Objective To study the correlation between chronic gastritis with benign mucosal nodular-change,Helicobacter pylori(H.pylori)infection and lymphoid follicles infiltration.Methods During July 1,2004 to June 30,2005 patients with chronic gastritis and benign mucosal nodular-change were identified by chromo-endoscopy with anabrosis indigo carmine staining at the antrum.Multiple biopsies were obtained for H.pylori detection with quick test and for pathology examination of mucosal lymphoid follicles formation and lymphocyte infiltration,as well as H.pylori infection.Results The patients were divided into nodular gastritis group,atrophy gastritis group and verrucous gastritis group with mean age of(31.00?11.62),(58.61?12.14)and(51.29?12.99)years old,respectively.The patients with nodular gastritis were the youngest(P

BACKGROUND: Many scholars have paid attentions on neural stem cells (NSCs), which are regarded as the cell source to repair the injured nervous tissues. And it is becoming a key point that NSCs will be obtained in an effective way.OBJECTIVE: To observe the characteristics of isolation, proliferation and differentiation of in vitro NSCs from subventricular zone (SVZ) and hippocampus of neonatal rats.DESIGN: Single-sample trial.SETTING: Department of Neurosurgery in the Third Affiliated Hospital of Sun Yat-sen University.MATERIALS: Ten SD rats aged 3 days, of either gender, were offered from the Experimental Animal Center of Sun Yat-sen University. Nestin antibody (rabbit-anti-rat), neurofilament (NF-200) antibody (rabbit-anti-rat), and glial fibrillary acidic protein (GFAP) antibody (mice-anti-rat) were all purchased from Sigma Company.METHODS: The experiment was carried out in the Laboratory of Histology and Embryology, Basic Medical College of Sun Yat-sen University from September to December in 2006. According to the ethical requirement, the serum-free DMEM/F12 medium containing basic fibroblast growth factor and epidermal growth factor was utilized to isolate and incubate NSCs from SVZ and hippocampus of neonatal rats. Then the proliferation and differentiation of NSCs in vitro were observed.MAIN OUTCOME MEASURES: Fluorescence immunocytochemistry was applied to detect the antigen of nestin expressed from NSCs, NF expressed from neuron cells and GFAP expressed from astrocytes. The differentiation of NSCs was identified.RESULTS: The cells isolated from SVZ and hippocampus of neonatal rats possessed the ability of proliferation and self-renewal. Through inverted microscope, nestin positive cells could be found in the cell clone sphere at passage 20 of cells. Cells induced to differentiate could express antigen of NF and GFAP by the attached cell clone sphere.CONCLUSION: The NSCs successfully isolated from SVZ and hippocampi of neonatal rats possess the ability of self-renewal, proliferation, and differentiation into neuron-like cells and astrocytes.

ObjectiveTo study the single nucleotide polymorphisms(SNPs) in the ORF26 gene of HHV-8 in Kaposi's sarcoma(KS),and to assess their correlations with the clinical phenotype and mucosal invasion of KS.MethodsHHV-8 DNA was extracted with phenol-chloroform-isoamyl alcohol from paraffin-embedded tissue specimens obtained from 32 cases of KS(including 26 classic and 6 AIDS-related KS).The ORF26 gene of HHV-8 was amplified by nested-PCR followed by bidirectional sequencing.The software DNAStar and program Clustal W were used to assess the SNPs in the ORF26 gene.Statistical analysis was carried out by using the Fisher's exact probability test.ResultsHHV-8 DNA was detected in 30 of the 32 tissue specimens,and in all of the 6 AIDS-related specimens.The predominant SNPs were 981 T/C(n =12),1086 C/T(n =12) and 1139 A/C(n =12) in the ORF26 gene of the 30 strains of HHV-8.No significant difference was observed in the distribution of SNPs in ORF26 between different phenotypes of KS or between KS with and without mucosal invasion.ConclusionThe ORF26 SNPs of HHV-8 seem unrelated to the clinical phenotypes or mucosal invasion of KS.

To compare the effects of four different intensive insulin therapies on blood glucose control and vascular endothelial function in newly-diagnosed type 2 diabetes.Patients were randomly divided to accept pre-meal insulin aspart 30 or pre-meal insulin aspart and glargine at bedtime or pre-meal Novolin-R and NPH at bedtime or continuous subcutaneous insulin aspart infusion.Capillary blood glucose determination and continuous glucose monitoring system were carried out,therapeutic time and total insulin dosage were recorded.Ultrasound was used to evaluate the vascular endothelial function.Glucose level,incidence of low glucose,potency ratio of the four groups were similar( P＞0.05 ) ; FMD and NMD were not significantly improved ( P =0.718,P =0.065 ).The short-term efficacy and safety of the four groups are similar.The short-term intensive insulin therapy has no obvious effect on vascular endothelial function.

