Animals ; Cognition ; Drugs, Chinese Herbal ; administration & dosage ; therapeutic use ; Electrocardiography ; Female ; Heart ; drug effects ; physiopathology ; Male ; Mice ; Mice, Inbred Strains ; Myocardium ; pathology ; Phytotherapy ; methods

Objective To determine the prevalence and characteristics of the del(GJB6-D13S1830) in Connexin30(Cx30) gene in children with prelingual deafness.Methods Forty-six prelingual deaf children and 30 children with normal comprehension were obtained,and the del(GJB6-D13S1830)in the Cx30 gene were screened by polymerase chain reaction(PCR) in 2 groups.Results Three cases of 46 deaf children were found to have heterozygous del(GJB6-D13S1830) in Cx30 gene.The rest deaf children and the normal controls did not harbor this deletion.Conclusion The heterozygous del(GJB6-D13S1830) in Cx30 gene is one of causes of prelingual deafness.

Objective To evaluate retrospectively the role of 18 F-fluorodeoxyglucose (FDG) PET/CT associated with MRI in the localization of epileptogenic foci. Methods Sixty-seven patients with medically resistant epilepsy were included from 2003 to 2008. All underwent 18F-FDG PET/CT and MRI for presurgical evaluation as well as post-surgical evaluation 12 to 65 months after operation. Based on postoperative seizure occurrence, patients were divided into two groups. One group was free of seizures ( Engel classification Ⅰ, Group 1) and the other was with postoperative seizure occurrence of any type ( Engel classification Ⅱ-Ⅳ, Group 2). X2-test or Fisher's exact test was used for the statistical analysis. Results About 71.6% (48/67) patients were defined as group 1, and 19 patients were group 2 ( 11 were Engel Ⅱ , 5 were Engel Ⅲ, and 3 were Engel Ⅳ ). In Group 1, no statistically significant difference was found between concordant (45/63) and discordant findings (3/4) with regard to 18F-FDG PET/CT and MRI images (Fisher's exact test, P ＞0.05). For 41 patients that showed focal abnormality both on MRI and 18F-FDG PET/CT, 80.5% (33/41) were found in group 1. For 20 patients that showed focal lesions on MRI while with multi-focal or generalized abnormal metabolism on 18F-FDG PET/CT, 11 (55.0%) were in group 1 and9 (45.0%) were group 2. There was no significant difference (33/41 vs 11/20, X2 =4.34, P ＜0.05 ). Conclusion 18F-FDG PET/CT associated with MRI may offer more helpful information for pre-surgical evaluation and prediction of prognosis of epileptic patients.

BACKGROUND: Long-term sustained release naltrexone has been reported in clinical application near one year that it can improve emotional state and relieve addiction; therefore, the effect of long-term sustained release naltrexone on memory restoration at neuropsychology level were explored. OBJECTIVE: To observe the effect of long-term sustained release naltrexone on memory ability of opioid addicts. DESIGN, TIME AND SETTING: A contrast observational study was performed at Drug Rehabilitation Centers of Wuhan, Changde, Zhengzhou, and Jiangyang between October and December 2006. Healthy controls were tested in Shenzhen Hospital of Peking University in October 2006. PARTICIPANTS: A total of 88 males with opioid addicts were divided into naltrexone group (n=35), compulsory detoxification group (n=26), and non-treatment group (n=27). Another 22 healthy subjects were considered as the controls. METHODS: At 6-12 months before testing, naltrexone (3.1 g) was subcutaneously implanted into bilateral abdominal wall in the naltrexone group; patients in the compulsory detoxification group underwent completely compulsory detoxification for 6 months, and the examination results, including diamorphine, methadone, and buprenorphine in urine, were negative on the immediately testing day. Event related potential and its wave form were recorded from the opioid addicts in the three groups and from healthy controls who finished semantic recognition between new and old words using portable-type event related potential working system. MAIN OUTCOME MEASURES: Correct rate and response time of semantic memory; latency and amplitude of language related potential-N400. RESULTS: ①There were significant differences in correct rate and response time between three expedmental groups and healthy control group (P ＜ 0.001 ); in addition, correct rate was significantly increased, and response time was significantly shortened in the naltrexone group compared to compulsory detoxification group and non-treatment group (P＜ 0.05). ② N400 latency in the three experimental groups was significantly longer than healthy control group (P ＜ 0.01), while N400 amplitude in the naltrexone group was increased, which was no significant difference compared to healthy control group (P> 0.05) but was significant difference compared to compulsory detoxification group and non-treatment group (P ＜ 0.01). CONCLUSION: Long-term sustained release naltrexone can effectively improve neural function and enhance semantic memory of the opioid addicts.

