Objective To study the effects of total saponins of Chaenomeles speciosa on release of β-hexosaminidase from rat basophilic leukemia-2H3 ( RBL-2H3 ) mast cells. Methods After rat RBL-2H3 mast cells were prepared, total saponins of Chaenomeles speciosa and the RBL-2H3 mast cells were co-cultured.The toxic effects of total saponins of Chaenomeles speciosa on mast cells were detected by MTT method, β-hexosaminidase release rate was measured by fluorescence quantitative spectrophotometric method, and cell supernatants of tumor necrosis factor-α( TNF-α) release were detected by ELISA. Results After total saponins of Chaenomeles speciosa were co-cultured with RBL-2H3 mast cells with different antigen stimulation, β-hexosaminidase release rates and the levels of TNF-α of mast cells significantly decreased compared with the control group. Conclusion Total saponins of Chaenomeles speciosa inhibit the degranulation of RBL-2H3 mast cells in a dose dependent manner, which provids basis for studying mechanism of inhibiting allergic reactions.

Objective To study the clinic effects and safety of budesonide suspension combined with tubertaline solution for nebulization therapy on infantile asthma.Methods Seventy-five cases with asthma were divided into 3 groups randomly,double-blinded and controlled,each group having 25 cases.Group A inhaling tubertaline solution(bricanyl),while group B inhaling pulmicort respules combined with bricanyl,group C inhaling budesonide suspension(pulmicort respules)only.Results In group A,16 cases was cure,3 cases was markedly improved,6 cases was failure,the total efficacy rate was 76 percent.In group B,22 cases was cure,2 cases was markedly improved,1 case failed,the total efficacy rate was 96 percent.While in group C,14 cases was cure,4 cases was markedly improved,7 cases failed,the total efficacy rate was 72 percent.The difference of efficacy rate between group A and group B was significant(P0.05).Conclusion Pulmicort respules combined with bricanyl for nebulising inhalation is effective and safety on infantile asthma and its effect is better than inhaling bude-sonide or tubertaline only.

ObjectiveTo evaluate the efficacy of short-segment transpedicular fixation combined with augmentation vertebroplasty in treatment of thoracolumbar burst fractures. MethodsFrom November 2006 to September 2009, 37 patients with thoracolumbar burst fracture were admitted and received transpedicular fixation combined with calcium sulfate cement augmentation vertebroplasty, and the clinical data including fracture types, complications and following-up results were collected for analysis. The multimethod evaluation strategies involved the anterior vertebral body height, the sagittal Cobb's angle, the restoration of nervous function, internal fixation failure, visual analogue scale (VAS) and Oswestry disability index (ODI) were retrospective analyzed. Results All patients were followed up for average 19 months (range, 14-37). There were no internal fixation failure, loss of reduction, neurological complications in all the patients. In 16 patients with partial neurologic deficits, 14 initially improved at the final follow-up, with no deterioration of neurologic functions. The mean time of calcium sulfate cement obvious absorption and union was 3 months and 5 months postoperatively, respectively. The anterior vertebral body height was 55.40％before surgery and 85.46％ after surgery on average, ended up with 82.35％. The sagittai Cobb's angle was improved from 22.45° to 6.86°, ended up with 9.66° on average. The mean VAS and ODI at the final followup were respectively 1.2 and 20.4 on average. ConclusionShort-segment transpedicular fixation combined with augmentation vertebroplasty appears to be effective in achieving stable biomechanics with high security,which seems to be a feasible option in the management of thoracolumbar burst fractures.

Appropriate selection and measurement of lead biomarkers of exposure are critically important for health care management purposes, public health decision making, and primary prevention synthesis. Lead is one of the neurotoxicants that seems to be involved in the etiology of psychologies. Biomarkers are generally classified into three groups: biomarkers of exposure, effect, and susceptibility.The main body compartments that store lead are the blood, soft tissues, and bone; the half-life of lead in these tissues is measured in weeks for blood, months for soft tissues, and years for bone. Within the brain, lead-induced damage in the prefrontal cerebral cortex, hippocampus, and cerebellum can lead to a variety of neurological disorders, such as brain damage, mental retardation, behavioral problems, nerve damage, and possibly Alzheimer's disease, Parkinsons disease, and schizophrenia. This paper presents an overview of biomarkers of lead exposure and discusses the neurotoxic effects of lead with regard to children and adults.
Alzheimer Disease ; chemically induced ; metabolism ; pathology ; physiopathology ; psychology ; Animals ; Behavior ; drug effects ; Biomarkers ; metabolism ; Brain ; metabolism ; pathology ; physiopathology ; Brain Diseases ; chemically induced ; pathology ; physiopathology ; Environmental Exposure ; adverse effects ; Humans ; Lead ; pharmacokinetics ; toxicity ; Lead Poisoning ; etiology ; metabolism ; pathology ; physiopathology ; psychology ; Neurotoxicity Syndromes ; etiology ; metabolism ; pathology ; physiopathology ; psychology ; Parkinson Disease, Secondary ; chemically induced ; metabolism ; pathology ; physiopathology ; psychology ; Schizophrenia ; chemically induced ; metabolism ; pathology ; physiopathology

