Adult ; Antidepressive Agents ; therapeutic use ; Bipolar Disorder ; blood ; drug therapy ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Interferon-gamma ; blood ; Interleukin-1 ; blood ; Interleukin-6 ; blood ; Male ; Middle Aged ; Perylene ; analogs & derivatives ; therapeutic use ; Phytotherapy ; Tumor Necrosis Factor-alpha ; metabolism

Objective To evaluate the reliability of gas sampling from the distal end of the tracheal tube for partial pressure of end-tidal CO2 (PETCO2) monitoring in neonates.Methods A total of 50 fullterm neonates,scheduled for elective abdominal surgery under general anesthesia,aged 1-28 days,weighing 2.55-4.00 kg,of ASA physical status Ⅰ or Ⅱ,were randomly divided into 2 groups (n =25 each) using a random number table:gas samples collected from proximal end of tracheal tube group (group P) and gas samples collected from distal end of tracheal tube group (group D).Epidural catheters of 1 mm in external diameter were used.One end of the catheter was connected to a tube for carbon dioxide sampling,and the other end was inserted into the endotracheal tube and advanced toward the distal hole of the tube.At 15 min of mechanical ventilation,blood samples were collected from the radial artery for record of PETCO2 and for blood gas analysis.Consistency test was performed between PETCO2 and partial pressure of arterial CO2 (PaCO2).Results PET CO2 was significantly lower than PaCO2 in the two groups.There was no significant difference in PaCO2between the two groups.PETCO2 was significantly higher in group D than in group P.Kappa was significantly higher in group D than in group P.Conclusion Gas sampling from the distal end of the tracheal tube is more reliable than gas sampling from the proximal end in monitoring PETCO2 in the neonates.

Objective To explore the diagnosis and therapy experience of vascular ring combined with tracheal compression in infants and neonates.Methods Sixteen cases(including 7 boys and 9 girls,aged 1 day to 12 months)with vascular ring combined with tracheal compression hospitalized in Guangdong General Hospital from Jun.2004 to Dec.2009 were enrolled.In these 16 children,13 cases had congenital heart malformations.All children underwent X-ray,echocardiography and spiral computed tomography examination.Nine cases received bronchoscopy study.Fifteen cases performed surgical division of vascular ring with cardiopulmonary bypass and 1 case underwent vascular ring division and tracheoplasty.Eleven cases received management of congenital heart defect simultaneously.Results Vascular ring anomalies included pulmonary artery sling in 5 children,right aortic arch-left ligmentum/aberrant left subclavian artery in 8 cases,double aortic arch in 1 case,innominate artery compression in 1 case,and pulmonary sling combined with right aortic arch-aberrant left subclavian artery in 1 case.There were 2 ring-sling complex cases in this study.The diagnosis of vascular ring were correctly made by echocardiography in 7 children and made by spiral computed tomography in all 16 cases.Two cases combined with tracheal ring died.In the follow-up study of 11 cases,5 cases were still vulnerable to wheezing.Conclusions The common presentation of tracheal compression in infants and neonates associated with vascular ring are tachypea,stridor,and dyspnea.Multi-slices spiral computed tomography is an important imaging modality.Surgical divisions of vascular ring are safe procedure in most cases and tracheal compression can be relieved by this operation.In patients with severe tracheal stenosis,tracheoplasty should be recommended.

