OBJECTIVETo study the effect of 1-tetrahydropalmatine (1-THP) on the spontaneous electric discharge (SED) induced by chronic dorsal root ganglion neurons compression.

METHODSUsing single fiber recording method, the SED of 84 neurons class A induced by compression were recorded. The effect of 1-THP on the SEDs and its relation with concentration were observed.

RESULTSIn the 84 SED of neurons, 25 showed periodical rhythmicity (PR) and 59 showed non-periodic rhythmicity (non-PR). 1-THP (100 micromol/L) inhibited SED in 16.0% (4/25) of neurons with PR and 67.8% (40/59) of neurons with non-PR (P < 0.01) in an effect-dose dependent manner, the higher the concentration of 1-THP, the more the inhibition, with quicker inhibiting in initiation and longer time needed for recovery. SED in 57.1% neurons were recovered 20 min after elution, but unrecovered even after 3 h in the others.

CONCLUSION1-THP shows inhibitory effect on the A-fiber SED induced by chronic dorsal root ganglion neurons compression.

Action Potentials ; drug effects ; Animals ; Berberine Alkaloids ; pharmacology ; Ganglia, Spinal ; drug effects ; injuries ; physiology ; Male ; Neurons ; drug effects ; physiology ; Rats ; Rats, Sprague-Dawley

Animals ; Aorta ; pathology ; Apolipoproteins E ; deficiency ; Atherosclerosis ; metabolism ; pathology ; Female ; Glycosides ; isolation & purification ; pharmacology ; Intercellular Adhesion Molecule-1 ; metabolism ; Mice ; Plants, Medicinal ; chemistry ; Polygonum ; chemistry ; Vascular Cell Adhesion Molecule-1 ; metabolism

Objective To identify mutations site and clinical characteristics of a familial hypercholesterolemia(FH) proband diagnosed clinically through DNA sequencing and family analysis in the proband and his family members of 3 generations.Methods Blood samples and clinical data of the kindred of total 29 from 3 generations members were collected.Proband had a physical examination electrocar-diogrom and vascular ultrasound.The proband and his family members took routine clinical exams,and genomic DNA was isolated.The promoter region and the 18 exons of low density liporotein receptor(LDLR) gene were screened by Touch down polymerase chain reaction -single strand conformation polymorphism(PCR-SSCP) and DNA sequencing.The result of sequencing were matched gene sequence published in the BLAST database.Results 1.Increased intima-media thickness and plaque were detected in the common carotid artery,right subclavian artery of the proband.Aortic valve regurgitation was found by echocardiography.2.No mutation R3500Q of ApoB100 was observed.3.Two heterozygous mutations in exon 10 and 13 of LDLR gene (W462X and A606T) were identified.The proband and 5 members of paternal relatives showed W462X heterozygosis mutation in exon 10 of LDLR gene which introduced the change from tryptophone to a new stop codon.The proband's mother and grandmother harboured A606T heterozygous mutation in exon 13 of LDLR gene due to a single base pair substitution of G for A in the codon for residue 1 879.Conclusions Disease causing mutations of proband are W462X and A606T compound heterozygosis mutation in exon 10 and 13 of LDLR gene inherited from mother and father.Proband shows homozyous phenotype though the genotype analysis indicates heterozygous mutations.

Objective To explore the role of xome apoptosis regulators during the development in rat cochlea.Methods The morphological development process of cochlea was obserred in Wistar rat aged between embryo day 13 to postnatal day 14 in this experiment.Survivin and caspase-3 Were respectively detested at protein and mRNA levels by immunohistochemistry and reverse transcription polymerage chain reaction(RT-PCR).Results The expression of survivin and cagpage-3 located in the bottom wall of the cochlear duct.Not only they widespread in the cell proliferation,but also they gyadually enhanced in the cell differentiation.Both of them had a crest-time.and survivin was prior to caspase-3.In organ of corti during adult time,caspase-3 Wag not present and survivin was only expressed.Conclusions During the development of the rat cochlea,both of them had similar location and trend.But they were derangement.This showed that beth of them participated in the cochlear morphological development.It wag suggested that the interaction between survivin and caspas-3 regulated the apoptosis,promoted the cochlear morphological development.

