In diabetes, glycation, tissue oxidation and endothelial function are all abnormal and predisposing to microvascular complications but interrelationships are complex with glycation appearing most direct.
Increased levels of NTBI become detectable 17-22 days after donation and increase further with storage time. This excess NTBI may promote bacterial infection in iron-loaded individuals.
Decreased serum vitamin E levels are found in homozygous sickle cell disease (SCD). Excessive transfusions may lead high non‐transferrin‐bound iron (NTBI). Hypothesizing a relationship between the two, vitamin E (measured using high performance liquid chromatography) was significantly lower in 30 SCD patients than in 30 age‐/sex‐matched controls (P < 0·001), but NTBI (bleomycin assay) was higher (P < 0·001). Vitamin E was lower in 10 transfused patients than in 20 non‐transfused patients (P < 0·001) with a significant inverse correlation between the NTBI and vitamin E (r = −0·58, P < 0·001). NTBI associated with iron overload in SCD may increase the potential for oxidative damage and low vitamin E activity may compound this effect.
There is an accumulation of evidence that shows a significant role of cancer stem cells in tumor initiation, proliferation, relapse, and metastasis. Nanog is the most important core transcription marker of stem cells, known by its role in maintaining pluripotency, proliferation, and differentiation. Therefore, this study aimed to examine the role of Nanog in breast cancer cell tamoxifen resistance and its implications in breast cancer treatment. In this study, the expression of the three core transcription markers Nanog, Oct3/4, and Sox2 were quantitatively evaluated using flow cytometry. Then, small interfering RNA (siRNA) against human Nanog was transfected into tamoxifen-resistant breast cancer cells via Lipofectamine 2000. Nanog gene expression in the cells was detected using reverse transcription polymerase chain reaction (RT-PCR). The change in cell proliferation was evaluated using the tetrazolium bromide method. An enzyme-linked immunosorbent assay was used to detect apoptosis of the transfected cells alone and in combination with 4-hydroxytamoxifen. The results showed a high level expression of Nanog, Oct3/4, and Sox2 in MDA-MB-231 and MCF7/tamoxifen resistant cells compared with MCF7/wild-type. siRNA-mediated Nanog gene silencing can efficiently inhibit cell proliferation and induce apoptosis of tamoxifen-resistant breast cancer cells. This study provides a basis for further study of the role of Nanog in developing resistance to tamoxifen, its implication in breast cancer management, and as a new strategy to enhance response to endocrine therapy.
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