AIM:To investigate the possible mechanism of magnolol on the damage of PC12 cell induced by the addition of 6-OHDA placed in an incubator for 24 h with rat's pheochromocytoma cell of adrenal medulla in the absence and presence of magnolol. METHODS:Cell viability was measured by MTT method. Reactive oxygen species (ROS) and aspartate-specific cysteine proteases-3 (Caspase-3) concentration(s) were assayed by fluorescence spectrophotometer. RESULTS:Cell activity declined sharply by the addition of 6-OHDA at concentration of 100 ?mol/L,the pre-treatment of magnolol(0.1~10 ?mol/L)could significantly increase the PC12 cell activity and prevent the increased ROS and caspase-3. CONCLUSION:Magnolol may protect the cell trauma induced by 6-OHDA,and the mechanism is related to inhibiting the 6-OHDA-induced elevation in intracellular ROS levels and reducing the caspase-3 activity.

Spotted fever caused by spotted fever group rickettsiae (SFGR) is found throughout China. During 2007–2008, 28 human SFGR isolates and 34 rat SFGR isolates including 15 isolates from Rattus fulvescens, 5 isolates from R. edwardsi, 7 isolates from Callosciurus erythraeus roberti and 7 isolates from Dremomys rufigenis) were obtained from L929 cell culture. Previous research indicated that the 62 strains of SFGR mentioned above shared not only the same serophenotype but also 100% of identity sequences of 16S rRNA, gltA, ompA, groEL and 17KD, which enabled us to apply multispacer typing (MST) to the 62 SFGR isolates in the study. Six primer pairs, which were used for typing of Rickettsia rickettsii and Rickettsia conorii, were chosen, and the results exhibited greater nucleotide polymorphisms among the 62 isolates tested. A total of 48 distinct genotypes were identified. The dominant genotype, represented by h3 isolates, accounted for 21.7% (13/60) of the isolates tested, and the remaining 47 genotypes were all unique. Phylogenetic analysis showed that all the 48 genotypes could be classified in the same clade, while the genetically related strain, R. heilongjiangensis, was close but not the same as the cluster. We concluded that the genetically diverse of spotted fever group rickettsiae strains are endemic in Chengmai County, Hainan Province, China.

Spotted fever caused by spotted fever group rickettsiae (SFGR) is found throughout China. During 2007—2008, 28 human SFGR isolates and 34 rat SFGR isolates including 15 isolates from Rattus fulvescens, 5 isolates from R.edwardsi, 7 isolates from Callosciurus erythraeus roberti and 7 isolates from Dremomys rufigenis) were obtained from L929 cell culture. Previous research indicated that the 62 strains of SFGR mentioned above shared not only the same serophenotype but also 100% of identity sequences of 16S rRNA, gltA, ompA, groEL and 17KD, which enabled us to apply multispacer typing (MST) to the 62 SFGR isolates in the study. Six primer pairs, which were used for typing of Rickettsia rickettsii and Rickettsia conorii, were chosen, and the results exhibited greater nucleotide polymorphisms among the 62 isolates tested. A total of 48 distinct genotypes were identified. The dominant genotype, represented by h3 isolates, accounted for 21.7% (13/60) of the isolates tested, and the remaining 47 genotypes were all unique. Phylogenetic analysis showed that all the 48 genotypes could be classified in the same clade, while the genetically related strain, R.heilongjiangensis, was close but not the same as the cluster. We concluded that the genetically diverse of spotted fever group rickettsiae strains are endemic in Chengmai County, Hainan Province, China.