Objective To evaluate the value of superb micro-vascular imaging( SMI) in evaluating the efficacy of uterine fibroids treated with high intensity focused ultrasound( HIFU) . Methods Forty patients with single fibroid were selected before and after HIFU treatment ,color Doppler flow imaging(CDFI) ,SMI and contrast-enhanced ultrasound ( CEUS ) pattern were used to detect the lesions . CEUS was used as standard . The correlation of different blood flow levels in the fibroids with SMI and the efficacy of HIFU were evaluated . Results Before HIFU treatment ,the blood flow signals of different degrees were found in the uterine fibroids . SMI showed that 4 fibroids( 10 .0％ ) were in the first degree ,21 fibroids( 52 .5％ ) were in the second degree and 15 fibroids ( 37 .5％ ) were in the third degree . CEUS showed that 8 fibroids ( 20 .0％ ) were hypo-enhanced ,19 fibroids( 47 .5％ ) were iso-enhanced and 13 fobroids(32 .5％ ) were hyper-enhanced . The correlation analysis showed that there was close relationship between the results of SMI and CEUS( Kappa = 0 .754 , P = 0 .00) . After HIFU treatment ,SMI and CEUS had no statistical difference in evaluating the efficacy of HIFU( P > 0 .05) . The ratio of non-perfused volume and the ratio of the volume reduction at 6 months after HIFU in the third degree of SMI were lower than those in the first and second degrees( P < 0 .05) . Conclusions There are some relationships between SMI and CEUS in evaluating the blood flow signal of uterine fibroids . SMI can prompt therapeutic efficacy of uterine fibroids ablated by HIFU and provide some clinical reference values .

OBJECTIVETo explore the electrophysiological effects of antiarrhythmic drugs on pacemaker cells of left ventricular outflow tract.

METHODSBy using conventional intracellular microelectrode technique to record action potentials, series antiarrhythmic drugs were used to investigate the electrophysiological features and regularities of spontaneous activity of left ventricular outflow tract.

RESULTS(1) Perfusion with 1 micromol/L quinidine resulted in a significant decrease in rate of pacemaker firing (RPF, P < 0.05), velocity of diastolic depolarization (VDD, P < 0.05), amplitude of action potential (APA, P < 0.05), and maximal rate of depolarization (V(max), P < 0.05), and a marked prolonging in 50% and 90% of duration of action potential (APD50 and APD90, P < 0.05). (2) 1 micromol/L lidocaine decreased RPF, VDD, MDP, APA and V(max) significantly (P < 0.05), shortened APD50 and APD90 notably (P < 0.05). (3) 1 micromol/L propafenone led to a significant decrease in RPF (P < 0.01), VDD (P < 0.05), APA (P < 0.05), V(max) (P < 0.01), and a marked prolonging in APD50 (P < 0.01) and APD90 (P < 0.05). (4) Application of 5 micromol/L propranolol resulted in a significant decrease in RPF and VDD (P < 0.01), MDP and APA (P < 0.01), V(max) (P < 0.05) and a notable prolonging in APD50 and APD90 (P < 0.05). (5) Perfusion with 1 micromol/L amiodarone resulted in a significant decrease in RPF and VDD (P < 0.01), APA (P < 0.01), V(max) (P < 0.05), a marked prolonging in APD50 (P < 0.01) and APD90 (P < 0.05). (6) 1 micromol/L verapamil significantly decreased RPF and VDD (P < 0.01), MDP and APA (P < 0.05), V(max) (P < 0.05), notably prolonged APD50 and APD90 (P < 0.01). (7) 50 micromol/L adenosine significantly decreased RPF and VDD (P < 0.05), APA (P < 0.05), V(max) (P < 0.01), markedly shortened APD50 and APD90 (P < 0.05).

CONCLUSIONAll kinds of antiarrhythmic drugs can decrease the autorhythmicity of guinea pig left ventricular outflow tract. By altering APD50 and APD90, they can affect effective refractory period (ERP) and having a significant effect on autorhythmicity of left ventricular outflow tract.

