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- 저자 : Nabil Zaid (검색결과 2 건)
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Soukaina Zouine,Farida Marnissi,Nada Otmani,Mohamed Bennani Othmani,Nabil Zaid,Kevin Kojok,Younes Zaid,Nadia Tahiri Jouti,Norddine Habti 한국유방암학회 2020 Journal of breast cancer Vol.23 No.1
Purpose: Aberrant glycosylation of the histo-blood group antigens (including the angina bullosa haemorrhagica [ABH]) is often observed during malignant transformation in most types of carcinomas. Data concerning their ethnic distributions are diverse which explains why their biological characteristics have to be studied in different populations. Our aim was to analyze the expression of the histo-blood group (specifically the ABH) antigens in breast carcinoma. Methods: The expression of the histo-blood group (specifically the ABH) antigens was studied in 109 patients with breast carcinoma using immunohistochemistry. Statistical analysis was performed using χ2 and Fisher analyses. Results: The loss of expression of histo-blood group (ABH) antigens in breast carcinoma was observed in 81.13% of patients with blood group O, 37.93% with blood group A, and 96.30% with blood group B. One key finding of this study was that the loss of expression of the ABH antigen was also observed in normal tissues adjacent to the tumor. The loss of expression was associated with higher tumor grade (p < 0.05). Expression of H antigen was observed in 50% of cases with loss of expression of B antigen and was associated with human epidermal growth factor receptor 2 (HER2) overexpression (p < 0.05). The loss of H antigen in patients with blood group O was associated with estrogen receptor expression (p < 0.001). Incompatible A antigen in tumor was expressed in 20.75% of patients with blood group O. Conclusion: Loss of the ABH antigens correlated with the Scarff-Bloom-Richardson histologic grading. H antigen was associated with HER2 overexpression in breast cancer. However, further studies are needed to determine the role of incompatible A antigen in mammary carcinogenesis.
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Doha Anka Idrissi,Nezha Senhaji,Asmae Aouiss,Loubna Khalki,Youssef Tijani,Nabil Zaid,Fatima Zahra Marhoume,Abdallah Naya,Mounia Oudghiri,Mostafa Kabine,Younes Zaid 대한약학회 2021 Archives of Pharmacal Research Vol.44 No.1
Ulcerative colitis (UC) and Crohn’s disease (CD)are chronic and multifactorial diseases that affect the intestinaltract, both characterized by recurrent inflammation ofthe intestinal mucosa, resulting in abdominal pain, diarrhea,vomiting and, rectal bleeding. Inflammatory bowel diseases(IBD) regroup these two disorders. The exact pathologicalmechanism of IBD remains ambiguous and poorly known. In genetically predisposed patients, defects in intestinalmucosal barrier are due to an uncontrolled inflammatoryresponse to normal flora. In addition to the genetic predisposition,these defects could be triggered by environmentalfactors or by a specific lifestyle which is widely accepted asetiological hypothesis. The involvement of the CD40/CD40Lplatelet complex in the development of IBD has been overwhelminglydemonstrated. CD40L is climacteric in cell signallingin innate and adaptive immunity, the CD40L expressionon the platelet cell surface gives them an immunologicalcompetence. The IL-1, a major inflammation mediator could be involved in different ways in the development of IBD. Here, we provide a comprehensive review regarding therole of platelet CD40/CD40L in the pathophysiologicaleffect of IL-1 in the development of Crohn’s disease (CD). This review could potentially help future approaches aimingto target these two pathways for therapeutic purposesand elucidate the immunological mechanisms driving gutinflammation.
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