Objective In order to investigate the relationship between hearing loss and diabetic peripheral neuropathy( DPN ) via comparing the pure tone thresholds and vibration perception threshold(VPT) in type 2 diabetic patients and control person without diabetes. Methods 173 subjects including 138 type 2 diabetic patients(DM)and 35 non-diabetes controls were examined for VPT and hearing threshold. Nerve conducting velocity ( NCV )including sensory nerve conducting velocity( SCV )and motorial nerve conducting velocity( MCV )of diabetic patients were determined. The participants were divided into three groups: control group (n = 35 ), DM group without peripheral neuropathy( non-PN group, n = 74 ), and DM group complicated with peripheral neuropathy (PN group,n = 64 ). The clinical characteristics, biochemical parameters , the incidence of sensorineural hearing loss ( SNHL),pure tone threshold, and VPT were compared among three groups. At last, the relationship between hearing thresholds and NCV were analyzed. Results The incidence of hearing impairment of sensorineural type was 29.69% in PN group, which was significantly higher than that of non-PN group( 17.57% )and control group( 17. 14% ). There was significant differences in age, duration of diabetes, glycolated hemoglobin (HbA1c), glycolated serum albumin ( GA), Fasting blood glucose( FPG), 2h postprandial blood glucose( PPG), VPT, and hearing threshold among the three groups( all P＜0. 05 ). The value of hearing threshold increased significantly( all P＜0. 05 ) in 3 VPT subgroups with VPT≤ 15 V, VPT 16-25 V, and VPT ＞25 V. The Spearman correlation analysis showed median NCV was negatively correlated with hearing threshold on 1.00, 2.00, 4. 00, and 8. 00 kHz ( All P ＜ 0. 05 ). The logistic regression analysis indicated that the age( regression coefficient =0. 088, P＜0. 01 ) was the independent risk factor of SNHL, median nerve MCV ( regression coefficient = -0. 135, P = 0. 046 ) was the important influencing factor of SNHL. Conclusion Diabetic patients are more likely to suffer from impaired middle-frequency and high-frequency hearing, DPN in patients is often complicated with hearing impairment. Age and median nerve MCV were major risk factors of SNHL in diabetic patients.

Objective To study the immune regulatory effect of natural killer cell(NKT) in the early stage of murine liver injury induced by type 5 adenovirus(Ad5). Methods Animal models were con-structed by injected C57BL/6 mice with 1.5×109-3×109 PFU Ad5 into the tail vein. Liver injury of mouse at day 0, 1, 2, 3, 4, 5 after infection was determined by HE staining and serum ALT/AST(alanine amin-otransferase/aspartate aminotransferase) level. Flow cytometry analysis was used to measure the proportion of lymphocytes, expression of Fas/FasL on the surface of NKT cells and level of IL-4, IFN-γ/in NKT cell plasma in the infected mouse liver. RT-PCR was applied to semi-quantify the chemokines and their receptors mRNA in infected mouse liver. Results NKT cells of mouse increased significantly at day 1 after infected with high titer Ads(3×109 PFU), expression of FasL on NKT cell and plasma IL-4, IFN-γ/level in NKT cells were also up-regulated, hence the obviously infiltration of lymphocytes in routine liver. Comparing with high titer Ads infection, low titer Ads infection (1.5×109 PFU) lead to little change of NKT cell proper-tion, and fewer infiltration of lymphocytes in murine liver. Hepatic chemokine RANTES, 1P-10, and MIP-1β mRNA expression in C57BL/6 was up-regulated 2 d after intravenous administration of 3×109 PFU Ad5. Corresponding chemokine receptor CCR5, CCR1, CXCR3 mRNA expression was up-regulated 3 d after in-fection. Conclusion NKT cells play an important role in lymphocytes recruitment into the liver of mouse in-fected with AdS, which may relate to up-regulatio of the plasma IL-4, IFN-γ level and expression of FasL of NKT cells, therefore facilitating the production of chemokines, e.g. IP-10 and Mig.

