Practical adhesion of rubber to aluminum is measured for various aluminum silanization treatments. In this study, 6-(3-triethoxysilylpropylamino)-1,3,5-triazine-2,4- dithiol (TES) was used as the coupling agent for preparing self-assembly monolayers (SAMs) on an aluminum surface. The structure and chemical composition of the SAMs were analyzed using Fourier transform infra-red spectroscopy (FT-IR) and X-ray photo-electron spectroscopy (XPS). The changes in the surface features of the aluminum surface due to TES treatment were investigated by atomic force microscopy (AFM). The adhesive properties of the silanized aluminum surface and EPDM rubber have been evaluated by a T-peel strength test. The results suggested that the Si-O-Al bonding at aluminum TES interface existed and a TES self-assembly monolayer was formed on the aluminum surface. More than 6.0 KN/m adhesion strength is obtained when the aluminum is silanized with 2.5 mmol/dm3 TES, cured at 160 °C and vulcanized with EPDM rubber at 160 °C for 30 min. It is suggested that the TES self-assembly monolayer is bound to aluminum through its ethoxysilyl functional group, and the thiol function group is strongly cross-linked to EPDM rubber, respectively.
Myocardial ischemia/reperfusion injury (MIRI), the major pathophysiology of cardiovascular disease, is a crucial therapeutic focus. To date, whether MIRI is centrally mediated and its underlying processing hierarchy remain elusive. We show that the electrical activity of the paraventricular nucleus (PVN) and rostral ventrolateral medulla (RVLM) neurons increased after MIRI in a mouse model. We identified a neural circuit involving glutamatergic projections from the paraventricular nucleus (GluPVN) to tyrosine hydroxylase–expressing neurons in the rostral ventrolateral medulla (THRVLM) that contributes to MIRI. Transneuronal tracing with neurotropic viruses indicated that the THRVLM neurons project directly to the spinal preganglionic neurons and then to the stellate ganglion, two critical neural nodes along the brain–heart axis. Chemogenetic inhibition of the GluPVN→THRVLM circuit or cervical sympathetic blockade reduced the level of norepinephrine in the heart and thereby prevented MIRI. Furthermore, pharmacological blockade of myocardium β-receptors also reduced MIRI. This brain–heart circuit that promotes MIRI represents a potential therapeutic target for MIRI treatment.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.