Objective To obtain acquired immunity evidence in hamsters elicited by third stage hookworm larvae of Necator americanas(NaL3).morphology changes of NaL3 and inflammatory responses in the skin and undedying subcutaneous tissue and muscles of hamsters were observed.Methods Hamsters were immunized subcutaneously with one dose of 150 NaL3 at 2 weeks earlier,and then challenged pereutaneously with 900 NaL3.Skins were excised from post-challenge hamsters at 6,24,72 hours and 1,2 weeks,and then examined under light microscopy.Non-immunized hamsters served as negative controls.Results In non-immunized hamsters the number of NaL3 were 15,33,11.0 and 0 at 6,24,72 hours and 1,2 weeks post-infection.No damaged or dead NaL3 section was observed.All NaL3 exhibited no structural damage and infihrating inflammatory cells were absent from the sunDunding tissues.There were no cutaneous changes.In contrast.the total number of Nak sections in the skin of immunized hamsters were 25,53,15,5 and 4 at 6,24,72 hours and 1,2 weeks post-challenge.Among these NaL3 sections,damaged and dead section number were 0,24,6,0,0 and 0,0,7,5,4.At 24 hours post-challenge the Nak exhibited cutieular swelling and damage.By 72 hours post-challenge pyknosis of the somatic cells nuclei and sparseness or loss of definition in the internal structures of NaL3 were seen.One or two weeks after chanenge,the NaL3 showed severe damage or even dead with remnants.Inflammatory responses including macrophages,epithelioid cells and eosinophils infiltrating and granulomata forming were mainly seen around the NaL3 sections in the skin of immunized hamsters.Conclusions Hamsters initially immunized with NaL3 exhibited obvious acquired immunity protection against percutaneously challenged infection as evidenced by vigorous inflammatory responses in the skin and underlying subcutaneous tissue and muscle.

Background and purpose:Chemotherapy plays an important role in the treatment of breast carcinoma by inhibiting the tumor growth and inducing the apoptosis.MAPK transduction pathway is closely related to proliferation and apoptosis of varieties of tumor cells,inhibition of MAPK pathway may increase the efficiency and decrease the toxicity of chemotherapy.Our study was to investigate the effect of MEK inhibitor PD98059 in response of breast cancer cell lines to Epirubicin.Methods:Human breast cancer cell lines MCF-7 and MCF-7/ADR were used as cell models.Epirubicin(EADM),PD98059(inhibitor of MAPK Kinase-MEK),or EADM+PD98059 was added into the culture medium,the expression of MEK2 and p-ERK were measured by Western blot,the growth of the two cell lines were measured by MTT.Results:ERK activity was elevated in MCF-7 after the treatment of EADM,the cells were more sensitive to EADM if combined with PD98059,while in MCF-7/ADR,ERK activity kept unchanged after EADM treatment,and PD98059 has no effect on the sensitivity of cells to EADM.Conclusion:MAPK signal transduction may be activated in some cells treated by EADM,adding inhibitor of MAPK signal transduction could improve the sensitivity of the cells to EADM.

