Toolbox from the EC FP7 HOSANNA project for the reduction of road and rail traffic noise in the outdoor environment

yesThis paper offers a brief overview of innovative methods for road and rail traffic noise reduction between source and receiver. These include using new barrier designs, planting of trees, treatments of ground and road surfaces and greening of building façades and roofs using natural materials, like vegetation, soil and other substrates in combination with recycled materials and artificial elements. The abatements are assessed in terms of numerically predicted sound level reductions, perceptual effects and cost–benefit analysis. Useful reductions of noise from urban roads and tramways are predicted for 1-m-high urban noise barriers and these are increased by adding inter-lane barriers. A 3 m wide 0.3 m high lattice ground treatment, a carefully planted 15-m-wide tree belt and replacing 50 m of paved areas by grassland are predicted to give similar reductions. Tree belts are shown to be very cost-effective and combining tall barriers with a row of trees reduces the negative impact of wind. Green roofs may significantly reduce the noise at the quiet side of buildings

Transrectal ultrasonography in Crohn's disease

En gastro-entérologie, l'ultrasonographie transrectale est un examen de premier choix dans la stadification des tumeurs anorectales. Dans la maladie de Crohn, l'ultrasonographie transrectale a mis en évidence des abcès et des fistules méconnus par les examens proctologiques. En outre, l'examen sonographique a détecté des anomalies de la paroi rectale et du sphincter anal. Ces anomalies peuvent précéder les lésions muqueuses (superficielles) et persister pendant la phase de guérison. La détection précoce des lésions anorectales dans la maladie de Crohn devrait faciliter un traitement rapide et adéqua

Involvement of nitric oxide in the inhibitory innervation of the human isolated colon

BACKGROUND: The exact nature of the inhibitory nonadrenergic noncholinergic (NANC) neurotransmitter in the human colon is still unknown. METHODS: The present study was designed to investigate the role of nitric oxide (NO) and adenosine 5'-triphosphate (ATP) in circular muscle strips of the human isolated colon. RESULTS: NO and ATP induced tetrodoloxin-resistant relaxations that mimicked those evoked by nerve stimulation. Apamin inhibited the response to ATP, had a variable effect on the relaxations to transmural stimulation, and had no effect on those to NO or nitroglycerin. NG-nitro-L-arginine (L-NNA) concentration dependently reduced the NANC nerve-mediated relaxations, but had no effect on those to ATP, NO, or nitroglycerin; the L-NNA resistant part of the NANC relaxation to nerve stimulation was further reduced by apamin. The inhibitory effect of L-NNA or the combination of L-NNA and apamin was prevented by L-arginine but not by D-arginine. CONCLUSIONS: These results suggest that NO and another substance, perhaps ATP, are involved in the inhibitory NANC neurotransmission in the circular muscle of the human colo

Evidence against ATP being the inhibitory transmitter released by nonadrenergic noncholinergic nerves in the canine ileocolonic junction

The nonadrenergic noncholinergic (NANC) relaxations in response to electrical stimulation and acetylcholine in the canine terminal ileum and ileocolonic junction were further characterized and the possible involvement of the putative NANC neurotransmitter ATP was investigated. During a norepinephrine-induced contraction, noncumulative administration of ATP and the nicotinic agonist, 1,1-dimethyl-4-phenylpiperazinium (DMPP) induced concentration-dependent relaxations in both the terminal ileum and ileocolonic junction; these responses were not inhibited by atropine, timolol or guanethidine. Desensitization to ATP blocked the ATP-induced relaxations, but not those to electrical stimulation or acetylcholine. All relaxations were abolished by tetrodotoxin. Theophylline or dipyridamole had no effect. Hexamethonium and desensitization to DMPP blocked the relaxations to acetylcholine and DMPP, but not those to electrical stimulation or ATP. The relaxations to acetylcholine, ATP and DMPP were inhibited by lidocaine. Thus, in the canine terminal ileum and ileocolonic junction, ATP induces NANC relaxations of neuronal origin, but ATP is unlikely to be the final NANC neurotransmitter mediating the relaxations to electrical stimulation or acetylcholine. These data also extend our previous observations on the presence of an inhibitory nicotinic innervation in these tissue

Acetylcholine is an indirect inhibitory transmitter in the canine ileocolonic junction

