Biomolecules & biomedicine最新文献

Coarctation of the aorta (CoA) ranks among the most prevalent congenital heart defects and poses a life-threatening risk if left undiagnosed. Herein, we utilized fetal heart quantification (HQ) technology to improve the prenatal prediction of CoA. A retrospective analysis was conducted on 64 fetal cases with suspected aortic arch constriction, identified through prenatal ultrasound findings between November 2020 and March 2022 at the Department of Ultrasound, Sir Run Run Shaw Hospital, Zhejiang University. According to the follow-up results, these cases were divided into two groups: 35 cases confirmed as CoA by postpartum surgery or induction, and 29 cases initially suspected of CoA prenatally but subsequently ruled out postnatally. Additionally, 88 cases of normal fetuses were randomly selected as the control group. Both conventional M-mode ultrasound techniques and Fetal HQ software were utilized for fetal analysis across all groups. Parameters related to the heart were measured, including fetal 4-CV length, width, Global Spherical Index (GSI), Mitral Annular Plane Systolic Excursion (MAPSE), areas and ratios of the left and right ventricles, as well as lengths and ratios of the left and right ventricles. Functional measurements of the left and right ventricles included ejection fraction (EF), fractional area change (FAC), global longitudinal strain (GLS), fractional shortening (FS), end-diastolic diameter (ED), and sphericity index (SI). Left ventricular (LV)-GLS, LV-FAC, LV-EF, and LV-EF Z-score could potentially differentiate between true CoA and false CoA or normal groups and serve as potential indicators for the clinical diagnosis of CoA. The receiver operating characteristic (ROC) curves indicated that LV-GLS and LV-EF Z-score have the greatest predictive power for CoA diagnosis. The segments 6-12 of FS in the confirmed CoA group were significantly lower than those in the false CoA and normal groups. Fetal HQ technology, by assessing changes in the size and shape of the heart, can provide relatively reliable parameter support for the prenatal diagnosis of fetal aortic coarctation.

Artificial intelligence (AI) has become a powerful tool in biochemistry, greatly enhancing research capabilities by enabling the analysis of complex datasets, predicting molecular interactions, and accelerating drug discovery. As AI continues to evolve, its applications in biochemistry are poised to expand, revolutionizing both theoretical and applied research. This review explores current and potential AI applications in biochemistry, with a focus on data analysis, molecular modeling, enzyme engineering...

The wider availability of continuous respiratory monitors and advanced data abstraction techniques has led to a substantial increase in understanding of postoperative opioid-induced respiratory depression (OIRD), particularly regarding its incidence, presentation, temporal distribution, and risk factors. Self-limited episodes of OIRD are relatively common, typically presenting as repetitive apneas beginning in the postoperative period and continuing through the first night after surgery. In contrast, life-threatening episodes of OIRD are rare and usually occur on the day of surgery. Traditional monitoring of patient vital signs may be insensitive in detecting OIRD, while healthcare staff may be more adept at recognizing the concurrent development of somnolence. Although obstructive sleep apnea (OSA) is a known risk factor for OIRD, a more comprehensive phenotype is emerging-elderly patients with debility and substantial comorbidity. These advances have significant implications for managing postoperative OIRD. This review will focus on how these new insights into OIRD have highlighted knowledge gaps and created opportunities for future research and practice initiatives.

It has been reported that long non-coding RNAs (lncRNAs) are involved in sepsis-induced liver injury, while the role of cancer susceptibility candidate 7 (CASC7) in liver injury induced by sepsis remains elusive. In our study, 62 patients and 55 healthy controls were enrolled from our hospital, from whom CASC7 and microRNA-217 (miR-217) in serum samples were detected by quantitative real-time PCR (qRT-PCR). Then the sepsis-induced liver injury mice model was established by lipopolysaccharide (LPS). The effect of CASC7 on liver injury induced by sepsis was confirmed by hematoxylin and eosin (HE) staining, ELISA assay, TUNEL assay, Annexin V-FITC apoptosis assay and cell counting kit-8 (CCK-8) assay, respectively. Besides, RNA pull-down, luciferase reporter gene assay, qRT-PCR, and western blot were used to evaluate the underlying mechanisms. In this study, lncRNA CASC7 was significantly increased while miR-217 was significantly decreased in patients with sepsis-induced liver injury compared with that in healthy controls. There was a negative association of CASC7 and miR-217 in serum samples from patients with sepsis-induced liver injury and healthy controls. CASC7 was upregulated in a time-dependent manner in liver tissues of LPS-treated mice. It was found that knockdown of CASC7 reduced the liver injury induced by LPS in mice. In vitro, LPS treatment enhanced cell apoptosis, while knockdown of CASC7 inhibited the role of LPS in cell apoptosis. Moreover, knockdown of CASC7 suppressed the LPS-enhanced tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β) expression. In addition, miR-217 was found to be a target of CASC7, and miR-217 mimic could reverse CASC7-promoted liver injury. Furthermore, toll-like receptor 4 (TLR4) was identified as the target of miR-217, and both CASC7 and miR-217 could downregulate the mRNA and protein level of TLR4. Additionally, TLR4 overexpression could reverse miR-217-inhibited or CASC7-promoted liver injury. Taken together, CASC7 contributes to the progression of LPS-induced liver injury via the miR-217/TLR4 axis.

