Ultrasound in paediatric surgery: A meta-analysis review of its influence on postoperative wound healing and infection rates.

Ultrasound (US) has traditionally been recognised for its imaging capabilities, but its emerging role as a therapeutic modality in postoperative wound management, especially in paediatric care, has garnered significant attention. This meta-analysis aimed to evaluate the influence of US on postoperative wound healing and infection rates in paediatric patients. From an initial pool of 1236 articles, seven were deemed suitable for inclusion. Postoperative wound healing was assessed using the Redness, Edema, Ecchymosis, Discharge, and Approximation (REEDA) scale. Notably, there was a significant difference in wound healing patterns between the US-treated and control groups (I2 = 94%, standardized mean difference [SMD]: -4.60, 95% confidence intervals [CIs]: -6.32 to -2.88, p < 0.01), as illustrated in Figure 4. Additionally, a marked difference in wound infection rates was observed between the groups (I2 = 93%, SMD: -5.86, 95% CIs: -9.04 to -2.68, p < 0.01), as portrayed in Figure 5. The findings underscore the potential benefits of US in enhancing postoperative wound healing and reducing infection rates in paediatric surgical settings. However, the application of US should be judicious, considering the nuances of individual patient needs and clinical contexts.

Rosiglitazone attenuates high glucose-induced proliferation, inflammation, oxidative stress and extracellular matrix accumulation in mouse mesangial cells through the Gm26917/miR-185-5p pathway.

Rosiglitazone (RSG) is widely used to reduce the amount of sugar in the blood of patients with diabetes mellitus. Diabetic nephropathy is the most common microvascular complication of diabetes. The role of RSG in diabetic nephropathy is not fully understood. Diabetic nephropathy model was constructed in high glucose (HG)-treated mouse mesangial cells. The effects of RSG on cell viability and cell cycle were investigated using cell counting kit-8 (CCK-8) assay and flow cytometry assay. Oxidative stress was assessed according to ROS production and SOD activity in cells. Inflammatory responses were assessed according to the releases of inflammatory cytokines. Extracellular matrix (ECM) accumulation was determined by the levels of fibronectin and collagen IV using western blot. The expression of Gm26917 and microRNA-185-5p (miR-185-5p) was detected by quantitative real-time polymerase chain reaction (qPCR). The interaction between Gm26917 and miR-185-5p was validated by dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and pull-down assay. RSG significantly inhibited HG-induced proliferation, oxidative stress, inflammatory responses and ECM accumulation in mouse mesangial cells. The expression of Gm26917 was induced by HG but weakened by RSG. Gm26917 knockdown alleviated HG-induced proliferation, oxidative stress, inflammatory responses and ECM accumulation in mouse mesangial cells, and Gm26917 overexpression partly abolished the effects of RSG. Moreover, miR-185-5p was a target of Gm26917, and miR-185-5p inhibition recovered proliferation, oxidative stress, inflammatory responses and ECM accumulation in mouse mesangial cells that were alleviated by Gm26917 knockdown. RSG ameliorated HG-induced mouse mesangial cell proliferation, oxidative stress, inflammation and ECM accumulation partially by governing the Gm26917/miR-185-5p pathway.

Phenotypic and Genotypic Alterations of Durancin GL-Resistant Enterococcus durans Strains.

The emergence and spread of bacteriocin-resistant bacteria threaten the efficiency of bacteriocin usage as food preservatives. In this experiment, 19 selected Enterococcus durans strains acquired resistance after exposure to durancin GL, and the mutants had similar intermediate levels of resistance. One wild-type E. durans KLDS 6.0603 and its two resistant mutants, E. durans KLDS 6.0603-2 and E. durans KLDS 6.0603-3, were used to characterize phenotypic and genotypic differences. Approximately 100 µg/mL of durancin GL can penetrate the cytoplasmic membrane of E. durans KLDS 6.0603, causing damage to bacterial cells, but cannot penetrate E. durans KLDS 6.0603-2 and KLDS 6.0603-3 membranes. Unsaturated fatty acid content in resistant strains was significantly increased compared with wild-type strains, indicating that the former has more fluidity of cell membrane than the latter. Decreased mannose phosphotransferase system gene expression (mptD) was observed in the two resistant strains. Results showed that the factors, including the increased unsaturated fatty acid and decreased mptD expression, could contribute to durancin GL resistance.

Comparative Genomic Analysis of Shrimp-Pathogenic Vibrio parahaemolyticus LC and Intraspecific Strains with Emphasis on Virulent Factors of Mobile Genetic Elements.

Vibrio parahaemolyticus exhibits severe pathogenicity in humans and animals worldwide. In this study, genome sequencing and comparative analyses were conducted for in-depth characterization of the virulence factor (VF) repertoire of V. parahaemolyticus strain LC, which presented significant virulence to shrimp Litopenaeus vannamei. Strain LC, harboring two circular chromosomes and three linear plasmids, demonstrated ≥98.14% average nucleotide identities with 31 publicly available V. parahaemolyticus genomes, including 13, 11, and 7 shrimp-, human-, and non-pathogenic strains, respectively. Phylogeny analysis based on dispensable genes of pan-genome clustered 11 out of 14 shrimp-pathogenic strains and 7 out of 11 clinical strains into two distinct clades, indicating the close association between host-specific pathogenicity and accessory genes. The VFDB database revealed that 150 VFs of LC were mainly associated with the secretion system, adherence, antiphagocytosis, chemotaxis, motility, and iron uptake, whereas no homologs of the typical pathogenic genes pirA, pirB, tdh, and trh were detected. Four genes, mshB, wbfT, wbfU, and wbtI, were identified in both types of pathogenic strains but were absent in non-pathogens. Notably, a unique cluster similar to Yen-Tc, which encodes an insecticidal toxin complex, and diverse toxin-antitoxin (TA) systems, were identified on the mobile genetic elements (MGEs) of LC. Conclusively, in addition to the common VFs, various unique MGE-borne VFs, including the Yen-Tc cluster, TA components, and multiple chromosome-encoded chitinase genes, may contribute to the full spectrum of LC virulence. Moreover, V. parahaemolyticus demonstrates host-specific virulence, which potentially drives the origin and spread of pathogenic factors.

