadi, Jawhari Fatima Zahra, Mohammed Kara, Amine Assouguem, Riaz Ullah, Mohamed A. Ibrahim, Ahmed Bari, Hafize Fidan, Lafraxo Soufyane, Abdellatif Alami, Amina Bari
The genus Pistacia, with its species having notable ecological, economic, and medicinal implications, demonstrates remarkable environmental adaptability. The central objective of the study is to analyze interspecific variations between Pistacia atlantica subsp. atlantica and Pistacia terebinthus across three distinct bioclimatic zones in the Middle Atlas region of Morocco. The methodology includes collecting dendrometric measurements and conducting macromorphological examinations on these two taxa, with a detailed analysis of 27 qualitative and quantitative variables. A micro-morphological analysis of leaves, using scanning electron microscopy (SEM), is employed to explore specific features such as size and stomatal density, as well as qualitative aspects like epidermal cell shape and trichomes. Dendrometric measurements have revealed that the canopy surface and the number of trunks per tree can serve as distinctive features between the two species. Regarding the sex ratio of Pistacia atlantica subsp. atlantica, 59% of the examined trees are males, primarily associated with the jujube tree in arid zones and the dwarf palm in humid areas. In contrast, female Pistacia terebinthus exhibit a similar percentage, predominantly associated with oak groves and cade juniper in their distribution areas. Principal component analysis of biometric measurements emphasized a significant disparity between the two species, representing 60.25% of the total variance. The use of SEM unveiled new features facilitating the identification of the two species. By leveraging the macromorphological and micromorphological variability of pistachio trees, we can qualify those best suited to diverse bioclimates. In this regard, we suggest incorporating them into reforestation and rehabilitation programs aimed at restoring our declining ecosystems.
{"title":"A comparative analysis of dendrometric, macromorphological, and micromorphological characteristics of Pistacia atlantica subsp. atlantica and Pistacia terebinthus in the middle Atlas region of Morocco","authors":"Mohammed Bassouya, Mohamed Chedadi, Jawhari Fatima Zahra, Mohammed Kara, Amine Assouguem, Riaz Ullah, Mohamed A. Ibrahim, Ahmed Bari, Hafize Fidan, Lafraxo Soufyane, Abdellatif Alami, Amina Bari","doi":"10.1515/biol-2022-0941","DOIUrl":"https://doi.org/10.1515/biol-2022-0941","url":null,"abstract":"The genus <jats:italic>Pistacia</jats:italic>, with its species having notable ecological, economic, and medicinal implications, demonstrates remarkable environmental adaptability. The central objective of the study is to analyze interspecific variations between <jats:italic>Pistacia atlantica</jats:italic> subsp. <jats:italic>atlantica</jats:italic> and <jats:italic>Pistacia terebinthus</jats:italic> across three distinct bioclimatic zones in the Middle Atlas region of Morocco. The methodology includes collecting dendrometric measurements and conducting macromorphological examinations on these two taxa, with a detailed analysis of 27 qualitative and quantitative variables. A micro-morphological analysis of leaves, using scanning electron microscopy (SEM), is employed to explore specific features such as size and stomatal density, as well as qualitative aspects like epidermal cell shape and trichomes. Dendrometric measurements have revealed that the canopy surface and the number of trunks per tree can serve as distinctive features between the two species. Regarding the sex ratio of <jats:italic>Pistacia atlantica</jats:italic> subsp. <jats:italic>atlantica</jats:italic>, 59% of the examined trees are males, primarily associated with the jujube tree in arid zones and the dwarf palm in humid areas. In contrast, female <jats:italic>Pistacia terebinthus</jats:italic> exhibit a similar percentage, predominantly associated with oak groves and cade juniper in their distribution areas. Principal component analysis of biometric measurements emphasized a significant disparity between the two species, representing 60.25% of the total variance. The use of SEM unveiled new features facilitating the identification of the two species. By leveraging the macromorphological and micromorphological variability of pistachio trees, we can qualify those best suited to diverse bioclimates. In this regard, we suggest incorporating them into reforestation and rehabilitation programs aimed at restoring our declining ecosystems.","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142247516","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}
