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Suspension bed are often used to treat and nurse the wounds of burn patients in clinic. Because of the suspension force, the patients′ activities are limited, and they stay in bed for a long time, which is very easy to cause foot drop, affecting the recovery of the patients. Aiming at this problem, we designed and made a foot drop prevention baffle made of stainless steel, which could withstand the buoyancy of the suspension bed, adjust the feet forwardly and backwardly, to the left and right according to the height of the patients and the distance of the feet to be separated, and keep the foot in a positive and external rotation position according to the comfort of the patients, which achieved good results in clinical application.
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Objective To study the relationship of placental expression of leptin and disease development in patients with pre-eclampsia.Methods The placental expression of leptin gene was determined in gestational hypertension(10 cases),mild pre-eclampsia(10 cases),Severe pre-eclampsia(10cases)and normal pregnant women(15 cases,control group)by reverse txanscription/polymerase chain reaction(RT/PCR).Meanwhile,24 hour urine protein and mean arterial blood pressure(MAP)were detected in patients with pre-eclampsia.Results The expression of leptin mRNA in placenta were significantly higher in severe and mild pre-eclarnpsia than that in normal pregnant women(0.507 ±0.036,0.476±0.023vs 0.441 ±0.030)(P＜0.01),meanwhile,in the severe pre-eclampsia was higher than that in the mild preeclampsia(P＜0.05).The difference was not significant between the gestafional hypertension(0.463±0.024)and the normal pregnant women(P＞0.05).There was a positive correlation between the placental leptin mRNA expression levels in pre-eclampsia and the 24 hour urine protein and MAP (P＜0.05).Conclusions The placental leptin mRNA expression levels in pre-eclampsia increase.The pre-eclampsia women placental hptin mRNA expression levels correlate with pathogenetie condition.The placental leptin mRNA expression levels in pre-eclampsia correlate,with disease development.
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BACKGROUND: It is commonly thought that the expression of tissue factor (TF) gene in human umbilical vein endothelial cells (HUVECs) could be induced by tumor necrosis factor(TNF-α) . But the intervention effect of monomer extract of radix salviae miltiorrhizae(764-3) on TF expression in duced by TNF-α in endothelial cells has not been reported and the mechanism is still unclear.OBJECTIVE: To investigate the intervention effect of 764 - 3 on TF expression and calcium ion( [Ca2+] i) induced by TNF-α in HUVECs so as to probe into the possible mechanism of 764 - 3 for preventing cardiovascular thromboembolic diseaseDESIGN: Randomized and controlled trial.SETTING: Laboratory of Department of Pathophysiology, Institute of Basic Medical Sciences, Peking Union Medical College MATERIALS: This study was conducted in the Department of Pathophysiology, Institute of Basic Medical Science, Peking Union Medical College,Chinese Academy of Medical Sciences from May 1998 to September 1999. Umbilical cord was chosen from Beijing Obstetrics and Gynecology Hospital.INTERVENTIONS: ECV304 cell strain and HUVECs were cultured in vitro. With gene recombination techniques, two luciferase reporter genes containing different length of human TF gene promoter were constructed. The two-luciferase reporter genes, together with the intracontrol plasmid pSV-3-gal were respectively cotransfected into cultured ECV304 and HUVECs.MAIN OUTCOME MEASURES: The activities of luciferase and βgalactosidase were detected in ECV304 and HUVECs treated by TNF-α or/and 764 -3. Taking Fluo- 3/AM as fluorescent indicator, [Ca2+]i in single HUVEC was observed with laser-scanning confocal microscope.RESULTS: The luciferase expression in the p - 244/ + 121 bp luc transfected endothelial cells was significantly increased when the cells were exposed to 100 U/mL TNF-α. The induction of TNF-α could be inhibited by 764 -3 ( P ＜ 0.05). The luciferaseexpression in the p - 111/+ 121 bp Luc transfected endothelial cells was significantly lower than that in the p - 244/+ 121 bp ones and at the same time, 764 -3 did not cause the significantly change of the luciferase expression. Under laser-scanning confocal microscope, TNF-α increased [Ca2 +] i in single HUVEC, but the effect was inhibited by 764 - 3.CONCLUSION: TF gene expression induced by TNF-α was inhibited by 764 - 3 in endothelial cells, which was dependent on the p-244/+ 121 bp,and [Ca2+ ]; might be involved in it.
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AIM: To investigate the influence of tumor necrosis factor ?(TNF ?) or angiotensin Ⅱ(Ang Ⅱ) on tissue factor(TF) gene expression and the regulatory effect of upstream sequence on TNF ? or Ang Ⅱ-induced TF gene transcription in human vascular endothelial cells.METHODS: TF mRNA in endothelial cells was analyzed by in situ hybridization. By means of gene recombinant technique, we constructed two luciferase reporter genes containing different upstream sequence of TF gene. The two luciferase reporter genes, together with the intracontrol plasmid pSV-?-gal were co-transfected respectively into cultured human vascular endothelial cells. The relative luciferase activities were detected.RESULTS: TNF? or Ang Ⅱ could increase the expression of TF mRNA in vascular endothelial cells. TNF? and AngⅡ could significantly increase the luciferase expression in the p-244/+121bp Luc transfected endothelial cells, respectively. The luciferase expression in the p-111/+121bp Luc transfected endothelial cells decreased significantly compared with that in the p-244/+121 bp Luc transfected endothelial cells and there was no significant difference compared with control group. CONCLUSION: Upstream sequence p-244/-112bp of TF gene may play an important regulatory role in TNF ? or AngⅡ-induced TF gene expression in human vascular endothelial cells.