Antiviral Agents ; therapeutic use ; China ; Hepatitis B ; drug therapy ; epidemiology ; immunology ; prevention & control ; therapy ; Hepatitis B Vaccines ; immunology ; Humans

China ; epidemiology ; Hepatitis, Viral, Human ; epidemiology ; Humans

Objective To explore the influencing factors of daunorubicin (DNR) induced apoptosis in Jurkat cells of acute lymphoblastic leukemia. Methods Jurkat cells were treated with different concentrations of DNR(0, 0.05, 0.1, 0.5 and 1 μg/mL)or pretreated with N-acetylcysteine (NAC). Cell proliferation was detected by MTT assay, cell apoptosis was observed by Hoechst/PI, reactive oxygen species (ROS) level and apoptosis were determined by flow cytometry, and the expression of survivin, bax, bcl-2 and bcl-xl mRNA was examined by RT-PCR. Results DNR siguificantly inhibited the proliferation of Jurkat cells. After treatment with 0, 0.05, 0.1, 0.5, 1 μg/mL DNR and pretreated with NAC for 24 h, ROS levels were (7.98±0.55)%, (8.88±0.86)%, (9.46±0.98)%, (17.48±2.98)%, (24.46±2.43)% and (11.59±1.29)%, respectively, and cell apoptosis rates were (11.41±1.44)%, (34.96±3.32)%, (45.58± 3.12)%, (84.19±2.65)%, (87.93±1.74)% and (80.47±0.63)%, respectively. After pretreatment with NAC, the levels of ROS were siguifieantly inhibited (P < 0.01). There was no significant difference in apoptosis rates between treatment with 0.5μg/mL DNR and pretreatment with NAC(P>0.05). The expression of bax mRNA was down regulated and the expression of survivin, bcl-2 and bcl-xl was up regulated (P < 0.05). Conclusion DNR can induce apoptosis of Jurkat cells. ROS may participate in the DNR induced Jurkat cell apoptosis, and apoptosis-related gene bax, bcl-2, bcl-xl and survivin may interact with ROS in the regulation of DNR induced Jurkat cell apoptosis.

OBJECTIVE: To explore whether there are beta-amyloid protein (Abeta) binding elements in heart-beneficial recipe (HBR, a compound traditional Chinese herbal medicine), which can ameliorate the cytotoxicity of Abeta. METHODS: The extract of HBR and Abeta(1-40) were co-precipitated, and the Abeta(1-40) in pellets was detected by immunoblotting. Affi-gel-Abeta(1-40) was constructed, and Affi-gel-Abeta(1-40) affinity elements from the extract of HBR were analyzed by high-performance liquid chromatography (HPLC). The assay of lactic dehydrogenase (LDH) release from the primary cultured rat cortex neurons was used to evaluate the cytotoxicity of Abeta(1-42), and the protection effects of the HBR serum and the Affi-gel-Abeta(1-40) treated HBR serum. RESULTS: Immunoblotting examination showed Abeta(1-40) could be co-precipitated with components of HBR following co-incubation, and the amount of Abeta(1-40) within pellets decreased when the HBR extract was diluted. Abeta(1-40) affinity elements from the extract of HBR, eluted from Affi-gel-Abeta(1-40) by glycine solution (pH=2.5), could be detected by HPLC-fluorescent detector system. The analysis of LDH release showed that exposure of neurons to 5 micromol/L Abeta(1-42) for 48 h caused a significant increase of LDH release in either a serum free or 10% serum contained culture condition (P<0.01). The rat HBR serum was able to suppress Abeta(1-42) induced LDH release (P<0.05), whereas Affi-gel-Abeta(1-40) treated HBR serum still maintained the ability to attenuate Abeta(1-42) induced LDH release although the effect was somewhat decreased compared with Affi-gel treated HBR serum. CONCLUSION: There are Abeta affinity components in HBR, which could not increase the Abeta cytotoxicity, but might be able to inhibit the cytotoxicity of Abeta. The results implied that the exploration of Abeta affinity elements from Chinese medicinal recipe which is effective for Alzheimer disease, might be an important direction in Alzheimer disease therapeutic research area.

Objective To investigate experience in nursing the patients with emergency traumatic injury combined with postoperative atelectasis. Method The clinical data of 11 patients with emergency traumatic injury combined with postoperative atelectasis were reviewed for summarizing the nursing experience. Result The clinical symptoms of all the 11 patients disappeared and the lungs reexpanded. Conclusion Careful observation of the disease conditions in order to prevent and treat atelectasis by airway humidification, sputum drainage and early exercises are effective for the cure of postoperative atelectasis.

