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1.
China Pharmacy ; (12): 3362-3364, 2017.
Artículo en Chino | WPRIM | ID: wpr-607094

RESUMEN

OBJECTIVE:To investigate the effects of mannitol combined with dexamethasone on related indexes of patients with infectious brain edema.METHODS:A total of 120 patients with infectious cerebral edema were divided into control group (60 cases) and observation group (60 cases) according to therapy plan.Control group was given Furosemide injection 20 mg+20% Mannitol injection 1 g/(kg,time)+0.9% Sodium chloride injection 10 mL intravenously,every 6 h,3 days later adjusting drug dose according to the disease condition of patients.Observation group was given Dexamethasone injection 10-20 mg+20% Mannitol injection 1 g/(kg·time)+ 0.9% Sodium chloride injection 10 mL intravenously,every 6 h,3 days later adjusting drug dose according to the disease condition of patients.A treatment course lasted for 7 d,and both groups were treated for 2 courses of treatment.The levels of NO,IL-1 and TNF-α,mortality and the occurrence of sequelae before and after treatment as well as the occurrence of ADR were observed in 2 groups.RESULTS:Before treatment,there was no statistical significance in the levels of NO,IL-1 or TNF-α between 2 groups (P>0.05).After treatment,the levels of NO,IL-1 and TNF-α in 2 groups were significantly lower than before treatment,and the observation group was significantly lower than the control group,with statistical significance (P<0.05).The incidence of mortality,sequelae and ADR in observation group were significantly lower than control group,with statistical significance (P<0.05).CONCLUSIONS:Mannitol combined with dexamethasone can reduce inflammatory factor level,the incidence of sequelae and mortality,without increasing the incidence of ADR.

2.
Artículo en Chino | WPRIM | ID: wpr-486170

RESUMEN

BACKGROUND:Immunotherapy with autologous immune cel s has been developed as a major adjuvant therapy for malignant tumors, but its mechanism of action has not been elucidated. OBJECTIVE:To investigate the relationship between cytokine-induced kil er cel secretion and apoptosis in human liver cancer stem cel s. METHODS:Human liver cancer stem cel s, HepG2 cel s, were isolated and enriched using serum-free suspension method. The peripheral blood mononuclear cel s from patients with liver cancer were induced byγ-interferon, CD3 monoclonal antibody and recombinant human interleukin-2 to form kil er cel s. Passage 1 liver cancer stem cel s were divided into control group (culture alone) and experimental group (co-culture of cytokines-induced kil er cel s and human liver cancer stem cel s). At 48 hours after culture, apoptosis in human liver cancer stem cel s was detected using flow cytometry, and expression of caspase-3 mRNA and protein was detected using RT-PCR and western blot, respectively. RESULTS AND CONCLUSION:The apoptotic rate in the control group was significantly lower than that in the experimental group (P<0.05). The expressions of caspase-3 at mRNA and protein levels were both higher in the experimental group than the control group (P<0.05). Experimental findings show that cytokines-induced kil er cel s can significantly promote apoptosis in human liver cancer stem cel s, and up-regulate the caspase-3 mRNA and protein expressions dramatical y.

3.
Chongqing Medicine ; (36): 3553-3555, 2015.
Artículo en Chino | WPRIM | ID: wpr-482659

RESUMEN

Objective To investigate the expression of proteinase active receptor 2(PAR2)protein in hepatocellular carcino-ma(HCC)and portal vessel tumor thrombosis(PVTT)to evaluate its clinical value.Methods Immunofluorescence,RT-PCR and Western blot were used to examine the expression of PAR2 protein in cancer tissue,tumor thrombosis and cancer-adjacent normal tissue from 21 patients with HCC.Results The expression pattern of PAR2 protein was different cancer tissue and cancer-adjacent normal tissue.PAR2 labeling index was significantly higher in cancer tissue and PVTT than cancer-adjacent normal tissue(P 0.05).Conclusion PAR2 is over-expressed in HCC and PVTT.PAR2 expression is re-lated with the development and progression of HCC.

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