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1.
J Diabetes Sci Technol ; 4(1): 145-50, 2010 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-20167178

RESUMO

BACKGROUND: Studies have shown that controlling blood glucose can reduce the onset and progression of the long-term microvascular and neuropathic complications associated with the chronic course of diabetes mellitus. Improved glycemic control can be achieved by frequent testing combined with changes in medication, exercise, and diet. Technological advancements have enabled improvements in analytical accuracy of meters, and this paper explores two such parameters to which that accuracy can be attributed. METHODS: Four blood glucose monitoring systems (with or without dynamic electrochemistry algorithms, codeless or requiring coding prior to testing) were evaluated and compared with respect to their accuracy. RESULTS: Altogether, 108 blood glucose values were obtained for each system from 54 study participants and compared with the reference values. The analysis depicted in the International Organization for Standardization table format indicates that the devices with dynamic electrochemistry and the codeless feature had the highest proportion of acceptable results overall (System A, 101/103). Results were significant when compared at the 10% bias level with meters that were codeless and utilized static electrochemistry (p = .017) or systems that had static electrochemistry but needed coding (p = .008). CONCLUSIONS: Analytical performance of these blood glucose meters differed significantly depending on their technologic features. Meters that utilized dynamic electrochemistry and did not require coding were more accurate than meters that used static electrochemistry or required coding.


Assuntos
Automonitorização da Glicemia/instrumentação , Automonitorização da Glicemia/normas , Técnicas Biossensoriais/instrumentação , Técnicas Biossensoriais/normas , Glicemia/análise , Calibragem , Diabetes Mellitus/sangue , Diabetes Mellitus/tratamento farmacológico , Eletroquímica/instrumentação , Eletroquímica/métodos , Processamento Eletrônico de Dados , Feminino , Humanos , Hipoglicemiantes/administração & dosagem , Insulina/administração & dosagem , Cinética , Masculino , Monitorização Ambulatorial/instrumentação , Monitorização Ambulatorial/normas , Valores de Referência , Reprodutibilidade dos Testes
2.
Hum Mol Genet ; 15(21): 3132-45, 2006 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-16984965

RESUMO

The variability in phenotypic presentations and the lack of consistency of genetic associations in mental illnesses remain a major challenge in molecular psychiatry. Recently, it has become increasingly clear that altered promoter DNA methylation could play a critical role in mediating differential regulation of genes and in facilitating short-term adaptation in response to the environment. Here, we report the investigation of the differential activity of membrane-bound catechol-O-methyltransferase (MB-COMT) due to altered promoter methylation and the nature of the contribution of COMT Val158Met polymorphism as risk factors for schizophrenia and bipolar disorder by analyzing 115 post-mortem brain samples from the frontal lobe. These studies are the first to reveal that the MB-COMT promoter DNA is frequently hypomethylated in schizophrenia and bipolar disorder patients, compared with the controls (methylation rate: 26 and 29 versus 60%; P=0.004 and 0.008, respectively), particularly in the left frontal lobes (methylation rate: 29 and 30 versus 81%; P=0.003 and 0.002, respectively). Quantitative gene-expression analyses showed a corresponding increase in transcript levels of MB-COMT in schizophrenia and bipolar disorder patients compared with the controls (P=0.02) with an accompanying inverse correlation between MB-COMT and DRD1 expression. Furthermore, there was a tendency for the enrichment of the Val allele of the COMT Val158Met polymorphism with MB-COMT hypomethylation in the patients. These findings suggest that MB-COMT over-expression due to promoter hypomethylation and/or hyperactive allele of COMT may increase dopamine degradation in the frontal lobe providing a molecular basis for the shared symptoms of schizophrenia and bipolar disorder.


Assuntos
Transtorno Bipolar/genética , Catecol O-Metiltransferase/genética , Metilação de DNA , Lobo Frontal/metabolismo , Regiões Promotoras Genéticas , Esquizofrenia/genética , Alcoolismo/genética , Substituição de Aminoácidos , Antipsicóticos/uso terapêutico , Transtorno Bipolar/tratamento farmacológico , Transtorno Bipolar/metabolismo , Estudos de Casos e Controles , Ilhas de CpG/genética , Epigênese Genética , Predisposição Genética para Doença , Cardiopatias/genética , Humanos , Polimorfismo Genético , Receptores de Dopamina D1/genética , Fatores de Risco , Esquizofrenia/tratamento farmacológico , Esquizofrenia/metabolismo
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