Risk factors for life-threatening complications of head and neck space infections: A systematic review and meta-analysis.

OBJECTIVE: The present systematic review was performed to identify risk factors associated with life-threatening complications of head and neck space infections (LCHNSI) within the included studies and assess the magnitude of their impact on patients. METHODS: We systematically searched PubMed, Web of Science, EmBase, Scopus and CNKI for articles that reported risk factors associated with life-threatening complications of head and neck space infections from inception to 14 December 2023. Only factors reported in at least three papers were considered in the meta-analysis. Pooled odds ratio (OR) and 95 % confidence interval (CI) were calculated using fixed effects model and random effects model. The between-study heterogeneity of effect size was quantified using the Q statistic and I2. In addition, subgroup analysis stratified by study characteristics and sensitivity analysis were performed to explore the potential sources of heterogeneity and the stability of the results. RESULTS: The review included a total of 29 studies. The results revealed that the risk factors which associated with LCHNSI were included diabetes mellitus (OR = 3.31, 95 % CI: 2.49-4.40), total leukocyte count(≥15 × 109/L) (OR = 1.21, 95 %CI: 1.04-1.42), multiple space involvement (OR = 4.32, 95 %CI: 3.47-5.38), combined systemic diseases (OR = 9.94, 95 %CI: 6.30-15.67), advanced age(≥60) (OR = 3.90, 95 %CI: 2.80-5.44), dyspnoea (OR = 23.39, 95 %CI: 12.41-44.10), high temperature(≥39°C) (OR = 3.23, 95 %CI: 2.02-5.17), retropharyngeal space involvement (OR = 3.62, 95 %CI: 2.06-6.35), parapharyngeal space involvement (OR = 4.62, 95 %CI: 2.27-9.42). CONCLUSIONS: According to the current analysis, diabetes mellitus, total leukocyte count(≥15 × 109/L), combined systemic diseases, multiple space involvement, advanced age(≥60), dyspnoea, high temperature (≥39 °C), retropharyngeal space involvement, parapharyngeal space involvement were the risk factors for LCHNSI. To mitigate the incidence of LCHNSI, clinical staff should carefully manage these risk factors, ensure prompt diagnosis, and implement timely preventive measures.

The Global Burden of Disease attributable to low physical activity and its trends from 1990 to 2019: An analysis of the Global Burden of Disease study.

Introduction: Low physical activity (LPA) is associated with several major non-communicable diseases (NCDs) and premature mortality. In this study, we aimed to assess the global burden and trends in disease attributable to LPA (DALPA) from 1990 to 2019. Methods: Annual age-standardized disability-adjusted life years (DALYs) and death rates of DALPA [all-cause and five specific causes (ischaemic heart disease, diabetes mellitus, stroke, colon and rectal cancer, and breast cancer)] by sex, age, geographical region and social deprivation index (SDI) score from 1990 to 2019 were available from the Global Burden of Disease (GBD) study 2019. The estimated annual percentage changes (EAPCs) were calculated to quantify the changing trend. A generalized linear model (GLM) was used to explore the relationship between DALYs/death rates of DALPA and sociodemographic factors. Results: Globally, in 2019, the age-standardized DALYs and death rates of DALPA were 198.42/100,000 (95% UI: 108.16/100,000-360.32/100,000) and 11.10/100,000 (95% UI: 5.66/100,000-19.51/100,000), respectively. There were 15.74 million (8.51-28.61) DALYs and 0.83 million (0.43-1.47) deaths attributable to LPA. Overall, age-standardized DALYs and death rates presented significant downward trends with EAPCs [-0.68% (95% CI: -0.85- -0.50%) for DALYs and -1.00% (95% CI: -1.13- -0.86%) for deaths] from 1990 to 2019. However, age-standardized DALYs and death rates of diabetes mellitus attributable to LPA were substantially increased [EAPC: 0.76% (95% CI: 0.70-0.82%) for DALYs and 0.33% (95% CI: 0.21-0.51%) for deaths]. In the 15-49 age group, DALPA presented significant upward trends [EAPC: 0.74% (95% CI: 0.58-0.91%) for DALYs and 0.31% (95% CI: 0.1-0.51%) for deaths]. The GLM revealed that higher gross domestic product and current health expenditure (% of GDP) were negatively associated with DALYs and death rates of DALPA. Conclusion: Although global age-standardized DALYs and death rates of DALPA presented downward trends, they still cause a heavy burden worldwide. These rates showed upward trends in the diabetic and 15-49 age groups, which need more attention and health interventions.

MiR-379-5p targets microsomal glutathione transferase 1 (MGST1) to regulate human glioma in cell proliferation, migration and invasion and epithelial-mesenchymal transition (EMT).

BACKGROUND: Glioma is one of the most malignant tumors worldwide. This study was aimed to study the effect of miR-379-5p/MGST1 on cell proliferation, migration, invasion and EMT in glioma. METHODS: RT-qPCR detected the expression of miR-379-5p and MGST1 in RNA level in glioma cell lines. Bioinformatic analysis was made to explore the associations between miR-379-5p and MGST1 while survival analysis was made with regards to MGST1 expression in glioma patients. Western blot analysis was applied to measure the EMT changes. MTT examined the cell viability. Transwell was used to detect the cellular invasion and migration. The binding sites between miR-379-5p and MGST1 were validated by luciferase reporter assays. RESULTS: miR-379-5p expression was lower in glioma cells. MiR-379-5p increase inhibited the viability, migration, invasion and EMT while inhibition of miR-379-5p showed a reverse effect. MGST1 inhibition curbed the cell functions. MiR-379-5p targeted and regulated MGST1 expression. Lower MGST1 is related to higher survival rate. CONCLUSION: miR-379-5p could regulate glioma cell viability, migration, invasion and EMT through MGST1, suggesting that miR-379-5p/MGST1 axis might function in the regulation of glioma progression.

