Objecfive To observe the changes of regional cerebral blood flow (rCBF) in systemic lupus erythematosus (SLE) patients with neuropsychiatrie disorders and evaluate rCBF SPECT imaging in the detection of neuropsychiatric problems in SLE patients.Methods Twenty neuropsychiatrie SLE patients were enrolled in the study and were performed SPECT rCBF imaging anti CT/MRI scans,respectively.Twenty SLE patients without neuropsychiatrie manifestatiuns (SLE) and 20 healthy volunteers also underwent SPECT rCBF imaging as controls.Semiquantitative analysis was conducted as designed by selecting 3 consecutive crosssections and delineating ROI,which generated HQ and the results were compared between with SLE and controls.Results SPECT rCBF findings were almormal in 20 NPSLE.in which 19 of the 20 with abnormal SPECT findings showed focal uptake defects the other patient showed increased foeal uptake.Four N PSLE patients had ahnormal CT/MRI scans findings.Compared with the methods of rCBF and CT/MRI imaging,the difference was significant (P＜0.01).Nineteen SLE patients without neuropsychiatrie manifestations had normal SPECT findings.the other 1 patient showed focal uptake defect.SPECT findings were all normal in 20 healthy volunteers.Temporal cortex was the most commonly involved region,followed by frontal cortex.Specific values generated from semiquantitative analysis (HQ) of temporal and frontal regions in neruopsychiatrie SLE patients were lower than that in SLE patients and healthy volunteers (P＜0.01 and P＜0.05).Conclusion SPECT rCBF imaging has the potential to be a sensitive tool to detect the neuropsyehiatric disordersin SLE patients,and has important value in helping for early diagnosis and therapy.Hypoperfusion on ECD-SPECT under the territory of the middle cerebral artery (MCA) is the most common observation,and which temporal and frontal regions are the most frequently involved regions in neruopsychiatrie SLE patients.

Objective To explore the effects of obesity on the survival,growth and proliferation of gastric cancer and apoptosis by in vivo experiments so as to clarify the relationship between obesity and gastric cancer. Methods High fat diet-induced obese mice model was established.MFC cells were inoculated subcutaneously into mice to establish xenograft tumor model;then tumor growth and peritoneal metastasis were observed for 2 weeks. At the end of in vivo experiments,serum insulin and visfatin concentrations were assayed by ELISA,and blood glucose was determined by glucometer.MFC cell proliferation and apoptosis,as well as the number and size of adipocytes in xenograft tumor tissues were analyzed by immunohistochemistry, TUNEL and HE staining, respectively.Results High fat diet-induced obese mice model was successfully established within 12 weeks,and 66.7% of mice in the model were obese.Obese mice had distinct metabolic changes manifested as weight gain,high blood glucose,high serum visfatin,hyperinsulinemia and insulin resistance.All mice survived and developed no metastasis.The tumors from obese mice had a larger volume,heavier weight and greater intra-tumoral adipocytes, and exhibited higher proliferation and reduced apoptosis rate compared to those of non-obese and lean mice.Both serum insulin and visfatin concentrations correlated positively with tumor proliferation and negatively with tumor apoptosis.In addition,tumor weight showed a significantly positive correlation with mice body weight.Effects of diet-induced obesity on gastric cancer were not related to the influence of diet,but to the degree of obesity. Conclusion The altered adipocytokine milieu and insulin resistance observed in obesity may lead directly to alterations in tumor microenvironment,thereby promoting the survival and growth of gastric cancer.

