Congresses as Topic ; Humans ; Liver Diseases

Objective To study the expression changes of matrix metalloproteinases (MMPs), protein kinase C (PKC) and nuclear factor-?B (NF-?B ) on the injured rabbit vascular smooth muscular cells (VSMC) transfected with tissue inhibitor of metalloproteinase-2 (TIMP-2) vector. Methods Lipofectin method was used to transfect TIMP-2 vector into VSMC, Western blot analysis to detect TIMP-2 peptides and zymography assay to determine MMPs. The activities of MMPs and NF-?B were detected by electrophoretic mobility shift assay (EMSA). The mRNA and protein expressions of PKC? were determined by RT-PCR and immunocytochemistry. Results The injured VSMC showed increased enzyme activity of MMP-2. There was very lower level expressions of PKC? and NF-?B in the normal VSMC but high in the injured VSMC. However, in injured VSMC transfected with TIMP-2 vector, the activity of MMP2/9 was suppressed and the expressions of PKC? and NF-?B decreased (P

Objective To investigate the effects of electrical stimulation on the expression of vascular endothelial growth factor(VEGF)mRNA and receptor FLK 1/KDR in a ischemic model of rat hindlimb. Methods The model of hindlimb ischemia on the right side was established by ligation of the superficial femoral artery in 10 rats. The rats were then randomized into an experimental group and a control group. The rats in the experimental group were intervened with electrical stimulation ( 25 Hz, 0.1 V) on the tibialis anterior (TA) of the right side, while those in the control group were not. RT PCR and immunohistological methods were used to detect the expressions of VEGF mRNA and protein in TA muscles. FLK 1/KDR was detected by means of Western blot and immunofluorescence. Results After 7 days of continuous stimulation, there was a significant increase in blood flow within the muscle. VEGF mRNA and VEGF protein had 4 fold and 2 fold increases, respectively, in the stimulated TA muscles as compared to the control(2.58 vs 0.93, 0.48 vs 0.24, P

Antineoplastic Agents ; adverse effects ; therapeutic use ; Diarrhea ; chemically induced ; Drug Delivery Systems ; methods ; Exanthema ; chemically induced ; Humans ; Leukopenia ; chemically induced ; Lung Diseases, Interstitial ; chemically induced ; Myocardial Infarction ; chemically induced ; Neoplasms ; drug therapy ; Tumor Lysis Syndrome ; etiology

Firing patterns of injured nerve fibers were recorded using the single-fiber firing recording technique. Under the same background firing pattern, three types of bursting were induced separately by EGTA, veratridine or high [Ca(2+)](o) in the same type of nerve fibers. The results suggest that different firing patterns are related to different stimuli, which means that each firing pattern carries corresponding neural information.
Action Potentials ; Animals ; Calcium ; pharmacology ; Egtazic Acid ; pharmacology ; Nerve Fibers ; drug effects ; pathology ; Rats ; Veratridine ; pharmacology

Hepatitis ; therapy ; Humans ; Liver Failure ; therapy ; Liver, Artificial

Humans ; Liver Failure ; complications ; therapy ; Prognosis

Hemoperfusion ; Humans ; Liver Failure ; therapy ; Liver, Artificial

Hepatocytes ; cytology ; Humans ; Liver Failure ; therapy ; Liver, Artificial

OBJECTIVEBased on the potential for nucleotide analogues to affect DNA polymerase-gamma, which controls the proliferation of mitochondria, this study aimed to determine whether long-term treatment with entecavir can cause damage to mitochondrial (mt)DNA in the peripheral blood mononuclear cells (PBMCs) of patients with chronic hepatitis B (CHB).

METHODSPatients with CHB were divided into three groups according to their history of treatment type and duration: (1) entecavir monotherapy for 2 years, n = 17; (2) entecavir monotherapy for 3 years, n = 17; (3) non-antiviral treatment as control, n = 18. PBMCs were isolated and used to assess the mtDNA content by quantitative real-time PCR of mitochondria-specific genes. Plasma malonaldehyde (MDA) and F2-isoprostanes were measured by enzyme linked immunosorbent assay. Plasma total antioxidant capacity (TAOC) was detected by spectrophotometry.

RESULTSThe relative quantity (RQ; of mtDNA to nuclear (n)DNA) was significantly lower in the 3-year treatment group (0.5+/-0.3) than in the control group (1.4+/-1.2; F = 5.233, P = 0.009). The RQ was also significantly lower in the 2-year treatment group (0.4+/-0.2) than in the control group (P = 0.004). The level of F2-isoprostanes (ng/mL) was significantly lower in the 3-year treatment group (1.2+/-0.5) than in the control group (3.6+/-2.9, P = 0.002) or the 2-year treatment group (2.4+/-1.3, P = 0.007). The TAOC was significantly different when compared among all three groups (F = 4.326, P = 0.019). The TAOC (IU/mL) in the 3-year treatment group (2.6+/-1.2) was significantly lower than in the control group (5.0+/-3.0 P = 0.005), but was not significantly different than that for the 2-year group (3.2+/-1.6, P = 0.227). The levels of MDA were not significantly different between any of the groups (F = 0.291, P = 0.749).

CONCLUSIONLong-term treatment with entecavir, up to 3 years, leads to decreased mtDNA content in PBMCs. Since no clinical manifestations of mtDNA toxicity were observed, the consequent damage to the mitochondrial function may be compensated for by yet unknown mechanisms.

Adult ; Antiviral Agents ; adverse effects ; DNA Damage ; drug effects ; DNA, Mitochondrial ; drug effects ; Female ; Guanine ; adverse effects ; analogs & derivatives ; Hepatitis B, Chronic ; blood ; Humans ; Leukocytes, Mononuclear ; cytology ; Male ; Middle Aged