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| Further characterization of altered microbiota in patients with inflammatory bowel diseases and linking dysbiosis with host genetic alterations in immunoregulation, innate microbial killing and barrier function are critical, so that individualized treatments to increase beneficial commensals and their metabolic products (probiotic and prebiotic administration) and diminish deleterious species such as adherent/invasive E. coli can be tailored for defined patient subsets. |
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- ·ÒëEPI: 204
- Ó¦Öú: 103 (¸ßÖÐÉú)
- ½ð±Ò: 15293.5
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°®ÓëÓêÏÂ: ½ð±Ò+1 2017-10-08 15:02:26
withoutsun(fjtony163´ú·¢): ½ð±Ò+5, ´ú·¢ 2017-11-15 17:02:45
fjtony163: ·ÒëEPI+1, ´ú·¢ 2017-11-15 17:02:52
°®ÓëÓêÏÂ: ½ð±Ò+1 2017-10-08 15:02:26
withoutsun(fjtony163´ú·¢): ½ð±Ò+5, ´ú·¢ 2017-11-15 17:02:45
fjtony163: ·ÒëEPI+1, ´ú·¢ 2017-11-15 17:02:52
|
Further characterization of altered microbiota in patients with inflammatory bowel diseases and linking dysbiosis with host genetic alterations in immunoregulation, innate microbial killing and barrier function are critical, so that individualized treatments to increase beneficial commensals and their metabolic products (probiotic and prebiotic administration) and diminish deleterious species such as adherent/invasive E. coli can be tailored for defined patient subsets. ½øÒ»²½²ûÃ÷Ñ×Ö¢ÐԽ᳦²¡»¼Õß΢ÉúÎï´ÔµÄ¸Ä±ä¼°Éú̬ʧµ÷ÓëÃâÒßµ÷½ÚµÄËÞÖ÷ÒÅ´«¸Ä±ä¡¢ÏÈÌìÐÔ΢ÉúÎïɱÉËºÍÆÁÕϹ¦ÄÜÖ®¼äµÄÁªÏµÖÁ¹ØÖØÒª£¬ÓÐÖúÓÚ¶ÔÌØ¶¨»¼ÕßÑÇȺ½øÐÐÌØ¶¨µÄ¸öÐÔ»¯ÖÎÁÆÒÔÔö¼ÓÓÐÒæ¹²Éú¾ú¼°Æä´úл²úÎï£¨ÒæÉú¾úºÍ´ÙÉúËØÖÎÁÆ£©ºÍ¼õÉÙÓк¦¾úÀàÈçÕ³¸½/ÇÖÏ®ÐԴ󳦸˾ú¡£ |
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