Objective To explore an effective and hidden incision scar method for epicanthus correction. Methods 80 patients of bi-lateral single eyelid with epicanthus were divided into group A,group B and group C. Twenty-five patients with 50 eyes of group A received“Z” plasty correction of epicanthus,25 cases with 50 eyes of group B received the traditional“Y-V” plasty correction of epicanthus,30 cases with 60 eyes of group C treated with modified “Y-V” plasty correction of epicanthus. The curative effective was observed. Results Three groups were followed up for 6~24 months, the appearances of 25 patients in group A were significantly improved,of whom 2 cases had uni-lateral recurrence,8 cases with obvious postoperative scar. The eyelid shapes of patients in group B were natural after surgery,12 cases with obvious scar. all patients in group C were found no postoperative hypertrophic scars. Conclusion The three surgical treatment were effec-tive for epicanthus,but the design approaches of“Z” plasty correction and“Y-V” plasty correction are more complex,and postoperative scar is obvious,meanwhile the modified “Y-V” plasty correction is simple with incision hidden good shape scar formation.

Objective:To find a feasible method to stimulate tumor-draining lymph node(TDLN) cells in clinic.Methods:CTL activity of TDLN cells induced by different stimulus (IL-2 group, IL-2+autologous tumor antigen group, IL-2+GM-CSF+IL-4+autologous tumor antigen group) was measured by the method of maximal LDH enzyme release. The mechanisms were explored by observation in morphology and detection of the CD83 positive rate of TDLN cells.Results:The level of growth of TDLN cells induced by (IL-2+GM-CSF+IL-4+autologous tumor antigen) was significantly higher than TDLN cells induced by IL-2 and (IL-2+autologous tumor antigen)(P

BACKGROUND:Bone marrow mesenchymal stem cells have the chemotaxis and homing role that promotes immune system reconstruction, eliminate residual lesions and prevent recurrence in patients.
OBJECTIVE:To observe therapeutic effect of human bone marrow mesenchymal stem cells transplantation into high-metastatic potential hepatocellular carcinoma animal models on metastatic potential of high-metastatic potential hepatocellular carcinoma.
METHODS:Nude mouse models of high-metastatic potential hepatocellular carcinoma were established in vivo. In the experimental group, 5×105 cells were injected via the tail vein on day 7 after tumor inoculation, twice a week. In the control group, cellculture medium, 0.2 mL per mouse, was injected by the tail vein. After the start of the experiment, tumor volume was measured every 4 days. After tumor inoculation for 14 days, 21 days, 28 days, 35 days, 42 days, animal models were sacrificed, and then tumor mass and body mass were recorded to calculate the inhibition rate. PCR was employed to detect osteopontin, bone sialoprotein, and integrinα Ⅴ mRNA expression, as wel as bcl-2, bax, caspase3 mRNA expression.
RESULTS AND CONCLUSION:The inhibition rate of tumor mass showed the best results in week 3. As time went on, the tumor inhibition rate was gradual y decreased. Metastasis-related biological factors showed a gradual down-regulated trend, indicating the polarization of tumor apoptotic indexes, that is, anti-apoptotic factor, bcl-2, showed a decreasing trend, while apoptotic factors, bax and caspase3, appeared to have a gradual y increased trend. These findings suggest that human bone marrow mesenchymal stem cells effects to inhibit high-metastatic potential hepatocellular carcinoma animal models appear to vary with time. After human bone marrow mesenchymal stem cells transplantation for 3 weeks, the inhibition performance on high-metastatic potential hepatocellular carcinoma is the best, and then it weakens with time. Human bone marrow mesenchymal stem cells are found to inhibit the metastatic potential of hepatocellular carcinoma.