Adult ; Female ; Graft vs Host Disease ; diagnosis ; Hepatitis, Autoimmune ; diagnosis ; Humans

AIM:To investigate the effect of tumor-suppressor RUNX3 on the transcription of apoptosis-related genes bcl-2,bax,caspase-3,caspase-8,caspase-9 in human gastric carcinoma cells BGC823,and to reveal the apoptosis molecular mechanism promoted by RUNX3. METHODS:The eukaryotic expression vector of human Runx3 gene pcDNA3.1-Runx3 was constructed. pcDNA3.1-Runx3 and blank vector pcDNA3.1 were transfected into BGC823 cells,respectively. After 48 h,the total mRNA and protein were acquired and the expression level of Runx3 was determined by RT-PCR and Western blotting. Then,the mRNA and protein expression of bcl-2,bax,caspase-3,caspase-8 and caspase-9 was determined by RT-PCR and Western blotting. ?-actin was used as a control. RESULTS:The eukaryotic expression vector pcDNA3.1-Runx3 was constructed successfully and transfected into BGC823 cells. RT-PCR and Western blotting confirmed that RUNX3 level was higher in pcDNA3.1-Runx3 transfected BGC823 cells than that in blank vector-transfected cells (P

Objective To observe the expressions of bone morphogenetic protein-2(BMP-2)and bone morphogenetie protein-7(BMP-7)in the synovial tissue of fluorosis rats and its correlation with pathogenic mechanism of fluorosis arthritis.Methods Thirty-two SD rats were randomly divided into 4 groups:the control group,low,moderate and high-dose fluoride group.The control group ate commou fodder.The low,moderate and high dose fluoride group were fed with fodder composed of 25%.35%and 68%of corn(containing fluorine of 148.00 mg/kg)in chronic endemic fluorosis region in Guizhou Province.After 140 days,the expressions of BMP-2 and BMP-7 protein were determined by immunohistochemistry and assayed the absorbanee by computer image-pattern analysis system.Light microscope was used to observe the synovial tissue by Hematoxin Eosin,and calculated the pathological integral of synovium according to pathological grade standard.Results The expressions of BMP-2 (32.50±2.73)and BMP-7(38.90±2.56)in the control group was spare.Compared with the control group,the expressions of BMP-2(59.43±5.12,79.82±6.41,101.76±7.56)and BMP-7(55.10±4.82,78.42±5.61,98.46± 6.05)in the synovial tissue was up-regulated in each experimental groups(P＜0.05),especially in the moderate dose and the high-dose groups(P＜0.05).Compared with the control group(0.54±0.21).the pathological integral of synovium increased(P＜0.05)in each experimental groups(1.04±0.98,4.69±1.28,8.60±2.07).The expressions of BMP-2 and BMP-7 in the synovial tissue was found to be positively related with the pathological integral of synovium(r=0.98,0.99,P＜0.05).Conclusion The BMP-2 and BMP-7 play an important role in the development of fluorosis arthritis,probably by affecting osteogenesis.

Objective: Non-small-cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR)-activating mutations have higher response rate and more prolonged survival following treatment with single-agent EGFR tyrosine kinase inhibitor (EGFR-TKI) compared with patients with wild-type EGFR. However, all patients treated with reversible inhibitors develop acquired re-sistance over time. The mechanisms of resistance are complicated. The lack of established therapeutic options for patients after a failed EGFR-TKI treatment poses a great challenge to physicians in managing this group of lung cancer patients. This study evaluates the in-fluence of EGFR-TKI retreatment following chemotherapy after failure of initial EGFR-TKI within at least six months on NSCLC pa-tients. Methods:The data of 27 patients who experienced treatment failure from their initial use of EGFR-TKI within at least 6 months were analyzed. After chemotherapy, the patients were retreated with EGFR-TKI (gefitinib 250 mg qd or erlotinib 150 mg qd), and the tumor progression was observed. The patients were assessed for adverse events and response to therapy. Targeted tumor lesions were as-sessed with CT scan. Results:Of the 27 patients who received EGFR–TKI retreatment, 1 (3.7%) patient was observed in complete re-sponse (CR), 8 (29.6%) patients in partial response (PR), 14 (51.9%) patients in stable disease (SD), and 4 (14.8%) patients in progres-sive disease (PD). The disease control rate (DCR) was 85.2%(95%CI=62%-94%). The median progression-free survival (mPFS) was 6 months (95%CI=1-29). Of the 13 patients who received the same EGFR-TKI, 1 patient in CR, 3 patients in PR, 8 patients in SD, and 2 patients in PD were observed. The DCR was 84.6%, and the mPFS was 5 months. Of the 14 patients who received another EG-FR-TKI, 0 patient in CR, 6 patients in PR, 6 patients in SD, and 2 patients in PD were observed. The DCR was 85.7%, and the mPFS was 9.5 months. Significant difference was found between the 2 groups in progression-free survival but not in response rate or disease control rate. Conclusion:Retreatment of EGFR-TKIs can be considered an option after failure of chemotherapy for patients who were
previously controlled by EGFR-TKI treatment.