Modified Autonomous Key Management Scheme with Reduced Communication/Computation Costs in MANET

The growing applications of mobile ad hoc networks (MANETs) have made related security issues much more important. B. Zhu et al. proposed a key management scheme using Shamir's secret sharing scheme to construct an Autonomous Key Management (AKM) hierarchy structure. However, Shamir's secret sharing in AKM to control key hierarchy incurs high message transmission costs. This paper modifies the secret sharing scheme and applies it to AKM to reduce communication and computation costs

Gastric carcinosarcoma with rhabdomyosarcomatous differentiation: a case report and literature review

Gastric carcinosarcoma with rhabdomyosarcomatous differentiation is a rare tumor. Herein, we report the case of a 34-year-old man with a history of dysphagia, upper abdominal fullness, and poor appetite. Endoscopic findings showed a large friable mass that originated from the gastric cardia and lesser curvature of the high body. Consequently, radical total gastrectomy with Roux-en-Y esophagojejunostomy was performed. Histopathological analysis of the resected specimen revealed that the mass had invaded the serosa without regional lymph node metastasis; moreover, the tumor was positive for desmin and myogenin. Finally, we conclude this report with literature review and discussion

(Benzonitrile-κN)chlorido[hydrido­tris(pyrazol-1-yl-κN 2)borato](triphenyl­phosphine-κP)ruthenium(II) ethanol solvate. Corrigendum

Corrigendum to Acta Cryst. (2009), E65, m438

Macrophage activation increases the invasive properties of hepatoma cells by destabilization of the adherens junction

AbstractTumor-associated macrophages play an important role in tumor progression, but whether they exert a tumor-progressive effect remains controversial. Here, we demonstrated that activated macrophage-conditioned medium (AMCM) obtained from RAW macrophages (RAW/AMCM) induced epithelial-mesenchymal transition (EMT) and stimulated the migratory and invasive activities of HepG2 cells, whereas control conditioned media had no effect. Epithelial-cadherin (E-cadherin) and β-catenin staining patterns were altered at the adherens junctions by RAW/AMCM treatment, with an approximately 50% decrease in E-cadherin and β-catenin in the cell membrane. Importantly, levels of β-catenin-associated E-cadherin were also decreased. Following RAW/AMCM treatment, enhanced activation of c-Src was seen prior to increased tyrosine phosphorylation of β-catenin, and this led to the destabilization of adherens junctions. Pretreatment of HepG2 cells with the Src kinase inhibitor, PP2, completely abolished the effects of RAW/AMCM on the EMT, migration, invasion, and expression and association of E-cadherin and β-catenin. AMCMs obtained from human THP-1 monocytes and mouse peritoneal macrophages also caused disassembly of the adherens junctions and migration of HepG2 cells. Furthermore, inhibition of the epidermal growth factor receptor (EGFR) with gefitinib partially prevented the downregulation of E-cadherin and β-catenin at the adherens junctions and migration behavior induced by RAW/AMCM. Our results suggest that activated macrophages have a tumor-progressive effect on HepG2 cells which involves the c-Src- and EGFR-dependent signaling cascades