Objective To clone, express and purify human PIF1 protein and analyze its ATPase activity. Methods The PIF1 cDNA was amplified by PCR from HeLa cell cDNA library and inserted to pET24b with histidine tag at its terminus to form pET24b-PIF1 plasmid. The recombinant pET24b-PIF1 plasmid was transformed to RosettaTM 2 (DE3) and the expression of PIF1 protein was monitored by SDS-PAGE analysis. By using fast protein liquid chromatograph (FPLC) system, the PIF1 protein was purified by affinity chromatograph and gel filtration. The ATPase activity of PIF1 was checked by thin layer chromatograph(TLC). Results The PIF1 protein was successfully cloned and expressed in E.coli. Conclusions The purification procedure of PIF1 protein was established using FPLC. The overexpressed and the purified PIF1 helicase has DNA and Mg2+ dependent ATPase activity.

BACKGROUND:Ankylosing spondylitis is an autoimmune disease involved in chronic systemic inflammation. Tumor necrosis factor and interleukin-6 levels increased in patients with ankylosing spondylitis. Inflammatory factors such as tumor necrosis factor and interleukin-6 can suppress CD36 expression in monocytes. OBJECTIVE: To analyze the correlation between CD36 expression in monocytes and ankylosing spondylitis. METHODS:A total of 84 newly diagnosed ankylosing spondylitis patients and 111 healthy individuals were included in this study. CD36 expressions in monocytes in ankylosing spondylitis patients and healthy individuals were tested using flow cytometer; meanwhile, biochemistry, immunology, routine blood examination and related inflammatory markers were determined between the two groups. RESULTS AND CONCLUSION:Results of baseline data in both groups demonstrated that CD36 fluorescence intensity in monocytes was significantly lower in patients with ankylosing spondylitis compared with healthy controls (P < 0.01). CD36 fluorescence intensity in monocytes was negatively correlated with C-reactive protein, erythrocyte sedimentation, interleukin-6 and tumor necrosis factor. In addition, CD36 fluorescence intensity in monocytes was negatively correlated with BASDAI score. Logistic regression analysis showed that erythrocyte sedimentation, interleukin-6, tumor necrosis factor and CD36 fluorescence intensity in monocytes were associated with ankylosing spondylitis, and risk factors for ankylosing spondylitis (P < 0.05). These findings confirm that inflammatory cytokine in patients with ankylosing spondylitis weakened the expression of CD36 in monocytes. There was a remarkable association between low expression of CD36 expression in monocytes and ankylosing spondylitis. CD36 expression of monocytes clinicaly may be considered to be an effective indicator to evaluate inflammation and disease activity in patients with ankylosing spondylitis.

Aim To explore the role of nicotinamide adenine dinucleotide phosphate ( NADPH ) oxidase in high glucose-induced injury in H9c2 cardiac cells. Methods H9 c2 cardiac cells were exposed to differ-ent concentrations of high glucose(5. 5 mmol·L-1 ,11 mmol · L-1 ,22 mmol · L-1 ,33 mmol · L-1 ,44 mmol ·L-1 , 55 mmol · L-1 ) for 24 h and different time pints of high glucose(0 h,12 h,24 h,36 h,48 h,72 h) . Cell viability was measured by MTT colorimetry, the protein expression of Bcl-2 , Bax and NADPH oxi-dase submits such as p22 phox , p47 phox and p67 phox were determined by western blotting. Results H9c2 cardi-ac cells exposure to high glucose for 24 h showed on decrease in cell survival and the Bcl-2 expression while an increase in the Bax expression ( P<0. 05 ) . Moreo-ver, high glucose could markedly up-regulate the activ-ity of NADPH oxidase characterized by the enhanced expression of p22 phox , p47 phox and p67 phox ( P<0. 05 ) . Conclusion Activating NADPH oxidase may play an important role in high glucose-induced injury in H9 c2 cells.

