BACKGROUND:Cardiopulmonary exercise test plays a significant role in the evaluation of cardiopulmonary function, but it is limited by expensive equipments and professional personnel, and moreover, the subjects need to bear the maximal exercise intensity. As a result, it is extremely urgent to find a submaximal exercise test characterized by simple operation, low cost and easy to be popularized and used. OBJECTIVE:To compare the maximal oxygen uptake in cardiopulmonary exercise test and 6-minute stair climbing and descending test. METHODS:Sixty-seven volunteers were recruited to undergo the cardiopulmonary exercise test using the Bruce protocol, and then, the maximal oxygen uptake was detected. After that, al the participants were subjected to 6-minute stair climbing and descending test, folowed by determination of the maximal oxygen uptake. RESULTS AND CONCLUSION:The maximal oxygen uptake in the cardiopulmonary exercise test was significantly higher than that in the 6-minute stair climbing and descending test (P < 0.01), and there was a highly positive correlation and consistency between the maximal oxygen uptakes in the two tests (r=0.911,P < 0.01). Therefore, 6-minute stair climbing and descending test can be used to detect the maximal oxygen uptake, which may become an effective method for evaluating cardiopulmonary function.

OBJECTIVETo study cellular and humoral immune status on prophase of severe hepatitis B (PSHB).

METHODS56 cases of PSHB patients, 40 cases of chronic hepatitis B (CHB) patients and 20 cases of healthy volunteers were enrolled for detection of CD3+, CD4+, CD8+ and CD3-/CD19+ (B cells) lymphocyte subsets in peripheral blood by flow cytometry. Serum IgG and complement C3 was detected by immunoturbidimetry and analyzed statistically.

RESULTSCompared with CHB group and healthy control group, percentage of lymphocyte subsets CD8+ were significantly lower in PSHB group (P < 0.01 or P < 0.05). While the percentage of lymphocyte subsets CD4+ and ratio of CD4+/CD8+ in PSHB group was obviously higher than those in CHB group (P < 0.+01 or P < 0.05). In addition, There was no significant difference on the percentage of B cell and level of serum IgG between PSHB group and CHB group (P > 0.05, while the level of serum complement C3 in PSHB group were significantly lower than those in CHB group and healthy control group (P < 0.01, P < 0.05).

CONCLUSIONPSHB has a certain degree of cellular immune dysfunction, which characterized by cellular immune function hyperfunction and humoral immune suppression.

Adult ; Antibodies, Viral ; immunology ; Complement C3 ; immunology ; Female ; Flow Cytometry ; Hepatitis B, Chronic ; immunology ; Humans ; Lymphocyte Count ; Male ; Middle Aged ; T-Lymphocyte Subsets ; cytology ; immunology ; Young Adult

The preliminary metabolic profile of total diterpene acid (TDA) isolated from Pseudolarix kaempferi was investigated by using in vivo and in vitro tests. Pseudolaric acid C2 (PC2) was identified as the predominant metabolite in plasma, urine, bile and feces after both oral and intravenous administrations to rats using HPLC-UV and HPLC-ESI/MS(n), and demethoxydeacetoxypseudolaric acid B (DDPB), a metabolite proposed to be the glucoside of PC2 (PC2G), as well as pseudolaric acid C (PC), pseudolaric acid A (PA), pseudolaric acid A O-beta-D glucopyranoside (PAG), pseudolaric acid B O-beta-D glucopyranoside (PBG) and deacetylpseudolaric acid A (DPA) originated from TDA could also be detected. It was demonstrated by tests that the metabolism of TDA is independent of intestinal microflora, and neither of pepsin and trypsin is in charge of metabolism of TDA, TDA is also stable in both pH environments of gastric tract and intestinal tract. The metabolites of TDA in whole blood in vitro incubation were found to be PC2, DDPB and PC2G, which demonstrated that the metabolic reaction of TDA in vivo is mainly occurred in blood and contributed to be the hydrolysis of plasma esterase to ester bond, as well as the glucosylation reaction. These results clarified the metabolic pathway of TDA for the first time, which is of great significance to the in vivo active form and acting mechanism research of P. kaempferi.