Fatal Outcome ; Herbicides ; poisoning ; Humans ; Injections, Intravenous ; Paraquat ; poisoning ; Poisoning ; mortality

Objective To establish a method of PKH26 labeled bone marrow-derived endothelial progenitor cells (EPCs) into rats with liver fibrosis and observe cell immigration and differentiation in the liver after transplantation.Methods Bone marrow-derived EPCs were isolated and cultured from rats with liver fibrosis,and then labeled with PKH26 in vitro.Under the scanning confocal microscopy and flow cytometry,PKH26 fluorescent labeling rate and cell survival rate were measured.EPCs of PKH26 fluorescent labeling were transplanted into rats with liver fibrosis via the tail vein,and the migration situation was observed in the liver.Endothelial cell markers CD31 and von willebrand factor (vWF) were detected by using immunofluorescence.Results The PKH26-labeled EPCs appeared red fluorescence and the labeling rate was 96.65 ％.As compared with unlabeled cells,the labeled cells grew well,and had no significant changes in the growth curve.After transplantation into the liver of rats,the PKH26 labeled cells were mainly distributed in blood vessel endothelium along fibers and hepatic sinusoids in hepatic lobule.Endothelial cell-specific antigens such as CD31 and vWF could be detected along the vascular walls.Conclusion PKH26 could be used to label and track EPCs in the liver of rats with liver fibrosis in vitro.The PKH26-labeled cells may migrate to the surrounding of the hepatic vessels and differentiate into mature endothelial cells.

Objective To evaluate the effect and pathological characters for patients with early esophageal carcinoma and intraepithelial neoplasia after endoscopic submucosal dissection (ESD). Methods 69 patients from January 2013 to January 2016 were treated with ESD at the early stage of esophageal carcinoma and intraepithelial neoplasia. The clinical features and the size of the lesions of all the patients were collected. Then analyzed postoperative complications and pathological characteristics. Results Among 69 cases, 16 were early esophageal cancer, 38 were high-grade esophageal neoplasia and 35 were low-grade esophageal neoplasia. The whole piece resection rate was 100.00 % (69/69), complete resection rate and curative resection rate was 95.65 % (66/69), respectively. The largest removal diameter is 7.0 cm. Biopsy accuracy was 69.57 % (48/69). Compared with biopsy, diagnostic accuracy with ESD specimens is higher. Conclusion The early esophageal carcinoma and intraepithelial neoplasia can be treated with ESD. ESD can resect lesions primarily, provide complete specimen for further pathological assessment and improve diagnostic accuracy.

Objective To understand the prevalence and the factors associated with depression and anxiety among patients attending the community-based methadone maintenance treatment(MMT) program.Methods 9 MMT clinics in 3 provinces were randomly selected,in which 1 301 MMT patients who met the criteria of recruitment were all interviewed.A cross-sectional study by administrative questionnaire was employed to investigate the demographics,drug abuse and MMT treatment status of the respondents.The 1301 respondents were also evaluated for depression and anxiety by SDS(Self-Rating Depression Scale) and SAS(Self-Rating Anxiety Scale) respectively.ANOVA and multivariate linear regressions analysis was used to verify the factors associated with depression and anxiety respectively.Results The prevalence of depression and anxiety among the MMT patients were 38.3%(498/1 301) and 18.4%(239/1 301).The multivariates linear regression analysis indicated that at the level of ?=0.05,gender,employment status were associated with depression,while gender,employnment status,educational level,drug abuse and methadone daily dosage were associated with anxiety.Conclusions There are certain proportions of MMT clients who suffer from depression and anxiety.The MMT clinic staff should put more emphasis on the efforts to reduce psychological disorders and its potential risks by enhancing psychological councelling,intervention and social support towards the MMT patients.

BACKGROUND:Previous studies have indicated that resistin stimulates a large set of chemokines in chondrocytes that are known to be important in inflammatory joint lesions.
OBJECTIVE:To further investigate the mechanism of co-regulation roles of transcription and post-transcription in the up-regulation of two chemokine genes CCL3 and CCL4 in chondrocytes in response to resistin.
METHODS:Human chondrocytes, T/C-28a2 and ATDC5 cels were cultured. The function of resistin on the chemokine genes, and the expression of C/EBPβ, nuclear factor-κB isoforms and chondrogenic specific miRNAs were tested by qPCR. The co-regulation of C/EBPβ and nuclear factor-κB was investigated by nuclear factor-κB inhibitor (IKK-NBD) and C/EBPβ inhibitor (SB303580) treatments, and subcelular localization was detected with or without resistin stimulation.
RESULTS AND CONCLUSION:Resistin could increase the expression of chemokine genes independently. Chondrocytes reacted in a non-restrictedly cel-specific manner to resistin; C/EBPβ inhibitor, nuclear factor-κB and some chondrogenic specific miRNAs in a combinatorial manner regulated chemokine gene expression. The activity of C/EBPβ was augmented by a transient increase in activity of nuclear factor-κB, and both transcription factors acted independently on the chemokine genes, CCL3 and CCL4.

