The effects of cigarette smoke extract (CSE) on the expression of heat stress protein 70 (Hsp70) in human bronchi smooth muscle cells were investigatedin vitro, and the changes in Hsp70 mRNA in the patients with chronic obstructive pulmonary disease and their significance were explored. Human bronchi smooth muscle cells were cultured with CSE at the different concentrations. The expression of Hsp70 mRNA and Hsp70 was detected by reverse translation-polymerase chain reaction (RT-PCR) and Western blotting respectively. Levels of Hsp70 mRNA and Hsp70 in lymphocytes from 20 patients with COPD and 20 healthy smoking control subjects were measured by RT-PCR and Western blotting. The results showed the expression of both Hsp70 mRNA and Hsp70 was decreased conformably in human bronchi smooth muscle cells treated with CSE at certain concentrationin vitro. The A values of the Hsp70 mRNA expression were 0.24±0.11 and 0. 42±0.13 respectively in COPD patients and healthy smoking controls with the difference being significant (P<0.01). There was also significant difference in theA values of the Hsp70 expression between COPD patients and healthy smoking controls (20.9±9.9 vs 44.8±15.3,P<0.01). The levels of Hsp70 mRNA had strongly positive correlation with Hsp70 protein (r=0.85,P<0.01). It was suggested that the expression of Hsp70 mRNA was in concordance with the expression of Hsp70, which could provide a basis on the study of Hsp70 gene regulation and Hsp70 gene in the development of COPD.

To explore the pharmacological effect of 3,4-dihydroxyacetophenone (DHAP) on the apoptosis of RAW264. 7 macrophage cells and the mechanism, RAW264. 7 macrophage cells were treated with 100 or 500 mg/L lipopolysaccharide (LPS), with or without 10⁻⁵ mol/LDHAP for 24 h. Trypan blue dye exclusion assay was used to assess cell viability. Cell apoptosis was morphological studied and flow cytometric assay was used. Tumor necrosis factor-α (TNF-α) level was measured by ELISA methods. IϰB protein was determined by Western blotting. Our results showed that in 100 mg/L LPS-stimulated macrophages, DHAP enhanced the cell apoptosis while in 500 mg/L LPS-stimulated macrophages, DHAP significantly inhibited the cell apoptosis. In both groups, DHAP increased the level of IκB but decreased the level of TNF-α. It is concluded that DHAP has dual effect on the apoptosis of RAW 264. 7 cells treated with different concentrations of LPS. This effect may be due to the inhibition of activation of NF-κB and autocrine production of TNFα. Our study suggests that DHAP may have anti-inflammatory effect on LPS-activated macrophages.

The effect of electroacupuncture (EA) on TRPM7 mRNA expression of focal cerebral ischemia in rats and further the role of EA in the relationship between TRPM7 and trkA pathway was investigated. Thirty SD rats were randomly divided into 5 groups: normal group, ischemia/reperfusion group, EA treated group (ischemic rats with EA treatment), TE infusion group (ischemic rats with EA treatment and TE buffer infusion), AS-ODN group (ischemic rats with EA treatment and antisense trkA oligonucleotide infusion). The stroke animal model was established by the modified method of middle cerebral artery occlusion. Antisense trkA oligonucleotide that blocked NGFs effects was injected into cerebroventricle before EA. The TRPM7 mRNA was detected by RT-PCR method. The results showed that there were low TRPM7 mRNA levels in cortex and hippocampus in normal group. Compared with normal group, TRPM7 mRNA expression was increased significantly in ischemia/reperfusion group (P<0.05). A significant reduction in the expression of TRPM7 mRNA was found in EA treated group in contrast to ischemia/reperfusion group (P<0.05). The expression of TRPM7 mRNA in AS-ODN group was remarkably increased compared with EA treated group and TE infusion group (P<0.05). The results indicated that TRPM7 channels in the ischemic cortex and hippocampus in rats might play a key role in ischemic brain injury. EA could reverse the overexpression of TRPM7 in cerebral ischemia/reperfusion rats. And the inhibitory effect of EA on TRPM7 channels might be through trkA pathway.

To study the expression of DNA repair enzyme hMTH1 mRNA and protein in hepatocellular carcinoma (HCC) tissues, tissues adjacent to the cancers, normal liver cells and hepatoma cell lines, and to investigate their function in the progress of HCC, semi-quantitative reverse-transcription polymerase chain reaction (RT-PCR) was employed to examine the expression of hMTH1 mRNA in matched HCC tissues (HT)/surrounding tissues (HST) of HCC, normal liver cell L02 and hepatoma cell lines SMMC7721, HepG2. hMTH1 protein was detected in corresponding HT as well as their HST by immunohistochemistry. Our results showed that the expression level of hMTH1 mRNA in HT was higher than that in HST (t=2.424,P<0.05). The expression level of hMTH1 mRNA in two hepatoma cell lines was higher than that in normal liver cell line (F=6.810,P<0.01). The expression of hMTH1 mRNA in SMMC7721 was similar to that in HepG2. hMTH1 protein was 88.2% (15 of 17) positive in HT and 82.4% (14 of 17) in HST. The protein level of hMTH1 in HT was correspondingly higher than in their HST (t=2.618,P<0.05). It is concluded that hMTH1 mRNA and protein were over-expressed in HCC and hepatoma cell lines. It may be one of the key events during the carcinogenesis, progression of HCC and may promote the malignant growth. These results suggest that hMTH1 plays a role in HCC and may be a candidate marker for the diagnosis of HCC.

To investigate the effects of ischemia-reperfusion on the levels of nitric oxide and nitric oxide synthase isoforms (nNOS and iNOS), rat organotypic hippocampus slice were cultured in vitro and subjected to ischemia by oxygen-glucose deprivation (OGD) for 30 min and then placed in the normal culture condition. The ischemia-reperfusion produced a time-dependent increase in nitrite levels in the culture medium. Reverse transcriptional-polymerase chain reaction showed augmented levels of mRNA for both nNOS and iNOS when compared with control at 12 h and remained increase at 36 h after OGD (P<0.05). The protein levels of both nitric oxide synthase isoforms increased significantly as determined by Western Blot. OGD also caused neurotoxicity in this model as revealed by the elevated lactate dehydrogenase (LDH) efflux into the incubation solution. The results suggest that organotypic hippocampus slice is a useful model in studying ischemia-reperfusion brain injury. NO and NOS may play a critical role in the ischemia-reperfusion brain damage in vitro.

