Objective To explore the role of oxidative stress in the initiation and development of experimental diabetic nephropathy.Methods Levels of MDA and the total SOD activity were tested in the whole kidney at 1 month,3 months and 6 months of experimental rat diabetes induced by streptozotocin.The pathological changes of diabetic rats were examined by light microscopy.Results The MDA level increased significantly in the diabetic group as compared to control group at all time intervals(2.16?0.57 vs 1.18?0.18,P

Objective: To investigate the expressions of estrogen receptor (ER) subtypes and c-met proto-oncogene in human endometrial carcinomas and to assess the clinical significance of ER and c-met in this carcinoma. Methods: Reverse transcription PCR (RT-PCR) was used to detect the expressions of ERα, ERβ and c-met proto-oncogene mRNA in 30 samples of endometrial carcinoma and 11 samples of normal endometrium. Results: The expression of ERα in endometrial carcinoma (0.70±0.40) was significantly reduced in comparison to that in normal endometrium (1.14±0.56, P<0.05). A similar finding was made for the expression of ERβ in carcinoma (0.24±0.18) versus normal tissues (0.48±0.20, P<0.05). In contrast, c-met mRNA expression was increased in endometrial carcinoma (1.45±0.72) compared to that in normal endometrium (0.42±0.31, P<0.01). A decrease tendency of the expression of ERα was also found from Stage I (0.82±0.41) to a more severe Stag II-III of endometrial carcinoma (0.42±0.17, P<0.05). The analysis of ERα and ERβ mRNA revealed a decrease tendency from shallow to deep invasion of the uterine muscles (P<0.05). We found that the expressions of ERα and ERβ were negatively correlated with c-met proto-oncogene with a coefficient correlation of -0.63 (P<0.01) and -0.32 (P<0.05), respectively. Conclusion: ERα and ERβ are both involved in mutagenic action of carcinogen. C-met proto-oncogene plays an important role in the carcinogenesis and development of endometrial carcinoma. C-met and ER expressions show a negative correlation in the development of endometrial carcinoma.

Objective: To investigate the expressions of estrogen receptor (ER) subtypes and c-met proto-oncogene in human endometrial carcinomas and to assess the clinical significance of ER and c-met in this carcinoma. Methods: Reverse transcription PCR (RT-PCR) was used to detect the expressions of ERα, ERβ and c-met proto-oncogene mRNA in 30 samples of endometrial carcinoma and 11 samples of normal endometrium. Results: The expression of ERα in endometrial carcinoma (0.70±0.40) was significantly reduced in comparison to that in normal endometrium (1.14±0.56, P<0.05). A similar finding was made for the expression of ERβ in carcinoma (0.24±0.18) versus normal tissues (0.48±0.20, P<0.05). In contrast, c-met mRNA expression was increased in endometrial carcinoma (1.45±0.72) compared to that in normal endometrium (0.42±0.31, P<0.01). A decrease tendency of the expression of ERα was also found from Stage I (0.82±0.41) to a more severe Stag II-III of endometrial carcinoma (0.42±0.17, P<0.05). The analysis of ERα and ERβ mRNA revealed a decrease tendency from shallow to deep invasion of the uterine muscles (P<0.05). We found that the expressions of ERα and ERβ were negatively correlated with c-met proto-oncogene with a coefficient correlation of -0.63 (P<0.01) and -0.32 (P<0.05), respectively. Conclusion: ERα and ERβ are both involved in mutagenic action of carcinogen. C-met proto-oncogene plays an important role in the carcinogenesis and development of endometrial carcinoma. C-met and ER expressions show a negative correlation in the development of endometrial carcinoma.

