Objective: To investigate the efficiency of the three attentional networks in attention deficit hyperactivity disorder (ADHD). Methods: Subjects were 25 children, aged 7 to 12 years, with DSM Ⅳ ADHD and 25 non ADHD controls matched by age, sex and IQ. Attentional networks tests were performed in all the subjects on an IBM compatible computer. Results: No differences were found between the ADHD children and the normal controls in alerting and orienting effects. However, ADHD children had a significantly larger executive control effect than their normal counterparts. The general accuracy of the ADHD children was significantly lower than that of the normal controls. Conclusion: ADHD children may have impairments in their executive control network of attention.

Objective To elucidate the role of programmed cell death factor 4(PDCD4)in mitochondrial dysfunction caused by sepsis-related vascular endothelial damage.Methods Cultured human umbilical vein endothelial cells(HUVECs)and mouse vascular endothelial cells(C166 cells)were transfected with a small interfering RNA targeting PDCD4 followed by treatment with lipopolysaccharide(LPS)alone or in combination with carbonyl cyanide 3-chlorophenylhydrazone(FCCP).The proteomic changes in the cells after PDCD4 knockdown were analyzed using LC-MS/MS technique.The mRNA expressions of PDCD4 and the genes associated with cell inflammation and apoptosis were detected with RT-PCR,and the expressions of FIS1,DRP1 and OPA1 proteins key to mitochondrial fission and fusion were determined using Western blotting.JC-1 and MitoSOX fluorescent probes were used to observe the changes in mitochondrial membrane potential and mitochondrial reactive oxygen species levels under by a laser confocal microscope.Results LPS stimulation of the cells significantly increased the mRNA expressions of interleukin-6(IL-6),tumor necrosis factor-α(TNF-α)and monocyte chemoattractant protein 1(MCP1)and enhanced the cellular expression of PDCD4(P<0.05).Proteomic analysis suggested a correlation between PDCD4 knockdown and changes in mitochondrial dynamics in the cells.LPS treatment significantly increased the expressions of mitochondrial fission proteins FIS1 and DRP1 and lowered the expression of the fusion protein OPA1 in the cells(P<0.05),causing also mitochondrial oxidative stress and reduction of the mitochondrial membrane potential(P<0.05).In HUVECs,treatment with FCCP significantly attenuated the protective effect of PDCD4 knockdown,which inhibited LPS-induced inflammation and oxidative stress and restored the balance between mitochondrial fission and fusion.Conclusion PDCD4 knockdown protects vascular endothelial cells against LPS-induced damages by repressing mitochondrial fission and oxidative stress,promoting mitochondrial fusion,and maintaining normal mitochondrial function.

Objective To elucidate the role of programmed cell death factor 4(PDCD4)in mitochondrial dysfunction caused by sepsis-related vascular endothelial damage.Methods Cultured human umbilical vein endothelial cells(HUVECs)and mouse vascular endothelial cells(C166 cells)were transfected with a small interfering RNA targeting PDCD4 followed by treatment with lipopolysaccharide(LPS)alone or in combination with carbonyl cyanide 3-chlorophenylhydrazone(FCCP).The proteomic changes in the cells after PDCD4 knockdown were analyzed using LC-MS/MS technique.The mRNA expressions of PDCD4 and the genes associated with cell inflammation and apoptosis were detected with RT-PCR,and the expressions of FIS1,DRP1 and OPA1 proteins key to mitochondrial fission and fusion were determined using Western blotting.JC-1 and MitoSOX fluorescent probes were used to observe the changes in mitochondrial membrane potential and mitochondrial reactive oxygen species levels under by a laser confocal microscope.Results LPS stimulation of the cells significantly increased the mRNA expressions of interleukin-6(IL-6),tumor necrosis factor-α(TNF-α)and monocyte chemoattractant protein 1(MCP1)and enhanced the cellular expression of PDCD4(P<0.05).Proteomic analysis suggested a correlation between PDCD4 knockdown and changes in mitochondrial dynamics in the cells.LPS treatment significantly increased the expressions of mitochondrial fission proteins FIS1 and DRP1 and lowered the expression of the fusion protein OPA1 in the cells(P<0.05),causing also mitochondrial oxidative stress and reduction of the mitochondrial membrane potential(P<0.05).In HUVECs,treatment with FCCP significantly attenuated the protective effect of PDCD4 knockdown,which inhibited LPS-induced inflammation and oxidative stress and restored the balance between mitochondrial fission and fusion.Conclusion PDCD4 knockdown protects vascular endothelial cells against LPS-induced damages by repressing mitochondrial fission and oxidative stress,promoting mitochondrial fusion,and maintaining normal mitochondrial function.

Objective: To establish the in vitro porcine gastric model of submucosal eminence lesion and to evaluate its application to endoscopic submucosal dissection(ESD). Methods: Silicone rubber impression materials and steel balls with diameters of 1 cm, 2 cm, and 3 cm were used to make three pairs of spherical cavities. And then raw ground beef was put into spherical cavities and boiled for 20 minutes to make spherical mass models. Six isolated porcine stomach with esophagus and duodenum were selected. The mass models with diameters of 1 cm, 2 cm and 3 cm were imbedded respectively into the submucosa of fundus, body, and antrum of porcine stomach through the incision on serosal layer. The submucosal masses were observed by endoscopy and endoscopic ultrasonography and ESD was performed. Results: A total of 18 mass models were constructed in 6 porcine stomachs, of which 17 models were successfully established and 1 failed. Typical endoscopic characteristics of gastric submucosal eminence lesions were found in 17 models. Endoscopic ultrasonography showed that these models originated from submucosal layer and demonstrated mixed echo. There were no significant differences between mucosa of lesions and that of surrounding areas. ESD was successfully performed in the porcine gastric models of submucosal eminence lesions, and all models were not broken or detached. Conclusion The in vitro porcine gastric model of submucosal eminence lesions can well replicate disease status and provide a suitable model for study on endoscopic therapy of submucosal eminence lesion and training of endoscopists.