To investigate the effect of P53 protein accumulation and p53 gene mutation in the pathogenesis of glioma and to study the role of MDM2, P53 and P16 protein in glioma formation and progression and their relationship with each other, LSAB immunohistochemical staining method and non-isotopic PCR-SSCP techniques were used to detect the expression of MDM2, P53 and P16 protein and p53 gene mutation in 48 cases of gliomas. The results showed that the positive expression rate of MDM2, P53 and the negative rate of P16 was 22.9%, 41.7% and 60.4%, respectively. The latter two in high grade (grade III, IV) gliomas had a significantly higher rate than in the low grade (grade II) gliomas. Moreover, the co-expression of MDM2 and P53 protein was confirmed in only 1 of 48 cases. No significant difference was found in the rate of the expression of MDM2 between high grade and low grade gliomas (P>0.1). PCR-SSCP results showed that mutation of 5–8 exons of p53 gene was detected in 17 out of 48 cases (35.42%). Mutation was detected in 16 of 20 cases of positive p53 expression, and another one was detected in 28 cases of negative expression cases. The correlation between p53 mutation and p53 mutation and p53 immunopositivity was observed in 89.6% of the cases. P53 gene mutation and the level of MDM2, P53 and P16 protein were not related to age, gender of the patients, tumor location and size. It is concluded that the mutation of p53 and deletion of p16 might play important roles in the tumorigenesis of gliomas and it was significantly associated with the grade of tumor differentiation. P53 protein accumulation can indirectly reflect p53 mutation. MDM2 amplification and overexpression might be an early event in the growth of human gliomas.

The effects of chloroquine on glial fibrillary acidic protein (GFAP), proliferation cell nuclear antigen (PCNA) and Cyclin D1 in hippocampus and cerebral cortex of rats with seizures induced by pentylenetetrazole (PTZ) were observed in the present study. Forty-eight male adult Sprague-Dawley (SD) rats were randomly divided into control group, chloroquine intervening group, and PTZ group. The behavior and electroencephalogram (EEG) were observed and recorded. GFAP and PCNA were examined with immunohistochemistry. The content of Cyclin D1 in hippocampus and cerebral cortex was inspected with Western blot. The results showed no seizure activity in the control group, severe seizure activity in the PTZ group (IV–V degree), and slight seizure activity (I–III degree) in the chloroquine intervening group (P<0.05). EEG recordings showed no epileptic spikes in the control group, high amplitude with fast frequency in the PTZ group, low-amplitude and slow frequency in the chloroquine intervening group. The expression of GFAP and the positive index of PCNA in the PTZ group were higher than those of control group (P<0.05 andP<0.01, respectively). No differences in GFAP expression and PCNA index were observed between chloroquine intervening and control groups (P>0.05). The content of Cyclin D1 in hippocampus and cerebral cortex was significantly higher in the PTZ group than in control and chloroquine intervening groups (P<0.05). Therefore, it is considered that chloroquine, by inhibiting the functions and proliferation of glial cells in the hippocampus and cerebral cortex, can alleviate the seizure activities. These results suggest that chloroquine may be an ideal anticonvulsant in preventing and treating epilepsy.

To investigate the expression of CD151 in human atherosclerosed artery and explore its clinical implications, Western blot and immunohistochemical techniques were used to determine the protein expression of CD151 in arterial tissues with atherosclerosis taken from 36 patients, including 26 cases who received bypass operation for peripheral artery atherosclerosis and 6 cases who died from coronary heart disease. The expression of CD151 in normal artery tissues from 15 healthy organ donators were also measured to serve as control. The results showed that expression of CD151 protein in atherosclerotic arteries was significantly higher than that in normal artery. In atherosclerotic arteries, CD151 expression was localized in vascular smooth muscle cells (VSMCs) in all tunica media and in partial subintima, while in normal artery, sparse expression was found in tunica media near adventitia. It is concluded that high CD151 protein expression in artery is associated with atherosclerosis and CD151 plays an important role in the atherosclerosis related to VSMC. The expression of CD151 in human atherosclerotic artery depends on the extent of atherosclerotic damage, its independent of risk factors.

To examine the protective effect of insulin on reoxygenation-induced injury and explore the underlying mechanisms, the model of anoxia/reoxygenation (A/R) injury was established by inducing anoxia for 2 h and reoxygenation for 4 h in cultured cardiomyocytes of neonatal rats. The rats were randomized to four groups receiving vehicle, insulin, LY294002, insulin plus LY294002 at the onset of reoxygenation after 2 h of anoxia. At the end of reoxygenation of 4 h, activity of lactate dehydrogenase (LDH) and content of malondialdehyde (MDA) were spectrophotometrically determined, apoptosis of cardiomyocytes were detected by using TUNEL and DNA Ladder, and Western blotting was employed to examine the expression of phosphorylated Akt in all groups. Our results showed that compared with vehicle-treated group, activities of LDH, contents of MDA, apoptosis index (AI) were significantly decreased, and expression of phosphorylated Akt was increased significantly in insulin-treated group. However, changes in LDH, MDA, AI and phosphorylated Akt resulting from insulin were attenuated or abolished by LY294002 (PI3K inhibitor). These data strongly suggest that early administration of insulin at reoxygenation protects cardiomyocytes from reoxygenation-induced apoptosis through PI3K/Akt signaling pathway.

The relationship between angiogenesis and eukaryotic translation initiation factor 4E (EIF4E) expression level in non-Hodgkin lymphoma (NHL) was studied. Mean microvessel density (MVD) and EIF4E were detected in 52 lymph node samples paraffin sections of patients with newly diagnosed NHL by the way of immunohistochemistry. Antisense EIF4E cDNA was cloned into plasmid pcDNA3. 1 (+) and transfected into Raji cells. A series of angiogenesis related factors, including vascular endothelial growth factor (VEGF), matrix metalloproteinases 9 (MMP-9) and tissue inhibitor of metalloproteinases-2 (TIMP-2) proteins were detected by Western blot. The results showed that: (1) The Expression of EIF4E and MVD was higher in aggressive lymphomas than in indolent lymphomas (P<0.05) and the expression of EIF4E was positively correlated with MVD in lymph node of NHL (r=0.695,P<0.01). (2) Antisense EIF4E eukaryocytic expression vector (pcDNA3. 1-EIF4Eas) was constructed successfully. (3) EIF4E, VEGF and MMP-9 were expressed at high levels in Raji cells as compared to normal human peripheral blood monocular cells (NHPMC), and blockage of EIF4E expression brought down the expression of VEGF and MMP-9. However, TIMP-2 was undetectable in Raji cells, although a moderate level of TIMP-2 was detected in NHPMC. It was concluded that the increased EIF4E expression was associated with aggressive property of NHL.

