[Detection and clinical significance of serum HBeAg and HBeAg/IC during the treatment of chronic hepatitis B patients with lamivudine].
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Publications and source records attributed to Hong Zhang.
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OBJECTIVE: To investigate the role of phospholipase A(2) (PLA(2)) in injury of lung complicated by acute pancreatitis (AP) and the therapeutic effect of verapamil, furthermore to explore its possible mechanism. METHODS: Eighty-two Sprague-Dawley rats both male and female were divided into three groups. AP was induced by injecting 3% sodium deoxycholate (1 ml/kg) into the biliopancreatic duct except the rats of sham operation group. Ten minutes after operation, rats were injected intraperitoneally with saline or verapamil, respectively. At 4 hours and 8 hours after treatment, the volume of as cites and pulmonary coefficient were measured. The amylase activity and calcium concentration in plasma and PLA(2) in ascites and homogenate of lung were determined. The survival time and mortality of rats in different groups were recorded, and the pathomorphism of pancreas and lung was observed under microscope. RESULTS: Verapamil reduced the mortality (P<0.05), and prolonged the survival time of rats with AP significantly (P<0.05), attenuated ascites volume, amylase activity and hypocalcemia in plasma, PLA(2) activity in ascites and lung homogenate, and ameliorated the inflammatory injury of pancreas and lung. CONCLUSION: The results suggest that PLA(2) plays a role in the injury of lung complicated by AP and verapamil possesses a therapeutic effect on the AP induced by sodium deoxycholate in rats, in which the mechanism might be due to inhibit PLA(2) activity by blocking calcium channel to ameliorate the damage of pancreas and lung which is induced by the overload of Ca(2+).
OBJECTIVE: To study the role of a protease inhibitor (ulinastatin) in protection of lung damage following hepatic ischemia/reperfusion in rat. METHODS: Thirty-two healthy male SD rats were randomly divided into four groups (n=8 in each group). Group A was served as sham-injury control group, group B rats were subjected to 90 minutes hepatic ischemia, and group C rats underwent 120 minutes reperfusion after 90 minutes ischemia of the liver. Ulinastatin (UTI) was administered to animals in group D which were reperfused 120 minutes after 90 minutes of ischemia of the liver. In addition to plasma malondialdehyde (MDA), broncho-alveolar lavage fluid protein (BALFP) content, and lung dry-to-wet weight ratios (D/W) were respectively examined in each group. The concentration of myeloperoxidase (MPO) in lung tissue was also measured. RESULTS: Compared to group A, plasma MDA, content of MPO in lung tissues and BALFP were significantly increased in both group B and group C, but they were much lower than those in group D. In addition, D/W was markedly decreased during hepatic ischemia and after 120 minutes reperfusion, while it was significantly increased in animals pretreated with UTI. CONCLUSION: Acute lung injury after hepatic ischemia and reperfusion is mainly induced by the oxidant stress, and neutrophil infiltration in the lung tissues is responsible for the damage under these conditions. Proteases inhibitors such as UTI might have antioxidation effects which attenuate lung injury induced by trauma to remote organs.
AIM: To investigate the effects of lipopolysaccharides (LPS, endotoxin) on the calcium content in pancreatic acinar cells and the origin of Ca2+ during calcium overload induced by LPS, further to explore the mechanism of LPS in inducing calcium overload and pancreatic acinar cell injury. METHODS: Male rat pancreatic acinar cells were isolated by collagenase digestion and loaded with Fluo-3/AM, then exposed to varying doses of LPS (from 1 mg/L to 20 mg/L). The dynamic change of [Ca2+]i in single pancreatic acinar cell in the absence and presence of Ca2+ in extracellular fluid was determined by laser scanning confocal microscopy. Cell viability was determined by MTT at different time points after treatment with LPS. RESULTS: Under physiological calcium concentration in extracellular fluid, LPS (10 mg/L) initiated a rapid, concentration-dependent rise in intracellular [Ca2+]i and consequent cell damage (P<0.05). LPS induced a slight rise of [Ca2+]i in the calcium-free extracellular fluid containing egtazic acid 1 mmol/L and addition of extracellular calcium in the presence of LPS resulted in a more immediate and remarkable rise of [Ca2+]i, which reached the peak value within 150 s and maintained the value sustainedly. Egtazic acid attenuated LPS-induced cell damage (P<0.05). The increase in intracellular [Ca2+]i preceded the pathological alteration of pancreatic acinar cells. CONCLUSION: LPS directly induced the injury and the disorder of calcium homeostasis in isolated rat pancreatic acinar cell. Calcium overload is an early event in the pathogenesis of LPS-induced cell damage. Origin of the [Ca2+]i in cytoplasma of pancreatic acinar cells during calcium overload is mainly due to the influx of extracellular Ca2+. Calcium homeostasis disorder may be one of the causes or at least an important mediator of LPS-induced pancreatic acinar cell damage.
