Objective [WT5”BZ]To evaluate the result of unilateral exploration for the treatment of hyperparathyroidism caused by parathyroid adenoma.[WT5”HZ]Methods[WT5”BZ] Clinical data of 20 cases from 1986 to 1999 were retrospectively analysed. Preoperative imaging examination was suggestive of unilateral lesion and unilateral exploration was performed accordingly.Results were compared with that of bilateral exploration.[WT5”HZ]Results[WT5”BZ] In 19 out of 20 cases the result of unilateral exploration was satisfactory making bilateral approach unnecessary except for one whose symptom was later proved to be caused by bilateral lesions.[WT5”HZ]Conclusions[WT5”BZ] The authors came to the conclusion that solitary adenoma is the most common cause of hyperparathyroidism in Chinese patients,hence unilateral exploration is of advantages. [WT5”HZ]

Objective　To evaluate the result of unilateral ex ploration for the treatment of hyperparathyroidism caused by parathyroid adeno ma.　Methods　Clinical data of 20 case s from 1986 to 1999 were retrospectively analysed. Preoperative imaging examinat ion was suggestive of unilateral lesion and unilateral exploration was performed accordingly.Results were compared with that of bilateral exploration.　Results　In 19 out of 20 cases the result of u nilateral exploration was satisfactory making bilateral approach unnecessary exc ept for one whose symptom was later proved to be caused by bilateral lesions.Conclusions　The authors came to the c onclusi on that solitary adenoma is the most common cause of hyperparathyroidism in Chin ese patients,hence unilateral exploration is of advantages.

AIM: Recombinant adenovirus possesses high transfection efficiency and wide host range. This study was designed to construct the recombinant adenovirus vector containing human vascular endothelial growth factor 165 (VEGF165), so as to lay a foundation for the subsequent gene transfection, microencapsulated genetically engineered cells and animal experiments. METHODS: The experiment was conducted in the Laboratory of Cardiothoracic Surgery (the National Key Laboratory), Changhai Hospital of The Second Military Medical University of Chinese PLA from January to May in 2007. Experiment materials: pAxCAwt.VEGF165 was provided by Institute of Cardiothoracic Surgery of Changhai Hospital. pAxCAwt.VEGF165 and DNA-TPC were cotransfected into human embryonic kidney 293 cells by lipofection method. Being propagated, recombinant replication-deficient adenovirus named Ad.VEGF165 was obtained. The target gene of recombinant adenovirus was identified by polymerase chain reaction (PCR) and restriction enzyme digestion. The titer of virus was detected by 50% tissue culture infective dose method. RESULTS: Construction of recombinant adenovirus Ad.VEGF165: The pAxCAwt.VEGF165 and DNA-TPC were successfully cotransfected into human embryonic kidney 293 cells by lipofection method, and replication-deficient adenovirus vectors coding for VEGF165 gene were generated. Identification of recombinant adenovirus Ad.VEGF165: Two fragments of PCR products (597 bp and 146 bp) were obtained by NcoI restriction enzyme. The result was consistent with that calculated with Gene Tool software. The virus titers was 2.2?1015 pfu/L. CONCLUSION: DNA-TPC and pAxCAwt.VEGF165 can be used to construct replication-deficient recombinant adenovirus Ad.VEGF165 in a high titer, low toxicity, high efficiency and safe transfection in vitro.

Objective:To investigate the effects of Chlamydia pneumoniae(Cpn) on SR-A1 and CD36 expression in THP-1-derived macrophages and role of c-Jun NH_2-terminal signal transduction pathway in the process.Methods:Cpn was propagated in Hep-2 cells.THP-1 monocytes were induced into macrophages by 160 nmol/L phorbol myristate acetate(PMA)for 48h,and were randomly allocated into four groups to be incubated continually: control group;Cpn infection group;Cpn and SP600125(a JNK inhibiter)group and SP600125 group.Lipid droplets in cytoplasm were observed by oil red O staining.The contents of intracellular cholesterol ester were detected by enzyme-fluorescence.The expression of SR-A1 and CD36mRNA and protein were determined by RT-PCR and Western blot, respectively. Results:THP-1-derived macrophages infected with Cpn resulted in large accumulation of lipid droplets and foam cell formation when co-cultured with LDL.Meanwhile,the expression of SR-A1 mRNA and protein were up-regulated by Cpn infection (P<0.05).However,the expressions of CD36 mRNA and protein in THP-1-derived macrophages infected with Cpn were unchanged.Moreover,the up-regulation of SR-A1 and foam cell formation induced by Cpn could be restrained by the JNK inhibiter SP600125 in a dose-dependent manner,and SP600125 had little impact on the expression of CD36 in THP-1-derived macrophages infected with Cpn.Conclusion:The up-regulation of SR-A1 but not CD36 expression is involved in mechanisms of Cpn inducing foam cell formation.And Chlamydia pneumoniae up-regulates the expression of SR-A1 via the JNK signal transduction pathway.This may be a novel mechanism for the foam cell formation induced by Cpn.