Objective To investigate the expression and clinical significance of T-cell receptor (TCR) Ⅴβ subfamily in hepatitis B virus (HBV)-related acute-on-chronic liver failure (HBV-ACLF) patients.Methods Twenty-eight patients with HBV-ACLF (HBV-ACLF group) and 32 patients with chronic hepatitis B flare (CHB-F group),who were treated in The Second People's Hospital from Oct.2010 to Mar.2012,and 20 healthy controls (HC group) were included in the study.Reverse transcriptase-polymerase chain reaction was used to detect the levels of TCR Ⅴβ subfamily and enzymelinked immunosorbent assay was used to detect the levels of serum cytokines [interleukin (IL)-2,IL-4,IL-6,IL-10,interferon (IFN)-γ and tumor necrosis factor (TNF)-α)] in the three groups.The comparison among three groups was done by one-way analysis of variance and the comparison between two groups was done by LSD-t test or rank sum test.Results The three groups had similar gender and age distribution (all P＞0.05).The HBV-ACLF group had significant different profiles of total bilirubin,albumin,prothrombin activity,international normalized ratio and cholesterol tatol compared with the CHB-F group (all P＜0.05).For patients in the HBV-ACLF group,the serum IL-2,IL-4,and IL-10 levels were lower(all P=0.000),and the IL-6 and IFN γ levels were higher than those of the HC group (all P=0.000).The IL-4,IL-10,and TNF-α levels in the CHB-F group were also significantly lower than those of the HC group (all P=0.000).Compared with the CHB-F group,the HBV-ACLF group had significantly lower IL-2,IL-10,and TNF-α levels (P=0.003,0.002,0.004),and higher IL-6 and IFN-γ levels (P=0.015,0.006).By one-way analysis of variance,there were significantly differences of △Ct1,△Ct5,△Ct7,△Ct12,△Ct15,△Ct20,△Ct22,and △Ct23 among the three groups (H=20.368,14.368,19.500,31.532,19.985,19.116,41.752 and 20.649,all P＜0.05).Conclusion The expression levels of TCR Ⅴβ subfamily and cytokines are changed in HBV-ACLF patients.

Objective To discuss the expression level of CUEDC2 protein and its connection with 24 h urinary albumin and serum creatinine iu db/db mice with diabetic nephropathy.Methods db/db mice were selected as experimental groups (n =10),and db/m mice as control (n =10).All mice were fed in barrier facilities under the same conditions.At week 24,all were sacrificed and the samples were collected for analyses.The histological changes were assessed by Hematoxylin-Eosin(HE) staining,periodic acid-Schiff (PAS) staining and Masson's trichrome (Masson) staining.The location and expression of CUEDC2 were measured by immunohistochemistry assays.24 h urinary albumin and serum creatinine were quantified by clinic lab in our hospital.Results Immunohistochemistry demonstrated that CUEDC2 was mainly located in the medulla tubules plasma cells.The results of HE staining revealed that there appeared glomerular number decreased,atrophy and inflammatory cell infiltration in the mice kidney of diabetic nephropathy group at the 24th week.The mesangial matrix expansion and renal tissue collagen deposition were significantly up-regulated in db/db mice compared with the normal control.As compared with the control group,the CUEDC2 protein expression and mRNA expression in db/db mice were significantly decreased than that in db/m mice (both P ＜ 0.05),and 24 h urinary albumin and serum creatinine were significantly increased.The correlation analysis showed CUEDC2 was negatively correlated with 24 h urinary albumin and serum creatinine (both P ＜ 0.05).Conclusion The expression of CUEDC2 in diabetic nephropathy mice kidney is significantly decreased and negatively correlated with the levels of 24 h urinary albumin and serum creatinine.

Objective To study the clinical characteristics and genetic cause of a Chinese family affected with paroxysmal kinesigenic dystonia(PKD).Methods The detailed clinical data and the blood samples of the affected patients with PKD and their relatives were collected.After genomic DNA was extracted from blood leukocytes,target linkage analysis Was performed using multiplex PCR by microsatellite marker's located in the reported critical region on chromosome 16.All exons and flanking regions of SCNN1G and ITGAL genes were amplified by PCR-sequence.Results In this three-generation 12 member family,5 individuals have been diagnosed as PKD.Target linkage analysis suggested the disease gene linked to chromosome 16.between D16S3396 and D16S3057 with two-point LOD score of 1.47 at recombination fraction(θ)=0.0.All affected individuals shared a common haplotype which co-segregated with the phenotype.Except for 8 reported SNPs,no pathologic sequence variants were found in candidate genes SCNN1G and ITGAL.Conclusions The studied family is genetically linked to the reported critical locus of PKD on chromosome 16.SCNN1G and ITGAL were ruled out as the causative genes for the studied pedigree.Further genetic analysis in this family may reveal new genetic cause responsible for PKD.

Objective To study the effects of CUEDC2 on renal interstitial fibrosis and inflammation response in rats with unilateral ureteral obstruction (UUO). Methods 30 Balb/c rats were randomly distributed into sham operation group(sham-vector),uuo operation group(uuo-vector) and CUEDC2 treatment group after uuo (uuo-cuedc2). Hematoxylin-eosin and Masson staining were used to measure renal pathology; Inflammation factors were quantified by ELISA; Immunohistochemistry was performed to measure the expression of CUEDC2;Protein expression of CUEDC2, Fibronectin, E-cadherin, Collagen I were detected by Western Blot. Results At 7 and 14d after operation, the area of interstitial fibrosis and expression of ICAM1,MCP1,IL1,IL8, Fibronectin and Collagen I in uuo-cuedc2 showed a marked decrease when compared to uuo-vector (p?0.05),the level of E-cadherin was significantly increased (P < 0.05). Conclusion CUEDC2 can inhibit renal interstitial fibrosis and decrease the expression of inflammation factors and Collagen deposition.