The plasma levels of inflammatory cytokine interleukin-6 (IL-6) and anti-inflammatory cytokine interleukin-10 (IL-10) in the patients with unstable angina or stable angina were determined and compared. In 30 patients with unstable angina and 22 patients with stable angina, plasma levels of IL-10 and IL-6 were detected by ELISA and plasma lipid parameters by lipid research clinical methods respectively. The results showed plasma levels of IL-10 were significantly lower in unstable angina group than in stable angina group (P=0.005), while those of IL-6 were significantly increased in unstable angina group as compared with those in stable angina group (P=0.039). There was a significantly negative correlation between IL-10 and IL-6 in patients with unstable angina (r=−0.41,P=0.003). In the unstable angina group, IL-6 levels were obviously positively correlated with TC (r=0.314,P=0.023), but not with TG and HDL. There were no significant correlations between IL-10 and plasma lipid parameters. It was suggested that the decreased IL-10 and increased IL-6 might be associated with the atheromatous plaque stability and progression of coronary heart diseases. IL-10 may play an important role in preventing coronary vascular lesions.

In this work, blank polylactic acid (PLA) nanoparticles with unstained surface were prepared by the nano-deposition method. On the basis of the preparation, the effect of surface modification on brain microvascular endothelial cells (BMECs) targeting was examined byin vivo experiments and fluorescence microscopy. The results showed that PLA nanoparticles are less toxic than PACA nanoparticles but their BMECs targeting is similar to PACA nanoparticles. The experiments suggest that drugs can be loaded onto the particles and become more stable through adsorption on the surface of PLA nanoparticles with high surface activity. The surface of PLA nanoparticles was obviously modified and the hydrophilicity was increased as well in the presence of non-ionic surfactants on PLA nanoparticles. As a targeting moiety, polysobate 80 (T-80) can facilitate BMECs targeting of PLA nanoparticles.

To study the effect of PD I administration on dopamine receptors (DR₁, DR₂) mRNAs expression in the lesioned striatum of the PD rat model and confirm if PD I has the effect of dopamine receptor agonist. The PD rats with unilateral 6-hydroxydopamine lesioned were administrated with PD I, L-dopa methyl/benserazide, L-dopa methyl/benserazide/PD I, normal saline respectively for 4 weeks and their behavioral changes were observed. Then the rats were sacrificed and RT-PCR technique was used to detect changes of dopamine receptors (DR₁, DR₂) mRNAs expression in the ipsilateral striatum 1 day after the last treatment. The results showed that treatment with PD I plus L-dopa resulted in a stable contralateral rotation behavior; treatment with L-dopa resulted in a progressively increased contralateral rotation behavior. Rotation behavior induced by anhydromorphine decreased with PD I or PD I plus L-dopa treatment. Treatment With L-dopa or PD I plus L-dopa, up-regulation of DR₁ mRNA and down-regulation of DR₂ mRNA were observed in the ipsilateral striatum which were more obvious than that treated with PD I or vehicle (P<0.05). It was concluded that long-term treatment with PD I could alleviate the behavior of PD rats. PD I had no apparent effect on the dopamine receptors (DR₁, DR₂) mRNAs expression in the ipsilateral striatum and the PD I has no agonist effect on dopamine receptors.

The aim of this investigation was to determine whether a PPARγ2 Pro12Ala polymorphism was associated with insulin resistance, β-cell function and hypertension in Chinese populations. 289 unrelated Chinese subjects first diagnosed Type 2 diabetes (HbAC1<6.0) were investigated, including 132 hypertensive diabetic (HTD) subjects, 157 normotensive diabetic (NTD) subjects. Blood pressure and anthropometric measurements were collected from all participants, as well as several venous blood samples during oral glucose tolerance test (OGTT). Biochemical measurements (high-density lipoprotein (HDL) and low-density lipoprotein-cholesterol (LDL), triglycerides) and PPARγ2 Pro12Ala genotype were also determined. And insulin resistance and β-cells function was assessed by HOMA-IR and HOMA-β respectively. The frequency of subjects bearing the Pro12Ala was lower in the hypertension group (3.03%) than in the non-hypertension group (5.7%) (P<0.05) after adjusted for age, BMI and gender. Hypertensive diabetic Pro12Ala subjects had lower fasting plasma glucose level (P=0.0127), and better glucose tolerance 60 min after oral glucose (P=0.0361). Moreover, plasma insulin concentrations at 60 min was lower than those without A variant (P=0.0275), and both hypertensive Ala/Pro in HOMA-β (P=0.0455) and AUC for insulin (P=0.0473) were higher, and HOMA-IR was lower (P=0.0375) as compared with hypertensive Pro/Pro subjects. No association was observed between Pro12Ala genotype and BMI, total cholesterol, HDL- cholesterol or triglycerides in either group. Our findings suggested that the Ala 12 allele of the PPARγ2 gene may improve insulin resistance and ameliorate β-cell function reserves in T2DM with hypertension, and protect patients from hypertension in T2DM. As an important thrifty gene, environment factors may exerts an effect of PPAR γ2 on glucose homeostasis and insulin resistance.

The expression of serum and glucocorticoid-induced protein kinase in the renal cortex of diabetic rats was examined, and the function of signal transduction mediated by SGK1 in diabetic nephropathy and its modulation by fluvastatin were also investigated. 24 male Wistar rats were randomly divided into normal control group (n=8), diabetic nephropathy group (n=8) and fluvastatin-treated diabetic nephropathy group (15 mg/kg/d,n=8). The metabolic parameters were measured at the 8th week. The expression of transforming growth factorβ₁ (TGF-β₁) and fibronectin (FN) was immunohistochemically examined. The expression of SGK1 was detected by RT-PCR and Western blot, and CTGF mRNA was assessed by RT-PCR. As compared to DN, blood glucose, 24-h urinary protein, Cer and kidney weight index were all decreased and the weight was increased obviously in group F. At the same time, mesangial cells and extracellular matrix proliferation were relieved significantly. The levels of cortex SGK1 mRNA and protein were up-regulated, and both TGF-β₁ and FN were down-regulated by fluvastatin. The mRNA of SGK1 was positively correlated with the CTGF, TGF-β₁, and FN. SGK1 expression is markedly up-regulated in the renal cortex of DN group and plays an important role in the development and progress of diabetic nephropathy by means of signal transduction. Fluvastatin suppressed the increased SGK1mRNA expression in renal cortex and postponed the development of diabetic nephropathy.

