Acupuncture Points ; Acupuncture Therapy ; Adult ; Aged ; Facial Muscles ; physiopathology ; Facial Paralysis ; physiopathology ; therapy ; Female ; Humans ; Male ; Middle Aged

Objective To observe the changes and relationships of glucose (Glu),insulin(Ins) ,insulin-like growth factor-1 (IGF-1) in newborn infant with hypixic-ischemic encephalopathy (HIE) and the protective role which Ins,IGF-1 worked on neuron.Methods HIE 50 cases,the quantity of IGF-1 in serum was detected by radioimmunoassay,the quantity of Ins in serum was detected by chemiluminescent immunoassay,the quantity of glucose in serum was detected by the instrument with type of Rokangquan TM accutive.The umbilical vein blood 2 mL were drawn from 20 cases of controls after birth.The indexes were detected by the same methods.Results 1.In acute period,the level of serum IGF-1 reduced obviously in newborn infants with HIE,and Glu increased obviously.There was a negative correlation between IGF-1 and Glu.The changes related with neonate complications.In rehabilited pe riod,the Glu get to normal,the IGF-1 was a little higher than that in acute period.but it still was lower than that of control group.There was negative correlation between IGF-1 and Glu.2.The level of Ins in serum of newborn infants with HIE had no obvious changes compairing with control group in acute period and rehabilited period.It had no relations with Glu,Ins.Conclusions It approves that IGF-1 and Glu in serum of newborn infants with HIE have obviously changed.This result will provide an academic base on treatment of HIE.

In the ApoE(-/-) mouse model of atherosclerosis (AS) stable plaque, the expression and location of intracellular tissue factor (TF) in the cellular components of AS stable plaque were investigated in order to explore the cellular mechanism of AS thrombosis. Pathological changes of the stable plaque were observed under a microscope. The expression of TF protein was examined in aortic stable plaque of mice by using immunohistochemistry. Color image planimetric system was used to analyze the histological components of the stable plaque and the TF distribution. Under the confocal microscope, the intracellular TF location in the stable plaque of mice was observed. The results showed the cellular area was the major part of stable plaque (67.36%+/-6.52%, P<0.01). The percentage of total area occupied by cellular area was significantly larger than atheromatous gruel and acellular area (P<0.01). Macrophages and smooth muscle cells (SMC) were major cells in the cellular area. The percentage of total area occupied by SMC was significantly larger than by macrophages (P<0.01). Multiple linear regression analysis showed there was a positive correlation between TF area and SMC area (r=0.616, P=0.008), and no correlation was found between TF area and macrophage area (r=0.437, P=0.08). Pictures of color image planimetric analysis of TF and SMC were merged to highlight areas with co-localization (yellow), it was concluded that the process could be a cell-mediated TF expression in the stable plaque. SMC may be the major source of TF in AS without plaque rupture.

Objective To study the relation between mitochondria damage and glutamate excitotoxicity in motor neuron disease.Methods Organotypic cerebral cultures were prepared from prefrontal brain of neonatal SD rats. Mitochondria was damaged by malonate sodium, and a NMDA receptor antagonist, MK-801 of 0.025,0.050,0.075,0.100 mmol/L, was respectively added into the cerebral cultures simultaneously in the protective experiment. The morphology of motor neurons was shown by Nissl and anti-high molecular weight filament (anti-NFH) immunohistochemical staining, and number of motor neurons was counted. The concentration of MDA in culture medium was measured by MDA assay. Results After exposed to malonate sodium (0, 1, 3, 5 and 7 mmol/L) for 1 week, the number of motor neurons in cerebral slices showed a dose-dependent decrease (49.78?4.30, 47.89?6.81, 25.67?6.18, 4.44?3.40, 1.22?1.99). The group treated with 3 mmol/L malonate sodium was selected as damage group. In protective experiment, the number of motor neurons in 0.050, 0.075 and 0.100 mmol/L MK-801-treated groups was significantly increased as compared with damage group, still less than that of controls. However, there was no difference of number of motor neurons among these three groups. The concentration of MDA in culture medium in normal control and 3, 5 mmol/L malonate sodium was (13.47?0.49), (15.87?0.74), (20.52?0.74) mmol/L. When treating cerebral cultures with 0.050 mmol/L MK-801 and 5 mmol/L malonate sodium simultaneously, the MDA was decreased to 14.45?0.78, close to normal level. Conclusion Glutamate excitotoxicity plays a role in motor neuron diseases caused by mitochondria damage, there exists a close relationship between glutamate exicitotoxicity and mitochondria damage.

