The gene and the amino acid sequence of the structural and regulatory region of thePseudomonas aeruginosa with different resistance patterns were analyzed. Six strains with different resistance patterns were selected and the AmpC β-lactamase was identified. The objective gene fragment was amplified by colonies PCR. The sequences of the PCR-products were analyzed. The DNA sequence of the structural gene ampC and the regulatory genes ampR, ampD and ampE was detected. The 6 strains and the wild-typePseudomonas aeruginosa are highly homogeneous in structural and regulatory region. Some new mutant points were found.

In order to further investigate the mechanisms of action of berberine (Ber), we assessed the effects of Ber on the mRNA expression of nitric oxide synthases (NOS) in rat corpus cavernosum. After incubation with Ber for 1 or 3 h respectively, the levels of NOS mRNA were examined by reverse transcription polymerase chain reaction (RT-PCR). Our results showed that there were iNOS and eNOS mRNA expression in rat corpus cavernosum. Ber enhanced eNOS mRNA expression in rat penis, but exhibited no effect on the expression of iNOS mRNA (P>0.05). The present study indicated that the relaxation of Ber involved the NO-cGMP signal thansduction pathway. The enhancing effect of Ber on eNOS mRNA expression might associated with its relaxation of corpus cavernosum.

The interaction of high-fat diet and the peptide YY (PYY) gene expression in diet-induced obesity and the mechanisms which predisposed some individuals to become obese on high-fat diet were explored. Thirty-six male SD rats were randomly divided into high-fat diet group (n=27) and chow fed control group (n=9). After 15 weeks of either a high-fat diet or chew fed diet, the high-fat diet group was subdivided into dietary induced obesity (DIO) and dietary induced obesity resistant (DIR) group according to the final body weight. Then the DIO rats were subdivided into two groups for a 8-week secondary intervention. One of the group was switched to chew fed diet, whereas the other DIO and DIR rats continued on the initial high-fat diet. Weight gain and food intake were measured, food efficiency was calculated, and the concentrations of plasma neuropeptide Y (NPY) and PYY were assayed. Hypothalamic NPY mRNA expression and PYY mRNA expression in ileum and colon was detected by RT-PCR. The results showed that at the end of 15th week, the levels of body weight and caloric intake were significantly higher in DIO group than in DIR or control group (P<0.01), while no significant difference was found between DIR and control group (P>0.05). The concentration of plasma PYY was significantly higher in DIR group than in DIO and CF group, while no significant difference was found between DIO and CF group (P<0.01). After switching the DIO rats to chow fed diet, their body weight gains were significantly lower than that of the DIO-HF group. The expression of PYY mRNA was increased in DIO-HF/CF rats than in DIO-HF rats, and the expression of hypothalamic NPY mRNA was decreased in DIO-HF/CF rats than in DIO-HF group. It was concluded that both dietary composition and PYY gene expression could potently alter the hypothalamic NPY expression and result in different susceptibility to obese and overeating. The decreased PYY was associated with the increased NPY expression and their predisposal to obese and overeating in rats.

To explore the expression of heme oxygenase-1 (HO-1) in the peripheral blood mononuclear cells (PBMCs) and its relationship with pulmonary ventilation function in asthmatic patients, 18 asthmatic patients and 18 healthy subjects were selected. HO-1 protein and mRNA levels in PBMCs were measured by immunohistochemical staining and reverse transcription-polymerase chain reaction (RT-PCR), respectively. Blood carbon monoxide Hb (COHb), serum total IgE and pulmonary ventilatory function were observed. Our results showed that the percentage of cells positive for immunohistochemical staining of HO-1 were significantly higher in asthmatic patients (41.72±7.44)% than that in with healthy subjects (10.45±4.36)% (P<0.001) and the optical density of PBMC HO-1 mRNA was higher in asthmatic patients (26.05±4.14) than that in healthy subjects (10.82±4.26) (P<0.001). The relation analysis showed that PBMC HO-1 protein and mRNA levels had significantly negative relation with FEV₁%, PEFR, MEFR_50%, respectively (r=−0.51–0.89,P<0.05–0.001, respectively) and a positive relation with COHb and serum total IgE (r =0.48–0.85, 0.05–0.001, respectively). It is concluded that the expression of PBMC HO-1 protein and mRNA increased significantly in asthmatic patients, and HO-1 may play a significant role in the pathogenesis of asthma. The expression of HO-1 may bear a relation with severity of asthma.

To obtain the recombinant tumor necrosis factor-α converting enzyme (TACE) ectodomain and use it as a selective molecule for the screening of TACE peptide inhibitors, the cDNA coding catalytic domain (T800) and full-length ectodomain (T1300) of TACE were amplified by RTPCR, and the expression plasmids were constructed by inserting T800 and T1300 into plasmid pET-28a and pET-28c respectively. The recombinant T800 and T1300 were induced by IPTG, and SDS-PAGE and Western blotting analysis results revealed that T800 and T1300 were highly expressed in the form of inclusion body. After Ni²⁺-NTA resin affinity chromatography, the recombinant proteins were used in the screening of TACE-binding peptides from phage display peptide library respectively. After 4 rounds of biopanning, the positive phage clones were analyzed by ELISA, competitive inhibition assay and DNA sequencing. A common amino acid sequence (TRWLVYFSRPYLVAT) was found and synthesized. The synthetic peptide could inhibit the TNF-α release from LPS-stimulated human peripheral blood mononuclear cells (PBMC) up to 60.3%. FACS analysis revealed that the peptide mediated the accumulation of TNF-α on the cell surface. These results demonstrate that the TACE-binding peptide is an effective antagonist of TACE.

The mechanisms of increased expression of toll-like receptor 4 (TLR-4) during the formation of foam cells were explored. Low density lipoprotein (LDL) was prepared by density gradient ultracentrifugation and oxidized by incubation with CuCl₂. The human monocytic leukemia cell line (THP-1) was cultured in RPMI1640. The differentiation of THP-1 cells into macrophages (MPs) was induced by using myristate acetate (PMA) for 48 h. The macrophages were then incubated with oxidized LDL (ox-LDL) to generate foam cells (FCs). The mRNA and protein expression levels of human TLR-4 were detected by immunocytochemistry, Western blotting and reverse transcription polymerase chain reaction (RT-PCR). The results showed that the TLR-4 mRNA and the protein expression levels were significantly increased during the differentiation of monocytes into macrophages (P<0.05) as well as during the formation of lipid-laden foam cells (P<0.05). It was concluded that the upregulation of human TLR-4 gene expression during the differentiation of monocytes into macrophages and the differentiation of macrophages into foam cells could increase TLR-4 protein synthesis dramatically, which may enhance the ability of foam cells inflammation reaction in atherosclerosis.

