Objective To investigate the existence and variance of quinolone-resistance genes in a group of pan-drug resistant of Acinetobacter baumannii ( A.baumannii ).Methods Twenty strains of pandrug resistant A.baumannii were isolated from patients registered in Affiliated Hospital of Nantong University from January 2011 to April 2011.Drug target genes to quinolone (gyrA,parC) and quinolone-resistance genes mediated by mobile genetic elements [ qnrA,qnrB,qnrS,aac(6')-Ⅰ b-cr,qepA] were analyzed by PCR and verified by DNA sequencing.Results In all 20 strains of A.baumannii,the sense mutation was found in the quinolone resistance-determining region of the gyrA gene in the form of TCA to TTA at codon 83 (Ser-83-Leu).Moreover,in the quinolone resistance-determining region of the parC gene sense mutation was found in the form of TCG to TTG at codon 80 (Ser-80-Leu) and 3 synonymous mutations were CCC to CCT at codon 40,GTA to GT]T at codon 41 and CGT to CGC at codon 44.And parC gene was a new mutation.However,mutations were not found in quinolone-resistance genes mediated by mobile genetic elements [ qnrA,qnrB,qnrS,aac( 6 ' )-Ⅰ b-cr,qepA ].Conclusion Quinolone-resistance-determining region play a key role in resistance to quinolones in this group of A.baumannii.To our knowledge,this is first report about the emergence of the new mutation of parC gene in China.

Apolipoprotein C3 (APOC3) is a multifunctional protein.Its concentration is positively correlated with triglyceride (TG) levels and is an independent risk factor for coronary heart disease (CAD) prediction and development.Recent studies showed that APOC3 could not only regulate triglyceride-rich lipoproteins (TRL) metabolism,but also regulated endothelial function,that is,it could induce endothelial dysfunction and disorders of lipid metabolism.Gradually,APOC3 induces atherosclerosis (AS),increases the risk of the occurrence of CAD and other related diseases.APOC3 polymorphisms are also closely related to related diseases.

Objective To investigate the expression of B-cell activating factor ( BAFF ) and its specific receptor BAFF-R in patients with B-cell non-Hodgkin′s lymphoma ( B-NHL) and to analyze the cor-relations between BAFF and the development of B-NHL.Methods RTQ-PCR and Western blot assay were used to measure the expression of BAFF and its specific receptor BAFF-R in patients with B-NHL.Fluores-cence immunocytochemical staining was used to determine the localization of BAFF and BAFF-R in Raji cells, a B-NHL cell line.The expression of BAFF in tumor tissues from patients with B-NHL of different his-tologic subtypes was measured by immunohistochemistry.WST proliferation and TUNEL assays were used to evaluate the effects of BAFF and BAFF-R on the proliferation, survival rate and apoptosis of Raji cells.Lin-ear correlations between the concentrations of lactate dehydrogenase ( LDH) and the expression of BAFF and BAFF at mRNA and protein levels in patients with B-NHL were analyzed.Results BAFF and its specific receptor BAFF-R were expressed in Raji cells and played an important role in the survival and proliferation of B-NHL cell line.The expression of BAFF in tumor cells from patients with B-NHL varied with the different histologic subtypes of B-NHL.Patients with small B-cell malignant lymphoma, large B-cell lymphoma ( LBCL) , mucosa-associated lymphoid tissue lymphoma ( MALT lymphoma) and follicular lymphoma showed higher levels of BAFF, while those with mantle cell lymphoma showed lower levels of BAFF.Compared with the healthy subjects, patients with B-NHL showed significantly increased expression of BAFF at mRNA and protein levels.The levels of LDH were closely related to the expression of BAFF at mRNA and protein lev-els.Conclusion BAFF and its specific receptor BAFF-R might play an important role in the growth and survival of malignant B cells.

Objective To investigate the enhancing effect of apolipoprotein C3 (APOC3) on THP-1 cell adhesion to aortas of mice.Methods Microsurgery was performed to separate the aorta of C57BL/6 mice in sterile condition.After stimulated by APOC3 (100 △g/ml) in vitro for 16 h,the aorta was allowed to adhere for 1 h with CFSE labeled THP-1 cells (1 ×106/ml).Then the adhesion effect was observed,and the expressions of vascular adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) were detected by immunohistochemical method.Results Adhesion effect of the mice aorta with THP-1 cells in the APOC3 stimulated group was stronger than the control group.Both the expressions of VCAM-1 and ICAM-1 in aortas were increased by APOC3,but the former was significantly up-regulated than the latter.Conclusion Apolipoprotein C3 could enhance THP-1 cell adhesion to aortas of mice.

ObjectiveTo investigate the activation of MAPK signal pathway in multiple myeloma and the regulation of BLyS expression levels through MAPK signal pathway; preliminarily study the role of MAPK signal pathway in the up-regulation of BLyS expression levels induced by IFN-γ.MethodsActivated MAPK pathway were detected by Western blot,while the expression of BLyS were detected with RT-PCR and Western blot,and Western blot investigated the effect of MAPK pathway on BLyS expression levels induced by IFN-γ.ResultsIn addition to the expression of ERK,JNK,p38,p-JNK was also expressed in MM cell lines,the MAPK pathway inhibitor targeting JNK SP600125 can down-regulate the expression of BLyS,and its activator anisomycin can up-regulate the expression of BLyS.SP600125 restrained the proliferation and survival of MM cells.ConclusionJNK/SAPK pathway was activated in MM cells; The activated degree of JNK/SAPK pathway and the expression level of BLyS was positively correlated.JNK/SAPK pathway play an important role in the up-regulation of BLyS expression levels induced by IFN-γ.

Objective To analyze the identification, drug resistance and clinical significance of a rare bacterium of Bordetella holmesii ( B. holmesii) to improve its detection and clinical diagnosis and treat-ment. Methods A strain isolated from a bacteremia case was identified by bacterial culture, biochemical tests and 16S rRNA gene sequencing. Mega 7. 0 software was used to conduct a similarity analysis of 16S rRNA gene sequences between the type strains of Bordetella spp. and the isolate, and then a phylogenetic tree was constructed. Antibiotic resistance of the isolate was determined by E-test. Changes in bacterial growth were measured after adding different concentrations of riboflavin or its inhibitor lumiflavin to the cul-ture medium. Results B. holmesii ABD2 was the pathogen causing bacteremia in the immunocompetent pa-tient. It was deposited under the number of CGMCC 1. 13721 in China General Microbiological Culture Col-lection Center (CGMCC), and the 16S rRNA gene sequences were deposited in National Center for Biotech-nology Information ( NCBI) with the accession number of KT828544. 1. Unrooted tree showed that the B. holmesii strain was highly homologous with B. pertussis. Antibiotic susceptibility test showed that the mini-mum inhibitory concentrations ( MIC) of piperacillin, ceftazidime, cefepime, imipenem, meropenem, cipro-floxacin, levofloxacin, gentamicin, amikacin, erythromycin, tetracycline and polymyxin B against the isolate were low, while the MIC values of cefazolin, cefuroxime, cefoxitin, cefotaxime, aztreonam and trime-thoprim-sulfamethoxazole were high. Riboflavin accelerated the growth of B. holmesii ABD2, while its inhibi-tor lumiflavin had an inhibitory effect. Conclusions As B. holmesii is hard to isolate and identify, limited clinical, microbiological and epidemiological data are available. It is an under-recognized pathogen with a considerable amount of information that remains to be studied.