Carcinoma, Squamous Cell ; genetics ; metabolism ; pathology ; Esophageal Neoplasms ; genetics ; metabolism ; pathology ; Gene Frequency ; Humans ; Lymphatic Metastasis ; Neoplasm Invasiveness ; Neoplasm Staging ; Polymorphism, Genetic ; Prognosis ; Proportional Hazards Models ; Risk Factors ; Survival Rate ; Tumor Necrosis Factor-alpha ; genetics ; metabolism

Animal Feed ; Animals ; Cysteamine ; Female ; Goats ; Mammary Glands, Animal ; growth & development ; physiology

Objective Choroidal neovascularization(CNV) is the main cause of blindness in over 50-years-old population. To establish an available CNV animal model is helpful for us to understand the pathogenesis and management of CNV. Purpose of present study was to observe the role of coagulation with different power of diode laser in laser-induced choroidal neovascularization model of Brown Norway (BN) rats. Methods Coagulation of 810 nm diode laser(8 - 10 spots for each eye) was performed in 36 male BN rats with the spot diameter 75 μm, shutter time 0. 1 s, power 120 mW, 140 mW and 160 mW, respectively, while 6 normal BN rats were used as contrast. CNV was evaluated by fundus examination, fundus fluorescein angiography (FFA), indocyanine green angiography(ICGA) and light microscope on day 1, 7, 14, 21, 28 and 56 after photocoagulation. Results CNV formed on the 7th day after photocoagulation in 120 mW, 140 mW and 160 mW groups and reached the peak on the 21st day according to FFA and ICGA manifestation. Incidence of CNV in 120 mW, 140 mW and 160 mW group was 51. 3%, 91. 8%, 88. 3% on FFA findings and 51.3%, 92.7%, 93.7% on ICGA findings, respectively. In 7 days after photocoagulation, inflammatory cells increased and CNV formed at the lesion. Photocoagulation plaque became thicker with pigment cells proliferating and migrating on 14 days. After that time, inflammatory cells decreased and more collagen fibers emerged. The CNV reminded till the 56th day after photocoagulation. Conclusion CNV model of BN rats can be successfully created using the different power of diode laser (from 120 through 160 mW). CNV rate under the laser coagulation with 140 mW is higher, indicating that the power of 140 mW may be a suitable parameter for diode laser-induced choroidal neovascularization model of BN rats.

Objective To detect the expression of CD133 in hepatic cell lines SMMC7721 and bcl-7402, and to investigate the possibility of CD133 as the surface marker of liver cancer stem cells. Methods The cell cycle and expression of CD133 in hepatic cell lines SMMC7721 and bcl-7402 were detected by flow eytometry. Magnetic cell sorting was used to isolate CD133-positive and CD133-negative cells. The differences in morphology, proliferation and differentiation between CD133-positive and CD133-negative cells were observed and analyzed by one-way ANOVA and u test. Results The percentages of CD133-positive cells in SMMC7721 and bcl-7402 cell lines were 0.7% -1.0% and 1.7% -8.9%, respectively. The percentages of CD133-positive cells in G0>/G1> phase in the 2 cell lines were 85.3% and 89.4%, which were significantly higher than CD133-negative cells and unsorted cells (F = 14.49, 38.84, P <0.05). The in vitro proliferation capability of CD133-positive cells was greater than that of CD133-negative cells and unsorted cells, especially during day 1-3 and day 5-7 (F =49.32,784.04, 89.91, 152.83, P < 0. 05). During the cultivation, the proportion of the CD133-positive cells decreased as time passed by, and the proportion of CD133-positive cells was nearly the same as unsorted cells on day 15 (u =O. 271, P <0.05). Conclusions CD133-positive ceils have strong capability of proliferation and differentiation in SMMC7721 and bcl-7402 cell lines in vitro. CD133 is one of the surface markers of liver cancer stem cells.

Objective Aliginic sodium diester(ASD) liposome was prepared and its aggregation stability was evaluated.Methods ASD liposome was made by reverse phase evaporating method from egg yolk lecithin,compared with blank liposome,the size distributions and mean particle diameters of ASD liposome and blank liposome were measured respectively before and after 40 hours heating under 37℃.Results Under the condition of n(PC)∶n(CHOL) = 1∶1,the mean size diameter of ASD liposome was 4.24?m.The mean size diameter of ASD liposome changed only 0.26?m after cultivation,however,the value of blank liposome was 1.35?m.Conclusion ASD loaded in the liposome enhanced the physical stability of the liposome.