To construct the specific siRNA expression vectors and investigate their effect on leptin and collagen I in HSC, which provide a new approach to the prevent and treat hepatic fibrosis. The five siRNAs against leptin gene were transcript synthesized intracellularly by expression templates of plasmid vector psiRNA-hH1 neo. The recombinant leptin siRNA plasmid vectors could express in eukaryocyte, and then to evaluate them by using enzyme cutting and sequencing. The recombinant plasmids were transfected into HSCs using Lipofectamine methods respectively. The cells were selected after growing in DMEM containing 300 μg/mL G418 for about 4 weeks. Gene expression of leptin and collagen I were showed by Western blot analysis and reverse transcription polymerase chain reaction (RT-PCR). Identification by enzyme cutting and sequencing showed that the leptin siRNA expression vectors were constructed successfully, and leptin siRNA could inhibit the leptin and collagen I gene expression effectively. It was concluded that RNA interference-mediated silencing of leptin gene diminished leptin and collagen I gene expression in HSCs. Furthermore, attenuated the extracellular matrix over-deposition at the same time. Leptin gene is ideal targets of gene therapy for liver fibrosis.

Hypermethylation of the promoter region is one of the major mechanism of tumor suppressor gene inactivation. In order to provide a research tool for the study on the function of MBD1 gene in DNA methylation and tumorigenesis, antisense MBD1 gene eukaryotic expression plasmid was constructed and transfected into human biliary tract carcinoma cell line QBC-939 to observe its effect on the expression of MBD1 mRNA and protein by using RT-PCR and FCM respectively. Following the transfection, the mRNA level of MBD1 gene decreased from 0.912±0.022 to 0.215±0.017, and the protein level of MBD1 gene also decreased from (80.19±5.05) % to (35.11±4.05) %. There were very significant differences in the expression both at the transcription and post-transcription levels of MBD1 gene between non-tranfection group and the antisense MBD1 gene eukaryotic expression plasmid transfection group (P<0.01). It was suggested that transfection with the antisense MBD1 gene cukaryotic expression plasmid can significantly reduce the expression level of MBD1 gene in QBC-939, and this study may provide a valid tool for the investigation of the function of MBD1 gene and its role in biliary tract carcinoma.

To reverse multidrug resistance (MDR) of HepG2 by anti-MDR1 hammerhead ribozyme, an anti-MDR1 hammerhead ribozyme was developed and delivered to P-gp-overproducing human hepatocarcinoma cell line HepG2 by a retroviral vector containing RNA polymerase III promoter. The expression of mdr1/Pgp and Rz was detected in HepG2, HepG2 multidrug-resistant cell line and HepG2 Rz-transfected cells by semi-quantitative RT-PCR and Western blot methods. Moreover, MTT assay was employed to detect the sensitivity of these ribozyme-transfected cells, and Rhodamine 123 (Rh123) was used to test the function of Pgp. The Rz-transfected HepG2 cells became doxorubicin-sensitive, which was concomitant with the decreased MDR1 expression. The study showed that the retrovirus vector encoding the anti-MDR1 ribozyme may be applicable to the treatment of MDR cells.

To investigate the effects of IL-5 on the expression of TGF-β1 in eosinophilsin vitro, eosinophils were incubated in the presence of the same concentrations of IL-4, IL-5 and IFNγ, different concentrations of IL-5 in vitro and changes of eosinophil viability were assessed by trypan blue exclusion. Non-cytokine was employed as a negative control. 16 h after the cultivation, supernatants and cells were assayed by using TGF-β1 specific ELISA and RT-PCR. The mRNA expression and protein expression of TGF-β1 in eosinophils stimulated with different cytokines was observed. The expression of TGF-β1 protein in eosinophils was increased significantly by IL-4 (433.67±9.86 vs 228.9±2.87) and IL-5 (403.72±7.60 vs 228.9±2.87,P<0.05), while decreased by IFNγ (178.47±2.60 vs 228.9±2.87). At the same time, the results demonstrated that the basal level of TGF expression was enhanced by IL-5 in all samples (P<0.05). The expression of TGF-β1 mRNA was 1.42, 1.70, 1.76-folds higher than that of the non-stimulated controls. It is concluded that IL-5 can up-regulate the expression of TGF-β1 in eosinophilsin vitro, which might have effect in eosinophil-associated chronic rejection.

The curcumin prodrugs, which could be selectively activated in tumor cells, were prepared to establish a basis for the targeted chemotherapy for cancer. On the basis of the molecular structure of curcumin, the N-maleoyl-L-valine-curcumin (NVC), N-maleoyl- glycine-curcumin (NGC) were chemically synthesized and identified by IR and NMR spectroscopy. After treatment with these two prodrugs for 6–24 h, the rates of growth inhibition on human bladder cancer EJ cells and renal tubular epithelial (HKC) cells were detected by MTT colorimetry. Our results showed that after the treatment with 20 μmol/L–40 μmol/L NVC and NGC for 6–24 h, the growth inhibitory effects on EJ cells were 6.71%–65.13% (P<0.05), 10.96%–73.01% (P<0.05), respectively, in both dose- and time-dependent manners. When compared with the curcumin of same concentrations, the growth inhibitory effects of these two prodrugs on HKC cells were significantly decreased (P<0.01). It is concluded that activation of curcumin prodrugs via hydrolysis functions of cellular esterase could inhibit the growth activities of tumor cells, and reduce the side effects on normal diploid cells. This provided a novel strategy for further exploration of tumor-targeted chemotherapeutic drugs.

To study the expression and significance of the serine protease Omi/HtrA2 in prostate cancer and benign prostatic hyperplasia. The expression of Omi/HtrA2 was assayed by means of immunohistochemical technique in 41 prostate cancer (Cap), 20 benign prostatic hyperplasia (BPH) and 10 normal prostate (NP) specimens. Omi/HtrA2 expression was positive in 30 (73.17%) prostate cancer specimens, and the positive rate of Omi/HtrA2 was lower in well differentiated than in poorly and moderately differentiated groups (P<0.05). By contrast, the cells in normal prostate and benign prostatic hyperplasia groups showed no or weak expression of Omi/HtrA2. Prostate cancer cells in vivo may need Omi/HtrA2 expression for apoptosis, and that Omi/HtrA2 expression might be involved in prostate cancer development.

