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This study investigates the combined effects of probiotics and omega-3 fatty acids on blood and liver function biomarkers, as well as gut microbiota diversity, in a high-fat diet (HFD)-induced obesity model in male mice. Cardiovascular diseases (CVD), often linked to obesity, are major global health issues driven by abnormal cholesterol and triglyceride levels in the blood. Omega-3 fatty acids, known to lower triglycerides and prevent CVD, and probiotics, which enhance gut microbiota balance and nutrient absorption, were evaluated for their combined effects. The experiment involved five groups of male C57BL/6J mice: a normal diet group, an HFD group, an HFD + probiotics group, an HFD + omega-3 group, and an HFD + combined probiotics and omega-3 group. Over six weeks, the combined treatment group showed significant reductions in body weight gain, a significant improvement in ALT levels (a key liver function biomarker), and enhanced anticoagulation markers, such as prothrombin time and activated partial thromboplastin time, compared to the HFD group. Gut microbiota analysis via 16S rRNA sequencing also revealed significant increases in microbial diversity in the combined treatment group. These findings suggest that co-administration of probiotics and omega-3 offers potential therapeutic benefits in reducing obesity-related metabolic dysfunctions by improving lipid metabolism, liver health, and blood circulation.

Mito-TEMPO is a well-known mitochondria-specific superoxide scavenger. However, the effect of Mito-TEMPO on porcine embryo development, to our knowledge, has not been studied yet. In the present study, porcine embryos were classified into two groups (G1 and G2) based on the cytoplasm lipid contents at the zygote stage. The development of blastocysts derived from G2 zygotes was reduced (G2:16.2 ± 7.9% vs G1: 26.5 ± 5.9%; 1.6-fold, p < 0.05) compared to those from G1 zygotes. In G2 embryos, the proportion of TUNEL-positive cells was also higher than that of G1 embryos. Superoxide in G2 embryos was significantly increased compared to that in G1 embryos. Mitochondrial membrane potential and ATP production were lower in G2 embryos than in G1 embryos. Phosphorylation of Drp1 at Ser 616 increased in G1 embryos during the cleavage stages compared to that in the zygote but was not significantly different in G2 embryos. Then, the effects of Mito-TEMPO were investigated in G2 embryos. Blastocyst formation rate (G2: 19.1 ± 5.1% vs G2 + Mito-TEMPO: 28.8 ± 4.0%; 1.5-fold, p < 0.05) and mitochondrial aggregation were recovered after superoxide reduction by Mito-TEMPO treatment. Thus, we showed that Mito-TEMPO improves blastocyst development by superoxide reduction in porcine embryos in vitro .

Peroxiredoxin 5 (Prdx5) is involved in pathophysiological regulation via the stress-induced cellular response. However, its function in the bone remains largely unknown. Here, we show that Prdx5 is involved in osteoclast and osteoblast differentiation, resulting in osteoporotic phenotypes in Prdx5 knockout ( Prdx5 Ko ) male mice. To investigate the function of Prdx5 in the bone, osteoblasts were analyzed through immunoprecipitation (IP) and liquid chromatography combined with tandem mass spectrometry (LC–MS/MS) methods, while osteoclasts were analyzed through RNA-sequencing. Heterogeneous nuclear ribonucleoprotein K (hnRNPK) was identified as a potential binding partner of Prdx5 during osteoblast differentiation in vitro. Prdx5 acts as a negative regulator of hnRNPK-mediated osteocalcin ( Bglap ) expression. In addition, transcriptomic analysis revealed that in vitro differentiated osteoclasts from the bone marrow-derived macrophages of Prdx5 Ko mice showed enhanced expression of several osteoclast-related genes. These findings indicate that Prdx5 might contribute to the maintenance of bone homeostasis by regulating osteoblast differentiation. This study proposes a new function of Prdx5 in bone remodeling that may be used in developing therapeutic strategies for bone diseases.

