Blood has always been the main sample in determining the different blood group types. However, in multiply-transfused patients, accurate red cell antigen typing by serology is a constant problem due to the exposure to donor‟s blood in patient‟s circulation making results unreliable. To overcome these problems, another source and technique for blood typing is needed. The main aim of this study was to investigate the genotype of red cells for RH (C, c, E, e), KEL (Kell, Celano), Kidd (JKA, JKB) and Duffy (FYA, FYB) using buccal swab and peripheral whole blood amongst multiply-transfused thalassaemia patients. Sixty-three of multiply-transfused thalassaemia patients from the Thalassaemia Clinic of Ampang Hospital and Universiti Kebangsaan Malaysia Medical Centre participated in this study. Paired samples consisting of peripheral whole blood and buccal swab samples were collected prior to the scheduled blood transfusion and on day 7 after the transfusion. Blood samples were subjected to serological phenotyping by tube method and DNA genotyping while buccal swab was subjected to DNA genotyping only. Blood genotyping was performed using TaqMan® Single Nucleotide Polymorphism Real Time Polymerase Chain Reaction (SNP RT-PCR) assays for RHEe, RHCc, Kidd, KEL and Duffy blood group systems. Complete data was available in 33 patients only. Discrepancies were found between the phenotype and genotype results for all blood groups tested in both pre- and post-transfusion samples. However, a full concordance of genotyping result between pre- and post-transfusion samples was observed. When comparing the genotyping results between different sampling methods, blood and buccal swab samples showed concordant results. Accurate red blood cell antigen profiling is important for patients requiring multiple transfusions. The SNP RT-PCR platform is a reliable alternative to the conventional method. Buccal samples offer a simple and inexpensive alternative collection method that may be used for accurate blood group genotyping when blood samples are unavailable.

Purpose: Intestinal fibrosis is a common complication of inflammatory bowel diseases. However, the possible involvement of epithelial-mesenchymal transition (EMT) has been scarcely investigated. This systematic review aims to search through research papers that are focusing on messenger RNA (mRNA) and protein expression profile in EMT in fistula or in intestinal fibrosis. Methods: Electronic exploration was performed until April 24, 2019 through PubMed, Ovid, Science Direct, and Scopus databases with the terms of “fistula” OR “intestinal fibrosis” AND “epithelial-mesenchymal transition”. Two independent reviewers scrutinized the suitability of the title and abstract before examining the full text that met the inclusion criteria. For each study, the sample types that were used, methods for analysis, and genes expressed were identified. The list of genes was further analyzed using DAVID (Database for Annotation, Visualization, and Integrated Discovery) and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway. Results: There were 896 citations found; however, only 3 studies fulfilled the requirements. Among the EMT-related genes, 5 were upregulated genes at mRNA level while 6 were at protein level. However, only 2 downregulated genes were found at each mRNA and protein level. Of the 4 inflammation-related genes found, 3 genes were upregulated at mRNA level and 1 at protein level. These genes were confirmed to be involved in the development of inflammatory induced fibrosis and fistula through EMT. Results from quantitative real-time polymerase chain reaction analysis were consistent with the process of EMT, confirmed by the western blot protein analysis. Conclusion: Many significant genes which are involved in the process of EMT in fistula and intestinal fibrosis have been identified. With high-end technology many more genes could be identified. These genes will be good molecular targets in the development of biomarkers for precision drug targeting in the future treatment of intestinal fibrosis and fistula.

Human papillomavirus type 16 (HPV-16) is a well-known etiological factor for cervical and oropharyngeal cancers. The E2 protein, the product of an early-transcribed gene in HPV–16, is postulated to cause the death of cancerous cells via p53-dependent and p53-independent pathways. The main aim of the present systematic review was to study the HPV 16-E2 protein as an apoptosis-inducer agent. A thorough search of MEDLINE/PubMed, Science Direct, Scopus, and EBSCOhost databases was conducted for relevant studies on HPV AND apoptosis OR cell death where HPV 16-E2 was involved. The search identified 967 publications. Eleven records dated from 1 January 1997 to 16 February 2022 were found to meet the inclusion criteria and were eligible for data extraction and inclusion. All studies concluded that HPV 16-E2 was able to induce cell death in transfected cells. E2 proteins from the high-risk HPV–16 were able to induce apoptosis through different apoptotic pathways depending on the location of the expressed gene. However, the mechanism was still unclear, and further studies are warranted.