Tohoku Journal of Experimental Medicine最新文献

This study evaluated the effectiveness of implementing an Enhanced Recovery after Surgery (ERAS) protocol in enhancing recovery outcomes following cesarean section (CS) in 200 women with gestational diabetes mellitus (GDM). The patients were randomized into an ERAS group or a Control group. The ERAS protocol differed from routine care by reducing preoperative fasting times, using targeted medications, employing neuraxial anesthesia and warming measures, initiating early feeding and mobilization, goal-directed fluid management, and earlier catheter removal to enhance recovery and minimize complications. Various outcome measures, including postoperative length of hospital stay (LOS) and time to achieve postoperative milestones, were assessed. Postoperative pain relief was evaluated using the visual analogue scale (VAS), while quality of life was assessed through the EuroQoL (EQ-5D-5L) survey. Patient satisfaction with nursing care was determined using the Patient Satisfaction with Nursing Care Quality Questionnaire (PSNCQQ). The ERAS group demonstrated significantly shorter postoperative LOS and achieved recovery milestones faster than the Control group. Postoperative pain relief outcomes were significantly improved in the ERAS group, with lower VAS scores for pain during rest and breastfeeding compared to the Control group. The ERAS protocol also effectively improved specific health dimensions and overall QOL following CS in patients with GDM. Furthermore, the ERAS group exhibited higher levels of patient satisfaction with postpartum nursing care quality compared to the Control group. Implementation of an ERAS protocol in CS for women with GDM significantly enhances postoperative recovery outcomes, including shorter hospital stay, improved pain relief, enhanced QOL, and increased patient satisfaction.

MiR-204-5p is involved in a variety of diseases related to thyroid dysfunction and pregnancy. However, the effect on subclinical hypothyroidism (SCH) during pregnancy remained unclear. We focused on the expression difference of serum miR-204-5p in pregnant women with subclinical hypothyroidism in the second trimester and evaluated the correlation between them in this study. One hundred normal pregnant women and 175 individuals diagnosed with SCH were enrolled. The miR-204-5p level was calculated by qRT-PCR and its relevance to serum thyroid stimulating hormone (TSH) was assessed by Pearson analysis. The predictive value was evaluated by receiver operator characteristic (ROC) curve. The risk factor of SCH was identified by multivariate logistic regression analysis. The miR-204-5p was obviously depressed in SCH group compared to control (P < 0.001) and was significantly negatively correlated to the serum TSH levels (r = -0.6082, P < 0.0001). ROC curve showed the potential predictive value while the area under the curve was 0.9153 with sensitivity of 90.29% and specificity of 86.00%. TSH (OR: 1.793, 95% CI: 1.072-2.998, P = 0.026) and miR-204-5p (OR: 0.528, 95% CI: 0.317-0.878, P = 0.014) were related to SCH risk in pregnant women. In both SCH group and low miR-204-5p group, individuals with respiratory distress syndrome (RDS) or depression possessed a higher proportion of adverse events during 32-38 gestational weeks. Depressed miR-204-5p was observed in SCH patients and was significantly negatively correlated to TSH level. MiR-204-5p was a risk factor for SCH in pregnant women. Additionally, depressed miR-204-5p might be related to the incidence of adverse pregnancy outcomes.

Acute lung injury (ALI) is an acute bilateral pulmonary infiltration disease, which may finally cause impairment and even loss of lung function. This study aimed to investigate the therapeutic potential and the mechanism of the Xuanfei Huazhuo decoction (XFHZ) against ALI in mice. The ALI mice stimulated by lipopolysaccharide (LPS) were subjected to the treatment of saline, 0.06, 0.11, and 0.22 mg/kg of XFHZ, and 10 mg/kg of fasudil, respectively, for seven consecutive days. It was found that XFHZ significantly attenuated LPS-induced pathological injury and mitochondrial dysfunction of vascular endothelial cells in the lung and suppressed LPS-mediated lung pulmonary edema (lung wet/dry weight ratio), the elevation of vascular permeability (increased total protein and albumin content in bronchoalveolar lavage fluid) and neutrophil infiltration. Microtubule stabilization, a process that could be regulated by GEF-H1, MYPT-1, Tau, and MAP-4, is critical for maintaining the endothelial cell barrier, of which disruption is a pathological hallmark of ALI. XFHZ reduced the expression of GEF-H1 and MYPT-1 at mRNA and protein levels and decreased Tau and MAP-4 protein expression in LPS-induced ALI. XFHZ also suppressed the increase of monomeric tubulin and the decrease of polymeric tubulin in injured lung induced by LPS. This study demonstrated that XFHZ can improve LPS-induced ALI by promoting microtubule stabilization, providing a theoretical basis for the clinical treatment of patients with ALI induced by different factors, including SARS-CoV-2 infection.