Objective To investigate the role of c-Jun N-terminal kinase (JNK) signal transduction pathway on the up-regulation of the expression of acyl-coenzyme A: cholesterol acyltransferasel (ACAT1) induced by Chlamydia pneumoniae (C. pn), and to discuss the mechanism of macrophages-derived foam cell formation induced by C. pn. Methods C. pn was propagated in Hep-2 cells. THP-1 monocytes were induced into macrophages by 160 nmol/L phorbol myristate acetate(PMA) for 48 h, and were randomly allocated into four groups to be incubated continually: control group, C. pn infection group, C. pn and SP600125 (a special JNK inhibitor)group and SP600125 group. Lipid droplets in cytoplasm were observed by oil red O staining. The contents of intracellular cholesterol ester were detected by enzyme fluorescence analysis. The expressions of ACAT1 mRNA and protein were determined by reverse transcriptase polymerase chain reaction(RT-PCR) and Western blot, respectively. Results Compared with the control group, the expressions of ACAT1 mRNA and protein were up-regulated in C. pn infection group [(4.16±0.26) vs. (2.17±0.18), (1.20±0.10)vs. (0.61±0.03), both P<0.05], and C. pn-induced foam cell formation was observed. The expressions of ACAT1 mRNA and protein and the foam cell formation were inhibited by SP600125 in a concentration-dependent manner (r = - 0.92, P<0.05; r= - 0. 96, P<0.05, respectively). Conclusions The up-regulation of ACAT1 expression is induced by C. pn via JNK signal transduction pathway, which is involved in the mechanism of C. pn-induced macrophage-derived foam cell formation.

AIM: To investigate the signal transduction mechanism of Chlamydia pneumoniae (Cpn) in down-regulating the expression of ATP binding cassette A1 (ABCA1) and ATP binding cassette G1 (ABCG1),the key molecules in cholesterol efflux and atherogenesis,from THP-1-derived macrophages. METHODS: Cpn was propagated in Hep-2 cells. THP-1 monocytes were induced into macrophages by 160 nmol/L phorbol myristate acetate (PMA) for 48 h,and were randomly allocated into 4 groups to incubate continually: control group,50 mg/L low density lipoprotein (LDL); Cpn infection group,Cpn (1×10~6 IFU) and 50 mg/L LDL; Cpn and SP600125 (a special JNK inhibiter) group,THP-1 macrophages were previously treated with different concentrations (1-20 μmol/L) of SP600125 for 1 h,and then infected with Cpn (1×10~6 IFU) and 50 mg/L LDL; SP600125 group,SP600125(20 μmol/L)and 50 mg/L LDL. The expressions of ABCA1/ABCG1 and peroxisome proliferator-activated receptor γ (PPARγ) from each group were detected then. The cholesterol efflux was detected by enzyme-fluorescence. The expressions of ABCA1/ABCG1 and PPARγ mRNA and protein were determined by RT-PCR and Western blotting,respectively. RESULTS: Cpn not only down-regulated the ABCA1/ABCG1 expression,but also down-regulated the expression of PPARγ,which regulated the ABCA1/ABCG1 genes transcriptions. However,the mentioned effects of Cpn infection were restrained by the special JNK inhibitor SP600125 in a dose-dependent manner. CONCLUSION: Chlamydia pneumoniae may down-regulate ABCA1/ABCG1 expression from THP-1-derived macrophages via JNK-PPARγ signal transduction pathway.

Objective To investigate the mechanisms of Chlamydia pneumoniae (C. pn)-induced foam cell formation, the expression of ATP binding cassette transporter AI ( ABCA1 ) and perexisome prolif-erator-activated receptor γ (PPARγ) were examined. Methods THP-1 monneytes were induced into mac-rophages after the addition of 160 nmol/L phorbol myristate acetate (PMA) for 72 h. THP-1-dorived macro-phages when co-cuhured 50 mg/L low density lipoprotein (LDL) were designated randomly in four groups: control (uninfected) group, C. pn infection group, rosiglitazone + C. pn infection group and rosiglitazone group. Lipid droplets in cytoplasm were observed by oil red O staining. The contents of intracellnlur choles-terol ester were detected by enzyme-flnoreseence. The expression of ABCA1, PPARγ, mRNA and protein were determined by RT-PCR and Western blot, respectively. Results C. pn down-regulated the expression of ABCA1, PPARγ at mRNA and protein levels in a concentration-dependent manner in THP-1-derived mac-rophages when co-incubated with LDL. Resiglitazone not only concentration-dependently alleviated the down-regulation of ABCA1 expression by C. pn infection (P<0.05), but also markedly suppressed the accumula- tion of lipid droplets and cholesteryl ester by C. pn at higher concentrations ( 10 and 20 μaol/L). Condu-sion C. pn induces foam cell formation by down-regulating the expression of ABCA1 via PPART pathway, which may provide a new evidence for the development and progression of atherosclerosis initiated by C. pn infection.

Objective To investigate the clinical value of 18 F?FDG PET/CT in staging multiple myeloma ( MM) and evaluating the glucose metabolic activity of MM. Methods A total of 25 MM patients ( 13 males, 12 females, age:39-67 years) from May 2010 to April 2015 were enrolled in this retrospective study. The SUVmax of each patient was recorded. D?S plus staging according to 18 F?FDG PET/CT was com?pared with the traditional D?S staging. The SUVmax and the percentage of plasmacytes of bone marrow of phase Ⅲ and non?phase Ⅲ ( phaseⅠand Ⅱ) according to D?S plus staging were compared. Two?sample t test and Wilcoxon rank sum test were used to analyze the data. Results In 25 MM patients, the range of SUVmax of lesions was 1.8-12?0 and the mean value was 5.15±2.74. According to D?S staging, the numbers of patients with phase Ⅰ,Ⅱ andⅢwere 7, 4 and 14, respectively. While the numbers were 3, 1 and 21 by D?S plus staging. Based on the D?S plus staging system, stages of 7 patients ( 28%, 7/25 ) were changed. According to the D?S plus staging system, the SUVmax between phaseⅢand non?phaseⅢpatients was significantly different (5.75±2.54 vs 3.00±0?70; t=2.12, P<0.05), while the percentage of plasma?cytes of bone marrow between the 2 groups had no significant difference ( 17. 50%( 4. 25%-41. 75%) vs 11?15%(10.25%-36.57%);z=0.05, P>0.05). Conclusion 18F?FDG PET/CT is of clinical importance for MM staging and metabolic activity assessment of MM.