AIM:To investigate the effect of RNA interference (RNAi)-mediated insulin-like growth factor 1 receptor ( IGF1R) gene silencing on the growth , migration, and invasion of hepatocellular carcinoma cells .METHODS:The most effective siRNA targeting IGF1R gene was designed and screened .After lentiviral expression vector pLVX-shR-NA2-IGF1R carrying the most effective siRNA sequence was constructed , it was transfected into 293T cells and packed into pLVX-shRNA2-IGF1R lentivirus.Huh7 and Hep3B cells were infected with the pLVX-shRNA2-IGF1R lentivirus to screen the positive clone Huh7 cells and Hep3B cells with the lentivirus .These Huh7 cells and Hep3B cells were cultured to ana-lyze the mRNA level of IGF1R, cell proliferation, cell cycle, cell apoptosis, cell migration/invasion, and the protein levels of IGF1R, Ki-67, p-AKT, p-ERK1, Gli1,β-catenin, cyclin D1, p21 and BCL-XL.RESULTS:The mRNA expression of IGF1R in Huh7 cells and Hep3B cells with pLVX-shRNA2-IGF1R lentivirus was significantly reduced .The proliferation of these cells was remarkably inhibited , and the number in G 1 phase was increased significantly .The percentages of apop-totic cells were increased markedly , and the number of cell migration/invasion was decreased markedly .The protein levels of IGF1R, Ki-67, p-AKT, p-ERK1, Gli1,β-catenin, cyclin D1, p21 and BCL-XL were decreased significantly compared with the blank control group and negative control group .CONCLUSION:The RNAi-mediated IGF1R gene silencing sig-nificantly suppresses the growth and the malignant biological characteristics of Huh 7 cells and Hep3B cells, which may be involved in the reduced protein levels of the above genes induced by down -regulation of IGF1R expression.

Objective To couple folate with chitosan and prepare folate-coupled chitosan by different connection ratio.Methods The folate-coupled chitosan was prepared by the reaction of the activated folate ester with the amine group on the chitosan.Then the folate-coupled chitosan was verified by infrared spectroscopy.The number of folates in each of the chitosans was measured by UV spectrophotometry.Results Infrared spectroscopy showed that the folate-coupled chitosan was prepared successfully,and the number of folates in each chitosan was approximately 3,10,20 and 30.Conclusion Coupling of folate with chitosan was successful,and folate-coupled chitosan by different connection ratio was successfully prepared.

AIM:To discuss the technique for preparing high-purity solanesol from tobacco. METHODS:The pre-treated tobacco leaves were extracted with mixed solvent of petroleum ether and ethanol,and saponified to obtain solanesol extract; The solanesol extract got through redissolution and dewaxing,then crystallized in the temperatare of -18 ℃; Finally purified by macroporous resin(YPR-Ⅱ,D-1300,HZ-816,HZ-802). RESULTS:The ratio of mixed solvent of petroleum ether and ethanol was 1 ∶ 4,ratio of liquid to materials was 1 ∶ 12,solanesol purity was about 32% after saponification,then crystallization made the purity up to 63. 4% ,finally purified through macroporous resin,the solanesol purity reached above 93. 6%. CONCLUSION:Through the general solvent extraction,saponification,crystallization and macroporous resin adsorption process,the solanesol purity of the product reaches higher than commonly expected values.

