Background/aim: Adenoid hypertrophy (AH) is one of the most frequent pediatric disorders. The aim of this study was to investigate the effects of TLR2-R753Q, TLR4-T399I, and TLR4-D299G polymorphisms in children with AH.
Materials And Methods: The variants of the TLR gene were determined by restriction fragment length polymorphism (PCR-RFLP) analysis in 60 patients with AH and in 50 healthy children. Data were analyzed with SNPStats and multifactor dimensionality reduction (MDR) software.
Results: We found that the presence of the G allele, the AG+GG and AG genotypes at TLR4-D299G, and the GGT haplotype were associated with AH in children (P = 0.013, P = 0.02, P = 0.038, and P = 0.001, respectively). On the contrary, no association was found between TLR2-R753Q and predisposition to AH. The CT genotype at TLR4-T399I showed a sex-specific association with AH, occurring only in boys with allergies (P = 0.0048). In addition, MDR analysis indicated a strong synergy between TLR gene markers contributing to AH. Allergic children with the diplotypes that included minor alleles of TLR4-D299G or TLR4-T399I had about a 4-fold increased risk for AH.
Conclusion: Common genetic variants of the gene encoding the TLR4 protein may have differential effects on AH and the presence of sex-specific allergy.
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http://dx.doi.org/10.3906/sag-1511-16 | DOI Listing |
Discov Oncol
January 2025
Gastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Introduction: Colorectal cancer (CRC) is the second most common cause of cancer-related deaths globally. The gut microbiota, along with adenomatous polyps (AP), has emerged as a plausible contributor to CRC progression. This study aimed to scrutinize the impact of the FadA antigen derived from Fusobacterium nucleatum on the expression levels of the ANXA2 ceRNA network and assess its relevance to CRC advancement.
View Article and Find Full Text PDFArch Dermatol Res
January 2025
Department of Genetics & Biotechnology, Graduate School of Biotechnology, College of Life Sciences, Kyung Hee University, Youngin, 17104, Republic of Korea.
Abnormal melanin synthesis within melanocytes can result in pigmentary skin disorders. Although pigmentation alterations associated with inflammation are frequently observed, the precise reason for this clinical observation is still unknown. More specifically, although many cytokines are known to be critical for inflammatory skin processes, it is unclear how they affect epidermal melanocyte function.
View Article and Find Full Text PDFZhongguo Dang Dai Er Ke Za Zhi
January 2025
PICU, Huai'an Maternal and Child Health Hospital Affiliated to Yangzhou University, Huai'an, Jiangsu 223002, China.
Objectives: To investigate the expression of soluble factor-related apoptosis ligand (sFasL) in peripheral blood and microRNA-147b (miR-147b) in monocytes in children with sepsis and their value in assessing prognosis.
Methods: A prospective study was conducted on 124 children with sepsis (sepsis group), 60 children with common infections (infection group), and 60 healthy children undergoing physical examinations (healthy control group). The independent risk factors for poor prognosis in children with sepsis were analyzed, and the value of serum sFasL and monocyte miR-147b in predicting poor prognosis in children with sepsis was assessed.
Hum Mol Genet
January 2025
Laboratory Medicine and Pathology, University of Minnesota, 420 Delaware Street SE, Minneapolis, MN, 55455, USA.
Background: Individuals with cystic fibrosis (CF; a recessive disorder) have an increased risk of colorectal cancer (CRC). Evidence suggests individuals with a single CFTR variant may also have increased CRC risk.
Methods: Using population-based studies (GECCO, CORECT, CCFR, and ARIC; 53 785 CRC cases and 58 010 controls), we tested for an association between the most common CFTR variant (Phe508del) and CRC risk.
BioData Min
January 2025
Department of Biomedical Informatics, Harvard Medical School, Boston, MA, 02115, USA.
Background: The mechanistic pathways that give rise to the extreme symptoms exhibited by rare disease patients are complex, heterogeneous, and difficult to discern. Understanding these mechanisms is critical for developing treatments that address the underlying causes of diseases rather than merely the presenting symptoms. Moreover, the same dysfunctional series of interrelated symptoms implicated in rare recessive diseases may also lead to milder and potentially preventable symptoms in carriers in the general population.
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