OBJECTIVE: To conduct a meta-analysis to determine the efficacy of peginterferon alpha (PEG-IFN α) therapy versus IFN α, adefovir dipivoxil (ADV) and entecavir (ETV) for HBeAg-positive chronic hepatitis B patients in China. METHODS: MEDLINE database and 3 main Chinese biomedical databases between 1966 and 2012 was retrieved. Two reviewers independently screened all reports to identify randomized controlled trials that evaluated PEG-IFN α therapy for the treatment of chronic hepatitis B in China. RESULTS: Fourteen trials met the eligibility criteria for this Meta analysis. PEG-IFN α therapy was more effective than IFN α therapy in achieving ALT normalization, serum HBV DNA clearance, HBeAg seroconversion, serum HBeAg clearance and fibrosis improvement in Chinese hepatitis B patients (P<0.05). PEG-IFN α was obviously superior to ETV in HBeAg seroconversion and serum HBeAg clearance (P<0.05), but the seroconversion rate was low. The combination therapy of PEG-IFN α and ADV was more effective than ADV monotherapy in ALT normalization, serum HBV DNA clearance and HBeAg seroconversion (P<0.05). PEG-IFN α showed no priority to other treatment regimes in HBsAg clearance. CONCLUSION Treatment with PEG-IFN α is safe and effective, and can be prescribed as firstline treatment options for chronic hepatitis B patients in China. Data are too limited to exclude a substantial benefit or harm of PEG-IFN α combination therapy for CHB patients in China.
Adenine ; analogs & derivatives ; therapeutic use ; Antiviral Agents ; therapeutic use ; China ; Drug Therapy, Combination ; Guanine ; analogs & derivatives ; therapeutic use ; Hepatitis B Surface Antigens ; Hepatitis B e Antigens ; Hepatitis B, Chronic ; drug therapy ; Humans ; Interferon-alpha ; therapeutic use ; Organophosphonates ; therapeutic use ; Polyethylene Glycols

Objective:To summarize the relationship between the clinicopathological features and prognosis of immunoglobulin A nephropathy (IgAN) after renal transplantation.Methods:A total of 34 patients with IgAN after renal transplantation confirmed by renal biopsy were enrolled. And another 34 patients with primary IgAN confirmed by initial renal biopsy were adopted as controls. Clinical and pathological features of two groups were compared to explore the relationship between clinicopathological features and prognosis of allograft IgAN.Results:As compared with primary IgAN group, renal function in allograft IgAN group included serum creatinine [(158.5±75.9) vs (84.8±26.8) umol/L], urea nitrogen [(9.7±6.1) vs (5.2±1.4) mmol/L], uric acid [(406.7±87.8) vs (359.0±92.6) umol/L], estimated glomerular filtration rate {(57.4±25.4) vs (91.2±28.6) [ml/(min·1.73m 2)]}. All were statistically significantly higher ( P<0.05) while other parameters showed no differences. Pathologically, the proportion of T1 type (50.0% vs 17.6%) of renal tubular atrophy/interstitial fibrosis was significantly higher in allograft IgAN group than control group ( P<0.05). Furthermore, univariate and multivariate Logistic regression analyses were performed between various pathological parameters and prognosis in allograft IgAN patients. It indicated that the degree of mesangial hyperplasia of patients with transplanted IgAN had a significantly negative impact on the prognosis. Conclusions:The clinicopathological features of patients with allograft IgAN show no difference from those of patients with primary IgAN. And among patients with allograft IgAN, those with severe mesangial hyperplasia often have a worse prognosis.

