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In order to improve the flame retardancy of knitted cotton fabrics and investigate the flame-retardant mechanism of the system formed by ammonium polyphosphate (APP) and chitosan (CS), flame-retardant knitted cotton fabrics coated with APP and CS were successfully prepared by layer by layer assembly. APP and CS formed the intumescent flame-retardant system, in which CS acted as the carbon source agent and APP acted as both the acid source and foaming agent. The surface micromorphologies before and after flaming of coated knitted cotton fabrics were exploited by scanning electron microscopy. The flammability, combustion behaviors, thermal degradation properties and flame-retardant mechanism of this system were investigated by vertical burning test, cone calorimetry test and thermogravimetric analysis coupled with Fourier transform infrared analysis in N2 atmosphere, respectively. Compared with the control sample, the deposition of APP and CS endowed the knitted cotton fabrics with improved flame retardancy, higher residual chars, lower heat release rate and total heat release, while increased the smoke production. Improved flame-retardant behaviors are attributed to the thermally stable residual chars, more release of inflammable gases and potential free radical scavengers (PO·) in the gaseous products, named the combination of the condensed-phase and gaseous-phase flame-retardant mechanism. [ABSTRACT FROM AUTHOR]

Purpose: Kinase interacting with stathmin (KIS) is a serine/threonine kinase involved in RNA processing and protein phosphorylation. Increasing evidence has suggested its involvement in cancer progression. The aim of this study was to investigate the role of KIS in the development of lung adenocarcinoma (LUAD). Dual luciferase assay was used to explore the relationship between KIS and SOX4, and its effect on ID1/β-catenin pathway. Methods: Real-time qPCR and western blot were used to assess the levels of KIS and other factors. Cell proliferation, migration, and invasion were monitored, and xenograft animal model were established to investigate the biological functions of KIS in vitro and in vivo. Results: In the present study, KIS was found to be highly expressed in LUAD tissues and cell lines. KIS accelerated the proliferative, migratory and invasive abilities of LUAD cells in vitro, and promoted the growth of LUAD in a mouse tumor xenograft model in vivo. Mechanistically, KIS activated the β-catenin signaling pathway by modulating the inhibitor of DNA binding 1 (ID1) and was transcriptionally regulated by SOX4 in LUAD cells. Conclusion: KIS, a target of SOX4, regulates the ID1-mediated enhancement of β-catenin to facilitate LUAD cell invasion and metastasis. [ABSTRACT FROM AUTHOR]