This study examined the effect of wild-type Smad3 gene on the osteoblastic differentiation of rat bone marrow-derived mesenchymal stem cellsin vitro. Bone marrow-derived mesenchymal stem cells (MSCs) were stably transfected with the complexes of pcDNA3. 0-Myc-Smad3 or pcDNA3. 0-Myc-Smad3ΔC and Lipofectamine reagent. Immunofluorescence staining was performed to evaluate the c-Myc signal in MSCs. The cell proliferation was detected by MTT method. To clarify the osteoblastic characteristics in stably transfected MSCs, alkaline phosphatase (ALP) mRNA and core binding factor α1 (Cbfa1) mRNA were investigated by RT-PCR, and ALP activity and mineralization were examined by p-nitrophenolphosphate method and alizarin red staining respectively. PD98059, a specific inhibitor of the ERK signaling pathway, was used to determine the role of ERK in Smad3-MSCs osteoblastic differentiation. c-Myc signal was detected in Smad3-MSCs and Smad3 ΔC-MSCs. The proliferation of Smad3-MSCs was slower than that of Smad3 ΔC-MSCs or V-MSCs. The relative levels of ALP mRNA and Cbfal mRNA in Smad3-MSCs, as well as ALP activity and mineralization, were markedly higher than those in Smad3 ΔC-MSCs or V-MSCs. Although ALP activity and mineralization were slightly lower in Smad3-MSCs treated with PD98059 than in those without PD98059 treatment, no significant difference was found between them (P>0.05). It is concluded that the wild-type Smad3 gene, which is a crucial component promoting bone formation, can inhibit the proliferation of MSCs and enhance the osteoblastic differentiation of uncommitted MSCs and the maturation of committed MSCs independent of the ERK signaling pathway.

To study the effect on regulation of cell cycle of osteosarcoma cell line MG63 tranceduced with exogenous p16ink4a and hRb1 genes, pIRES-p16ink4a-hRbl, PIRES-p16ink4a and pIRES-hRb1 plasmids were constructed by gene recombination technology. The recombinant plasmid was transferred into osteosarcoma cell line MG63 by metafectene, and the resistant clones were selected by G418 selective medium. mRNA and protein expression of osteosarcoma cell line were assayed by RT-PCR and Western-Blot respectively. Cell cycle and apoptosis were analyzed by subG1 flow cytometric. Cell proliferation was tested by MTT. In the genome of these transfected target cells, the expression of p16ink4a and hRb1 mRNA and protein were detected respectivelyin vitro. It was demonstrated with subG₁ flow cytometric analysis and MTT method that p16ink4a and hRb1 genes cooperation more significantly inhibited cell growth and induced a more marked G1 arrest and apoptosis than p16ink4a/hRb1 alone (P<0.01). Coexpression of exogenous p16ink4a with hRb1 broke the regulatory feedback loop of p16ink4a-cyclinD₁/CDK-hRb1 and played a more significant role in inhibiting cell growth as well as inducing cell apoptosis than p16ink4a or hRb1 did alonein vitro.

To investigate the estrogen receptor(ER) expression in cartilage cell in the development of osteoarthritis induced by bilateral ovariectomy in guinea pig and to find their relationship. 30 two-month-old female guinea pigs were randomly divided into two groups (n=15 each): sham operation (control) group and ovariectomized group (OVX); Scanning electorne microscope (SEM) and transmission electron microscope (TEM) were obtained to analysis the cartilage degeneration of the hind limb knee joint after 6 and 12 weeks of ovariectomy. Dextran-Coated-Charcoal (DCC) was taken to quantitively detect the expression of ER. The serum levels of estrogen and gestone were detected by immune contest assay. The results showed that ER do exist in the cartilages of the guinea pigs, with higher expression in the control group than in OVX group at the same time point (P<0.05). It was increased also at 12 th week after operation than that of preoperation. The blood serum levels of estrogen and gestone showed a similar tendency to the expression of ER. Joint cartilage degeneration detected by SEM and TEM could be found at 6 th week, but severe degenerative lesions at 12 th week in the OVX group compared with the control group (P<0.01). The data suggested that bilateral ovariectomy in guinea pig lead to severe osteoarthritis which mighgt be related to the lower serum level of estrogen and the downregulation of the expression of ER in the cartilage also.

To modify the surface property of poly lactide-co-glycolide (PLGA) by biomimetic mineralization to construct a new kind of artificial bone. PLGA films and 3-diamensional (3-D) porous scaffolds hydrolyzed in alkaline solution were mineralized in SBF for 14 days. The morphology and composition of the mineral grown on PLGA were analyzed with SEM, FTIR and XRD. The porosity of the scaffolds was detected by using the liquid displacement method. The compressive strength of the scaffolds was detected by using a Shimadzu universal mechanic tester. An obvious mineral coating was detected on the surface of films and scaffolds. The main component of the mineral was carbonated hydroxyapatite (HA) similar to the major mineral component of bone tissues. The porosity of the un-mineralized and mineralized porous scaffolds was (84.86±8.52) % and (79.70±7.70) % respectively. The compressive strength was 0.784±0.156 N/mm² in un-mineralized 3-D porous PLGA and 0.858±0.145 N/mm² in mineralized 3-D porous PLGA. There were no significant differences between the mineralized and un-mineralized scaffolds (P>0.05) in porosity and biomechanics. Biomimetic mineralization is a suitable method to construct artificial bone.

To study the effects of Icariin on expression of osteopontin (OPN) mRNA and type I collagen in rat osteoblastsin vitro and to explore its possible mechanisms in preventing osteoporosis. OB was isolated from calvaria of new-born new-born fetal Sprague-Dawley (SD) rats by means of modified sequential collagenase digestion and incubated in MEM medium and the cell morphology was observed under inverted phase contrast microscope, OB was identified by alkaline phosphatase (ALP) staining. Different concentration (0.1 μg/mL, 1.0 μg/mL, 10 μg/mL) of Icariin was added to the OB and incubated. The effect of Icariin on the proliferation and osteogenesis of OB was monitored by MTT analysis. The expression of type I collagen was estimated with immunohistochemistry techniques. The expression levels of mRNA of OPN in the cells in every group were examined by reverse-transcriptase polymerase chain reaction (RT-PCR). The expression of OPN mRNA and type I collagen was strengthened gradually with the increase of Icariin concentration and peaked with 10 μg/mL Icariin on the 5th day. Icariin could significantly promote the expression of OPN mRNA and type I collagen in rat osteoblastsin vitro. The levels of expression of OPN mRNA and type I collagen were changed with different concentration of Icariin. Icariin could effectively prevent and treat osteoporosis and promote the bone formation.

