Biomolecules & biomedicine最新文献

{"title":"Mechanistic insights into Y-Box binding protein-1 mediated regulation of lipid metabolism and oxidative stress in NAFLD via INHBE/TNF-β pathway.","authors":"Zhi Ren, Rui Wang, Jun Wei, Zhenzeng Ma, Xiquan Ke","doi":"10.17305/bb.2024.11249","DOIUrl":"10.17305/bb.2024.11249","url":null,"abstract":"<p><p>Nonalcoholic fatty liver disease (NAFLD) is a prevalent liver disorder that has emerged as a significant public health concern. This study aimed to investigate the mechanisms by which Y-box binding protein-1 (YB1) knockdown influences lipid metabolism and oxidative stress in palmitic acid (PA)-induced NAFLD LO2 cells. The expression of YB1 was analyzed using the GSE89632 dataset from the Gene Expression Omnibus (GEO) database. RNA sequencing was performed, followed by Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, and protein-protein interaction (PPI) network analyses to identify differentially expressed genes (DEGs). Quantitative real-time PCR (QRT-PCR), Western blotting, flow cytometry, and various biochemical assays were used to evaluate gene expression, lipid accumulation, and oxidative stress. Our results demonstrated that YB1 is highly expressed in NAFLD. RNA sequencing revealed 798 DEGs between the shCtrl and shYB1 groups, with 190 genes upregulated and 608 genes downregulated. Notably, we observed an increase in Inhibin beta E (INHBE) expression, while EGR1, GDF15, NUPR1, and FOSB were decreased in NAFLD LO2 cells. YB1 knockdown, particularly when combined with INHBE suppression, significantly enhanced cell viability, improved lipid metabolism, and reduced reactive oxygen species (ROS) accumulation and malondialdehyde (MDA) content. The downstream mechanism was primarily associated with TNF-β signaling. Specifically, we observed decreased levels of TGF-β1, p-Smad2, and p-Smad3 following YB1 and INHBE knockdown. Furthermore, INHBE overexpression reversed the beneficial effects induced by YB1 knockdown. In conclusion, YB1 knockdown improves lipid metabolism and reduces oxidative stress in NAFLD LO2 cells, largely through the INHBE/TNF-β signaling pathway. These findings provide valuable insights into novel therapeutic strategies for managing NAFLD.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1528-1539"},"PeriodicalIF":0.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12097399/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142924201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prediction of post-insertion infections related to totally implantable subcutaneous venous access ports in tumor patients using a nomogram.","authors":"Sen Wang, Heng Zong, Lei Tang, Yuandong Wei","doi":"10.17305/bb.2024.11583","DOIUrl":"10.17305/bb.2024.11583","url":null,"abstract":"<p><p>Totally implantable subcutaneous venous access ports (TISVAPs) are essential for long-term central venous chemotherapy, delivering medication directly into the central veins of patients. While they play a critical role in reducing patient discomfort, TISVAPs pose a notable risk of post-insertion infections-particularly concerning for oncology patients with compromised immune systems due to aggressive treatment regimens. Our research addresses this issue by developing a predictive nomogram to estimate the risk of TISVAP-associated infections. The model is based on independent risk factors identified in our study: a history of diabetes, the type of chemotherapy, peripheral blood leukocyte count (WBC), and serum albumin levels. Using retrospective clinical data from 309 oncology patients who underwent TISVAP implantation at a tertiary A-grade comprehensive hospital, we divided the dataset into training (n = 246) and validation (n = 63) subsets. Through logistic and Lasso regression analyses, we identified the independent risk factors associated with infections. The resulting interactive nomogram demonstrated strong accuracy and reliability, with C-indexes of 0.82 and 0.835 for the training and validation sets, respectively. This tool equips healthcare providers to proactively identify high-risk patients and tailor preventive strategies accordingly. Ultimately, our research aims to enhance patient outcomes and improve the quality of life for those undergoing long-term venous chemotherapy.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1601-1609"},"PeriodicalIF":0.