The present study aimed to find out dynamic changes of apoptosis in human cytomegalovirus (HCMV) infected cells and the influence of HCMV infection on activation of caspase-3 and the expression of apoptosis-regulating genes, bcl-2 and fas mRNA. The sequential changes of apoptotic cell rate in high and low MOI (MOI=2.5 and 0.25 respectively) of HCMV infected human embryonic lung fibroblasts (HELFs) at 1 h, 12 h, 24 h, 36 h, 48 h, 72 h and 96 h post-infection were measured by flow cytometry. The expression levels of caspase-3 protein and bcl-2 and fas mRNA in HCMV infected cells (MOI=0.25) at 72 h post-infection were detected by Western blot andin situ hybridization methods, respectively. It was found that the ratio of apoptotic cells in normal controls was consistently lower, but the rates in low and high MOI infected cells were gradually increased with time prolonged, reached peak at 96 h (8.85%) and 72 h (25.63%), respectively. By Western blot analysis, only a narrow band of 32 kD (1 kD=0.992 1 ku) procaspase-3 was found in normal cells, but a wider procaspase-3 band and a much wider band of 17 kD proteins (p17) appeared in the infected cells. Meanwhile, the expression of bcl-2 mRNA was higher and that of fas mRNA was lower in the normal HELF cells, whereas there were significantly lower bcl-2 mRNA and higher fas mRNA expression levels in HCMV infected cells. It was concluded that HCMV was a stronger inducer of apoptosis in HELF cells. Caspase-3, as the marker of undergoing apoptosis, was expressed increasingly and activated in the infected cells, indicating its action in HCMV-inducing apoptosis. Down-regulating bcl-2 mRNA expression and up-regulating fas mRNA expression were also involved in the mechanism of HCMV-induced apoptosis.

The regulation of astroglia on synaptic plasticity in the CA1 region of rat hippocampus was examined. Rats were divided into three groups: the newly born (<24 h), the juvenile (28–30 days) and the adult groups (90–100 days), with each group having 20 animals. The CA1 region of rat hippocampus was immunohistochemically and electron-microscopically examined, respectively, for the growth of astroglia and the ultrastructure of synapses. The high performance liquid chromatography was employed to determine the cholesterol content of rat hippocampus. In the newly-born rats, a large number of neurons were noted in the hippocampal CA1 region of the newly-born rats, and few astroglia and no synaptic structure were observed. In the juvenile group, a few astroglias and some immature synapses were found, which were less than those in adult rats (P<0.01). The cholesterol content was 2.92±0.03 mg/g, 11.20±3.41 mg/g and 12.91±1.25 mg/g for newly born, the juvenile and the adult groups, respectively, with the differences among them being statistically significant (P<0.01). Our study suggests that the astrocytes may play an important role in the synaptic formation and functional maturity of hippocampal neurons, which may be related to the secretion of cholesterol from astrocytes.

To explore the possibility and condition of differentiation of bone marrow mesenchymal cells (BMSCs) to neural cellsin vitro, BMSCs from whole bone marrow of rats were cultured. The BMSCs of passage 3 were identified with immunocytochemical staining of CD44(+), CD71(+) and CD45(−). There were type I and type II cells in BMSCs. Type I BMSCs were spindle-shaped and strong positive in immunocytochemical staining of CD44 and CD71, whereas flat and big type II BMSCs were lightly stained. The BMSCs of same passage were induced to differentiate into neural cells by β-mercaptoethanol (BME). After induction by BME, the type I BMSCs withdrew to form neuron-like round soma and axon-like and dendrite-like processes, and were stained positively for neurofilament (NF). The type II BMSCs did not change in the BME medium and were negatively or slightly stained of NF.

The hypoglycemic activity and its mechanism of Jatrorrhizine (Jat) were studied. The normal mice and alloxan-induced hyperglycemic mice were given with different doses of Jat. Blood glucose and liver glycogen levels were determined by spectrophotometry with glucose-oxidase and iodine reagents respectively. The levels of blood lactic acid (LC) and liver lactate dehydrogenase (LDH) activity were measured to explore the effect of Jat on anaerobic glycolysis. Succinate dehydrogenase (SDH) activity in liver was measured to evaluate the effect of Jat on aerobic glycolysis in liver. It was found that Jat (50 mg/kg, 100 mg/kg) could significantly decrease blood glucose level in a dose-and time-dependent manner in both normal and alloxan-diabetic mice, increase the activity of SDH, but had no significant effects on the LC level and LDH activity. Jat could significantly reduce the content of liver glycogen in normal mice. Moreover, Jat could inhibit the platelet aggregation in rabbitsin vitro in a dose-effect relationship. It was concluded that Jat induced the pronounced decrease in blood glucose in normal and hyperglycemic mice. The hypoglycemic activity of Jat may be attributed to the enhancement of aerobic glycolysis.

The correlation between pulmonary endothelin receptors and alveolar-arterial oxygen gradient (A-aDO₂) in rats with hepatopulmonary syndrome was investigated. Animals were divided into 2 groups: Sham-operated (Sham) group and common bile duct ligation (CBDL) group. Arterial blood gas was evaluated by a blood gas analyzer. The concentrations of ET-1 in blood and lung tissue sample were evaluated by radioimmunoassay. The distribution and expression of two kinds of subtype receptor of ET-1, ETRA and ETRB were examined byin situ hybridization. The results showed that the level of A-aDO₂ was higher in CBDL group were both higher than in Sham group (P<0.05). There was no significant difference in averageA of ETRA between two groups by imaging analysis (0.21±0.06vs 0.22±0.08,P>0.05), while that of ETRB was higher in CBDL group than in Sham group (0.58±0.16vs 0.28±0.07,P<0.05). The expression of ETRB in lung was positively correlated with A-aDO₂(P<0. 05). It was concluded that the widened A-aDO₂ may be related with enhancement of the expression of ETRB in lung.

The effect of acute ischemia on the electrophysiological characteristics of the three layers myocardium of caninein vivo was investigated. Twelve canines were divided into two groups randomly: acute ischemia (AI) group and sham operation (SO) group. By using the monophasic action potential (MAP) technique, MAP and effective refractory period (ERP) of the three layers myocardium were measured by specially designed plunge needle electrodes and the transmural dispersion of repolarization (TDR) and transmural dispersion of ERP (TDE) were analyzed. The results showed that in the AI group, MAP duration (MAPD) was shortened from 201.67±21.42 ms to 169.50±13.81 ms (P<0.05), but ERP prolonged to varying degrees and TDE increased during ischemia. In the SO group, MAPD and ERP did not change almost. Among of the three layers myocardium of canine, MAPD was coincident in two groups. It was concluded that during acute ischemia, MAPD was shortened sharply, but there was no significant difference among of the three layers myocardium. The prolonged ERP was concomitant with increased TDE during acute ischemia, which may play an important role in the occurrence of arrhythmias induced by acute ischemia. These findings may have important implications in arrhythmogenesis.