This study was purpose to investigate apoptosis pathway of leukemia K562 cells induced by anticoagulant fraction from Agkistrodon acutus venom (AVVC-1). The mitochondrial transmembrane potential (ΔΨm) of leukemia K562 cells was detected by flow cytometry with JC-1 single staining. The expression of cytochrome C in the mitochondrial of leukemia K562 cells was analyzed by Western blot after AVVC-1 treatment. The distribution of cytochrome C in leukemia K562 cells was measured by immuno-fluorescence test. The results showed that the potential of mitochondrial membrane decreased after treatment with different concentrations of AVVC-1 (12.5, 25, 50, 100 µg/ml) for 6 h (P < 0.01). The expression level of cytochrome C protein in mitochondria obviously declined after treatment with 30 µg/ml AVVC-1 for 48 h, and the fluorescent intensity of cytochrome C in cytosol was enhanced at the same time. It is concluded that AVVC-1-induced K562 cell apoptosis is related with mitochondrial damage, and cytochrome C may be a useful agent for investigating human leukemia therapy by using AVVC-1.
Agkistrodon ; Animals ; Apoptosis ; drug effects ; Cytochromes c ; metabolism ; Humans ; K562 Cells ; Membrane Potential, Mitochondrial ; drug effects ; Mitochondria ; metabolism ; Snake Venoms ; pharmacology

Humans ; Musculoskeletal Manipulations ; Periarthritis ; physiopathology ; therapy ; Shoulder Joint ; physiopathology

OBJECTIVE: To observe the effect and the mechanism of Chrysanthemum morifolium Ramat on apoptosis of bovine aortic smooth muscle cells. METHODS: Vascular smooth muscle cells were isolated from thoracic aorta of fetal calf and cultured, then incubated with different concentration of Chrysanthemum morifolium Ramat. Apoptosis was measured by flow cytometry. SOD and MDA were measured by spectrophotometer. RESULTS: We found that: (1) the number of apoptotic cells was reduced from (4.425+/-0.624)% to (2.875+/-0.640)% in Chrysanthemum morifolium Ramat group, in a concentration dependent manner; (2) the value of SOD was increased from (1.683+/-0.149)X10(4) U/L to (2.297+/-0.230)X104 U/L and the value of MDA was reduced from(166.454+/-56.805)&mgr;mol/L to (73.068+/-27.203)&mgr;mol/L in Chrysanthemum morifolium Ramat group, also in a concentration dependent manner. CONCLUSION: Chrysanthemum morifolium Ramat can inhibit apoptosis of vascular smooth muscle cells in a concentration-dependent manner.

OBJECTIVETo explore cell death and apoptosis in rat hippocampal neurons at different time points after ischemia, hypoxia and reperfusion injury and to elucidate time window characteristics in ischemia neuronal injury.

METHODSHippocampal neurons were obtained from rat embryo and were cultured in vitro. The ischemia and reperfusion of cultured rat hippocampal neurons were simulated by oxygen-glucose deprivation (OGD) and recovery. OGD at different time points (0.25 h to 3.0 h) and then the same recovery (24 h) were prepared. Annexin V-PI staining and flow cytometry examined neuron death and apoptosis at different time after injury.

RESULTSAfter OGD and recovery, both necrosis and apoptosis were observed. At different times after OGD, there were statistically significant differences in neuron necrosis rate (P < 0.05), but not in apoptosis rate (P > 0.05). At recovery, survival rate of hippocampal neurons further decreased while apoptosis rate increased. Furthermore, apoptosis rates of different time differed greatly (P < 0.05). Apoptosis rate gradually increased with significant difference among those of different time points (P < 0.05). However, 2 h after ischemia, apoptosis rate decreased markedly.

CONCLUSIONSApoptosis is an important pathway of delayed neuron death. The therapeutic time window should be within 2 h after cerebral ischemia and hypoxia.

Animals ; Apoptosis ; physiology ; Brain Ischemia ; pathology ; Cell Death ; physiology ; Cell Hypoxia ; Cells, Cultured ; Disease Models, Animal ; Female ; Fetus ; cytology ; Flow Cytometry ; Hippocampus ; pathology ; Neurons ; pathology ; Pregnancy ; Pregnancy, Animal ; Probability ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; pathology ; Sensitivity and Specificity ; Time Factors

OBJECTIVETo construct an eukaryotic expression vector carrying rat brain-derived neurotrophic factor receptor trkB gene.

