This study aims to compare the diagnostic performance of colloidal gold immunochromatographic assay (GICA) with culture-based screening for antepartum detection of Group B Streptococcus (GBS). This prospective study was conducted in a tertiary hospital in South China, performing GBS screening on women at 35-37 weeks of gestation. GICA and direct bacterial culture were separately performed on paired rectovaginal swabs. Decisions about intrapartum antibiotic prophylaxis (IAP) were based on the GBS positive results by either GICA or culture. The detection rate for GBS colonization was 7.5% (31/414) by the culture and 16.4% (68/414) by the GICA, with significant difference (p<0.001). Kappa value between the two methods was 0.516 (p<0.001), suggesting moderate concordance. Against the reference standard of direct culture, the GICA showed a sensitivity of 90.3%, specificity of 89.6%, positive predictive value (PPV) of 41.2%, negative predictive value (NPV) of 99.1%, and accuracy of 89.6%. Among individuals with positive GICA, the culture-positive group was associated with significantly higher proportion of IAP and lower relative risk of adverse pregnancy outcomes compared to the negative group. The GICA demonstrates 90% sensitivity and specificity in detecting maternal GBS colonization compared to culture. This rapid test may be considered as a promising alternative, particularly for emergency labor and large-scale screening in resource-limited settings. However, the clinical overuse of IAP should be concerned.

Aicardi-Goutières syndrome (AGS) is a progressive multisystem disorder marked by early-onset encephalopathy. This report investigates the genetic basis of AGS in a newborn from consanguineous parents with microcephaly, recurrent hemorrhagic strokes, brain calcifications, leukodystrophy, epilepsy, anemia, thrombocytopenia, and left ventricular hypertrophy. Next-generation sequencing-based targeted gene panel testing for epilepsy c.65-13G>A variant in the RNASEH2B gene. Both parents were identified as carriers of the heterozygous mutation, confirming autosomal recessive inheritance. RNA analysis showed that this variant created a new splice site, leading to an 11-base-pair extension in exon 2. This alteration caused a frameshift (p.Glu22Valfs*7) and subsequent truncation of the RNASEH2B protein. This case highlights the severe neurological manifestations of AGS in newborns and elucidates the pathogenic mechanism of a newly identified intronic RNASEH2B variant.

Esophageal squamous cell carcinoma (ESCA) is a prevalent malignant tumor with poor prognosis. Interleukin 2 receptor beta (IL2RB) has been implicated in various cancers; however, its role in ESCC remains unclear. We analyzed IL2RB expression in clinical samples and cell lines. The impact of IL2RB on tumor progression was assessed using gain- and loss-of-function approaches, along with in vivo tumor models. In addition, we explored the effect of IL2RB on the immune microenvironment and its potential to modulate the JAK1/STAT5 pathway. IL2RB was found to be significantly upregulated in ESCC tissues compared to normal tissues. Functional studies revealed that IL2RB knockdown inhibited tumor cell proliferation, migration, and invasion, as well as epithelial-mesenchymal transition (EMT). IL2RB was shown to reshape the tumor immune microenvironment by inducing CD8+T cell depletion. Mechanistic investigations indicated that IL2RB activates the JAK1/STAT5 pathway, thereby promoting ESCC progression. Our findings demonstrate that IL2RB plays a critical role in ESCC progression and immune evasion, suggesting its potential as a therapeutic target. Further studies are warranted to explore the clinical application of IL2RB targeting in ESCC treatment.

Islet β-cell dysfunction and insulin resistance are associated with obesity-associated type 2 diabetes mellitus. Short-chain fatty acids (SCFAs) are important regulatory factors for energy metabolism. We aimed to determine the effects of butyric acid (BA) on β-cell apoptosis in type 2 diabetes. A db/db transgenic mouse model and lipopolysaccharide (LPS)-stimulated β-cell model were used to determine the effects of BA on β-cells. The viability and apoptosis of β cells were determined using the MTT assay and flow cytometry, respectively. The expression of inflammatory factors IL-1β, TNF-α, IL-6, and IL-10 was measured using quantitative PCR. Activation of the NF-κB signaling pathway was detected by quantitative PCR and Western blotting. Fasting plasma glucose (FPG), fasting insulin (FINS), total cholesterol (TC), and triglyceride (TG) levels were assessed to evaluate glycolipid metabolism. Intestinal flora and SCFA analyses were performed to explore the changes in the gut microbiota. Butyric acid treatment notably suppressed LPS-induced expression of pro-inflammatory cytokines and improved β-cell apoptosis. The levels of TC, TG, FPG, and FINS were significantly elevated in diabetic mice and decreased after BA treatment. The expression of the β-cell regulatory genes Maf-A and Foxo1 was notably decreased in diabetes, and BA treatment restored their expression levels. Butyric acid notably alleviated β-cell apoptosis and the secretion of inflammatory cytokines in diabetes by suppressing NF-κB signaling. Butyric acid improves the intestinal flora of diabetic mice, suggesting its potential as a novel therapeutic agent for diabetes.

