Objective To assess differences in brain activation between active and passive movement of the right hand using blood oxygen level-dependent functional magnetic resonance imaging (BOLD-fMRI). Methods Nine healthy adult right handed volunteers were studied. fMRI was performed with active and passive finger-to-finger movement. Results Right hand active and passive movement produced significant activation in the contralateral sensorimotor cortex ( SMC ), the contralateral premotor cortex ( PMC ), bilaterally in the supplementary motor area (SMA) and in the ipsilateral cerebellum. The activated brain areas were centered on the contralateral SMC and PMC and located more forward during active movement than during passive movement. The contralateral SMC was the most strongly and the most frequently activated brain area. The contralateral posterior parietal cortex (PPC) was less relevant to the hand movements. Unlike active movement, passivemovement activated more areas in the posterior central gyrus than in the anterior central gyrus. Conclusions Both active and passive movement significantly activate the brain areas which are responsible for hand movement, but there are some differences in the locations of the cortex areas activated and in the incidence activation except in the contralateral SMC.

Data analysis poses a significant challenge to the large-scale proteomics studies. Based on the structured and controlled vocabularies-Gene Ontology (GO), and the GO annotation from related databases, a strategy composed of several programs and local databases is developed to identify the functional distribution and the significantly enriched functional categories of the proteomic expression profile. It would be helpful for understanding the overall functions of these identified proteins and supply the fundamental information for further bioinformatics exploration. This strategy has been successfully used in the Human Fetal Liver (HFL) proteomic research, which is available online at http://www.hupo.org.cn/GOfact/.

ObjectiveTo investigate whether γδ T cells act as a regulatory factor during respiratory syncytial virus (RSV) infections was responsible for the subsequent changes in asthmatic-type inflammation in allergic mice.MethodsMice were sensitized and challenged with OVA,and infected intranasaly with RSV before or after OVA sensitization.Lung sections were stained with HE for determination of inflammatory reaction.Real-time RT-PCR was used to analyze the expression of cytokine mRNA of γδ T cells in the lung and spleen of tested mice.The number of γδ T cells in the spleen and lung of BALB/c mice was determined by flow cytometry.Adoptive transfer of γδ T cells was performed to identify the role of γδ T cells in allergic asthma.ResultsOVA-sensitized and challenged mice exhibited significantly peribronchial inflammation with larger number of mononuclear cells and granulocytes in the lung tissue sections.RSV infection before OVA-sensitization diminished the grade of inflammatory responses induced by OVA treatment.The expression of IFN-γ mRNA was increased siguificantly in RSV-infected,OVA-sensitized mice.In contrast,the level of IL-4 mRNA was diminished.The number of total γδ T cells as well as activated γδ T cells was decreased in the spleen and lung of OVA-sensitized mice by prior RSV infection.Adoptive transfer of γδ T cells obtained from OVA-sensitized and challenged mice induced a slight inflammation in the lung of normal mice,and enhanced inflammatory responses in RSV-infected OVA-sensitized mice.Conclusionγδ T cells may play an important role in the development of allergen-induced allergic airway inflammation.

Objective: To explore the clinical and anatomical characteristics of coronary slow lfow (CSF) in relevant patients.
Methods: We summarized the patients without coronary angiography (CAG) proved coronary stenosis (stenosis < 40%) while with TIMI indicated CSF in our hospital from 2013-01 to 2015-01. The patients were divided into 2 groups: CSF group, n=56 patients having at least 1 major coronary artery with TIMI frame counts > 27 and Control group,n=55 patients with normal coronary lfow. The related laboratory indexes were examined and relationship between MCV and CSF was studied by multi-logistic regression analysis.
Results: In CSF group, MCV 90.4 (87.48, 92.65) fL and RDW-CV 12.5 (12.30, 13.18) % were lower than those in Control group 92.3 (90.1, 94.3) fL and 13(12.7, 13.4) %,P<0.05; while MCHC 337 (332, 347) g/L and the number of left circumlfex distal braches involved 3 (2, 4) were higher than those in Control group 327.5 (322, 338) g/L and 2 (2, 3),P<0.05. Multi-logistic regression analysis showed that MCV was negatively related to CSF (partial regression coefficient= -0.138, P=0.015), Spearman rank correlation analysis presented that MCV was negatively related to TIMI frame counts (r= -0.201, P=0.009).
Conclusion: Deformability of red blood cells might be involved in pathogenesis of CSF in relevant patients.

