The importance of ancillary insurance benefits by members of Medicare risk contract insurance plan

Thesis (D.Sc.D.)--Boston University, Henry M. Goldman School of Dental Medicine, 2000.Includes bibliographical references (leaves 63-75)

Interleukin (IL)-17A and IL-17F and asthma in Saudi Arabia: mRNA transcript levels and gene polymorphisms

Asthma is a multifactorial disorder and both genetic and environmental factors contribute to its development. The present study explored cytokines interleukin (IL)-17A and IL17F levels as usable parameters for the diagnosis of asthmatics Saudi patients. Blood samples were collected from 100 asthma patients and 100 matched controls. The transcript mRNA levels in whole blood were determined by real-time reverse-transcription polymerase chain reaction. Expression studies showed that levels of IL17A and IL17F were significantly higher in asthma patients compared to controls [IL17A: 1.112 (2.088) vs 0.938 (1.363)]; IL17F: 0.707 (1.33) vs 0.667 (0.590). The mRNA transcripts of IL17A and IL17F were positively and significantly correlated in all subjects examined in this study: controls as well as asthma patients (r = 0.455, P < 0.01 for controls and r = 0.644, P < 0.01 for patients). These findings suggest that asthma is characterized by an elevation of cytokines IL17A and IL17F and the measurement of their expression can be a valuable parameter for the diagnosis of asthma.Keywords: Asthma, interleukin-17F (IL17F), interleukin-17A (IL17A), gene expression, real time-polymerase chain reaction (RT-PCR), Saudi Arabia.African Journal of Biotechnology Vol. 12(23), pp. 3615-362

Association of MUTYH and colorectal cancer

Mutations in the MUTYH gene have been reported to be associated with increased risk of developing colorectal cancer. In this study, we confirmed this association using original data on 928 colorectal cancer cases and 845 healthy controls from Scotland. We then conducted a meta-analysis from published data on the association between mutations at MUTYH and colorectal cancer risk. We show for the first time a small but significant mono-allelic effect with a genotype relative risk (GRR) of 1.27 (95% confidence interval (CI): 1.01–1.61), and confirm and give a more precise estimate of the strong bi-allelic effect with an estimated GRR of 117 (95% CI: 74–184). This study underscores the need for large sample sizes in order to identify small gene effects when the disease allele frequency is low

Genetic variants in MUTYH are not associated with endometrial cancer risk

Hereditary non-polyposis colorectal cancer (HNPCC), also known as Lynch syndrome, is an autosomal dominant inherited predisposition to a number of epithelial cancers, most notably colorectal and endometrial cancer. Outside of the context of Lynch syndrome there is little evidence for an autosomal dominant or recessive condition that predisposes to endometrial cancer. Recently, genetic variants in MUTYH have been associated with a recessive form of colorectal cancer, known as MUTYH associated polyposis or MAP. MUTYH is involved in base excision repair of DNA lesions and as such a breakdown in the fidelity of this process would necessarily not be predicted to result in a specific disease. At present there is little information about the role of MUTYH in other types of cancer and only one report indicating a possible relationship with endometrial cancer

Role of PCNA-dependent stimulation of 3′-phosphodiesterase and 3′–5′ exonuclease activities of human Ape2 in repair of oxidative DNA damage

Human Ape2 protein has 3′ phosphodiesterase activity for processing 3′-damaged DNA termini, 3′–5′ exonuclease activity that supports removal of mismatched nucleotides from the 3′-end of DNA, and a somewhat weak AP-endonuclease activity. However, very little is known about the role of Ape2 in DNA repair processes. Here, we examine the effect of interaction of Ape2 with proliferating cell nuclear antigen (PCNA) on its enzymatic activities and on targeting Ape2 to oxidative DNA lesions. We show that PCNA strongly stimulates the 3′–5′ exonuclease and 3′ phosphodiesterase activities of Ape2, but has no effect on its AP-endonuclease activity. Moreover, we find that upon hydrogen-peroxide treatment Ape2 redistributes to nuclear foci where it colocalizes with PCNA. In concert with these results, we provide biochemical evidence that Ape2 can reduce the mutagenic consequences of attack by reactive oxygen species not only by repairing 3′-damaged termini but also by removing 3′-end adenine opposite from 8-oxoG. Based on these findings we suggest the involvement of Ape2 in repair of oxidative DNA damage and PCNA-dependent repair synthesis