Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026986 (myelodysplastic syndrome)
 14,926 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve aliphatic methacrylates with a carboxylic group [succinate (2 MES, 5 MPeS and 10 MDS), methylsuccinate (2 MEMS, 5 MPeMS and 10 MDMS), maleate (2 MEM, 5 MPeM and 10 MDM) and citraconate (2 MEC, 5 MPeC and 10 MDC)] were synthesized by the addition of four dicarboxylic acid anhydrides to each of three different alkylene chain length hydroxy methacrylates to investigate the relationship between the methacrylate structure and its bonding to tooth. The bond strength of methacrylates to polished tooth surface decreased with increasing alkylene chain lengths under dry conditions, but water immersion reduced this change. The bond strength of succinate and maleate to polished tooth surface was higher than that of methylsuccinate and citraconate under dry conditions. All methacrylates showed high bond strength to etched enamel, with maleate showing the highest bond strength. On the other hand, the bond strength of 2 MEM and 5 MPeM to etched dentin was markedly high, and about 5 microns thick resin reinforced dentin at the interface between etched dentin and resin (2 MEM or 5 MPeM) was observed by SEM and EPMA analysis.
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PMID:[Adhesion of dental resin to tooth structure--syntheses and adhesion to tooth structure of various aliphatic methacrylates with a carboxylic group]. 270 Feb 51

Hypermethylation of CpG islands within the promoter region is one of the mechanisms by which genes are inactivated and may be one of the reason for silencing of cell cycle control or DNA-mismatch repair genes in myelodysplastic syndrome (MDS). Since the function of cell cycle control genes including the cyclin-dependent kinase inhibitors known as p15(INK4b) and p16(INK4a), as well as p14(ARF) which blocks MDM-2 (an inhibitor of p53), the retinoblastoma (RB1) protein and the mismatch repair gene MGMT is critical for hematopoietic proliferation and differentiation, we performed methylation specific polymerase chain reaction (MSP) in low-density, non-adherent bone marrow cells from 49 patients with MDS. In addition, expression of p15(INK4b) and RB1 was analysed by quantitative real-time PCR. From selected patients, we analyzed the methylation pattern of cell cycle control genes in CD34+ bone marrow cells. Thirty-nine of 49 cases (80%) had at least one of five genes methylated in our MDS samples by analysing low-density non-adherent bone marrow cells. The frequency of p15(INK4b) methylation was 34 of 49 samples (69%). The incidence of methylation of both p14(ARF) and p16(INK4a) was four of 49 (8%). RB1 gene was methylated in seven samples (14%) and each patient had RA. Interestingly, none of these genes were methylated in the purified CD34+ hematopoietic stem cells from the MDS patients. Furthermore, all our RARS patients had a methylated p15(INK4b) promoter correlating with non-detectable expression of this gene in bone marrow cells from those patients. These results indicate that hypermethylation of cell cycle control genes in MDS may occur late during the differentiation of myelodysplastic stem cells.
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PMID:Comparative analysis of hypermethylation of cell cycle control and DNA-mismatch repair genes in low-density and CD34+ bone marrow cells from patients with myelodysplastic syndrome. 1668 76