This study aimed to investigate the presence of antibiotic susceptibility patterns and bacterial profiles of some multi-drug-resistant bacteria isolated from the effluents of Kolladiba and Debark Hospitals. Sixteen samples were collected from Kolladiba and Debark Hospitals in North Gondar, Ethiopia, to investigate the presence of multi-drug-resistant bacteria. To assess susceptibility patterns, well-isolated bacterial colonies were subjected to seven antibiotics. The selected resistant isolates were characterized using morphological and biochemical tests. Plasmid DNA analysis of the isolates was also performed. Out of a total of 28 bacterial isolates, 12 were found to be multi-drug resistant. Among the tested antibiotics, erythromycin was the most resistant antibiotic, while novobiocin was the most effective antibiotic. A plasmid profile study of the isolates revealed both the presence and absence of plasmids. The number of plasmids ranged from zero to four, with plasmid sizes of 100, 900, 1,000, 1,400, 1,500, and 1,800 base pairs. This study concluded that effluents from both hospitals have high number of multi-drug-resistant isolates. The genes responsible for multi-drug resistance in bacterial isolates under this study could be either plasmid-mediated or chromosomal DNA-mediated. The presence of multi-drug-resistant bacteria in these effluents should not be overlooked.
{"title":"Profile and antimicrobial susceptibility patterns of bacteria isolated from effluents of Kolladiba and Debark hospitals","authors":"Tamene Milkessa Jiru, Ewunetu Ayanaw","doi":"10.1515/biol-2022-0960","DOIUrl":"https://doi.org/10.1515/biol-2022-0960","url":null,"abstract":"This study aimed to investigate the presence of antibiotic susceptibility patterns and bacterial profiles of some multi-drug-resistant bacteria isolated from the effluents of Kolladiba and Debark Hospitals. Sixteen samples were collected from Kolladiba and Debark Hospitals in North Gondar, Ethiopia, to investigate the presence of multi-drug-resistant bacteria. To assess susceptibility patterns, well-isolated bacterial colonies were subjected to seven antibiotics. The selected resistant isolates were characterized using morphological and biochemical tests. Plasmid DNA analysis of the isolates was also performed. Out of a total of 28 bacterial isolates, 12 were found to be multi-drug resistant. Among the tested antibiotics, erythromycin was the most resistant antibiotic, while novobiocin was the most effective antibiotic. A plasmid profile study of the isolates revealed both the presence and absence of plasmids. The number of plasmids ranged from zero to four, with plasmid sizes of 100, 900, 1,000, 1,400, 1,500, and 1,800 base pairs. This study concluded that effluents from both hospitals have high number of multi-drug-resistant isolates. The genes responsible for multi-drug resistance in bacterial isolates under this study could be either plasmid-mediated or chromosomal DNA-mediated. The presence of multi-drug-resistant bacteria in these effluents should not be overlooked.","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142195245","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}
Diabetic cardiomyopathy (DCM) is identified as a progressive disease that may lead to irreparable heart failure. Toll-like receptor (TLR) signaling is believed to be implicated in the pathogenesis of DCM. This study intended to explore the potential impact of Toll-like receptor 4 (TLR4) on DCM in vitro and in vivo. Streptozotocin and HG medium were utilized to induce diabetes in animal and cell models, respectively. Selective TLR4 inhibitor TAK-242 and calcium/calmodulin-dependent protein kinase-II (CaMKII) inhibitor KN-93 were employed to explore the involvement of TLR4/CaMKII in DCM. TLR4 expression was increased in DCM hearts, while inhibition of TLR4 activation by TAK-242 improved cardiac function, attenuated heart hypertrophy, and fibrosis, as well as reduced oxidative stress and proinflammatory cytokine levels in rats, which were confirmed by Doppler echocardiography, hematoxylin and eosin staining, and Masson Trichome staining and specific enzyme-linked immunosorbent assay kits. Besides, the expression of hypertrophy-related molecules and oxidative stress damage were also inhibited by TAK-242. Furthermore, TAK-242 treatment reduced CaMKII phosphorylation accompanied by decreased expression of NOD-like pyrin domain-containing protein 3, gasdermin D (GSDMD), The N-terminal domain of Gasdermin D (GSDMD-N), apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC) and Caspase-1 both in vivo and in vitro. Similar positive impacts on HG-induced pyroptosis were also observed with KN-93 treatment, and this was achieved without affecting TLR4 expression. Collectively, our work suggested that TAK-242 demonstrated substantial benefits against DCM both in vivo and in vitro, potentially attributed to the suppression of the TLR4-mediated CaMKII/NLRP3 pathway activity.