Adult ; Female ; Humans ; Intestinal Neoplasms ; Male ; Middle Aged ; Sarcoma, Myeloid

A L-histidine producing mutant was derived from Corynebacterium glutamicum HZ4221(TRA R DCP R AMT R histidase - )by means of mutagenesis with N-methy-N′-nitro- N-nitrosoguanidine(NTG).Contrast to original strain,the amount of histidine accumulation reached to a level of 5.31g/L in a medium containing 80g/Lglucose and 30g/L ammonium sulfate after cultured for 72 hours; the transketolase activity reduced to a degree of 15.7%.The utilization of the carbon sources,genetic stability,effect of metal ions were also been investigated in this paper.

In this paper, metabolic networks of the Corynebacterium glutamicum GWY020 and the two de-rivatives carrying additional mutations HUI821and GUI089 were established and modified. The concentra-tions of extra-cellular metabolites were determined under sub-steady-state (50 h~52 h) of the batch culture. The metabolic flux distribution maps of the three strains were obtained, compared and analyzed. These re-sults indicate that the introduction of analog supersensitive marker or analog resistant marker skew the metabolic flux towards the formation of L-Arginine. This study revealed the usefulness of the metabolic flux analysis as a tool for verification of existing production strains. The analysis may play an important role in helping us to rationally re-design metabolism for further improvement of fermentation process.

Objective Analysis of the etiological factors and the diagnostic methods of fever of unknown origin(FUO)in order to avoid misdiagnosis and missed diagnosis.Methods One hundred and twenty-eight patients with FUO were collected from our hospital.Results A final diagnosis was established in 118(92.2%)patients by using serological methods,bacteriological methods,body fluid test,bone marrow examination,tissue biopsy and diagnositic therapy.Infection(62.5%),connective tissue diseases(16.1%),malignancies(11.0%)were found to be the common causes of the fever in these patients while infection was the main cause of FUO in our research.The major pathogens responsible for the infec tion was bacteria,followed by virus and tuberculosis.Adult Still's disease was the most common connective tissue diseases in these patients.Lymphoma,malignant histocytosis and leukemia were the main forms of malignancy.Conclusion Infectious diseases was the most common cause of FUO while connective tissue disease and malignant tumors are also important in the pathogenesis of FUO.

Epidemiological surveys show that folic acid can prevent prostate cancer, but fortified folic acid may increase the risk of the malignancy. The physician data queries from the National Cancer Institute of the USA describe folate as protective against prostate cancer, whereas its synthetic analog, folic acid, is considered to increase prostate cancer risk when taken at levels easily achievable by eating fortified food or taking over-the-counter supplements. We review the current literature to examine the effects of folate and folic acid on prostate cancer, help interpret previous epidemiologic data, and provide a clarification regarding the apparently opposing roles of folate for patients with prostate cancer. A literature search was conducted in Medline to identify studies investigating the effect of nutrition and specifically folate and folic acid on prostate carcinogenesis and progression. In addition, the National Health and Nutrition Examination Survey database was analyzed for the trends in serum folate levels before and after mandatory fortification. Folate likely plays a dual role in prostate carcinogenesis. There remains some conflicting epidemiologic evidence regarding folate and prostate cancer risk. However, there is growing experimental evidence that higher circulating folate levels can contribute to prostate cancer progression. Further research is needed to clarify these complex relationships.
Dietary Supplements ; adverse effects ; Disease Progression ; Folic Acid ; analogs & derivatives ; blood ; pharmacology ; Food, Fortified ; Humans ; Male ; Nutrition Surveys ; Nutritional Status ; Prostatic Neoplasms ; blood ; chemically induced

Animals ; Apoptosis ; physiology ; Carcinoma, Squamous Cell ; drug therapy ; physiopathology ; prevention & control ; Cyclooxygenase 2 ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors ; therapeutic use ; Head and Neck Neoplasms ; drug therapy ; physiopathology ; prevention & control ; Humans ; Membrane Proteins ; Neoplasm Invasiveness ; Neoplasm Metastasis ; drug therapy ; Neovascularization, Pathologic ; drug therapy ; metabolism ; Prostaglandin-Endoperoxide Synthases ; metabolism