ライフサイエンスコーパス: mucosal atrophy

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1 is preserved in TLR4KO-TPN mice and prevents mucosal atrophy.

2 a signaling from IECs attenuates TPN-induced mucosal atrophy.

3 F-alpha) expression that ultimately produces mucosal atrophy.

4 liferation decreased in control, and in both mucosal atrophy (22% decline) and mucosal hypertrophy (1

5 ral nutrition (TPN), resulting in intestinal mucosal atrophy and decreased epithelial barrier functio

6 with significantly higher scores for gastric mucosal atrophy and intestinal metaplasia than those wit

7 Manipulating this pathway may prevent mucosal atrophy and maintain the mucosal barrier in cond

8 GSH) depletion, hair loss, skin erosion, gut mucosal atrophy, and depletion of mucins.

9 ypical celiac lesion (the crypt hyperplastic mucosal atrophy) as it generally unfolds: the increased

10 way may well explain many of the findings of mucosal atrophy associated with TPN.

11 to study this interaction as TPN results in mucosal atrophy due to decreased IEC proliferation and i

12 portant targets for interventions to prevent mucosal atrophy during prolonged ileus or fasting.

13 ted previously, IGF-I, but not GH, prevented mucosal atrophy during TPN, although GH elevated plasma

14 impaired, and trophic feeding to prevent gut mucosal atrophy has become a standard treatment of criti

15 cosa in two patients, 4 and 7 years old, and mucosal atrophy in a 22-year-old.

16 testinal epithelial cells caused significant mucosal atrophy in the small intestine, as indicated by

17 We identified the novel finding of decreased mucosal atrophy in TLR4 knockout (TLR4KO) mice receiving

18 Mucosal atrophy induced by FM reduces total intestinal a

19 clear and has not been studied in a model of mucosal atrophy induced by total parenteral nutrition (T

20 hat drives the initiation and progression of mucosal atrophy, metaplasia, and dysplasia toward gastri

21 development of the proinflammatory state and mucosal atrophy observed in TPN-treated mice.

22 utions of TNF-alpha signaling to TPN-induced mucosal atrophy remain unclear.

23 deficiency in the pathogenesis of intestinal mucosal atrophy under pathological conditions.

24 ts; however, TPN is associated with profound mucosal atrophy, which may adversely affect clinical out

25 lays a central role in mediating TPN-induced mucosal atrophy without intact epidermal growth factor r

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