Platelet-rich Plasma Promotes Restoration of the Anterior Vaginal Wall for the Treatment of Pelvic Floor Dysfunction in Rats.

STUDY OBJECTIVE: To determine the efficacy of using platelet-rich plasma (PRP) for vaginal wall repair in rats with vaginal wall impairment induced by vaginal distension (VD). DESIGN: A single-blind, randomized study. SETTING: A certified animal research facility. ANIMALS: Twenty-four female Sprague Dawley rats. INTERVENTIONS: Female Sprague Dawley rats were divided into sham (n = 8), VD (n = 8), and VD + PRP (n = 8) groups. Vaginal tissues from the VD group were dissected at 28-day post injury. VD + PRP rats received vaginal PRP injections on the 1st, 7th, 14th, and 21st day after VD and sacrificed on the 28th day. MEASUREMENTS AND MAIN RESULTS: Urodynamic tests were performed in all rats. Immunohistochemistry was used to evaluate matrix metalloprotease-2 (MMP-2) and matrix metalloprotease-9 (MMP-9). Masson's staining was used to evaluate collagen fibers and calculate collagen volume fraction. Collagen fiber damage was confirmed in the VD group, evidenced by thinner and sparse distribution of collagen fibers, with significantly higher MMP-2 and MMP-9 expression than the sham group (p <.05). The collagen fiber damage in the vaginal wall likely led to pelvic floor dysfunction (PFD), evidenced by significantly decreased bladder leak-point pressure (p <.01) and abdominal leak-point pressure (p <.01) in the VD group compared with the sham group. After completion of the PRP treatment, a significantly higher collagen volume fraction (p <.01) and significantly increased bladder leak-point pressure (p <.05) and abdominal leak-point pressure (p <.01) were achieved in the VD + PRP compared with the VD group, thus indicating repair of the vaginal wall and improvement of PFD. CONCLUSION: PRP injections facilitate the regeneration of vaginal wall tissue, particularly collagen fiber, after VD, leading to functional improvement of PFD. Findings support the feasibility of using PRP as a novel treatment for PFD.

Single-nucleotide Polymorphism rs17860041 A/C in the Promoter of the PPIA Gene is Associated with Susceptibility to Kawasaki Disease in Chinese Children.

Background: Kawasaki disease (KD) is an acute systemic vasculitis of unknown etiology. Cyclophilin A (CypA), also known as PPIA, has been identified to play a vital role in the pathogenesis of cardiovascular or inflammatory diseases. However, no studies have examined the relationship between single-nucleotide polymorphisms (SNPs) in the peptidylprolyl isomerase A (PPIA) and the development of KD and KD with or without coronary artery lesions (CALs). Objective: The present study was conducted to evaluate whether PPIA SNPs are associated with susceptibility to KD or CALs in KD. Methods: Three PPIA SNPs were genotyped in 101 KD patients and 105 healthy controls from a Chinese population. The allele and genotype frequencies were compared between the case and control groups, as well as in KD patients with and without CALs. Results: The data revealed a significant difference in the genotype and allele frequencies of rs17860041 A/C between KD patients and normal controls. Compared to the rs17860041 CC genotype, the AC genotype demonstrated a consistently beneficial roles in reducing the KD incidence. Furthermore, the allele frequency of C in the KD group was higher than that in the control group (P < .05). Haplotype analysis for PPIA polymorphisms (rs10951772 A/G, rs17860041 A/C, and rs4720485 A/T) also confirmed this association in KD patients and normal controls. Conclusion: A PPIA promoter SNP (rs17860041 A/C) confers susceptibility to KD in Chinese children and was identified as an important marker of KD in this study.

Therapeutic effect of myofascial trigger point electroacupuncture technology on the treatment of overactive bladder syndrome in female. / 电针刺激肌筋膜触发点治疗女性膀胱过度活动症的临床疗效.

OBJECTIVES: To explore the therapeutic effect of myofascial trigger point electroacupuncture technology on treating female overactive bladder syndrome. METHODS: Forty female patients with overactive bladder were randomly divided into 2 groups: an experimental group and a control group. The experimental group was treated with myofascial trigger point electroacupuncture therapy combined with solifenacin succinate while the control group was only treated with solifenacin succinate. Patients in both groups were treated for 12 weeks. The overactive bladder symptom score (OABSS), urinary urgency score and urination frequency of 24 h in the 2 groups were compared to analyze the therapeutic effect. RESULTS: Before the comprehensive treatment, there was no significant difference between the experimental group and the control group (P>0.05). After 2 and 12 weeks of continuous treatment, the OABSS, urinary urgency symptoms score and 24 h urination frequency in the experimental group and the control group were lower than those before the treatment, and the degree of decline in the experimental group was more obvious, with significant difference (P<0.05). CONCLUSIONS: Treating overactive bladder syndrome in women with myofascial trigger point electroacupuncture combined with solifenacin succinate can significantly improve the OABSS and improve the life quality of the patients.

The Relationship of COX-2 Gene Polymorphisms and Susceptibility to Kawasaki Disease in Chinese Population.

