OBJECTIVETo explore the molecular mechanism in the formation of unstable plaques.

METHODSThe cDNA microarray E-MTAB-2055 was downloaded from ArrayExpress database to screen the differentially expressed genes in 24 ruptured plaques against 24 stable plaques. Functional enrichment analysis was conducted to define the biological processes and pathways involved in disease progression. The protein-protein interaction network was constructed to identify the risk modules with close interactions. Five pairs of carotid specimens were used to validate 3 differentially expressed genes of the risk modules by real-time PCR.

RESULTSA total of 439 genes showed differential expression in our analysis, including 232 up-regulated and 207 down-regulated genes according to the data filter criteria. Immune-related biological processes and pathways were greatly enriched. The protein-protein interaction network and module analysis suggested that TYROBP, VCL and CXCR4 might play critical roles in the development of unstable plaques, and differential expressions of CXCR4 and TYROBP in carotid plaques were confirmed by real-time PCR.

CONCLUSIONOur study shows the differential gene expression profile, potential biological processes and signaling pathways involved in the process of plaque rupture. TYROBP may be a new candidate disease gene in the pathogenesis of unstable plaques.

Adaptor Proteins, Signal Transducing ; genetics ; Disease Progression ; Down-Regulation ; Gene Expression Profiling ; Humans ; Membrane Proteins ; genetics ; Oligonucleotide Array Sequence Analysis ; Plaque, Atherosclerotic ; genetics ; Protein Interaction Maps ; Real-Time Polymerase Chain Reaction ; Receptors, CXCR4 ; genetics ; Transcriptome ; Up-Regulation ; Vinculin ; genetics

OBJECTIVETo improve the diagnosis and treatment of primitive neuroectodermal tumors (PNET) of the pancreas.

METHODSOne patient with PNET of the pancreas was reported in this article. The corresponding literatures on the diagnosis and treatment was reviewed.

RESULTSThe patient was diagnosed as pancreatic PNET by her clinical, microscopic, and immunohistochemical features as well as cytogenetic analysis after the resection of the tumor located in the uncinate process in PUMC Hospital. Radiochemotherapy was given after the operation for 8 months and no recurrence was observed. Since PNET of pancreas have no specific clinical symptoms and most patients have jaundice and/or abdominal pain, the diagnosis depended on the immunohistochemical features of positive P30/32(MIC2) and at least two of the neural markers. The cytogenetic analysis showed translocation mainly harbored the characteristic t (11; 22) (q24; q12). Since pancreatic PNET were highly aggressive, early chemotherapy, close follow-up, and immediate surgical interventions were required as early as possible.

CONCLUSIONPNET can occur in pancreas, and diagnosis and treatment should be made as early as possible to improve the outcome.

Child ; Combined Modality Therapy ; Female ; Follow-Up Studies ; Humans ; Neuroectodermal Tumors, Primitive ; diagnosis ; therapy ; Pancreatic Neoplasms ; diagnosis ; therapy

Aim To investigate the effect of baicalein on the reversal of multidrug resistance ( MDR) media-ted by breast cancer resistance protein ( BCRP) in hu-man breast cancer MCF-7/MX cells, and explore the possible mechanisms. Methods MTT assay was per-formed to determine the cytotoxicity of baicalein and susceptibility of chemotherapeutic drugs. The protein expression levels of BCRP, p-p38 MAPK and NF-κB p65 were determined by Western blot. Results MCF-7/MX cells were not only resistant to MX but cross-re-sistant to 5-FU and DDP, and the resistance index was 70. 45, 6. 68 and 21. 47, respectively. 2. 5, 5μmol· L-1 of baicalein could increase the sensitivity to above chemotherapeutic agents and decrease the expression levels of BCRP, p-p38 MAPK and NF-κB p65 in MCF-7/MX cells. Conclusion Baicalein can effec-tively reverse MDR of MCF-7/MX by down-regulating BCRP expression through p38/MAPK and NF-κB path-ways.

AIM:To investigate the effects of baicalein on pulmonary arterial hypertension(PAH)induced by monocrotaline(MCT)in rats,and its molecular mechanism was further explored.METHODS: Male SD rats(n=28) were randomly divided into 4 groups: control group, MCT group, MCT+baicalein 50 mg/kg group and MCT +baicalein 100 mg/kg group.The PAH model was established by subcutaneous injection of MCT.After 2 weeks of modeling,the rats in baicalein treatment groups were gavaged baicalein 50 and 100 mg· kg -1· d-1for 14 d,the rats in control group were administered with saline.After 4 weeks of modeling,right ventricular systolic pressure(RVSP),right ventricular hypertro-phy index(RVHI)and right ventricular mass index(RVMI)were detected.Masson staining was used to detect the degree of lung fibrosis.The pathomorphological changes of the pulmonary vessels were observed by HE staining.Western blot was used to detect the expression of α-smooth muscle actin(α-SMA)in the lung tissue and the phosphorylation p 38,ERK and JNK in the artery.RESULTS:Compared with the control group,RVSP, RVHI and RVMI increased significantly in the MCT group(P<0.01).Pulmonary fibrosis and the thickening of pulmonary artery wall were observed.α-SMA was up-regulated and p38,ERK and JNK was activated significantly(P<0.01).Compared with the MCT group,baicalein(50 and 100 mg/kg)significantly decreased the RVSP,RVHI and RVMI(P<0.01).Lung fibrosis was reduced and the vas-cular wall thickening was decreased in baicalein-treated groups.Baicalein(50 and 100 mg/kg)inhibited the phosphoryla-tion of p38,ERK and JNK compared with the MCT group(P<0.01).CONCLUSION:Baicalein ameliorates MCT-in-duced PAH by the inhibition of pulmonary artery wall thickening at least partially via MAPK signaling pathway.