Objective To evaluate the effects of different levels of neuromuscular blockade(NMB)on transcranial electric motor-evoked potentials(TCeMEPs)during idiopathic scoliosis.Methods Thirty American Society of Anesthesiologists physical status Ⅰ or Ⅱ patients of both sexes,aged 11-23 yr,weighing 31-62 kg,scheduled for elective idiopathic scoliosis under general anesthesia,were enrolled in the study.NMB was monitored with train of four(TOF)-Watch SX.The levels of partial NMB were classified into 5 states according to TOF ratio(TOFR)and TOF counts:1 or 2 TOF counts(TOF1),3 TOF counts and TOFR≤15%(TOF2),TOFR 16%-25%(TOF3),TOFR 26%-50%(TOF4),TOFR 51%-75%(TOF5) and TOFR>75%(no NMB).Each state was maintained for 10 min.Failure and false-positive findings in TCeMEP monitoring,development of unexpected body movement and satisfaction with NMB were recorded.Results Compared with no NMB,the failure and false-positive rates of TCeMEP monitoring were significantly increased,the incidence of unexpected body movement was decreased,and the rate of satisfactory NMB was increased at TOF1,TOF2 and TOF3(P<0.05),no significant change was found in failure or false-positive rates of TCeMEP monitoring at TOF4 and TOF5(P>0.05),and the incidence of unexpected body movement was decreased and the rate of satisfactory NMB was increased at TOF4,the rate of satisfactory NMB was increased at TOF5(P<0.05),and no significant change was found in the incidence of unexpected body movement at TOF5(P>0.05).Compared with those at TOF4,no significant change was found in the failure or false-positive rates of TCeMEP monitoring(P>0.05),the incidence of unexpected body movement was significantly increased,and the rate of satisfactory NMB was decreased at TOF5(P<0.05).Conclusion Maintaining TOFR at 26%-50% the partial NMB during surgery does not affect TCeMEP monitoring during idiopathic scoliosis and meets the intra-operative NMB requirements simultaneously,and it is the optimum NMB for this type of surgery.

OBJECTIVETo investigate the effects of β-elemene in suppressing the proliferation and apoptosis of SGC7901 gastric cancer cells in vitro and explore the underlying mechanisms.

METHODSUsing MTT assay, flow cytometry, and clonogenic survival assay, we assessed the effects of β-elemene on the viability, apoptosis, cell cycle distribution, and clonogenic survival of gastric cancer SGC7901 cells and gastric mucosal epithelial GES-1 cells. Western blotting was employed to determine the changes in the protein expression profiles in SGC7901 cells in response to β-elemene treatment.

RESULTSβ-elemene significantly suppressed the cell viability and increased the apoptosis of SGC7901 cells, and these effects were less obvious in GES-1 cells. β-elemene decreased clonogenic survival of SGC7901 cells, increased the proportion of G2/M phase cells, decreased the expression of Bcl-2, and increased the expression of Bax and cleaved caspase-3. β-elemene did not obviously affect the expression of total p21-activated protein kinase 1 (Pak1) but decreased the level of phospho-Pak1 (Thr423) and phospho-ERK1/2 (Thr202/Tyr204) in SGC7901 cells.

CONCLUSIONβ-elemene inhibits the proliferation and induces apoptosis of gastric cancer cells possibly by inhibiting Pak1/ERK signaling and regulating apoptosis-associated proteins such as Bcl-2 and Bax.

Apoptosis ; Apoptosis Regulatory Proteins ; metabolism ; Cell Cycle ; Cell Division ; Cell Line, Tumor ; drug effects ; Cell Proliferation ; Cell Survival ; Humans ; Sesquiterpenes ; pharmacology ; Signal Transduction ; Stomach Neoplasms ; pathology

OBJECTIVETo explore the significance of plasma levels of mannan-binding lectin (MBL)-associated serine protease 2 (MASP2) in children with upper respiratory tract infection (URTI).

METHODSA total of 103 children with URTI and 35 healthy children were examined for plasma levels of MASP2 and C-reactive protein (CRP). According to CRP levels, white blood cell count (WBC), stage of infection, and administration of treatments, the children with URTI were divided into the elevated CRP group (n=48) and the normal CRP group (n=54), elevated WBC group (n=61) and normal WBC group (n=40), the early stage of infection without treatment group (n=68) and mid-late stage of infection with treatment group (n=35).

