Abdominal Neoplasms ; complications ; metabolism ; pathology ; surgery ; Adult ; Dendritic Cell Sarcoma, Follicular ; complications ; metabolism ; pathology ; surgery ; Diagnosis, Differential ; Female ; Humans ; Ki-1 Antigen ; metabolism ; Leukocytosis ; complications ; metabolism ; pathology ; surgery ; Receptors, Complement 3b ; metabolism ; Receptors, Complement 3d ; metabolism ; Young Adult

OBJECTIVETo investigate the effects of asymmetric dimethylarginine (ADMA) on ACAT-1 expression and cholesterol content in THP-1-derived macrophages and foam cells.

METHODSTHP-1 cells were induced to differentiate into macrophages and further into foam cells. The macrophages and foam cells were exposed to different concentrations (0, 3.75, 7.5, 15, and 30 µmol/L) of ADMA for varying time lengths (6, 12, and 24 h), and the changes in ACAT-1 mRNA and protein levels in the cells were measured with RT-PCR and Western blotting. The cellular cholesterol content was measured with enzyme-linked colorimetry assay.

RESULTSIn THP-1-derived macrophages and foam cells, the expression levels of ACAT-1 mRNA and protein and cellular cholesterol content increased significantly in response to ADMA treatment in a time- and concentration-dependent manner.

CONCLUSIONADMA may play an important role in inducing foam cell formation from macrophages. ACAT-1 inhibition targeting the macrophages and foam cells may serve as a potential therapeutic target in the treatment of atherosclerosis.

Acetyl-CoA C-Acetyltransferase ; metabolism ; Arginine ; analogs & derivatives ; pharmacology ; Cell Line ; Cholesterol ; analysis ; Foam Cells ; cytology ; metabolism ; Humans ; Macrophages ; cytology ; drug effects ; metabolism ; Monocytes ; cytology ; drug effects ; RNA, Messenger ; genetics ; Up-Regulation

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

In this paper, the five strains of Polygonatum odoratum were used as the experimental materials to test the supercooling point, freezing point, the degree of supercooling, the transition stage time, cooling time and water composition of the plant tissue. The cold resistance of P. odoratum was analyzed with the Gray Correlation Method. The results showed that the cold resistances of the five strains of P. odoratum were different, and the water content of plant tissue had some relevance with freezing point and supercooling point, whereas, it could not be measured when the moisture content was too low. The order of cold resistance of the five strains of P. odoratum was ZJCY, DYYZ, XYYZ, CYYZ and JZ I.
Cold Temperature ; Plant Roots ; chemistry ; physiology ; Polygonatum ; chemistry ; classification ; physiology ; Water ; analysis

OBJECTIVETo develop a screening system for more rapid and sensitive mutation detection of autosomal dominant polycystic kidney disease (ADPKD) gene 1 (PKD1) by using denaturing high-performance liquid chromatography (DHPLC) protocol.

METHODSUsing genomic DNA as templates extracted from blood samples of 19 Han pedigrees with 67 family members, the complete codon areas were amplified by long-range PCR and nested PCR in succession, and then the PCR products were analyzed by DHPLC. The mutations from screened abnormal PCR products were confirmed by DNA sequencing, and then compared with the mutations identified by single strand conformation polymorphism (SSCP) before.

RESULTSThere were 14 mutations found in this study, including 10 missense, 1 insertion, 1 deletion and 2 nonsense mutations. Besides 12 mutations identified before, mutations nt32819G>A and nt37137T>C were the novel mutations found. The mutation detection ratio was 73.7%.

CONCLUSIONThis developed system via DHPLC can be used as a more effective approach for mutation detection of autosomal dominant polycystic kidney disease PKD1 in Hans.

Adult ; Asian Continental Ancestry Group ; genetics ; Base Sequence ; China ; Chromatography, High Pressure Liquid ; methods ; DNA Mutational Analysis ; Family Health ; Female ; Humans ; Male ; Middle Aged ; Mutation ; Pedigree ; Polycystic Kidney, Autosomal Dominant ; diagnosis ; ethnology ; genetics ; Polymerase Chain Reaction ; Polymorphism, Single-Stranded Conformational ; TRPP Cation Channels ; genetics