Objective To investigate the effects of high flow hemodialysis (HFHD) on cardiac function in uremia patients. Methods A prospective randomized controlled study was conducted. Sixty patients who were diagnosed with uremia, taken maintenance hemodialysis (MHD) and 30 healthy controls admitted to the Second People's Hospital of Guiyang from December 2014 to June 2015 were enrolled. They were randomly divided into two groups:HFHD group (HFHD three times a week) and the routine hemodialysis group (HD group, HD three times a week), with 30 in each group. Patients in each group were received hemoperfusion and hemofiltration once a month. Before the treatment and 6 months after the treatment, venous blood from all the patients were collected for testing the brain natriuretic peptide (BNP), cardiac troponin T (cTnT) and the ultrasound cardiograph were done at the same period by a special person, the left ventricular end diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD), the left ventricular end diastolic volume (LVEDV), left ventricular end systolic volume (LVESV), left ventricular posterior wall thickness (LVPWT), interventricular septum thickness (IVST), early and late diastolic blood flow to the largest ratio (E/A), left ventricular ejection fraction (LVEF), left ventricular mass index (LVMI) were recorded. Results Compared with the health control group, BNP, cTnT, LVEDD, LVESD, LVESV, LVPWT, IVST were significantly increased, LVEDV were significantly lowered before treatment in the HD group and HFHD group. But no significant differences in the above indexes and E/A, LVEF, LVMI between two groups were found. Compared with the data before treatment, the BNP, LVPWT were significantly lowered after treatment in HD group [BNP (ng/L): 641.50±60.09 vs. 2676.20±454.30, LVPWT (mm): 10.57±1.16 vs. 12.57±1.41, both P < 0.05]. The BNP, LVPWT were significantly lowered in HFHD group as compared with HD group [BNP (ng/L): 253.10±48.77 vs. 641.50±60.09, LVPWT (mm): 9.29±1.08 vs. 10.57±1.16, both P < 0.05]; in addition, the cTnT, IVST, LVMI were significantly lowered after the treatment in HFHD group compared with those before treatment [cTnT (μg/L): 0.014±0.005 vs. 0.028±0.011, IVST (mm): 7.81±1.69 vs. 11.04±2.23, LVMI (g/m2): 149.10±15.77 vs. 158.70±17.25, all P < 0.05], and the LVEF were significantly increased in HFHD group as compared with those before treatment (0.574±0.068 vs. 0.528±0.082, P < 0.05). Conclusion HFHD has obvious advantages than the routine HD in improving cardiac function of uremia patients.

Objective To study the effect and mechanisms of berberine (BBR) on the proliferation of papillary thyroid cancer K1 cells induced by high glucose.Methods K1 cells were cultured under 5.5 mmol/L or 25 mmol/L glucose condition with or without different concentration of BBR (0,10,40 and 80 μmol/L) for 24 hours.The proliferations of K1 cells in each condition were detected by MTT.Western blot was used to measure the expression of nuclear factor erythroid 2-related factor 2 (Nrt2),phosphoinositide 3-kinase (PI3K),protein kinase B (Akt) and phosphorylated-Akt (p-Akt).The distribution pattern of Nrf2 in K1 cells was determined using immunofluorescent staining.Results Compared with 5.5 mmol/L condition,the proliferation rate [(126.64 ± 5.41) ％ vs (87.31 ± 3.67) ％],expression levels of PI3K (0.425 ±0.019 vs 0.272 ±0.039),p-Akt/Akt (0.446 ±0.021 vs 0.168 ±0.035) and Nrf2 (0.597 ± 0.014 vs 0.308 ± 0.026),and Nrf2 distribution (93.0％ vs 23.1％) in nuclear of K 1 cells under 25 mmol/L condition were significantly elevated,respectively (all P ＜0.01).Addition of BBR in 25 mmol/L condition dose dependently (10,40,80 μmol/L) lowered the proliferation rate of K1 cells [(111.76 ± 4.10)％,(70.03 ±2.18)％,(32.41 ±3.76)％ vs (126.64 ±5.41)％,all P＜0.05],and suppressed the expression of PI3K,p-Akt/Akt,Nrf2,and Nrf2 nuclear distribution (P ＜ 0.05).Conclusions BBR dose dependently inhibited the proliferation of high glucose-induced K1 cells.This effect was associated with the suppression on of PI3K/Akt signaling activation,Nrf2 expression and its nuclear translocation.