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AIM: To investigate the effects of norepinephrine(NE)on vascular endothelial cell damage in-duced by lipopolysaccharides(LPS).METHODS: Human umbilical vein endothelial cells(HUVEC-12)were cultured with LPS at 100 mg/L to establish the cell damage model.Real-time PCR and Western blot were used to determine the ex-pressions of VE-cadherin at mRNA and protein levels.The levels of TNF-α,IL-1β,IL-2 and IL-10 in culture supernatant were measured by ELISA.The reactive oxygen species(ROS)production in the endothelial cells was detected by ROS as-say kit.RESULTS: LPS decreased both mRNA and protein levels of VE-cadherin accompanied by increased levels of TNF-α,IL-1β,IL-2 and intracellular ROS,and decreased level of IL-10 in the endothelial cells.NE reversed the expres-sion of VE-cadherin at mRNA and protein levels under the condition of LPS treatment in a dose -dependent manner,and al-so alleviated the intracellular oxidative stress.CONCLUSION: NE reverses the endothelial damage induced by LPS, which may be related to the up-regulation of VE-cadherin level and the decreases in oxidative stress and inflamatory media-tors.
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Objective To discuss the incidence and risk factors of pressure ulcer in surgical patients of our hospital.Methods Totally 10 737 surgical patients were recruited.The patients were assessed by the Braden Scale. The incidence of pressure ulcer in patients with the Braden score lower than 18 was recorded.Besides,the data of patients with pressure ulcers on admission were also collected.All risk factors in patients with pressure ulcer were ana-lyzed.Results The incidence rate of pressure ulcer in surgical patients was 0.54%.The incidence of pressure ulcer was highest in department of Neurosurgery(1.46%),followed by the department of Orthopedics(0.61%),which was significantly higher than other departments,the difference was statistically significant(P <0.05).Single factor analy-sis indicated that age,smoking,nutrition,diabetes,paralysis,and large,urinary incontinence,consciousness,operation situation,serum albumin,use of analgesics,presence of caregivers contributed to pressure ulcer,the difference was sta-tistically significant(P <0.05).Multivariable logistic regression analysis showed that age,diabetes,paralysis,con-sciousness,albumin levels,use of analgesic,presence of caregivers were independent risk factors of pressure ulcers in patients.Conclusion There are many factors affecting the incidence of pressure ulcer,while age,diabetes,paralysis, consciousness,albumin levels,use of analgesic,presence of caregivers are independent risk factors of pressure ulcers.
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<p><b>OBJECTIVE</b>This study examined the effect of rapamycin, an inhibitor of mammalian target of rapamycin (mTOR), on eukaryotic initiation factor (eIF- 4E) expression in rat myocardial fibroblasts infected by Coxsackievirus B3 (CVB3) in order to identify the drug target for treatment of viral myocarditis.</p><p><b>METHODS</b>Primary cultured rat myocardial fibroblasts were treated with CVB3 with multiplicity of infection (MOI=0.5 PFU/cell). The experiment consisted of four groups in which the cultured rat fibroblasts cells were treated with CVB3, rapamycin (10 nM) and CVB3 + rapamycin or placebo (control). Experimental model of CVB3-infected myocardial fibroblasts was confirmed by detection of CVB3 mRNA expression with RT-PCR and observation of morphological changes of the infected cells with microscopy. eIF-4E expression was determined by both RT-PCR and Western Blot methods.</p><p><b>RESULTS</b>Morphological changes were found in the fibroblasts treated with MOI 0.5 PFU/cell of CVB3 by transmission electron microscope and the viral particles were found in the cytoplasm. CVB3 mRNA was expressed in CVB3-infected fibroblasts after 1, 2, and 3 days after infection and 2 days after passage. The gray scale values of the eIF- 4E /beta -actin in the control, the CVB3, the rapamycin and the CVB3+rapamycin groups were 0.73 +/- 0.07, 0.87 +/- 0.03, 0.32 +/- 0.03 and 0.56 +/- 0.04 respectively detected by RT-PCR, and were 0.79 +/- 0.09, 1.35 +/- 0.12, 0.55 +/- 0.04, and 0.62 +/- 0.07 respectively detected by Western blot. EIF- 4E expression in the CVB3 group was higher than that in the control group. Both the rapamycin and the CVB3+rapamycin groups had lower eIF- 4E expression than the control and the CVB3 groups.</p><p><b>CONCLUSIONS</b>CVB3 can infect myocardial fibroblasts and up-regulate the eIF- 4E expression in rat myocardial fibroblasts. Rapamycin can inhibit eIF- 4E expression and may be a potential medicine for treatment of viral myocarditis. It was suspected that mTOR/eIF- 4E signal pathway in rat myocardial fibroblasts might play an important role in the pathogenesis of viral myocarditis.</p>