RESULTSPlasma MASP2 levels was significantly higher in URTI group than in the healthy control group (P<0.001) and showed a close correlation with age (r=0.302, P<0.01). Plasma MASP2 level was significantly correlated with CRP level in elevated CRP group (r=0.310, P<0.05) but not in normal CRP group (P>0.05), correlated with WBC in elevated WBC group (r=0.392, P<0.01) but not in normal WBC group (P>0.05), and was significantly higher in early stage infection without treatment group than in mid-late stage of infection with treatment group (P<0.01). MASP2, MBL2 and CRP genes had a common binding site for the transcription factor HNF-4α.

CONCLUSIONSMASP2 may be an acute-phase protein, and its plasma level might serve as a new reference index in the diagnosis of URTI in children.

C-Reactive Protein ; metabolism ; Case-Control Studies ; Child ; Humans ; Leukocyte Count ; Mannose-Binding Protein-Associated Serine Proteases ; metabolism ; Respiratory Tract Infections ; blood

Objective To investigate the effects ofβ-elemene in suppressing the proliferation and apoptosis of SGC7901 gastric cancer cells in vitro and explore the underlying mechanisms. Methods Using MTT assay, flow cytometry, and clonogenic survival assay, we assessed the effects ofβ-elemene on the viability, apoptosis, cell cycle distribution, and clonogenic survival of gastric cancer SGC7901 cells and gastric mucosal epithelial GES-1 cells. Western blotting was employed to determine the changes in the protein expression profiles in SGC7901 cells in response toβ-elemene treatment. Resultsβ-elemene significantly suppressed the cell viability and increased the apoptosis of SGC7901 cells, and these effects were less obvious in GES-1 cells.β-elemene decreased clonogenic survival of SGC7901 cells, increased the proportion of G2/M phase cells, decreased the expression of Bcl-2, and increased the expression of Bax and cleaved caspase-3. β-elemene did not obviously affect the expression of total p21-activated protein kinase 1 (Pak1) but decreased the level of phospho-Pak1 (Thr423) and phospho-ERK1/2 (Thr202/Tyr204) in SGC7901 cells. Conclusion β-elemene inhibits the proliferation and induces apoptosis of gastric cancer cells possibly by inhibiting Pak1/ERK signaling and regulating apoptosis-associated proteins such as Bcl-2 and Bax.

Absteact:Objective To explore the significance of plasma levels of mannan-binding lectin (MBL)-associated serine protease 2 (MASP2) in children with upper respiratory tract infection (URTI). Methods A total of 103 children with URTI and 35 healthy children were examined for plasma levels of MASP2 and C-reactive protein (CRP). According to CRP levels, white blood cell count (WBC), stage of infection, and administration of treatments, the children with URTI were divided into the elevated CRP group (n=48) and the normal CRP group (n=54), elevated WBC group (n=61) and normal WBC group (n=40), the early stage of infection without treatment group (n=68) and mid-late stage of infection with treatment group (n=35). Results Plasma MASP2 levels was significantly higher in URTI group than in the healthy control group (P<0.001) and showed a close correlation with age (r=0.302, P<0.01). Plasma MASP2 level was significantly correlated with CRP level in elevated CRP group (r=0.310, P<0.05) but not in normal CRP group (P>0.05), correlated with WBC in elevated WBC group (r=0.392, P<0.01) but not in normal WBC group (P>0.05), and was significantly higher in early stage infection without treatment group than in mid-late stage of infection with treatment group (P<0.01). MASP2, MBL2 and CRP genes had a common binding site for the transcription factor HNF-4α. Conclusion MASP2 may be an acute-phase protein, and its plasma level might serve as a new reference index in the diagnosis of URTI in children.

