Pub Date : 2024-08-23eCollection Date: 2024-01-01DOI: 10.1515/biol-2022-0852
Lei Chen, Cong Tong, Xiangan Zhao, Chunfang Xu
The aim of the present study is to explore the potential prediction value of neutrophil-to-lymphocyte ratio (NLR) or peripheral blood platelet-to-lymphocyte ratio (PLR) for rebleeding in patients with esophagogastric variceal bleeding (EVB). We have enrolled 80 rebleeding patients with EVB and 113 EVB patients without rebleeding in the present study. The lymphocyte, platelet counts, the PLR, and the NLR of the candidates were calculated, and receiver-operating characteristic curve was drawn to examine whether NLR or PLR is a sensitive biomarker for distinguishing rebleeding patients from the EVB patients. We observed that NLR and PLR were all significantly increased in rebleeding patients with EVB compared with the non-rebleeding patients (p < 0.01); moreover, the area under the curve of NLR and PLR was 0.7037 (95% confidence interval [CI], 0.6281-0.7792) and 0.7468 (95% CI, 0.6793-0.8144), respectively, suggesting that NLR or PLR is a sensitive biomarker for distinguishing non-rebleeding patients from the rebleeding patients. We reported that NLR and PLR were significantly increased in the peripheral blood of patient with esophagogastric variceal rebleeding, suggesting that NLR and PLR may be potential early diagnostic and prognostic markers for the rebleeding among patients with EVB.
{"title":"Neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio as potential diagnostic markers for rebleeding in patients with esophagogastric variceal bleeding.","authors":"Lei Chen, Cong Tong, Xiangan Zhao, Chunfang Xu","doi":"10.1515/biol-2022-0852","DOIUrl":"10.1515/biol-2022-0852","url":null,"abstract":"<p><p>The aim of the present study is to explore the potential prediction value of neutrophil-to-lymphocyte ratio (NLR) or peripheral blood platelet-to-lymphocyte ratio (PLR) for rebleeding in patients with esophagogastric variceal bleeding (EVB). We have enrolled 80 rebleeding patients with EVB and 113 EVB patients without rebleeding in the present study. The lymphocyte, platelet counts, the PLR, and the NLR of the candidates were calculated, and receiver-operating characteristic curve was drawn to examine whether NLR or PLR is a sensitive biomarker for distinguishing rebleeding patients from the EVB patients. We observed that NLR and PLR were all significantly increased in rebleeding patients with EVB compared with the non-rebleeding patients (<i>p</i> < 0.01); moreover, the area under the curve of NLR and PLR was 0.7037 (95% confidence interval [CI], 0.6281-0.7792) and 0.7468 (95% CI, 0.6793-0.8144), respectively, suggesting that NLR or PLR is a sensitive biomarker for distinguishing non-rebleeding patients from the rebleeding patients. We reported that NLR and PLR were significantly increased in the peripheral blood of patient with esophagogastric variceal rebleeding, suggesting that NLR and PLR may be potential early diagnostic and prognostic markers for the rebleeding among patients with EVB.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11365466/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110490","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 : 2024-08-23eCollection Date: 2024-01-01DOI: 10.1515/biol-2022-0933
Anagha Bindu, Sudipa Bhadra, Soubhagya Nayak, Rizwan Khan, Ashish A Prabhu, Surajbhan Sevda
Bioelectrochemical biosensors offer a promising approach for real-time monitoring of industrial bioprocesses. Many bioelectrochemical biosensors do not require additional labelling reagents for target molecules. This simplifies the monitoring process, reduces costs, and minimizes potential contamination risks. Advancements in materials science and microfabrication technologies are paving the way for smaller, more portable bioelectrochemical biosensors. This opens doors for integration into existing bioprocessing equipment and facilitates on-site, real-time monitoring capabilities. Biosensors can be designed to detect specific heavy metals such as lead, mercury, or chromium in wastewater. Early detection allows for the implementation of appropriate removal techniques before they reach the environment. Despite these challenges, bioelectrochemical biosensors offer a significant leap forward in wastewater monitoring. As research continues to improve their robustness, selectivity, and cost-effectiveness, they have the potential to become a cornerstone of efficient and sustainable wastewater treatment practices.