糖尿病心肌病（DCM）被认为是一种进展性疾病，可能导致无法挽回的心力衰竭。据信，Toll 样受体（TLR）信号传导与 DCM 的发病机制有关。本研究旨在探讨 Toll 样受体 4 (TLR4) 在体外和体内对 DCM 的潜在影响。研究分别利用链脲佐菌素和 HG 培养基在动物和细胞模型中诱导糖尿病。采用选择性TLR4抑制剂TAK-242和钙/钙调蛋白依赖性蛋白激酶II（CaMKII）抑制剂KN-93来探讨TLR4/CaMKII在DCM中的参与。多普勒超声心动图、苏木精和伊红染色、Masson Trichome 染色和特异性酶联免疫吸附测定试剂盒证实，TLR4 在 DCM 心脏中表达增加，而 TAK-242 可抑制 TLR4 的活化，从而改善大鼠的心脏功能，减轻心脏肥大和纤维化，降低氧化应激和促炎细胞因子水平。此外，TAK-242还抑制了肥大相关分子的表达和氧化应激损伤。此外，TAK-242 还能降低 CaMKII 的磷酸化，同时减少体内和体外 NOD-like pyrin domain-containing protein 3、gasdermin D (GSDMD)、The N-terminal domain of Gasdermin D (GSDMD-N)、apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC) 和 Caspase-1 的表达。KN-93 处理对 HG 诱导的热凋亡也有类似的积极影响，而且这是在不影响 TLR4 表达的情况下实现的。总之，我们的研究表明，TAK-242 对体内和体外的 DCM 均有显著疗效，这可能是由于它抑制了 TLR4 介导的 CaMKII/NLRP3 通路的活性。
{"title":"TAK-242 alleviates diabetic cardiomyopathy via inhibiting pyroptosis and TLR4/CaMKII/NLRP3 pathway","authors":"Xiaolong Zhao, Jing Zhang, Feng Xu, Longqi Shang, Qingquan Liu, Chunjian Shen","doi":"10.1515/biol-2022-0957","DOIUrl":"https://doi.org/10.1515/biol-2022-0957","url":null,"abstract":"Diabetic cardiomyopathy (DCM) is identified as a progressive disease that may lead to irreparable heart failure. Toll-like receptor (TLR) signaling is believed to be implicated in the pathogenesis of DCM. This study intended to explore the potential impact of Toll-like receptor 4 (TLR4) on DCM <jats:italic>in vitro</jats:italic> and <jats:italic>in vivo</jats:italic>. Streptozotocin and HG medium were utilized to induce diabetes in animal and cell models, respectively. Selective TLR4 inhibitor TAK-242 and calcium/calmodulin-dependent protein kinase-II (CaMKII) inhibitor KN-93 were employed to explore the involvement of TLR4/CaMKII in DCM. TLR4 expression was increased in DCM hearts, while inhibition of TLR4 activation by TAK-242 improved cardiac function, attenuated heart hypertrophy, and fibrosis, as well as reduced oxidative stress and proinflammatory cytokine levels in rats, which were confirmed by Doppler echocardiography, hematoxylin and eosin staining, and Masson Trichome staining and specific enzyme-linked immunosorbent assay kits. Besides, the expression of hypertrophy-related molecules and oxidative stress damage were also inhibited by TAK-242. Furthermore, TAK-242 treatment reduced CaMKII phosphorylation accompanied by decreased expression of NOD-like pyrin domain-containing protein 3, gasdermin D (GSDMD), The N-terminal domain of Gasdermin D (GSDMD-N), apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC) and Caspase-1 both <jats:italic>in vivo</jats:italic> and <jats:italic>in vitro.</jats:italic> Similar positive impacts on HG-induced pyroptosis were also observed with KN-93 treatment, and this was achieved without affecting TLR4 expression. Collectively, our work suggested that TAK-242 demonstrated substantial benefits against DCM both <jats:italic>in vivo</jats:italic> and <jats:italic>in vitro</jats:italic>, potentially attributed to the suppression of the TLR4-mediated CaMKII/NLRP3 pathway activity.","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142195247","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}
Exercise training can significantly improve skeletal muscle mitochondrial function and has been proven to be highly relevant to alterations in skeletal muscle DNA methylation. However, it remains unclear whether late-in-life exercise has an effect on promoter methylation of PGC-1α, a key regulator of mitochondrial biogenesis. Here we employed two distinct exercise modalities, constant medium intensity exercise training (CMIT) and high-intensity interval exercise training (HIIT), to investigate their impacts on PGC-1α expression and methylation regulation in skeletal muscle of aged mice. The results revealed a notable decrease in PGC-1α expression in skeletal muscle of aged mice, accompanied by elevated methylation levels of the PGC-1α promoter, and increased DNA methyltransferase (DNMT) protein