OBJECTIVETo explore the effect of Bushen Huoxue Compound (BHC) on lactate dehydrogenase (LDH) leakage, expressions of vascular endothelial growth factor (VEGF) and VEGF mRNA in retinal Muller cells under high glucose condition or advanced glycosylation end products (AGEs) condition by using serum pharmacological method.

METHODSThe retinal Müller cells of 5-7 days post-natal Sprague Dawley (SD) rats were cultured with modified enzyme-digestion method. Purified retinal Muller cells were cultured in normal conditions, high glucose condition (50 mmol/L) or AGEs (50 mg/L and 100 mg/L) conditions, and BHC-containing serum was added to culture medium. The LDH leakage and VEGF expressions were measured by enzyme-linked immunosorbent assay (ELISA). In addition, the relative expression of VEGF mRNA was tested by reverse transcription polymerase chain reaction (RT-PCR).

RESULTSCompared with the normal control group, expressions of VEGF and VEGF mRNA were significantly increased in the high glucose group, the low dose AGEs group and the high dose AGEs group (all P < 0.01). The LDH leakage was obviously increased in the high dose AGEs group, when compared with the normal control group and the high glucose group (P < 0.01). The LDH leakage, expressions of VEGF and VEGF mRNA were obviously decreased by BHC-containing serum both in high glucose and AGEs conditions (P < 0.05, P < 0.01). BHC-containing serum had no significant effect on the LDH leakage and expressions of VEGF and VEGF mRNA in normal conditions (P > 0.05).

CONCLUSIONSAGEs intervention could obviously lower the stability of Müller cell membrane. Up-regulated expressions of VEGF and VEGF mRNA in cultured Müller cells could be induced by AGEs or high glucose. BHC-containing serum could stabilize the stability of Müller cell membrane, inhibit the transcription of VEGF mRNA and decrease the protein expression of VEGF, which might be one of important mechanisms for preventing and treating diabetic retinopathy.

Animals ; Cells, Cultured ; Diabetic Retinopathy ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Ependymoglial Cells ; Glucose ; L-Lactate Dehydrogenase ; RNA, Messenger ; Rats ; Rats, Sprague-Dawley ; Vascular Endothelial Growth Factor A

Objective To explore the effect of carvedilol on ACE2 gene and protein expression in chronic heart failure rats after myocardial infarction.Methods The heart failure model was induced by acute myocardial infarc- tion (AMI) through ligating the left anterior descending coronary artery.One month after operation,rats were randomized to receive placebo or carvedilol 2 mg/(kg?d),by gavage.Sham-operated rats were used as the control group.Hemodynamies,body mass and left ventrieular mass index,plasma and myocardial level of angiotensin Ⅱ were determined.ACE2 gene and protein expression was assessed by using RT-PCR and Western Blot.Results The mortality of placebo and Carvedilol groups were 20%,compared with 0% in sham operated rats.Carvedilol significantly improved LVEDP,LVSP,+dp/dt_(max) and-dp/dt_(min) in CHF rats but all the hemodynamics data were still inferior than that of controls.Plasma and myocardial angiotensin Ⅱ level were increased significantly in CHF placebo rats than those of control rats (plasma Ang Ⅱ:CHF:194?19 vs controls:132?15 ng/L,myocardium Ang Ⅱ:CHF:6.7?0.4 vs control:3.8?0.3 ng/g,P

The interaction between Gliotoxin and bovine serum albumin (BSA) was studied by the fluo-rescence, Circular Dichroism (CD) and ultraviolet visible (UV-Vis) techniques. The fluorescent experiment showed that the intrinsic fluorescence of BSA was quenched by the binding of gliotoxin in a static quenching procedure, with an association constant of 7.2?103 L/mol and in hydropobic forces. And the CD spectrum revealed that gliotoxin effected the conformation of BSA by increased the mass of ?-helix.