Objective To investigate the relationship between the single nucleotide polymorphisms(SNPs) of disrupted in schizophrenia 1 (DISC1) gene and autism in Chinese Han children.Methods Genome-wide SNP genotyping was performed by using Illumina HumanHap CNV370-Duo Chip in 278 autistic trios,157 autistic individuals and 435 healthy controls.Genotype data of SNPs within DISC1 gene were selected.The association between these SNPs loci and autism was analyzed through case-control association analysis and family-based transmission disequilibrium test.Results Fifty-two SNPs were involved for further analysis.1.Case-control association analysis showed that 6 SNPs (rs4658939,rs2793093,rs10495309,rs2492367,rs1 1122362,rs1073179) and 7 haplotypes (AGAAAG constructed with rs823163-rs823161-rs4658933-rs1417585-rs10864693-rs6541281,GGG and AAA constructed with rs4658939-rs2793093-rs10495309,GG and AG constructed with rs2492367-rs12046794,GAA constructed with rs9432040-rs2356606-rs1 1122362 and GG constructed with rs9431714-rs1073179) had significant differences between autistic patients and controls(x2 =4.704,4.915,5.568,8.087,4.043,5.183,5.369,5.295,4.440,5.304,7.615,4.018,4.811,P =0.030,0.027,0.018,0.005,0.044,0.023,0.021,0.021,0.035,0.021,0.006,0.045,0.028).2.In the transmission disequilibrium test analysis,2 SNPs (rs4658945,rs11122362) and 2 haplotypes (AG constructed with rs10495310-rs4658945,GAA constructed with rs9432040-rs2356606-rs11122362) showed significant transmission disequilibrium(x2=4.445,5.400,3.973,5.126,P =0.035,0.020,0.046,0.024).Conclusions The polymorphism of rs11122362 and GAA haplotype constructed with rs9432040-rs2356606-rs11122362 are associated with autism,and DISC1 gene is a susceptibility gene for autism in Chinese Han children.

Objective:To investigate the effects of establishment of a trauma center on the therapeutic efficacy for patients with severe multiple injuries.Methods:A retrospective study was conducted in the patients who had been treated at The Second Affiliated Hospital, University of South China for severe multiple injuries from October 2015 to September 2019. They were assigned into 2 groups. The study group included 102 patients who had been treated after establishment of our trauma center (from October 2017 to September 2019) while the control group 126 patients who had been treated before establishment of our trauma center (from October 2015 to September 2017). The 2 groups were compared in terms of time for emergency treatment (from admission to emergency surgery or ICU), ICU stay, hospital stay, total medical costs and mortality.Results:There was a significant difference between the 2 groups in time for emergency treatment [51 (47, 57) min for the study group versus 97 (87, 107) min for the control group] ( P<0.05). There were no significant differences between the 2 groups in ICU stay [4 (1.8, 9.3) d versus 4 (2.0, 10.0) d], hospital stay [25.5 (15.8, 39.0) d versus 21.5 (12.8, 41.5) d], or total medical costs [￥41,259.0 yuan (￥26,950 yuan, ￥81,599 yuan)] ( P>0.05). There was a significant difference between the 2 groups in mortality [12.7% (13/102) for the study group versus 24.6% (31/126) for the control group] ( P<0.05). Conclusion:Establishment of a trauma center can effectively shorten time for emergency treatment, improve treatment efficacy and reduce mortality for patients with severe multiple injuries.

The recombinant plasmid pCI-TSLC1 carrying TSLC1 gene was stably transfected into human hepatocellular carcinoma cell line HepG2. Cell proliferation was analyzed by MTT assay. The ability of migration was determined by transwell and FACSort flow cytometry was used to detect the cell cycle distribution and apoptosis. Western blotting revealed that H4 expressed higher amounts of TSLC1 protein than H15 and H0 did. The growth of TSLC1-transfected cells was significantly suppressed in vitro, and the ability of migration was reduced as well. The re-expression of TSLC1 could induce cell apoptosis. It was concluded that TSLC1 strongly inhibited the growth and ability of migration of HepG2 cell line in vitro and also induced apoptosis, suggesting that TSLC1 could reduce the tumorigenicity of human hepatocellular carcinoma cell line HepG2 in vitro, which provided a basis for further exploring the roles of TSLC1 in hepatocellular cellular carcinoma.
Apoptosis/*genetics ; Cell Adhesion Molecules/*genetics ; Cell Proliferation ; Hep G2 Cells ; Immunoglobulins/*genetics ; Neoplasm Invasiveness/genetics ; Transfection ; Tumor Suppressor Proteins/*genetics