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12097388/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142959717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alleviating the IL-1β-stimulated extracellular matrix degradation in osteoarthritis, and chondrocyte inflammation by <i>Morinda officinalis</i> polysaccharide via the SIRT6/NF-κB pathway.","authors":"Dongfang Zhao, Shuqin Xing, Jiao Qi, Zhiqiang Wei, Jianghai Huang, Jigao Sun, Xinzhu Wen, Yafei Wang","doi":"10.17305/bb.2024.11437","DOIUrl":"10.17305/bb.2024.11437","url":null,"abstract":"<p><p>Morinda officinalis polysaccharide (MOP) is a major active component of Morinda officinalis, known for its roles in supporting bone health and reducing oxidation and inflammation. However, no studies to date have specifically examined the effects of MOP on interleukin-1β (IL-1β)-stimulated chondrocyte inflammation or the progression of osteoarthritis (OA). To investigate, cell counting kit-8 assays were performed to evaluate MOP's impact on the viability of human chondrocytes (C28/I2 cells). Cell damage was assessed using flow cytometry and Hoechst 33258 fluorescent staining. Inflammatory factor levels were measured via western blot and ELISA, while extracellular matrix (ECM) degradation was analyzed through immunofluorescence. The involvement of the NF-κB pathway and its regulation by Sirtuin 6 (SIRT6) were also explored using western blot. Following IL-1β treatment, C28/I2 cell viability decreased, inflammatory factor secretion increased, and ECM degradation was observed. MOP counteracted these effects by mitigating IL-1β-induced cell damage, preventing ECM degradation, and reducing inflammatory factor secretion, in a dose-dependent manner. Furthermore, IL-1β treatment suppressed SIRT6 expression, whereas MOP upregulated it. Notably, silencing SIRT6 diminished MOP's protective effects on C28/I2 cells and reversed MOP's suppression of the NF-κB pathway. In conclusion, MOP alleviates IL-1β-induced C28/I2 cell injury by inhibiting the NF-κB pathway through activation of SIRT6. This, in turn, reduces the inflammatory response, prevents ECM degradation, and ultimately slows OA progression.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1610-1620"},"PeriodicalIF":0.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12097393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-term smoking contributes to aging frailty and inflammatory response.","authors":"Huijin Hou, Yidi Chai, Ting Zhang, Yue Liang, Lan Huang, Xu Cao, Shufang Liang","doi":"10.17305/bb.2024.11722","DOIUrl":"10.17305/bb.2024.11722","url":null,"abstract":"<p><p>In recent years, the health challenges linked to frailty in the elderly, particularly those worsened by cigarette smoke, have become more pronounced. However, quantitative studies examining the impact of smoking dosage on frailty in this population remain limited. To address this gap, we developed a model using smoke-exposed elderly mice. Fifteen-month-old C57BL/6J mice were exposed to smoke from two burning cigarettes for 15 min in a whole-body chamber. This exposure occurred 4, 6, and 8 times daily for 30 days, representing low, medium, and high smoking dosages, respectively. Frailty levels were assessed through rotation and grip strength tests, alongside lung histopathology and inflammatory factor protein expression analyses across the three dosage groups. Additionally, we used the Gene Expression Omnibus (GEO) database to validate the correlation between frailty and inflammation in elderly smokers, facilitating cross-comparisons between animal model findings and human sample data. Our results show that mice exposed to high-dose smoking were significantly more prone to frailty, with notable reductions in maximal grip strength (P < 0.01) and drop time (P < 0.001). Among human samples, 69.2% of elderly smokers exhibited a frailty phenotype, compared to just 15.4% of nonsmokers. Both smoking-exposed mice and elderly smokers demonstrated upregulation of tumor necrosis factor-α (TNF-α) and interleukin-1 β (IL-1β) in lung tissue and serum. Mechanistically, this upregulation activates the NF-κB signaling pathway. Our findings quantitatively link smoking-induced frailty to increased levels of TNF-α and IL-1β, providing experimental evidence for the diagnosis and prevention of frailty in elderly populations.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1647-1662"},"PeriodicalIF":0.