This study is to investigate the anti-tumor activities of a novel cyclophosphamide derivate 4, 6-diphenyl cyclophosphamide (9b) in vivo and in vitro, and its possible mechanism of action. The inhibitory effects of 9b on human hepatoma cell line HepG2, human breast carcinoma cell line MCF-7 and human myeloid leukemia cell line K562 were measured by MTT assay in vitro. Cell cycle distribution and apoptotic rate were evaluated by flow cytometry. To evaluate the anti-tumor effect of 9b in vivo, mouse model bearing inoculated H22 tumor was established. The results indicated that 9b could inhibit the proliferation of HepG2, MCF-7 and K562 cells in a dose and time dependent manner. The ICo50 values of 9b were 32.34 micromol.L-1 to HepG2 cells, 87.07 micromol.L-1 to MCF-7 cells and 149.10 micromol.L-1 to K562 cells after incubation for 48 h. The results of flow cytometry indicated that after being treated for 48 h with different concentrations of 9b, the ratios of HepG2, MCF-7 cells at the Go/G1 phase and K562 cells at the G0/Gl phase and G2/M phase increased significantly compared with control group, and the apoptotic rate increased with the increase of the concentration of 9b. 9b could significantly reduce tumor weight of H22 solid tumor mouse model in vivo. To summarize, 9b showed significantly anti-tumor activity in vivo and in vitro, of which the mechanism might be associated with the change of cell cycle distribution and induction of tumor cell apoptosis.
Animals ; Antineoplastic Agents, Alkylating ; chemistry ; pharmacology ; Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Cyclophosphamide ; analogs & derivatives ; chemistry ; pharmacology ; Dose-Response Relationship, Drug ; Female ; Humans ; Inhibitory Concentration 50 ; Liver Neoplasms, Experimental ; pathology ; Male ; Mice ; Molecular Structure ; Random Allocation ; Tumor Burden ; drug effects

This study examined the effect of electro-acupuncture (EA) combined with transcranial magnetic stimulation (TMS) therapy at different time windows on learning and memory ability of rats with cerebral infarction and the underlying mechanism. Two hundred SD rats were randomly divided into four groups: normal group, sham-operated group, model group and EA+TMS group, and each group was then divided into five sub-groups in terms of the different time to start treatment post operation: 6, 12, 24, 48 and 72 h. Cerebral infarction models were established in the model and the EA+TMS groups by left middle cerebral artery occlusion/reperfusion (MCAO/R). After treatment for 14 d, the Morris water maze test was applied to examine the spatial learning and memory abilities of rats. In infarcted area, the expression of caspase-3 was immunohistochemically detected, and real-time fluorescent quantitative PCR was used to measure the expression of Bcl-2 mRNA. The results showed that in EA+TMS group compared with model group at the same treatment time windows, the escape latency was substantially shortened, the expression of caspase-3 was considerably decreased and the expression level of Bcl-2 mRNA significantly increased (P<0.05). In the EA+TMS sub-groups, the escape latency was shortest, the expression level of caspase-3 lowest, and the expression level of Bcl-2 mRNA highest at the treatment time window of 24 h. It was concluded that EA combined with TMS can promote neurological function of rats with cerebral infarction by increasing the expression level of Bcl-2 mRNA and decreasing the expression of caspase-3. The best time window is 24 h after perfusion treatment to ischemia.

Objective To evaluate the efficacy and safety of radiotherapy combined with concurrent and then adjuvant temozolomide in the patient with glioblastoma.Methods The databases of PubMed,Cochrane library,Medline and OVID were retrieved according to the Cochrane systematical assessment method.The included literatures were performed the quality evaluation and the meta analysis was performed after extracting the data.Results The summary of comparison between temozolomide group and radiotherapy group in the included studies showed that the 12-month overall survival rate[RR 1.22,95 ％ CI(1.01,1.47),P=0.04]and 24-month overall survival rate[RR 2.65,95 ％ CI(1.53,4.40),P＜0.01]had statistically significant differences;the 12-month pregrossion free survival rate[RR 2.59,95 ％CI(1.53,4.40),P=0.000 4] and 24-month pregrossion free survival rate[RR 6.77,95 ％ CI (2.82,16.26),P＜ 0.01] also showed statistically significant difference.The results of adverse reaction events revealed that the hematological toxic reactions in the temozolomide group had statistical difference between the concurrent therapy period and radiotherapy period [RR 3.21,95％CI(1.89,5.46),P＜0.01];which in the temozolomide group had statistical difference between the concurrent period and adjuvant period [RR 0.48,95 ％ CI(0.36,0.65),P＜0.01);but the non-hematological toxic reaction had no statistical difference[RR 1.11,95％CI(0.72,1.70),P=0.64].Conclusion Radiotherapy combined with concurrent and then adjuvant temozolomide therapy improves the overall and progression free survival period in the patient with glioblastoma,the higher occurrence rate of hematologic toxic reactions is correlated with temozolomide treatment drugs.