{"title":"Bioelectrochemical biosensors for water quality assessment and wastewater monitoring.","authors":"Anagha Bindu, Sudipa Bhadra, Soubhagya Nayak, Rizwan Khan, Ashish A Prabhu, Surajbhan Sevda","doi":"10.1515/biol-2022-0933","DOIUrl":"10.1515/biol-2022-0933","url":null,"abstract":"<p><p>Bioelectrochemical biosensors offer a promising approach for real-time monitoring of industrial bioprocesses. Many bioelectrochemical biosensors do not require additional labelling reagents for target molecules. This simplifies the monitoring process, reduces costs, and minimizes potential contamination risks. Advancements in materials science and microfabrication technologies are paving the way for smaller, more portable bioelectrochemical biosensors. This opens doors for integration into existing bioprocessing equipment and facilitates on-site, real-time monitoring capabilities. Biosensors can be designed to detect specific heavy metals such as lead, mercury, or chromium in wastewater. Early detection allows for the implementation of appropriate removal techniques before they reach the environment. Despite these challenges, bioelectrochemical biosensors offer a significant leap forward in wastewater monitoring. As research continues to improve their robustness, selectivity, and cost-effectiveness, they have the potential to become a cornerstone of efficient and sustainable wastewater treatment practices.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11365470/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110486","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 : 2024-08-23eCollection Date: 2024-01-01DOI: 10.1515/biol-2022-0932
Lijun Xing, Yun Chen, Tingting Zheng
Hepatocellular carcinoma (HCC) is among the most common malignant liver tumors. Despite progress in anticancer drugs and surgical approaches, early detection of HCC remains challenging, often leading to late-stage diagnosis where rapid disease progression precludes surgical intervention, leaving chemotherapy as the only option. However, the systemic toxicity, low bioavailability, and significant adverse effects of chemotherapy drugs often lead to resistance, rendering treatments ineffective for many patients. This article outlines how nanoparticles, following functional modification, offer high sensitivity, reduced drug toxicity, and extended duration of action, enabling precise targeting of drugs to HCC tissues. Combined with other therapeutic modalities and imaging techniques, this significantly enhances the diagnosis, treatment, and long-term prognosis of HCC. The advent of nanomedicine provides new methodologies and strategies for the precise diagnosis and integrated treatment of HCC.
{"title":"Research progress of nanoparticles in diagnosis and treatment of hepatocellular carcinoma.","authors":"Lijun Xing, Yun Chen, Tingting Zheng","doi":"10.1515/biol-2022-0932","DOIUrl":"10.1515/biol-2022-0932","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is among the most common malignant liver tumors. Despite progress in anticancer drugs and surgical approaches, early detection of HCC remains challenging, often leading to late-stage diagnosis where rapid disease progression precludes surgical intervention, leaving chemotherapy as the only option. However, the systemic toxicity, low bioavailability, and significant adverse effects of chemotherapy drugs often lead to resistance, rendering treatments ineffective for many patients. This article outlines how nanoparticles, following functional modification, offer high sensitivity, reduced drug toxicity, and extended duration of action, enabling precise targeting of drugs to HCC tissues. Combined with other therapeutic modalities and imaging techniques, this significantly enhances the diagnosis, treatment, and long-term prognosis of HCC. The advent of nanomedicine provides new methodologies and strategies for the precise diagnosis and integrated treatment of HCC.