Objective: To report a newly designed method for treating supracondylar fracture of the humerus,and to inquire into the problems of cubitus varus deformity and joint stiff.Methods:Based on a review of anatomy,a new method which called tension band with sphenoid-shaped osteotomy through posterior approach was designed and applied for 46 cases of patients in clinic.The clinical effect was compared with effect of crossing Kirchner's wire.Results:The tension band with sphenoid-shaped osteotomy was a better method and can abide by anatomical and biomechanical principles.After follow-up for 12-36 months,curative effect was estimated as follow:30 cases were excellent,14 cases good and 2 cases poor according to Home's evaluation.Conclusions:It is a better methods in treating supracondylar fracture of the humerus following advantages including simple,reliable fixation and early mobilization etc.

Objective To investigate risk factors of Alzheimer's patients with aspiration pneumonia and inter-vention,to provide a reference for clinical treatment.Methods From January 2013 to June 2014,322 patients with Alzheimer's disease were selected,the incidence of aspiration pneumonia was analyzed,and the age,gender,depression Tian water test grading,underlying diseases,aspiration and other potential factors were analyzed to get risk factors of aspiration pneumonia,and summarized countermeasures.Results Multivariate analysis showed that underlying disea-ses (95%CI =1.694 -5.319,P =0.011),invasive procedures(95%CI =1.884 -6.362,P =0.001),depression Tian water test grade(95%CI =2.184 -9.636,P =0.000),malnutrition(95%CI =2.501 -11.114,P =0.000), Glasgow Coma Scale(95%CI =1.271 -3.569,P =0.011),were risk factors for Alzheimer patients with aspiration pneumonia(P <0.05).Conclusion Alzheimer's patients with inhalation pneumonia have multiple risk factors,more expectoration should be done for caring,e.g.oral care,in order to reduce the probability of pneumonia.

AIM:To investigate the effect of tert-butylhydroquinone ( tBHQ) on the replicative senescence of bone marrow mesenchymal stem cells (BMSCs).METHODS: Late stage BMSCs were continuously treated with tBHQ at concentration of 30 μmol/L for 4 weeks and the cells were used for the following assays immediately .The proteasomal ac-tivity was determined by chemiluminescence method .The samples were subjected to CCK-8 assay and BrdU incorporation as well as flow cytometry analysis for analyzing the cell vitality and proliferation .Percentage of senescent cells was detected by senescence-associatedβ-galactosidase ( SA-β-Gal) staining.The expression of P53 was measured by Western blot .RE-SULTS:After the continuous treatment of tBHQ (30 μmol/L) for 4 weeks, the proteasomal activity of late stage BMSCs increased by 21.96%±1.98%(P<0.05).The cell vitality and survival were significantly increased with the increases in tBHQ doses till 40 μmol/L, and no cytotoxicity reaction with the increased dose of tBHQ till 120 μmol/L was observed . BrdU-positive cells, which represented the cell proliferation , were significantly increased (P<0.05).The proliferation in-dex was also significantly increased by flow cytometry analysis (P<0.05).The SA-β-Gal positive cells and the expression of P53 were decreased (P<0.05).CONCLUSION:tBHQ delays the proteasome dysfunction associated senescence pro-gress of BMSCs by increasing the proteasomal activity .

