Objective To investigate the disease situation of adult carotid atherosclerosis in water-related endemic fluorosis areas in Heilongjiang province in 2008 so as to explore the relationship between water-related endemic fluorosis and incidence of carotid atherosclerosis disease. Methods A total of 266 participants over the age of 40 from four villages in Zhaozhou county with water fluoride ≥ 1.0 mg/L in a fluorosis area and 283 residents over the age of 40 from four villages in Tailai county with water fluoride ＜ 1.0 mg/L in a nonfluorosis area were investigated. A portable-type B mode color ultrasound was used to examine the left carotid artery of all participants.The carotid atherosclerosis was diagnosed and graded through the ultrasonograms. Results The prevalence rates of carotid atherosclerosis in the 4 fluorosis villages(Xinfeng, Taipingshan, Baochan and Houzheng villages) were 47.3% (35/74), 63.5%(40/63), 73.3%(33/45) and 60.7%(51/84), respectively, and in the 4 nonfluorosis villages(Hala,Qianxing, Sanjia and Ailin villages) were 32.7% (17/52), 32.9% (24/73), 39.2% (31/79) and 30.4% (24/79),respectively. The prevalence rates of carotid atherosclerosis in every villages standardized by age were 47.3% ,63.5%,73.3% ,60.7% and 34.7% ,36.3% ,43.0% ,41.3%, respectively. Statistic method used was Wilcoxon two sample test and the differences were significant(T = 26, P ＜ 0.05 ). Total carotid atherosclerosis positive rate standardized by age in the 4 fluorosis villages was significantly higher than that in the 4 nonfluorosis villages[57.5%(153/266) ,37.8% (107/283), x2 = 21.36, P ＜ 0.01 ]. After standardized by age, the severity of carotid atherosclerosis was significantly different between fluorosis villages and nonfluorosis villages (x2 = 36.15, P ＜ 0.01 ). Conclusion The prevalence rate of carotid atherosclerosis in endemic fluorosis area is higher than that in nonfluorosis area.

OBJECTIVETo explore the role of sTRAIL in the pathogenesis of HBV infection in human being.

METHODSsTRAIL in 153 patients' sera was examined with ELISA. Correlations between sTRAIL and liver functional parameters were analysed.

RESULTSThe levels of sTRAIL in patients with various clinical types of hepatitis B as well as primary hepatocellular carcinoma were all higher than that in normal persons and became almost normal in recovering stage cases. In acute and chronic HBV infection, sTRAIL level was negatively correlated with ALT, AST and total bilirubin levels, and positively correlated with serum albumin.

CONCLUSIONThe results indicated that higher level of sTRAIL expression is correlated with liver damage, and apoptosis induced by sTRAIL is one of the mechanisms of liver damage in HBV infection.

Adolescent ; Adult ; Aged ; Alanine Transaminase ; blood ; Aspartate Aminotransferases ; blood ; Enzyme-Linked Immunosorbent Assay ; Female ; Hepatitis B ; blood ; Hepatitis B, Chronic ; blood ; Humans ; Liver Cirrhosis ; blood ; virology ; Liver Neoplasms ; blood ; virology ; Male ; Middle Aged ; Serum Albumin ; analysis ; TNF-Related Apoptosis-Inducing Ligand ; blood ; Young Adult

Objective To investigate the relationship between drinking-water type of endemic arsenicosis and adult carotid artery atherosclerosis. Methods In 2009, 285 participants aged over 40 from drinking-water type of endemic arsenism areas and 293 residents aged over 40 from control areas were investigated in Yingxian county,Shanxi province. Portable-type B mode color ultrasound was used to examine the carotid artery of all participants.The carotid atherosclerosis were diagnosed and graded through the ultrasonograms. Content of water arsenic and hair arsenic of 10 people randomly selected in every villages were detected. Results A total of 5 villages with drinkingwater type of endemic arsenicosis as observation group and 5 villages without drinking-water type of endemic arsenicosis as control group were investigated. The prevalence rates of adult carotid atherosclerosis within observation group were 35.09%(20/57), 55.74%(34/61), 38.46%(20/52), 36.51%(23/63) and 46.15%(24/52), respectively,and standardized prevalence rates were 32.5%, 33.8%, 34.9%, 46.2% and 47.3%, respectively and the prevalence rates of adult carotid atherosclerosis within control group were 18.18%(10/55), 30.77%(16/52), 20.00%(10/50),18.67% (14/75) and 21.31% ( 13/61 ), respectively; the standardize prevalence rates were 22.4%, 17.7%, 10.7%,24.6%, 18.9%, respectively. The standardize prevalence rates were higher in observation group [39.50%(113/285) ]than that in control group[39.50%(113/285), T = 26, P ＜ 0.01 ]. The severity of adult carotid atherosclerosis (composition of 4 - 7 scores ) was compared between observation group [ 17.70%(20/113 )] and control group [ 14.06% (9/64) ], and the difference was insignificant(x2 = 0.26, P ＞ 0.05). Conclusions The prevalence rate of carotid atherosclerosis in drinking-water type of endemic arsenicosis areas is higher than that of the control areas.The study provides evidence that arsenic poisoning can cause atherosclerosis.