Objective: To explore mechanism of lung injury of rats induced by inhalation of white smoke from burning smoke pot. Methods: Forty-eight Sprague Dawley rats were divided into control group (n=12) and injury group (n=36) according to the random number table. Rats in injury group were placed in smoke-induced injury experimental equipment fulled with white smoke from burning smoke pot for 5 minutes to make lung injury, and rats in control group were placed in smoke-induced injury experimental equipment fulled with air for 5 minutes to make sham injury. Six rats in injury group at post injury hour (PIH) 6, 24, and 72 and six rats in control group at PIH 72 were collected to observe pathological changes of lung tissue and pathological score of rats in the two groups by hematoxylin-eosin staining, to detect expression of nuclear factor-κB (NF-κB) p65 mRNA in lung tissue of rats by reverse transcriptional polymerase chain reaction, and to detect content of tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and IL-6 in lung tissue of rats by enzyme-linked immunosorbent assay. Data were processed with one-way analysis of variance and t test. Results: At PIH 72, lung tissue structure of rats in control group was clear and complete, with no inflammatory cell infiltration. At PIH 6, there was edema, hemorrhage, and inflammatory cell infiltration in lung tissue of rats in injury group. At PIH 24, edema, hemorrhage, and inflammatory cell infiltration in lung tissue of rats in injury group aggravated. At PIH 72, area of edema in lung tissue of rats in injury group was enlarged, with obvious hemorrhage and inflammatory cell infiltration. At PIH 6, 24, and 72, pathological score of lung tissue of rats in injury group was (3.43±0.86), (5.39±0.93), and (9.99±0.84) points, respectively, obviously higher than that of rats in control group at PIH 72 [(2.11±0.20) points, t=3.659, 8.450, 22.355, P<0.05]. As time post injury prolonged, pathological scores of lung tissue of rats in injury group were significantly increased (F=121.244, P<0.01). At PIH 6, 24, and 72, expression of NF-κB p65 mRNA in lung tissue of rats in injury group was 15.5±4.3, 25.9±1.8, 30.9±3.5 respectively, significantly higher than that of rats in control group at PIH 72 (7.8±0.8, t=4.315, 20.445, 14.408, P<0.01). As time post injury prolonged, expression of NF-κB p65 mRNA in lung tissue of rats in injury group gradually increased (F=32.691, P<0.01). At PIH 6, 24, and 72, content of TNF-α, IL-1β, and IL-6 in lung tissue of rats in injury group was significantly higher than that of rats in control group at PIH 72, respectively (t=7.650, 8.968, 6.827, 6.726, 8.978, 3.460, 5.420, 13.289, 16.438, P<0.01). At PIH 24, content of TNF-α and IL-1β in lung tissue of rats in injury group was higher than that of rats in the same group at PIH 6 and 72, respectively (t=3.409, -2.549, 4.047, -4.100, P<0.05). At PIH 24 and 72, content of IL-6 in lung tissue of rats in injury group was respectively higher than that of rats in the same group at PIH 6 (t=8.273, 9.711, P<0.05). Conclusions After inhaling white smoke from burning smoke pot, rats are inflicted with lung injury by increasing expression of NF-κB p65 mRNA and content of TNF-α, IL-1β, and IL-6, and induce pathological changes of edema, hemorrhage, and inflammatory cell infiltration of lung tissue.

OBJECTIVE: To determine the effect of transforming growth factor-β1 (TGF-β1) on the expression of telomerase in hepatic stellate cells (HSCs) in rats and the role of TGF-β1 in the development of liver fibrosis. METHODS: Primary HSCs were isolated from normal rats by density gradient separation and divided into 2 groups for culturing. The morphology of HSCs was identified by the inverted fluorescence microscope. The purity of HSCs was identified by immunohistological expression and fluorescence analysis. One group of HSCs was treated with different concentrations (0, 0.1, 1, and 10 ng/mL) of TGF-β1 for 24 h, while the other group was treated with 1 ng/mL TGF-β1 and cultured for 3, 6, and 9 days. The mRNA expression of telomerase reverse transcriptase (TERT) was assessed and compared by polymerase chain reaction. RESULTS: Cell morphology showed that TGF-β1 triggered the differentiation of HSCs from a quiescent phenotype into highly activated myofibroblasts. TERT mRNA expression in the primary HSCs showed slight increase with the culture time, though with no statistical difference between the results at various time points (P>0.05). TGF-β1 at 0.1 ng/mL did not significantly affect the TERT mRNA level compared with the 0 ng/mL group, while 1 ng/mL and 10 ng/mL TGF-β1 significantly decreased the level of TERT mRNA (P<0.05). TGF-β1 at 1 ng/mL had only weak effect on TERT mRNA expression after the 3 day treatment compared with the 0 ng/mL group (P>0.05). TGF-β1 at 1 ng/mL significantly inhibited TERT mRNA expression 6 days after the treatment (P<0.05). TGF-β1 inhibited the expression of TERT mRNA level in the HSCs in both dose- and time-dependent manner. CONCLUSION TGF-β1 may contribute to the transdifferentiation of HSCs by reducing TERT levels to develop hepatic fibrosis.
Animals ; Cell Transdifferentiation ; Cells, Cultured ; Hepatic Stellate Cells ; drug effects ; metabolism ; RNA, Messenger ; Rats ; Telomerase ; metabolism ; Transforming Growth Factor beta1 ; pharmacology