BACKGROUND: Kawasaki disease (KD) is an acute systemic vasculitis that predominantly affects children, and it can result in coronary artery lesions. Cyclooxygenase-2 (COX-2) is involved in the conversion of arachidonic acid to prostaglandin H2, an important precursor of several prostaglandins. The aim of this study was to examine the association between COX-2 gene polymorphisms and susceptibility to KD. METHODS: A total of 276 subjects (136 KD and 140 controls) were recruited. The analysis of two single nucleotide polymorphisms rs689466 (-1195G/A) and rs20417 (-765G/C) was respectively detected with polymerase chain reaction sequence-based typing methods. RESULTS: Polymorphisms of rs689466 were significantly different between the normal controls and KD patients (χ2 = 6.070 and 5.435, both p < 0.05). The frequencies of AA genotype and A allele of rs689466 in Kawasaki disease group were higher than that of control group (χ2 = 4.832, p = 0.028, OR = 1.832, 95%CI = 1.064-3.124; χ2 = 5.435, p = 0.028, OR = 1.491, 95%CI = 1.065-2.088). CONCLUSION: This study provides the first evidence supporting an association between COX-2 gene polymorphisms and susceptibility of KD. The AA genotype and A allele of rs689466 confer predisposing factors to KD.

Adjunctive Treatment With Eslicarbazepine Acetate for Adults and Children With Focal-Onset Epilepsy: A Meta-Analysis.

Background: The efficacy and tolerability of eslicarbazepine acetate (ESL) in adults and children with focal-onset epilepsy (FOE) according to the dose remain to be validated. A meta-analysis based on randomized controlled trials (RCTs) was therefore conducted as a summary. Methods: Relevant RCTs were collected by systematic searching the electronic databases of PubMed, Cochrane's Library, Embase, Wanfang and CNKI from inception to May 16, 2022. The random-effect model was adopted to pool the results by incorporating the possible heterogeneity. Efficacy outcomes including responsive rate and effective rate, defined as cases with 50 and ≥75% reduction in seizure frequency compared to baseline, were determined, respectively. Incidence of severe adverse events (AE) leading to drug discontinuation was also evaluated. Results: Ten studies including 2,565 people with epilepsy contributed to the meta-analysis. For adults, ESL 400 mg/d did not improve the response rate or the effective rate; ESL 800 mg/d was associated with improved response rate (odds ratio [OR] 2.16, 95% confidence interval [CI]: 1.65-2.83, p < 0.001) and effective rate (OR 2.16, 95% CI: 1.41-3.30, p < 0.001) without significantly increased severe AE (OR 1.58, 95% CI: 0.90-2.78, p = 0.11); ESL 1,200 mg/d improved response rate (OR 2.49, p < 0.001) and effective rate (OR 3.09, p = 0.04), but significantly increased severe AE (OR 3.72, p < 0.001). For children, ESL also did not significantly improve the response rate (OR 1.76, p = 0.22) or the effective rate (OR 2.17, p = 0.13). Conclusion: ESL 800 mg/d is effective and well-tolerated as adjuvants for adults with FOE. Efficacy of ESL in children with FOE should be further evaluated.

Mannose inhibits proliferation and promotes apoptosis to enhance sensitivity of glioma cells to temozolomide through Wnt/ß-catenin signaling pathway.

BACKGROUND: Temozolomide (TMZ) is generally applied for glioma treatment, while drug resistance of TMZ limits its therapeutic efficacy. Mannose exerts evident anti-tumor effect. We intended to investigate whether mannose enhanced TMZ sensitivity to glioma and examined the underlying mechanism. METHODS: MTT and clone formation assays were performed to detect cell viability and proliferation. Cell apoptosis was measured by flow cytometry. The protein and gene expression levels were detected by Western blot and qRT-PCR assays. Xenograft glioma model was established to explore the influence of mannose in vivo. RESULTS: Mannose inhibited glioma cell growth, which was facilitated by knockdown of phosphomannose isomerase (PMI) while reversed by overexpression of PMI. Mannose enhanced the sensitivity of glioma cells to TMZ, indicated by the further inhibited cell viability and colony formation and the aggravated cell apoptosis, which was reversed by overexpression of O6-methylguanine DNA methyltransferase (MGMT). Furthermore, mannose and TMZ inhibited MGMT expression and Wnt/ß-catenin activation. Moreover, activating Wnt/ß-catenin pathway blocked anti-proliferative effect induced by mannose and TMZ, which was further suppressed by overexpressed MGMT. Mannose inhibited glioma growth, suppressed Ki67 and downregulated MGMT and ß-catenin in vivo. CONCLUSION: Mannose inhibited MGMT to enhance sensitivity of glioma cells to TMZ, with Wnt/ß-catenin pathway involvement. Our data suggested that mannose could be an innovative agent to improve glioma treatment, particularly in TMZ-resistant glioma with high MGMT.

Metabolic Control of Epilepsy: A Promising Therapeutic Target for Epilepsy.

Epilepsy is a common neurological disease that is not always controlled, and the ketogenic diet shows good antiepileptic effects drug-resistant epilepsy or seizures caused by specific metabolic defects via regulating the metabolism. The brain is a vital organ with high metabolic demands, and epileptic foci tend to exhibit high metabolic characteristics. Accordingly, there has been growing interest in the relationship between brain metabolism and epilepsy in recent years. To date, several new antiepileptic therapies targeting metabolic pathways have been proposed (i.e., inhibiting glycolysis, targeting lactate dehydrogenase, and dietary therapy). Promising strategies to treat epilepsy via modulating the brain's metabolism could be expected, while a lack of thorough understanding of the role of brain metabolism in the control of epilepsy remains. Herein, this review aims to provide insight into the state of the art concerning the brain's metabolic patterns and their association with epilepsy. Regulation of neuronal excitation via metabolic pathways and antiepileptic therapies targeting metabolic pathways are emphasized, which could provide a better understanding of the role of metabolism in epilepsy and could reveal potential therapeutic targets.