Objective To investigate the relationship between sonic hedgehog(SHH)signaling pathway and chronic pancreatitis.Methods Thirty Wistar rats were randomly divided into the model group,experimental control group and blank control group,and there were 10 rats in each group.Trinitrobenzene sulfonic acid was infused into the pancreatic duct of the rats to induce pancreatitis in the model group.The pancreatic duct of the rats in the experimental control group were infused with 0.9％ sodium chloride solution.No treatment was performed on rats in the blank control group.The serum levels of bilirubin and amylase of the 3 groups were determined,and the histopathological alterations were studied.Expressions of patched-1(PTCH-1),smoothened (SMO)and SHH were detected by immunohistochemistry.All data were analyzed using the analysis of variance or Student's t test.Results The levels of total bilirubin(TBil)in the model group,experimental control group and blank control group from day 1 to day 35 were(3.17 ±0.21)μmol/L-(9.28 ±2.15)μmol/L,(3.44 ±0.54)μmol/L-(3.76 ± 0.15)μmol/L,(2.45 ± 0.32)μmol/L-(3.27 ± 1.43)μmol/L,respectively.The levels of amylase in the model group,experimental control group and blank control group were(1124 ± 143)U/L-(1522 ± 169)U/L,(1123 ± 104)U/L-(1007 ± 141)U/L,(1014 ± 115)U/L-(1013 ± 142)U/L,respectively.Compared with the experimental group and the blank control group,the serum levels of TBil and amylase in the model group were increased significantly from day 7 to day 35(F =14.81,16.27,18.13,11.49,17.91;11.54,10.24,12.64,21.11,15.38,P ＜ 0.05),and fibrotic proliferation of pancreatic tissues were found at day 35;the expressions of PTCH-1,SMO and SHH in the pancreatic tissue was increased significantly in the model group.Conclusion SHH signaling pathway is activated in the tissue of pancreatitis in rats,it might play an important role in the genesis of pancreatitis.

At present,the fashions,methods and means of medical genetics teaching have fallen behind the development of the subject.Under the patterns of net-teaching,the construction of net-teaching database is an important tache to develop teaching favourably,improve the quality and efficiency of teaching fleetly.This paper introduces the process of constructing a net-teaching database for medical genetics,the applications and characters of the database in teaching.

Purpose To observe therapeutic effect of electroacupuncture Neixiyan (Ex-LE 4 ) and Dubi (ST 35) in treating osteoarthritis of knee joint. Method All the 120 cases were randomly divided into electroacupuncture and control groups, 60 cases in each group,and they were given electroacupuncture and Ritalin slowreleased tablet respectively, and pain, mobility and swelling degree of knee joint were observed before and after treatments. Results In treatment group, the average score increased by 18, while in control group, it increased by 12.33 ( P < 0. 05 ) after treatment. Conclusion Therapeutic effect of electroacupuncture Neixiyan (Ex-LE 4) and Dubi (ST 35) in treating osteoarthritis of knee joint was better than that of administration of Ritalin slow-released tablet.