METHODSUsing the total RNA isolated from rat brain as template, the trkB gene was amplified by reverse-transcription-polymerase chain reaction (RT-PCR) with a pair of specific primers which contained the restrictive sites of EcoR I and BamH I. The amplified fragment of trkB gene was digested with EcoR I and BamH I, and then subcloned into cloning vector pMD18-T and expression vector pEGFP-C2 respectively. The recombinant plasmids were identified by restriction endonuclease enzyme analysis and PCR.

RESULTSThe amplified DNA fragment was about 1461 bp in length. Enzyme digestion and PCR analysis showed that the gene of trkB had been successfully cloned into vector pMD18-T and pEGFP-C2.

CONCLUSIONSThe trkB gene of rat has been amplified and cloned into the eukaryotic expression vector pEGFP-C2.

Animals ; Brain-Derived Neurotrophic Factor ; genetics ; pharmacology ; Cloning, Molecular ; methods ; Eukaryotic Cells ; Female ; Gene Expression Regulation ; Genetic Therapy ; methods ; Genetic Vectors ; Male ; Models, Animal ; RNA ; analysis ; Rats ; Rats, Wistar ; Receptor, trkB ; genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Schwann Cells ; cytology ; Sensitivity and Specificity ; Templates, Genetic ; Transfection

Objective To discuss the effect of breast cancer anti-estrogen resistance 1(BCAR1) knockdown on the expression of P38 and p-P38 in lung cancer cell line A549. Methods A549 cells (control group), A549 cells with RNAi letiviral vector of BCAR1 (interference group) and A549 cells with negative control letiviral vector (negative group) were cultured. Western blot was used to detect the expression of P38 and p-P38. The prolifera-tion,cell cycle,migration and invasion were measured by colony formation assay,flow cytometer,transwell experi-ment and scratch adhesion test,respectively. Results p-P38 expression in interference group cells was significant-ly lower than that in other two group cells(P<0.05).G1phase of interference group cells was significantly increas-ing than that in other two group cells(P<0.05).The proliferation,migration and invasion of interference group cells were all significantly suppressed as compared with that of other two group cells(P<0.05). Conclusions BCAR1 knockdown decreases p-P38 expression and inhibits proliferation,migration and invasion of A549 cells.

OBJECTIVETo observe the effect of Yangxueqingnao particles on rat vascular smooth muscle cell (VSMC) proliferation induced by lysophosphatidic acid (LPA).

METHODSThe amount of (3)H-TdR ((3)H-thymidine) admixed in cultured rat VSMC was measured and mitogen-activated protein kinase (MAPK) activity and lipid peroxidation end product malondialdehyde (MDA) content of the VSMC were assayed.

RESULTS1x10(-9), 1x10(-8), 1x10(-7) mol/L LPA in a concentration dependent manner, induced the amount of (3)H-TdR admixed, MAP kinase activity, and MDA content of the cultured rat VSMC to increase. However, 5%, 10%, and 15% Yangxueqingnao serum preincubation resulted in a decrease of 23.0%, 42.0%, and 52.0% (P<0.01) respectively in the amount of (3)H-TdR admixed, a decline in VSMC MAP kinase activity of 13.9% (P<0.05), 29.6% (P<0.01), and 48.9% (P<0.01) respectively, and also, a decrease in MDA content of VSMC of 19.4%, 24.7%, and 43.2% (P<0.01) respectively, in the 1x10(-7) mol/L LPA-treated VSMC.

CONCLUSIONSLPA activates the proliferation and lipid peroxidation of VSMC in a concentration dependent manner. The LPA-induced VSMC proliferation is related to the activity of MAP kinases, enzymes involved in an intracellular signalling pathway. The results of the present study showed that Yangxueqingnao particles can effectively inhibit LPA-induced VSMC proliferation, MAP kinase activation, and reduce lipid peroxidative lesion.

Animals ; Cell Proliferation ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Extracellular Signal-Regulated MAP Kinases ; metabolism ; Lysophospholipids ; pharmacology ; Male ; Malondialdehyde ; metabolism ; Muscle, Smooth, Vascular ; cytology ; drug effects ; metabolism ; Rats ; Rats, Sprague-Dawley