The effects of L-carnitine, as an ingredient of cardioplegia solution, on cardiac function and cardiomyocyte apoptosis in patients undergoing heart valve replacement operation were investigated. Twenty-three cases undergoing heart valve replacement with cardiopulmonary bypass (CPB) were randomly allocated into two groups: L-carnitine group (n=12, 12 g/L L-carnitine was put in the ST. Thomas cardioplegia) and control group (n=11, identical to the L-carnitine group except that normal saline was administered instead of L-carnitine). Serum cardial troponin I (cTnI) levels, the left ventricular ejection fraction (LVEF), and cardiac index (CI) were measured perioperatively. A bit of myocardial tissue obtained from right atria was taken before CPB and by the end of intracardiac procedure to undergo electron microscopy examination and estimate apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL). From the end of CPB to 3 days after operation, the serum levels of cTnI in the L-carnitine group was significantly lower than that in the control group (P<0.05). Heart color ultrasonogram showed that the CI index and LVEF at 7th day postoperatively in the L-carnitine group were significantly higher than in the control group (P<0.05). Compared to the control group, L-carnitine significantly alleviated the morphologic changes of cardiac muscle cells (electron microscopy examination) and decreased the amounts of apoptotic cardiac muscle cells (TUNEL). Furthermore, the dosage of vasoactive drugs used after operation was significantly less in the L-carnitine group (P<0.01). It was concluded that L-carnitine cardioplegia solution could improve cardiac function in patients undergoing heart valve replacement operation and alleviate CPB-mediated apoptosis of cardiac muscle cells.

A mammalian expression plasmid pcDNA3. 1-hCC10 was constructed and identified, then CC10 protein expression in A549 lung cancer cell line was detected. A 273 bp cDNA fragment was amplified from the total RNA of normal lung tissue by using RT-PCR and cloned into expression plasmid cDNA3. 1, and the recombinant plasmid was identified by employing double digestion restriction enzymesHind III andBamH I and the cDNA sequence was assayed by the Sanger dideoxymediated chain termination method. The segment was then transfected into the A549 lung cancer cell line. The protein expression of CC10 was detected by immunofluorescence and Western blot. Our results showed that the cDNA fragment included the entire coding region (273 bp). The recombinant eukaryotic cell expression vector of pcDNA3. 1-hCC10 was successfully constructed, and the sequence of the insert was identical to the published sequence. A549 cells line transfected with the pcDNA3. 1-hCC10 expressed high level of CC10 protein. The recombinant plasmid cDNA3. 1-hCC10 may serve as an effective tool for the study of tumorogenesis and tumor treatment.

To investigate the expression and significance of CD28 and CTLA4 on T cells in bone marrow of aplastic anemia (AA) mice,in vitro bone marrow mononuclear cells (BMMNCs) were activated through being incubated with PHA (15 μg/mL). The expression of CD28 and CTLA4 on T cells incubated with or without PHA was detected by two-color flow cytometry. The expression of CD28 and CTLA4 was significantly increased after PHA stimulation. In the AA mice, the expression of CD28 with or without PHA stimulation was both higher than that in the normal mice (bothP<0.01), but the expression of CTLA4 with or without PHA stimulation showed no significant difference in comparison to that in the normal mice (bothP>0.05). In the AA mice, there were more activation and activated potential of T cells than the normal, and the abnormal expression of CD28 and CTLA4 may participate in immunological disorder mediated by T cells.

The effect of ligustrazine on the expression of CD31 in syngenic bone marrow transplantation (BMT) mice was studied. Fifty-six Balb/c mice were divided into 3 groups: normal control group, BMT control group, and ligustrazine treated group. Syngenic BMT mouse models were established according to the literatures. In BMT control group and the ligustrazine treated group, the mice were given respectively orally 0.2 mL saline and 2 mg ligustrazine twice a day. On the 7th, 14th, and 21st day after BMT, the mice were killed. The expression of CD31 on the surface of bone marrow nuclear cells (BMNC) was detected by flow cytometry. Peripheral blood leukocytes, platelets and BMNC were counted. Histological observation of bone marrow was made. The results showed that in ligustrazine treated group the peripheral blood leukocytes, platelets and BMNC counts, and the expression of CD31 on the day 7, 14, 21 after BMT were higher than in BMT control group (P<0.01 orP<0.05). In conclusion, ligustrazine could obviously enhance the CD31 expression on the surface of BMNC after syngenic BMT in mice, which may be one of the mechanisms underlying the ligustrazine accelerating hematopoietic reconstitution in syngenic BMT.

The HL-60 cells were transfected with chk1 antisense and sense chain, and 24 h later subjected to irradiation. Twenty-four h after irradiation, the changes in the chk1 protein expression was assayed by Western blot, and the cell cycles and apoptosis rate detected by FCM. The irradiated apoptosis sensitivity was increased by antisense blocking of chk1 gene in HL-60 cell line with the apoptosis rate being 26.31%, significantly higher than that by the sense blocking (10.34%, 0.025<P<0.05). In HL-60 cells transfected with chk1 antisense chain, the G₂/M phase arrest was attenuated and the cells in G₂/M phase were accounted for 38.42%, significantly lower than those of the cells transfected with chk1 sense chain (54.64%, 0.005<P<0.01). It was concluded that antisense blocking of chk1 gene could increase the apoptosis sensitivity to irradiation.

The antinephritic effect of lipo-prostaglandin E₁, prostaglandin E₁ incorporated in lipid microspheres was investigated using an experimental model of mesangial proliferative glomerulonephritis (MsPGN). Twenty-two female rats were randomly divided into nephritic group (N,n=6), lipo-prostaglandin E₁ treated group (NL,n=8) and control group (C,n=6). Lipo-prostaglandin E₁ was given intravenously at 40 μg·kg⁻¹·d⁻¹ from the 6th week to the 8th week. Twenty-four h urinary protein contents and blood creatinine (Cr) were determined and the pathological changes were observed in the experiment. The expression of proliferating cell nuclear antigen (PCNA), extracellular matrix (fibronectin, FN; collagen type IV, Col IV) and transforming growth factorβ₁ (TGFβ₁) was detected by using immunohistochemistry. The results showed that lipo-prostaglandin E₁ significantly inhibited the glomerular histopathological changes as well as the elevation of plasma Cr (P<0.05). The overexpression of PCNA, FN, Col IV and TGFβ₁ were also obviously inhibited in group NL as compared with the group N (P<0.01). It was suggested that lipo-prostaglandin E₁ could improve renal function, inhibit the proliferation of glomerular cells and reduce the deposition of extracellular matrix, which may be related to the down-regulation of the TGFβ₁ expression.