Objective:To explore the role and mechanism of long non-coding RNA KCNQ1 overlapping transcript 1 (LncRNA KCNQ1OT1) in the migration, proliferation and invasion of hepatocellular carcinoma (HCC).Methods:The experimental method was conducted. The expression levels of LncRNA KCNQ1OT1 in HCC tissues and normal liver tissues in the StarBase database were collected. The experimental methods including real-time quantitative PCR, cell transfection, scratch assay, CCK8 assay, Transwell assay, Western blot were used to determine the expression, migration, proliferation, invasion of LncRNA KCNQ1OT1 in HCC cells and its relationship with phosphatidylinositol 3-kinase/phosphorylated AKT Protein (PI3K /p-AKT) signaling pathways. Observation indicators: (1) expression of LncRNA KCNQ1OT1 in HCC tissues and normal liver tissues; (2) the migration of HepG2, SMCC-7721 and MHCC-97H HCC cells after LncRNA KCNQ1OT1 gene knockdown; (3) the proliferation and invasion of HepG2, SMCC-7721 and MHCC-97H HCC cells after LncRNA KCNQ1OT1 gene knockdown; (4) effects of LncRNA KCNQ1OT1 gene knockdown on PI3K/p-AKT signaling pathways. Measurement data with normal distribution were expressed as Mean± SD, and comparison between groups was analyzed using the t test. The Kaplan-Meier method was used to calculate survival rates and draw survival curves. Results:(1) Expression of LncRNA KCNQ1OT1 in HCC tissues and normal liver tissues. The expression levels of LncRNA KCNQ1OT1 in 374 HCC tissues and 50 normal liver tissues from StarBase database were 3.320±0.017 and 1.470±0.025, respectively, showing a significant difference ( t=5.24, P<0.05). Results of gene expression profile interactive analysis showed that the 30-month disease-free survival rates of HCC patients with high and low expression levels of LncRNA KCNQ1OT1 were 41% and 55%, respectively, with a significant difference ( χ2=6.209, P<0.05). The relative expression of LncRNA KCNQ1OT1 in HepG2, SMCC-7721and MHCC-97H cells were 1.470±0.042, 3.300±0.032, 4.040±0.031, respectively, versus 1.000±0.022 in normal liver cells (LO2), showing significant differences ( t=17.66, 95.40, 114.20, P<0.05). (2) The migration of HepG2, SMCC-7721 and MHCC-97H HCC cells after LncRNA KCNQ1OT1 gene knockdown. ① Results of cell transfection showed that the relative expression levels of LncRNA KCNQ1OT1 in HepG2, SMCC-7721 and MHCC-97H cells after LncRNA KCNQ1OT1 gene knockdown were 0.350±0.016, 0.310±0.020, 0.380±0.018, respectively, versus 1.000±0.021, 1.000±0.018, 1.000±0.019 in the negative control cells, showing significant differences ( t=23.40, 28.15, 22.32, P<0.05). ② Results of scratch assay showed that the healing rates of HepG2, SMCC-7721, MHCC-97H cells after LncRNA KCNQ1OT1 gene knockdown were 85.0%±1.9%, 75.0%±1.8%, 90.0%±1.7%, respectively, versus 100.0%±2.0%, 95.0%±1.8%, 72.0%±1.7% of the negative control cells, showing significant differences ( t=31.35, 47.36, 38.42, P<0.05). ③ Results of Transwell assay showed that the vertical migration rates of HepG2, SMCC-7721, MHCC-97H cells after LncRNA KCNQ1OT1 gene knockdown were 195±10, 205±12, 85±8, respectively, versus 520±11, 430±7, 405±20 of the negative control cells, showing significant differences between them ( t=922.30, 458.20, 708.40, P<0.05). (3) The proliferation and invasion of HepG2, SMCC-7721 and MHCC-97H HCC cells after LncRNA KCNQ1OT1 gene knockdown. ① Results of CCK8 assay showed that 72-hour optical densities of HepG2, SMCC-7721, MHCC-97H cells after LncRNA KCNQ1OT1 gene knockdown were 1.370±0.018, 1.240±0.016, 1.360±0.020, respectively, versus 0.900±0.023, 1.740±0.032, 1.230±0.025 of the negative control cells, with significant differences ( t=10.79, 12.00, 7.56, P<0.05). ② Results of Transwell assay showed that the invasion numbers of HepG2, SMCC-7721, MHCC-97H cells after LncRNA KCNQ1OT1 gene knockdown were 186±12, 155±7, 75±9, respectively, versus 505±1, 245±8, 300±15 of the negative control cells, showing significant differences ( t=955.90, 163.40, 530.90, P<0.05). (4) Effects of LncRNA KCNQ1OT1 gene knockdown on PI3K/p-AKT signaling pathways. Resluts of Western blot showed that the relative repression levels of PI3K in HepG2, SMCC-7721, MHCC-97H cells after LncRNA KCNQ1OT1 gene knockdown were 0.447±0.009, 0.430±0.012, 0.354±0.006, respectively, versus 0.820±0.017, 0.850±0.012, 0.531±0.001 of the negative control cells, showing significant differences ( t=18.94, 25.72, 27.46, P<0.05). The relative repression levels of p-AKT in HepG2, SMCC-7721, MHCC-97H cells after LncRNA KCNQ1OT1 gene knockdown were 0.343±0.015, 0.410±0.012, 0.579±0.006, respectively, versus 0.546±0.012, 0.620±0.012, 0.830±0.012 of the negative control cells, showing significant differences ( t=10.78, 12.86, 19.02, P<0.05). Conclusions:LncRNA KCNQ1OT1 plays an important role in the occurrence and development of HCC. LncRNA KCNQ1OT1 gene knockdown can inhibit the PI3K/AKT signaling pathways, so it can significantly inhibit the proliferation, migration and invasion of HCC cells.

OBJECTIVEThe purpose of this study was to investigate the blood lead level of 3 - 5 year old children living in the cities in China and to provide scientific data for making policy on environmental lead pollution for children health protection.

METHODSSix thousand five hundred and two vein blood samples from 3 - 5 year old children in nineteen cities of nine provinces were sampled. Inductively coupled plasma-mass spectrometry (ICP-MS) were employed to determine lead level in whole blood after microwave digestion for sample preparation and questionnaire survey was also performed. Data were analyzed with multiple regression on factors which affecting blood lead levels.

RESULTSResults showed that mean blood lead level was 88.3 micro g/L for 3 - 5 year old children living in the cities in China and mean blood lead level of boys (91.1 micro g/L) was higher than that of girls (87.3 micro g/L). Twenty-nine point nine one per cent of the children's blood lead level exceeded 100 micro g/L. The research finding showed: (1) higher blood lead levels had negative effects on children's physical growth, language ability etc. (2) behavior of parents had certain effects on children's blood lead levels. (3) blood lead levels of children were affected by unhealthy habits.

CONCLUSIONSProblem of childhood lead poisoning in China has become more serious. During the past ten years, blood lead levels of children has been increased in China while decreasing in developed countries. Blood lead levels of children in China are higher than that of developed countries, which called for special concern by government and society.

Child, Preschool ; China ; Environmental Pollutants ; blood ; Female ; Humans ; Lead ; blood ; Male ; Mass Spectrometry ; Sex Factors ; Urban Health ; Urban Population

Genetics ; Laboratories ; Technology ; standards ; United States