Objective: To detect the changes of serum level of connective tissue growth factor (CTGF) in patients with ST-segment elevation myocardial infarction (STEMI) and to study the correlation between CTGF level and the maximal activity of creatine kinase-MB (CK-MB). Methods: Our research included 2 groups of patients: STEMI group and unstable angina (UA) group. All patients were treated in our hospital from 2013-07 to 2014-06,n=50 in each group. In STEMI group, the serum levels of CTGF were examined by ELISA at 24h, 2, 7, 14 days of onset, and in UA group, CTGF level was examined at 24h of onset. The CK-MB activity levels were measured in STEMI group at the same time points by immunosuppression method. Results: The serum level of CTGF in UA patients at 24 h of onset was (10.34 ± 2.00) ng/mL, and in STEMI patients were (16.76 ± 3.17) ng/mL at 24h, (29.87 ± 4.90) ng/mL at 2d, (45.02 ± 8.35) ng/mL at 7d and (31.61 ± 4.40) at 14d. The CTGF levels in STEMI group at different time points were all higher than UA group at 24h of onset,P<0.01. In STEMI group, the CTGF levels were increasing from 24h to 7d, then decreasing at 14d, allP<0.01. In STEMI group, the highest protein concentration of CTGF was positively related to the maximal activity of CK-MB at 7 days of onset (r=0.859,P=0.000). Conclusion: CTGF expression has been up-regulated in STEMI patients which might be related to myocardial ifbrosis. The protein level of CTGF is related to MI size, it shows certain predictive value in relevant patients.

BACKGROUND:Nerve growth factor has been shown to play an important role in bone healing, but little is reported on the effect of growth factor composite scaffolds via the immediate implantation in the repair of canine bone defects. OBJECTIVE:To analyze the effect of nerve growth factor composite scaffolds via the immediate implantation for the repair of canine bone defects. METHODS:Nerve growth factor composited strontium apatite scaffolds were prepared. Canine mandibular defect models were established and divided into three groups, fol owed by implanted with composite scaffold (experimental group), strontium apatite (positive control group), or nothing (blank control group). The three-dimensional CT reconstruction and hematoxylin-eosin staining of canine mandibular bone defects were observed. RESULTS AND CONCLUSION:In the blank control group, there were few new bones surrounding bone defect. Trabecular bones spread from the defect center to the surrounding tissues in the experimental and positive control groups. The bone density, volume, thickness, and implant-bone contact were significantly increased, while the trabecular separation was significantly decreased in the experimental group compared with the positive control and blank control groups (P<0.05), and al above indicators in the positive contro group were significantly higher than those in the blank control group (P<0.05). Hematoxylin-eosin staining showed that in the experimental group, there were a large number of new bones that contacted with the surrounding bones closely, and trabecular bones arranged regularly. In the positive control group, newborn osteoid, trabeculare, and a smal amount of debris were found. In the blank control group, few new bones were connected with the surrounding bones untightly and trabecular bone arranged irregularly. These results indicate that the nerve growth factor composite scaffold can promote the bone regeneration in the canine bone defects after immediate implantation.

BACKGROUND:Now experimental and clinical research on suitable bone substitutes for alveolar bone defects after dental implantation is an issue of concern.OBJECTIVE:To study the therapeutic effect of titanium core/bone morphogenetic protein (BMP) composite material on alveolar bone defects after immediate implant placement.METHODS:Twenty-four New Zealand rabbits were randomly assigned into normal group (no intervention),experimental group or control group.Animal models of bone femoral greater trochanter defect were made in the experimental and control groups.Dental implant and titanium core/BMP composite material were implanted in the experimental group,while dental implant and titanium core were implanted in the control group.Percentage of CD4+,CD8+ T lymphocytes,natural killer cell activity and interleukin 2 level were detected at postoperative 4 weeks;bone mineral density and osteogenesis around the implant were detected at postoperative 16 weeks through X-ray and histological examinations.RESULTS AND CONCLUSION:X-ray results showed that the bone mineral density in the experimental group was significantly higher than that in the control group (P ＜ 0.05).Histological results showed that in the experimental group,different degrees of cell lysis around the composite,more bone cells and bone matrices were found,implant-bone osseointegration formed well,and red-dyed mature bone tissues were detective inside the implant.Compared with the experimental group,lower number of bone cells and fibrocytes were found in the control group.Additionally,the percentage of CD4+ and CD8+ T lymphocytes,natural killer cell activity and interleukin 2 level in the experimental group were significantly lower than those in the control group (P ＜ 0.05).To conclude,the titanium core/BMP composite material can effectively repair alveolar bone defects after immediate implant placement to guide the growth of bone cells.

Objective: To explore the association between methylenetetrahydrofolate reductase (MTHFR) C677T and A1298C gene polymorphisms and toxicity of Methotrexate(MTX) chemotherapy in pediatric acute lymphoblastic leukemia (ALL). Methods: From January 2015 to June 2018, 128 pediatric patients with ALL in southern Fujian who were admitted at the First Affiliated Hospital of Xiamen University were selected.Their peripheral blood 2 mL was collected and genomic DNA was extracted.The MTHFR genotype was detected by polymerase chain reaction(PCR) direct sequencing method, and the clinical significance of HD-MTX on ALL children with toxic and side effects was evaluated according to the National Cancer Institute-Common Toxicity Criteria. Results: Among 128 children, 54 cases(42.2%) presented rash, 48 cases (37.5%)with mucosal lesions, 51 cases (39.8%) with liver function damage, 23 cases (18.0%) with renal function damage, 52 cases (40.6%) with gastrointestinal reactions, 38 cases (29.7%)with leukopenia, 34 cases (26.6%) with thrombocytopenia and 63 cases (49.2%) with hemoglobin reduction.There was no significant difference in the incidence of MTX adverse reactions (rash, mucosa lesions, liver and renal function damage, gastrointestinal reaction, leukopenia, hemoglobin decrease and thrombocytopenia) between the MTHFR C677T and A1298C polymorphisms (all P>0.05). The different clinical risk (MTX dose) of the children was not statistically signi-ficant in the MTHFR C677T and A1298C genotypes and allele frequencies (χ²=2.573, 2.264, 1.615, 0.267; all P>0.05). There was no significant difference among the abnormal incidence of MTX at 24 h, 48 h and 72 h (all P>0.05). Conclusions MTHFR C677T and A1298C polymorphisms do not seem to be good markers of MTX-related toxicity and/or outcome in pediatric ALL in southern Fujian, and its clinical application still needs further discussion.