Fabry disease (FD) is a lysosomal storage disorder in which α-galactosidase (GLA) deficiency leads to a build-up of globo-triaosylceramide (Gb3) in various cell types. Gb3 accumulation leads to the abnormalities of microvascular function associated with FD. Previously, we discovered significant abnormalities in vascular endothelial cells (VECs) derived from FD-induced pluripotent stem cells. We then used a cell-based system to screen a group of clinical compounds for candidates capable of rescuing those abnormalities. Lomerizine was one of the most promising candidates because it alleviated a variety of FD-associated phenotypes both in vitro and in vivo. Lomerizine reduced mitochondria Ca 2+  levels, ROS generation, and the maximal respiration of FD-VECs in vitro. This led to a suppression of the endothelial-to-mesenchymal transition (EndMT) and rescued FD-VEC function. Furthermore, FD-model mice (Gla−/−/TSP1Tg) treated orally with lomerizine for 6 months showed clear improvement of several FD phenotypes, including left ventricular hypertrophy, renal fibrosis, anhidrosis, and heat intolerance. Thus, our results suggest lomerizine as a novel candidate for FD therapy.

It has been reported that chitosan has a hemostatic effect and an antibiotic activity. This study aimed to evaluate the efficacy and feasibility of using a chitosan tampon (Hemoblock-Tampon) in preventing hemorrhage and enhancing wound healing after the loop electrosurgical excision procedure (LEEP).This single-blind, prospective, randomized study included 62 consecutive patients who underwent LEEP for cervical intraepithelial neoplasia. A chitosan tampon (31 patients; treatment group), or a general tampon (31 patients; control group) was applied to the uterine cervix immediately after LEEP. One patient in the treatment group declined to participate in this study. Thus, 30 patients in the treatment group and 31 patients in the control group completed this study. For objective analysis of hemorrhage in the postoperative 2 weeks, the amounts of bleeding were checked daily with a pictorial blood assessment chart. We evaluated vaginal discharge, abdominal pain, and impairment in daily living during the postoperative 2 weeks using 5 visual analogue scale questionnaires.The bleeding count was significantly lower in the treatment group than in the control group (21.37 ± 16.86 vs. 40.52 ± 16.55, p  = 0.0014). The sum of the scores of the 5 questionnaires was significantly lower in the treatment group than in the control group (6.53 ± 2.84 vs. 8.59 ± 2.88, p  = 0.0079). The incidence of vaginal discharge was significantly lower in the treatment group than in the control group (20.0% vs. 48.4%, p  = 0.0207). According to logistic regression, only the use of chitosan tampon reduced the risk of moderate to severe vaginal bleeding 2 weeks after surgery (Odd ratio, 0.213; 95% confidence interval, 0.06–0.76; p  = 0.0172). Complete healing of the uterine cervix occurred in 86.7% of patients in the treatment group and in 61.3% of patients in the control group at 4 weeks after surgery ( p  = 0.0255).The use of chitosan tampons can reduce hemorrhage, vaginal discharge, abdominal pain, and impairment of daily living after LEEP. Moreover, chitosan tampon may help enhance wound healing.

Infection with the human pathogen Vibrio vulnificus leads to the generation of reactive oxygen species (ROS) via NAD(P)H oxidase (Nox) in host cells. In the present study, we employed mutant V. vulnificus strains to identify an essential virulence factor responsible for this ROS generation. We found that repeats-in-toxin A1 (RtxA1) expressed by V. vulnificus acts via Nox1 to induce significant ROS generation in the intestine epithelial cells, which ultimately results in cell death. Furthermore, RtxA1 modulates the small GTPase Rac2, which is known to play an important role in the activation of Nox. When mice were infected by the oral method, in contrast with the wild-type bacteria, an RtxA1-deficient V. vulnificus mutant was unable to induce ROS generation within the intestine and failed to cause death. These findings strongly suggest that RtxA1-induced Rac2 expression is a critical step underlying the pathogenicity of V. vulnificus

The incidence of myocardial infarction, among the causes of cardiovascular morbidity and mortality, is increasing globally. In this study, left ventricular (LV) dysfunction, including LV systolic and diastolic function, was investigated in a rat myocardial ischemia/reperfusion injury model with echocardiography. The homoisoflavanone sappanone A is known for its anti-inflammatory effects. Using echocardiography, we found that sappanone A administration significantly improved LV systolic and diastolic function in a rat myocardial ischemia/reperfusion injury model, especially in the early phase development of myocardial infarction. Based on myocardial infarct size, serum cardiac marker assay, and histopathological evaluation, sappanone A showed higher efficacy at the doses used in our experiments than curcumin and was evaluated for its potential to improve LV function.

