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The Genetic Basis of NEC Susceptibility
Published in David J. Hackam, Necrotizing Enterocolitis, 2021
Lovya George, Wei Yu, Alain Cuna, Venkatesh Sampath
Polymorphisms in the FUT2 gene, which result in differing phenotypes of secreted fucosylated glycans on mucosa, have important implications in host–microbiome interactions. The FUT2 nonsecretor phenotype has been associated with alterations in the gut microbiome (66), with some studies demonstrating that it confers genetic susceptibility to Crohn disease (67). Morrow et al. (68) investigated the non-secretor status (AA) of the FUT2 polymorphism (428G→A) and found no evidence of association between this variant and NEC or surgical NEC. However, when salivary secretion of H-antigen was used to determine nonsecretor status, a positive association with NEC was found. Demmert et al. (69) investigated the same FUT2 polymorphism in a large prospective cohort of 2406 very low-birth-weight (VLBW) infants and found no association of this polymorphism with NEC. These differing results can possibly be explained by the varied influence of the FUT2 genotype on the secretor phenotype, which is also influenced by epigenetic changes and not always concordant with genotypes.
Cellular Components of Blood
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The ABO antigens are complex oligosaccharide (carbohydrates) (Figure 51.9). The core antigen is the H antigen, which is a precursor with L-fucose as the terminal sugar. The A antigen is formed when N-acetylgalactosamine is added to the terminal group of the H antigen. The B antigen results when D-galactose is added to the H antigen.
Histoplasmosis
Published in Rebecca A. Cox, Immunology of the Fungal Diseases, 2020
The specificity of antibody responses to H. capsulatum can be established by use of the ID test in which reference Histoplasma antigen and antiserum reagents are used. The diagnostic value of precipitin antibodies in this disease was first noted by Heiner.153 Of the multiple antigens present in histoplasmin, the two which have been designated H and M are specific for H. capsulatum. The occurrence of precipitin antibody to the H antigen, either alone or in combination with antibody to the M antigen, provides strong, if not definitive evidence of histoplasmosis, but occurs in less than 27% of patients.147,150,154,155 Reactivity to the M antigen is demonstrable in approximately 75% of patients with histoplasmosis, but does not differentiate between active or inactive disease and may result from histoplasmin skin testing in sensitized persons.154–156
Forward and reverse typing discrepancy and crossmatch incompatibility of ABO blood groups: cause analysis and treatment
Published in Hematology, 2023
Hongmei Qiu, Xuechun Wang, Yan Shao
ABO subtype, also known as ABO variant, is associated with the following blood group test results: (1) forward and reverse ABO blood group typing discrepancy; (2) consistent forward and reverse ABO blood group typing with forward blood group typing response intensity ≤ 3 + or reverse blood group typing response intensity ≤ 2, as seen in the two cases of subtype AB in this study. Anti-H agglutination intensity is the major criterion for defining ABO subtypes. From strong to weak, the H antigen of each blood group is O>A2>B>A1>A2B>A1B. The antigen identification method was determined based on the results of the absorption and diffusion test in which the absorptive capacity of subtypes was lower than that of normal red blood cells but the diffusion capacity was higher [10]. The absorption and diffusion tests are typically used to detect ABO subtypes when there are discrepancies between forward and reverse ABO blood group typing, or when forward blood group typing is O. This method, however, has a few drawbacks. An additional genetic test based on molecular biology is recommended if possible.
Association between ABO blood type and type I endometrial cancer: a retrospective study
Published in Journal of Obstetrics and Gynaecology, 2023
Shiyuan Wei, Tingting Yi, Zhenbo OuYang, Jiawen Wu
The ABO gene is located on chromosome 9 (9q34), and contains seven exons that span more than 18 kb of genomic DNA (Hong et al. 2021). This gene encodes glycosyltransferases that catalyse the addition of a single sugar to the H antigen to form the A and B antigens. ABO blood type antigens are not only expressed on the surface of erythrocytes, but also on the surface of epithelial cells such as the digestive tract, skin and genitourinary tract (Abegaz 2021). Therefore, the distribution of blood groups in tumour patients and the normal population can be compared to assess the genetic tendency of tumour (Rummel and Ellsworth 2016). In recent years, many studies have shown that ABO blood types can affect the occurrence and development of various pathogenic processes and may be related to tumour susceptibility (Alexandra et al. 2022), and even Coronavirus Disease 2019 (COVID-19) (Zhao et al. 2021). In 1985, Aird et al. (Giannopoulos et al. 1985) first reported an association between blood type and renal cell carcinoma. Later studies reported the relationship between ABO blood type and various cancers, which suggested that human blood group antigens may affect the incident of cancer (Huang et al. 2017, Bothou et al. 2019, Mao et al. 2019, Song et al. 2019). Furthermore, a genome-wide study found that the ABO gene locus is significantly related to the development of pancreatic cancer (Amundadottir et al. 2009).
The Interface of Vibrio cholerae and the Gut Microbiome
Published in Gut Microbes, 2021
Jennifer Y. Cho, Rui Liu, John C. Macbeth, Ansel Hsiao
Only a limited number of host genetic factors have been associated with susceptibility and resistance to cholera. The ABH blood group antigens found on the surface of numerous cell types, and specifically the O phenotype that expresses an unmodified H antigen, have been associated with increased severity of cholera symptoms. Indeed, the prevalence of O blood group is low in the Ganges River Delta, a historically significant focal center of cholera infection, suggesting that cholera-associated selective pressures may have driven evolutionary changes in human populations.50 A growing body of work, however, has focused on the gut microbiome, the co-evolving native microbial community of the gut. Limitations in the ability to define, culture, and manipulate microbial populations in animal systems have stymied detailed molecular characterization of microbe–microbe and microbe–host interactions in the context of infection and colonization. However, a growing body of work, leveraging advances in germ-free animal systems and multi-omic approaches applied to commensal microbial communities, has elucidated several molecular mechanisms underlying the role of human microbiome structure in susceptibility to V. cholerae infection.