Objective Our objective was to design a new type of bedpan (inflatable, bed urinal) and compare its effect with common bedpan. Methods We divided 144 patients with bone fracture and lying in bed into the test group and the control group with 72 cases in each group from May 2006 to February 2007. Inflatable bed urinals were used in the test group and common bedpans were used in the control group. The pain alleviation, comfort degree, staining of bed sheet and skin injury were observed and evaluated in each group. Results Application of inflatable bed urinal was superior to common bedpan in the following aspects: alleviation of pain, comfort degree, staining of bed sheets and skin injury. Conclusions Adoption of inflatable bed urinal could alleviate pain, prevent the incidence of complication and reduce the workload of nurses.

Objective To evaluate the effect of high-level spinal cord injury(SCI)on the expression of mitochondrial voltage-dependent anion channel 2(VDAC2)in rat cardiomyocytes.Methods Forty-eight pathogen-free healthy adult male Sprague-Dawley rats,weighing 200-250 g,were divided into 2 groups(n=24 each)using a random number table:sham operation group(group S)and high-level SCI group(group H).The animals were anesthetized with intraperitoneal chloral hydrate and subjected to SCI using the modified Allen weight-drop method in group H.The spinal cord was only exposed in group S.At 6,12,24 and 48 h after SCI(T1-4),6 rats in each group were randomly selected and sacrificed,and myocardial specimens were collected from the cardiac apex for microscopic examination of the cell morphology(with a transmission electron microscope) and for determination of cell apoptosis(by TUNEL assay),expression of Bax,Bcl-2 and VDAC2 protein and mRNA in cardiomyocytes(by Western blot and real-time polymerase chain reaction,respectively).The apoptosis rate and ratios of Bax/Bcl-2 protein and mRNA were calculated.Results Compared with group S,the apoptosis rate and ratios of Bax/Bcl-2 protein and mRNA were significantly increased at T1-4,the expression of VDAC2 protein and mRNA was significantly down-regulated at T2-4(P<0.05 or 0.01),and the pathologic changes of cardiomyocytes were aggravated in group H.Conclusion The mechanism of myocardial damage is related to down-regulation of mitochondrial VDAC2 expression in cardiomyocytes and promotion of cell apoptosis in rats with high-level SCI.