OBJECTIVETo investigate the proliferation of tissue-engineered cartilage cells stimulated by different intensities of compressive stress.

METHODSHuman embryonic cartilage cells were seeded into type II collagen sponge scaffold. The cells of the pressure groups were stimulated by different compression rate (0-5%, 0-10%, and 0-20%) at a cyclical frequency of 0.1 Hz. The cells of the control group were cultured without pressure. Gross observation, histological section, MTT assay and flow cytometry were used to observe the morphology, cell number and distribution and detect the cell proliferation and cell cycle.

RESULTSTissue-engineered cartilage cells in 0-10% group showed the largest size and greatest thickness with normal morphology. Tissue biopsies showed the largest number of cartilage cells with more uniform distribution, close alignment, more matrix secretion. The cartilage cell activity was significantly enhanced and the percentage of S phase cells significantly increased in the pressure group compared with those in the control group, and such changes were especially obvious in 0-10% group in which the S phase cells increased by 59.0% compared with that in the control group.

CONCLUSIONThe proliferation of tissue-engineered cartilage cells is regulated by the cyclic stress intensity, and a pressure frequency of 0.1 Hz with compression rate of 0-10% can better promote the cell proliferation.

Cell Proliferation ; Cells, Cultured ; Chondrocytes ; cytology ; Humans ; Stress, Mechanical ; Tissue Engineering ; Tissue Scaffolds

AIMTo investigate the synergetic effect and the mechanism of antitumor action of the antibiotic lidamycin in combination with cisplatin in vitro.

METHODSCytotoxicity of the drugs was measured by clonogenic assay. Chromatin condensation was observed by co-staining with fluorescent dyes, Hoechst 33342 and propidium iodide. Apoptotic sub-G1 was detected by flow cytometry and DNA ladder was observed using agarose gel electrophoresis. Bcl-2 protein level was detected by Western blot assay.

RESULTSBy using clonogenic assay, lidamycin in combination with cisplatin was found to have synergetic effects on the proliferation of human hepatoma BEL-7402 cells. The data showed that BEL-7402 cells treated with cisplatin and lidamycin in combination produced internucleosomal DNA fragmentation analysed by agarose gel electrophoresis. The results of flow cytometry showed that cisplatin and lidamycin administrated in combination showed no obvious change in G1 phase distribution compared with single treatment. However, this combination reduced the S phase arrest and reversed the reduction of G2/M phase induced by single treatment. The results also showed that there was 11.3% or 9.37% of cells undergoing apoptosis in BEL-7402 cells treated with cisplatin or lidamycin, respectively, while it showed 32.4% of apoptotic cells in combination treatment. Cisplatin, lidamycin and combination of cisplatin and lidamycin was shown to induce typical chromatin condensation in BEL-7402 cells. The study showed that 0.5 mumol.L-1 cisplatin or 1 x 10(-4) mumol.L-1 lidamycin alone decreased Bcl-2 protein level, while lidamycin in combination with cisplatin strongly inhibited expression of Bcl-2 proteins in BEL-7402 cells.

CONCLUSIONThe results suggest that lidamycin enhancement of cisplatin-induced apoptosis associates with decrease of Bcl-2 protein expression, which may be useful for cancer chemotherapy.