In order to explore the role of connective tissue growth factor (CTGF) in the pathogenesis of renal tubulointerstitial fibrosis, 48 Wistar rats were randomly divided into sham-operated and unilateral ureteral obstruction (UUO) group. On the postoperative day 1, 3, 7 and 14, the rats were killed and the kidneys were removed. The renal tubulointerstitial injury index was evaluated according to the MASSON staining. The mRNA levels of CTGF, transforming growth factor-β1 (TGF-β1), collagen I (col I), and plasminogen activator inhibitor-1 (PAI-1) were detected using reverse transcriptional-polymerase chain reaction (RT-PCR). Immunohistochemistry was performed to evaluate the protein expression of the above factors, and the relations among them were analyzed. Quantitative expression of CTGF protein in the kidneys was also assessed using Western blot. The results showed that TGF-β1 mRNA level was increased at first day after UUO, followed by a marked elevation of CTGF mRNA level, which began to increase 3 days after UUO (P<0.01). With the progression of the disease, the mRNA expression of CTGF, col I and PAI-1 was increased progressively. Immunohistochemistry revealed that the CTGF protein expression was significantly increased in fibrotic areas and tubular epithelial cells 3 days after UUO. On the post-UUO day 7, the protein level of CTGF was positively related to the renal tubulointerstitial injury index (r=0.62,P<0.01), the expression of TGF-β1 (r=0.85,P<0.01), col I (r=0.78,P<0.01), and PAI-1 (r=0.76,P<0.01). Upon Western blot analysis, CTGF protein expression began to increase 3 days after UUO, and appeared progressively throughout the time course (P<0.01, as compared with sham-operated group). It is concluded that CTGF can be induced by TGF-β and mediate various profibrotic actions of this cytokine, such as increasing extracellular matrix (ECM) synthesis and decreasing ECM degradation. The increased expression of CTGF may play a crucial role in the development and progression of tubulointerstitial fibrosis.

The role of protease activated receptor-2 (PAR-2) in the renal tubulointerstitial lesion induced by unilateral ureteral obstruction (UUO) was explored. Mice were sacrificed on the day 1, 3, 5, 7, 10, 14 and 21 after UUO. The expression of PAR-2 mRNA and protein and α-smooth muscle actin (α-SMA) protein in tubulointerstitium was detected by RT-PCR and immunohistochemistry at each time point, respectively. The results showed that the PAR-2 expression in renal tubulointerstitium was increased progressively starting form 24 h to the day 14 post-ligation, and it was significantly associated with the relative volume of interstitium and the positive area of α-SMA. PAR-2 was mainly expressed in renal tubule epithelial cells, especially in proximal tubular cells. It also located in renal capillary ansa, interstitial infiltrate cells and fibroblasts. It was concluded that PAR-2 was active in interstitial and tubular cells in the early phase of fibrotic process and played an important role in mediating the tubulointerstitial lesion after UUO.

To evaluate the efficacy and safety of risedronate sodium in treatment of postmenopausal osteoporosis, one-year randomized, double blind clinical trial was performed among 54 women with postmenopausal osteoporosis. The changes were compared in bone mineral density (BMD), bone metabolism markers and adverse events after 12 months oral administration of risedronate sodium. BMD was measured by dual energy X-ray absorptionmetry (DEXA) and bone turnover marker was detected. The results showed that there was a significant increase in BMD of the lumbar spine (3.29%±1.18%, 4.51%±1.64% respectively) after 6 and 12 months in the risedronate treatment group versus placebo control group (−0.62%±0.24%, 0.48%±0.18% respectively). Bone turnover was decreased to a stable nadir over 6 and 12 months for resorption markers [N-telopeptide (NTx),P<0.05] and over 12 months for formation marker (ALP,P<0.05; BGP,P<0.05). The safety profile of risedronate sodium was similar to that of placebo. There were no trends toward increased frequency of any adverse experience except for gastrointestinal symptoms (7.1%), rash (7.1%) and hematuria (3.6%), which were usually mild, transient, and resolved with continued treatment. It was concluded that risedronate was an efficacious and safe drug in treatment of postmenopausal osteoporosis.

The expression of TNF-_α in the liver at different periods postSchistosoma japonica infection and the effect on liver fibrosis after supplementary injection of these cytokines were investigated. The mice infected with schistosome cercariae were divided into 3 groups: normal control group, TNF-_α-untreated infection group and TNF-_α-treated infection group. ABC immunohistochemistry and pathologic image multimedia quantification system were applied to dynamically detect the activity of TNF-_α. The results showed that the levels of TNF-_α in the liver in TNF-_α-untreated infection group were slowly decreased with prolongation of infection time (from 8th, 11th, 14th to 18th week), while in the TNF-_α-treated infection group, those were increased significantly after intraperitoneal injection of TNF-_α at 6th week after infection. At first to 8th week after the final injection of TNF-_α, the intrahepatic TNF-_α levels in the TNF-_α-treated infection group were significantly higher than in the other two groups (P<0.01), and the granulomatous inflammation and fibrosis in the liver were also milder in the normal control group. It was concluded that at the early stage ofSchistosoma japonica infection mouse liver mainly released Th1 cytokine and TNF-_α from Th1 activated macrophages. Six weeks after infection (post egg deposition), exogenous supplement with intraperitoneal injection of TNF-_α could induce the enhanced expression of Th1 cytokines and alleviate the liver granulomatous inflammation and fibrosis.

The relationship between immune vasculitis and atherosclerosis was studied. The experimental model of weanling rabbits for immune vasculitis was reproduced by intravenous injection of 10% bovine serum albumin. There were 6 groups: group A, 25 weanling rabbits with immune vasculitis subject to coronary arteriography; group B, 10 normal mature rabbits subject to coronary arteriography; group C, 10 weanling rabbits subject to coronary arteriography; group D, 8 weanling rabbits with vasculitis and cholesterol diet; group E, 8 weanling rabbits receiving single cholesterol diet; group F: 8 weanling rabbits receiving basic diet. Four weeks later, coronary arteriography was performed in groups A, B and C. The rabbits in groups D, E and F were sacrificed for the study of pathological changes in the coronary artery after 12 weeks. The results showed that the dilatation of coronary artery occurred in 6 rabbits of group A, but in groups B and C, no dilatation of coronary artery appeared. In comparison with group E, more severe atherosclerosis occurred in group D, showing the thickened plaque, fibrous sclerosis and atherosclerotic lesion. Percentage of plaques covering aortic intima, incidence of atherosclerosis of small coronary arteries and degree of stenosis of coronary arteries were significantly higher in group D than in group E, (P<0.01). No atherosclerosis changes were found in group F. It was concluded that in the acute phase, the serum immune vasculitis can induce the dilatation of coronary artery of some weanling rabbits, and aggravate the formation of atherosclerosis in rabbits fed with cholesterol diet. Immune vasculitis is a new risk factor of atherosclerosis and ischemic heart disease.

