Decreased synapse-associated proteins are associated with the onset of epileptic memory impairment in endothelial -deficient mice.

Accumulating evidence indicates that epilepsy has a higher risk of inducing memory impairment and dementia. However, the underlying onset mechanism remains unclear. Here, we found that mice with spontaneous epilepsy induced by endothelial CDK5 deficiency exhibited hippocampal-dependent memory impairment at 6 months of age, but not at 2 months of age.

Ozone pollution in Chinese cities: Assessment of seasonal variation, health effects and economic burden.

The ground-level ozone (O) concentration in the urban regions of China has become an increasingly noticeable environmental problem in recent years. Many epidemiological studies have reported the association between O pollution and mortality, only a few studies have focused on the O-related mortality and corresponding economic effects at the Chinese city and province level. This study reports the seasonal variation of ground-level O in 338 cities of China during the year 2016 and evaluates its effect on premature mortality and economic loss.

PM-related health and economic loss assessment for 338 Chinese cities.

China is in a critical stage of ambient air quality management after global attention on pollution in its cities. Industrial development and urbanization have led to alarming levels of air pollution with serious health hazards in densely populated cities. The quantification of cause-specific PM-related health impacts and corresponding economic loss estimation is crucial for control policies on ambient PM levels.

Spatial-temporal patterns of PM concentrations for 338 Chinese cities.

Air pollution has become a major concern in cities worldwide. The present study explores the spatial-temporal patterns of PM (particles with an aerodynamic diameters ≤2.5μm) and the variation in the attainment rate (the number of cities attaining the national PM standard each day) at different time-scales based on PM concentrations.

Wogonin exacerbates the cytotoxic effect of oxaliplatin by inducing nitrosative stress and autophagy in human gastric cancer cells.

Background: Gastric cancer remains one of the leading cause of death in the world. Drug combinations are potential approaches to provide more efficient treatments that minimize side effects.

Purpose: We investigated the pharmacological effects of the combination of wogonin with oxaliplatin on gastric cancer cells in vitro and in vivo.

Endothelial ErbB4 deficit induces alterations in exploratory behavior and brain energy metabolism in mice.

Aims: The receptor tyrosine kinase ErbB4 is present throughout the primate brain and has a distinct functional profile. In this study, we investigate the potential role of endothelial ErbB4 receptor signaling in the brain.

Results: Here, we show that the endothelial cell-specific deletion of ErbB4 induces decreased exploratory behavior in adult mice.

Retrospective analysis of tigecycline shows that it may be an option for children with severe infections.

Aim: This study assessed the efficacy and safety of tigecycline in children with life-threatening infections.

Methods: We retrospectively reviewed the clinical records of patients treated with tigecycline from June 2012 to May 2014 in a Chinese tertiary centre.

Results: The study comprised 24 patients (14 male) with a median age of four years (range, 50 days-12 years).

Visualizing peroxynitrite fluxes in endothelial cells reveals the dynamic progression of brain vascular injury.

Accumulating evidence suggests that formation of peroxynitrite (ONOO(-)) in the cerebral vasculature contributes to the progression of ischemic damage, while the underlying molecular mechanisms remain elusive. To fully understand ONOO(-) biology, efficient tools that can realize the real-time tracing of endogenous ONOO(-) fluxes are indispensable. While a few ONOO(-) fluorescent probes have been reported, direct visualization of ONOO(-) fluxes in the cerebral vasculature of live mice remains a challenge.

Nitrosative stress induces peroxiredoxin 1 ubiquitination during ischemic insult via E6AP activation in endothelial cells both in vitro and in vivo.

Aims: Although there is accumulating evidence that increased formation of reactive nitrogen species in cerebral vasculature contributes to the progression of ischemic damage, but the underlying molecular mechanisms remain elusive. Peroxiredoxin 1 (Prx1) can initiate the antioxidant response by scavenging free radicals. Therefore, we tested the hypothesis that Prx1 regulates the susceptibility to nitrosative stress damage during cerebral ischemia in vitro and in vivo.

The disturbance of hippocampal CaMKII/PKA/PKC phosphorylation in early experimental diabetes mellitus.

Background: Defining the impact of diabetes and related risk factors on brain cognitive function is critically important for patients with diabetes.

Aims: To investigate the alterations in hippocampal serine/threonine kinases signaling in the early phase of type 1 and type 2 diabetic rats.

Methods: Early experimental diabetes mellitus was induced in rats with streptozotocin or streptozotocin/high fat.

The γ-secretase blocker DAPT reduces the permeability of the blood-brain barrier by decreasing the ubiquitination and degradation of occludin during permanent brain ischemia.

Background: Tight junction protein degradation is a principal characteristic of the blood-brain barrier (BBB) damage that occurs during brain ischemia.

Aims: We investigated the mechanisms of occludin degradation that underlie permanent middle cerebral artery occlusion (pMCAO) in rats.

Methods And Results: Western blot and Co-immunoprecipitation data indicated ubiquitination and degradation of occludin in brain after pMCAO, which was consistent with ZO-1 degradation in penumbra regions as observed at 24 h after pMCAO.

Ischemic injury promotes Keap1 nitration and disturbance of antioxidative responses in endothelial cells: a potential vasoprotective effect of melatonin.

Clinical epidemiology has indicated that the endothelial injury is a potential contributor to the pathogenesis of ischemic neurovascular damage. In this report, we assessed S-nitrosylation and nitration of Keap1 to identify downstream nitric oxide redox signaling targets into endothelial cells during ischemia. Here, oxygen-glucose deprivation (OGD) exposure initiates the nuclear import of Keap1 in endothelial cells, which interacted with nuclear-localized Nrf2, as demonstrated through co-immunoprecipitation and immunocytochemical assay.

[Effect of chronic lead exposure on expression of autophagy-associated proteins in rat hippocampus].

Objective: To investigate the effects of chronic lead exposure on expression of autophagy-associated proteins in rat hippocampus.

Methods: SD rats were randomly divided into three groups: control group was given distilled water, lead-exposed groups were given 0.5 g/L (low-dose) or 2.

Expression profiling of Ca(2+)/calmodulin-dependent signaling molecules in the rat dorsal and ventral hippocampus after acute lead exposure.

The septal and temporal poles of the hippocampus differ markedly in their anatomical organization, but whether these distinct regions exhibit differential neurochemical profiles underlying lead (Pb(2+)) neurotoxicity remains to be determined. In the present study, we examined changes in the expression of Ca(2+)/calmodulin-dependent enzymes, including calpain, calcineurin, phospho-CaMKII (Thr286) and neuronal nitric oxide synthase (nNOS), in the rat dorsal and ventral hippocampus (DH and VH) after acute Pb(2+) exposure. Five days after Pb(2+) exposure, we observed constitutively active forms of calcineurin (45 kDa and 48 kDa) in ventral portions of the hippocampus, a result consistent with the observed calpain activation that is indicated by the breakdown of spectrin in this region.