expressions. However, both forms of exercise training significantly corrected PGC-1α epigenetic changes, increased PGC-1α expression, and ameliorated skeletal muscle reduction. Furthermore, exercise training led to elevated expression of proteins related to mitochondrial biogenesis and energy metabolism in skeletal muscle, improving mitochondrial structure and function. In conclusion, late-in-life exercise improved skeletal muscle function, morphology, and mitochondria biogenesis, which may be associated with hypomethylation in promoters of PGC-1α and increased content of skeletal muscle PGC-1α. Notably, there was no clear difference between HIIT and CMIT in PGC-1α expression and skeletal muscle function.
{"title":"Hypomethylation in promoters of PGC-1α involved in exercise-driven skeletal muscular alterations in old age","authors":"Qiaowei Li, Qin Liu, Zhong Lin, Wenwen Lin, Feng Huang, Pengli Zhu","doi":"10.1515/biol-2022-0959","DOIUrl":"https://doi.org/10.1515/biol-2022-0959","url":null,"abstract":"Exercise training can significantly improve skeletal muscle mitochondrial function and has been proven to be highly relevant to alterations in skeletal muscle DNA methylation. However, it remains unclear whether late-in-life exercise has an effect on promoter methylation of PGC-1α, a key regulator of mitochondrial biogenesis. Here we employed two distinct exercise modalities, constant medium intensity exercise training (CMIT) and high-intensity interval exercise training (HIIT), to investigate their impacts on PGC-1α expression and methylation regulation in skeletal muscle of aged mice. The results revealed a notable decrease in PGC-1α expression in skeletal muscle of aged mice, accompanied by elevated methylation levels of the PGC-1α promoter, and increased DNA methyltransferase (DNMT) protein expressions. However, both forms of exercise training significantly corrected PGC-1α epigenetic changes, increased PGC-1α expression, and ameliorated skeletal muscle reduction. Furthermore, exercise training led to elevated expression of proteins related to mitochondrial biogenesis and energy metabolism in skeletal muscle, improving mitochondrial structure and function. In conclusion, late-in-life exercise improved skeletal muscle function, morphology, and mitochondria biogenesis, which may be associated with hypomethylation in promoters of PGC-1α and increased content of skeletal muscle PGC-1α. Notably, there was no clear difference between HIIT and CMIT in PGC-1α expression and skeletal muscle function.","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142195246","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}
The cardiometabolic index (CMI) is an emerging and effective indicator for predicting the presence of metabolic-associated fatty liver disease (MAFLD). This study aims to investigate the relationship between CMI and MAFLD using data from NHANES 2017–2020. In this cross-sectional study, a total of 3,749 subjects were included. The study conducted a thorough analysis of CMI with three multivariate logistic regression models, subgroup analyses, and restricted cubic splines (RCS) were utilized. Using multifactorial logistic regression as the primary method of analysis, we found that a higher CMI was also significantly associated with an increased risk of MAFLD (OR = 1.45, 95% CI (1.05–2.01)). This result was further visualized by the RCS curve: There was a non-linear positive correlation between CMI and MAFLD incidence (the turning point is CMI = 0.4554). These findings were strongly reinforced by subsequent subgroup and sensitivity analyses. There is a robust positive relationship between the CMI and the risk of MAFLD, providing valuable clinical benefits for early detection and screening of MAFLD. It is important to highlight the presence of a non-linear association between CMI and MAFLD, with an inflection point identified at CMI = 0.4554.
