Carbon dioxide (CO2) capture using solid sorbents has been recognized as a very promising technology that has attracted intense attention from both academic and industrial fields in the last decade.

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The connective tissue growth factor known as CCN2 is an inducible, profibrotic molecule that becomes aberrantly expressed in mechanical overload-bearing tissues. In this study, we found that CCN2 gene expression is rapidly induced in cyclically stretched bladder smooth muscle cells (SMCs) in vitro and in the detrusor muscle of a mechanically overloaded bladder in a rat model of experimental urethral obstruction. The activity of CCN2 promoter constructs, transiently transfected into cultured SMCs, was increased (up to 6-fold) by continuous cyclic stretching. Molecular analyses of the CCN2 promoter by serial construct deletions, cis-element mutagenesis, and electrophoretic mobility shift assays revealed that a highly conserved NF-B binding site located within the CCN2 proximal promoter region is responsible for the activation of the promoter by stretch. Chromatin immunoprecipitation assays showed that NF-B binds to the endogenous CCN2 promoter in both stretched cells and mechanically overloaded bladder tissues. Furthermore, stretch-dependent CCN2 promoter activity was significantly reduced upon inhibition of either phosphatidylinositol 3-kinase, p38 stress-activated kinase, or RhoA GTPase and was completely abolished upon inhibition of actin polymerization. Concordantly, actin polymerization was increased in either mechanically stretched cells or overloaded bladder tissues. Incubation of cultured SMCs with a cell-penetrating peptide containing the N-terminal sequence, Ac-EEED, of smooth muscle ␣-actin, altered both actin cytoskeleton organization and stretch-mediated nuclear relocation of NF-B, and subsequently, it reduced CCN2 promoter activity. Thus, mechanical stretch-induced changes in actin dynamics mediate NF-B activation and induce CCN2 gene expression, which probably initiates the fibrotic reactions observed in mechanical overloadassociated pathologies.

This paper is a continuation of an effort to build an organized operator theory in H 2 (D 2 ). It studies self-commutators for certain operator pairs and defines some numerical invariants for submodules. The fringe operator, which captures much of the information of the pairs, is defined in the last section and is used to establish an equality which connects the numerical invariants to traces of the self-commutators.