نفاذية معوية (Arabic Wikipedia)

Analysis of information sources in references of the Wikipedia article "نفاذية معوية" in Arabic language version.

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  • Thoma YM، Anderson JM، Turner JR (2012). Johnson LR، وآخرون (المحررون). Tight Junctions and the Intestinal Barrier. Academic Press. ج. 1. ص. 1043–. ISBN:978-0-12-382027-3. مؤرشف من الأصل في 2023-08-15. {{استشهاد بكتاب}}: |عمل= تُجوهل (مساعدة)

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  • Fasano, A. (فبراير 2012). "Leaky Gut and Autoimmune Diseases". Clinical Reviews in Allergy & Immunology (Review). ج. 42 ع. 1: 71–78. DOI:10.1007/s12016-011-8291-x. PMID:22109896. S2CID:4088994.
  • Leonard MM، Sapone A، Catassi C، Fasano A (2017). "Celiac Disease and Nonceliac Gluten Sensitivity: A Review". JAMA (Review). ج. 318 ع. 7: 647–656. DOI:10.1001/jama.2017.9730. PMID:28810029. S2CID:205094729. Previous studies have shown that gliadin can cause an immediate and transient increase in gut permeability. This permeating effect is secondary to the binding of specific undigestible gliadin fragments to the CXCR3 chemokine receptor with subsequent release of zonulin, a modulator of intercellular tight junctions. This process takes place in all individuals who ingest gluten. For the majority, these events do not lead to abnormal consequences. However, these same events can lead to an inflammatory process in genetically predisposed individuals when the immunologic surveillance system mistakenly recognizes gluten as a pathogen.
  • Näslund E، Hellström PM (سبتمبر 2007). "Appetite signaling: from gut peptides and enteric nerves to brain". Physiology & Behavior. ج. 92 ع. 1–2: 256–62. DOI:10.1016/j.physbeh.2007.05.017. PMID:17582445. S2CID:230872.
  • Suzuki T (فبراير 2013). "Regulation of intestinal epithelial permeability by tight junctions". Cellular and Molecular Life Sciences. ج. 70 ع. 4: 631–59. DOI:10.1007/s00018-012-1070-x. PMID:22782113. S2CID:16512214.
  • Heyman M، Abed J، Lebreton C، Cerf-Bensussan N (سبتمبر 2012). "Intestinal permeability in coeliac disease: insight into mechanisms and relevance to pathogenesis". Gut (Review). ج. 61 ع. 9: 1355–64. DOI:10.1136/gutjnl-2011-300327. PMID:21890812. S2CID:42581980. Changes in intestinal paracellular and transcellular permeability appear secondary to the abnormal immune reaction induced by gluten. Gliadin was suggested to increase junction permeability to small molecules through the release of prehaptoglobin-2. Environmental triggers of CD other than gliadin may also promote changes in permeability. Intestinal infection and iron deficiency can stimulate the expression of the transferrin receptor (TfR) CD71 in enterocytes. ... Once established, the alterations in intestinal permeability, notably the retro-transport of IgA-gliadin peptides, might self-sustain the inflammatory immune responses and perpetuate a vicious circle.

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  • Thoma YM، Anderson JM، Turner JR (2012). Johnson LR، وآخرون (المحررون). Tight Junctions and the Intestinal Barrier. Academic Press. ج. 1. ص. 1043–. ISBN:978-0-12-382027-3. مؤرشف من الأصل في 2023-08-15. {{استشهاد بكتاب}}: |عمل= تُجوهل (مساعدة)
  • Rao JN, Wang JY (1 Jan 2010). "Intestinal Architecture and Development" (بالإنجليزية). Morgan & Claypool Life Sciences. Archived from the original on 2021-04-22. {{استشهاد بدورية محكمة}}: الاستشهاد بدورية محكمة يطلب |دورية محكمة= (help)