BackgroundDeath-associated protein kinase1 (DAPK1) is an important tumor suppressor gene. DNA methylation can inactivate genes, which has often been observed in the carcinogenesis of cervical cancer. During the past several decades, many studies have explored the association between DAPK1 promoter methylation and cervical cancer. However, many studies were limited by the small samples size and the findings were inconsistent among them. Thus, we conducted a meta-analysis to assess the association between DAPK1 promoter methylation and cervical cancer.MethodsWe systematically searched eligible studies in the PubMed, Web of Science, EMBASE and CNKI databases. Using meta-regression, subgroup analysis and sensitivity analysis, we explored the potential sources of heterogeneity. The odds ratio (OR) and 95% confidence interval (95% CI) were calculated by Meta-Analysis in R.ResultsA total of 15 studies from 2001 to 2012, comprising 818 tumor tissues samples and 671 normal tissues samples, were analyzed in this meta-analysis. The frequencies of DAPK1 promoter methylation ranged from 30.0% to 78.6% (median, 59.3%) in cervical cancer tissue and 0.0% to 46.7% (median, 7.8%) in normal cervical tissue. The pooled OR was 19.66 (95%CI = 8.72–44.31) with the random effects model, and heterogeneity was found through the sensitivity analysis. The I2 = 60% (P = 0.002) decreased to I2 = 29.2% (P = 0.144) when one heterogeneous study was excluded, and the pooled OR increased to 21.80 (95%CI = 13.44–35.36) with the fixed effects model.ConclusionThe results suggested a strong association between DAPK1 promoter methylation and cervical cancer. This study also indicated that DAPK1 promoter methylation may be a biomarker during cervical carcinogenesis that might serve as an early indication of cervical cancer.
Context Sepsis is a systemic inflammatory disease; pristimerin exhibits strong antibacterial, anti-inflammatory and antioxidant properties. Objectives We explored whether pristimerin protected against cognitive dysfunction and neuroinflammation in C57BL/6 J mice with sepsis-induced brain injuries. Materials and methods Sepsis was induced by intraperitoneal administration of 2 mg/kg lipopolysaccharide (LPS). C57BL/6 J mice were separated into four groups ( n = 10 per group): positive control, negative control, pristimerin 10 mg/kg and pristimerin 100 mg/kg. Pristimerin was administered orally for 28 days prior to LPS administration and for six days thereafter. Behavioural changes were assessed one day after LPS administration using the Morris water maze and via neurological dysfunction scoring. Molecular pathogenesis was explored by measurement of malondialdehyde, superoxide dismutase, reactive oxygen species and inflammatory cytokine levels in mouse brains. Neuronal apoptosis was evaluated using the TUNEL assay. The levels of p-Akt/Akt, p-PI3K/PI3K, mTOR, Bax, Bcl-2 and caspase-3 proteins were determined via Western blotting. Results Pristimerin improved cognitive function and reduces the neurological score to 1.15 ± 0.03. Pristimerin significantly reduced all cytokine levels: TNF-α by 18 ± 0.6 pg/mg, IL-1β by 43 ± 1.3 pg/mg and IL-6 by 34 ± 1.12 pg/mg. There was significant ( p < 0.01) improvement in PI3K/Akt signalling and histopathological changes in the brain tissue of sepsis induced brain injured rats. Conclusions Pristimerin ameliorated neuronal injury by regulating PI3K/Akt signalling in mice with sepsis-induced brain injuries. Pristimerin may merit further development for clinical applications.
ObjectivesInflammation plays an important role in the development of depression after stroke. Monocyte-to-HDL Cholesterol Ratio (MHR) recently emerged as a novel comprehensive inflammatory indicator in recent years. This study aimed to investigate whether there is a relationship between MHR levels and post-stroke depression (PSD).MethodsFrom February 2019 to September 2021, patients with acute ischemic stroke (AIS) were recruited within 7 days post-stroke from the two centers and blood samples were collected after admission. The 17-item Hamilton Depression Scale (HAMD-17) was used to measure depressive symptoms at 3 months after stroke. Patients were given the DSM-V criteria for diagnosis of PSD.ResultsOf the 411 enrolled patients, 92 (22.38%) patients were diagnosed with PSD at 3-months follow-up. The results also showed significantly higher level of MHR in patients with depression [0.81 (IQR 0.67–0.87) vs. 0.61 (IQR 0.44–0.82), P < 0.001] at admission than patients without depression. Multivariate logistic regression revealed that MHR (OR 6.568, 95% CI: 2.123–14.565, P = 0.015) was an independent risk factor for the depression at 3 months after stroke. After adjustment for potential confounding factors, the odds ratio of PSD was 5.018 (95% CI: 1.694–14.867, P = 0.004) for the highest tertile of MHR compared with the lowest tertile. Based on the ROC curve, the optimal cut-off value of MHR as an indicator for prediction of PSD was projected to be 0.55, which yielded a sensitivity of 87% and a specificity of 68.3%, with the area under the curve at 0.660 (95% CI: 0.683–0.781; P = 0.003).ConclusionElevated level of MHR was associated with PSD at 3 months, suggesting that MHR might be a useful Inflammatory markers to predict depression after stroke.
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