Objective:To investigate the effect of metformin and arsenic trioxide on KG1a cells proliferation of acute myeloid leukemia and its possible mechanism.Methods:CCK-8 method was used to detect the killing effect of metformin,arsenic trioxide and combined application on KG1a cells.Annexin V-FITC/P1 Dual Stain Flow Cytometry was used to detect the effect of combined application on apoptosis of KG1 a cells.Western blot was used to detect the expression of intracellular apoptosis-,autophagy-related protein.Results:Metformin and arsenic trioxide alone or in combination could inhibit the proliferation of KG1 a cells and induce apoptosis of KG1 a cells,and the proliferation inhibition rate and apoptosis rate in the combined drug group were higher than those in the drug group alone(P＜0.05).The combination of drugs induced upregulation of Caspase 8 protein and P62 protein expression and was higher than that in the drug group alone(P＜0.05).Conclusion:Metformin can synergize with arsenic trioxide to kill KG1a cells,and its mechanism of action may be related to inducing apoptosis and enhancing autophagy.

Objective To investigate the effects of panax notoginseng saponins (PNS) on early-stage apoptosis in steonecrosis of rabbit femoral head .Methods The 24 rabbits were randomly divided into three groups :normal control group ,model group ,and PNS group .In model group ,equine serum (10 mL/kg) and methylprednisolone (40 mg/kg) were injected alternatively to induce osteonecrosis of the femoral head .In PNS group ,PNS (50 mg/kg , i .v .) was administered continuously before methylprednisolone management .In control group ,the rabbits were fed routinely .TUNEL method was used to detect apoptotic cells .Caspase-3 activity in the femoral head was measured by caspase-3 assay kit . Immunohistochemistry method and Western blot analysis were applied to detect the expressions of Bcl-2 and Bax .Results In model group ,typical appearance of apoptotic cells was observed in the femoral head by TUNEL staining (P< 0 .05) .PNS treatment significantly inhibited cell apoptosis of the femoral head in model group .Furthermore ,pretreatment with PNS significantly reversed the inhibition of Bcl-2 expression , augmentation of Bax expression and caspase-3 activity ( P< 0 .05 ) . Conclusion PNS could up-regulate the expression of Bcl-2 ,down-regulate that of Bax ,reduce the activity of caspase-3 ,and inhibit cell apoptosis of the femoral head .

Ion channelopathies are the mainly etiopathogenisis of inherited arrhythmia. Those arrhythmia syndromes are commonly caused by ion channel gene mutation, which can be classified as sodium,potassium and calcium ion channel mutation.Changes in the genes encoding for cardiac ion channel subunits produce modification in the function of the channels, and cause the dysfunctions of cardiac electrical activity; and the clinical manifestation is malignant arrhythmia.
Animals ; Arrhythmias, Cardiac ; genetics ; physiopathology ; Channelopathies ; genetics ; physiopathology ; Humans ; Ion Channels ; genetics ; physiology ; Mutation

Anticoagulants ; therapeutic use ; Child ; Coagulants ; blood ; Heparin, Low-Molecular-Weight ; therapeutic use ; Humans ; Purpura, Schoenlein-Henoch ; blood ; drug therapy ; Signal Transduction ; Thromboplastin

The objectives of this study are to prepare resveratrol loaded mixed micelles composed of poloxamer 403 and poloxamer 407, and optimize the formulation in order to achieve higher drug solubility and sustained drug release. Firstly, a thin-film hydration method was utilized to prepare the micelles. By using drug-loading, encapsulation yield and particle size of the micelles as criteria, influence of three variables, namely poloxamer 407 mass fraction, amount of water and feeding of resveratrol, on the quality of the micelles was optimized with a central composite design method. Steady fluorescence measurement was carried out to evaluate the critical micelle concentration of the carriers. Micelle stability upon dilution with simulated gastric fluid and simulated intestinal fluid was investigated. The in vitro release of resveratrol from the mixed micelles was monitored by dialysis method. It was observed that the particle size of the optimized micelle formulation was 24 nm, with drug-loading 11.78%, and encapsulation yield 82.51%. The mixed micelles increased the solubility of resveratrol for about 197 times. Moreover, the mixed micelles had a low critical micelle concentration of 0.05 mg · mL(-1) in water and no apparent changes in particle size and drug content were observed upon micelles dilution, indicating improved kinetic stability. Resveratrol was released from the micelles in a controlled manner for over 20 h, and the release process can be well described by Higuchi equation. Therefore, resveratrol-loaded poloxamer 403/407 mixed micelles could improve the solubility of resveratrol significantly and sustained drug release behavior can be achieved.
Drug Carriers ; chemistry ; Fluorescence ; Kinetics ; Micelles ; Particle Size ; Poloxamer ; chemistry ; Solubility ; Stilbenes ; chemistry ; Water