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12097404/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143030318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A preliminary study on the prognostic significance of cysteine-rich EGF ligand domain 2 protein (CRELD2) in patients with triple negative breast cancer.","authors":"Mehmet Zahid Kocak, Murat Araz, Siddika Findik, Aykut Demirkiran, Mustafa Korkmaz, Melek Karakurt Eryilmaz, Mehmet Artac","doi":"10.17305/bb.2024.11865","DOIUrl":"10.17305/bb.2024.11865","url":null,"abstract":"<p><p>The cysteine-rich epidermal growth factor ligand domain 2 protein (CRELD2) is associated with pathways that regulate epithelial-to-mesenchymal transition, a critical process driving cancer metastasis. This study aimed to determine the prognostic value of CRELD2 status on survival outcomes in triple-negative breast cancer (TNBC). Seventy patients were included in the study. Thirty-four patients were metastatic, and 36 patients were non-metastatic. CRELD2 protein expression in tumor tissue was determined by immunohistochemical staining (IHC). The patients were divided into two groups: CRELD2 positive and negative groups. Clinicopathological features and survival outcomes were compared between the groups. In the survival analysis of the non-metastatic patient group, five-year overall survival (OS) rate was 91.7% in the CRELD2-positive patient group and 91% in the negative group (P = 0.91). Median progression free survival (PFS) was 9.4 (95% confidence interval [CI]: 6.4-12.4) months in the CRELD2-positive group and 11.9 (95% CI: 8.2-18.6) months in the CRELD2-negative group (P = 0.04). The median OS was 17.2 (95% CI: 13.7-22.3) months in the CRELD2-positive group and 24.7 (95% CI: 21.8-29.6) months in the CRELD2-negative group (P = 0.02). In multivariate analysis, CRELD2 status (negative vs positive) (hazard ratio [HR]: 0.50, 95% CI: 0.38-0.96, P = 0.02) was determined to be a risk factor for OS and CRELD2 status (negative vs positive) (HR: 0.82, 95% CI: 0.33-0.96, P = 0.01) was defined as a risk factor for PFS in patients with metastatic TNBC. This is the first clinical study to determine the effect of CRELD2 on survival and as a prognostic marker in patients with triple metastatic breast cancer. These results need to be validated prospectively with a large sample size.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1663-1671"},"PeriodicalIF":0.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12097403/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143048931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between triglyceride-glucose (TyG) index and risk of depression in middle-aged and elderly Chinese adults: Evidence from a large national cohort study.","authors":"Zhang-Yang Xu, Hong Zheng, Zi-Jun Pan, Shou-Yi Hu, Yun-Xia Wang, Wen-Jun Su","doi":"10.17305/bb.2024.11800","DOIUrl":"10.17305/bb.2024.11800","url":null,"abstract":"<p><p>Insulin resistance (IR) has been proposed as a contributing factor to major depressive disorder (MDD), with previous studies reporting a positive correlation between triglyceride-glucose (TyG) a proxy indicator of IR and MDD. However, limited information is available regarding their longitudinal association. This study aimed to clarify the connection between TyG levels and depression risk, as well as explore its predictive potential. A total of 3021 participants without a prior history of depression were recruited from the China Health and Retirement Longitudinal Study and followed for seven years. Participants were categorized into tertiles based on their TyG levels. The cumulative hazard of depression was analyzed using Kaplan-Meier curves, while cox regression analyses and multivariable-adjusted restricted cubic spline (RCS) curves were employed to assess the relationship between TyG levels and depression risk. Stratified analyses across various subgroups were also conducted to confirm the robustness of the conclusions. Over the follow-up period, 1782 participants (58.9%) developed depression, with incidence rates of 30.2%, 34.0%, and 35.8% in tertiles 1, 2, and 3, respectively. After adjusting for confounding factors, each 1-unit increase in TyG was associated with a significantly higher risk of depression. RCS curve analysis revealed a compelling dose-response relationship between TyG levels and depression susceptibility. These findings indicate that elevated TyG levels are strongly associated with an increased risk of depression and could serve as a reliable biomarker for assessing depression risk. These insights provide valuable guidance for developing more effective strategies for the prevention and treatment of depressive disorders.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1621-1630"},"PeriodicalIF":0.