Incisional hernia after minimally invasive gastrectomy in gastric cancer patients

Purpose@#Although there are several studies on the incidence and risk factors for incisional hernia (IH) after open surgery, data about IH after minimally invasive surgery (MIS) for gastric cancer is rare. This study aimed to identify the incidence and risk factors for IH after MIS in gastric cancer patients. @*Methods@#We analyzed the clinicopathologic data of patients who had laparoscopic or robotic gastric cancer surgeries between January 2006 and July 2019 at National Cancer Center, South Korea. Risk factors for development of IH were investigated with univariate and multivariate analyses. @*Results@#A total of 2,769 patients underwent laparoscopic-assisted or robot-assisted gastrectomy with extracorporeal gastric resection and reconstruction, while 1,469 underwent totally laparoscopic or totally robotic gastrectomy (TLRG) with intracorporeal gastric resection and reconstruction. IH repair was performed in 23 patients (0.5%) after gastric cancer surgery. In the multivariate analysis, female sex (odds ratio [OR], 5.23; 95% confidence interval [CI], 2.03–13.43; p = 0.001), high body mass index (BMI) of ≥25 kg/m2 (OR, 4.23; 95% CI, 1.73–10.35; p = 0.002), larger tumor size (OR, 21.67; 95% CI, 5.37–87.34; p < 0.001), and intracorporeal procedure (OR, 5.63; 95% CI, 2.15–14.61; p < 0.001) were independent significant risk factors for IH. @*Conclusion@#IH after MIS for gastric cancer is not common. Female sex, high BMI, large tumor size, and intracorporeal procedure were significant risk factors for it in this study. Therefore, in patients with risk factors, surgeons should cautiously close the abdominal wall access wound after MIS for gastric cancer, to prevent IH.

Incisional hernia after minimally invasive gastrectomy in gastric cancer patients

Purpose@#Although there are several studies on the incidence and risk factors for incisional hernia (IH) after open surgery, data about IH after minimally invasive surgery (MIS) for gastric cancer is rare. This study aimed to identify the incidence and risk factors for IH after MIS in gastric cancer patients. @*Methods@#We analyzed the clinicopathologic data of patients who had laparoscopic or robotic gastric cancer surgeries between January 2006 and July 2019 at National Cancer Center, South Korea. Risk factors for development of IH were investigated with univariate and multivariate analyses. @*Results@#A total of 2,769 patients underwent laparoscopic-assisted or robot-assisted gastrectomy with extracorporeal gastric resection and reconstruction, while 1,469 underwent totally laparoscopic or totally robotic gastrectomy (TLRG) with intracorporeal gastric resection and reconstruction. IH repair was performed in 23 patients (0.5%) after gastric cancer surgery. In the multivariate analysis, female sex (odds ratio [OR], 5.23; 95% confidence interval [CI], 2.03–13.43; p = 0.001), high body mass index (BMI) of ≥25 kg/m2 (OR, 4.23; 95% CI, 1.73–10.35; p = 0.002), larger tumor size (OR, 21.67; 95% CI, 5.37–87.34; p < 0.001), and intracorporeal procedure (OR, 5.63; 95% CI, 2.15–14.61; p < 0.001) were independent significant risk factors for IH. @*Conclusion@#IH after MIS for gastric cancer is not common. Female sex, high BMI, large tumor size, and intracorporeal procedure were significant risk factors for it in this study. Therefore, in patients with risk factors, surgeons should cautiously close the abdominal wall access wound after MIS for gastric cancer, to prevent IH.