[The value of determination of serum myoglobin in estimation of degree of illness and prognosis of patients with sepsis in Xining area].

OBJECTIVE: To investigate the value of determination of serum myoglobin (MYO) in estimation of the degree of illness and prognosis of patients with sepsis in Xining area. METHODS: Serum MYO was measured and acute physiological and chronic health estimationII (APACHEII) score was evaluated in 30 cases with sepsis within 24 hours of admission to emergency intensive care unit (EICU), and their correlation was analyzed. The patients were divided into two groups, survival group and death group according to the result within 28 days. The MYO and APACHEII score were analyzed in both groups. All cases were divided into three groups: namely <500 (n=10), 500-1 000 (n=14), >1 000 µg/L (n=6) groups, according to serum MYO value, and APACHEII score and dead case were compared among three groups. RESULTS: Sixteen patients survived, and 14 patients died. The level of serum MYO and APACHEII score were significantly lower in survival group than death group [MYO (µg/L): 607.85±499.40 vs. 976.21±370.10, APACHEII score: 15.50±4.43 vs. 18.93±3.63, t(1)=2.28, t(2)=2.29, both P<0.05]. With the elevation of serum MYO, the dead case was increased in sepsis patients (the dead case in MYO<500, 500-1 000, >1 000 µg/L groups was 2, 7, 5 cases, respectively,χ(2)=5.94, P<0.05), but there was no difference in APACHEII score among three groups. There was significant positive correlation between serum MYO and APACHEII score (r=0.407, P<0.05). CONCLUSION: Determination of serum MYO can reflect degree of illness and prognosis of sepsis patients in Xining area.

The prevalence and risk factors of sarcopenia in patients with type 2 diabetes mellitus: a systematic review and meta-analysis.

BACKGROUND: Sarcopenia was a frequent chronic complication in patients with type 2 diabetes mellitus (T2DM), and previous evidence showed conflicting results regarding the prevalence and risk factors of sarcopenia in T2DM. In the current study, we aimed at systematically exploring the prevalence and risk factors of sarcopenia in patients with T2DM. METHODS: PubMed, Embase, and Cochrane Central Register of Controlled Trials were systematically searched to identify observational studies which investigated the prevalence and risk factors of sarcopenia in patients with T2DM. The quality of individual included studies was evaluated using The Newcastle-Ottawa scale. Pooled effects regarding prevalence and associated factors were calculated using random-effects models. The potential publication bias was assessed via funnel plot and Egger test. RESULTS: Twenty-eight studies involving 16,800 patients were included in our meta-analysis. The pooled prevalence of sarcopenia in patients with T2DM was 18% (95% CI 0.15-0.22; I2 = 97.4%). The pooled results showed that elder age (OR 4.73; 95% CI 4.30-5.19; I2 = 85.6%), male gender, chronic hyperglycemia (higher HbA1c) (OR 1.16; 95% CI 1.05-2.47; I2 = 99.2%) and osteoporosis (OR 1.16; 95% CI 1.05-2.47; I2 = 99.2%) was predictors for sarcopenia, whereas patients with lower BMI (OR 1.16; 95% CI 1.05-2.47; I2 = 99.2%) and metformin administrations (OR 1.16; 95% CI 1.05-2.47; I2 = 99.2%) were not prone to get sarcopenia. The funnel plot and statistical tests showed no obvious publication bias. CONCLUSIONS: Sarcopenia was frequent in T2DM patients. Elder age, male gender and chronic hyperglycemia, Osteoporosis were significant risk factors for Sarcopenia. Lower BMI and metformin administrations were associated with lower risk of sarcopenia.

Metformin Inhibits Proliferation of Human Thyroid Cancer TPC-1 Cells by Decreasing LRP2 to Suppress the JNK Pathway.

OBJECTIVE: To uncover the potential effect of metformin on proliferation and apoptosis of thyroid cancer TPC-1 cell line, and the underlying mechanism. METHODS: Viability, apoptosis and LRP2 level in TPC-1 cells treated with different doses of metformin for different time points were determined. Besides, protein levels of p-JNK1 and c-Jun N-terminal kinases (JNK) in metformin-treated TPC-1 cells were detected by Western blot. Regulatory effects of LRP2 on the JNK pathway and cell viability in metformin-treated TPC-1 cells were assessed. RESULTS: Viability in TPC-1 cells gradually decreased with the treatment of increased doses of metformin either for 24 h or 48 h. The apoptotic rate was concentration-dependently elevated by metformin treatment. Relative levels of LRP2 and p-JNK1 were concentration-dependently downregulated by metformin treatment. In addition, overexpression of LRP2 partially abolished the inhibitory effect of metformin on the viability of TPC-1 cells. CONCLUSION: Metformin treatment suppresses the proliferative ability and induces apoptosis of TPC-1 cells by downregulating LRP2 to block the JNK pathway.