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12097402/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The association between plasma levels of Sestrin2 and risk factors of cardiovascular diseases in healthy and diabetic adults: A study of Qatar Biobank data.","authors":"Shahenda Abdelsalam, Muhammad Ammar Zahid, Hicham Raïq, Hanan Abunada, Ahad Elsayed, Aijaz Parray, Abdelali Agouni","doi":"10.17305/bb.2024.11418","DOIUrl":"10.17305/bb.2024.11418","url":null,"abstract":"<p><p>This study examines the association between serum Sestrin2 (SESN2) levels and cardiovascular disease (CVD) risk factors in healthy and diabetic adults, using data from the Qatar Biobank (QBB). A total of 844 participants were included, with 518 in the diabetic cohort and 326 in the healthy cohort. Clinical characteristics, cardiometabolic markers, and SESN2 levels were measured, and binomial logistic regression analyses were conducted to assess the associations between SESN2 and various health indices. Diabetic patients had significantly lower SESN2 levels compared to healthy controls (5.49 ± 5.94 vs 8.25 ± 7.57 ng/mL, P < 0.001). A significant negative correlation was observed between SESN2 and HbA1c (-0.19, P = 0.0006), insulin (-0.19, P = 0.0006), HOMA-IR (-0.17, P = 0.0024), C-peptide (-0.18, P = 0.0012), triglycerides (TG)/HDL ratio (-0.12, P = 0.0283), and the pulsatility index (PI) (-0.15, P = 0.006). In healthy individuals, higher SESN2 levels were associated with lower odds of elevated HbA1c (adjusted odds ratio [AOR] = 0.33, P = 0.00), insulin (AOR = 0.23, P = 0.00), HOMA-IR (AOR = 0.58, P = 0.06), C-peptide (AOR = 0.56, P = 0.04), and TG (AOR = 0.37, P = 0.03). In contrast, diabetic patients showed a positive correlation between SESN2 and insulin (0.15, P = 0.0005), HOMA-IR (0.11, P = 0.0106), and C-peptide (0.12, P = 0.0048). Participants in the highest SESN2 tertile had increased risks for high BMI (AOR = 1.96, P = 0.05), high TG (AOR = 1.57, P = 0.04), high NT-proBNP (AOR = 7.27, P = 0.01), and high fibrinogen (AOR = 1.92, P = 0.03). These findings suggest that while high SESN2 levels are cardioprotective in healthy individuals, they may indicate higher cellular stress in diabetics. Determining optimal SESN2 levels could help assess CVD risk, particularly in diabetic patients.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1479-1490"},"PeriodicalIF":0.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12097390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142786897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"hUC-MSC extracellular vesicles protect against hypoxic-ischemic brain injury by promoting NLRP3 ubiquitination.","authors":"Shanshan Xiao, Ying Lv, Xuejing Hou, Shuqiang Qu","doi":"10.17305/bb.2024.10706","DOIUrl":"10.17305/bb.2024.10706","url":null,"abstract":"<p><p>Hypoxic-ischemic brain injury (HIBD) is a major cause of neonatal mortality and long-term neurological deficits, with limited treatment options. Extracellular vesicles (EVs) from human umbilical cord mesenchymal stem cells (hUC-MSC-EVs) have shown promise in neuroprotection, but the mechanisms remain unclear. This study explores how hUC-MSC-EVs protect neonatal rats from HIBD. hUC-MSC-EVs were isolated, characterized, and administered to neonatal rats subjected to HIBD. Behavioral reflexes and brain infarction were assessed, along with cellular and molecular analyses of hippocampal tissue. An in vitro oxygen-glucose deprivation/reoxygenation (OGD/R) model was used to simulate ischemic conditions in rat primary microglia. Results demonstrated that hUC-MSC-EVs significantly improved neurological outcomes, reduced brain infarction, and decreased microglial activation and pyroptosis. These effects were linked to the inhibition of NLRP3 inflammasome activation and enhanced ubiquitination via the protein kinase A (PKA) pathway. Blocking PKA partially reversed these protective effects. Here we highlight that hUC-MSC-EVs provide neuroprotection by regulating the NLRP3 inflammasome, offering a potential therapeutic strategy for HIBD. These findings expand the understanding of EV-mediated neuroprotection and suggest broader applications for ischemia-related conditions, with potential for clinical translation.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1553-1570"},"PeriodicalIF":0.