To investigate the expression of cyclooxygenase-2 (COX-2) in ovarian cancer cell lines, RT-PCR and immunocytochemistry were used to detect the expression of COX-2 in 5 ovarian cancer cell lines. The expression of COX-2 mRNA and protein was detected in all 5 cell lines. It is suggested that COX-2 is expressed in ovarian cancer cell lines, which provides a basis for the chemoprevention of ovarian cancer.

In order to characterize their relationship through clinicopathological comparison between IgA nephropathy and Henoch-Schönlein purpura nephritis (HSPN), 31 children with IgA nephropathy aged between 3 to 15 years and 120 children with HSPN aged between 4 to 15 years were compared with each other in clinical manifestation, blood biochemistry, serum immunology and followup study. Renal pathological findings under light microscope, immunofluorescence and electronic microscope were analyzed and also compared between 31 children with IgA nephropathy and 32 biopsied children with HSPN. The results showed that the onset age was over 12 years in 25.8% children with IgA nephropathy, but only 10% in HSPN (P<0.05). The clinical patterns of IgA nephropathy and HSPN were similar, but extra-renal manifestations were more often in HSPN, all of them had skin purpura, 59% had gastrointestinal symptoms and 47% suffered from arthralgia, compared with only abdominal pain in 3.2% children with IgA nephropathy. The renal pathological investigation showed global sclerosis in 35.5% of IgA nephropathy and 3.1% of HSPN, mesangial sclerosis in 41.9% of IgA nephropathy and 6.3% of HSPN, but endothelial proliferation in 65.6% of HSPN and 29% of IgA nephropathy (allP<0.01). Thin basement membrane nephropathy was only found in 6.5% children with IgA nephropathy, no in HSPN. The electronic dense deposits in HSPN were sparse, loose and wildly spread in glomerular mesangium, subendothelial area and even intra basement membrane, but it was dense, lumpy and mostly limited in mesangium and paramesangium in IgA nephropathy. Predominant IgA deposits were found in 81.2% of HSPN, and overwhelming IgG deposits in 12.5% of HSPN with relatively weak IgA deposits, moreover 6.3% of HSPN showed linear IgG deposits in glomerular capillary. Totally 71.9% of HSPN had IgG deposits in glomeruli and only 19.4% of IgA nephropathy showed glomerular IgG deposits (P<0.01). No IgG deposit was observed in 81.6% of IgA nephropathy, among them most showed IgA and IgM and/or C3 deposits, moreover overwhelming IgG deposits and linear IgG deposits couldn't be found in IgA nephropathy. Mean 20 months follow-up showed complete remission in 72.5% of HSPN, but only 19.4% in IgA nephropathy after 34 months follow-up. Moreover, 64.5% of IgA nephropathy had consistent hematuria and proteinuria and 16.1% had active nephritides (P<0.05). It was concluded that significant clinico-pathological difference was found between HSPN and IgA nephropathy, which didn't support the one disease entity hypothesis. HSPN and IgA nephropathy are probably two diseases with similar immune abnormalities.

The expression and activity of NF-κB in the synovium of collagen-induced arthritis (CIA) rats was detected in order to investigate the possible therapeutic effects of triptolide on rheumatoid arthritis (RA). The experimental Wistar rat model of CIA was set up by intradermal injection of emulsion of bovine collagen II and the successful rate of setting-up models was evaluated by arthritis index (AI). Rats were grouped randomly into three groups: normal, model and treatment group. The expression of TNF-α and IL-6 in synovial fluid was detected by ELISA, and the expression and activity of NF-κB in synovium by immunohistochemistry method and by electrophoretic mobility shift assay (EMSA) respectively. As compared with normal group, the expression of TNF-α and IL-6 in synovia (P<0.05), and the expression and activity of NF-κB (P<0.05) in synovium were increased in model group. There was statistical difference in above-mentioned indexes between model group and treatment group. Triptolide may play a protective role in RA via downregulating the expression and activity of NF-κB in synovium.

The effects of active antiendotoxin chemical fraction isolated fromRadix Isatidis (fraction D) on TNF-α and IL-8 secretion in HL-60 cells induced by lipopolysaccharide (LPS) were studied. The appropriate densities of cell suspension and fraction D solution were determined by MTT colorimetric method. Fraction D and LPS were added to HL-60 cell suspension with three different methods respectively. The contents of TNF-α and IL-8 in the cultured supernatant induced by LPS were detected by using ELISA method. The results showed that the absorbance (A) was directly proportional to the number of cells and the linearity was good in the range from 0.25×10⁵ to 2×10⁵ cell/mL cell suspension. The fraction D significantly inhibited the oversecretion of TNF-α and IL-8 in HL-60 cells induced by LPS at the concentration of 7.812 mg/mL which had no cytotoxicity. It was indicated that the antiendotoxin mechanism of the active fraction fromRadix Isatidis was contributed to the inhibition of the oversecretion of cytokines induced by LPS.

The anti-tumor effect and mechanism of SEA-Fab' coupled protein on gastric tumor was studied. The target cell Walker-256 was treated with SEA-Fab' synthesized chemically or SEA respectively for 24 h, 36 h or 72 h. PBMC+Walke-256 cells served as controls. The apoptotic index of SEA-Fab' against effector cells was detected. In the mouse gastric cancer models (n=60), SEA-Fab', SEA and normal saline was injected in experimental group, SEA group and control group respectively. The occurrence and weight of tumor was observed. The results showed that the apoptotic index was significantly higher in the SEA-Fab' (34.6%–68.9%) and SEA group (15.5%–31.9%) than in PBMC+Walker-256 group (5.5%–12.8%) with the difference being significant (P<0.01). And there was significant difference between SEA-Fab' group and SEA group (P <0.01). The tumor weight in SEA-Fab', SEA and control groups was 3.64±0.53 g, 0.78±0.26 g and 0.49±0.17 g respectively with the difference being statistically significant between the SEA-Fab' group, SEA group and the control group (P<0.01). In the SEA-Fab's and SEA groups, there were CD4⁺ T and CD8⁺ T cell infiltrates, but in the control group, no or few T lymphocytes were seen in the mouse tumor tissue. It was concluded that SEA-Fab' was more effective to activate T lymphocytes to kill the tumor cells than SEA used alone. It was feasibility by using the monoclonal antibody as carrier to perform the targeted immunotherapy of gatric tumor.