Objective To perform a spatial analysis of myocardium uhrastructure and the activity of mitochondrial succinate dehydrogenase in sub-acute Keshan disease. Methods Myocardium samples were collected from the cases with sub-acute Keshan disease and non-myocarditis(control), and their ultrastructure was observed under electron microscope. The density of mitochondrion volume and cristal membrane and its volume were measured by a point-counting method, while mitochondrion volume was estimated by water displacement method, succinate dehydrogenase activity of mitochondrion by iron-copper method in sub-acute Keshan disease and non-myocarditis cases. Results The volume ratio of mitochondrion to the cell on myoeardium [(47.79±6.20)%], the area ratio of mitochondrion to sarcoplasm [(55.06±6.50) %], mitochondrion to myofibrils [(1.43±0,41)%], mitochondrion section area[(0.78±0.15)μm2], and ratio of the lesion of cristal membrane area to the matrix area and mitochondrion volume[(67.14±13.96)%, (44.62±13.44)%]in sub-acute Keshan disease group were obviously higher than those in control [(33.20±7.62)%, (38.07±9.43)%, (0.71±0.33)%, (0.44±0.07)μm2, (14.11± 12.51)%, (9.34±11.28)%; t = 3.75,7.93,6.61,36.40,52.65,37.51, all P < 0.05]. The volume ratio of myofibrils to cell[(34.52±5.12)%]and the area ratio of cristae mitochondria to matrix[(32.43±14.42)%]in sub-acute Keshan disease group was obviously less than those in control [(48.51±4.30)%, (86.04±12.37)%; t = 9.85, 53.46, both P < 0.05)]. Succinate dehydrogenase activity was negative in sub-acute Keshan disease group. Conclusions Myocardium ultrastructure changes in sub-acute Keshan disease including the increase of volume and areas of mitochondria and the damage of the cristal membrane in mitochondria. Succinate dehydrogenase activity is decreased or even disappeared.

Objective To investigate the effects of ciprofloxacin on dermal collagen synthesis and profibrotic gene expressions in an experimental mouse model of scleroderma induced by bleomycin. Methods Experimental mouse models of scleroderma were established by subcutaneous injection of bleomycin into the dorsal skin of 15 BALB/c mice for 4 consecutive weeks. Then, the mouse models were randomly and equally divided into 3 groups to be topically treated with 1% ciprofloxacin cream (ciprofloxacin group), 2.5% asiaticoside cream (asiaticoside group)and cream vehicle (model group)respectively for 5 consecutive weeks. Five mice firstly injected with sterile phosphate buffered saline (PBS)for 4 weeks then topically treated with cream vehicle for 5 weeks served as the blank control group. After the 5-week topical treatment, all the mice were sacrificed, skin specimens were resected from the dorsal skin of them, and subjected to HE staining and Masson staining. Further more, an immunohistochemical assay was performed to measure the expressions of type I collagen (COL-1), matrix metalloproteinase-1 (MMP1) and tissue inhibitor of matrix metalloproteinase-1 (TIMP1), semi-quantitative reverse transcription PCR to quantify the expressions of connective tissue growth factor (CTGF), transforming growth factor-β1 (TGFβ1)and Smad3 genes, and alkaline hydrolysis-spectrophotometry to determine the level of hydroxyproline in skin. Statistical analysis was carried out by one-way analysis of variance and the least significant difference(LSD)test with the SPSS 17.0 software. Results Compared with the blank control group, the model group showed increased dermal thickness at injection sites (432.76 ± 93.74 μm vs. 301.69 ± 79.47 μm, P < 0.01). Masson staining revealed thick and dense collagen bundles in an irregular arrangement in the dermis in the model group, which was consistent with dermal fibrosis in scleroderma. The total content of collagen and staining intensity of COL-1, MMP1 and TIMP1 were all significantly decreased in the ciprofloxacin group and asiaticoside group compared with the model group (F = 1628.54, 33.29, 84.82, 224.81, respectively, all P < 0.01), while no significant changes were observed in dermal thickness (both P > 0.05). Moreover, compared with cream vehicle, asiaticoside down-regulated the expressions of the three profibrotic genes(CTGF, TGFβ1 and Smad3)to different extents (all P < 0.05), while ciprofloxacin only inhibited the expressions of TGFβ1 and Smad3 genes (both P < 0.05)with no significant effect on CTGF gene expression (P > 0.05). Conclusion Ciprofloxacin may counteract dermal fibrosis by inhibiting the TGFβ1/Smad3 pathway and modulating the unbalanced expressions of MMP1 and TIMP1.

Objective To investigate the relationship between eosinophil and in-stent restenosis in acute coronary syndrome patients. Methods One hundred and fifity-one ACS cases werenenrolled in this study. According to the results of coronary angiography (the stented segment lumen loss over 50% was judged to be ISR), patients were divided into the restenosis group and the non-restenosis group. Results Based on the logistic analysis, no significant association was found between eosinophil and ISR, and even after adjustment of related risk factors (P > 0.05). The stratification analysis showed that the high level of eosinophil might increase the risk of ISR in ACS patients with history of hypertension (P = 0.038) and myocardial infarction (P = 0.032). Conclusion Eosinophil may be associated with the risk of ISR in ACS patients with history of hypertension and myocardial infarction. The underlying mechanisms need to be elucidated in further study.