OBJECTIVE: To explore the significance of the panel-reactive antibody (PRA) detection in renal transplantation. METHODS: Enzyme-linked immunosorbent assay (ELISA) was used to measure the PRA levels in 641 patients with renal transplantation, of whom 570 were examined preoperatively while 71 postoperatively. RESULTS: Of the 570 cases examined preoperatively for PRA levels, 490 cases were negative of PRA in which acute rejection occurred in 35 cases (7.14%) after the transplantation, while in the 68 cases with slightly positive PRA as detected preoperatively, acute rejection occurred in 36 cases (52.9%). Among the 12 cases with positive PRA assay both before and after the operation, acute rejection took place in 10 cases (83.3%). As for the 71 patients receiving postoperative PRA detection, 59 were PRA-negative, among whom acute rejection occurred in only 3 cases (5.08%), while 7 (58.3%) out of the 12 PRA-positive experienced episodes of acute rejection. CONCLUSION: PRA-positive recipients of the renal transplantation have higher risks of acute rejection of the graft, and PRA detection both before and after the operation may be of great importance.
OBJECTIVE: To investigate the effects of smoke inhalation injury on the phagocytic function of rat alveolar macrophages and neutrophil apoptosis. METHODS: Wistar rats inflicted with smoke inhalation injury were employed in the study. Fifty-four Wistar rats were randomly divided into normal control (N, n = 6) and inhalation injury (I, n = 48) groups. Alveolar macrophages were harvested from the BALF (bronchoalveolar lavage fluid) in I group of rats at 2, 6, 12 and 24 postburn hours (PBHs) and on 2, 3, 4 and 5 postburn days (PBDs). The dynamic change in the phagocytosis of chicken erythrocytes by alveolar macrophages in vitro was observed. The positive rate of myeloperoxidase (MPO) staining of alveolar macrophages (AMs) by MPO staining method was observed, so as to indirectly reflect neutrophil apoptosis and the phagocytosis o apoptotic neutrophils by AMs. Furthermore, the dynamic change in the inflammatory cell apoptosis within BALF was monitored by flow cytometry. RESULTS: (1) he phagocytosis of chicken erythrocytes by AMs was decreased during early postburn stage (2 - 6 PBHs) but recovered after 12 PBHs. (2) The positive MPO staining of AMs was increased gradually after injury and reached top level at 24 PBHs, but decreased during 2 - 5 PBDs. (3) The apoptotic rate within BALF was around 3.02% - 12.95% and rose to peak value at 24 PBHs. CONCLUSION: There was increased apoptosis of inflammatory cells within BALF. The resolution process of inflammation after smoke inhalation injury involved neutrophil apoptosis and the phagocytosis of apoptotic neutrophils by AMs.
OBJECTIVE: To analyze the speech characters with computation complexity. METHOD: Voices of 51 testees spoke the same paragraph were recorded and the same sentence of voice waveform was intercepted as source data. There were two kinds of sample voices: same testee speaking the same sentence at different time and different testee speaking the same sentence. RESULT: The computation complexity curves of the different testee were obviously distinguishing, while those of the same testee were almost the same. In a 2D embedded space the computation complexity features of individual testee differs with others even if testees speak the same sentences. CONCLUSION: This complexity features might be applied to speaker recognition system and using complexity method to analyze speech signals has wide application prospect.