Dexmedetomidine (DEX) exerts neuroprotective effects following ischemic stroke (IS) by regulating several pathways, such as extracellular signal-regulated kinase 1 and 2 pathway and Ca2⁺-stromal interaction molecule 1/Orai calcium release-activated calcium channel protein 1 pathway, according to previous studies. However, the underlying mechanisms are not entirely elucidated yet. The purpose of this study was to investigate the impact of DEX on inhibiting neuron damage during IS, and the potential mechanism. Hippocampal neurons (HT22 cells) were treated with oxygen-glucose deprivation/reoxygenation (OGD/R) in the presence of 1 _μM DEX, 10 _μM LY294002 [a protein kinase B (AKT) inhibitor], or their combination. DEX increased viability and reduced apoptosis in OGD/R-stimulated hippocampal neurons. DEX reduced lactate dehydrogenase (LDH) and reactive oxygen species (ROS), but increased superoxide dismutase (SOD) and mitochondrial membrane potential (MMP) in OGD/R-stimulated hippocampal neurons. These discoveries indicated that DEX mitigated OGD/R-triggered oxidative stress in hippocampal neurons. DEX increased phosphorylated-AKT/AKT and phosphorylated-mammalian target of rapamycin (mTOR)/mTOR in OGD/R-stimulated hippocampal neurons, which suggested that DEX activated the AKT/mTOR pathway. LY294002 inhibited the AKT/mTOR pathway and viability, but enhanced apoptosis and oxidative stress in OGD/R-stimulated hippocampal neurons. Notably, LY294002 reversed the effect of DEX on the above-mentioned processes in OGD/R-stimulated hippocampal neurons. In conclusion, DEX inhibits OGD/R-triggered hippocampal neuron injury by activating the AKT/mTOR pathway, which is conducive to attenuating IS progression.

Ovarian cancer has been regulated by microRNAs (miRNAs). Dysregulation of miR-487b-3p has been observed in several cancers. Present research was performed to explore the expression and function of miR-487b-3p in ovarian cancer. Differentially expressed miRNAs (DEmiRNAs) have been selected from GSE131790 dataset. miR-487b-3p level in epithelial ovarian cancer (EOC) patients has been verified by qRT-PCR. Effect of miR-487b-3p for EOC has been explored in SKOV3 and A2780 cells. Cell proliferation was assessed by Cell Counting Kit-8 conducted to assess the cell viability. Cell apoptosis rate was examined by flow cytometer. Transwell experiment was conducted to assess the migration and invasiveness of cells. Target gene of miR-487b-3p was predicted by databases. Target association was certified by double luciferase experiment. miR-487b-3p was upregulated in EOC patients. High miR-487b-3p could diagnose the onset of EOC (area under ROC curve (AUC) = 0.924, sensitivity = 88.79%, specificity = 84.8%). High FIGO stage (P = 0.023) and low differentiation grade (P = 0.044) were more frequently discovered in high miR-487b-3p group. miR-487b-3p could facilitate the cell viability, migration, invasiveness and inhibit the apoptosis of EOC cells. Ferrochelatase (FECH) is a direct target gene of miR-487b-3p. FECH was decreased in EOC tissues and passively related to miR-487b-3p. FECH could reverse the function of miR-487b-3p for EOC cells. Upregulated miR-487b-3p in EOC patients had high diagnostic value for EOC. miR-487b-3p facilitated EOC development via FECH.

Alcohol-induced osteoporosis (AOP) is a condition characterized by decreased bone mass and increased fracture risk due to excessive alcohol consumption. This study aimed to investigate the impact of ethanol on osteogenic differentiation through the KDM6B/BMP2 axis in AOP pathogenesis. Bone marrow mesenchymal stem cells (BMSCs) were cultured and exposed to ethanol to simulate AOP conditions. The expression levels of KDM6B, BMP2, and osteogenic markers were evaluated using RT-PCR, Western blotting, and immunohistochemistry. Osteogenic differentiation was assessed through alkaline phosphatase (ALP) activity assay and Alizarin Red staining experiment. The regulatory role of KDM6B in BMP2 demethylation was investigated using Chromatin Immunoprecipitation (ChIP) assay for H3K27me3 methylation levels. KDM6B and BMP2 expression was found decreased in AOP bone samples, and a positive correlation between KDM6B and BMP2 expression was observed. Ethanol treatment resulted in the downregulation of KDM6B, BMP2, and osteogenic markers in BMSCs, while upregulation of KDM6B rescued these phenomena. Moreover, ethanol treatment elevated the H3K27me3 methylation level of BMP2 promotor region, which was also reversed by KDM6B upregulation. Meanwhile, downregulation of BMP2 reversed the pro-osteogenic effects of KDM6B upregulation. KDM6B inhibits the H3K27me3 methylation of BMP2 to promote osteoblast differentiation and therefore ameliorates alcohol-induced osteoporosis.