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The aim of the present study was to investigate the prevalence and genotyping of Toxoplasma gondii in Iranian human immunodeficiency virus (HIV)-positive patients using multilocus-nested polymerase chain reaction restriction fragment length polymorphism (Mn-PCR-RFLP). A total of 102 serum samples obtained from infected patients were collected from the laboratory centres in northern Iran. Anti-T. gondii antibodies and deoxyribonucleic acid (DNA) detection were accomplished by an enzyme-linked immunosorbent assay and PCR. The Mn-PCR-RFLP method was used for the genotyping of T. gondii. Overall, 68.6% (70/102) and 11.7% (12/102) of the individuals were tested positive for anti-T. gondii immunoglobulin G and T. gondii DNA, respectively. Complete genotyping was performed on 10/12 (83.3%) PCR-positive samples. Accordingly, the samples were classified as genotype #1 (type II clonal; n = 3, 30%), genotype #2 (type III clonal; n = 2, 20%), genotype #10 (type I clonal; n = 2, 20%), genotype #27 (type I variant; n = 1, 10%), genotype #35 (type I variant; n = 1, 10%) and genotype #48 (type III variant; n = 1, 10%). The results were indicative of the high frequency of the type I and type I variant of T. gondii strains in HIV-positive patients in northern Iran. Given the high prevalence of T. gondii and frequency of pathogenic types (pathogen in laboratory mice) in the patients, special measures should be taken to prevent the possible increased incidence of encephalitis by T. gondii.
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http://dx.doi.org/10.1017/S0031182019001598 | DOI Listing |
Theor Appl Genet
September 2025
Plant Breeding, Wageningen University & Research, P.O. Box 386, 6700 AJ, Wageningen, The Netherlands.
Potato bolters are caused by excision of a transposon from the StCDF1.3 allele, resulting in a somatic mutant with late maturity. Somatic mutations during vegetative propagation can lead to novel genotypes, known as sports.
View Article and Find Full Text PDFNat Metab
September 2025
Department of Clinical and Biomedical Sciences, Faculty of Health and Life Sciences, University of Exeter, Exeter, UK.
Young-onset monogenic disorders often show variable penetrance, yet the underlying causes remain poorly understood. Uncovering these influences could reveal new biological mechanisms and enhance risk prediction for monogenic diseases. Here we show that polygenic background substantially shapes the clinical presentation of maturity-onset diabetes of the young (MODY), a common monogenic form of diabetes that typically presents in adolescence or early adulthood.
View Article and Find Full Text PDFNat Commun
September 2025
Shanghai Yao Yuan Biotechnology Ltd (Drug Farm), Shanghai, China.
ROSAH (retinal dystrophy, optic nerve edema, splenomegaly, anhidrosis, and headache) syndrome is a rare genetic disease caused by variants in alpha-kinase 1 (ALPK1) resulting in downstream pro-inflammatory signaling mediated by the TIFA/TRAF6/NF-κB pathway. Here, we report the design of an ALPK1 inhibitor, DF-003, with pharmacokinetic properties suitable for daily oral dosing. In biochemical assays, DF-003 potently inhibits human ALPK1 (IC = 1.
View Article and Find Full Text PDFBone
September 2025
Department of Bone and Mineral Research, Research Institute, Osaka Women's and Children's Hospital, Osaka Prefectural Hospital Organization, Izumi, Osaka, 594-1101, Japan. Electronic address:
Hypophosphatasia (HPP) is caused by inactivating variants of ALPL, the gene encoding tissue non-specific alkaline phosphatase (TNSALP). In order to deepen our understanding of the pathogenic mechanisms of HPP, we herein generated ALPL-knockout (KO) human induced pluripotent stem (iPS) cells by applying CRISPR/Cas9-mediated gene deletion to an iPS clone derived from a healthy subject. We analyzed two ALPL-KO clones, one ALPL-hetero KO clone, and a control clone isogenic except for ALPL.
View Article and Find Full Text PDFCell Genom
September 2025
Institute of Pathology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany; Center for Molecular Medicine Cologne, University of Cologne, Cologne, Germany. Electronic address:
Inherited genetic variants contribute to Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC), but it is unknown which cell types are involved in this process. We performed single-cell RNA sequencing of BE, EAC, and paired normal tissues and integrated genome-wide association data to determine cell-type-specific genetic risk and cellular processes that contribute to BE and EAC. The analysis reveals that EAC development is driven to a greater extent by local cellular processes than BE development and suggests that one cell type of BE origin (intestinal metaplasia cells) and cellular processes that control the differentiation of columnar cells are of particular relevance for EAC development.
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