BACKGROUND:Amniotic cells are mainly composed of amniotic epithelial cells and amniotic mesenchymal cells, which have multi-differentiation potential and can be transformed into neurons as wel as synthesize and release biological y active substances and neurotrophic factors. In preliminary studies, amniotic cells that are transplanted into the brain can significantly promote the regeneration of brain neurons. OBJECTIVE:To explore the role of amniotic cells in mouse brain cells after ischemia-reperfusion injury. METHODS:The model of cerebral ischemia-reperfusion injury was established in Babl/c mice using occlusion of bilateral common carotid arteries, and then brain cells were separated from mice. Amniotic cells were isolated from mouse placenta. Brain cells from Balb/C mice co-cultured with amniotic cells served as experimental group, and brain cells cultured with PBS as control group. RESULTS AND CONCLUSION:The viability of brain cells in the experimental group was significantly higher than that in the control group (P<0.05). There was no difference in necrotic rate of brain cells between the experimental and control groups after 24 and 72 hours co-culture (P>0.05);after 48 hours co-culture, however, the necrotic rate of brain cells was significantly lower in the experimental group than the control group (P<0.05). In cellcycle, the experiment group showed increased S phase cells;while, the control group exhibited increased G 1 phase cells and decreased S phase cells. G 2 phase cells had no changes in number in both two groups. Through the above results, amnion cells can be proved to protect and promote the regeneration of brain cells of Balb/C mice with ischemia-reperfusion injury, and inhibit cellnecrosis and apoptosis.

Objective To explore the heredity susceptibility of children to Kawasaki disease (KD) through studying expression and genomic density polymorphism of peripheral erythrocyte complement receptor-1 (ECRI). Methods Thirty cases of KD patients and 28 cases of healthy children were included in this study. The rates of red blood cell (RBC)-C3bRR and RBC-ICR were detected by method described elsewhere. The ECR1 activity and genomic density polymorphism were detected by Hind Ⅲ restriction enzyme digestion polymerase chain reaction-restriction fragment length polymorphism. Results Rates of RBCoC3bRR of KD patients during the acute phase was significantly lower than that of the control group (P < 0.01), and remained lower than the control group during the recovering phase (P < 0.05). The rates of RBC-ICR were significantly higher in KD patients than that of the control group (P < 0.05). Frequencies of HL and LL genotypes of KD patients were more than those of the control group (P < 0.01). A significant difference was found in the frequency distribution of ECR1 genotype between the two groups (P < 0.01). L allele frequency in the patient group was higher than that in the control group. Conclusions Depressed RBC immune function in KD patients may be linked to the high frequency of L allele, which implies the genomic density polymorphism of ECR1 play an important role in determining susceptibility to Kawasaki disease. (J Clin Pediatr,2010,28(2):160-163)

A 23-year-old male patient developed vesicles on the scrotum 5 years prior to this presentation.Then,vesicles gradually affected the whole scrotum,whick easily ruptured due to friction.Physical examination showed diffuse millet-sized vesicles on the scrotum with milky white fluids,and exudates with chyle-like appearance.Histopathological examination revealed proliferating and dilated lymphatic vessels with different sizes of lumens in the dermis.Immunohistochemical study showed positive staining for D2-40 and CD31.The patient was diagnosed with scrotal lymphangioma,and received photodynamic therapy with aminolevulinic acid.After the treatment,the number of vesicles markedly decreased,and no obvious exudates were observed.During 1 year of follow up,no scars or other complications occurred,and no obvious relapse was found.

Objective:To investigate the possible role of long non-coding RNA (LncRNA) 00602 in promoting browning in adipocytes induced by adenovirus type 36 (Ad36).Methods:According to Ad36 infection, adipose tissue samples of obese patients were divided into Ad36-negative group and Ad36-infected group. Realtime fluorescent quantitative PCR (qRT-PCR) was used to detect the changes in the expression of LncRNA00602 mRNA in omental adipose tissue of the two groups, and analyze the differences between the two groups. The correlation between waist-to-hip ratio, systolic blood pressure, diastolic blood pressure, fasting blood glucose, triacylglyceride and other indicators of the patients in the group with LncRNA00602 mRNA expression were analyzed. HE staining was used to detect the size of adipocytes in the omental adipose tissue of the Ad36 negative group and the Ad36 infection group. qRT-PCR and Western blotting were used to detect the mRNA and protein expression levels of uncoupling protein 1 (UCP1) and PR domain containing 16 (PRDM16) in omental adipose tissue of two groups of patients. Human adipose-derived stem cells (hADSC) were isolated and cultured, using Ad36 to induce differentiation, and divided into control group and LncRNA00602 knockdown group. On 0, 2, and 4 days after LncRNA00602 knockdown, fluoroboron dipyrrole (BODIPY) and mitochondrial red fluorescence (Mito-Tracker Red) were used to stain intracellular lipid droplets and mitochondria. At the same time, qRT-PCR and Western blotting were used to detect changes in the expression of UCP1 and PRDM16.Results:The expression of LncRNA00602 gene in the Ad36 infection group was higher than that in the Ad36 negative group (all P<0.05). The expression of LncRNA00602 in the Ad36 negative group was not significantly different from the above clinical indicators, while the expression of LncRNA00602 was negatively correlated with serum fasting blood glucose and triacylglyceride ( r=-0.522, -0.486, P<0.05) in the Ad36 infection group; HE staining showed that the average adipocyte area of the Ad36 infection group was smaller than that of the Ad36 negative group. At the same time, UCP1 and PRDM16 gene expression were higher than the negative group (all P<0.05). At the cellular level, on the 2nd and 4th days after knockdown of LncRNA00602, the lipid droplet area of adipocytes in the LncRNA00602 knockdown group was larger than that of the control group, the number of mitochondria decreased compared with the control group, and difference was statistically significant ( P<0.05 or P<0.01); Compared with the control group, there was significantly lower expression of the browning marker genes UCP1, PRDM16, and protein in the adipocytes in the LncRNA00602 knockdown group (all P<0.05). Conclusion:In Ad36-induced adipocyte differentiation, LncRNA00602 may positively regulate the expression of UCP1, PRDM16 and lipid droplet metabolism, and promote the browning of adipocytes.

OBJECTIVES: Intracerebral hemorrhage (ICH) has the highest mortality and disability rates among various subtypes of stroke. Previous studies have shown that the gut microbiome (GM) is closely related to the risk factors and pathological basis of ICH. This study aims to explore the causal effect of GM on ICH and the potential mechanisms. METHODS: Genome wide association study (GWAS) data on GM and ICH were obtained from Microbiome Genome and International Stroke Genetics Consortium. Based on the GWAS data, we first performed Mendelian randomization (MR) analysis to evaluate the causal association between GM and ICH. Then, a conditional false discovery rate (cFDR) method was conducted to identify the pleiotropic variants. RESULTS: MR analysis showed that Pasteurellales, Pasteurellaceae, and Haemophilus were negatively correlated with the risk of ICH, whileVerrucomicrobiae, Verrucomicrobiales, Verrucomicrobiaceae, Akkermansia, Holdemanella, and LachnospiraceaeUCG010 were positively correlated with ICH. By applying the cFDR method, 3 pleiotropic loci (rs331083, rs4315115, and rs12553325) were found to be associated with both GM and ICH. CONCLUSIONS There is a causal association and pleiotropic variants between GM and ICH.
Humans ; Genome-Wide Association Study ; Gastrointestinal Microbiome/genetics* ; Genetic Predisposition to Disease ; Cerebral Hemorrhage/genetics* ; Stroke