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11365471/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110491","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 : 2024-08-23eCollection Date: 2024-01-01DOI: 10.1515/biol-2022-0920
Yanbin Zhu, Shufeng Huang, Dan Chai, Lei Liang
Gestational diabetes mellitus (GDM) is a metabolic disease that occurs during pregnancy. Herein, we investigate G protein-coupled receptor 1 (GPR1) in mediating GDM through the phosphorylation of serine/threonine kinase (AKT) pathway. Thirty pregnant SD rats were grouped into: normal pregnancy control group (NC), GDM model group, and GDM model + high-dose GPR1 antagonist treatment (GDM + Ari) group. GDM model was established, and the GDM + Ari group adopted GPR1 antagonist aripiprazole. The blood glucose level, insulin level, and insulin resistance (IR) were detected. The expression and phosphorylation of GPR1, AKT, and extracellular signal-regulated kinase (ERK) in placental tissue were detected using reverse transcription-polymerase chain reaction (RT-PCR) and western blotting (WB). The serum insulin concentration, glucose concentration, and glycated hemoglobin concentration during pregnancy in GDM group SD rats were significantly higher than those in the NC group (P < 0.05). The expression and phosphorylation levels of GPR1, AKT, and ERK in the placental tissue of SD pregnant rats in the GDM group were significantly lower than those in the NC group. Furthermore, compared with the GDM group, the expression of GPR1, AKT, and ERK in placental tissue was significantly reduced in the GDM + Ari group, while simultaneously enhancing the blood glucose level and IR level. In addition, the survival number, body weight, and malformation rate of the offspring of the GDM + Ari group were significantly improved, and there was no significant effect on the number of offspring. The expressions of GPR1, AKT, and ERK in placental tissue exhibited a significant decrease, while the glucose level and IR were observed to increase in the GDM + Ari group. Enhancing the expression of GPR1 may activate AKT phosphorylation to alleviate GDM. GPR1 could potentially serve as a novel target for diabetes treatment, offering new insights into managing GDM.
妊娠糖尿病(GDM)是一种发生在妊娠期的代谢性疾病。在此,我们研究了 G 蛋白偶联受体 1(GPR1)通过丝氨酸/苏氨酸激酶(AKT)磷酸化途径介导 GDM 的情况。将 30 只妊娠 SD 大鼠分为:正常妊娠对照组(NC)、GDM 模型组和 GDM 模型 + 大剂量 GPR1 拮抗剂治疗组(GDM + Ari)。建立 GDM 模型,GDM + Ari 组采用 GPR1 拮抗剂阿立哌唑。检测血糖水平、胰岛素水平和胰岛素抵抗(IR)。采用反转录聚合酶链反应(RT-PCR)和免疫印迹(WB)技术检测胎盘组织中 GPR1、AKT 和细胞外信号调节激酶(ERK)的表达和磷酸化情况。GDM 组 SD 大鼠妊娠期血清胰岛素浓度、血糖浓度和糖化血红蛋白浓度均显著高于 NC 组(P < 0.05)。GDM组SD妊娠大鼠胎盘组织中GPR1、AKT和ERK的表达和磷酸化水平明显低于NC组。此外,与 GDM 组相比,GDM + Ari 组胎盘组织中 GPR1、AKT 和 ERK 的表达明显降低,同时血糖水平和 IR 水平升高。此外,GDM + Ari 组后代的存活数、体重和畸形率均有明显改善,而对后代数量无明显影响。GDM + Ari 组胎盘组织中 GPR1、AKT 和 ERK 的表达明显降低,而葡萄糖水平和 IR 则明显升高。增强 GPR1 的表达可激活 AKT 磷酸化,从而缓解 GDM。GPR1 有可能成为治疗糖尿病的新靶点,为控制 GDM 提供新的思路。