Aminoglycosides ; pharmacology ; Antibiotics, Antineoplastic ; pharmacology ; Antineoplastic Agents ; pharmacology ; Apoptosis ; Carcinoma, Hepatocellular ; pathology ; Cisplatin ; pharmacology ; Drug Synergism ; Enediynes ; Humans ; Liver Neoplasms ; metabolism ; pathology ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; S Phase ; drug effects ; Tumor Cells, Cultured

Hepatitis ; immunology ; Humans ; Liver Cirrhosis ; immunology ; Receptors, Complement ; blood

OBJECTIVETo investigate the effect of leptin on collagen systhesis in wounded rats.

METHODSThirty male Wistar rats, weight (180 +/- 20)g, were randomly divided into three groups (n = 10) by weight: normal depilation group, wound control group and leptin treatment group and ten rats were included in each group. A full-thickness defect measuring 2 x 2.5 cm was made in the back of rats in wound control group and leptin treatment group. Each wound in rats of leptin treatment group was applied topically with 0.1 ml leptin solution (2.0 microg leptin), daily for 7 days and that of wound control group with equivalent saline solution. All rats were killed and then granulation tissues samples and skin were collected to examine the synthesis of collagen.

RESULTSHydroxyproline content in granulation tissues of in leptin treatment group (33.92 +/- 3.09) mg/g were significantly increased than those in control group (29.55 +/- 3.59 mg/g, P < 0.05). The mRNA expressions of collagen I and III were significantly enhanced in leptin treatment group (0.96 +/- 0.09, 0.09 +/- 0.06) than those in control group (0.80 +/- 0.03, 0.08 +/- 0.03). The levels of type I and III collagen were significantly increased in leptin treatment group than those in control group.

CONCLUSIONLeptin applied topically can accelerate wound healing through enhancing gene expression of type I and III collagen and synthesis of collagen in wound tissue.

Administration, Cutaneous ; Animals ; Collagen Type I ; genetics ; metabolism ; Collagen Type III ; genetics ; metabolism ; Leptin ; administration & dosage ; therapeutic use ; Male ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Wistar ; Wound Healing ; drug effects ; Wounds and Injuries ; drug therapy

Objective To investigate the imaging findings of the lacerating injury of the lung. Methods Ten patients of lung lacerating injury were examined by X-ray and CT within 1—5 h after injury. X-ray(2—5 times)and CT(3—5 times)examinations were repeated for 7 patients.Results The lung lacerating injury involved 10 sides and 14 lung lobes(21 lesions in total)in the 10 cases,among which 1 case involved the right upper lobe with 1 lesion,2 cases in the right lower lobe with 2 lesions,1 case in the right upper and lower lobes with 2 lesions for each lobe,3 cases in the left lower lobe with 9 lesions,and 3 cases in both the left upper and the lower lobes with 7 lesions.The X-ray findings were cavity-like shadows with smooth margin in 9 lesions(9/21),and patchy shadows of fogging margin in 12 lesions(12/21).The CT imaging findings included 6 pulmonary hematomas(6/21),and 15 cavitary lesions with air-fluid levels (15/21).In the 15 cavitary lesions,CT revealed 14 single cavities and 2 small cavities within a big cavity. On dynamic follow-up observation,the cavity was the biggest in 1—5 h after injury,but the hematoma was the biggest in 2—3 days after injury.Hematomas tended to absorb slower than the cavities.After 16— 32 days,all lesions revolved into small patchy or stripe-like shadows with slightly increased density. Conclusion Cavitary lesion with air-fluid level is the characteristic imaging finding of lung lacerating injury.CT surpasses X-ray plain film in revealing the details of lung lacerating injury.