The heat shock proteins (HSPs) 70 and HSP 27 expression in patients with non-small cell lung cancer (NSCLC) was studied and the relationship between HSP 70 and HSP 27 with the clinicopathological features of NSCLC was investigated. The expression of HSP 70 and HSP 27 was detected in tumor tissues from 60 patients with NSCLC by S-P immunohistochemistry. The findings were analyzed in combination with the histological types, histopathological differentiation, lymph node metastasis, patients clinical stages, smoking history and gender. The results showed that of the 60 NSCLC tissue specimens studied, the immunoreactivity of HSP 70 and HSP 27 was detected in 47 (78.3%) and 43 (71.7%) specimens, respectively. A positive correlation was found between the overexpression of HSP 70 and HSP 27. The histopathological differentiation, lymph node metastasis, clinical stages and smoking history were correlated to the expression of HSP 70, but not to the expression of HSP 27. No statistical significance was observed in histological types and gender with respect to both HSP 70 and HSP 27 expression. It is suggested that the HSP 70 expression is a powerful and significant prognostic indicator and is related to histopathological differentiation, lymph node metastasis, patients' clinical stages, smoking history, whereas HSP 27 expression is not.

Neuropathic pain has been hypothesized to be the result of aberrant expression and function of sodium channels at the site of injury. To investigate the effects of NaV1.8 antisense oligonucleotide on the expression of sodium channel mRNA in dorsal root ganglion (DRG) neurons in chronic neuropathic pain. 24 Sprague-Dawley rats weighing 200–260 g were anesthetized with the intraperitoneal injection of 300 mg·kg⁻¹ choral hydrate. The CCI model was made by loose ligation of sciatic nerve trunk by 4-0 chromic gut. The mechanical and thermal pain threshold were measured before operation and 1, 3, 5, 7, 9, 11, 13 days after operation. A PE-10 catheter was implanted in subarachnoid space at lumbar region. On the 7th postoperative day the animals were randomly divided into 4 groups. The drugs were injected intrathecally twice a day for 5 consecutive days in group 2–4. The animals were decapitated 14 days after the surgery. The L4–L6 DRG of the operated side was removed and crushed, and total RNA was extracted with Trizol reagent. The contralateral side was used as control. The change of NaV1.8 sodium channel transcripts was determined by RT-PCR. Pain threshold was significantly lowered after CCI as compared with that in control group and was elevated 3 days after antisense oligonucleotide injection. Sensory neuron specific TTX-R sodium channel NaV1.8 transcript was down-regulated after antisense oligonucleotide injection at the dosage of 45 μg as compared with that in CCI group (P<0.01), and it was even greater at the dosage of 90 μg. The intrathecally injected NaV1.8 antisense oligonucleotide can reduce the mechanical allodynia and thermal hyeralgesia partially by downregulating the SNS transcript expression.

To investigate the effect of propofol on the release of glutamate and γ-aminobutyric acid (GABA) from rat hippocampal synatosomes, synaptosomes was made from hippocampus and incubated with artificial cerebrospinal fluid (aCSF). With the experiment of Ca²⁺-dependent release of glutamate and GABA, dihydrokainic acid (DHK) and nipectic acid were added into aCSF. For the observation of Ca²⁺-independent release of glutamate and GABA, no DHK, nipectic acid and Ca²⁺ were added from aCSF. The release of glutamate and GABA were evoked by 20 μmol/L veratridine or 30 mmol/L KCl. The concentration of glutamate and GABA in aCSF was measured by using high-performance liquid chromatography (HPLC), 30, 100 and 300 μmol/L propofol significantly inhibited veratridine-evoked Ca²⁺-dependent release of glutamate and GABA (P<0.01 orP<0.05). However, propofol showed no effect on elevated KCl-evoked Ca²⁺-dependent release of glutamate and GABA (P>0.05). Veratridine or elevated KCl evoked Ca²⁺-independent release of glutamate and GABA was not affected significantly by propofol (P>0.05). Propofol could inhibit Ca²⁺-dependent release of glutamate and GABA. However, it has no effect on the Ca²⁺-independent release of glutamate and GABA.

To assess the left ventricular longitudinal regional myocardial systolic function by strain imaging (SI) echocardiography and to study the relationship between regional myocardial systolic function and left ventricular structure in patients with hypertrophic cardiomyopathy (HCM). SI echocardiography were performed in 18 patients with HCM and 17 healthy subjects. For each wall, regional myocardial systolic strain was analyzed at the basal, mid, and apical level respectively. And the peak systolic strain was measured. Our results showed that the patients with HCM had reduced peak systolic strain at almost each segment of different walls when compared with healthy subjects. There was significant correlation between the mid-septum peak systolic strain and the thickness of IVS, so was the correlation between the mid-septum peak systolic strain and the IVS to LVPW thickness ratio. This study demonstrated that the left ventricular longitudinal regional myocardial systolic function was abnormal in HCM, and this kind of abnormalities existed extensively in hypertrophic and non-hypertrophic cardiac segments. The degrees of left ventricle hypertrophy and asymmetry are related to the myocardial regional systolic function in HCM.

To study the changes in every part of the β-adrenergic signal transduction pathway and their effects on ischemic preconditioning of rat myocardiumin vivo. SD rats were divided into three groups: IP group, I/R group and CON group. The IP group was further divided into PC1−, 2−, 3−, and PC1+, 2+, 3+ groups according to preconditioning procedure. The rats received surgical procedure and underwent left coronary artery occlusion and reperfusion. We analyzed the infarct size by TTC staining, measured serum myocardial enzymes, studied the β-AR Bmax and Kd by radioligand binding assay of receptors, checked the activity of AC and PKA by the method of biochemistry and examined the content of cAMP by radioimmunoassay. The infarct area was much smaller in the IP group than in the I/R group (P<0.001), while the enzymes were significantly higher in I/R (P<0.001). The Bmax of β-AR in IP was much higher than that in I/R (P<0.001), but no difference in Kd could be seen between IP and I/R groups. In IP, the activity of AC and PKA and the content of cAMP were higher than those in I/R (P<0.05, 0.002 and 0.001, respectively). In the procedure of preconditioning, the content of cAMP and the activity of PKA showed the characteristic of cyclic fluctuation. Ischemic preconditioning can protect the heart from necrosis and reduce endo-enzyme leakage. The system of β-adrenergic signal transduction pathway probably takes part in the protection effect of the IP, which might be clicited by the PKA.

