Objective To observe the abnormality on behavioral ability of transgenic mice for HRX-EEN fusion gene.Methods Transgenic mice for HRX-EEN fusion gene(transgenic group,n=12)and C57/BL mice(control group,n=12)were tested in hidden platform training(day 1 to day 4)and probe trial testing(day 5)in Morris water maze in which ability of spatial learning and retention was assessed.Results In hidden platform training,the latencies of transgenic group were longer than those in control group,and significant differences were observed between the two groups for day 2,3 and 4(P

Objective To study the influence of sivelestat sodium on platelets activity,injury and count during cardiopulmonary bypass (CPB)in dogs.Methods Twelve adult health dogs were randomly divided into control group (group C,n=6)and sivelestat sodium group (group S,n=6). Sivelestat sodium at 15 mg/kg was administrated intravenously before the establishment of CPB and then was maintained intravenously at 10 mg·kg-1·h-1 to the end of CPB in the group S,and the same volume of saline was used in the group S.The levels of neutrophil elastase (NE),malondialdehyde (MDA),granular membrane protein-140 (GMP-140),thromboxaneB2 (TXB2 ),the count of plate-lets and the hematocrit (Hct)were measured before CPB,15 and 45 min after cross-clamping and 30, and 60 min after aortic unclamping in both groups.Results The levels of NE,GMP-140,TXB2 at T2-T5 and MDA at T3-T5 were significantly higher than those at T1 in both groups;moreover the lev-els were significantly lower in group S than group C (P<0.05).The levels of Plt at T2-T5 were sig-nificantly lower than those at T1 in both groups;moreover the levels were significantly higher in group S than group C (P <0.05).Conclusion Sivelestat sodium reduced the levels of plasma NE, MDA,GMP-140,TXB2 inhibited the activation of Plt,and decreased the injury and consumption of Plt,which presents the protective effects for Plt during CPB.

OBJECTIVETo investigate the effect of distraction osteogenesis (DO) in the treatment of severe mandibular micrognathia with severe obstructive sleep apnea and hypopnea syndrome (OSAHS).

METHODS19 cases of severe mandibular micrognathia with OSAHS were treated by DO. All the patients received PSG and MSCT examination before and after DO to evaluate the therapeutic effect and changes in the upper airway.

RESULTSAccording to the evaluation standard, 17 cases were cured and 2 cases improved markedly. The sagittal distance and area, transverse distance and area of the upper airway increased markedly after DO. The volume of upper airway increased from (15 572.03 +/- 3 370.11) mm3 to (21 182.69 +/- 4 533.15) mm3.The airway change happened mainly in velopharyngeal region and the lingopharyngeal region, but not in the laryngopharyngeal region.

CONCLUSIONSDO can treat severe mandibular micrognathia patients with OSAHS effectively by enlarging the volume of upper airway,especially in the velopharynx and glossopharyngeum region. The MSCT plays an effective and important role.

Adolescent ; Adult ; Child ; Child, Preschool ; Female ; Humans ; Male ; Mandible ; surgery ; Micrognathism ; complications ; surgery ; Osteogenesis, Distraction ; methods ; Sleep Apnea, Obstructive ; complications ; surgery ; Young Adult

Adult ; Female ; Humans ; Magnetic Resonance Imaging ; Neuroma, Acoustic ; pathology ; surgery

12E7 Antigen ; Adolescent ; Adult ; Antigens, CD ; metabolism ; Biomarkers, Tumor ; metabolism ; Brain Neoplasms ; secondary ; Cell Adhesion Molecules ; metabolism ; Child ; Child, Preschool ; Diagnosis, Differential ; Extremities ; Female ; Follow-Up Studies ; Humans ; Immunohistochemistry ; In Situ Hybridization, Fluorescence ; Infant ; Ki-67 Antigen ; metabolism ; Male ; Neuroectodermal Tumors, Primitive ; metabolism ; pathology ; Oncogene Proteins, Fusion ; metabolism ; Repressor Proteins ; metabolism ; Sarcoma, Ewing ; metabolism ; pathology ; Sarcoma, Synovial ; diagnosis ; metabolism ; pathology ; surgery ; Soft Tissue Neoplasms ; diagnosis ; metabolism ; pathology ; surgery ; Vimentin ; metabolism ; Young Adult