The metabolic profile of pseudolaric acid B (PB) was investigated by using in vivo and in vitro tests. Pseudolaric acid C2 (PC2) was identified as the specific metabolite of PB in plasma, urine, bile and feces using HPLC and HPLC-ESI/MS(n) after both oral and intravenous administration to rats, and almost no prototype was detected in all kinds of samples. The metabolic behaviors of PB orally administered in rats treated with antibiotics to eliminate intestinal microflora were identical with those in untreated rats, demonstrating that the metabolism of PB is independent of intestinal microflora. PB was stable in 48 h respective incubation with artificial gastric juice and artificial intestinal juice, suggesting that neither pepsin nor trypsin is in charge of metabolism of PB, and also demonstrating that PB is stable in both pH environments of gastric tract and intestinal tract. In vitro research on metabolism of PB in rat liver microsomes incubation revealed that little PB was metabolized and that the proposed metabolites were the demethoxy and demethoxydecarboxy products of the prototype. The amount of metabolites was extremely low compared with the prototype, indicating that liver microsomes are not responsible for the metabolism of PB either. PB was gradually metabolized into PC2 during 1 h in whole blood incubation in vitro, and the metabolic process showed dynamically dependent manner with incubation time. Once absorbed into blood, PB was quickly metabolized into PC2, accordingly, little prototype was detected in all kinds of samples. The metabolism was attributed to the rapid hydrolysis of C-19 ester bond by plasma esterase. These results clarified the metabolic pathway of PB for the first time, which was of great significance to identify the in vivo active form and interpret acting mechanism of the active compounds of P. kaempferi.

Objective To investigate the effects of recombinant human augmenter of liver regeneration (rhALR) on renal inflammation in acute kidney injury (AKI) induced by renal ischemia reperfusion (IR). Methods SD rats were randomly divided into sham-operated group,IR group,rhALR1 group (100 μg/kg) and rhALR2 group (200 μg/kg).Both renal pedicles of rats were identified and occluded with microvascular clamps for 60 min to induce acute kidney injury (AKI).Blood urea nitrogen and serum creatinine levels were evaluated using a Hitachi 747 automatic analyzer. For histological examination, sections were stained with HE. The activity of myeloperoxidase (MPO) was detected by spectrophotometer.Expression of TNF-α,ICAM-1,MCP-1 was determined by Western blotting. Results Blood urea nitrogen,serum creatinine levels and the injury of kidney were improved significantly in rhALR group as compared with IR group (all P＜ 0.05).They were improved more significantly in rhALR2 group as compared to in rhALR1 group (all P＜0.05).The protein levels of TNF-α,ICAM-1,MCP-1 and the activity of MPO in kidneys from the sham-operated rats were low,and increased significantly after renal ischemia reperfusion injury (all P＜0.05).After treated with rhALR,the expression of TNF-α,ICAM-1,MCP-1 and the activity of MPO were decreased significantly in kidneys as compared to those in IR group (all P＜0.05),which decreased more significantly in rhALR2 group than those in rhALR1 group (all P＜ 0.05). Conclusions nhALR can protect kidneys from ischemia reperfusion injury in rats.The mechanism may be associated with the inhibition of renal inflammatory cells infiltration and down-regulated expressions of YNF-α,ICAM-1 and MCP-1 in the kidney.

Kazakh of Xinjiang is the region with a high incidence of esophageal cancer,genetic research is quite active in recent years.Through the research on biological activity of P53,RB gene during esophageal cancer process.We tried to find potential differences in the national heredity susceptibility and so to support treatment and the research.