{"title":"G protein-coupled receptor 1 participating in the mechanism of mediating gestational diabetes mellitus by phosphorylating the AKT pathway.","authors":"Yanbin Zhu, Shufeng Huang, Dan Chai, Lei Liang","doi":"10.1515/biol-2022-0920","DOIUrl":"10.1515/biol-2022-0920","url":null,"abstract":"<p><p>Gestational diabetes mellitus (GDM) is a metabolic disease that occurs during pregnancy. Herein, we investigate G protein-coupled receptor 1 (GPR1) in mediating GDM through the phosphorylation of serine/threonine kinase (AKT) pathway. Thirty pregnant SD rats were grouped into: normal pregnancy control group (NC), GDM model group, and GDM model + high-dose GPR1 antagonist treatment (GDM + Ari) group. GDM model was established, and the GDM + Ari group adopted GPR1 antagonist aripiprazole. The blood glucose level, insulin level, and insulin resistance (IR) were detected. The expression and phosphorylation of GPR1, AKT, and extracellular signal-regulated kinase (ERK) in placental tissue were detected using reverse transcription-polymerase chain reaction (RT-PCR) and western blotting (WB). The serum insulin concentration, glucose concentration, and glycated hemoglobin concentration during pregnancy in GDM group SD rats were significantly higher than those in the NC group (<i>P</i> < 0.05). The expression and phosphorylation levels of GPR1, AKT, and ERK in the placental tissue of SD pregnant rats in the GDM group were significantly lower than those in the NC group. Furthermore, compared with the GDM group, the expression of GPR1, AKT, and ERK in placental tissue was significantly reduced in the GDM + Ari group, while simultaneously enhancing the blood glucose level and IR level. In addition, the survival number, body weight, and malformation rate of the offspring of the GDM + Ari group were significantly improved, and there was no significant effect on the number of offspring. The expressions of GPR1, AKT, and ERK in placental tissue exhibited a significant decrease, while the glucose level and IR were observed to increase in the GDM + Ari group. Enhancing the expression of GPR1 may activate AKT phosphorylation to alleviate GDM. GPR1 could potentially serve as a novel target for diabetes treatment, offering new insights into managing GDM.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11365467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110488","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 : 2024-08-16eCollection Date: 2024-01-01DOI: 10.1515/biol-2022-0935
Dian Zhang, Jiawen Li, Chao Zhang, Jinliang Xue, Peihao Li, Kai Shang, Xiao Zhang, Baoping Lang
Many cancers exhibit resistance to chemotherapy, resulting in a poor prognosis. The transcription factor NRF2, activated in response to cellular antioxidants, plays a crucial role in cell survival, proliferation, and resistance to chemotherapy. This factor may serve as a promising target for therapeutic interventions in esophageal carcinoma. Recent research suggests that NRF2 activity is modulated by ubiquitination mediated by the KEAP1-CUL3 E3 ligase complex, highlighting the importance of deubiquitination. However, the specific deubiquitinase responsible for regulating NRF2 in esophageal cancer remains unknown. In this study, a novel regulator of the NRF2 protein, Ubiquitin-Specific Protease 35 (USP35), has been identified. Mechanistically, USP35 modulates NRF2 stability through enzymatic deubiquitination. USP35 interacts with NRF2 and facilitates its deubiquitination. Knockdown of USP35 leads to a notable increase in NRF2 levels and enhances the sensitivity of cells to chemotherapy. These findings suggest that the USP35-NRF2 axis is a key player in the regulation of therapeutic strategies for esophageal cancer.