OBJECTIVE: To screen for proteins interacting with novel gene AngRem104. METHODS: The yeast strain AH109 was transformed with AngRem104-pGBKT7/c-myc, and yeast-mating was utilized to screen for interacting proteins with AngRem104 in pretransformed human kidney cDNA library. RESULTS: AngRem104 protein was expressed and there was no self-activation and toxicity in AH109. Seven proteins that interacted with AngRem104, including eukaryotic translation elongation factor 1 alpha 1, glucocorticoid receptor AF-1 specific elongation factor, beta 2-microglobulin, BBS2 and four of cell metabolism related proteins, were identified. CONCLUSION: The novel gene AngRem104 may interact with the proteins, which may interfere with cell metabolism, disturb the balance between transcription factors, or may be involved in some immunity related and hereditary diseases. This investigation provides functional clues for further exploration of the novel gene, AngRem104.
OBJECTIVE: To observe the effects of combined use of losartan and fosinopril in the treatment of early diabetic nephropathy. METHODS: Fifty-seven patients with diabetic nephropathy were divided equally into group A with treatment with losartan (50 mg) and fosinopril (10 mg) daily, group B with daily losartan treatment (50-100 mg), and group C with fosinopril treatment at the daily dose of 10-20 mg. After the 6-month medication, the patients underwent examinations for changes in the mean arterial blood pressure (MABP), serum creatinine (SCr), blood urea nitrogen (BUN) and 24-h urine protein excretion. RESULTS: Losartan or fosinopril used alone or in combination significantly lowered MABP, 24-h urine protein excretion, SCr and BUN in the patients ( P < 0.05 or P < 0.01). In spite of the absence of significant differences between the patient groups, combination use of the two drugs produced the most obvious reduction of the parameters measured. CONCLUSION: Combined use of losartan and fosinopril may decrease MABP, 24-h urine protein excretion, SCr and BUN to a greater extent than the use of losartan or fosinopril alone.
OBJECTIVE: To observe in vitro changes of endothelial cells after confrontation with tumor cells. METHODS: Dynobeads were used to isolate the endothelial cells from the rat lung. Mouse dendritic cell sarcoma cells (DCS), human gastric carcinoma cells (BGC-823) and mouse lung adenocarcinoma cells (LA795) were added to the endothelial cells when the latter was at the confluence phase. Phase contrast microscope, scanning electro-microscope, immunohistochemistry, transwell and fluorescence dye transfer were used to detect morphological and functional changes of the endothelial cells. RESULTS: Endothelial cells may look like cobble stones or long spindle shaped. Direct contact of tumor cells with endothelial cells induced round vascular-like space formation between confluent endothelial cells. Tumor cells were often found at the newly appeared spaces. Tumor cell conditioned medium could support the growth and promote the locomotion of endothelial cells through transwell. It was observed that luciffer yellow was directly transported from tumor cells to endothelial cells. CONCLUSIONS: Tumor cells can directly induce morphological and functional changes in endothelial cells. Direct intercellular communication between tumor cells and endothelial cells is present.
OBJECTIVE: To investigate the nasal carriage of antibiotic-resistant pneumococci in children of < 5 years old in the following four cities, Beijing, Shanghai, Guangzhou and Xi'an. METHODS: A total of 647 pneumococci strains were isolated and detected. Minimal inhibition concentrations (MICs) of antibiotics were determined by E-test. Disk diffusion test was used for the measurement of antimicrobial susceptibility. RESULTS: Prevalence of penicillin non-susceptible Streptococcus pneumoniae in the four cities was 41%, with Guangzhou (60.8%) ranking first, followed by Xi'an (45%), Shanghai (37%) and Beijing (25.9%). The majority of penicillin non-susceptibility isolates (23.9% - 53.8%) had a low level of resistance (MIC 0.64 - 1.5 microg/ml). The most sensitive antimicrobials in terms of percentage of susceptible organisms were amoxicillin-clavulanic acid (99.4%), followed by ceftriaxone (92.1%); cefurxime and cefaclor were slightly more sensitive than penicillin with susceptibility of 74.8% and 77.9%. Erythromycin, tetracycline and TMP-SMZ were highly resistant (83.6%, 82.1% and 76.2% respectively). Among erythromycin resistant isolates, 100% were resistant to azithromycin, 98.6% to clarithromycin, 97.2% to roxithromycin and spiramycin, and 96.6% to clindamycin. 97.2% (141/145) were typical of the macrolides-lincosamides-streptogramons B (MLSB) resistance phenotype, and 2.8% (4/145) were M phenotype. The group of PRSP was with significantly higher rates of non-susceptibility for ceftriaxone (18.4%), cefurxime (58.6%), cefaclor (53.4%), compared with the group of PEN-S (0.5%, 1.8% and 0.2%, respectively) and the rate of multi-drug resistance in the isolates of PRSP group (92.9%) was significantly higher than that of PEN-S group (59.2%). CONCLUSION: The rates of penicillin and multi-drug resistance among isolates of pneumococci carried nasally in are high children and the high prevalence of multi-drug resistance in the Chinese population may be becoming one of the most serious problems in this century.
