Common Polymorphisms Within QPCT Gene Are Associated with the Susceptibility of Schizophrenia in a Han Chinese Population.

A recent genome-wide association study conducted in Caucasians has identified glutaminyl-peptide cyclotransferase (QPCT) gene as a susceptibility gene for schizophrenia, as its common single nucleotide polymorphism (SNP) rs2373000 was significantly associated with the risk of this disease. To date, this finding has not been validated in other populations or ethnic groups. The aim of this study was to investigate the association of common SNPs spanning QPCT gene with the susceptibility of schizophrenia in a Han Chinese population comprising 440 schizophrenia patients and 450 control subjects.

TSNARE1 polymorphisms are associated with schizophrenia susceptibility in Han Chinese.

t-SNARE domain containing 1 gene (TSNARE1) is located at human chromosome 8q24.3, and may play a crucial role in intracellular protein transport and synaptic transmission. Recently, a large-scale meta-analysis of genome-wide association study dataset identified that rs10098073 and rs4129585, two single nucleotide polymorphisms (SNPs) within TSNARE1, were closely associated with the risk of schizophrenia in Caucasians.

rs11098403 polymorphism near NDST3 is associated with a reduced risk of schizophrenia in a Han Chinese population.

A recent genome-wide association study indicated that rs11098403, a single nucleotide polymorphism in the vicinity of NDST3, was strongly associated with the risk of schizophrenia in Caucasians. However, this relation has not been validated in other populations or ethnic groups. Herein, we conducted a case-control study to investigate the association of rs11098403 polymorphism with the schizophrenia risk in a Han Chinese population comprising 440 schizophrenia patients and 450 control subjects.

Upregulation of TREM2 ameliorates neuropathology and rescues spatial cognitive impairment in a transgenic mouse model of Alzheimer's disease.

Triggering receptor expressed on myeloid cells 2 (TREM2) gene is a recently identified susceptibility gene for Alzheimer's disease (AD), as its low-frequency variants increase the risk of this disease with an odds ratio similar to that of an APOE ɛ4 allele. To date, the expression and biologic functions of TREM2 under AD context remain largely unknown. Using APPswe/PS1dE9 mice, a transgenic model of AD, we showed that TREM2 was upregulated in microglia during disease progression.

Triggering receptor expressed on myeloid cells 2 knockdown exacerbates aging-related neuroinflammation and cognitive deficiency in senescence-accelerated mouse prone 8 mice.

As a major characteristic of aging process, neuroinflammation is involved in the pathogenesis of several aging-related diseases including Alzheimer's disease (AD). Triggering receptor expressed on myeloid cells 2 (TREM2) is a newly identified risk gene for AD, which regulates inflammatory process in peripheral tissues via modulating the release of inflammatory cytokines. However, the role of TREM2 in aging-related neuroinflammation, cognitive deficiency, and AD-like neuropathology is unclear so far.

Activation of double-stranded RNA-dependent protein kinase inhibits proliferation of pancreatic β-cells.

Double-stranded RNA-dependent protein kinase (PKR) is revealed to participate in the development of insulin resistance in peripheral tissues in type 2 diabetes (T2DM). Meanwhile, PKR is also characterized as a critical regulator of cell proliferation. To date, no study has focused on the impact of PKR on the proliferation of pancreatic β-cells.

Early activation of nSMase2/ceramide pathway in astrocytes is involved in ischemia-associated neuronal damage via inflammation in rat hippocampi.

Background: Ceramide accumulation is considered a contributing factor to neuronal dysfunction and damage. However, the underlying mechanisms that occur following ischemic insult are still unclear.

Methods: In the present study, we established cerebral ischemia models using four-vessel occlusion and oxygen-glucose deprivation methods.

Elevated toll-like receptor 3 inhibits pancreatic β-cell proliferation through G1 phase cell cycle arrest.

Activation of the innate and acquired immune systems plays an important role in chronic inflammatory diseases and conditions such as obesity, insulin resistance, type 2 diabetes mellitus and atherosclerosis, with additional roles in regulation of cell proliferation and survival. Here, we provide evidence that TLR3 can respond to nutrient signals and induce loss of β-cell mass through induction of G1 cycle arrest. Activation of TLR3 by polyinosinic-polycytidylic acid [poly (I:C)] was shown to trigger the decline of cyclin D1/2 protein levels in pancreatic β-cell lines, which could be reversed by the proteasome inhibitor MG132.

[Protective effect of H2S pretreatment on cerebral ischemia-reperfusion injury and its mechanisms in rats].

Objective: To investigate the protective effect of H2S pretreatment after cerebral schemia/reperfusion injury and its mechanisms in rats.

Methods: The rat model of global cerebral ischemia/reperfusion injury was established by bilateral common carotid arteries occlusion combined with hemorrhagic hypotension.30 rats were randomly divided into four groups(1)sham group(n=5),in which rats received sham surgery only,with their bilateral vertebral artery and bilateral common carotid artery exposed but without ischemia treatment;(2)global cerebral ischemia/reperfusion model group(IR group,n=5),in which the global cerebral ischemia was induced by 10-min occlusion of bilateral common carotid arteries combined with hypotension;(3)H2S pretreatment group(n=15),in which H2S(12,24,48 Μmol/kg)was intraperitoneally injected before operation;(4)NaCl pretreatment group(n=5),in which the rats were intraperitoneally injected with saline 30 minutes before operation.

MiR-21 involve in ERK-mediated upregulation of MMP9 in the rat hippocampus following cerebral ischemia.

Matrix metallinoprotease-9 (MMP9) plays a key role in the pathogenesis of post-ischemic blood brain barrier (BBB) disruption and the formation of lesions after cerebral ischemia. In this study we investigate the effect of brain-specific miRNAs on MMP-9 protein level in the rat hippocampus following cerebral ischemia and its underlying mechanism. Cerebral ischemia significantly upregulated miR-21 and -224 in the hippocampus; however, expression of miR-122 and -338-3p was not significantly affected by ischemia.