Background Accumulating studies have suggested that gut microbiota (GM) dysbiosis and vitamin D3 deficiency each play an important role during the progression of hypertension (HTN). However, few studies have characterized the underlying interaction between GM shift and vitamin D3 deficiency in HTN patients. Hypothesis This study aimed to evaluate the possible crosstalk between GM dysbiosis and vitamin D deficiency in the pathogenesis of HTN. Methods In a cohort of 34 HTN patients and 15 healthy controls, we analyzed the fecal microbiota products, GM composition, and the interaction between GM and vitamin D3. Results Vitamin D3 was significantly decreased in feces of HTN patients (P = .006, vs controls) and was correlated with altered GM, including decreased Shannon index (R2 = 0.1296, P = .0111) and Pielou evenness (R2 = 0.1509, P = .0058). Moreover, vitamin D3 positively correlated with HTN‐reduced bacterial genera, including Subdoligranulum (R2 = 0.181, P = .0023), Ruminiclostridium (R2 = 0.1217, P = .014), Intestinimonas (R2 = 0.2036, P = .0011), Pseudoflavonifractor (R2 = 0.1014, P = .0257), Paenibacillus (R2 = 0.089, P = .0373), and Marvinbryantia (R2 = 0.08173, P = .0464). Partial least squares structural equation modeling showed that 27.7% of the total effect of gut microbiome on HTN was mediated by limiting vitamin D production. Finally, receiver operating characteristic curve analysis revealed the predictive capacity of differential gut microbiome signatures and decreased vitamin D3 to distinguish HTN patients (AUC = 0.749, P = .006). Conclusions Our findings suggest that the GM dysbiosis contributing to the development of HTN might be partially mediated by vitamin D3 deficiency. Future studies involving the underlying mechanism and intervention strategies targeting microbiome composition and vitamin D3 to counteract the progression of HTN are warranted.

In the present study, the effect of fatty acid synthase (FASN) inhibition on cell invasion and migration in vitro was investigated. A recombinant plasmid containing a microRNA targeting the FASN gene was used to inhibit FASN expression in U2‑OS cells. Cell migration and invasion were investigated using wound healing and Transwell invasion assays. We found that cell invasion and migration were suppressed by inhibiting FASN. In addition, the effect of inhibition of FASN on phosphorylation of Akt was investigated by detecting the expression levels of pAkt using western blot analysis. Furthermore, protein expression levels of nuclear factor‑κB (NF‑κB; p65) and matrix metalloproteinase (MMP)‑2 and ‑9 were also measured by western blot analysis. Results demonstrated that expression levels of pAkt, NF‑κB (p65) and MMP‑2 and ‑9 proteins were reduced significantly by inhibiting FASN. Therefore, we confirmed that inhibition of FASN by RNA interference suppresses osteosarcoma cell metastasis via downregulation of the phosphoinositide 3‑kinase/Akt/NF‑κB signaling pathway in vitro.

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Nasopharyngeal carcinoma (NPC) is a common malignancy of the nasopharynx, and radioresistant represents the main obstacle in NPC treatment. Malignant transformation of normal cells is driven by genetic and epigenetic changes, which are primarily manifested as changes in miRNA levels and DNA methylation status. microRNA (miR)-613 plays an inhibitory role in several types of cancer. Herein, the current study sought to explore the roles of miR-613 in NPC cell radiosensitivity. miR-613 expression patterns in NPC tissues were detected, and its correlation with clinical indexes was analyzed. NP-69 and C666-1 cell lines were selected for cellular experimentation. Radioresistant cell line C666-1R was obtained by fractionated radiation. Cell viability, survival fraction, and apoptosis were detected by CCK-8, colony formation assay, and flow cytometry. The binding relation between miR-613 and DNMT3B was verified by dual-luciferase and RIP assays. miR-613 was lowly expressed in NPC tissues and cells, with lower expression levels in C666-1R than C666-1, and further correlated with lymph node metastasis, tumor size, and tumor metastasis. miR-613 overexpression reduced C666-1R cell viability and survival fraction and increased apoptosis, while C666-1 cells with silencing miR-613 presented the opposite trends. miR-613 targeted DNMT3B. miR-613 and DNMT3B overexpression led to enhanced C666-1R cell viability and survival fraction and decreased apoptosis. miR-613 reduced TIMP3 methylation and elevated TIMP3 protein level by inhibiting DNMT3B. miR-613 enhanced NPC radiosensitivity by inhibiting the DNMT3B/TIMP3/STAT1/FOXO1 pathway. Collectively, miR-613 inhibited DNMT3B, reduced TIMP3 methylation, and increased TIMP3 protein level, thus inhibiting the STAT1/FOXO1 pathway and enhancing the radiosensitivity of NPC cells.

Objective This study aimed to identify the factors relevant for developing a scale to estimate the prognosis of patients with epilepsy. Methods This study followed 141 patients with newly or previously diagnosed epilepsy for between four and nine years. The patients were divided into three groups on the basis of their outcomes during the follow-up period: patients that were seizure-free without anti-epileptic drugs (AEDs) (group A, n = 48), patients with pharmacoresponsive epilepsy (group B, n = 52), and patients with pharmacoresistant epilepsy (group C, n = 41). The predictors of the prognosis of epilepsy were determined using logistic regression models and optimum subsets regression, and a scale for estimating the prognosis of epilepsy (SEPE) was developed. Results The SEPE was able to distinguish between better and worse outcomes for the three groups. A score ≤3 on the SEPE predicted that a patient would become seizure-free without the use of AEDs, with a specificity of 67% and a sensitivity of 50%. A score ≤4 on the SEPE predicted that a patient may have a positive outcome; scores in this range were assigned to 97.9% of patients that were seizure-free without the use of AEDs and 65% of patients with pharmacoresponsive epilepsy, with a specificity of 80%, a sensitivity of 81%. Scores ≥6 on the SEPE predicted a poor outcome. Conclusion Of the patients with a SEPE score ≤3, some were able to become seizure-free without the use of AEDs, while for other patients, it may be possible that AED use can be discontinued. Patients with a SEPE score ≤4 have the potential to achieve long-term remission. Patients with a SEPE score ≥6 are more likely to have pharmacoresistant epilepsy.