Objective To evaluate the association between methylenetetrahydrofolate reductase (MTHFR) gene C677T polymorphism and susceptibility to methotrexate (MTX) adverse reaction in children with acute lymphoblastic leukemia (ALL) chemotherapy. Method The data bases of The Cochrane Library, PubMed, EMbase, EMCC, OVID, CNKI, VIP and WanFang Data were searched for relevant articles published in English and Chinese up to March 2016. Two researchers independently screened literature, extracted data, and assessed bias risk in the included studies. The RevMan 5.3 and Stata 12 software were used to analyze the association between gene polymorphism and the adverse reaction of MTX chemotherapy with the recessive, dominance, co-dominance, addition and allele gene model respectively. Results A total of 12 studies were included and all of them were case-control study, with 1419 cases in case group and 2188 cases in control group. The results of meta-analysis showed that the MTHFR gene polymorphism was unrelated to the untoward effect of neutropenia, thrombocytopenia, hemoglobin reduction, mucosal damage and liver function damage during MTX chemotherapy in children with ALL under the 5 analytical models. Under the co-dominance gene model, the association between MTHFR polymorphism C677T and overall adverse reaction of MTX was statistically significant (OR=1.39, 95％CI: 1.02～1.91, P=0.04). In the recessive gene model, the C677T polymorphism of MTHFR was associated with a reduced risk of gastrointestinal adverse reactions during MTX chemotherapy (OR=3.31, 95％CI: 1.03～10.59, P=0.04). In the dominance gene model, the C677T polymorphism of MTHFR was associated with a reduced risk of skin damage induced by MTX chemotherapy (OR=3.05, 95％CI: 1.25～7.41, P=0.01). Conclusion There is no significant association between the C677T polymorphism of MTHFR and the adverse effects of MTX chemotherapy, butfurther studies with larger sample size are needed.

Objective To verify the molecular mechanism of Qiangxin Decoction in treating CHF,which was created by Professor Lu Jianqi,a famous old Chinese medicine and Qihuang scholar in Guangxi,based on network pharmacological methods,molecular docking technology and animal experiments.Methods Firstly,TCMSP database and related literatures were searched to find the important compounds of Qiangxin decoction;Through TCMSP database and STITCH database,find the target of Qiangxin Tang;Get the main target points of CHF with the help of GeneCards,DisGeNET,OMIM and other databases;The Venny platform was selected to obtain the intersection target of the two;Using STRING platform and Cytoscape 3.6.1,build a"component target"network and a PPI network of Qiangxin Tang target CHF target;The DAVID 6.8 database was used for GO enrichment analysis and KEGG pathway enrichment analysis;Use AutoDock Vina software for molecular docking.Finally,the model of CHF after AMI was established by ligating the anterior descending branch of left coronary artery in rats,and the expression of core target protein was detected by Western blot.Results 185 important active components including quercetin,kaempferol,luteolin,tanshinone iia and naringenin were obtained from the analysis of network pharmacological results.The core targets were signal transduction and transcription activation factor 3(STAT3),mycobacterium tuberculosis regulatory protein(RELA),phosphorylated protein kinase 1(AKT1)100 therapeutic targets,such as mitogen activated protein kinase 1(MAPK1)and interleukin-6(IL-6),preliminarily indicate that Qiangxin decoction may regulate cytokine mediated signal pathway,positive regulation of gene expression,response to hypoxia The reaction to lipopolysaccharide,drug and other biological processes play a role in the treatment of CHF.The results of molecular docking showed that the important compounds of Qiangxin Tang had strong binding ability to the core target;The results of animal experiments showed that the components of Qiangxin decoction could significantly reduce the phosphorylation expression level of STAT3 protein and MAPK1 protein and the expression level of IL6 protein(P<0.05).The high dose group of Qiangxin Decoction was slightly better than the low dose group.Conclusion This study preliminarily clarified that Qiangxin decoction can play a role in treating CHF by reducing the phosphorylation of STAT3 protein and MAPK1 protein and the expression level of IL6 protein,and also verified that Qiangxin decoction has the characteristics of multiple components,multiple targets,and multiple ways of synergistic effect in treating CHF.Animal experiments provide experimental theoretical basis for clinical doctors to treat CHF and further research.