The prognostic significance of Bcl-2 expression in colorectal cancer has been intensively studied, however, the results were controversial in the whole group of colorectal cancer patients. We proposed that one of the main reasons for such controversial results may be that Bcl-2 played variable roles in the subgroup of patients. We, therefore, investigated the prognostic importance of Bcl-2 expression by using immunohistochemistry in the various subgroups of 147 patients with colorectal cancer. Among these tumours, 85 (58%) expressed Bcl-2 protein and 62 (42%) were negative. Bcl-2 expression was positively related to DCC expression (p=0.0002). Survival analyses in the subgroups of the patients showed that lack of Bcl-2 expression was related to a worse prognosis in the male patients (p=0.02) but not in female patients (p=0.53), in the patients with DNA diploid tumours (p=0.005) not in the patients with non-diploid tumours (p=0.46), and in the patients with ras negative tumours (p=0.01) not in the patients with ras positive tumours (p=0.25). Bcl-2 expression was not related to prognosis in the total group of the patients (p=0.20). In conclusion, Bcl-2 protein may play variable prognostic roles in the subgroups of the patients with colorectal cancer. Analysis of Bcl-2 expression in the tumour may be of value in predicting prognosis and therapeutic response.
We chose Hela cells as research object and studied the cytotoxicity generated by cyclophosphamide, an antitumor drug, after cell electroporation by the use of electromagnetic pulses. Comparison between the electroporation group and the contrast group revealed the greatly enhanced cytotoxicity of the electroporation group, indicating that under some conditions electromagnetic pulses can enhance the cytotoxicity of antitumor drugs. The results of this study provide reliable evidences and a feasible approach for clinical treatment of tumor.
OBJECTIVE: To establish a mouse model of HCV core expression and investigate the toxicity of HCV core protein or the possible pathogenic effects. METHODS: A series of vaccinia viral expression vectors were engineered to express 5' portion of HCV genes including 5' non-translated region (NTR), core protein, and portion of the E1 gene. These HCV sequences were fused to a luciferase reporter gene and inserted into a vaccinia virus expression vector (pSC11) adjacent to the vaccinia virus promoter, p7.5. The recombinant DNA constructs were packed into infectious recombinant chimeric viruses. The expression of HCV core protein was examined in cultured cells after infection with these viruses. Death of the infected mice was investigated by specific correlation to the expression of HCV core protein and its expression levels. RESULTS: The recombinant virus (VNCE-LUA) expressed HCV core protein and an envelopeluciferase fusion protein in cultured cells. When Balb/c mice were inoculated intraperitoneally with more than 10(7) pfu per mouse of VNCE-LUA, death occurred immediately. The mortality was dependent on the amount of VNCE-LUA virus inoculated. All mice inoculated with 3 x 10(8) pfu of VNCE-LUA died within 4 days of infection and 50% of mice inoculated with 3 x 10(7) pfu of VNCE-LUA died within 7 days of infection. No death occurred in mice inoculated with 3 x 10(8) pfu of a control recombinant vaccinia virus, which expressed luciferase but not the HCV core and envelope proteins. Deletion of core sequences from VNCE-LUA rapidly reduced the mortality of infected mice whereas deletion of envelope sequence did not. SCID mice infected with VNCE-LUA died 2-3 days after infection, suggesting that the HCV-core induced mortality is not dependent on host T- or B-cell responses to core protein. CONCLUSIONS: HCV core protein can be lethal to mice when expressed in vivo and this specific lethality is independent of T-cells or B-cells. The findings and model itself provide a useful tool for further investigation on potential pathological effects as well as the potential toxicity of the HCV core protein.