Objective To explore the association between polymorphisms of interferon-gamma gene intron 1 at position+874 (IFN-γ+874) gene and the susceptibility of HBV and/or HCV infection with different clinical outcomes. Methods IFN-γ+874 gene SNP were detected in 277 subjects including 79 chronic HBV/HCV coinfections,69 individuals only with HBV infection,55 individuals only with HCV infection and 74 controls,by sequence specific primers-PCR (SSP-PCR). Hepatocellular injury as suggested by alanine aminotransferase (ALT) was detected by Beckman LX-20. The status of viral particles in serum was determined by RT-nPCR. The possible association of the polymorphism of IFN-γ+874 with the susceptibility of HBV and/or HCV infection and the outcome of these infections were analyzed. Results (1) IFN-γ+874 AA frequency in individuals with chronic HBV,HCV,HBV/HCV coinfections were significant higher than that in controls (X~2=16.15,P=0.01); OR (95% CI) of IFNγ+874 AA in chronic infection with HBV,HCV,HBV/HCV coinfections appeared to be 2.70 (1.24-5.92),3.22 (1.43-7.25) and 4.02 (1.88-8.55) compared with + 874 TA. No significant differences were found among HBV,HCV,HBV/HCV coinfections (X~2=1.97,P=0.73). There were no significant association of IFN-γ +874 A/T allele frequency with HBV and/or with HCV infection (X~2=4.87,P=0.18). (2)The clinical outcomes of mild chronic hepatitis (CH),moderate/severe CH and cirrhosis with HBV and/or HCV infection were associated with IFN-γ+874 AA [X~2＝14.17,P＝0.03;OR＝3.09(1.51-6.33),3.85 (1.70-8.70),3.14 (1.08-9.17)]. No significant relationships were found between IFN-γ+874 A/T allele frequency and the clinical outcome of HBV/HCV infection (X~2＝6.07,P＝0.11). (3)There were no significant associations of IFN-γ+874 genotype/allele frequency with HCV duplication (X~2=2.36,P=0.31). (4) There were no significant associations of IFN-γ+874 genotype/allele frequency with abnormal ALT (X~2=0.15,P=0.93). Conclusion These results suggested that polymorphisms in the IFN-γ +874 had some influence on chronic HCV and/or HBV infection,and on the outcome of HCV and/or HBV infections. IFN-γ+874 AA genotype and T allele were possible risk to chronic HBV and/or HCV infections and to the outcomes of HBV and/or HCV infection. However,IFN-γ+874 TA genotype might serve as possible protective factors to them.

Objective To study the relationship between polymorphisms in interleukin-2gene at position-330 (IL-2-330) and the clinical outcome of hepatitis B virus (HBV) and/or hepatitis C virus (HCV) infection. Methods 277 subjects were recruited including 79 chronic HCV co-HBV infection, 55 chronic HCV infection, 69 chronic HBV infection and 74 controls. Single nucleotide polymorphisms of IL-2-330 was investigated by restricted fragment long polymorphism-PCR (RFLP-PCR). Hepatocellular injury, as revealed by alanine aminotransferase (ALT) was detected by Beckman LX-20 analyzer. The presence of hepatitis C viral particles in serum was determined by RT-nPCR. Results ( 1 ) IL-2-330 polymorphisms showed close association with persistent HBV and/or HCV infection. IL-2-330 TT was associated with an increased risk, but IL-2-330 GG with a reduced risk of persistent HBV and/or HCV infection (χ2=14.24, P=0.03 ) with ORs (95%CI) as 7.14(2.13-23.81 ), 3.46 (1.17-10.02) and 2.93 (1.15-7.46) respectively. However,IL-2-330 TT/GG did not significantly differ between patients with HBV and/or HCV infection (χ2=2.09, P=0.72). IL-2-330 T allele was associated with an increased risk, but the -330G allele was associated with a reduced risk of chronic HBV/HCV infection (χ2=12.33,P=0.01),with ORs (95% CI) as 2.26 (1.39-3.69) , 1.82 ( 1.09-3.03 ) and 1.73 ( 1.10-2.73 ) respectively. (2) IL-2-330polymorphisms showed significant association with the outcome of HBV and HCV infection ( χ2=13.52, P=0.04). IL-2-330 TT was associated with an increased risk, but-330 GG with a reduced risk of mild CH, moderate/severe CH, and cirrhosis. The ORs (95%CI) appeared to be 3.33(1.75-6.32), 3.31 (1.75-6.26), 11.23 (3.09-40.76) respectively. IL-2-330 T allele was associated with an increased risk, but the -330 G allele was associated with a reduced risk of mild CH, moderate/severe CH and cirrhosis (χ2= 12.32, P=0.01 ), with ORs as 1.86(1.32-2.63), 1.71 (1.27-2.31) and 2.77(1.57-4.89) respectively. (3) The polymorphisms of IL-2-330 showed no association with HCV RNA replication (χ2=0.83, P=0.66; χ2=0.20, P=0.66). The polymorphisms of IL-2-330 were not significantly associated with abnormal ALT ( χ2= 1.10, P=0.58; χ2=0.08, P=0.78). Conclusion These results suggested that IL-2-330 TT/T was associated with an increased risk, but IL-2-330GG/G was associated with reduced risk of persistent HBV and/or HCV infection, and with the development of mild CH,moderated/severe CH,and cirrhosis.