To investigate a new kind of tumor tracer^99mTc-YIGSR developed from a five amino structure (YIGSR) of the Laminin-chain, which can bind to the laminin receptors of tumor specifically, and radiolabeled with MAG₃. (1) Preparation of the^99mTc-YIGSR probe: with S-Acetly-NH₃-MAG₃ as the chelator and with proper reductants YIGSR was labeled with^99mTc; (2) Cell culture and viability measurement: EAC was maintained in RPMI 1640 supplemented with calf serum; the trypan blue exclusion was applied to calculate the cell viability; (3) Study of the cell dynamic: The EAC's uptake of^99mTc-YIGSR and^99mTc-MIBI was observed at 37 °C and 22 °C, respectively. (1) The labeling efficiencies of^99mTc-YIGSR and^99mTc-MIBI were (62±3)% and (96±2)%, respectively; (2) The cell viability was declined with time of incubation; (3) At 37 °C, the EAC'S uptake of^99mTc-YIGSR and^99mTc-MIBI reached the peak of (43.16±2.4)% and (24.4±1.8)% at 60 min, respectively; and at 22 °C, the highest uptake was (26.5±2.1)% and (9.47±1.9)% at 60 min, respectively. Thein vitro study suggests that^99mTc-YIGSR is superior to^99mTc-MIBI in cell uptake and has potential value in tumor imaging.

Membrane-type 1 matrix metalloproteinase (MT1-MMP/MMP-14) plays crucial roles in tumor cell growth, invasion, and angiogenesis. To clarify whether the endogenously expressed MT1-MMP in metastatic human ovarian carcinoma cell lines SKOV3 plays a critical role in tumor cell invasiveness, antisense MT1-MMP cloned in cukaryotic expression vector pMMP14as was transferred into SKOV3 cells. 48h after transfection, decreased expression of endogenous MT1-MMP protein was detected in pMMP14as-transfected SKOV3 cells and the activation of pro-MMP2 was inhibited markedly. The mean percentage of invasive cells was (62.50±5.30)% in pMMP14as-transfected cells, which was obviously less than that (97.20±6.90) % in the control. Thus, antisense MT1-MMP effectively inhibited the endogenous MT1-MMP expression and the invasiveness in SKOV3 cells, suggesting that MT1-MMP may be a therapeutic target molecule for human invasive ovarian cancers.

To investigate the effect of magnesium sulfate on the fetal rats of FGR and the expression of caspase-3 in the placenta of maternal rat; To explore the mechanism of using magnesium sulfate to cure the FGR. Establish model of FGR by a way of passive smoking: giving the maternal rats different agent of magnesium sulfate by subcutaneous injection: low agent group (300 mg/kg). high agent group (600 mg/kg). Concentration of magnesium sulfate was monitored. The expression of caspase-3 was measured by RT-PCR and immunohistochemistry technology. Both of the concentrations of magnesium sulfate in high and low agents group are higher than the FGR group (P<0.01); the weight of the placenta and fetal rat in high agent group are higher than the FGR group (P<0.05 andP<0.01); the expression of mRNA and protein of caspase-3 in the two agent group is higher than the FGR group (P<0.05 respectively); concentration of magnesium sulfate in the maternal rat blood correlate to the weight of fetal rat (r=0.899,P=0.038) and the expression of caspase-3 in the placenta of maternal rat (r=−0.747,P=0.033;r=−0.915,P=0.001). The research suggests that the weight of fetal rat could be increased by treatment of magnesium sulfate. Because it would imfrmove the placental function by depressing the expression of caspase-3.

The purpose is to study the prophylactic and therapeutic effect of the traditional Chinese Medicine (TCM)-Jinyebaidu (JYBD) to guinea pig cytomegalovirus (GPCMV) intrauterine infection. The virus-free female and male guinea pigs were screened with nest-polymerase chain reaction (N-PCR). After inbred, pregnant guinea pigs were selected and divided into 3 groups randomly: 5 guinea pigs of the blank control group were not given either GPCMV or JYBD. 31 guniea pigs of the positive control group were inoculated 1 mL (10⁷ TCID₅₀) suspension of GPCMV intraperitoneal. 10 guniea pigs of the experimental group were inoculated GPCMV firstly and then perfused stomach with JYBD for 14 days, (Dosage in accordance with the modulus of the weight ratio of human to guniea pig). The effects of JYBD on the intrauterine infection of GPCMV were observed. The results showed that JYBD could decrease the maternal infection rate from 100% (31/31) to 50 % (5/10) (P<0.001), the intrauterine infection rate from 100% (72/72) to 75% (21/28) (P<0.001), and the rate of abnormal outcome of pregnancy from 64.4% (29/45) to 25.0% (7/28) (P<0.001), the infective symptoms being relieved. It can be concluded that traditional Chinese medicine-JYBD can prevent and treat GPCMV intrauterine infection, and can be expected a prophylactic drug for HCMV intrauterine infection.

To investigate the level of serum IL-10 in allergic rhinitis patients and the correlation between IL-10 and serum total IgE (TIgE). 50 allergic rhinitis patients and 30 normal subjects were involved in the study. The levels of serum IL-10 and TIgE were measured by enzyme-linked immunosorbent assay (ELISA), and the correlation between serum IL-10 and TIgE was analyzed. In the allergic rhinitis group, the levels of serum IL-10 and TIgE were 8.34±2.48 pg/mL and 142.6±28.2 KU_Λ/L. In the normal control group, they were 12.86±2.88 pg/mL and 47.2±12.2 KU_Λ. There were significant differences between the two groups (P<0.01); and the level of serum TIgE in the patients was negatively correlated with that of IL-10 (r=−0.46,P=0.02). The level of serum IL-10 was significantly decreased in allergic rhinitis patients, which was beneficial to the synthesization of IgE. IL-10 plays an important role in the episode of allergic rhinitis.

To observe the glial reactions surrounding facial motor neurons following facial nerve anastomosis. At 1, 7, 21 and 60 d following facial nerve anastomosis, the recovery process of facial movement was observed, the glial fibrillary acidic protein (GFAP) immunoreactivity was analyzed by a combined method of fluorescent retrograde tracing and immunofluorescent histochemical staining, and the ultrastructure of astrocytes were observed under a transmission electron microscope (TEM), respectively. Postoperatively the function of facial muscles could not return to normal, often accompanied with hyperkinetic syndromes such as synkinesis at the late stage. Motor neurons in every facial subnucleus could be retrogradely labeled by fluoro-gold (FG), and displayed an evident somatotopic organization. Normally there was a considerable number of GFAP-positive cells in non-nucleus regions but few inside the facial nucleus region. Postoperatively the GFAP immunoreactivity in the anastomotic side increased significantly, but gradually decreased at the late stage. The ultrastructure of astrocytes in our experiment showed that the sheet-like process of astrocytes invested and protected the injured facial motor neurons. The present study shows that reactive astrocytes undergo some characteristic changes during the process of facial nerve injury and regeneration. The plastic change at the late stage may be involved in the mechanism of synkinesis.