{"title":"The deubiquitinating enzyme USP35 regulates the stability of NRF2 protein.","authors":"Dian Zhang, Jiawen Li, Chao Zhang, Jinliang Xue, Peihao Li, Kai Shang, Xiao Zhang, Baoping Lang","doi":"10.1515/biol-2022-0935","DOIUrl":"10.1515/biol-2022-0935","url":null,"abstract":"<p><p>Many cancers exhibit resistance to chemotherapy, resulting in a poor prognosis. The transcription factor NRF2, activated in response to cellular antioxidants, plays a crucial role in cell survival, proliferation, and resistance to chemotherapy. This factor may serve as a promising target for therapeutic interventions in esophageal carcinoma. Recent research suggests that NRF2 activity is modulated by ubiquitination mediated by the KEAP1-CUL3 E3 ligase complex, highlighting the importance of deubiquitination. However, the specific deubiquitinase responsible for regulating NRF2 in esophageal cancer remains unknown. In this study, a novel regulator of the NRF2 protein, Ubiquitin-Specific Protease 35 (USP35), has been identified. Mechanistically, USP35 modulates NRF2 stability through enzymatic deubiquitination. USP35 interacts with NRF2 and facilitates its deubiquitination. Knockdown of USP35 leads to a notable increase in NRF2 levels and enhances the sensitivity of cells to chemotherapy. These findings suggest that the USP35-NRF2 axis is a key player in the regulation of therapeutic strategies for esophageal cancer.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11330172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000487","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 : 2024-08-16eCollection Date: 2024-01-01DOI: 10.1515/biol-2022-0908
Chun Jiang, Peng Wang, ZhenWei Tan, Yin Zhang
Recent scientific investigations have revealed the intricate mechanisms underlying bone formation, emphasizing the essential role of long non-coding RNAs (lncRNAs) as critical regulators. This process, essential for skeletal strength and functionality, involves the transformation of mesenchymal stem cells into osteoblasts and subsequent deposition of bone matrix. lncRNAs, including HOX transcript antisense RNA (HOTAIR), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), differentiation antagonizing non-coding RNA (DANCR), and maternally expressed gene 3 (MEG3), have emerged as prominent players in this regulatory network. HOTAIR modulates osteoblast differentiation by interacting with chromatin-modifying enzymes, while MALAT1 regulates osteogenic differentiation through microRNA interactions. DANCR collaborates with Runx2 to fine-tune osteoblast differentiation, and MEG3 orchestrates multiple signaling pathways crucial for bone formation. Moreover, other lncRNAs such as H19, lncRNA for enhancing osteogenesis 3, rhabdomyosarcoma 2-associated transcript, urothelial cancer associated 1, taurine up-regulated gene 1, and nuclear enriched abundant transcript 1 contribute to the complex regulatory network governing osteoblast activities. Understanding the precise roles of these lncRNAs offers promising avenues for developing innovative therapeutic strategies targeting bone-related disorders like osteoporosis. Overall, this review summarizes the pivotal role of lncRNAs in bone formation, highlighting their potential as targets for future research endeavors aimed at advancing therapeutic interventions in bone diseases.
{"title":"Long non-coding RNAs in bone formation: Key regulators and therapeutic prospects.","authors":"Chun Jiang, Peng Wang, ZhenWei Tan, Yin Zhang","doi":"10.1515/biol-2022-0908","DOIUrl":"10.1515/biol-2022-0908","url":null,"abstract":"<p><p>Recent scientific investigations have revealed the intricate mechanisms underlying bone formation, emphasizing the essential role of long non-coding RNAs (lncRNAs) as critical regulators. This process, essential for skeletal strength and functionality, involves the transformation of mesenchymal stem cells into osteoblasts and subsequent deposition of bone matrix. lncRNAs, including HOX transcript antisense RNA (HOTAIR), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), differentiation antagonizing non-coding RNA (DANCR), and maternally expressed gene 3 (MEG3), have emerged as prominent players in this regulatory network. HOTAIR modulates osteoblast differentiation by interacting with chromatin-modifying enzymes, while MALAT1 regulates osteogenic differentiation through microRNA interactions. DANCR collaborates with Runx2 to fine-tune osteoblast differentiation, and MEG3 orchestrates multiple signaling pathways crucial for bone formation. Moreover, other lncRNAs such as H19, lncRNA for enhancing osteogenesis 3, rhabdomyosarcoma 2-associated transcript, urothelial cancer associated 1, taurine up-regulated gene 1, and nuclear enriched abundant transcript 1 contribute to the complex regulatory network governing osteoblast activities. Understanding the precise roles of these lncRNAs offers promising avenues for developing innovative therapeutic strategies targeting bone-related disorders like osteoporosis. Overall, this review summarizes the pivotal role of lncRNAs in bone formation, highlighting their potential as targets for future research endeavors aimed at advancing therapeutic interventions in bone diseases.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11330173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000486","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}