Objective To study the damage to striatum in patients perorally addicted to compound codeine phosphate solution by using the brain dopamine transporter SPECT imaging. Methods Patients p erorally addicted to compound codeine phosphate solution ( n = 29 ) and addicted to heroin ( n = 27 ), as well as healthy volunteers (n = 31 ) were included in the study. Each of them underwent dopamine transporter (DAT) SPECT imaging with 99Tcm-2β-[N, N'-bis-( 2- mercaptoethyl ) ethylenediamino] methyl, 3β-(4-chlorophenyl)tropane (99Tcm-TRODAT-1). The striatum volume (V, cm3), mass (m, g) and radiactivity ratio (Ra) of striatum to whole brain were calculated using physio-mathematical modeling method.R esults Bilateral striatum of healthy volunteers showed typical "panda eyes" pattern and the distribution of DAT was uniform and symmetrical. Bilateral striatum of patients addicted to compound codeine phosphate showed impaired tracer uptake, similar to those addicted to heroin. The V, m and Ra of bilateral striatum of patients addicted to compound codeine phosphate were (23.68 ±4.94) cm3, (24.87 ±5.19) g and (5.01 ±0. 88 ) %, respectively, which were significantly lower than those of healthy controls: ( 35.39 ± 4.42 ) cm3,(37.16 ±4.64) g and (7.93 ±0.86)% (t = -9.69, -9.69, - 13.01, all P =0.000), but significantly higher than those addicted to heroin: ( 18.87 ± 4.66 ) cm3, ( 19.81 ± 4.90 ) g and (4.26 ± 1.02 ) % ( t =3.74, 3.74, 2.96, P = 0.000, 0.000, 0.005 ). Conclusion Long-term peroral intake of compound codeine phosphate solution may damage the function of cerebral striatum, which is someway similar to though less severe than, the impairment caused by heroin.

AIMTo observe the injured effect of homocysteine (HCY) on cardiomyocytes and investigate its signal transduction mechanism as well as the key regulatory link.

METHODSCardiomyocytes were isolated from neonatal Wistar rats. After incubation with HCY, the survival rate of cardiomyocytes was determined by trypan blue stained assay, while the apoptosis rate was measured by TUNEL and FCM. Western blot and EMSA were used to tested ERK2 protein phosphorylation and NF-kappaB active expression in cardiomyocytes, respectively.

RESULTSThe survival rate of cardiomyocytes treated with HCY was reduced significantly in dose- and time- dependent manner. It was found that 10(-3) mol/L HCY could increase the apoptosis rate of cardiomyocytes to the peak (7.65%) at 4 h stress. Several HCY levels revealed the strong inhibitory effect on ERK2 protein phosphorylation, especially, 10(-3) mol/L HCY decreased the level of active ERK2 expression to 3.04% of control at 4 h (P < 0.01). NF-kappaB activation was also inhibited significantly by several HCY level for different time in cardiomyocytes.

CONCLUSIONHCY plays an important role in injury of cardiomyocytes and apoptosis is a form of HCY-induced injury to cardiomyocytes. HCY can block ERK2 protein phosphorylation and NF-kappaB activation, which contribute to the injury of cardiomyocytes.

Animals ; Apoptosis ; drug effects ; Cells, Cultured ; Homocysteine ; pharmacology ; Myocytes, Cardiac ; drug effects ; metabolism ; NF-kappa B ; metabolism ; Rats ; Rats, Wistar ; Signal Transduction

To investigate the effect of stress on homocysteine metabolism in the rat and explore the mechanism as well as the key regulatory link of stress-induced hyperhomocysteinemia, male Wistar rats were treated with restraint stress while control rats received routine treatment. By HPLC-fluorometry, the homocysteine level in rat plasma was determined. Cystathionine beta-synthase (CBS) activity in blood, heart, liver and kidney was measured by radioisotope assay using [(14)C]-serine as the labeled substrate. Total RNA was isolated from rat liver after restraint stress. RT-PCR and Northern blot were used to estimate the level of CBS mRNA. The results showed that hyperhomocysteinemia was induced by restraint stress. The highest CBS enzyme activity was seen in rat livers. A decrease in hepatic activities of CBS was found in restraint stress rats. The 29.4% +/-2.5% reduction in the activity of CBS was accompanied by a 44.1% +/-3.4% decrease in its mRNA level. CBS enzyme activity was slightly elevated in the kidney of stressed rats while it was almost undeterminable in the cardiovascular system. The study suggests that stress leads to an inhibition of the transsulfuration pathway in homocysteine metabolism. The hepatic CBS influenced by stress at the level of transcription exerts a profound effect on the circulating levels of homocysteine. The liver is the key organ where stress affects homocysteine metabolism.
Animals ; Down-Regulation ; Homocysteine ; metabolism ; Hyperhomocysteinemia ; blood ; etiology ; Male ; Rats ; Rats, Wistar ; Restraint, Physical ; Stress, Physiological ; complications ; metabolism

Hemangioma ; pathology ; Humans ; Joint Diseases ; pathology ; Male ; Middle Aged ; Synovial Membrane ; pathology