OBJECTIVES:To analyze the prevalence of plasmid‐mediated quinolone resistance (PMQR) determinants in ciprofloxacin‐nonsusceptible Escherichia coli and Klebsiella pneumoniae isolated from patients at a tertiary care hospital in Korea. METHODS: A total of 102 nonduplicate isolates of ciprofloxacin‐intermediate or ciprofloxacin‐resistant E coli (n=80) and K pneumoniae (n=22) from blood cultures were obtained. The qnr ( qnrA, qnrB , qnrS ), aac(6′)-Ib-cr , qepA and oqxAB genes were detected using polymerase chain reaction (PCR) and confirmed using direct sequencing. To determine whether the PMQR‐positive plasmid was horizontally transferable, conjugation experiments were performed. RESULTS: Of the 102 isolates, 81 (79.4%) had one or more PMQR genes; these consisted of 59 (73.8%) E coli and 22 (100%) K pneumoniae isolates. The qnr genes were present in 15 isolates (14.7%): qnrB4 was detected in 10.8% and qnrS1 was detected in 3.9%. The aac(6′)-Ib-cr , qepA and oqxAB genes were detected in 77.5%, 3.9% and 10.8%, respectively. In conjugation experiments, PMQR genes were successfully transferred from seven (8.6%) isolates. The range of minimum inhibitory concentrations of ciprofloxacin for these seven transconjugants increased to 0.5 mg/L to 1 mg/L, which was 16‐ to 33‐fold that of the recipient E coli J53 bacteria. CONCLUSIONS: PMQR genes were highly prevalent among ciprofloxacin‐nonsusceptible E coli and K pneumoniae from blood cultures in the authors’ hospital. Therefore, it is necessary to monitor for the spread of PMQR genes of clinical isolates and to ensure careful antibiotic use in a hospital setting.

Background Peroxiredoxin V (Prdx V) plays a major role in preventing oxidative damage as an effective antioxidant protein within a variety of cells through peroxidase activity. However, the function of Prdx V is not limited to peroxidase enzymatic activity per se. It appears to have unique function in regulating cellular response to external stimuli by directing interaction with signaling protein. In this study, we identified Prdx V interacting partners in mouse kidney under hypoxic stress using immunoprecipitation and shotgun proteomic analysis (LC-MS/MS). Results Immunoprecipitation coupled with nano-UPLC-MS E shotgun proteomics was employed to identify putative interacting partners of Prdx V in mouse kidney in the setting of hypoxia. A total of 17 proteins were identified as potential interacting partners of Prdx V by a comparative interactomics analysis in kidney under normoxia versus hypoxia. Dihydrolipoamide branched chain transacylase E2 (DBT) appeared to be a prominent candidate protein displaying enhanced interaction with Prdx V under hypoxic stress. Moreover, hypoxic kidney exhibited altered DBT enzymatic activity compared to normoxia. An enhanced colocalization of these two proteins under hypoxic stress was successfully observed in vitro. Furthermore, peroxidatic cysteine residue (Cys48) of Prdx V is likely to be responsible for interacting with DBT. Conclusions We identified several proteins interacting with Prdx V under hypoxic condition known to induce renal oxidative stress. In hypoxic condition, we observed an enhanced interaction of Prdx V and DBT protein as well as increased DBT enzymatic activity. The results from this study will contribute to enhance our understanding of Prdx V’s role in hypoxic stress and may suggest new directions for future research.