In order to study the expression of transformation suppressor gene RECK and MMP-9 in hilar cholangiocarcinomas and its clinical significance, and explore the roles of RECK gene in metastasis and invasion of hilar cholangiocarcinoma, the expression levels of RECK, and MMP-9 mRNA were detected by using reverse transcription-polymerase reaction in 42 paraffin-embedded samples of hilar cholangiocarcinoma and 10 samples of benign bile duct diseases. The results showed that in hilar cholangiocarcinoma tissues, the expression of RECK gene was 0.235±0.062, significantly lower than in normal bile duct tissue (0.533±0.024,P<0.05). In hilar cholangiocarcinoma tissues, the expression of MMP-9 (0.528±0.039) was significantly higher than in the normal tissues (0.311±0.032,P<0.05). The expression of RECK gene was closely related to the intrahepatic and surrounding organs invasion (P<0.05). It was concluded that RECK gene could inhibit the expression of MMP-9 in hilar cholangiocarcinomas and closely correlated with the biological behaviors. The abnormal expression of RECK gene might be one of the molecular mechanisms of hilar cholangiocarcinoma metastasis.

The change and the role of MAPK cascade pathway and P53 pathway after liver transplantation were explored. Thirty-four punctured donor liver specimens and 10 normal liver specimens were classified as group A (no rejection,n=10), group B (mild/moderate acute rejection,n =10), group C (serious acute rejection,n=8), group D (chronic rejection/fibrosis,n=6) and group E (control,n=10). By using immunohistochemistry, the expression levels of mitogen activated protein kinase (MAPK), Ras and P53 proteins, and byin situ hybridization, MAPK and ras mRNA expression levels were detected. The results showed that the expression levels of MAPK and Ras proteins were increased by turns in groups A, B and C, and decreased by turns in groups D and E. The protein expression of P53 was higher in the treated groups. The expression of Ras, HSP70 mRNA was identical as that of protein. It is suggested that the MAPK cascade pathway and P53 pathway can protect the hepatocytes by different mechanisms after liver transplantation. MAPKs cascade pathway repairs hepatocyte injury or accelerates hepatocytes into proliferation or differentiation. P53 pathway blocks cell cycle within G1 phase to make hepatocyte repair or apoptosis to reduce disorder differentiation.

The effects of cyclosporine A (CsA) on Angiontensin II (Ang II)-induced protein contents, c-fos protein levels and cytosolic Ca²⁺ level ([Ca²⁺]i) in cultured cardiomyocytes of neonatal rats were observed. Total protein contents were determined by Bradford method. The expression of c-fos protein was detected by Western blot. [Ca²⁺]i labeled with fluorescent probe Fluo-3/AM was measured under a laser scanning confocal microscope. The results revealed that as compared with control, the total protein contents were increased in cardiomyocytes treated with Ang II (10⁻⁷ mol/ L), which could be inhibited by CsA in a dose-dependent manner. It was found that Ang II could increase the c-fos protein expression, which could be inhibited by CsA in a dose-dependent manner. Ang II induced the [Ca²⁺]i elevation in cardiomyocytes. CsA did not influence the resting intracellular Ca²⁺, but inhibited significantly the Ang II-induced [Ca²⁺]i elevation. It was concluded that CsA can suppress the Ang II-induced c-fos protein expression and [Ca²⁺]i elevation in single cardiomyocyte, which might pay a role in the prevention of Ang II-induced cardiomyocyte hypertrophy by CsA.

To identify the best suture techniques for the tendon repair, the biomechanical properties of tendons sutured by different methods were dynamically examined. 140 chickens were divided into 2 groups equally: group A and group B. The tendon of the right side was subjected to injury-repair process, and the tendons of the left sides served as controls in both groups. In group A, “figure-of-8” suture, modified Kessler suture and Bunnell suture were used for the 2nd to 4th paws respectively, while in group B, Kleinert suture, Tsuge suture and Ikuta suture were used. On the day 0, 3, 7, 14, 21, 28, 42 after operation, 10 animals were sacrificed and the flexor tendons of both sides were harvested for strength test. The results showed that the initial strength of the repaired tendons and the strength after 6 weeks following tendon cut were far below those of intact tendons, irrespective of suture techniques used. With the 6 techniques, theP_max of tendons repaired by Tsuge suture was increased continually, reaching the highest value on the 42nd day. TheP_max of tendons sutured by the modified Kessler suture was slightly lower than that by Tsuge suture, but it was increased steadily in healing. The tendons repaired by figure-of-8 suture yielded the lowestP_max. It was concluded that Tsuge suture and modified Kessler suture were the best techniques for tendon repair.

To investigate the role of ligustrazine on relaxation of the isolated rabbit corpus cavernosum tissuein vitro, the effects of ligustrazine on the corpus cavernosum were observed by using experimental method of smooth muscle strips. Concentration-responses to phenylephine (PE) and KCl were recorded. The results showed that ligustrazine concentration-dependently depressed the contraction response of smooth muscle strips induced by PE. The maximum percentage relaxation of cavernosal strips by ligustrazine was 74.1%±6.2% (compared with control: 21.9%±5.6%P<0.01). Ligustrazine concentration-dependently reduced the amplitude of the contraction induced by cumulative doses of PE or KCl, shifted the cumulative concentration response curves of PE and KCl to the right and depressed their maximal responses. It was concluded that ligustrazine could significantly relax the cavernosal muscle contraction induced by PEin vitro. The results suggested that ligustrazine inhibited calcium ion influx.

The changes in excitability and autorhthmicity of bladder detrusor in experimental noninsulin dependent diabetes mellitus (NIDDM) rats were observed. Sixty-nine NIDDM rats as NIDDM group and 69 normal rats as control group were enrolled into this experimental study. At 6th, 10th, 14th, 18th, 22nd and 26th week after the rats were injected last time, the changes in the excitability and autorhthmicity of detrusor stripsin vitro were observed. The results showed that the threshold of the tension which made the detrusor strips contract was significantly higher in NIDDM group (0.716±0.325 g) than in control group (0.323±0.177 g) (F=59. 63,P<0.001). At different stages, the threshold of the tension resulting the contract of the detrusor strips in NIDDM group was also higher than in control group. At 18th week after STZ injection, the frequency of spontaneous contract of the detrusor strips in NIDDM was significantly higher than in control group (P<0.05), whereas at 22nd week, that in NIDDM group was significantly lower than in control group (P<0.05). It was concluded that the decreased excitability of the bladder detrusor was the earliest and most obvious changes in bladder function in diabetes rats and the autorhthmicity had also changed at the early stage of diabetic bladder.

