BackgroundVarious signs of activation of microglia have been reported in schizophrenia, and it is hypothesized that microglia activation is closely associated with the neuropathology of schizophrenia.MethodsNeonatal intrahippocampal injection of lipopolysaccharide (LPS), an activator of microglia, was performed in rats at postnatal day 7 (P7), and they were separately given saline, risperidone (0.5 mg/kg), minocycline (40 mg/kg) or a combination of both of them at P42 for consecutive 14 days. Behavioral changes (locomotion activity, social interaction, novel object recognition and prepulse inhibition) were examined and the number of microglia was assessed by using immunohistochemistry in adulthood.ResultsThe adult rats in LPS-injected group showed obvious behavioral alteration (e. g. deficits in social interaction, novel object recognition and prepulse inhibition) and a dramatic increase of number of activated microglial cells in the hippocampus and other brain regions such as cerebral cortex and thalamus compared to those in saline-injected group. Interestingly, application of either minocycline, risperidone or both of them significantly rescued behavioral deficits and attenuated microglia activation.ConclusionOur results suggest that inhibition of microglia activation may be one of mechanisms underlying the antipsychotic effect of minocycline and risperidone.

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Abnormal hemodynamics is thought to contribute to the increased risk of contrast-induced nephropathy (CIN) and mortality. However, few studies focused on patients without abnormal hemodynamics (defined as hypotension, intra-aortic balloon pump usage) and reduced left ventricular ejection fraction (LVEF < 40%). Our study was to explore the impact of CIN on mortality in patients with acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI) with relative stable hemodynamics. In this observational study, we included 696 patients with AMI undergoing PCI without reduced LVEF and abnormal hemodynamics. The end point was long-term, all-cause mortality. During the mean follow-up of 2.79 years, CIN was detected in 110 (15.8%) patients. The total all-cause mortality was higher in CIN group than that in non-CIN group (24% vs 3.4%, P < .001). In the multivariate Cox analysis, CIN was an independent predictor of worse outcomes (adjusted hazard ratio [HR]: 2.97, 95% confidence interval: 1.46-6.06, P < .001) and significantly associated with long-term mortality, so did renal insufficiency (adjusted HR: 4.40, P < .001) and use of β-blockers (adjusted HR: 0.33, P < .001). Among patients with AMI, CIN independently predicted long-term mortality following PCI, regardless of LVEF impairment and abnormal hemodynamics.