The objective of this study was to investigate the relationship between low attenuation area (LAA) scores, pulmonary function parameters, and clinical prognosis in patients with chronic obstructive pulmonary disease (COPD). COPD patients were divided into four LAA-based grades. Various lung function parameters were measured and correlated with LAA scores. Patient symptoms were examined using the St. George's Respiratory Questionnaire (SGRQ) and exercise capacity using the 6-min walk test (6MWT). Statistical analysis determined the significance of differences. Higher levels of LAA were associated with decreased lung function and airflow limitations, suggesting a positive relationship between the two. Clinical symptom scores increased as COPD severity based on LAA stratification worsened. Reduced exercise capacity was shown by a substantial decline in 6MWT scores as COPD severity increased. As LAA scores increased, SGRQ scores increased, indicating a decreased quality of life (QOL). The study demonstrated a relationship between LAA scores and COPD severity. High LAA scores were associated with poor lung function, worse clinical symptoms, limited exercise capacity, and lower QOL. These findings show that LAA scores are clinically relevant for disease severity assessment and COPD management. Further research is required to determine LAA scores' prognostic significance in disease progression and treatment response to enhance COPD therapy.
{"title":"Association of low attenuation area scores with pulmonary function and clinical prognosis in patients with chronic obstructive pulmonary disease.","authors":"Xiangli Tang, Chentao Xu, Tianjin Zhou, Yanfei Qiang, Yingzhe Wu","doi":"10.1515/biol-2022-0871","DOIUrl":"10.1515/biol-2022-0871","url":null,"abstract":"<p><p>The objective of this study was to investigate the relationship between low attenuation area (LAA) scores, pulmonary function parameters, and clinical prognosis in patients with chronic obstructive pulmonary disease (COPD). COPD patients were divided into four LAA-based grades. Various lung function parameters were measured and correlated with LAA scores. Patient symptoms were examined using the St. George's Respiratory Questionnaire (SGRQ) and exercise capacity using the 6-min walk test (6MWT). Statistical analysis determined the significance of differences. Higher levels of LAA were associated with decreased lung function and airflow limitations, suggesting a positive relationship between the two. Clinical symptom scores increased as COPD severity based on LAA stratification worsened. Reduced exercise capacity was shown by a substantial decline in 6MWT scores as COPD severity increased. As LAA scores increased, SGRQ scores increased, indicating a decreased quality of life (QOL). The study demonstrated a relationship between LAA scores and COPD severity. High LAA scores were associated with poor lung function, worse clinical symptoms, limited exercise capacity, and lower QOL. These findings show that LAA scores are clinically relevant for disease severity assessment and COPD management. Further research is required to determine LAA scores' prognostic significance in disease progression and treatment response to enhance COPD therapy.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11330171/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000485","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 : 2024-08-06eCollection Date: 2024-01-01DOI: 10.1515/biol-2022-0909
Lili Huang, Wenjing Wu, Xiaoqin Wang
Diabetic kidney disease (DKD) is one of the main microvascular complications of diabetes mellitus, as well as the leading cause of end-stage renal disease. Intestinal microbiota has emerged as a crucial regulator of its occurrence and development. Dysbiosis of the intestinal microbiota can disrupt the intestinal mucosal barrier, abnormal immunological response, reduction in short-chain fatty acid metabolites, and elevation of uremic toxins, all closely related to the occurrence and development of DKD. However, the underlying mechanisms of how intestinal microbiota and its metabolites influence the onset and progression of DKD has not been fully elucidated. In the current review, we will try to summarize the microecological mechanism of DKD by focusing on three aspects: the intestinal microbiota and its associated metabolites, and the "gut-kidney axis," and try to summarize therapies targeted at managing the intestinal microbiota, expecting to provide theoretical basis for the subsequent study of the relationship between intestinal homeostasis and DKD, and will open an emerging perspective and orientation for DKD treatment.
