0.975). The deviation of medical decision level was within 1.6. Conclusion Comparison among various analyzers were improved after the other analyzers corrected by the one comparable analyzer through the result of the fresh serums determined by it.

Objective To determine the changes of peripheral levels of T helper cell cytokines of patients with chronic hepatitis B (CHB) during antiviral treatment,and to further explore its clinical significance.Methods The plasma levels of interleukin (IL)-2,IL-6,IL-10,interferon (IFN)-γ and tumor necrosis factor(TNF)-α of thirty-three CHB patients during antiviral treatment (entecavir) were measured using enzyme linked immunosorbont assay (ELISA).And their biochemical indicators of liver function were determined.The differences of cytokines levels before and after antiviral treatment were compared using ANOVA.The correlations between the changes of cytokines and alanine transaminase (ALT),hepatitis B virus (HBV) DNA levels were analyzed.Results Levels of IFNγ before and 12,24,48 weeks after treatment were (5.98±2.77),(5.95±3.37),(2.93±2.15) and (9.29±4.65) pg/mL,respectively (F=3.845,P＜0.05),which were positively correlated with ALT levels (r =0.396,P＜0.05).Both TNF-α and IL-10 levels declined after antiviral treatment,which were significantly different at different time points (F=20.156 and 16.695,respectively; both P＜0.05),and both levels of TNF-α and IL-10 were positively correlated with ALT levels (r=0.354and 0.316,respectively; both P＜0.05) and positively correlated with HBV DNA levels (r=0.382and 0.386,respectively; both P＜0.05).While both IL-2 and IL-6 levels were not significantly different between before and after antiviral treatment (F=0.010 and 0.932,respectively; both P＞0.05).The serum levels of ALT and HBV DNA before and after antiviral treatment were all significantly different (F=17.69 and 198.98,respectively; both P＜0.05),which declined gradually during treatment and were positively correlated (r =0.581,P＜0.05).Conclusions IL-10,IFNγand TNF-α may be involved in the pathologic process of CHB,and closely related to the deterioration of the disease.Monitoring plasma levels of these cytokines during antiviral treatment could be useful to understand the immune status and evaluate the efficacy of antiviral drugs.

Objective To observe the effect of the three active ingredients of a Chinese traditional medicine compound named Kang Fu Ling( KFL) against PC12 cells oxidative damage induced by microwave radiation.Methods PC12 cells were differentiated into neuros induced by nerve growth factor ( NGF ) .PC12 cells were incubated for 48 hours after astragalosides,total paeony glycoside and tanshinones were added at different concentrations (1, 3, or 9 μg/ml) .The cells in the control group were cultivated with the only medium of the same volume.Then, cells were irradiated with 30 mW/cm2 microwave for 6 minutes.The morphology of PC12 cells was observed under an inverted microscope soon before and after irradiation and the cell viability was measured by methylthiazolyl tetrazolium ( MTT) colorimetry.Reactive oxygen species ( ROS ) was determined using active oxygen probe 2′, 7′-dichlorodihyarofluolescen diacetde ( DCFH-DA ) while malonyldialdehyde(MDA) was measured in the homogenate of PC12 cells through thiobarbituric acid ( TBA) reactive substance assay.Results The cell morphology of each group showed no obvious difference.6 h after irradiation, the viability of irradiation control group measured by MTT declined apparently(P<0.01)compared with the normal control group.The 3 μg/ml astragalosides treatment group increased the viability of PC12 cells after microwave exposure ( P <0.01).The contents of ROS and MDA were increased after irradiation(P<0.01).However, in the three active ingredients of Kang Fu Ling treatment groups, both ROS and MDA were much lower than in irradiation control group.Conclusion Astragalosides, total paeony glycoside and tanshinones, which are the three active ingredients of Kang Fu Ling, all have protective effect against PC12 cell injury caused by microwave radiation,possibly by scavenging free radicals and reducing oxidative stress injury.