To investigate the clinical use of π graft in total arterial revascularization and its outcomes, a retrospective analysis of 23 patients out of 1000 patients undergoing total arterial coronary bypass surgery with a π graft between September 1994 and December 2004 was performed. In the selected patients for the management of triple vessel disease with middle diagonal/intermediate ramus disease such that a skip with the left internal mammary artery (LIMA) or radial artery (RA), the main stem of π graft, to the left anterior descending coronary artery (LAD) will not work and the right internal mammary artery (RIMA) or right gastroepiploic artery (RGEA) cannot pick up the diagonal/intermediate ramus, hence the LAD and diagonal/intermediate ramus were grafted with a mini Y graft using the distal segment of LIMA, RIMA, RA or RGEA, together with the bilateral internal mammary artery (BIMA) or LIMA-RA T graft to compose π graft. Twenty-three patients (18 males, 5 females) underwent the π graft procedure. There were no deaths or episodes of myocardial infarction, stroke, and deep sternal wound infection. One patient required reopening for controlling bleeding. Until the end of 2004, during a mean follow-up of 81.0±28.4 months, no angina needing re-intervention or operative therapy or coronary related death occurred. In conclusion, in patients with specific coronary artery anatomy/stenosis, the BIMA (sometimes LIMA with RA or RGEA) π graft can be successfully performed for total arterial revascularization with good midterm outcomes.

In order to investigate the effect of nerve growth factor (NGF) on the proliferation of rabbit corneal endothelial cells and epithelial cells, thein vitro cultured rabbit corneal endothelial cells and epithelial cells were treated with different concentrations of NGF. MTT assay was used to examine the clonal growth and proliferation of the cells by determing the absorbency values at 570 nm. The results showed that NGF with three concentrations ranging from 5 U/mL to 500 U/mL enhanced the proliferation of rabbit corneal endothelial cells in a concentration-dependent manner. 50 U/mL and 500 U/mL NGF got more increase of proliferation than that of 5 U/mL NGF did. Meanwhile, 50 U/mL and 500 U/mL NGF could promote the proliferation of the rabbit corneal epithelial cells significantly in a concentration-dependent manner. However, 5 U/mL NGF did not enhance the proliferation of epithelial cells. It was suggested that exogenous NGF can stimulate the proliferation of both rabbit corneal endothelial and epithelial cells, but the extent of modulation is different.

By using RT-PCR and immunohistochemistry, the expressions of transforming growth factorβ₂(TGF-β₂) mRNA, proliferating cell nuclear antigen (PCNA) and fibronection (FN) protein in lens epithelial cells (LECs) of age-related nuclear and cortex cataract were detected and compared. The results of RT-PCR revealed that the expression of TGF-β₂ mRNA was higher in cortex cataract than in nuclear cataract. Immunohistochemistry demonstrated that the expression of PCNA protein was lower and the expression of FN protein was higher in cortex cataract than in nuclear cataract. It was suggested that TGF-β₂, PCNA and FN might take important parts in the process of age-related cataract. Cortex cataract was related to the transdifferentiation of LECs, and nuclear cataract to the proliferation of LECs.

In order to provide a rational research basis for detection of resistance ofNeisseria gonorrhoeae transferable resistance (mtr) efflux system, plasmid pET-28a(+) encoding mtrC gene was constructed and the related target protein was expressed inEscherichia coli (E. coli) DE3. The fragments of mtrC gene ofNeisseria gonorrhoeae from the standard strains were amplified and cloned into prokaryotic expression plasmid pET-28a(+) with restriction endonuclease to construct recombinant pET-mtrC which was verified by restriction endonuclease and DNA sequencing. The recombinant was transformed intoE. coli DE3 to express the protein mtrC induced by IPTG. The results showed mtrC DNA fragment was proved correct through restriction endonuclease and DNA sequencing. Its sequence was 99.5% homologus to that published on GeneBank (U14993). A 48. 5 kD fusion protein which was induced by IPTG was detected by SDS-PAGE. It was concluded that the construction of prokaryotic expression plasmid of mtrC protein ofNeisseria gonorrhoeae was correct and the fusion protein was successively expressed inE. coli.

The ATP2C1 gene mutation in one case of familial benign chronic pemphigus was investigated. One patient was diagnosed as familial benign chronic pemphigus by pathology, ultrastructural examination and clinical features. Genomic DNA was extracted from blood samples. Mutation of ATP2C1 gene was detected by polymerase chain reaction (PCR) and DNA sequencing. The results showed that deletion mutation was detected in ATP2C1 gene in this patient, which was 2374delTTTG. No mutation was found in the family members and normal individuals. It was concluded that the 2374delTTTG mutation in ATP2C1 gene was the specific mutation for the clinical phenotype for this patient and was a de novo mutation.

The effects of oligosaccharide and creatine (Cr) supplementation on glucose, lactic acid and urea nitrogen levels in blood and activity of serum creatine kinase (CK) were explored. Twenty CUBA male athletes were divided into 4 groups: group A (supplementation of Cr alone), group B (supplementation of oligosaccharide), group C (supplementation of oligosaccharide and Cr) and group D (placebo control group). By using orthogonal L4 table (2³), the experiment was performed. There were factors including oligosaccharide (carbohydrate, CHO), Cr and their correlation. Each factor had two levels: supplementation and no-supplementation. The results showed that the supplementation of CHO or Cr alone, combined supplementation of CHO and Cr could significantly reduce the glucose, urea nitrogen levels in blood and serum CK activity after competition in the athletes. Moreover, the effects of combined supplementation of CHO and Cr were more satisfactory. It was concluded that supplementation of CHO and Cr could promote the recovery of physical performance and athletic abilities after athletics in basketball athletes.

The measurement of coronary flow velocity reserve (CFVR) by transthoracic Doppler echocardiography (TTDE) with invasive intracoronary Doppler flow wire technique (ICD) was validated and the pathological factors which influence CFVR in patients with angiographically normal coronary arteries were analyzed. CFVR was determined successfully in left anterior descending artery (LAD) in 37 of 40 patients with angiographically normal coronary arteries (men 22, women 15, age 20–75 years, mean age 54±12 years). Coronary flow velocity was measured in the distal LAD by TTDE with contrast enhancement at baseline and during intravenous adenosine infusion of 140 μg/kg per min within 48 h after ICD technique. Average peak velocity at baseline (APVb), average peak velocity during hyperemia (APVh) and CFVR determined from TTDE were correlated closely with those from ICD measurements (APVb: y=0.64x+5.04,r=0.86,P<0.001; APVh: y=0.63x+14.36,r=0.82,P<0.001; CFVR: y=0.65x+0.92,r=0.88,P<0.001). For CFVR measurements, the mean differences between TTDE and ICD methods were 0.12±0.39. CFVR in patients with history of hypertension was significantly lower than that in patients without history of hypertension (P<0.05). Intravascular ultrasound (IVUS) was performed in 34 patients. Plaque formation was found in LAD by IVUS in 17 (50%) patients. No significant difference in CFVR was found between the patients without plaque formation (3.11±0.49) and those with plaque formation (2.76±0.53,P=0.056). It is suggested that TTDE with contrast enhancement provides reliable measurement of APV and CFVR in the distal LAD. The early stage of atherosclerosis could be detected by IVUS, which may be normal in angiography. CFVR is impaired in patients with history of hypertension compared with that in patients without history of hypertension.

