Following the reports of its teratogenicity,thalidomide was banned from the market in the 1960s.Later,researches discovered the teratogenicity was caused by inhibiting angiogenesis,and at that time the antiangiogenesis effect was considered an important factor in anti-tumour.Since then,many other anti-tumour mechanisms of thalidomide had been revealed and thalidomide was considered a kind of potential antitumor drug and was researched widely.This article focuses on the anti-tumour mechanisms of thalidomide and its use in combination therapy for the treatment of solid tumor.

Circulating tumor cell (CTC) is a kind of malignant tumor cells shed from the primary tumor into the circulation caused by spontaneity or surgical operation and puncture. With the development of CTC analysis recently, the detection methods have been gradually diversified. As a new biomarker, CTC plays a significant role in the diagnosis, therapeutic effect monitoring and prognosis of tumors. This paper mainly introduces the enrichment and analysis technology of CTC, and explore the relationship between CTC and tumors.

Objective:To explore the therapeutic effect of nicorandil based on routine medication on stable coronary heart disease (CHD) .Methods :A total of 100 inpatients diagnosed as stable CHD were enrolled ,randomly and e-qually divided into nicorandil group (received nicorandil 5mg based on routine medication ,three times/d) and rou-tine treatment group .After discharge ,patients were followed up for six months .Angina pectoris frequency ,ECG , serum level of high sensitive C reactive protein (hsCRP) and 6min walking distance (6MWD) were compared be-tween two groups before and after follow up .Results:After six-month follow up ,compared with routine treatment group ,there were significant improvements in clinic therapeutic effect (48% vs .74% ) and ECG therapeutic effect (78% vs .96% ) in nicorandil group , P<0.05 all;compared with before follow-up ,there were significant reduc-tions in angina pectoris frequency and serum hsCRP level ;and significant rise in 6MWD in both groups , P<0.05 all;compared with routine treatment group ,there were significant reductions in angina pectoris frequency [ (10.35 ± 1.51) times/week vs .(9.95 ± 1.65) times/week] and hsCRP level [ (1.12 ± 0.51) mg/L vs .(0.95 ± 0.43) mg/L];and significant increase in 6MWD [ (342.38 ± 35.64) m vs .(388.64 ± 32.43) m] in nicorandil group , P<0.05 all .Conclusion:Nicorandil can effectively reduce the attack number of angina pectoris of stable coronary heart disease and serum hsCRP level ,increase exercise tolerance and improve clinical therapeutic effect .

Objective:To explore the effect of gingko flavonoids on the content of SOD and MDA and cardiac function in the rats with heart failure. Methods:Totally 40 male Sprague-Dawley rats were randomly divided into 5 groups by random number table meth-od, namely the blank group, the model group, low-dose gingko flavonoids group, high-dose gingko flavonoids group and metoprolol group. Except the blank group, all the other groups were subcutaneously injected 300 mg·kg-1 isopropyl adrenaline for two days to make the heart failure model. After that, metoprolol group was given metoprolol 20 mg·kg-1 ·d-1 , the ginkgo flavonoids group was given 250 or 500 mg·kg-1 ·d-1 ginkgo flavonoids extract, the other groups were given physiological saline with the same volume, and the treatment course was 8 weeks. After the treatment, cardiac function indices ( IVST, LVPWT, LVEDD, LVESD and LVEF) , SOD and MDA levels in cardiac muscle tissue and the pathological integral, and myocardial pathologic morphology characteristics were deter-mined. Results:LVEDD and LVESD of the two ginkgo flavonoids groups and metoprolol group were obviously improved compared with those of the model group, while LVEF, IVST and LVPWT were significantly decreased (P<0. 05), showing that the cardiac function was improved after the treatment. The levels of SOD were raised, while MDA and the pathological integral were decreased significantly in the two ginkgo flavonoids groups compared with those of the model group (P<0. 05), with a dose-dependant relationship. Conclu-sion:Ginkgo flavonoids have certain protective effect in heart failure rats, and the mechanism may be related to reducing the level of lipid peroxidation and improving the body antioxidant enzyme activity.

Kawasaki disease is a disease based on systemic vasculitis, which has become the most common disease in children with acquired heart disease, but its etiology and pathogenesis remain unclear.The homeostasis of the gut microbiota plays an important role in the maturation of the body′s immune system and immune regulation.The disorder of the gut microbiota is involved in a variety of inflammatory and immune diseases in children.Studies have found that there are changes in the composition of gut microbiota in children with Kawasaki disease.Gut microbiota disorders are related to the occurrence and development of Kawasaki disease, with the immune system function affected.Various mechanisms such as intestinal mucosal barrier dysfunction, immune inflammation, oxidative stress and metabolite effects promote the pathogenesis of Kawasaki disease.This article reviews the research on the relationship between gut microbiota and Kawasaki disease.

Objective To explore the treatment to craniocerebral injury.Methods 6 patients suffered from serious, developing head injury with epidural and subdural hematoma were processed by cone socket hematoma drainage in ward before hematoma was eliminated.Results Hematoma drainage can be performed within 20 min after hospitalization. No case died and no infection occured. The score of Glasgow Outcome Scale were Ⅴ(2 cases), Ⅳ(2 cases),Ⅲ(1 case) and Ⅱ(1 case) 3 months after operation.Conclusion Cone socket hematoma drainage in ward is a good method to treat craniocerebral injury.

China ; Foundations ; Integrative Medicine ; Natural Science Disciplines

Humans ; Integrative Medicine ; Medicine ; Medicine, Chinese Traditional

Objective To investigate the influence of NS-398, a selective cyclooxygenase(COX)-2 inhibitor, on the proliferation and apoptosis of colorectal cancer cell HT-29, and to explore its potential mechanism. Methods Cultured HT-29 cells were treated with NS-398. MTT assay and flow cytometry were used to measure the proliferation and apoptosis. RT-PCR analysis was performed to measure the level of COX-2 mRNA expression at different time points in HT-29 cells. The expression of prostaglandin (PG)E2,Cyclin D1 and Bcl-2 were measured by ELISA and Western blot, respectively.Results High expression of COX-2 mRNA was detected in colorectal cancer cell line HT-29 and no obvious change of COX-2 mRNA was found after the treatment of NS-398 . NS-398 inhibited the cells proliferation and induced apoptosis in a dose-and time-dependent manner, and resulted in a significant down-regulation of Cyclin D1, Bcl-2 and PGE2.Conclusions Our results show that NS-398 may inhibit the proliferation and induce apoptosis of colon cancer cell lines HT-29 through decreasing expression of Cyclin D1 and Bcl-2 . COX-2 activity rather than its mRNA expression was related to NS-398-mediated pathway on HT-29 cells. This may be a new interfering target of selective COX-2 inhibitor on colon cancer.

Objective To observe the effect of ionizing radiation on the expressions of TLR4 and adaptor protein MyD88 in mouse peritoneal macrophages in the Toll-mediated signal transduction pathways.Methods 160 male Kunming white mice were randomly divided into 16 groups(ten each group):sham-irradiation and five groups after 4,8,16,24 and 48 h X-ray irradiation for time-course experiments;sham-irradiation and nine groups after 0.05,0.075,0.100,0.200,0.500,1.000,2.000,4.000,6.000 Gy irradiation for dose-effect experiments.Flow cytometry was used to detect the expressions of TLR4 and MyD88 after whole body irradiation (WBI) with X-rays.Results Both of TLR4 and Myd88 expressed more than shamirradiation after 0.075 and 2.000 Gy WBI for 4 h,and the expressions of them reached the peak at 16 h or 4 h after WBI(P