The effects of cholinergic agents, electrical stimulation and vasoactive intestinal polypeptide (VIP) were studied on transverse muscle strips of the canine ileum, ileocolonic junction and colon. Acetylcholine, methacholine and carbachol caused concentration-dependent contractions in the three gut tissues. Only acetylcholine (greater than 10(-5) M) evoked transient relaxations in the ileum and the ileocolonic junction before the onset of contractions. During contractions by noradrenaline, acetylcholine induced relaxations, which were enhanced by atropine; electrical stimulation also caused frequency-dependent relaxations. Propranolol or naloxone did not affect the relaxations. Hexamethonium, cocaine or lidocaine inhibited the relaxations induced by acetylcholine but not those evoked by electrical stimuli. Tetrodotoxin inhibited all relaxations, VIP did not evoke relaxation in the ileocolonic junction. These data indicate that acetylcholine stimulates nicotinic receptors on non-adrenergic non-cholinergic neurons, which do not release VIP or opioids. It is thus suggested that there is a nicotinic inhibitory innervation at the canine ileum and ileocolonic junctio

Alpha 2-adrenoceptor-mediated modulation of the nitrergic innervation of the canine isolated ileocolonic junction.

1. The effects of specific alpha-adrenoceptor agonists and antagonists on electrically-evoked non-adrenergic non-cholinergic (NANC) relaxations, previously demonstrated as nitrergic, were investigated in isolated circular muscle strips of the canine ileocolonic junction. 2. During a substance P-induced contraction and in the presence of atropine and guanethidine, the specific alpha 1-adrenoceptor agonist, phenylephrine and antagonist, prazosin, as well as the specific alpha 2-adrenoceptor antagonist, yohimbine, had no effect on the NANC relaxations evoked by electrical field stimulation. In contrast, clonidine and the more specific alpha 2-adrenoceptor agonist, UK-14,304, significantly reduced the electrically-induced relaxations, preferentially those in response to low frequency stimulation. The inhibitory effect of UK-14,304 on these relaxations was antagonized by yohimbine. 3. During a noradrenaline-induced contraction, clonidine, but not UK-14,304 significantly augmented the relaxations to electrical stimulation. 4. The adrenoceptor agonists and antagonists used had no effect on concentration-response curves to NO or on the relaxation induced by nitroglycerin. 5. These results indicate that stimulation of prejunctional alpha 2-adrenoceptors inhibits the nitrergic NANC relaxations induced by field stimulation and thus suggest prejunctional regulation of nitric oxide release via alpha 2-adrenoceptors in the canine ileocolonic junction

Nitric oxide as an inhibitory non-adrenergic non-cholinergic neurotransmitter

Inhibitory non-adrenergic non-cholinergic (NANC) nerves are thought to be important in the autonomic innervation of the gastrointestinal tract and other organ systems. The nature of their neurotransmitter is still debated. Speculation that nitric oxide (NO), formed from L-arginine in neuronal structures and other cells, could act as a neurotransmitter, is not yet supported by demonstration of its release upon nerve stimulation. Using a superfusion bioassay, we report the release of a vasorelaxant factor upon stimulation of the NANC nerves in the canine ileocolonic junction. Several pieces of evidence, including the selectivity of the bioassay tissues, chemical instability, inactivation by superoxide anion and haemoglobin, inhibition by NG-nitro-L-arginine (L-NNA) and potentiation by L-arginine all indicated that NO accounted for the biological activity of this transferable NANC facto

Pharmacological characterization of 5-hydroxytryptamine receptors in the canine terminal ileum and ileocolonic junction

The effects of 5-hydroxytryptamine (5-HT), the 5-HT1-like receptor agonist 5-carboxamidotryptamine and the 5-HT3 receptor agonist 2-methyl-5-hydroxytryptamine were studied on circular muscle strips of the canine terminal ileum and ileocolonic junction. Serial administration of 5-HT or of 5-carboxamidotryptamine induced slow tonic contractions that at higher concentrations of 5-HT (10(-4)-3 x 10(-4] were preceded by an initial relaxation and a fast phasic contraction. The concentration-response curves to both agonists were competitively shifted to the right by the mixed 5-HT1/5-HT2 receptor antagonist methysergide. The initial relaxation and fast phasic contraction were inhibited by the 5-HT3 receptor antagonist ICS 205-930 and tetrodotoxin. Atropine blocked the fast phasic contraction, but enhanced the relaxation. During acetylcholine-induced contractions, 5-HT and 2-methyl-5-hydroxytryptamine (greater than or equal to 10(-5) M), but not 5-carboxamidotryptamine, evoked relaxations that were blocked by ICS 205-930 and tetrodotoxin, but not by adrenoceptor antagonists. Thus, in the canine terminal ileum and ileocolonic junction, 5-HT stimulates neuronal 5-HT3 receptors and excitatory 5-HT1-like receptors located on smooth muscle. Stimulation of the 5-HT3 receptors results in an acetylcholine-mediated contraction and a relaxation mediated by an as yet unknown nonadrenergic noncholinergic neurotransmitte