Objective To investigate the role of endothelial progenitor cells ( EPCs ) transplantation in rats with sepsis induced by endotoxin ( lipopolysaccharides, LPS ). Methods Sixty clean grade Sprague-Dawley ( SD ) rats with genetic background were divided into three groups according to random number table method:control group, model group, and EPCs transplantation group, with 20 rats in each group. The sepsis model was reproduced by intravenous delivery of LPS 5 mg/kg. Rats in control group were injected with the same amount of normal saline. EPCs were isolated, and cultured and identified were fluorescently labeled with the green fluorescent protein ( GFP ) adenoviral transfection method. The EPC transplantation group was injected with LPS, then a fluorescently labeled EPCs suspension was injected via the tail vein 1 hour later. The expression of fluorescent markers of EPCs was detected with both small animal in vivo imaging instrument and frozen section. Seven days after transplantation, abdominal aorta blood was collected to determine interleukins ( IL-6 and IL-10 ) in peripheral blood with enzyme linked immunosorbent assay ( ELISA ), and the lung, liver, and kidney tissues were harvested, the wet/dry ratio of the lung ( W/D ) was calculated, and hematoxylin and eosin ( HE ) staining was performed to observe, the change in histopathology. Toll-like receptor 4 ( TLR4 ) mRNA expression in lung, liver, and kidney tissues was determined with real-time reverse transcription-polymerase chain reaction ( RT-PCR ). Results The positive rate of EPCs cells with double marking of CD133 and CD34 was 99.0% at the 5th generation of subculture by using flow cytometry. After the transplantation of EPCs labeled with the green fluorescent protein, the appearance of fluorescence indicated that EPCs were mainly localized in the chest, and a stronger fluorescence was observed near the blood vessels. EPCs transplantation could significantly reduce the inflammatory cell infiltration and cell damage in lung, liver, and kidney tissue in septic rats. Compared with control group, the expression of IL-6 and IL-10 in the peripheral blood, W/D ratio, and TLR4 mRNA in lung, liver, and kidney were increased significantly in the model group. Compared with model group, the expressions of IL-6 and IL-10 in the peripheral blood were significantly reduced after EPCs transplantation [ IL-6 (μg/L ):2.127±0.118 vs. 2.664±0.438, IL-10 ( ng/L ): 24.5±3.9 vs. 31.5±3.8, both P < 0.01 ]. EPCs transplantation reduced the W/D ratio of lung, liver and kidney tissues ( lung: 4.68±0.24 vs. 5.48±0.15, liver: 3.33±0.11 vs. 3.94±0.09, kidney: 4.08±0.20 vs. 4.84±0.21, all P < 0.05 ], and down-regulated the expression of TLR4 mRNA ( ×103, lung: 782±131 vs. 1 136±126, liver: 39.1±14.0 vs. 69.2±8.7, kidney: 52.2±15.2 vs. 83.5±17.1, all P < 0.01 ). Conclusions EPCs can enter the lung, liver and kidney tissues of the rat successfully after transplantation of EPCs via vein. EPCs transplantation can down-regulate pro-inflammatory process, help to recover the balance of pro-and anti-inflammatory processes, alleviate the damage to the lung, liver, and kidney tissue significantly.

Objective:To prepare highly purified Staphylococcal enterotoxin B(SEB) by affinity chromatography and test its activities.Methods:Anti-SEB McAb(1D2) purified by precipitation method with caprylic acid was coupled to Sepharose 4B. And then the SEB was isolated using an affinity chromatography column. In addition, we analyzed the superantigen activity and antigen activity of SEB.Results:The purification efficiency of SEB was 60.71% by affinity chromatography. Its purity was higher than those of standard preparation and the SEB purified by ion change chromatography. At the same time, the purified SEB by affinity chromatography possesses favourable activities of superantigen and antigen.Conclusion:McAb affinity chromatography could be used for purification of SEB with high efficiency.

According to the results of quantum chemistry calculation and the present research status in the relationship between the structures and the functions of DT, the E154 in DT catalyzing domain was mutated to aspartic acid and arginine in order to study the effects of the alteration on the biological activities. By means of gene site-direct mutation, two mutated genes were prepared and the high performance expression was obtained in E.coli system. The results of toxcity studies indicated that the acute toxicity in guinea pig and cytotoxicities of mutant E154D increased slightly in compared with those of recombination wild toxin, and contrarily, those of E154R decreased obviously.

Aim To explore the effect of adenylate cyclase(AC) antagonists SQ22536 and agonist forskolin on acute lung injury induced by lipopolysaccharide.Methods ICR mice were randomly divided into normal saline control group(N group), model group(group L), dexamethasone group(group D),AC antagonists s(group SQ) and AC agonist group(group F).The ALI mouse model was induced by instilling intratracheally with LPS(2 mg·kg-1), and 6 h later, the lung tissue and alveolar lavage fluid(BALF) were harvested, pathological changes in lung were observed, white blood cell and neutrophil, albumin content in BALF and myeloperoxidase(MPO) activity of lung tissue homogenate were determined, and tumor necrosis factor α(TNF-α), interleukin-1β(IL-1β), interleukin 6(IL-6) and cAMP content in lung homogenates were detected by ELISA.Results Compared with normal saline group, a large number of neutrophils infiltrated around the pulmonary vessel and airway 6 h after LPS intratracheal instillation in model group.White blood cells and neutrophils and protein content increased in BALF;MPO activity and cAMP levels increased in lung tissues.In the lung tissue TNF-α and IL-6, IL-1β content increased, compared with model group.Forskolin could improve the pathological changes of lung tissue, reduce the total number of leukocytes, number of neutrophils and protein content in BALF, and reduce MPO activity and TNF-α content in lung tissue, at the same time it increased the cAMP content;SQ22536 had no significant effect when compared with model group.Conclusion AC agonists have protective effects on LPS-induced acute lung injury in mice, and the mechanism may be related to elevating cAMP levels, inhibiting neutrophil adhesion and chemotaxis and reducing inflammatory factor levels.