{"title":"Non-linear associations between cardiovascular metabolic indices and metabolic-associated fatty liver disease: A cross-sectional study in the US population (2017–2020)","authors":"Meimei Xu, Sibo Han, Qiaomei Wu, Shihong Ma, Huiying Cai, Mengqi Xue, Fengling Liu, Xiaozhen Xiao, Xiaoshuang Chen, MeiZhen Lin","doi":"10.1515/biol-2022-0947","DOIUrl":"https://doi.org/10.1515/biol-2022-0947","url":null,"abstract":"The cardiometabolic index (CMI) is an emerging and effective indicator for predicting the presence of metabolic-associated fatty liver disease (MAFLD). This study aims to investigate the relationship between CMI and MAFLD using data from NHANES 2017–2020. In this cross-sectional study, a total of 3,749 subjects were included. The study conducted a thorough analysis of CMI with three multivariate logistic regression models, subgroup analyses, and restricted cubic splines (RCS) were utilized. Using multifactorial logistic regression as the primary method of analysis, we found that a higher CMI was also significantly associated with an increased risk of MAFLD (OR = 1.45, 95% CI (1.05–2.01)). This result was further visualized by the RCS curve: There was a non-linear positive correlation between CMI and MAFLD incidence (the turning point is CMI = 0.4554). These findings were strongly reinforced by subsequent subgroup and sensitivity analyses. There is a robust positive relationship between the CMI and the risk of MAFLD, providing valuable clinical benefits for early detection and screening of MAFLD. It is important to highlight the presence of a non-linear association between CMI and MAFLD, with an inflection point identified at CMI = 0.4554.","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142195244","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}
Dendritic cells (DCs) play a crucial role in bridging innate and adaptive immune responses. They are widely distributed in various tissues and organs, including the eyes. In the ocular context, permanent DCs are present at the peripheral edge of the retina and the peripapillary area in an immature state. However, during the inflammatory process, DCs become activated and contribute to the development of uveitis. This review focuses on introducing the characteristics and status of DC-induced uveitis, exploring factors that can influence the status of DCs, and discussing feasible methods for treating DCs in both experimental autoimmune uveitis animal models and humans. It emphasizes the importance of further research on molecular pathways and signaling pathways that regulate the function of DCs. For example, investigating molecules such as cytotoxic T-lymphocyte-associated protein 4, which inhibits the B7-CD28 co-stimulatory interaction, can help improve immune homeostasis. The aim is to identify new therapeutic targets and develop targeted strategies for DCs, such as DC vaccine therapy or the use of immune modulators. These approaches can be tailored to the immune characteristics and disease manifestations of individual patients, enabling personalized treatment strategies. This may include the personalized design and precise medication of DC therapy, with the ultimate goal of improving treatment efficacy while minimizing adverse reactions.
