BackgroundAlloantibody production is one of the most challenging complications in transfusion‐dependent thalassaemia patients. Haemolytic anaemia, an increase in blood consumption, difficulty in haematopoietic stem cell transplantation and reduced quality of life are consequences of alloimmunisation. The most predisposed antigens (Ags) for alloantibody development are Rh and Kell blood group Ags.ObjectiveThe aim of the present study is to evaluate any correlation between HLA‐DRB1 alleles and Rh and Kell alloantibodies.Materials and MethodsFifty‐two non‐responders (control) and 54 responders (case) were enrolled in this study. Alloantibody detection was performed using the tube method. Genotyping of HLA‐DRB1*01 and HLA‐DRB1*15 was conducted by single‐specific primer‐polymerase chain reaction.ResultsIn the responder group, 77.8% were hyper‐responders (more than one alloantibody), and only 22.2% were mono‐responders. Most detected alloantibodies were Anti‐K (94.4%), followed by Anti‐E (64.8%), Anti‐C (29.6%) and Anti‐D (25.9%). There was a significant difference in HLA‐DRB1*15 between responder and non‐responder groups, 73.7% vs 26.3%, respectively. (P = .029, OR = 3.290; 95%CI). Our results showed that HLA‐DRB1*15 was more frequent in hyper‐responders than mono‐responders (92.9% vs 7.1%) (P = .007). The greatest HLA‐DRB1*15 was seen in Anti‐K (P = .014, odds ratio [OR = 3.784]; 95% confidence interval [CI]) and Anti‐E (P = .011, OR = 3.609; 95%CI) alloantibodies. There is no association between HLA‐DRB1*01 and alloimmunisation.ConclusionOur findings showed that there is a significant correlation between HLA‐DRB1*15 and Anti‐K and Anti‐E alloantibodies. These findings can be useful in detecting susceptible thalassaemic patients and improving transfusion management.
Colorectal cancer is the third most common cancer. The activity of the Sonic hedgehog pathway is increased in patients with colorectal cancer. bFGF and Cyclopamine could act as Shh pathway inhibitors. But, by considering the dual role of bFGF on the growth of cancer cells, this study aimed to evaluate the simultaneous effect of bFGF and Cyclopamine, on apoptosis in the HT-29 cell line. Cell viability was performed using MTT assay. The apoptosis rate was measured using Annexin V-FITC/PI flow cytometry. Clonogenic assay was performed. The gene expression was investigated using Real-Time PCR method. The bFGF decreased the expression of apoptotic genes. But, the Cyclopamine increased the expression of apoptotic genes and decreased the colony formation ability. Simultaneous treatment with bFGF and Cyclopamine was associated with decreased expression of anti-apoptotic genes and decreased colony formation ability. Despite the anti-apoptotic effect of bFGF on cancer cells, it increased the anti-cancer effect of Cyclopamine, which can be due to the existence of a less-known signaling pathway between bFGF and Shh to inhibit growth, so it is important to investigate its exact mechanisms.
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