Objective To study the treatment effect by addition of granulocyte-colony-stimulating factor (G-CSF) that could reduce the level of residual disease in patients with Ph-positive chronic myeloid leukemia (CML) who appeared to have achieved a suboptimal response to imatinib (IM) alone. Methods Eleven patients with CML who had achieved≥ 35 % Ph-negativity on treatment of IM were enrolled. The initial dose of imatinib was 400 mg or 600 mg orally daily, and G-CSF, 5 μg/kg subcutaneously daily. The administration of G-CSF was postponed or interrupted in the event of leukocytosis (leukocytes ≥ 30 ×109/L) until the whitecell count fell ＜20 × 109/L. Efficacy was assessed by serial monitoring of blood levels of bcr-abl transcripts.Treatment with G-CSF was discontinued if the patient did not achieve a reduction in the transcript level of at least 0.5 log after 6 months. For patients whose bcr-abl transcript levels continued to decline but had not yet reached molecular remission, treatment was designed to continue for 1 to 6 months. Results Of 11 evaluable patients, nine had an appreciable decline in bcr-abl transcript levels(include 7 cases the reduction was greater than 1 log and 2 cases the reduction was greater than 0.5 log), 2 cases the reduction was lower than 0.5 log.In 7 cases the reduction was greater than 1 log, including five patients who did not achieved complete cytogenetic response and two patients achieved complete molecular responses. No bleeding episodes occurred.No patient discontinued therapy because of toxicity and there were no treatment-related deaths. Conclusion The addition of G-CSF should be considered safely and successfully for patients who fail to obtain optimal response to IM alone and this approach deserves further evaluation.

Objective To investigate the mechanisms modulating the functions of dendritic cells (DCs) and suppressing the activation and proliferation of T cells by transforming growth factor-β (TGF-β).Methods Mouse splenic DCs were purified with CD11c+ immunomagnetic beads and the purity of isolated DCs were detected by flow cytometry.Gene chip was used to detect gene expression in DCs after stimulation with TGF-β, and then real-time PCR was performed to analyze the differentially expressed genes in microarray at mRNA level.The activation and proliferation of CD4+ T cells which were co-cultured with DCs after stimulation with TGF-β were detected by flow cytometry.Results The purity of DCs reached over 95% after isolation.TGF-β down-regulated the expression of cell surface markers CD53, CD69, CD33, CD74 and CD93 on DCs;decreased the expression of chemokines Ccl3, Ccl5, Ccl9, Ccl6, Ccl17, Cxcl10, Ccl22, Ccl4, Ccr7, Ccl2, Cxcl9 and Ccl7;inhibited the expression of inflammatory cytokines IL-2ra, IL-12rb2, IL-15ra, IL-1b and IL-15.Moreover, the DCs-mediated activation and proliferation of CD4+ T cells were suppressed by TGF-β.Conclusion TGF-β inhibits the DCs-mediated activation and proliferation of CD4+ T cells by suppressing the expression of surface markers on DCs and down-regulating the expression of chemokines and inflammatory cytokines.

Objective To assess the toxicity risks of diphenylchlorarsine (DA) to environments, human beings and livestock. Methods Totally 120 mice were randomly divided into 6 groups and given DA by gastric gavage at the doses of 32, 30, 28, 26, 24, 22 mg/kg respectively for LD_(50) of DA in mice. The toxicity of DA in rat skin were evaluated by smearing 50 ?l DA at the concentrations of 140, 70, 35, 17.5, and 8.8 mg/ml to an area of 4 cm2, and that of eyes exposure was carried out by dropping 10 ?l DA of 140.7, 70, 7, 0.7 mg/ml in rat eyes. The counterpart skin area and eyes served as control. Results LD_(50) of DA in mice was 28.07 mg/kg, the estimated doses for no-observed-adverse-effect levels (NOELs) were 8.8 mg/ml (0.44 mg) to the skin and 0.7 mg/ml (0.014 mg) to the eyes respectively. Conclusion DA can induce the injuries on the liver, kidneys, esophagus and stomach. High concentration of DA can cause inflammation of the skin and lens opacification, even blind.