树突状细胞（DC）在连接先天性免疫反应和适应性免疫反应方面发挥着至关重要的作用。它们广泛分布于各种组织和器官，包括眼睛。在眼部，永久性 DCs 以未成熟状态存在于视网膜外周边缘和毛细血管周围区域。然而，在炎症过程中，DCs 会被激活并导致葡萄膜炎的发生。本综述重点介绍了DC诱发葡萄膜炎的特点和现状，探讨了影响DC现状的因素，并讨论了在实验性自身免疫性葡萄膜炎动物模型和人类中治疗DC的可行方法。报告强调了进一步研究调节 DC 功能的分子通路和信号通路的重要性。例如，研究细胞毒性T淋巴细胞相关蛋白4等抑制B7-CD28共刺激相互作用的分子有助于改善免疫稳态。研究的目的是确定新的治疗靶点，开发针对直流电的策略，如直流电疫苗疗法或使用免疫调节剂。这些方法可根据个体患者的免疫特征和疾病表现进行定制，从而实现个性化治疗策略。这可能包括直流电疗法的个性化设计和精确用药，最终目标是提高疗效，同时最大限度地减少不良反应。
{"title":"Overview of dendritic cells and related pathways in autoimmune uveitis","authors":"Fan Zhao, Jing-Sheng Yu","doi":"10.1515/biol-2022-0887","DOIUrl":"https://doi.org/10.1515/biol-2022-0887","url":null,"abstract":"Dendritic cells (DCs) play a crucial role in bridging innate and adaptive immune responses. They are widely distributed in various tissues and organs, including the eyes. In the ocular context, permanent DCs are present at the peripheral edge of the retina and the peripapillary area in an immature state. However, during the inflammatory process, DCs become activated and contribute to the development of uveitis. This review focuses on introducing the characteristics and status of DC-induced uveitis, exploring factors that can influence the status of DCs, and discussing feasible methods for treating DCs in both experimental autoimmune uveitis animal models and humans. It emphasizes the importance of further research on molecular pathways and signaling pathways that regulate the function of DCs. For example, investigating molecules such as cytotoxic T-lymphocyte-associated protein 4, which inhibits the B7-CD28 co-stimulatory interaction, can help improve immune homeostasis. The aim is to identify new therapeutic targets and develop targeted strategies for DCs, such as DC vaccine therapy or the use of immune modulators. These approaches can be tailored to the immune characteristics and disease manifestations of individual patients, enabling personalized treatment strategies. This may include the personalized design and precise medication of DC therapy, with the ultimate goal of improving treatment efficacy while minimizing adverse reactions.","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142195253","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}
Yun Wang, Yi Xu, Tun Zhao, Ya-Jun Ma, Wei Qin, Wen-Li Hu
Intensive care unit-acquired weakness (ICU-AW) is prevalent in critical care, with limited treatment options. Certain microRNAs, like miR-542, are highly expressed in ICU-AW patients. This study investigates the regulatory role and mechanisms of miR-542 in ICU-AW and explores the clinical potential of miR-542 inhibitors. ICU-AW models were established in C57BL/6 mice through cecal ligation and puncture (CLP) and in mouse C2C12 myoblasts through TNF-α treatment. In vivo experiments demonstrated decreased muscle strength, muscle fiber atrophy, widened intercellular spaces, and increased miR-542-3p/5p expression in ICU-AW mice model. In vitro experiments indicated suppressed ATG5, ATG7 and LC3II/I, elevated MDA and ROS levels, decreased SOD levels, and reduced MMP in the model group. Similar to animal experiments, the expression of miR-542-3p/5p was upregulated. Gel electrophoresis explored the binding of polyethyleneimine/mesoporous silica nanoparticles (PEI/MMNs) to locked nucleic acid (LNA) miR-542 inhibitor (LNA-542). PEI/MMNs@LNA-542 with positive charge (3.03 ± 0.363 mV) and narrow size (206.94 ± 6.19 nm) were characterized. Immunofluorescence indicated significant internalization with no apparent cytotoxicity. Biological activity, examined through intraperitoneal injection, showed that PEI/MMNs@LNA-542 alleviated muscle strength decline, restored fiber damage, and recovered mitochondrial injury in mice. In conclusion, PEI/MMNs nanoparticles effectively delivered LNA-542, targeting ATG5 to inhibit autophagy and alleviate mitochondrial damage, thereby improving ICU-AW.
