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Varicella-zoster virus (VZV) lurks in cranial nerves and other brain ganglias after infection. Because middle cerebral artery (MCA) receives the ipsilateral trigeminal ganglia afferent innervations, the reactivated VZV infects the adventitia and intima of cerebral artery wall probably through this way and causes vascular inflammation, finally resulting in artery remodeling, vessel occlusion, and ischemia. In fact, there is a growing clinical recognition that there is an association between VZV reactivation and subsequent stroke. Here, we showed a case of ischemic stroke secondary to varicella-zoster virus meningoencephalitis and reviewed the literature to emphasize the importance of VZV-associated vasculopathy.

Depression is a common co-morbidity in asthma, worsening asthma control and impairing quality of life. Previous studies have reported a higher risk of cognitive deficit in depression, yet little research has focused on the level of cognition in asthmatic patients with depression. Evidence shows that inflammation may play an important role in both asthma and depression. Cerebral white matter injury, possibly induced by inflammation, has been associated with depression. This study assesses cognitive function in patients with asthma and a depression comorbidity, compared to patients with asthma only or depression only.Four groups were studied: Asthma comorbid Depression group (A + D,A + D group showed the highest incidence of cognitive deficit, with the cognitive domain particularly affected. Compared to N group, serum levels of IL-6, HMGB1, Netrin-1, MBP and MOG were significantly elevated in A + D group. MOG level negatively correlated with the MoCA score.Patients with comorbidities presented with more severe cognitive deficits and higher levels of inflammatory cytokines. Cerebral white matter injury may account for the cognitive deficit in patients and MOG could be a potential biomarker for this process.

The mevalonate cascade is a key metabolic pathway that regulates a variety of cellular functions and is thereby implicated in the pathophysiology of most brain diseases, including neurodevelopmental and neurodegenerative disorders. Emerging lines of evidence suggest that statins and Rho GTPase inhibitors are efficacious and have advantageous properties in treatment of different pathologic conditions that are relevant to the central nervous system. Beyond the original role of statins in lowering cholesterol synthesis, they have anti-inflammatory, antioxidant and modulatory effects on signaling pathways. Additionally, Rho GTPase inhibitors and statins share the mevalonate pathway as a common target of their therapeutic actions. In this review, we discuss potential mechanisms through which these drugs, via their role in the mevalonate pathway, exert their neuroprotective effects in neurodegenerative and neurodevelopmental disorders.

The present study observed and compared the biological behaviour of HepG2 cells prior and subsequent to the overexpression of activating transcription factor 3 (ATF3). Experiments investigating the cytological function by which ATF3 affects liver cancer cells were also performed. MTT, Transwell and flow cytometry assays were used to observe and detect the biological behaviour of HepG2 cells with and without lentivirus (LV)-ATF3-enhanced green fluorescent protein (EGFP) infection. The effects of ATF3 overexpression on cell proliferation, migration, apoptosis and cell cycle progression were evaluated. The LV-ATF3-EGFP overexpression vector was successfully constructed, and the HepG2 cells were successfully infected with the vector. Following ATF3 overexpression, cell proliferation was decreased, the rate of cell apoptosis was accelerated and cell cycle progression was slowed (P0.05), although there was a trend towards a gradual decrease. In conclusion, ATF3 exerted suppressive effects in HepG2 cells, potentially by inhibiting cancer cell growth, accelerating cell apoptosis, and blocking cell cycle progression. Intervention targeting ATF3 expression may represent a novel approach for the prevention and treatment of human liver cancer.

Background Numerous studies report that cancer prevalence in patients with schizophrenia might be different from the general population, but findings remain controversial. Aim Our updated meta-analysis of cohort studies aims to analyze the data from cohort studies concerning the incidence risk of overall cancer and some site-specific cancers in patients with schizophrenia. Method We performed a systemic search through electronic databases. Cohort studies evaluating and describing the cancer incidence among patients with schizophrenia were included. Pooled risk ratios (RRs) were calculated for assessing the incidence risk of cancer. Results There were 16 cohort studies included in this meta-analysis, which combined a total of 480,356 participants with schizophrenia and 41,999 cases of cancer. Results showed that there was a slight significant decreased overall risk ratio of cancer incidence among patients with schizophrenia (RR = 0.90, 95% CI 0.81–0.99). When stratified by cancer site and gender, there were significant decreased incidence risk rates of colorectal cancer (RR = 0.82, 95% CI 0.69–0.98) and prostate cancer (RR = 0.55, 95% CI 0.42–0.71) in those patients, moreover, the incidence rate of colorectal cancer decreased significantly in male patients (RR = 0.89, 95% CI 0.81–0.98), and the incidence rate of lung cancer increased significantly in female patients (RR = 1.12, 95% CI 1.01–1.25). Conclusions The incidence risk of some cancers was reduced in patients with schizophrenia. Gender and type of cancer were two important confounding factors contributed to the heterogeneity that required adjustment in our cancer incidence meta-analysis.

Prostaglandin E 2 (PGE