Future of IBD pathogenesis: how much work is left to do?
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Etiology of inflammatory bowel disease: a unified hypothesisCD69 is the crucial regulator of intestinal inflammation: a new target molecule for IBD treatment?Expression of PPAR γ in intestinal epithelial cells is dispensable for the prevention of colitis by dietary abscisic acid.Efficacy profiles for different concentrations of Lactobacillus acidophilus in experimental colitis
P2860
Future of IBD pathogenesis: how much work is left to do?
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2008 nî lūn-bûn
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2008年の論文
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2008年論文
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2008年論文
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2008年論文
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2008年論文
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2008年論文
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2008年论文
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2008年论文
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2008年论文
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name
Future of IBD pathogenesis: how much work is left to do?
@en
type
label
Future of IBD pathogenesis: how much work is left to do?
@en
prefLabel
Future of IBD pathogenesis: how much work is left to do?
@en
P2860
P356
P1476
Future of IBD pathogenesis: how much work is left to do?
@en
P2093
Claudio Fiocchi
P2860
P304
P356
10.1002/IBD.20659
P478
14 Suppl 2
P577
2008-10-01T00:00:00Z