ObjectiveTostudytheinhibitioneffectof c-mycASODN(antisense oligodeoxynucleotide) and 5-FU (5-fluorouracil) on the expression of c-myc gene and the proliferation of human hepatomacellsHEPG-2. MethodsAfter treatedbyliposomemediatedc-mycantisense phosphorothioate oligodeoxynucleotide (APSODN) and 5-FU, the growth inhibition rate was detected by MTT assay, the expression of c-myc mRNA was detected by RT-PCR and immunohistocehemical methods HEPG-2cells. The cell cycle was analyzed by flow cytometric analysis. The morphological changes were observed by fluorescence staining and cellular genome electrophoresis. ResultsAfter sealing c-myc gene with ASODN,the growth of cells was repressed and the effect was time-dependent and dose-dependent ( P = 0. 02 ). The ability of proliferation decreased, the expression of c-myc gene was inhibited on transcription and translation levels; 5-FU can induce apoptosis of hepatoma cells HEPG-2 dramatically with the dose of 10 μ mol/L, when treated by both c-myc ASODN and 5-FU, HEPG-2 cells was induced apoptosis in a cooperative style ( P =0. 01 ).ConclusionsThe liposome mediated c-myc (APSODN) and 5-FU can inhibit the proliferation of HEPG-2 cells by inhibiting the expression of c-myc gene and can induce apoptosis of hepatoma cells HEPG-2 in a cooperative style. c-myc ( APSODN ) can increase the sensitivity of 5-FU to hepatoma cells and decrease the effective concentration of 5-FU.

Objective To observe the clinical effect of modified Zhisou powder and Symbicort Turbuhaler simultaneously on patients with Cough Variant Asthma. Methods 120 patients with Cough Variant Asthma were randomly recurited into two groups. 60 patients in the treatment group were treated with modified Zhisou powder and Symbicort Turbuhaler; 60 patients in the control group were treated with Symbicort Turbuhaler. 4 weeks was a therapeutic course in both group. Results The markedly controlled rate (MCR) (clinical control+excenence)of the treatment group was 83.3%, obviously surpassed the control group (70.0%) (P＜0.05); There was obvious improvement of cough, expectoration, breath lessness and throaty pruritus after the therapy in both groups, but it was much better in the treatment group than the control group(P＜0.05). The pulmonary function was significantly improved after treatment in both groups(FEV1, FEV1% and PEF, P＜0.05). The improvement showed significant difference between the two groups(P＜0.05). There was obvious decrease of EOS, IL-5 and ECP in both groups. The decrease of ECP and IL-5 in the treatment group was greater than the control group(P＜0.01). Conclusion The therapy of modified Zhisou powder and Symbicort Turbuhaler has advantage over pure western therapy.

Objective: To study the possible role and way of ALR in the immune regulation in vitro. Methods: The proliferation of spleen mononuclear cells of rat was detected with 3H-TdR method in vitro under the following different treatments:(1)the administration of the different concentration of rALR with 5 ?g/ml ConA at same time;(2)the addition of 30 ?g/ml ALR after 5 ?g/ml ConA pretreatment in 10 h and 32 h, respectively;(3)the addition of 5 ?g/ml ConA after 30 ?g/ml ALR pretreatment until 30 h. Cyclosporin A and the supernatant from cultures of yeast were used as positive and negative controls, respectively. The IL-2 levels in the supernatants from the mononuclear cells by various treatments were detected with RIA test kit. Results: rALR inhibited the proliferation and the production of IL-2 of the mononuclear cells from rat spleen stimulated by ConA dose-dependently. The mononuclear cell proliferations were still inhibited by 30 ?g/ml rALR after stimulated by ConA for 10 h or 32 h, but the pretreatment of 30 ?g/ml rALR for 30 h had no influence on the reactivity of mononuclear cell to ConA compared with control. Conclusion: rALR could inhibit in dose-dependent way the proliferation of mononuclear cells from rat spleen stimulated by ConA in vitro, but it couldn’t influence the rest mononuclear cells. This suggests that the rest mononuclear cells might not express the receptor of ALR.

OBJECTIVE To give details of the resistance of Staphylococcus aureus infection to various types of drugs.METHODS The laboratory data of resistant S.aureus from Nov 2005 to Dec 2006 were investigated and analyzed and compared the results to the standard sample.RESULTS The sequence of the antibacterial agents resistant to the S.aureus in decreasing order was azithromycin(91.66%),penicillin(88.57%),ceftazidime(87.50%) and amoxicillin(73.53%) with the age distribution of the sufferers from 31-40 years old. It was found 23.86% patients(42 samples) had the positive rate in prostatic fluid of 32.95%.CONCLUSIONS Based on the patient conditions,provide the appropriate drug treatment would avoid the occurrence of resistant S.aureus.