OBJECTIVETo provide guidance for the high-dose methotrexate (HD-MTX) treatment of pediatric acute lymphoblastic leukemia (ALL), and to understand the impact of SLCO1B1c.521T>C (rs4149056) variant on methotrexate (MTX) pharmacokinetics and clinical outcome in children with ALL.

METHODEighty-two children with ALL in Division of Hematology of Wuhan Children's Hospital from January 2008 to February 2013 were enrolled. All patients were genotyped for rs4149056 single nucleotide polymorphism (SNP) into wild-type group (TT genotype) and variant group (TC/CC genotype). According to the ALL-BFM 2000 protocol, all patients received intravenous infusion of MTX every ten days at 3 to 5 g/m(2). Leucovorin rescue was performed after 36 hours of the MTX administration and its dose was adjusted according to the MTX plasma concentration at 48 hours. The concentrations of MTX and its metabolite at 24, 48 and 72 h were determined by high performance liquid chromatography with solid phase extraction. Population pharmacokinetic parameters were estimated by the NLME software. The pharmacokinetics, toxicity and leucovorin rescue was compared. The relapse rate within 5 years and event-free survival were followed up.

RESULTEighty-two pediatric patients were classified into two groups: variant group including 20 TC genotype carriers and one CC genotype carrier, wild-type group included 61 patients with TT genotype. Compared with wild-type group, plasma concentration of MTX at 48 and 72 h increased significantly [48 h: (1.00±1.41) vs.(0.34±0.17) µmol/L, t=2.131, P=0.046; 72 h: (0.31±0.26) vs.(0.08±0.04) µmol/L; t=3.995, P=0.001]. Area under the concentration time curve (AUC48-∝) of MTX significantly increased in variant group [(23.18±19.91) vs.(5.66±2.01) h·µmol/L] (t=4.025, P=0.001). Time above the MTX safety threshold (TC>0.1 µmol/L) increased significantly in variant group [(95.3±22.0) vs.(67.1±7.5) h, t=5.880, P<0.001]. Rescue dosage of leucovorin in variant group was higher than that in wild-type group [(312.7±287.8) vs.(140.6±27.5) mg/m2, t=2.614, P=0.017]. The children carrying rs4149056 C allele suffered from a higher frequency of serious adverse effect [gastrointestinal toxicity: 33% (7/21) vs. 5% (3/61);hepatic toxicity: 24% (5/21) vs. 2% (1/61)]. The difference was statistically significant (χ2=9.275, 8.289, all P<0.05). Hospital stay of variant group was significantly longer than that of wild-type [(4.95±1.43) vs. (4.05±0.22) d, t=2.881, P=0.009]. The relapse rate within 5 years of variant group and wild-type group were 9% (2/21) and 13% (8/61), respectively. There were no significant differences in the event-free survival between the two groups (χ2=0.001, P=0.971).

CONCLUSIONThe SLCO1B1 c.521T>C variant was an important determinant of MTX pharmacokinetics. An appropriate leucovorin dose raise in variant group was beneficial to reducing the serious toxicity and did not affect the long-term clinical outcome.

Alleles ; Antineoplastic Combined Chemotherapy Protocols ; Asparaginase ; Child ; Daunorubicin ; Disease-Free Survival ; Genotype ; Humans ; Leucovorin ; administration & dosage ; Methotrexate ; administration & dosage ; pharmacokinetics ; Organic Anion Transporters ; genetics ; Polymorphism, Genetic ; Polymorphism, Single Nucleotide ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; drug therapy ; genetics ; Prednisone ; Solute Carrier Organic Anion Transporter Family Member 1b1 ; Treatment Outcome ; Vincristine