Protective effect of 4,4'-diaminodiphenylsulfone against paraquat-induced mouse lung injury

Although 4,4'-diaminodiphenylsulfone (DDS, dapsone) has been used to treat several dermatologic conditions, including Hansen disease, for the past several decades, its mode of action has remained a topic of debate. We recently reported that DDS treatment significantly extends the lifespan of the nematode C. elegans by decreasing the generation of reactive oxygen species. Additionally, in in vitro experiments using non-phagocytic human fibroblasts, we found that DDS effectively counteracted the toxicity of paraquat (PQ). In the present study, we extended our work to test the protective effect of DDS against PQ in vivo using a mouse lung injury model. Oral administration of DDS to mice significantly attenuated the lung tissue damage caused by subsequent administration of PQ. Moreover, DDS reduced the local expression of mRNA transcripts encoding inflammation-related molecules, including endothelin-1 (ET-1), macrophage inflammatory protein-1alpha (MIP-1alpha), and transforming growth factor-beta (TGF-beta). In addition, DDS decreased the PQ-induced expression of NADPH oxidase mRNA and activation of protein kinase Cmicro (PKCmicro). DDS treatment also decreased the PQ-induced generation of superoxide anions in mouse lung fibroblasts. Taken together, these data suggest the novel efficacy of DDS as an effective protective agent against oxidative stress-induced tissue damages.

Suppression of ROS generation by 4,4'-diaminodiphenylsulfone in non-phagocytic human diploid fibroblasts

The action mode of 4,4'-diaminodiphenylsulfone (DDS) is still under debate, although it has long been used in treatment of several dermatologic diseases including Hansen's disease. In this study, we tested the effect of DDS as an antioxidant on paraquat-induced oxidative stress in non-phagocytic human diploid fibroblasts (HDFs). Overall, preincubation of HDFs with DDS prevented the oxidative stress and the resulting cytotoxic damages caused by paraquat in these cells. The specific effects of DDS in paraquat-treated HDFs are summarized as follows: a) reducing the expression of NADPH oxidase 4 (NOX4) by inhibiting paraquat-induced activation of PKC; b) inhibiting paraquat-induced decreases in mitochondrial complex protein levels as well as in membrane potentials; c) consequently, inhibiting the generation of cytosolic and mitochondrial superoxide anions. Taken together, these findings suggest that DDS would suppress the radical generation in non-phagocytic HDFs during oxidative stress, and that DDS might have the extended potential to be used further in prevention of other oxidative stress-related pathologies.

Alterations of epinephrine-induced gluconeogenesis in aging

The effects of glucagon and epinephrine on gluconeogenesis in young (4 month) and old (24 month) Fisher 344 rat hepatocytes were compared. In contrast to glucagon, which had a similar effect on gluconeogenesis in both young and old cells, epinephrine caused a smaller increase in gluconeogenesis in old rat hepatocytes than in young hepatocytes. beta2 adrenergic receptor (beta2-AR) expression slightly decreased in aged rat liver, and there were differences between young and old hepatocytes in their patterns of G protein coupled receptor kinases, which are involved in the activation of beta2-AR receptor signal desensitization. The major isoform of the kinase changed from GRK2 to GRK3 and the expression of beta-arrestin, which is recruited by the phosphorylated beta2-AR for internalization and degradation, increased in aged rat liver. GRK3 overexpression also decreased the glucose output from young rat hepatocytes. We conclude that an age-associated reduction in epinephrine-induced gluconeogenesis occurs through the epinephrine receptor desensitizing system.

Alterations of epinephrine-induced gluconeogenesis in aging

The effects of glucagon and epinephrine on gluconeogenesis in young (4 month) and old (24 month) Fisher 344 rat hepatocytes were compared. In contrast to glucagon, which had a similar effect on gluconeogenesis in both young and old cells, epinephrine caused a smaller increase in gluconeogenesis in old rat hepatocytes than in young hepatocytes. beta2 adrenergic receptor (beta2-AR) expression slightly decreased in aged rat liver, and there were differences between young and old hepatocytes in their patterns of G protein coupled receptor kinases, which are involved in the activation of beta2-AR receptor signal desensitization. The major isoform of the kinase changed from GRK2 to GRK3 and the expression of beta-arrestin, which is recruited by the phosphorylated beta2-AR for internalization and degradation, increased in aged rat liver. GRK3 overexpression also decreased the glucose output from young rat hepatocytes. We conclude that an age-associated reduction in epinephrine-induced gluconeogenesis occurs through the epinephrine receptor desensitizing system.