The chronological and spatial rules of changes during focal cerebral ischemia and reperfusion in different brain regions with magnetic resonance diffusion-weighted imaging (DWI) in a model of occlusion of middle cerebral artery (MCAO) and the development of cytotoxic edema in acute phase were explored. Fifteen healthy S-D rats with MCA occluded by thread-emboli were randomly divided into three groups. 15 min after the operation, the serial imaging was scanned on DWI for the three groups. The relative mean signal intensity (RMSI) of the frontal lobe, parietal lobe, lateral cauda-putamen, medial cauda-putamen and the volume of regions of hyperintense signal on DWI were calculated. After the last DWI scanning, T₂WI was performed for the three groups. After 15 min ischemia, the rats was presented hyperintense signals on DWI. The regions of hyperintense signal were enlarged with prolonging ischemia time. The regions of hyperintense signal were back to normal after 60 min reperfusion with a small part remaining to show hyperintense signal. The RMSIs of parietal lobe and lateral cauda-putamen were higher than that of the frontal lobe and medial cauda-putamen both in ischemia phase and recanalization phase. The three groups were normal on T₂WI imaging. DWI had good sensitivity to acute cerebral ischemia, which was used to study the chronological and spatial rules of development of early cell edema in ischemia regions.

Whether the localized flow acceleration occurs in the resting stenotic left anterior descending coronary artery was explored and its value for detection of coronary stenosis estimated. Blood flow in the left anterior descending coronary arteries in 45 patients was detected by transthoracic color Doppler echocardiograph and multipoint pulse Doppler spectrums were recorded in the same segment. The ratio of the maximal peak diastolic velocity to the minimal peak diastolic velocity was calculated. The ratio ≥1.5 was the cutoff value for the presence of localized acceleration flow. There were 23 patients with localized acceleration flow examined by echocardiography. Twenty of them were found to have luminal diameter stenosis (60%–98%) in the left anterior descending coronary arteries by coronary angiography and 3 patients were normal. There were 22 patients without localized acceleration flow examined by echocardiography. Eighteen of them had no or <60% stenosis. Four patients had serious stenosis (≥95%) or occluded segments in the left anterior descending coronary arteries on coronary angiography. The ratio of the maximal peak diastolic velocity to the minimal peak diastolic velocity was significantly higher in patients with left anterior descending coronary artery stenosis than that in those without stenosis (1.9±0.3 (vs 1.3±0.2,P<0.01) and it correlated significantly with left anterior descending coronary artery stenosis (r=0.77,P<0.01). The specificity by using the ratio≥1.5 for stenosis detection was 85.7% (18/21), and the sensitivity was 83.3% (20/24). This study demonstrated that local blood flow velocity was increased in the resting stenotic left anterior descending coronary artery. Transthoracic color Doppler echocardiography is a reliable noninvasive method to detect localized acceleration flow in the left anterior descending coronary artery stenosis and it is useful in the noninvasive diagnosis of stenosis in the left anterior descending coronary artery.

In order to study MR features of the regenerative nodule (RN) and dysplastic nodule (DN) of the cirrhotic liver, 26 cases of cirrhotic liver with RNs and DNs, of which 8 cases accompanied with hepatocellular carcinoma, were subjected to MRI. Eighteen of 26 cases underwent additional enhanced MRI with administration of Gd-DTPA on T1WI and 10 of the 18 cases did additional SPIO (Feridex) enhancement on T2WI. Clinical data showed normal level of α-fetoprotein in 18 cases except 8 cases accompanied with HCC. The results showed that 12 cases had RNs with nodules measuring <1 cm. The MR appearance of those RNs showed isointensity on T1WI and hypointensity on T2WI. The intensity of those RNs was isointense to the surrounding hepatic parenchyma on enhanced MRI with administration of Gd-DTPA or SPIO. Among the 14 cases of DNs, 8 cases had nodules measuring 1–3 cm in size and 6 had macroregenerative nodule measuring >3 cm. In 8 cases with DNs measuring 1–3 cm in size, 5 cases appeared hyperintense on T1WI and hypointense on T2WI as well as the enhancement as that of nodules with <1 cm in size; and the remaining 3 cases appeared hypointense on T1WI and hyperintense on T2WI, and were not isointense to the surrounding hepatic parenchyma on enhanced MRI but hyperintense on SPIO enhanced MRI. In 6 cases of macroregenerative nodule measuring >3 cm in size, 2 cases appeared hyperintense to the surrounding hepatic parenchyma on T1, T2WI and enhanced MRI; 4 cases showed hyperintense on T1WI, and hypointense on T2WI and enhanced MRI. Sometimes, normal vessels were seen to pass through the surface of macroregenerative nodules. It was suggested that RNs of cirrhosis had features on MRI that usually allow distinction from hepatocellular carcinoma but not always from dysplastic nodules (DNs). A helpful distinction between HCC and DNs is that the latter are almost never hyperintense on T2WI. Additionally, low grade DNs appear hypointense on SPIO enhanced MRI.

The different sera proteomic components between uremia patients and normal subjects were studied through two-dimensional gel electrophoresis technique. Immobilized pH gradient two-dimensional polyacrylamide gel electrophoresis (2DE), silver staining, ImageMaster 2D 5.0 analysis software, matrix assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF-TOF-MS) and IPI human database searching were used to separate and identify the proteome of the sera from the patients with uremia. The results showed that satisfactory 2DE patterns of the serum proteins were obtained. Twenty-six protein spots showed significant difference in quantity in uremia patients, and 20 protein spots were identified by MALDI-TOF-TOF-MS. It was concluded that good reproducibility could be obtained by applying immobilized pH gradient 2DE to separate and identify the proteome in serum, which provided the foundation for the further study on uremia toxins pertaining to protein.

The demand for knowledge of productive health and the current status of productive health services provided by relevant governmental institutions were qualitatively and quantitatively studied. The study identified the key factors that influenced the demand for the productive health services and results of the services. It also discussed the effective approaches to control, planning and sustainable development of the reproductive health services for the floating populations.

Data communication and sharing of five level network of Public Health Information System, i.e. nation, province, district (city), county, and town, as far as to the countryside level were described, and how to apply the three solutions, i.e. Access VPN, Intranet VPN, and Extranet VPN of VPN technique to achieve the appropriation of the public network was also presented.