The mechanism of apoptosis induced by SIRT1 deacetylase inhibitors in both human breast cancer MCF-7 and MCF-7 doxorubicin-resistant cells was studied. MTT assay was used to detect growth-inhibitory effect on the cells. Protein expression was detected by Western blotting. Chromatin condensation was detected by a fluorescent microscope after Hoechst 33342 staining. Cell cycle distribution was analyzed with flow cytometry. Apoptotic cells were detected with Annexin V staining. Nicotinamide (NAM) and Sirtinol, two SIRT1 deacetylase inhibitors, exhibited the similar growth-inhibitory effects on MCF-7/DOX cells and MCF-7 cells, but no potentiation of DOX activities. The arrest at G2/M phase was detected by flow cytometry in both MCF-7 and MCF-7/DOX cells after NAM treatment. Activation of caspase pathway in MCF-7 cells, such as the cleavages of PARP, caspase-6, -7, -9, were observed after exposure to NAM 50 mmol x L(-1), accompanied by the occurrence of chromatin condensation and Annexin V positive cells. However, the cleavages of PARP, caspase-6 and -7 in MCF-7/DOX cells delayed after exposure to NAM for 24 h and obviously increased at 48 h with appearance of chromatin condensation and Annexin V positive cells. SIRT1 deacetylase inhibitors show no cross resistance to MCF-7 drug-resistant cells, and the similar growth-inhibitory actions of them to MCF-7 sensitive and drug-resistant cells by which it is mediated by activation of apoptotic caspase pathway.
Apoptosis ; drug effects ; Benzamides ; pharmacology ; Breast Neoplasms ; metabolism ; pathology ; Caspases ; metabolism ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Doxorubicin ; pharmacology ; Drug Resistance, Multiple ; drug effects ; Drug Resistance, Neoplasm ; drug effects ; Enzyme Inhibitors ; pharmacology ; Female ; Humans ; Naphthols ; pharmacology ; Niacinamide ; pharmacology ; Sirtuin 1 ; antagonists & inhibitors

OBJECTIVETo investigate the effect of ADMA on macrophage migration inhibitory factor (MIF) expression and tumor necrosis factor-α (TNF-α) and IL-8 secretion in THP-1 monocyte-derived macrophages. METHIDS: THP-1 monocytes were induced to differentiate into macrophages by a 24-h incubation with 160 nmol/L PMA. The THP-1 monocyte-derived macrophages were exposed to different concentrations of ADMA for 24 h, and the changes in MIF mRNA and protein expressions were analyzed with RT-PCR and Western blotting, respectively. Enzyme-linked immunosorbent assay was used to detect the levels of TNF-α and IL-8 in the supernatant of THP-1-derived macrophages following ADMA treatments.

RESULTSADMA obviously up-regulated MIF mRNA and protein expressions in THP-1-derived macrophages in a concentration- dependent manner. Exposure of the cells to 15 µmol/L ADMA for 24 h showed the most potent effect in up-regulating MIF mRNA and protein expressions. ADMA treatment also resulted in a dose-dependent increase of the levels of TNF-α and IL-8 in the culture supernatant of the macrophages, and the peak levels occurred following the treatment with 15 µmol/L ADMA.

CONCLUSIONADMA can up-regulate MIF expression and induce TNF-α and IL-8 secretion in THP-1 monocyte-derived macrophages.

Arginine ; analogs & derivatives ; pharmacology ; Cell Differentiation ; Cell Line ; Humans ; Interleukin-8 ; secretion ; Intramolecular Oxidoreductases ; genetics ; metabolism ; Macrophage Migration-Inhibitory Factors ; genetics ; metabolism ; Macrophages ; cytology ; metabolism ; Monocytes ; cytology ; Phenanthrenes ; pharmacology ; RNA, Messenger ; genetics ; metabolism ; Tumor Necrosis Factor-alpha ; secretion

OBJECTIVETo investigate the effect of mitochondrial permeability transition pore inhibitor cyclosporine A (CsA) on lipopolysaccharide (LPS)-induced acute lung injury in mice.

METHODSAll male ICR mice were randomly divided into five groups (n = 24): control group, LPS group, dexamethasone group, cyclosporine A(CsA) group and CsA + atractyloside(Atr) group. Six hours after treatment with LPS, the activity of lactate dehydrogenlase (LDH) in bronchoalveolar lavage fluid (BALF) and level of tumor necrosis factor-alpha (TNF-alpha) in lung tissue were detected. The lung wet weight/dry weight ratio and the pulmonary capillary permeability index were also detected.

RESULTSIn contrast to LPS group, the mitochondrial permeability transition pore inhibitor CsA induced a decrease in LDH activity in the BALF and TNF-alpha level in lung tissue, lung wet weight/dry weight ratio and the pulmonary capillary permeability index were declined. Atractyloside, the activator of mitochondrial permeability transition pore, almost abolished the role of CsA on LPS-induced lung injury.

CONCLUSIONThese results suggested that CsA plays the protective effect on LPS-induced lung injury in mice, it is likely through inhibiting the opening of mitochondrial permeability transition pore.

Acute Lung Injury ; chemically induced ; physiopathology ; prevention & control ; Animals ; Cyclosporine ; pharmacology ; L-Lactate Dehydrogenase ; metabolism ; Lipopolysaccharides ; Male ; Mice ; Mice, Inbred ICR ; Mitochondrial Membrane Transport Proteins ; antagonists & inhibitors ; Protective Agents ; pharmacology ; Tumor Necrosis Factor-alpha ; metabolism

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.