{"title":"Analysis of the microecological mechanism of diabetic kidney disease based on the theory of \"gut-kidney axis\": A systematic review.","authors":"Lili Huang, Wenjing Wu, Xiaoqin Wang","doi":"10.1515/biol-2022-0909","DOIUrl":"10.1515/biol-2022-0909","url":null,"abstract":"<p><p>Diabetic kidney disease (DKD) is one of the main microvascular complications of diabetes mellitus, as well as the leading cause of end-stage renal disease. Intestinal microbiota has emerged as a crucial regulator of its occurrence and development. Dysbiosis of the intestinal microbiota can disrupt the intestinal mucosal barrier, abnormal immunological response, reduction in short-chain fatty acid metabolites, and elevation of uremic toxins, all closely related to the occurrence and development of DKD. However, the underlying mechanisms of how intestinal microbiota and its metabolites influence the onset and progression of DKD has not been fully elucidated. In the current review, we will try to summarize the microecological mechanism of DKD by focusing on three aspects: the intestinal microbiota and its associated metabolites, and the \"gut-kidney axis,\" and try to summarize therapies targeted at managing the intestinal microbiota, expecting to provide theoretical basis for the subsequent study of the relationship between intestinal homeostasis and DKD, and will open an emerging perspective and orientation for DKD treatment.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11306963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141907310","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 : 2024-08-06eCollection Date: 2024-01-01DOI: 10.1515/biol-2022-0928
Xuan Zhang, Fang Li, Botao Yang, Wei Zhang, Yingchun Wang
The incidence rate of gestational diabetes mellitus (GDM) remains high among pregnant women in the second trimester of pregnancy. However, the main clinical approach to alleviate the symptoms of GDM is to control the diet. Our study explored the therapeutic effects of omega-3 fatty acids (ω-3 FAs) on GDM at the cellular and animal levels. We found that ω-3 FAs can promote the transformation of M0 macrophages into anti-inflammatory M2 macrophages. The transformed M2 macrophages promoted β-oxidation and reduced hepatocyte lipid synthesis (P < 0.05), thereby promoting hepatic function and preventing the excessive accumulation of lipid droplets in the hepatocyte cell line HepG2. Supplementation of ω-3 FAs in pregnant GDM mice significantly reduced fasting blood glucose levels, glucose tolerance test, and insulin tolerance test indices, and lipid accumulation in the liver and effectively prevented the occurrence of liver fibrosis (P < 0.05). These therapeutic effects may be mediated through the anti-inflammatory effects of ω-3 FAs (P < 0.05). ω-3 FAs also had positive effects on the offspring of pregnant GDM mice, as demonstrated by reduced birth mortality and improved glycemic stabilization (P < 0.05). In conclusion, this study provides a possible translational medicine strategy for the treatment of GDM.
