Dunaevskij Zhurchat Ruchji Noti
A simple and practical synthesis of soluble hexa- peri-hexabenzocoronene ( HBC) from readily available hexaphenylbenzene ( HPB) is described. In this simple procedure, the substitution of the free para positions of the propeller-shaped HPB with tert-butyl groups and the oxidative cyclodehydrogenation to planar HBC is achieved in a one-pot reaction using ferric chloride both as a Lewis acid catalyst and as an oxidant in excellent yields.
Propisi pomogut podgotovit k pismu ruku rebenka 6-7 let, razvit navyki raboty s rabochej tetradju, sformirovat prostranstvennye otnoshenija. Propisi mozhno ispolzovat v obrazovatelnom protsesse detskogo sada ili pri podgotovke rebenka k shkole v. Cvetnie bukvi russkogo alfavita dlya raspechatki.
The ready availability of HBC allows the isolation of its pure cation-radical salt using a variety of chemical oxidants such as antimony pentachloride and triethyloxonium and nitrosonium hexachloroantimonate salts.
• Perivagal application of capsaicin (1% solution) is considered to cause selective degeneration of vagal afferent (sensory) C fibres and has been used extensively to examine the site of action of many gastrointestinal (GI) neuropeptides. • The actions of both capsaicin and GI neuropeptides may not be restricted to vagal afferent fibres, however, as other non‐sensory neurones displayed sensitivity to capsaicin and brainstem microinjections of these neuropeptides induce GI effects similar to those obtained upon systemic application. • The present study used immunohistochemical, biophysical and functional approaches to test the hypothesis that perivagal capsaicin induces degeneration of vagal efferents controlling GI functions. • Our data indicate that perivagal application of capsaicin induces degeneration of vagal efferent motoneurones and decreased vagal motor responses.
Treatment with perivagal capsaicin cannot therefore be considered selective for vagal afferent C fibres and, consequently, care is needed when using perivagal capsaicin to assess the mechanism of action of GI neuropeptides. Abstract Perivagal application of capsaicin (1% solution) is considered to cause a selective degeneration of vagal afferent C fibres and has been used extensively to examine the site of action of many gastrointestinal (GI) neuropeptides. The actions of both capsaicin and GI neuropeptides may not be restricted to vagal afferent fibres, however, as other non‐sensory neurones have displayed sensitivity to capsaicin and brainstem microinjections of these neuropeptides induce GI effects similar to those obtained upon systemic application.
Perivagal application of capsaicin (1% solution) is considered to cause selective degeneration of vagal afferent (sensory) C fibres and has been used extensively to examine the site of action of many gastrointestinal (GI) neuropeptides. Symplur Signals for Research. The trusted research platform for healthcare social media. Conduct explorative research with advanced NLP, healthcare optimized machine learning and sentiment algorithms.
The aim of the present study was to test the hypothesis that perivagal capsaicin induces degeneration of vagal efferents controlling GI functions. Experiments were conducted 7–14 days after 30 min unilateral perivagal application of 0.1–1% capsaicin. Immunohistochemical analyses demonstrated that, as following vagotomy, capsaicin induced dendritic degeneration, decreased choline acetyltransferase but increased nitric oxide synthase immunoreactivity in rat dorsal motor nucleus of the vagus (DMV) neurones. Electrophysiological recordings showed a decreased DMV input resistance and excitability due, in part, to the expression of a large conductance calcium‐dependent potassium current and the opening of a transient outward potassium window current at resting potential. Furthermore, the number of DMV neurones excited by thyrotrophin‐releasing hormone and the gastric motility response to DMV microinjections of TRH were decreased significantly.
Our data indicate that perivagal application of capsaicin induced DMV neuronal degeneration and decreased vagal motor responses. Treatment with perivagal capsaicin cannot therefore be considered selective for vagal afferent C fibres and, consequently, care is needed when using perivagal capsaicin to assess the mechanism of action of GI neuropeptides. Introduction Capsaicin (CAP), applied systemically or perivagally, has been used for many years to induce a supposedly selective degeneration of sensory neurones and fibres, including vagal afferents, via actions at TRPV1 receptors (;; ). In particular, perivagal application of CAP is considered to cause selective degeneration of vagal afferent C fibres and has been used extensively to examine the site of action of many gastrointestinal (GI) neuropeptides.