Selecting an appropriate therapy for osteonecrosis of the jaws management based on current literature is a rational decision that can help lead to a proper treatment plan.
Altitude hypoxia induces an increase in erythropoiesis. Some of the factors involved in the control of altitude polycythemia were studied. Ten subjects (4 women, 6 men) were exposed for 3 wk to extreme altitude (6,542 m). Blood was withdrawn in normoxia (N) and after 1 wk (H1), 2 wk (H2), or 3 wk (H3) at 6,542 m for the measurement of serum erythropoietin (EPO), blood hemoglobin (Hb), hematocrit (Hct), intraerythrocyte folate (Fol), and plasma ferritin (Fer) concentrations. Renal blood flow (RBF) and absolute proximal reabsorption rate (APR) were measured by the p-aminohippuric acid and lithium clearance, respectively, in N and H2 conditions. O2 supply to the kidneys was calculated using RBF and arterial O2 content (CaO2). After an initial sharp increase in EPO, it decreased at H2 and H3. Hct and Hb increased from N to H1 and H2 and then unexpectedly decreased from H2 to H3. Mean corpuscular Hb content (MCHC = Hb/Hct) was lower in all H than in N conditions. Increase in EPO at H1 varied from 3- to 134-fold among individuals. Women showed a smaller increase in Hct and Hb and a greater decrease in MCHC. Two women showed a large increase in EPO without increase in Hb. Fol was not modified by altitude hypoxia. Fer showed a marked decrease in H1 and H3 compared with N. Hb was positively related to Fer in hypoxia. Iron intake in food was markedly decreased during the 2-wk ascent to 6,542 m. EPO was inversely related to CaO2 and positively related to APR.(ABSTRACT TRUNCATED AT 250 WORDS)
Epigenetic alterations such as DNA methylation have been implicated in the development and progression of various cancers. DNA methylation consists of the reversible addition of a methyl group to the carbon 5 position of cytosine in CpG dinucleotides and is considered essential for normal embryonic development. However, global genomic hypomethylation and aberrant hypermethylation of regulatory regions of tumor suppressor genes have been associated with chromosomal instability and transcription repression, respectively, providing neoplastic cells with a selective advantage. DNA methyltransferases are the enzymes responsible for the addition of methyl groups to CpG dinucleotides, which, together with histone modifiers, initiate the events necessary for transcription repression to occur. It has been demonstrated that increased expression of DNA methyltransferases may contribute to tumor progression through methylation-mediated gene inactivation in various human cancers. Given their importance, this article reviews the main epigenetic mechanisms for regulating transcription and its implications in cancer development. Cancer 2011;117:677-87. V C 2010 American Cancer Society.KEYWORDS: epigenesis, DNA methylation, methyltransferases, histone code.Heritable and reversible mechanisms known as epigenetic alterations do not require direct alterations of DNA sequences, but they can be responsible for modifying gene expression and are related to cancer development.1-6 Although the genetic information provides the sequence for protein synthesis, the epigenetic information provides instructions on how, where, and when the genetic information will be used. 7Several epigenetic mechanisms regulate gene expression: DNA methylation, modifications of histone proteins, and functional noncoding RNA. 1 The major form present in mammalian cells is DNA methylation, which is the covalent addition of a methyl group to the carbon-5 position of cytosine predominantly in the CpG dinucleotide. 7,8 This cytosine modification pattern can be transmitted through cell division and may contribute to gene inactivation in cancer. 3,4 DNA methylation is essential for normal embryonic development and has a variety of important functions, such as the regulation of gene expression, control of cell differentiation and development, chromatin modification, mutation accumulation, silencing of endogenous retroviruses, preservation of chromosomal integrity, genomic imprinting control, and X chromosome inactivation.7,9-13 Initially discovered as a mechanism for the control of development, it plays an important role in many tumor types.14 Genomic methylation patterns are frequently altered in tumor cells, with global hypomethylation accompanying region-specific hypermethylation sites. When hypermethylation occurs within the promoter of a tumor suppressor gene, it can silence expression of the associated gene and provide the cell with a growth advantage in a manner akin to deletions or mutations. 7,10,15 This review summarizes the main epigenetic mechanisms involv...
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