To study the effect of tTG fully phosphorothioated antisense oligodeoxynucleotides (tTG-ASDON) on tTG expression in cultured bovine trabecular meshwork cells (BTMCs)in vitro and explore a new treatment alternative for primary open angle glaucoma (POAG), the ASDON₁ and ASDON₂ complementary to the protein codogram region of tTG were designed, synthesized and phosphorothioated according to the secondary structure of tTG. The ASDON₁ and ASDON₂ were embedded in Lipofectamine and transfected into BTMCs. The untreated group served as negative controls. The expression of tTG in the mRNA and protein level were measured by semi-quantitative RT-PCR and immunohistochemical technique-Supervision method respectively. Our results showed that both the mRNA and the protein of tTG with tTG-ASDON₁ and tTG-ASDON₂ were significantly decreased as compared with that of the controls (P<0.05). On the other hand, no significant difference was found between the ASDON₁ group and the ASDON₂ group. It is concluded that the expression of tTG mRNA and protein in cultured BTMC are down-regulated by tTG-ASDON. As a result, tTG-ASDON may be used for the treatment of POAG through the inhibitory effect on the expression of tTG.

To evaluate the inhibiting effect of Homoharringtonine (HHT) on the corneal haze after excimer laser photorefractive keratectomy (PRK) in rabbits. 18 healthy rabbits which underwent PRK were randomly divided into three groups (A, B and C). The refractive degree of ablation was −10.0DS in each group. Group A was locally treated with a piece of filter paper soaked with 1 mg/mL HHT for 5 min, and then the entire cornea was repeatedly irrigated with balance solution: Group B was dropped with 0.1 mg/mL HHT after PRK for 3 months; Group C was the control group. Corneal haze, histopathology, response, ect. were investigated. The corneal haze was significantly less in group A, while the difference between group B and group C was insignificant. Keratocytes and fibrocytes in corneal stroma were more active up to 3 months in group B and group C. Intraoperative use of topical HHT can reduce corneal haze after PRK in rabbits.

To evaluate the effect of dexamethasone on the expression of aquaporin-1 (AQP-1) in cultured bovine trabecular meshwork cells, bovine trabecular meshwork cells were cultured in vitro and reproduced to the third and the fourth generation, then treated with dexamethasone at the concentrations of 5, 25, 50, 250 μg/L respectively for 7 days. Immunohistochemical technique-supervision method was employed to measure, and image analysis system to analyze the expression of AQP-1 in normal cultured bovine trabecular meshwork cells and those treated with dexamethasone. In normal bovine trabecular meshwork cells, the grayscale of AQP-1 positive staining was 167.94±1.18, while it was 168.92±0.91, 176.72±1.80, 180.64±1.31, 185.64±1.58 in cells treated with 5, 25, 50, 250 μg/L concentrations of dexamethasone. When the concentration of dexamethasone was higher than 25 μg/L, the expression of AQP-1 was significantly inhibited (P<0.05). The regulation of AQP-1 expression by dexamethasone in cultured bovine trabecular meshwork cells in vitro may be one of causes that retard the aqueous outflow in glucocorticoid- induced glaucoma.

In this study, the effect of cyclosporin A (CsA) eye drop on keratoconjunctivitis Sicca (KCS) and its mechanism were studied. The KCS models were established by injecting Pertussis vaccine, complete freund's adjuvant (CFA) and antigen of conjunctiva from isotype mice. Then the KCS models were treated with cyclosporin A eye drop. Changes in breaking-up time (BUT), lacrimal secretion in 30 min and diversion in 24 h were measured. The percentage of beaker cells, the lymphocytic infiltration in conjunctiva were observed. The expression levels of Aquaporin-3 (AQP3) in conjunctiva epithelial cells, beaker cells and accessory lacrimal gland were immunohistochemically detected. The results showed that there were significant differences in BUT, the percentage of beaker cells, lacrimal secretion in 30 min, the lymphocytic infiltration and the expression of AQP3 between the experimental group and an control group. It was concluded that CsA eye drop exerts marked therapeutic effect on KCS by inhibiting T lymph cells, increasing the goblet cells and AQP3 expression in conjunctiva.

To detect the expression of telomerase subunits (human telomerase reverse transcriptase, human telomerase associated protein 1 and human telomerase RNA) in gastric cancer and to examine the role that different telomerase subunits play in the gastric carcinogenesis, reverse transcription-polymerase chain reaction (RT-PCR) was used to detect telomerase subunits messenger RNA in 24 samples of gastric cancer and corresponding non-cancerous tissue. The results showed that the positive rate of hTERT mRNA from gastric cancer and corresponding non-cancerous tissues was 100% and 25%, respectively. The former was significantly higher than the latter (χ²=26.4,P<0.01). The positive rate of hTEP1 mRNA from gastric cancer and corresponding non-cancerous tissues was 100% and 91.7%, respectively and no significant difference was found between them (χ²=2.1,P>0.05). The positive rates of hTR for gastric cancer and corresponding non-cancerous tissues were both 100% and no significant difference existed between them. It is concluded that in contrast to hTEP1 and hTR, the up-regulation of hTERT mRNA expression may play a more important role in the development of gastric cancer.

In order to study the susceptibility of murine vaginal mucosa to Candida albicans under different conditions, vaginal lavage fluid and vaginal tissue of mice were observed and compared between murine models with normal immune system (estrogen-treated mice) and immunosuppressed murine model, and between primary infection model of vaginal candidiasis and secondary infection one. The average level of colony forming unit (CFU) from the immunosuppressed group was higher than that from estrogen-treated group at each time point and the peak time was delayed. The differences between the two groups were statistically significant (P<0.05) from the fourths day after inoculation. A significant difference existed in the average level of CFU between the control group and the estrogen-treated group (P<0.05), and between the control group and the immuosuppressed group (P<0.01). It was concluded that the vaginal mucosa from the immunosuppressed mice is more susceptible to Candida albicans and no difference is found in susceptibility between mice with primary infection and secondary infection.