ObjectiveTo determine the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism in Han ethnic patients with type 2 diabetes in Chenzhou area of Hunan province,and to assess the assoeiation between this polymorphism and diabetes.MethodsThis study was cross-sectional designed.Samples were taken by random sampling method from diabetes, prediabetes and euglycemia subjeers.ACE gene polymorphism I/D were examined by PCR.Genotype was classified as I1, ID, or DD based on positive or negative insertion/deletion allele.ResultsThis study showed significant differences of ages (X2 =32.09, P ＜0.01), body mass index (BMI) (X2 =16.10, P ＜0.01), family history (X2 =20.42, P ＜0.01) and serum triglyceride (F =21.289, P ＜0.01) among three groups, and diabetes group tended to have higher value.Frequency of genotype II, ID, DD were 72(56.3％) ,52(40.6％) and 4(3.1％) in diabetes, 64(64.0％) ,30(30.0％) and 6(6.0％) in pre-diabetes subjects, 81 (72.3％),29(25.9％)和 2(1.8％) in euglycemia subjects, consecutively.Chi-square analysis showed statistically significant association between ID + DD vs.Ⅱ genotype and diabetes (x2 = 6.68, P ＜ 0.05).Logistic regression analysis showed four variables that significantly influence to diabetes, namely ACE gene polymorphism, family history of diabetes, BMI, and serum triglyceride level.ConclusionsACE ID + DD genotype had significant relationship with diabetes in Chenzhou Han ethnic population, Hunan province, China.

Objective To explore the developmental characteristics of different functional levels of autism and the diffe-rence in children. Methods A total of 159 autistic children aged 13-71 months including 85 high-functioning autistic (HFA) chil-dren and 74 low-functioning autistic (LFA) children were evaluated for their developmental characteristics by the development scales from the psycho-educational profile-revised (PEP-R). Results Within the same age group, both HFA and LFA children had obvious unbalance in individual ability development (H=41.68~113.51, P<0.01). Impaired cognitive performance is most common in HFA children. The development of cognitive performance was inconsistent with cognitive expression while the gross motor development was normal. The ability development in LFA children were all impaired, especially in imitation, cogni-tive performance and cognitive expression. With increasing age, the scores of imitation, perception, cognitive performance, cog-nitive expression and overall development quotient were increased gradually in HFA children (P<0.05) while the scores of cogni-tive performance and overall development quotient were decreased in LFA children. Conclusions Autistic children tend to have abnormal developmental progress and order, and individual ability development varies by functional level in autistic children with increasing age.

Objective:To understand and determine the biological properties of Chlamydia pneumonia (Cpn) hypothetical protein Cpn0423 and the mechanisms of which involved in Cpn0423-induced inflammatory response. Methods:The biological properties of Cpn0423 gene were analyzed using bioinformatic software. The subcellular localization of nucleotide-binding oligomerization domain-like receptor 2 (NOD2) in bone marrow-derived macrophages (BMDMs) was detected by confocal microscope. NOD2-siRNA was used to inhibit the expression of NOD2 at mRNA level. Cpn0423-induced macrophage inflammatory protein 2 (MIP-2) and IL-6 production in BMDMs were detected by ELISA. PCR was performed to detect Cpn0423 DNA in bronchoalveolar lavage fluid (BALF) of Cpn-positive patients.Results:The homology between Cpn0423 and other type Ⅲ secretion system effector proteins of Chlamydia ranged from 85% to 93%. NOD2-siRNA could effectively inhibit the expression of NOD2 at mRNA level in BMDMs ( P<0.001). Moreover, Cpn0423-induced production of MIP-2 [(920.5±99.1) pg/ml vs (130.1±11.5) pg/ml, P<0.001] and IL-6 [(266.2±58.4) pg/ml vs (165.7±21.5) pg/ml, P<0.001] in BMDMs were decreased following NOD2-siRNA pre-treatment. Cpn0423 DNA was detected in the BAlF of 83.3% (10/12) of Cpn-positive cases, but not in Cpn-negative cases. Conclusions:Cpn0423 induced inflammatory response in host cells through NOD2 pathway, which was closely related to the chronic inflammatory injury caused by Cpn.