In this study, the rat type 2 diabetes mellitus (T2DM) model was established through tail vein injection with low dose of streptozotocin (STZ) and high fat diet for 8 weeks, and then treated with Jiaotai Pill. The oral glucose tolerance test (OGTT), fasting serum insulin (FINS), free fatty acid(FFA) levels and blood lipid were assayed. HOMA-IR was calculated. Pancreatic pathology was performed. And pancreatic triglyceride (TG) content was examined by the lipid extraction method. Pancreatic islet cell apoptosis were detected by terminal dexynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL). According to the results, the model group showed abnormal OGTT, increased FINS, HOMA-IR, FFA, lipid disorder, obvious fat accumulation and significantly increased TG content in pancreatic tissues, and enhanced pancreatic islet cell apoptosis. Compared with the model group, the Jiaotai Pill group displayed improved OGTT, reduced FINS, HOMA-IR, FFA, recovered lipid disorder, decreased fat accumulation and significantly declined TG content in pancreatic tissues, and lowered pancreatic islet cell apoptosis. In summary, Jiaotai pill could effectively treat type 2 diabetes in rats. Its mechanism may be related to the reduction in pancreatic fat accumulation and islet cell apoptosis.
Animals ; Apoptosis ; drug effects ; Diabetes Mellitus, Type 2 ; drug therapy ; metabolism ; physiopathology ; Drugs, Chinese Herbal ; administration & dosage ; Fats ; metabolism ; Glucose Tolerance Test ; Humans ; Islets of Langerhans ; cytology ; drug effects ; Male ; Pancreas ; drug effects ; metabolism ; Rats ; Rats, Wistar

Ten compounds were isolated from the artificially induced dragon's blood of Dracaena cambodiana by various column chromatographies on silica and sephadex LH-20 gel. Based on spectral analysis of NMR and MS, their structures were identified as 3, 4-dihydroxyallylbenzene (1), 3', 4', 5'-trimethoxycinnamylalcohol (2), pinoresinol (3), (2R)-7, 4'-dihydroxy-8-methylflavane (4), (2R)-7,4'-dihydroxy-5-methoxy-8-methylflavane(5),(2S)-7,3'-dihydroxy-4'-methoxy-8-methylflavane(6) ,(2S)-4',7-dihydroxy-6, 8-dimethylflavane(7), 4,2',4'-trihydroxychalcone(8), 4,4'-dihydroxy-2-methoxydihydrochalcon(9) and Cambodianin E (10). Antibacterial activity assay showed that compounds 1, 4 and 10 have inhibitory effect on Fusarium oxysporum f. sp. cuben, Fusarium oxysporum f. sp. niveum, Fusarium oxysporum f. sp. vasinfectum and Ralstonia solanacearum.
Antifungal Agents ; chemistry ; isolation & purification ; pharmacology ; Dracaena ; chemistry ; Drugs, Chinese Herbal ; chemistry ; isolation & purification ; pharmacology ; Fusarium ; drug effects ; Molecular Structure ; Plant Extracts ; chemistry ; isolation & purification ; pharmacology ; Spectrometry, Mass, Electrospray Ionization

OBJECTIVETo establish a near-infrared qualitative analysis model to identify the authenticity of Polygonum multiflo- rum and distinguish processed products Polygoni Multiflori Radix.

METHODThe NIR spectra were peformed on over 30 batches of P. multiflorum and Polygoni Multiflori Radix samples and the adulterants Cynanchum bungei, Pteroxygonum giraldii, Polygonum cillinerve to establish the qualitative discriminant model and the conformity test model of Polygonum multifiorum , and cluster analysis was used to analyze the samples from different origins.

RESULTThe model is able to identify correctly P. multiflorum with its counterfeit, and distinguish between P. multiflorum and Polygoni multiflori Radix.

