1,721,244 research outputs found
Role of enteric glial S100 protein in intestinal inflammation
No full textInvited lecture about the role of the enteroglial-derived S110 beta protein in the control of gastrointestinal inflammation
Impact of genetic polymorphisms on the pathogenesis of achalasia: an age-dependent paradigm?
No full textA wealth of evidence supports the concept that achalasia represents an autoimmune disorder in which a triggering factor (probably a virus) is the starter of an uncontrolled myenteric ganglionitis leading to neurodegeneration. The reasons whereby this process occurs only in some individuals and at the oesophageal level are unknown, but it is reasonable to assume that some genetic influence may affect the achalasia phenotype, making some individuals more or less susceptible to the disease. Association studies between achalasia and polymorphisms of genes involved in the regulation of immune responses may help to explain the complexity of achalasia pathogenesis and progression
Food intake and gastrointestinal motility. A complex interplay.
No full textThe complex network between the central nervous system and the enteric nervous system plays a pivotal role in preparing the digestive tract to receive food, process it to activate digestion and control food intake itself. This field has always stimulated researchers and is now receiving notable impetus by the availability of sophisticated technologies able to provide an increasing amount of complex data. This article describes recent findings that underline the role of feeding and the gastrointestinal system in regulating food intak
Regolazione della sensibilità viscerale del tratto digestivo superiore ed inferiore mediata dal sistema serotoninergico.
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Visceral hypersensitivity in functional disorders of the upper gastrointestinal tract.
No full textVisceral hypersensitivity is now recognised as a major pathophysiological mechanism in functional gastrointestinal disorders of the upper gastrointestinal tract. In patients with non-cardiac chest pain and functional dyspepsia, a high prevalence of visceral hypersensitivity has been indeed observed. In these patients, luminal physiological stimuli can be perceived as unpleasant or even painful. Although the fine mechanisms underlying such “aberrant perceptions” are yet not fully clarified, it is thought that an altered activation of the gut-wall receptors, an altered conduction of sensory inputs at the level of neural pathways, or an impaired processing of the sensations at the level of brain, may occur along the brain–gut axis. So far, drugs able to reduce hypersensitivity, that target each of the constituents of the stimuli–perception chain, have the therapeutic potential to reduce visceral hypersensitivity and, thus, to improve the symptoms. In this context, the availability of new agonists/antagonists to neurotransmitters offers a new exciting tool for the treatment of functional disorders of the upper gastrointestinal tract
Nicotinamide methylation and hepatic energy reserve.
No full textIn liver diseases the reduction of hepatic energy reserve may affect many metabolic pathways that require ATPR e.g. the synthesis of pyridine nucleotides from nicotinamide (NAM). When exogenous NAM is poorly utilized in this synthesis, it follows a dissipative metabolic pathway and is excreted in urine as N-methyinicotinamide (NMN).
Recently we reported a significant increase of NMN production and excretion in cirrhotic patients in basal condition and after NAM oral load. The aim of this study was to verify NAM methylation in relation to liver content of ATP and glycogen during rat liver in vitro perfusion with or without metabolic stress. The stress was obtained by a 15 min delay in Krebs medium perfusion of isolated liver. The metabolic stress significantly reduced the liver content of ATP The production of NMN in the stressed rat liver is significantly higher than in normal liver. The NAM liver methylation is inversely related to ATP (r = -0.74; p < 0.01) and glycogen (r = -0.53; p < 0.05) levels.
In conclusion this study suggests that the increase of NMN production in cirrhotic patients may depend on the energy crisis of liver cel
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