Objective To explore the molecular mechanism in the formation of unstable plaques. Methods The cDNA microarray E-MTAB-2055 was downloaded from ArrayExpress database to screen the differentially expressed genes in 24 ruptured plaques against 24 stable plaques. Functional enrichment analysis was conducted to define the biological processes and pathways involved in disease progression. The protein-protein interaction network was constructed to identify the risk modules with close interactions. Five pairs of carotid specimens were used to validate 3 differentially expressed genes of the risk modules by real-time PCR. Results A total of 439 genes showed differential expression in our analysis, including 232 up-regulated and 207 down-regulated genes according to the data filter criteria. Immune-related biological processes and pathways were greatly enriched. The protein-protein interaction network and module analysis suggested that TYROBP, VCL and CXCR4 might play critical roles in the development of unstable plaques, and differential expressions of CXCR4 and TYROBP in carotid plaques were confirmed by real-time PCR. Conclusion Our study shows the differential gene expression profile, potential biological processes and signaling pathways involved in the process of plaque rupture. TYROBP may be a new candidate disease gene in the pathogenesis of unstable plaques.

Objective To explore the molecular mechanism in the formation of unstable plaques. Methods The cDNA microarray E-MTAB-2055 was downloaded from ArrayExpress database to screen the differentially expressed genes in 24 ruptured plaques against 24 stable plaques. Functional enrichment analysis was conducted to define the biological processes and pathways involved in disease progression. The protein-protein interaction network was constructed to identify the risk modules with close interactions. Five pairs of carotid specimens were used to validate 3 differentially expressed genes of the risk modules by real-time PCR. Results A total of 439 genes showed differential expression in our analysis, including 232 up-regulated and 207 down-regulated genes according to the data filter criteria. Immune-related biological processes and pathways were greatly enriched. The protein-protein interaction network and module analysis suggested that TYROBP, VCL and CXCR4 might play critical roles in the development of unstable plaques, and differential expressions of CXCR4 and TYROBP in carotid plaques were confirmed by real-time PCR. Conclusion Our study shows the differential gene expression profile, potential biological processes and signaling pathways involved in the process of plaque rupture. TYROBP may be a new candidate disease gene in the pathogenesis of unstable plaques.

BACKGROUNDHypertrophic obstructive cardiomyopathy (HOCM) carries an increased risk for sudden cardiac death. No data regarding the percutaneous transseptal myocardial ablation (PTSMA) and epicardial left ventricular pacing (LVP) were reported.

METHODSSeven patients with recurrent symptoms and increased resting left ventricular outflow tract pressure gradient (LVOTG) after PTSMA and another 14 patients with HOCM without history of PTSMA were studied. Both resting and dobutamine stress echocardiography, PTSMA and LVP were routinely performed.

RESULTSIn patients without previous PTSMA procedure, mild reduction of resting LVOTG was detected at 5 minutes after left ventricular pacing, and this reduction became significant at 10 minutes. All patients were divided into successful and unsuccessful groups according to their response to LVP. In contrary to patients in unsuccessful group, resting and R-S2 stimuli-induced LVOTG during PTSMA procedure were decreased dramatically ((9 +/- 5) mmHg vs (58 +/- 12) mmHg, (12 +/- 2) mmHg vs (113 +/- 27) mmHg, P < 0.001). Analysis of Logistic regression demonstrated that only LVOTG level during left ventricular pacing was an independent factor predicting the reduction of LVOTG immediately after PTSMA (odds ratio (OR), 0.59; 95% CI 2.67 to 5.82; P = 0.0002).

CONCLUSIONLeft ventricular endocardial temporary pacing plays a critical role in predicting acute effect on the reduction of LVOTG immediately after PTSMA procedure.

Adult ; Cardiac Pacing, Artificial ; Cardiomyopathy, Hypertrophic ; diagnostic imaging ; physiopathology ; therapy ; Catheter Ablation ; Echocardiography ; Female ; Humans ; Logistic Models ; Male ; Middle Aged ; Pressure ; Ventricular Function, Left