The use of sustainable metal-based catalysts for the synthesis of five-membered ring containing cyclic carbonates from epoxides and carbon dioxide is critically reviewed. Coverage is restricted to catalysis by the abundant metals: sodium, potassium, aluminium, calcium, titanium and iron and the relative merits and limitations of each catalyst syste m are compared.

Background & Aims Rifaximin is used to treat patients with functional gastrointestinal disorders, but little is known about its therapeutic mechanism. We propose that rifaximin modulates the ileal bacterial community, reduces subclinical inflammation of the intestinal mucosa, and improves gut barrier function to reduce visceral hypersensitivity. Methods We induced visceral hyperalgesia in rats, via chronic water avoidance or repeat restraint stressors, and investigated whether rifaximin altered the gut microbiota, prevented intestinal inflammation, and improved gut barrier function. Quantitative polymerase chain reaction and 454 pyrosequencing were used to analyze bacterial 16S rRNA in ileal contents from the rats. Reverse transcription, immunoblot, and histologic analyses were used to evaluate levels of cytokines, the tight junction protein occludin, and mucosal inflammation, respectively. Intestinal permeability and rectal sensitivity were measured. Results Water avoidance and repeat restraint stress each led to visceral hyperalgesia, accompanied by mucosal inflammation and impaired mucosal barrier function. Oral rifaximin altered the composition of bacterial communities in the ileum (Lactobacillus species became the most abundant) and prevented mucosal inflammation, impairment to intestinal barrier function, and visceral hyperalgesia in response to chronic stress. Neomycin also changed the composition of the ileal bacterial community (Proteobacteria became the most abundant species). Neomycin did not prevent intestinal inflammation or induction of visceral hyperalgesia induced by water avoidance stress. Conclusions Rifaximin alters the bacterial population in the ileum of rats, leading to a relative abundance of Lactobacillus. These changes prevent intestinal abnormalities and visceral hyperalgesia in response to chronic psychological stress.

The vagus nerve conveys primary afferent information produced by a meal to the brainstem. Serotonin (5‐HT), which abounds in intestinal enterochromaffin cells, is released in response to various stimuli. We have recently demonstrated that 5‐HT released from intestinal enterochromaffin cells activates 5‐HT3 receptors on vagal afferent fibres to mediate luminal non‐cholecystokinin‐stimulated pancreatic secretion. The present study was designed to evaluate the responses of vagal sensory neurons to intraluminal osmotic stimulation and luminal infusion of maltose, glucose or 5‐HT. We investigated the role of endogenous 5‐HT in signal transmission evoked by luminal stimuli to activate vagal sensory neurons. The discharges of vagal primary afferent neurons innervating the intestine were recorded from rat nodose ganglia. Luminal factors such as intestinal osmotic stimuli and perfusion of carbohydrates elicited powerful vagal nodose responses. Electrical subdiaphragmatic vagal stimulation activated 364 single units; 40 of these responded to intestinal mucosal stimuli. Of these 40, 30 responded to intraduodenal perfusion of hyperosmolar NaCl (500 mosmol l−1), 27 responded to tap water (5 mosmol l−1) and 20 and 19 responded to maltose (300 mM) and glucose (277.5 mM), respectively. The 5‐HT3/4 antagonist tropisetron (ICS 205‐930) or 5‐HT3 antagonist granisetron abolished luminal stimuli‐evoked nodose neuronal responses. Intraluminal infusion of 10−5 and 10−4 M 5‐HT elicited increases in vagal afferent discharge in 25 and 31 units, respectively, by activating the 5‐HT3 receptors. Acute subdiaphragmatic vagotomy, intestinal mucosal application of the local anaesthetic lidocaine (lignocaine) or administration of 5‐HT3 antagonist each abolished the luminal 5‐HT‐induced nodose neuronal responses. In contrast, distension‐sensitive neurons did not respond to duodenal infusion of 5‐HT. Pharmacological depletion of 5‐HT stores using p‐chlorophenylalanine (PCPA), a 5‐HT‐synthesis inhibitor, abolished luminal factor‐stimulated nodose neuronal responses. In contrast, pretreatment with 5,7‐dihydroxytryptamine (5,7‐DHT), a specific 5‐HT neurotoxin that destroys 5‐HT‐containing neurons without affecting 5‐HT‐containing mucosal cells, had no effect on these responses. These results suggested that the nodose neuronal responses to luminal osmolarity and to the digestion products of carbohydrates are dependent on the release of endogenous 5‐HT from the mucosal enterochromaffin cells, which acts on the 5‐HT3 receptors on vagal afferent fibres to stimulate vagal sensory neurons.

No abstract