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12097387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142911262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of plasma endocan levels with metabolic parameters and predictive value of endocan for the development of complications in patients with type 2 diabetes mellitus: An observational study.","authors":"Kenana Ljuca, Mensura Aščerić, Olivera Batić-Mujanović, Svjetlana Loga-Zec, Nadina Ljuca, Emir Bećirović, Samir Bejić, Predrag Jovanović, Minela Bećirović","doi":"10.17305/bb.2024.11512","DOIUrl":"10.17305/bb.2024.11512","url":null,"abstract":"<p><p>The aim of the current research was to investigate the association between plasma endocan levels and metabolic control parameters, as well as to evaluate its predictive value for clinical complications in patients with type 2 diabetes mellitus (DMT2). A total of 100 DMT2 patients participated in this prospective observational study. Plasma endocan levels were significantly elevated in DMT2 patients with HbA1c > 7% (1.38 ± 0.33 vs 0.68 ± 0.23 ng/mL; P < 0.0001), compared to patients with HbA1c ≤ 7%. Patients with plasma endocan concentrations >1.10 ng/mL (median value of 1.10 ng/mL) demonstrated significantly higher levels of metabolic parameters: body mass index (BMI), HbA1c (%), fasting glucose level, LDL cholesterol, total cholesterol, triglycerides, along with significantly lower HDL cholesterol levels. Furthermore, patients with plasma endocan levels >1.10 ng/mL were found to have an increased risk for the following complications: retinopathy (relative risk [RR]: 2.7500; 95% confidence interval [CI]: 1.2150-6.2244; P = 0.0152, nephropathy (RR: 2.0952; 95% CI: 1.2294-3.5710; P = 0.0065), neuropathy (RR: 1.9945; 95% CI: 1.2025-3.3081; P = 0.0075), angina pectoris (RR: 2.4881; 95% CI: 1.0865-5.6979; P = 0.0311, hypertension (RR: 1.1372; 95% CI: 1.0060-1.2856; P = 0.0398), cardiomyopathy (RR: 2.6190; 95% CI: 1.1507-5.9612; P = 0.0218), myocardial infarction (RR: 9.4286; 95% CI: 1.2742-69.7697; P = 0.0280) and stroke (RR: 4.4638; 95% CI: 1.3765-14.4758; P = 0.0127). Correlation analysis revealed that plasma endocan levels were positively correlated with HbA1c (%) (r = 0.856, P < 0.0001), fasting glucose level (r = 0.631, P < 0.0001), LDL (r = 0.347, P = 0.0004), cholesterol (r = 0.282, P = 0.0045), and triglycerides (r = 0.366, P = 0.0002). Conversely, plasma endocan levels were negatively correlated with HDL cholesterol (r = -0.429, P < 0.0001). In conclusion, higher plasma endocan levels were strongly associated with poor metabolic control in DMT2 patients and exhibited significant predictive value for both microvascular and macrovascular complications.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1522-1527"},"PeriodicalIF":0.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12097385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142886546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Obstetric-specific compared to general early warning system for predicting severe postpartum maternal morbidity.","authors":"Neža Pezdirc, Tatjana Stopar Pintarič, Miha Lučovnik","doi":"10.17305/bb.2024.11679","DOIUrl":"10.17305/bb.2024.11679","url":null,"abstract":"<p><p>Severe maternal morbidity is a major global health concern, and early identification of at-risk postpartum women is essential to improving outcomes. We aimed to compare the predictive values of the Modified Early Obstetric Warning System (MEOWS) versus the non-obstetric general Early Warning System (EWS) for predicting severe maternal morbidity in postpartum women. We retrospectively reviewed hospital documentation of 723 postpartum women admitted to the obstetric high dependency unit between October 2020 and March 2021. Severe maternal morbidity was defined using the American College of Obstetricians and Gynecologists' criteria. We assessed the sensitivity, specificity, positive and negative predictive values, as well as positive and negative likelihood ratios, of the MEOWS and the EWS for predicting severe postpartum maternal morbidity. Twenty-four (3.3%) women included in the study met the criteria for severe maternal morbidity. Hypertensive complications and obstetric haemorrhage were the most prevalent causes of maternal morbidity. The sensitivity of the MEOWS was 92%, specificity 62%, positive predictive value 8%, and negative predictive value 100%. The positive likelihood ratio was 2.4, while the negative likelihood ratio was 0.1. In comparison, the EWS had a sensitivity of 63%, specificity of 66%, positive predictive value of 6%, and negative predictive value of 98%. The positive likelihood ratio for the EWS was 1.8, and the negative likelihood ratio was 0.6. The obstetric-specific early warning system proved to be superior for the early prediction of severe postpartum maternal morbidity compared to the general non-obstetric warning system.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1517-1521"},"PeriodicalIF":0.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12097397/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142847450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}