Osteoporotic femoral neck fractures (OFNFs) pose a significant orthopedic challenge in the elderly population, accounting for up to 40% of all osteoporotic fractures and leading to considerable health deterioration and increased mortality. In addressing the critical need for early identification of osteoporosis through routine screening of femoral neck bone mineral density (FNBMD), this study developed a user-friendly prediction model aimed at men aged 50 years and older, a demographic often overlooked in osteoporosis screening. Utilizing data from the National Health and Nutrition Examination Survey (NHANES), the study involved outlier detection and handling, missing value imputation via the K nearest neighbor (KNN) algorithm, and data normalization and encoding. The dataset was split into training and test sets with a 7:3 ratio, followed by feature screening through the least absolute shrinkage and selection operator (LASSO) and the Boruta algorithm. Eight different machine learning algorithms were then employed to construct predictive models, with their performance evaluated through a comprehensive metric suite. The random forest regressor (RFR) emerged as the most effective model, characterized by key predictors such as age, body mass index (BMI), poverty income ratio (PIR), serum calcium, and race, achieving a coefficient of determination (R²) of 0.218 and maintaining robustness in sensitivity analyses. Notably, excluding race from the model resulted in sustained high performance, underscoring the model's adaptability. Interpretations using Shapley additive explanations (SHAP) highlighted the influence of each feature on FNBMD. These findings indicate that our predictive model effectively aids in the early detection of osteoporosis, potentially reducing the incidence of OFNFs in this high-risk population.

Colorectal adenocarcinoma (COAD) is a significant cause of cancer-related mortality worldwide, necessitating the identification of novel therapeutic targets and treatments. This research aimed to investigate the role of ARL3 in COAD progression and to explore the effects of Piperine on ARL3 expression, cell proliferation, epithelial-mesenchymal transition (EMT), and endoplasmic reticulum (ER) stress. Bioinformatics analysis of The Cancer Genome Atlas (TCGA)-COAD, GSE39582, and GSE44861 datasets assessed ARL3 expression levels. Immunohistochemical data from the Human Protein Atlas (HPA) database confirmed ARL3 overexpression in COAD. The association of ARL3 with COAD clinical parameters and prognosis was also examined. COAD cells were treated with Piperine, and in vitro assays evaluated cell proliferation, apoptosis, EMT marker expression, and ER stress (ERS) responses. ARL3 overexpression in COAD correlated with poor prognosis and varied across pathological stages. Piperine treatment inhibited COAD cell proliferation in a concentration- and time-dependent manner, as indicated by reduced Ki-67 levels and decreased colony-forming ability. Piperine induced S-phase cell cycle arrest and facilitated apoptosis in COAD cells, evidenced by changes in Bax, Bcl-2, cleaved caspase-3, and cleaved Poly (ADP-ribose) polymerase (PARP) levels. Moreover, Piperine downregulated ARL3 expression in COAD cells, thereby suppressing transforming growth factor beta (TGF-β)-induced EMT. Additionally, Piperine attenuated the ARL3-mediated ER stress response, significantly reducing binding immunoglobulin protein (BiP), inositol-requiring enzyme 1 alpha (p-IRE1α), activating transcription factor 6 (ATF6), and C/EBP homologous protein (CHOP) levels. Piperine exerts anti-cancer effects in COAD by modulating ARL3 expression, disrupting cell cycle progression, inhibiting the EMT pathway, and regulating ERS. These findings suggest that Piperine holds promise as a therapeutic agent for COAD through its targeting of ARL3.

