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Message de lalamed posté le 03-05-2009 à 17:26:10 (S | E | F)
est ce que quelqu'un pourrait m'aider à corriger un speech en anglais, c'est vraiment très urgent, parce que je ne sais pas si j'ai bien formulé les phrases, merci d'avance pour vos réponses, voici mon texte:
Good morning. I’m going to present you my work which concerns the bioavailability of cit in the sepsis.
Cit is an amino acid that is not incorporated into proteins, however it have several roles, like marker of intestinal and renal functions, it’s an alternative to arg supplementation, it can stimulate muscle protein synthesis and limit the progress of atherosclerosis.
The intestinal absorption of cit was demonstrated by only 2 studies: the first one is realized in 1992, it’s demonstrated that the cit transport across the intestinal barrier is na+ dependent and the second study realized in our laboratory demonstrate that the cit uptake by cultured enterocyte are accomplied by na+ dependent system B0,+ and by na+ independent system that include 2 transporters b0,+ and L.
Then, the exogenous cit can be absorbed efficiently by the gut. The cit can be provided also from the dietary gln and arg. 13% of gln is converted on cit in the intestine.
Cit pass by the blood circulation in the kidney where it is converted to arg by arginosuccinate synthase and arginosuccinate lyase, after that the arg is released in the blood stream for use by other tissues. As regards arg, 11.5% of arg absorbed by the gut pass in the liver for ureagenesis.
However, in the catabolic aggression like the sepsis, the activation of the macrophages by the bacteria or by her products endotoxin leads to release of several inflammatory mediators and in particular pro inflammatory cytokines. This last one is responsible in disturbance of organism metabolism and in particular with the activation of inducible nitric oxide synthase and the alteration of amino acid absorption by the gut. To clarify this phenomenon, several studies demonstrated that the intestinal absorption of amino acid is decreased in endotoxemic animals.
These inflammatory mediators induce also the degradation of the muscle proteins for the release of arg because the endogenous synthesis may not suffice to meet metabolic demands. In this situation the arg becomes an essential amino acid and then the supplementation of nutrition with arg would seem logical. However arg are largely metabolized by the liver that release urea. And on the other hand a large quantity of arg activates iNOS that produce NO that have a detrimental role in the sepsis (NO play a major role in the hypotension). So the therapeutic alternative may be the cit that can be metabolized to arg by the kidney with an adequate quantity.
Then, the question that we arise is: in the sepsis, the bioavailability of cit can be preserved or not
For that the first objective of the study is: the regulation of cit uptake in the intestinal cells by the catabolic and anabolic stimuli.
For this purpose, we used caco-2 cells as intestinal cells model. The cells are seeds into polycarbonate filter. After 21 days, the caco-2 cells are differentiated and then had 2 poles: apical with the brush border and basolateral.
The caco-2 cells are incubated with different cytokines: tnf alpha, interleukin 1 beta and interferon gamma ate period varying from 6 to 48 hours, with different doses of lps for 24 hours and also with 5 nM of insulin for 2 hours. After cells treatment, the uptake study can be initiated by addition in the apical side 200
M of cit that contains10
M of radiolabeled cit during 5 min. the radioactivity is measured, the content of protein is quantified and the result are expressed as pourcentage of cit transport in stimulated and unstimulated cells.
The first result demonstrates the effect of lipopolysaccharides. The abscissa axis represents different doses of lps and the ordinate axis is the percentage of cit uptake in stimulated and unstimulated cells, then, in this graph, we don’t observe variation of cit uptake in stimulated cells.
Then, we examined the effect of pro-inflammatory cytokines on cit uptake. Abscissa axis represents incubation times and ordinate axis represents percentage of cit uptake.
The first graph represents the effect of TNF and we observe that the cit uptake is unaffected at various times of incubation except minor increase at 24h.
The second graph represents the effect of il-1b and we don’t observe variation of cit uptake compared to the control at all times explored.
The same result is observed on cells incubated with interferon. The uptake of citrulline is unaffected with inf.
Thus, the pro inflammatory cytokines have no effect on cit uptake with the exception of minor increase of cit absorption in the presence of TNF at 24h.
After that we explored the effect of anabolic stimuli the insulin, and also we didn’t observe a modification of cit uptake in the presence of insulin.
We conclude that is likely that the inflammation does not alter this parameter of the cit bioavailability. The same results are observed in another cell types like macrophage, aortic smooth muscle cells and neural cells.
Those promising results are not decisive because they are other factors that can alter the activity of amino acid transporters. For that the second objective of the study is the determine the bioavailability of cit compared of those of arg and gln in endotoxemic rats
For this, we used 36 sprague dawley male rats. The animals are acclimated for a period of 7 days. After that, rats were randomized on 6 groups. The 3 first groups are lps with the grp 1 is cit, group 2 is arg and group 3 is gln. The last 3 groups is the group control with cit arg and gln.
The group lps were injected intraperitoneally with lps at dose 7.5 mg/kg during 12hours.
After that, the amino acids cit, arg and gln are administrated by gavage.
The blood samples were collected via caudal catheter at interval 0 to 10h after oral administration. And the plasma amino acid is measured by ion exchange chromatography
The preliminary control study with n=3 was performed to assess the pharmacokinetic of cit in control rat. We observe that the plasma cit concentration reached a maximum at 2 hours and decrease to the baseline level at 10h
Modifié par lucile83 le 03-05-2009 17:36
Un peu long aussi,non?