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Objective:1. To detect any change in the PTEN/Akt/FoxO1 signaling pathway in the muscles of rats with chronic hypoxia-hypercapnia treated using neuromuscular electrical stimulation (NMES), and 2. To document the role of chronic hypoxia-hypercapnia in inducing muscle atrophy.Methods:Thirty-two male Sprague-Dawley rats were randomly divided into a control group, a model group, a mock stimulation group, and an NMES group, each of eight. All of the rats in the model group, the mock stimulation group and the NMES group were placed in a hypoxia-hypercapnia chamber with a 9-11% O 2 and 5.5-6.5% CO 2 atmosphere for 8h per day and 7d per week, lasting 4 weeks. The control group were placed in a similar chamber with normal air. In the last 2 weeks, after the 8h in the chamber, the NMES group were given 30min of electrical stimulation at 100Hz to the calf muscles of their bound lower limbs. The mock stimulation group were only bound without any electrical stimulation. After the 4-week intervention, the gastrocnemius muscles were resected and their cross-sectional areas (CSAs) were observed using hematoxylin-eosin staining. Immunohistochemistry and western blotting were employed to detect the protein expression of phosphatase and tensin (PTEN), p-Akt, Akt and FoxO1. Results:Compared with the control group, a significant decrease was observed in the average CSA and in the expression of p-Akt and Akt in the model group, while a significant increase was found in the average protein expression of PTEN and FoxO1. Compared with the model group, there was a significant increase in the average CSA, as well as the average expression of p-Akt and Akt in the NMES group, but a significant decrease in the average expression of PTEN and FoxO1.Conclusion:Neuromuscular electrical stimulation can relieve muscle atrophy from chronic hypoxia-hypercapnia by inducing skeletal muscle protein synthesis through regulating the PTEN/Akt/FoxO1 signaling pathway, at least in rats.
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Objective@#To analyze the effect of detail nursing in enteral nutrition in patients with severe craniocerebral injury.@*Methods@#A total of 96 patients with severe craniocerebral injury admitted to ICU department were divided into 2 groups of 48 cases according to the Stochastic numerical table method. Both groups were treated with enteral nutrition. During the treatment, the control group was given routine care, and the observation group was given detailed nursing, and the two groups were compared.@*Results@#The incidence of abdominal distension, constipation and diarrhea in the observation group was 4.17% (2/48) and 2.08% (1/48) lower than 16.67% (8/48) and 16.67% (8/48) in the control group, the difference was statistically significant (χ2=4.019, 4.414, P<0.05). The Glasgow Coma Scale (GCS) score was 9.45±1.42, which was significantly higher than 7.19±1.36 of the control group (t=7.963, P<0.05). Compared with the control group, the serum total protein (62.67±3.69) g/L, serum albumin (35.56±2.08) g/L, and peripheral lymphocyte count (1.68±0.15)×109 were significantly higher than (59.15±3.55) g/L, (31.62±2.17) g/L, (1.49±0.26)×109 in the control group (t=4.763, 9.081, 4.385, P<0.05).@*Conclusion@#During the period of enteral nutrition therapy for patients with severe craniocerebral injury, detailed nursing is helpful to reduce the related complications, improve the degree of illness, and improve the nutritional status of the body.
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Objective To analyze the effect of detail nursing in enteral nutrition in patients with severe craniocerebral injury. Methods A total of 96 patients with severe craniocerebral injury admitted to ICU department were divided into 2 groups of 48 cases according to the Stochastic numerical table method. Both groups were treated with enteral nutrition. During the treatment, the control group was given routine care, and the observation group was given detailed nursing, and the two groups were compared. Results The incidence of abdominal distension, constipation and diarrhea in the observation group was 4.17% (2/48) and 2.08% (1/48) lower than 16.67% (8/48) and 16.67% (8/48) in the control group, the difference was statistically significant ( χ2=4.019, 4.414, P<0.05). The Glasgow Coma Scale (GCS) score was 9.45 ± 1.42, which was significantly higher than 7.19 ± 1.36 of the control group (t=7.963, P<0.05). Compared with the control group, the serum total protein (62.67±3.69) g/L, serum albumin (35.56±2.08) g/L, and peripheral lymphocyte count (1.68 ± 0.15)×109 were significantly higher than (59.15 ± 3.55) g/L, (31.62 ± 2.17) g/L, (1.49 ± 0.26)×109 in the control group (t=4.763, 9.081, 4.385, P<0.05). Conclusion During the period of enteral nutrition therapy for patients with severe craniocerebral injury, detailed nursing is helpful to reduce the related complications, improve the degree of illness, and improve the nutritional status of the body.
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<p><b>AIM</b>To study the expression of leptin receptor (OB-R) and neuronal damage following focal ischemia/reperfusion in rats.</p><p><b>METHODS</b>20 adult male Wistar rats were divided into four groups randomly: sham-operated 24 h,72 h control group and ischemic/reperfusion 24 h, 72 h experiment group. Focal ischemia/reperfusion model was made with MCAO. Immunohistochemistry and immunoelectron microscope were used to observe the expression of OB-R of the cortex and neuronal damage.</p><p><b>RESULTS</b>The positive cells of OB-R were found in pyramidal cells of the parietal cortex, choroid plexus and blood vessel endothelium. Compared with sham-operated group, significant reduction of OB-R positive cells in the pyramidal cells was observed in the ischemia/reperfusion rats 24 hours after cerebral ischemia (P < 0.05). The positive cells of OB-R of sham-operated 72 h group reduced further (P < 0.01). Histochemistry and electron microscope showed neuronal damage in the core area of cerebral ischemia in the late period was more obvious than in the early period.</p><p><b>CONCLUSION</b>The early and delayed ischemia/reperfusion neuronal damage were accompanied with reduction of OB-R expression. Thus, it is worth to study the effect of OB-R in cerebral ischemia.</p>