Absteact:Objective To explore the significance of plasma levels of mannan-binding lectin (MBL)-associated serine protease 2 (MASP2) in children with upper respiratory tract infection (URTI). Methods A total of 103 children with URTI and 35 healthy children were examined for plasma levels of MASP2 and C-reactive protein (CRP). According to CRP levels, white blood cell count (WBC), stage of infection, and administration of treatments, the children with URTI were divided into the elevated CRP group (n=48) and the normal CRP group (n=54), elevated WBC group (n=61) and normal WBC group (n=40), the early stage of infection without treatment group (n=68) and mid-late stage of infection with treatment group (n=35). Results Plasma MASP2 levels was significantly higher in URTI group than in the healthy control group (P<0.001) and showed a close correlation with age (r=0.302, P<0.01). Plasma MASP2 level was significantly correlated with CRP level in elevated CRP group (r=0.310, P<0.05) but not in normal CRP group (P>0.05), correlated with WBC in elevated WBC group (r=0.392, P<0.01) but not in normal WBC group (P>0.05), and was significantly higher in early stage infection without treatment group than in mid-late stage of infection with treatment group (P<0.01). MASP2, MBL2 and CRP genes had a common binding site for the transcription factor HNF-4α. Conclusion MASP2 may be an acute-phase protein, and its plasma level might serve as a new reference index in the diagnosis of URTI in children.

Objective To investigate the effects ofβ-elemene in suppressing the proliferation and apoptosis of SGC7901 gastric cancer cells in vitro and explore the underlying mechanisms. Methods Using MTT assay, flow cytometry, and clonogenic survival assay, we assessed the effects ofβ-elemene on the viability, apoptosis, cell cycle distribution, and clonogenic survival of gastric cancer SGC7901 cells and gastric mucosal epithelial GES-1 cells. Western blotting was employed to determine the changes in the protein expression profiles in SGC7901 cells in response toβ-elemene treatment. Resultsβ-elemene significantly suppressed the cell viability and increased the apoptosis of SGC7901 cells, and these effects were less obvious in GES-1 cells.β-elemene decreased clonogenic survival of SGC7901 cells, increased the proportion of G2/M phase cells, decreased the expression of Bcl-2, and increased the expression of Bax and cleaved caspase-3. β-elemene did not obviously affect the expression of total p21-activated protein kinase 1 (Pak1) but decreased the level of phospho-Pak1 (Thr423) and phospho-ERK1/2 (Thr202/Tyr204) in SGC7901 cells. Conclusion β-elemene inhibits the proliferation and induces apoptosis of gastric cancer cells possibly by inhibiting Pak1/ERK signaling and regulating apoptosis-associated proteins such as Bcl-2 and Bax.

[Abstract] Objective: To investigate the pathogenesis of prostate cancer by analyzing the associated hub gene modules of prostate cancer and identifying key transcription factors and genes that affect these modules. Methods: WGCNA (weighted gene co-expressed network analysis) was used to identify hub gene modules associated with important clinicopathological features of prostate cancer, such as pathological staging, Gleason grading etc. The OPOSSUM online tool was used to analyze the transcription factors enriching and regulating those genes. Pathway enrichment analysis and protein-protein interaction network analysis were used to identify key genes in prostate cancer. Finally, the effects of these genes on clinical features and disease-free survival (DFS) of prostate cancer patients were analyzed. Results: Three hub modules were identified, and they were highly associated with pathologic T stage, pathologic N stage and Gleason grading of prostate cancer, respectively. Further screening revealed 13 key dysregulated transcription factors that participated in the regulation of these three hub modules. The differentially expressed genes regulated by the 13 key transcription factors were significantly enriched in Calcium signaling pathway, cGMP-PKG signaling pathway and cAMP signaling pathway. 14 key genes (PRKG1, PRKG2, CYSLTR2, GRPR, CHRM3, ADCY5, ADRA1D, EDNRA, EDNRB, CYSLTR2, AGTR1, GRPR, GRIA1 and OXT) were at important nodes in the gene network. Among them, the high expression of ADRA1A, PRKG2, CHRM3, ADRA1D and EDN3 significantly extended the DFS of patients with prostate cancer (all P<0.01). Conclusion: ADRA1A, PRKG2, CHRM3, ADRA1D and EDN3 are regulated by key dysregulated transcription factors and highly associated with clinical features of prostate cancer. Their high expressions will significantly prolong the DFS of prostate cancer patients, which may shed light to the discovery of mechanism in prostate adenocarcinoma.