Staphylococcus epidermidis, a coagulase-negative staphylococcus, is a prevalent skin commensal that has increasingly been recognized as a significant pathogen, particularly in hospital environments, where it is associated with device-related infections. The emergence of multi-drug resistance and its ability to form biofilms complicate the clinical management of infections caused by this organism, posing a growing public health concern. This study aimed to investigate the nasal carriage of S. epidermidis among healthy young individuals and to analyze its antibiotic resistance patterns, resistance genes, and biofilm formation capabilities. Nasal swabs were collected from 40 undergraduate students at Mahasarakham University, Thailand, aged between 20 and 22 years. A total of 38 isolates were confirmed as S. epidermidis through both phenotypic and molecular characterization. Antibiotic susceptibility testing demonstrated resistance to various classes of antimicrobials, including beta-lactams, macrolides, and tetracyclines. Notably, five isolates exhibited methicillin resistance S. epidermidis (MRSE). Resistance genes, such as mecA, ermA, tetM, tetL, and tetK, were identified across the isolates, contributing to the observed resistance profiles. Biofilm formation assays revealed that most isolates displayed weak to moderate biofilm formation, with only one isolate demonstrating strong biofilm-forming capacity. Genetic analysis indicated a significant correlation between biofilm formation and the presence of the icaA gene, which is crucial for biofilm production. This study suggests the necessity for ongoing surveillance of nasal carriage of S. epidermidis to enhance understanding of its role in the dissemination of antimicrobial resistance and biofilm-associated infections, particularly within healthcare settings.

Pulmonary artery smooth muscle cell (PASMC) dysfunction is the central pathogenic mechanism in pulmonary hypertension (PH). This study explored the mechanism of action of RUNX1, a potential therapeutic target for PH, in PASMCs. A PH mouse model was used to investigate the impacts of RUNX1 knockdown on hemodynamics, right ventricular hypertrophy (RVH), and pulmonary artery remodeling (hematoxylin-eosin [H&E] staining). Isolated PASMCs were transfected with RUNX1- or chromobox 5 (CBX5)-related vectors and then subjected to cell function assays. Immunoprecipitation was used to detect molecular binding and ubiquitination. RUNX1 knockdown reduced right ventricular systolic pressure (RVSP), RVH, and pulmonary artery remodeling in mice with PH. Knockdown of RUNX1 or CBX5 suppressed proliferation, invasion, and migration and stimulated apoptosis in PASMCs under hypoxia. RUNX1 enhanced ubiquitin-specific protease 15 (USP15) promoter activity. USP15 bound to CBX5 and reduced CBX5 ubiquitination, thereby promoting CBX5 expression. CBX5 overexpression promoted the proliferation and movement of hypoxic PASMCs with reduced RUNX1 expression and decreased their apoptosis. In conclusion, RUNX1 knockdown inhibits USP15 transcription to promote the ubiquitination and degradation of CBX5, thereby alleviating PH in mice and reducing hypoxia-induced PASMC dysfunction.

To assess the diagnostic accuracy of two-dimensional shear wave elastography (2-D SWE) and point shear wave elastography (pSWE) in detecting liver fibrosis stages in patients with metabolic dysfunction-associated steatotic liver disease (MASLD), a comprehensive search was conducted across four databases up to February 9, 2024. A bivariate random-effects model was used to analyze the diagnostic accuracy of the methods. After screening, 13 studies involving pSWE included 1527 patients, while nine studies involving 2-D SWE included 1088 patients. The areas under the summary receiver operating characteristic (SROC) curves for diagnosing significant fibrosis (F ≥ 2), advanced fibrosis (F ≥ 3), and cirrhosis (F = 4) using pSWE and 2-D SWE were as follows: 0.84 (95% CI 0.80-0.87), 0.91 (95% CI 0.88-0.93), and 0.94 (95% CI 0.91-0.95) for pSWE; 0.83 (95% CI 0.79-0.86), 0.85 (95% CI 0.82-0.88), and 0.89 (95% CI 0.86-0.91) for 2-D SWE, respectively. The pooled sensitivity for pSWE and 2-D SWE for stages F ≥ 2, F ≥ 3, and F = 4 were 0.71 (95% CI 0.63-0.78), 0.81 (95% CI 0.72-0.88), and 0.81 (95% CI 0.63-0.91) for pSWE, and 0.77 (95% CI 0.68-0.84), 0.80 (95% CI 0.72-0.87), and 0.92 (95% CI 0.75-0.98) for 2-D SWE, respectively. The pooled specificity of pSWE and 2-D SWE for these stages were 0.83 (95% CI 0.76-0.88), 0.87 (95% CI 0.81-0.92), and 0.91 (95% CI 0.86-0.94) for pSWE, and 0.76 (95% CI 0.66-0.84), 0.76 (95% CI 0.69-0.82), and 0.83 (95% CI 0.78-0.85) for 2-D SWE, respectively. In conclusion, both 2-D SWE and pSWE demonstrated high diagnostic performance in identifying various stages of liver fibrosis in MASLD patients.

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 c...