{"title":"Omega-3 fatty acids prevent gestational diabetes mellitus via modulation of lipid metabolism.","authors":"Xuan Zhang, Fang Li, Botao Yang, Wei Zhang, Yingchun Wang","doi":"10.1515/biol-2022-0928","DOIUrl":"10.1515/biol-2022-0928","url":null,"abstract":"<p><p>The incidence rate of gestational diabetes mellitus (GDM) remains high among pregnant women in the second trimester of pregnancy. However, the main clinical approach to alleviate the symptoms of GDM is to control the diet. Our study explored the therapeutic effects of omega-3 fatty acids (ω-3 FAs) on GDM at the cellular and animal levels. We found that ω-3 FAs can promote the transformation of M0 macrophages into anti-inflammatory M2 macrophages. The transformed M2 macrophages promoted β-oxidation and reduced hepatocyte lipid synthesis (<i>P</i> < 0.05), thereby promoting hepatic function and preventing the excessive accumulation of lipid droplets in the hepatocyte cell line HepG2. Supplementation of ω-3 FAs in pregnant GDM mice significantly reduced fasting blood glucose levels, glucose tolerance test, and insulin tolerance test indices, and lipid accumulation in the liver and effectively prevented the occurrence of liver fibrosis (<i>P</i> < 0.05). These therapeutic effects may be mediated through the anti-inflammatory effects of ω-3 FAs (<i>P</i> < 0.05). ω-3 FAs also had positive effects on the offspring of pregnant GDM mice, as demonstrated by reduced birth mortality and improved glycemic stabilization (<i>P</i> < 0.05). In conclusion, this study provides a possible translational medicine strategy for the treatment of GDM.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11306960/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141907312","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 : 2024-08-06eCollection Date: 2024-01-01DOI: 10.1515/biol-2022-0936
Weilin Shao, Yan Feng, Jin Huang, Tingyu Li, Shengguai Gao, Yihao Yang, Dongqi Li, Zuozhang Yang, Zhihong Yao
Osteosarcoma (OS) is the most common primary malignant bone tumor in children and adolescents, and is characterized by high heterogeneity, high malignancy, easy metastasis, and poor prognosis. Recurrence, metastasis, and multidrug resistance are the main problems that limit the therapeutic effect and prognosis of OS. PI3K/AKT/mTOR signaling pathway is often abnormally activated in OS tissues and cells, which promotes the rapid development, metastasis, and drug sensitivity of OS. Emerging evidence has revealed new insights into tumorigenesis through the interaction between the PI3K/AKT/mTOR pathway and non-coding RNAs (ncRNAs). Therefore, we reviewed the interactions between the PI3K/AKT/mTOR pathway and ncRNAs and their implication in OS. These interactions have the potential to serve as cancer biomarkers and therapeutic targets in clinical applications.
骨肉瘤(Osteosarcoma,OS)是儿童和青少年最常见的原发性恶性骨肿瘤,具有异质性高、恶性程度高、易转移、预后差等特点。复发、转移和多药耐药是制约OS治疗效果和预后的主要问题。PI3K/AKT/mTOR信号通路通常在OS组织和细胞中异常激活,从而促进了OS的快速发展、转移和药物敏感性。新的证据显示,通过 PI3K/AKT/mTOR 通路与非编码 RNA(ncRNA)之间的相互作用,人们对肿瘤发生有了新的认识。因此,我们回顾了 PI3K/AKT/mTOR 通路与 ncRNA 之间的相互作用及其在 OS 中的影响。这些相互作用有可能成为癌症生物标志物和临床应用中的治疗靶点。
{"title":"Interaction of ncRNAs and the PI3K/AKT/mTOR pathway: Implications for osteosarcoma.","authors":"Weilin Shao, Yan Feng, Jin Huang, Tingyu Li, Shengguai Gao, Yihao Yang, Dongqi Li, Zuozhang Yang, Zhihong Yao","doi":"10.1515/biol-2022-0936","DOIUrl":"10.1515/biol-2022-0936","url":null,"abstract":"<p><p>Osteosarcoma (OS) is the most common primary malignant bone tumor in children and adolescents, and is characterized by high heterogeneity, high malignancy, easy metastasis, and poor prognosis. Recurrence, metastasis, and multidrug resistance are the main problems that limit the therapeutic effect and prognosis of OS. PI3K/AKT/mTOR signaling pathway is often abnormally activated in OS tissues and cells, which promotes the rapid development, metastasis, and drug sensitivity of OS. Emerging evidence has revealed new insights into tumorigenesis through the interaction between the PI3K/AKT/mTOR pathway and non-coding RNAs (ncRNAs). Therefore, we reviewed the interactions between the PI3K/AKT/mTOR pathway and ncRNAs and their implication in OS. These interactions have the potential to serve as cancer biomarkers and therapeutic targets in clinical applications.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11306965/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141907311","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}