CONCLUSIONNear-infrared spectroscopy can be applied in the identification of P. multiflorum, which could be used to screen Chinese herbal medicine preliminarily.

Drugs, Chinese Herbal ; chemistry ; Plant Roots ; chemistry ; Polygonum ; chemistry ; Spectroscopy, Near-Infrared ; methods

OBJECTIVETo investigate the effect of salidroside on hypoxia-induced apoptosis of corpus cavernosum smooth muscle cells (CCSMCs) in rats.

METHODSRat CCSMCs were cultured in vitro by the enzyme digestion method and identified by immunofluorescent staining of anti-alpha-SMA and anti-Desmin. The non-toxic dose of salidroside was determined by MTT assay. Low-oxygen mixed gas (1% O2, 5% CO2, and 94% N2) was piped into a modular incubator chamber to induce hypoxia. The CCSMCs were divided into a normal, a hypoxia, and a 32 microg/mL salidroside intervention group. The apoptosis of the CCSMCs was detected by flow cytometry and the expression of the caspase-3 protein determined by Western blot.

RESULTSThe majority of the CCSMCs were positive for alpha-SMA and Desmin at immunofluorescent staining. Salidroside at < 32 microg/ml produced no obvious toxicity to CCSMCs. Compared with the normal control group, the rates of early and late apoptosis of CCSMCs were both increased significantly in the hypoxia group ([12.77 +/-1.41]% vs [18.69 +/- 1.29]%, P < 0.01 and [14.63 +/- 2.00]% vs [21.03 +/- 1.530]% , P < 0.05). Western blot showed a markedly increased expression of cleaved caspase-3 (P < 0.01). Intervention with 32 microg/ml salidroside significantly reduced hypoxia-induced early apoptosis of CCSMCs ([13.46% +/- 1.87]%, P < 0.01) and decreased the expression of cleaved caspase-3 (P < 0.01).

CONCLUSIONSalidroside can reduce the expression of cleaved caspase-3 and inhibit hypoxia-induced apoptosis of CCSMCs in rats.

Animals ; Apoptosis ; drug effects ; physiology ; Caspase 3 ; metabolism ; Cell Hypoxia ; physiology ; Cells, Cultured ; Glucosides ; pharmacology ; Humans ; Male ; Myocytes, Smooth Muscle ; cytology ; drug effects ; enzymology ; Penis ; cytology ; drug effects ; Phenols ; pharmacology ; Rats

OBJECTIVEExtracellular signal-regulated kinases (ERKs) can be activated by calcium signals. In this study, we investigated whether calcium-dependent kinases were involved in ERKs cascade activation after global cerebral ischemia.

METHODSCerebral ischemia was induced by four-vessel occlusion, and the calcium-dependent proteins were detected by immunoblot.

RESULTSLethal-simulated ischemia significantly resulted in ERKs activation in N-methyl-D-aspartate (NMDA) receptor-dependent manner, accompanying with differential upregulation of Src kinase and Ca2+/calmodulin-dependent protein kinase II (CaMKII) activities. With the inhibition of Src family tyrosine kinases or CaMKII by administration of PP2 or KN62, the phosphorylation of ERKs was impaired dramatically during post-ischemia recovery. However, ischemic challenge also repressed ERKs activity when Src kinase was excessively activated.

CONCLUSIONSrc family tyrosine kinases and CaMKII might be involved in the activation of ERKs mediated by NMDA receptor in response to acute ischemic stimuli in vivo, but the intense activation of Src kinase resulted from ischemia may play a reverse role in the ERKs cascade.

Analysis of Variance ; Animals ; Brain Ischemia ; enzymology ; pathology ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases ; metabolism ; Disease Models, Animal ; Extracellular Signal-Regulated MAP Kinases ; metabolism ; Gene Expression Regulation ; physiology ; Hippocampus ; cytology ; enzymology ; Male ; Neurons ; enzymology ; pathology ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate ; metabolism ; Signal Transduction ; physiology ; Statistics, Nonparametric ; src-Family Kinases ; metabolism