Animals ; Anti-Arrhythmia Agents ; pharmacology ; Electrocardiography ; Guinea Pigs ; Heart Ventricles ; drug effects

Enterotoxins ; analysis ; Humans ; Microbial Sensitivity Tests ; Staphylococcal Food Poisoning ; microbiology ; Staphylococcal Protein A ; analysis ; Staphylococcus aureus ; isolation & purification

Objective To observe the effects of cell cycle inhibitor on astrocytic proliferation and scar formation and to study neuronal apoptosis after focal cerebral ischemia in rats.Methods Ischemic model was established by photochemistry method.T_2-weighted MRI was performed on the 3rd, 7th, and 30th day after focal cerebral ischemia.The expression of glial fibrillary acidic protein(GFAP)and apoptosis was observed by immunofluorescence.The protein levels of GFAP and proliferation cell nuclear antigen (PCNA), CyelinA and CyclinB1 were measured by Western blotting from the ischemic and sham animals finished on the 3rd, 7th, and 30th day.Results A marked and significant reduction of brain infarction volume was found in Olomoucine-treated ischemic animals(2.27%?0.28% , 1.87%?0.19%, 1.08%? 0.18%)as compared with controls(5.10%?0.35%, 4.60%?0.26%, 3.96%?0.28%, P

OBJECTIVETo investigate molecular mechanism of tanshinone II A inducing differentiation and apoptosis in acute promyelocytic leukemia NB4 cells.

METHODNB4 cells were cultured in vitro and treated with tanshinone II A and observed cellular morphology, cell category and the cellular proliferation. DNA microarray technique was used to analyze the gene expression profiles of NB4 cells induced by tanshinone II A.

RESULT92.8% of NB4 cells treated with 0.5 mg x L(-1) tanshinone II A were induced into mature neutrophils, in which myetocytes and melamyetocytes were 27.0%, banded and segmented neutrophits 68.2%. Cell growth were inhibited. cDNA microarray showed the enormously expressed 183 genes including 23 differentiation associated genes, and other interrelated genes.

CONCLUSIONTanshinone II A inducing differentiation in NB4 cells may be via regulation of many kinds of genes, especially differentiation associated genes expression. This partially explained the molecular mechanism of tanshinone II A inducing differentiation.

Cell Differentiation ; drug effects ; Cell Line, Tumor ; Diterpenes, Abietane ; Drugs, Chinese Herbal ; pharmacology ; Gene Expression Regulation, Leukemic ; drug effects ; Humans ; Leukemia, Promyelocytic, Acute ; drug therapy ; genetics ; metabolism ; Phenanthrenes ; pharmacology

OBJECTIVETo explore the role of monitoring sex chromosome chimeric status by fluorescence in situ hybridization (FISH) in the identification of leukemic extramedullary relapse and post-transplant lymphoproliferative disease (PTLD) in acute lymphocytic leukemia (ALL) after allogeneic hematopoietic stem cell transplantation (allo-HSCT).

METHODSSix ALL patients who received sex-mismatched allo-HSCT and manifested extravisceral lymphadenectasis or local lump were investigated. The sex chromosome chimeric status in tumor tissues and bone marrows (BM) were monitored by FISH, and EBV-RNA in the tumor tissues were detected by in situ hybridization (ISH).

RESULTSThe sex chromosomes in BM of all 6 patients were 100% donor-derived. Among the sex chromosome chimeric status of tumor tissues, three patients were mainly recipient-derived, and the percentage of sex chromosomes derived from recipients were 100%, 100% and 98.0%, respectively, and then they were diagnosed leukemic extramedullary relapse. The other 3 patients were donor-derived, the percentage was 98.5%, 96.0% and 91.5%, respectively, and were diagnosed PTLD. EBV-RNA and latent membrane protein (LMP-1) were positive in 2 patients with PTLD and negative in the other 4 patients. One patient with extramedullary relapse obtained partial remission, one with PTLD gained complete remission, and the others died eventually after therapy.

CONCLUSIONMonitoring the sex chromosome chimeric status by FISH is an effective method to distinguish leukemic extramedullary relapse from PTLD in ALL received sex-mismatched donor HSCT.

Adolescent ; Adult ; Female ; Hematopoietic Stem Cell Transplantation ; Humans ; In Situ Hybridization, Fluorescence ; methods ; Lymphoproliferative Disorders ; pathology ; surgery ; Male ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; pathology ; physiopathology ; surgery ; Recurrence ; Sex Chromosomes ; genetics ; physiology ; Transplantation Conditioning ; Young Adult