{"title":"PEI/MMNs@LNA-542 nanoparticles alleviate ICU-acquired weakness through targeted autophagy inhibition and mitochondrial protection","authors":"Yun Wang, Yi Xu, Tun Zhao, Ya-Jun Ma, Wei Qin, Wen-Li Hu","doi":"10.1515/biol-2022-0952","DOIUrl":"https://doi.org/10.1515/biol-2022-0952","url":null,"abstract":"Intensive care unit-acquired weakness (ICU-AW) is prevalent in critical care, with limited treatment options. Certain microRNAs, like miR-542, are highly expressed in ICU-AW patients. This study investigates the regulatory role and mechanisms of miR-542 in ICU-AW and explores the clinical potential of miR-542 inhibitors. ICU-AW models were established in C57BL/6 mice through cecal ligation and puncture (CLP) and in mouse C2C12 myoblasts through TNF-α treatment. <jats:italic>In vivo</jats:italic> experiments demonstrated decreased muscle strength, muscle fiber atrophy, widened intercellular spaces, and increased miR-542-3p/5p expression in ICU-AW mice model. <jats:italic>In vitro</jats:italic> experiments indicated suppressed ATG5, ATG7 and LC3II/I, elevated MDA and ROS levels, decreased SOD levels, and reduced MMP in the model group. Similar to animal experiments, the expression of miR-542-3p/5p was upregulated. Gel electrophoresis explored the binding of polyethyleneimine/mesoporous silica nanoparticles (PEI/MMNs) to locked nucleic acid (LNA) miR-542 inhibitor (LNA-542). PEI/MMNs@LNA-542 with positive charge (3.03 ± 0.363 mV) and narrow size (206.94 ± 6.19 nm) were characterized. Immunofluorescence indicated significant internalization with no apparent cytotoxicity. Biological activity, examined through intraperitoneal injection, showed that PEI/MMNs@LNA-542 alleviated muscle strength decline, restored fiber damage, and recovered mitochondrial injury in mice. In conclusion, PEI/MMNs nanoparticles effectively delivered LNA-542, targeting ATG5 to inhibit autophagy and alleviate mitochondrial damage, thereby improving ICU-AW.","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142195252","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}
Non-Hodgkin lymphoma (NHL) limited to the larynx is very rare. The authors present the clinical diagnosis and treatment of four patients with laryngeal NHL. Case 1 was diagnosed with glottic, subglottic, and tracheal mucosa-associated lymphoid tissue (MALT) lymphoma, and was treated with radiotherapy and chemotherapy after surgery. Case 2 was diagnosed with laryngeal MALT lymphoma and underwent radiotherapy. Case 3 was diagnosed with angioimmunoblastic T-cell lymphoma, and was treated with radiotherapy and chemotherapy. Case 4 had MALT lymphoma in the glottic area with a malignant thyroid tumor, and was treated with radiotherapy and chemotherapy after surgery. More reports and research on this disease are needed.
局限于喉部的非霍奇金淋巴瘤（NHL）非常罕见。作者介绍了四例喉 NHL 患者的临床诊断和治疗。病例 1 被诊断为声门、声门下和气管粘膜相关淋巴组织（MALT）淋巴瘤，手术后接受了放疗和化疗。病例 2 被诊断为喉 MALT 淋巴瘤，接受了放疗。病例 3 被诊断为血管免疫母细胞 T 细胞淋巴瘤，接受了放疗和化疗。病例 4 患有声门区 MALT 淋巴瘤并伴有恶性甲状腺肿瘤，手术后接受了放疗和化疗。我们需要对这种疾病进行更多的报道和研究。
{"title":"Laryngeal non-Hodgkin lymphoma: Report of four cases and review of the literature","authors":"Xin Tang, Dingting Wang, Huajun Feng, Gang Qin","doi":"10.1515/biol-2022-0937","DOIUrl":"https://doi.org/10.1515/biol-2022-0937","url":null,"abstract":"Non-Hodgkin lymphoma (NHL) limited to the larynx is very rare. The authors present the clinical diagnosis and treatment of four patients with laryngeal NHL. Case 1 was diagnosed with glottic, subglottic, and tracheal mucosa-associated lymphoid tissue (MALT) lymphoma, and was treated with radiotherapy and chemotherapy after surgery. Case 2 was diagnosed with laryngeal MALT lymphoma and underwent radiotherapy. Case 3 was diagnosed with angioimmunoblastic T-cell lymphoma, and was treated with radiotherapy and chemotherapy. Case 4 had MALT lymphoma in the glottic area with a malignant thyroid tumor, and was treated with radiotherapy and chemotherapy after surgery. More reports and research on this disease are needed.","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142195251","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}
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