Objective:To observe the correlation of platelet activation and the inflammatory factors in patients with coronary heart disease (CHD).Methods:A total of 150 patients with CHD were divided into three groups according to the guideline of ACC/AHA:Stable angina pectoris (SAP) group (n=47,aspirin 100 mg/d); Unstable angina pectoris(UAP) group (n=50,aspirin 100 mg/d+Dalteparin 5000 U Q12 h); Acute myocardial infarction (AMI) group (n=53,aspirin 100 mg/d+Dalteparin 5000 U Q12 h+Plavix 75 mg/d).53 healthy adults served as the Control group.The fast blood sugar,lipid,platelet count,platelet aggregation of plasma,fibrinogen,high sensitivity C reactive protein (hs-CRP) of plasma,and 11-dehydro thromboxane B_2 (11-DH-TXB_2) of urine were detected upon patients' admission.Results:The level of plasma hs-CRP in groups of SAP,UAP and AMI(4.25±2.95 mg/l,7.61±6.11 mg/l,15.46±8.22 mg/l)were significantly higher than that in Control group(2.07±1.28 mg/l,P<0.05).The max rate of platelet aggregation induced by ADP in groups of UAP and AMI were significantly higher than that in Control and SAP groups(74.35±8.91%,73.88±8.35% vs.66.22±7.51%,68.67±6.87%,P<0.05).There were significant differences in the max rate of platelet aggregation induced by arachidonic acid (AA) and 11-DH-TXB_2 of urine in different groups (P<0.05).The level of plasma hs-CRP in all patients with CHD were significantly positively correlated with the max rate of platelet aggregation induced by ADP (r=0.473,P=0.000),AA(r=0.434,P=0.000) and 11-DH-TXB_2 of urine (r=0.554,P=0.000).Conclusion:There were significant relationship between the levels of plasma hs-CRP,11-DH-TXB_2 and the max rate of platelet aggregation,which indicating inflammation might induce platelet aggregation in CHD patients.

Pheochromocytoma and paraganglioma are rare neuroendocrine tumors. Because of the abnormal secretion of catecholamine, the risk of disease is high. At present, the choice of drug treatment for these diseases is still controversial. The further understanding of the research has showed that the different molecular subtypes have different carcinogenic mechanism and therapeutic response. And a variety of corresponding targeted drugs have entered the clinical trial stage, showing a certain therapeutic potential. This article reviews the current treatment and the progress of targeted drugs for pheochromocytoma and paraganglioma.

Objective:To understand the expression levels of γδT cells and CD4 + CD25 + regulatory T cells in the peripheral blood of HIV-infected/AIDS patients, and explore the correlation and possible relationship between γδT cells and CD4 + CD25 + regulatory T cells in the progression of HIV infection/AIDS Mechanism. Methods:Immunofluorescent monoclonal antibody labeling technology and flow cytometry were used to detect 12 cases of AIDS, 19 cases of intermediate HIV infection, 15 cases of early HIV infection, and 30 cases of healthy physical examination in peripheral blood CD3 + T cells and CD4 + The expression levels of T cells, CD8 + T cells, γδT cells, CD4 + CD25 + regulatory T cells; Pearson was used to analyze the correlation between γδT cells and CD4 + CD25 + regulatory T cells. Results:The expression (Mean± SD, %) of γδT cells in the peripheral blood of the AIDS group, the mid-stage HIV infection group, the early HIV infection group and the healthy control group were: 4.46±1.37, 3.59±0.67, 3.12±0.33, 1.73±0.36, group The time ratio, F=6.091, P=0.018. The expression (Mean± SD, %) of CD4 + CD25 + regulatory T cells in the peripheral blood of the AIDS group, the mid-stage HIV infection group, the early HIV infection group, and the healthy control group were: 10.28±1.94, 7.37±1.03, 6.68±0.58, 4.03±0.82, ratio between groups, F=13.568, P=0.002. The comparison of γδT and CD4 + CD25 + regulatory T cells among the four groups is statistically significant, AIDS group>HIV mid-infection group>HIV early infection group>control group. In terms of correlation, γδT, CD4 + CD25 + regulatory T cells are negatively correlated with CD4 + T cells ( r value are -0.982, -0.712, P value are 0.001, 0.002, respectively), and positively correlated with CD8 + T cell counts ( r value are 0.873 , 0.809, P value are 0.000 and 0.000 respectively); γδT cells are positively correlated with CD4 + CD25 + regulatory T cells ( r=0.911, P=0.000). Conclusions:HIV infection induces the proliferation of γδT cells and CD4 + CD25 + regulatory T cells, both of which participate in the immune response caused by HIV infection. γδT cells are positively correlated with CD4 + CD25 + regulatory T cells, and the two may have a synergistic effect.