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Naguib M. Zoheir Mona S. Hamdy Mervat M. Khorshied Nelly N. Abulata Mehry El Sobky Amr M. Saleh Hussein M. Khairy 《Comparative clinical pathology》2013,22(2):203-207
Deep vein thrombosis (DVT) is a common multi-factorial disease, with serious short- and long-term complications, and a potential fatal outcome. Many genes are involved in determining the interindividual variation in traits that define the onset and progression of disease, as well as the response to treatment. Several association studies have designed the relationship between factor XII C46T polymorphism and the risk of arterial and venous thrombosis. Some studies reported that FXII gene polymorphism is not associated with venous thrombosis, whereas other studies found an increased risk of venous thrombosis in carriers of a FXII-T variant. We constructed an age–gender–ethnic–matched case–control study including 52 DVT patients and 100 healthy volunteers. C46T polymorphism of the coagulation factor XII was carried out using allelic discrimination assay by real-time polymerase chain reaction for patients and controls, while plasma factor XII activity was detected by one-step clotting assay. FXII C46T genotyping in DVT patients revealed that 34.6% were heterozygous harboring the FXII-CT heterotype and 3.85% were homozygous; FXII-TT homotype, with no statistically significant difference in the distribution of the mutant genotypes between DVT patients and the control group. FXII activity was significantly reduced in DVT patients harboring the mutant genotypes. In the present study, FXII C46T gene polymorphism was not associated with increased risk of deep venous thrombosis. 相似文献
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Eugen Dhimolea Ricardo de Matos Simoes Dhvanir Kansara Aziz Al’Khafaji Juliette Bouyssou Xiang Weng Shruti Sharma Joseline Raja Pallavi Awate Ryosuke Shirasaki Huihui Tang Brian J. Glassner Zhiyi Liu Dong Gao Jordan Bryan Samantha Bender Jennifer Roth Michal Scheffer Constantine S. Mitsiades 《Cancer cell》2021,39(2):240-256.e11
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Geir Bjørklund Nagwa A. Meguid Afaf El-Ansary Mona A. El-Bana Maryam Dadar Jan Aaseth Maha Hemimi Joško Osredkar Salvatore Chirumbolo 《Journal of molecular neuroscience : MN》2018,66(4):492-511
Autism spectrum disorder (ASD) is a neurodevelopmental disorder afflicting about one in every 68 children. It is behaviorally diagnosed based on a triad of symptoms, including impairment in communication, impairment in sociability and abnormal and stereotypic behavior. The subjectivity of behavioral diagnosis urges the need for clinical biomarker tests to improve and complement ASD diagnosis and treatment. Over the past two decades, researchers garnered a broad range of biomarkers associated with ASD and often correlating with the severity of ASD, which includes metabolic and genetic biomarkers or neuroimaging abnormalities. Metabolic biomarkers are either involved in key pathways such as a trans-sulfuration pathway or produced due to the derangement of these pathways in the case of oxidative stress. Recent studies reported several genetic abnormalities related to ASD, encompassing various mechanisms, from copy number variations (CNVs) and single nucleotide polymorphisms (SNPs) to chromosomal anomalies. However, it is still premature to consider these genetic variants as true biomarkers for ASD, due to their low reproducibility and regional-specific nature. Herein, we comprehensively review state of the art about major biomarkers reported in ASD and the association of some biomarkers with ASD symptoms and severity. It is important to establish those biomarkers to be able to help in the diagnosis and to optimize the treatment of ASD. 相似文献
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