Sevoflurane protects the liver from ischemia-reperfusion injury by regulating Nrf2/HO-1 pathway.

We aimed to investigate the role and mechanism of sevoflurane (SEV) preconditioning in liver ischemia-reperfusion (I/R) injury. In vivo, rats were randomly divided into Sham group, I/R rat model group, I/R + SEV group and SEV group. In vitro, hypoxia-reoxygenation (H/R) cell model were established. Hematoxylin-Eosin (H&E) and TUNEL assay were used to evaluate the degree of tissue damage and detect apoptosis in rats, respectively. HO-1, nuclear Nrf2 and cytosolic Nrf2 expressions were detected by immunohistochemical staining, Western blot analysis and quantitative real-time PCR (qRT-PCR), respectively. Contents of Lactate dehydrogenase (LDH), malondialdehyde (MDA), and reactive oxygen species (ROS) were determined by corresponding kits. Inflammatory factor levels, cell viability, apoptosis were detected by enzyme-linked immunosorbent assay (ELISA), MTT assay, and flow cytometry, respectively.In the I/R group, liver damage was severe, apoptosis-positive cells were increased, HO-1 and nuclear Nrf2 expressions were increased, and cytosolic Nrf2 expression was decreased. After SEV pretreatment, the degree of liver injury and apoptosis in rats were significantly reduced, HO-1 and nuclear Nrf2 expressions were increased significantly, and cytosolic Nrf2 expression was decreased. 4% SEV had the best mitigating effect on H/R-induced liver cell damage, as evidenced by reduced contents of LDH and MDA, decreased inflammatory factors, a lowered apoptosis rate, inhibited ROS production, effectively promoted Nrf2 nucleation, and activated Nrf/HO-1 pathway. ML385 pretreatment significantly inhibited the effect of SEV on hepatocytes.Sevoflurane protects the liver from ischemia-reperfusion injury by regulating the Nrf2/HO-1 pathway.

Propofol Protects Against Hepatic Ischemia Reperfusion Injury via Inhibiting Bnip3-Mediated Oxidative Stress.

Propofol (PRO) protects against hepatic ischemia/reperfusion (I/R) injury. Bnip3 is involved in the I/R-induced injury. This study investigated whether the effect of PRO on hepatic hypoxia/reoxygenation (H/R) injury was realized through regulating Bnip3. After establishing a hepatic ischemia reperfusion (I/R ) injury model in mice, the serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were determined by an automatic biochemical analyzer. The histopathology and apoptosis of liver tissues were detected by hematoxylin-eosin and TUNEL staining. After the H/R liver cells were cultured and treated with PRO, the viability, apoptosis, reactive oxygen species (ROS) production, and the levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), TNF-α, and IL-6 were detected by MTT, flow cytometry, colorimetry, and ELISA. The expressions of Bnip3 and apoptosis-related factors in I/R mouse liver tissues and H/R cells were determined by immunohistochemical assay, immunofluorescence, Western blot, or RT-qPCR. PRO ameliorated the abnormal histopathology, reduced cell apoptosis and the levels of AST, ALT, Bnip3, Cleaved Caspase-3, and Bax, but upregulated the Bcl-2 level in the liver tissues of I/R mice. In H/R liver cells, PRO promoted the cell viability, downregulated the levels of LDH, MDA, TNF-α, IL-6, and reduced ROS production. Moreover, PRO promoted the downregulated expressions of cytosolic Bnip3, total Bni3p, Cleaved Caspase-3, and Bax and upregulated the Bcl-2 level. siBnip3 reversed the effect of H/R on the liver cells, and its overexpression also reversed the effect of PRO on H/R-induced liver cells. PRO protects against hepatic I/R injury via inhibiting Bnip3.

Long noncoding RNA nuclear-enriched abundant transcript 1 regulates proliferation and apoptosis of neuroblastoma cells treated by cisplatin by targeting miR-326 through Janus kinase/signal transducer and activator of transcription 3 pathway.

Neuroblastoma is a common malignancy and frequently affects children, leading to a low survival rate. Long noncoding RNAs (lncRNAs) are reported to be closely related to cancer progression. The purpose of this study was to explore a novel mechanism of lncRNA nuclear-enriched abundant transcript 1 (NEAT1) in neuroblastoma. NEAT1 was upregulated in neuroblastoma cell lines (IMR32 and SK-N-SH). Overexpression of NEAT1 increased proliferation inhibited by cisplatin and decreased apoptosis promoted by cisplatin. MicroRNA-326 (miR-326) was a target of NEAT1 and miR-326 reintroduction abolished the effects of NEAT1 overexpression on cell proliferation and apoptosis. Moreover, NEAT1 overexpression activated Janus kinase/signal transducer and activator of transcription 3 (JAK1/STAT3) signaling pathway through absorbing miR-326. Besides, NEAT1 overexpression promoted tumor growth in vivo through stimulating the expression of p-JAK1 and p-STAT3 but inhibiting miR-326 expression. NEAT1 accelerated proliferation and weakened apoptosis of neuroblastoma cells treated by cisplatin by targeting miR-326 through activating JAK1/STAT3 signaling pathway, suggesting that NEAT1 was a potential biomarker against neuroblastoma.