OBJECTIVE: To investigate the effect of Ca(2+) on lipopolysaccharide (LPS)-induced NF-kappa B activation in pancreatic acinar cells and the role of NF-kappa B in LPS-induced acinar cell injury. METHODS: Male rat pancreatic acinar cells were isolated by collagenase digestion, then exposed to varying concentrations of LPS (from 1 to 20 mg/L) in the presence or absence of EGTA. At various time points (30 minutes, 1 hour, 2 hours, 4 hours and 10 hours) after treatment with the agents, cell viability was determined by MTT. Nuclear translocation of NF-kappa B's subunit p65 was visualized by immunofluorescence staining and nuclei protein was extracted to perform EMSA which was used to assay the activity of NF-kappa B binding to the DNA sequence containing the recognition site of NF-kappa B. RESULTS: LPS induced cell damage in a time- and concentration-dependent manner while EGTA attenuated LPS-induced cell damage (P < 0.05). NF-kappa B p65 immunofluorescence staining had increased intensity in the cytoplasm and indicated that nuclear translocation occurred within 30 minutes and its zenith was reached at 1 hour after LPS (10 mg/L) treatment. Testing of NF-kappa B DNA binding activity showed the same alteration phase as p65 immunofluorescence staining. NF-kappa B activation preceded the pathological alteration of pancreatic acinar cells. The Ca(2+) chelator EGTA inhibited LPS-induced NF-kappa B activation. CONCLUSIONS: NF-kappa B activation is an important early event in LPS-induced injury to pancreatic acinar cells. Ca(2+) is an important mediator in the process of LPS-induced NF-kappa B activation.
OBJECTIVE: To observe the sensitivity change of SMMC-7721 cells transfected with antisense DNMT1 gene fragment to tumor necrosis factor related apoptosis inducing ligand (TRAIL) and its mechanism. METHODS: Cell survival rate was measured by trypan blue, apoptosis rate by TUNEL method and the expression of bcl-2, bax and bad by flow cytometry. RESULTS: Cell survival rate of SMMC-7721 cells transfected with antisense DNMT1 gene fragment was markedly lower than that transfected with sense DNMT1 gene fragment or empty vector (P < 0.05 and 0.01), but the apoptosis rate was on the contrary (P < 0.05 or 0.01). The expression of bax and bad (especially the former), but not bcl-2 of SMMC-7721 cells transfected with antisense DNMT1 gene fragment was markedly higher than those of SMMC-7721 cells transfected with sense DNMT1 gene fragment or empty vector. CONCLUSION: The sensitivity of SMMC-7721 cells to TRAIL can be enhanced by the transfection of antisense DNMT1 gene fragment, which may be related to the increase of bax and bad expression.
This article reports the experiment studies on treating the S-180 sarcomas of KM mice with high-intensity electric pulse and antitumor drug (cyclophosphamide). The results showed that the experimental group of electric field combined with drug has the best effect on tumor, compared with the control group. In addition, electric field can inhibit the formation of vas Capillaries and decrease the supply of nutrition for tumor cell. In conclusion, electric field has inhibited the growth of tumor.
OBJECTIVE: Using animal anemia models to observe the antianemia effect of Shengxuesu, and to afford an experimental basis for preventing and treating anemia. METHOD: Rat model of iron deficiency induced by denutrition and mouse model of nemorrhagic anemia by blood lefting were established. Indices of hemoglobin(HB), red blood cell count(RBC), hematocrit(HCT), mean corpuscular hemoglobin count(MCHC), serum iron(SI), serum ferritin (SF) and total iron-binding capacity(TIBC) were monitored. RESULT: A dosage of Shengxuesu 0.5-2 g.kg-1 was given to the rat model of hypoferric anemia by gavage for 15 days, and to the mouse model of hemorrhagic anemia by gavage for 7 days. The result shows that HB, RBC, HCT, MCHC in blood and iron, ferroprotein in serum were elevated significantly; but total bounding iron in serum was decreased. Meanwhile, diet amount, diet consumption and general activity of the model rats were increased.