Activation of p38-mitogen-activated protein kinase contributes to ischemia reperfusion in rat brain.

Inflammation plays an important role in cerebral ischemia reperfusion, which can cause severe damage to the brain and may lead to cerebral hemorrhage transformation. p38-mitogen-activated protein kinase (p38mapk) has been implicated in the etiology of a number of diseases because it is a cause of inflammation, but comparatively little research has been carried out into its role in the etiology of ischemia reperfusion. We investigated the expression of p38mapk in cerebral ischemia reperfusion to gain a better understanding of its potential role in hemorrhagic transformation (HT). One hundred rats were randomly divided into three groups: an ischemia reperfusion group, an ischemia group, and a sham-operated group. We carried out neurological deficit assessments, infarct volume measurements, histopathological examinations, and immunohistochemistry analyses. p38mapk was overexpressed in the ischemia reperfusion group, which exhibited severe tissue damage and greater edema than the other two groups. These results suggest that p38mapk plays an important role in cerebral ischemia reperfusion, and may be one of the causes of HT.

Interleukin-10 polymorphisms associated with susceptibility to acute myeloid leukemia.

We investigated the association between polymorphisms in interleukin-10 (IL-10) -1082G/A (rs1800896), -819T/C (rs1800871), and -592A/C (rs1800872) and the risk of acute myeloid leukemia (AML) in a Chinese population. A total of 167 primary AML cases and 328 healthy control subjects were recruited at the First People's Hospital of Yunnan Province between March 2009 and January 2012. The polymorphisms rs1800896, rs1800871, and rs1800872 were genotyped by polymerase chain reaction-restriction fragment length polymorphism. Multivariate regression analyses showed that subjects carrying the rs1800871 CC genotype and C allele had a significantly increased risk of AML, with adjusted odds ratios (95% confidence intervals) of 1.72 (1.01-2.97) and 1.38 (1.04-1.81), respectively. Those carrying the rs1800872 G allele had a slightly increased risk of AML, with an adjusted odds ratio (95% confidence interval) of 1.30 (1.01-1.72). Moreover, genotyping results demonstrated that subjects carrying both the rs1800871 C allele and rs1800872 G allele had a moderately increased risk of AML, indicating that the 2 genotypes had a synergistic effect on AML risk (odds ratio = 2.03, 95% confidence interval = 1.24- 3.15). Our results demonstrated that polymorphisms in rs1800871 and rs1800872 enhance the risk of AML, and these 2 single nucleotide polymorphisms have a synergistic effect on AML risk.