Osteoporosis is a common disorder marked by bone loss, fragility, and fractures. microRNAs (miRNAs) are highlighted as potential regulators of osteoblast differentiation, and exosomes carrying miRNAs from bone marrow stromal cells (BMSCs) are applied to treatment. Herein, we aimed to clarify the role of miR-17 and BMSCs in ovariectomized rats with osteoporosis. After establishment of an osteoporosis animal model, miR-17 and BARX2 expression in ovariectomized rat tissues and osteoblasts were detected. Osteoblasts were transfected with mimics and inhibitor and co-cultured with BMSCs, whilst cell proliferation and differentiation were evaluated. miR-17 was poorly expressed in ovariectomized rat tissue, while BARX2 was up-regulated. Overexpression of miR-17 induced decreased BARX2 expression but enhanced proliferation and differentiation of osteoblasts in osteoporotic rats. Importantly, the presence of BMSCs also facilitated osteoblast differentiation and decreased BARX2 expression, which was abolished by addition of exosome inhibitors. Mechanistically, miR-17 targeted BARX2 expression to up-regulate ALP and Co1-I in osteoporosis. Collectively, miR-17 delivered by BMSC exosomes promotes osteogenic differentiation and induces bone healing in osteoporosis through BARX2 regulation. The combined use of exosome inhibitors confirmed the therapeutic effect of BMSCs and BMSC exosomes containing miRNAs on various diseases.

This study aimed to evaluate the effect of a novel intrauterine infusion of autologous platelet-rich plasma (PRP) on endometrial condition and clinical outcomes in patients with thin endometrium undergoing frozen-thawed embryo transfer (FET) cycles. A prospective randomized controlled trial was conducted with 70 patients diagnosed with thin endometrium at the Reproductive Medicine Center of Shenzhen Maternal and Child Health Hospital from January 2022 to June 2023. The patients were randomly divided into two groups: a single PRP infusion group and a PRP combined with endometrial microstimulation (EM+PRP) group. Endometrial thickness and classification were assessed before and after treatment. Clinical outcomes, including human chorionic gonadotropin (HCG) positivity rate, embryo implantation rate, clinical pregnancy rate, and early miscarriage rate, were analyzed. Baseline characteristics, including pre-treatment endometrial thickness, were comparable between groups. Both groups showed a significant increase in endometrial thickness after treatment (P<0.05). The EM+PRP group exhibited a greater improvement in post-treatment endometrial thickness compared to the single PRP group (P<0.05). Endometrial morphology showed improvement in both groups, but the difference was not statistically significant (P>0.05). No significant differences were found between the two groups in terms of HCG positivity rate, embryo implantation rate, clinical pregnancy rate, or early miscarriage rate. Both EM+PRP and single PRP intrauterine infusion effectively increased endometrial thickness and improved clinical outcomes in patients with thin endometrium. The combined EM+PRP therapy showed potential for greater efficacy in improving endometrial condition, warranting further research in larger, multicenter studies.

Atherosclerosis (AS) represents a life-threatening condition involving vascular inflammation and posing a high risk of death, yet effective therapeutic strategies remain limited. This research focused on elucidating the regulatory function of the long noncoding RNA H19 (lncRNA H19) in AS and its underlying molecular mechanisms. To conduct the research, an AS mouse model induced by a high-fat diet and a vascular smooth muscle cell (VSMC) model exposed to oxidized low-density lipoprotein (ox-LDL) treatment were respectively constructed. There were significant aortic pathological changes and increased foam cell formation in the AS group versus the Control group. ox-LDL treatment effectively enhanced VSMC proliferation, VSMC migration, foam cell formation, and inflammatory cytokine secretion (TNF-α and IL-6), along with decreased microRNA-107 (miR-107) expression, while simultaneously increasing CD40 expression in VSMCs, all of which were reversed by knockdown of H19. Additionally, inhibition of miR-107 increased the migration and proliferation, inflammatory cytokine secretion, as well as foam cell formation in ox-LDL-treated VSMCs subjected to H19 knockdown. Moreover, miR-107 was confirmed to directly target CD40, and CD40 overexpression mitigated H19 knockdown-induced effects on ox-LDL-treated VSMCs. H19 regulates the progression of AS by modulating the CD40/CD40L axis through regulation of miR-107. Targeting H19/miR-107 and CD40/CD40L may serve as a potential treatment strategy for AS.

Atherosclerosis (AS) contributes significantly to the development of cardiovascular disease. Despite recent advances in medical treatment, the outcomes for patients with AS are still unsatisfactory. This study aims to enhance our understanding of AS and pave the way for the development of more effective therapeutic approaches to improve patient outcomes and ultimately reduce the burden of this devastating condition. An AS cell model was established using oxidized low-density lipoprotein (OX-LDL) administration to human vascular smooth muscle cells (HVSMCs), followed by injection with oe-NC, oe-FUS, oe-Sfrp5, or oe-FUS+ oe-Sfrp5. Western blot, Transwell assay, CCK8 assay, Oil Red O staining assay, and ELISA were used to elucidate the mechanisms of the FUS/Sfrp5/Wnt5 pathway in our model of AS. In this study, both FUS and Sfrp5 inhibited Wnt5a expression. In addition, FUS inhibited lipid droplet formation and migration capacity of OX-LDL-induced HVSMCs, and FUS and Sfrp5 may have a synergistic effect in controlling Wnt5a in AS. These results highlight the potential therapeutic value of targeting the FUS and Sfrp5 pathway to control AS progression. The findings suggest that FUS and Sfrp5 may have a synergistic effect in controlling Wnt5a in AS.