With the deepening of China′s healthcare reform, cost control of medical consumables has become an important means to alleviate the problem of " high medical cost" . Through analysis of the difficulties of medical consumables cost control and mechanism loopholes in such control, the authors proposed a whole-process control practice, in terms of assessment, procurement, use, supervision, assessment and evaluation, and recommend on formulating whole-process cost control measures at both government and hospital levels.

OBJECTIVETo assess the association between single nucleotide polymorphisms (SNPs) of calcium channel β 2 subunit (CACNB2) gene and essential hypertension (EH) in ethnic Han Chinese in Wenzhou area, and to study the influence of rs7069292 alleles on gene expression with luciferase reporter technique.

METHODSSixty hundred and thirty seven Han Chinese with EH and 600 normal controls were enrolled. Genotypes of 6 SNP within CACNB2 gene including rs2228645, rs2357928, rs7069292, rs7099380, rs10764319 and rs11014166 were determined with matrix assisted laser desorption ionization/time of flight mass spectrometer (MALDI-TOF MS). A luciferase reporter gene plasmid containing the fragment flanking rs7069292 (-2831 bp to -2460 bp) in the 5' regulatory region of CACNB2 was constructed.

RESULTSCompared with the control, CT and TT genotypes for the rs7069292 locus were significantly more common in EH group (5.20% vs. 2.17%, 2.59% vs. 1.08%, P< 0.05). CC genotype was not found. Promoter activity for allele C of the rs7069292 locus was significantly increased compared with allele T (P< 0.05). No significant difference was detected for other 5 SNPs in terms of genotypes and allele frequency.

CONCLUSIONThe rs7069292 CT polymorphism of the CACNB2 gene is associated with EH in ethnic Han Chinese from Wenzhou area. A T>C mutation may affect the expression of CACNB2.

Aged ; Alleles ; Base Sequence ; Calcium Channels, L-Type ; genetics ; Case-Control Studies ; Cell Line ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Humans ; Hypertension ; genetics ; Male ; Middle Aged ; Polymorphism, Single Nucleotide

OBJECTIVETo analyze clinical manifestation and genetic mutations in 8 Chinese pedigrees featuring hereditary dysfibrinogenemia.

METHODSProthrombin time(PT), activated partial thromboplastin time(APTT), thrombin time(TT), calibration of plasma protamine sulfate against TT, fibrinogen (Fg) activity, coagulation factors II, V, VII, VIII, IX, X, XI and XII of all probands and their family members were detected with an automatic blood coagulation analyzer; D-dimer(D-D) and fibrin(ogen) degradation products(FDPs) were also dtected by automatic blood coagulation analyzer, Fg antigen were detected with an immunoturbidimetry method. Exons of fibrinogen genes FGA, FGB and FGG and flanking sequences were amplified by polymerase chain reaction(PCR) and sequenced.

RESULTSAll of the probands showed normal levels of FDPs, D-dimer(D-D) and activity of coagulation factor II,V,VII, VIII, IX,X,XI, XII. Plasma PT and APTT were normal or slightly prolonged. Prolonged TT was found in all of the probands, whilst TT was not significantly shortened by protamine sulfate. Fg antigen was within the normal range, but Fg activity was significantly decreased. The Fg antigen/activity ratio was greater than 2. One proband has carried a heterozygous variant of the FGA gene g.1233G>A(p.A α Arg35His). Four have carried a heterozygous mutation of the FGB gene g.9692A>G(p.Bβ Asn190Ser). The remaining 3 had heterozygous substitution of FGG gene g.10819G>A(p.γ Arg301His). In addition, 2 polymorphisms (p.A α Thr331Ala) and p.B β Arg478Lys) were identified in FGA and FGB genes.

CONCLUSIONp.A α Arg35His, p.B β Asn190Ser and p. γ Arg301His are responsible for the inherited dysfibrinogenemia in the 8 Chinese pedigrees. p.B β Asn190Ser is firstly reported in China. p.B β Asn190Ser and p. γ Arg301His may be mutation hot spot in the Chinese population.

Afibrinogenemia ; blood ; genetics ; Fibrin Fibrinogen Degradation Products ; analysis ; Fibrinogen ; analysis ; genetics ; Humans ; Pedigree