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1.
Sheng Wu Yi Xue Gong Cheng Xue Za Zhi ; 28(3): 592-6, 2011 Jun.
Artigo em Chinês | MEDLINE | ID: mdl-21774230

RESUMO

Neonatal jaundice is a common neonatal disease. Severe jaundices lead to kernicterus that affects intellectual development of infants or even causes death. Timely and early prediction is vital to the treatment and prevention. This paper presents a jaundice predictor, which uses C8051F020 as the core of single-chip microcomputer (SCM) system with prediction algorithms proven by a large number of clinical trials. The jaundice predictor can reduce the incidence rate of jaundice, alleviate the condition of infants with jaundice, improve the quality of perinatal, with predicting pathologic neonatal jaundice effectively and calling attention to the prophylactic treatment. In addition, compared with the existing transcutaneous jaundice meters, the new predictor has a smaller size, a lighter weight, more user-friendly, and easier to use by hand-holding.


Assuntos
Bilirrubina/sangue , Desenho de Equipamento/métodos , Icterícia Neonatal/diagnóstico , Microcomputadores , Fotometria/métodos , Algoritmos , Humanos , Recém-Nascido , Icterícia Neonatal/sangue
2.
J Biotechnol ; 233: 17-25, 2016 Sep 10.
Artigo em Inglês | MEDLINE | ID: mdl-27373958

RESUMO

Clostridium kluyveri is unique in fermenting ethanol and acetate to butyrate, caproate, and H2. The genes encoding butyrate-producing enzymes, including electron-bifurcating butyryl-CoA dehydrogenase/electron transfer flavoprotein complex and NADH-dependent reduced ferredoxin:NADP(+) oxidoreductase, form a cluster, which is preceded by a gene annotated as the transcriptional regulator Rex. Northern blotting and RT-PCR experiments indicated that the gene cluster forms a large transcriptional unit that possibly includes several small transcriptional units. The deduced Rex protein contains a winged helix DNA-binding domain and a Rossmann fold potentially interacting with NAD(H). Bioinformatics analysis revealed that Rex can bind the promoter regions of numerous genes, which are involved in carbon and energy metabolism, including NADH oxidation, hydrogen production, ATP synthesis, butyrate formation, and succinate metabolism. Rex may regulate the transcription of genes encoding certain transcriptional regulators and transporters. Electrophoretic mobility shift and isothermal titration calorimetry assays revealed that Rex specifically formed protein-DNA complexes with the promoter regions of target genes, which could be inhibited by NADH but restored by an excess amount of NAD(+). These results suggest that Rex plays a key role in the carbon and energy metabolism of C. kluyveri as a global transcriptional regulator in response to the cellular NADH/NAD(+) ratio.


Assuntos
Clostridium kluyveri/genética , Clostridium kluyveri/metabolismo , Regulação Bacteriana da Expressão Gênica/genética , Genes Bacterianos/genética , Proteínas de Bactérias/genética , Proteínas de Bactérias/metabolismo , Butiratos/metabolismo , Oxirredução
3.
Neurosci Lett ; 367(3): 355-9, 2004 Sep 09.
Artigo em Inglês | MEDLINE | ID: mdl-15337265

RESUMO

Previous studies have demonstrated that c-Jun NH2-terminal protein kinase (JNK) plays a crucial role in neuronal apoptosis. Here, we report that indirubin-3'-oxime, a known effective inhibitor of cyclin-dependent kinases (CDKs) and glycogen synthase kinase 3-beta (GSK-3beta), has a significant inhibitory effect on JNK. Kinase assay showed that indirubin-3'-oxime directly inhibited the activity of all three isoforms of JNK (JNK1, and JNK3) in vitro, with half inhibition dose (IC50) of 0.8 microM, 1.4 microM, and 1.0 microM, respectively. In cerebellar granule neurons (CGNs), indirubin-3'-oxime blocked c-Jun phosphorylation induced by potassium withdrawal and prevented CGNs from apoptosis in a dose dependent manner. However, inhibitors of CDKs and GSK-3beta were ineffective in reducing c-Jun phosphorylation both in vitro and in vivo, suggesting that indirubin-3'-oxime prevents c-Jun phosphorylation independent of its inhibition on CDKs and GSK-3beta. Our studies give further supports for JNK-targeting strategy in preventing neuronal apoptosis.


Assuntos
Apoptose , Cerebelo/citologia , Indóis/farmacologia , Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo , Neurônios/efeitos dos fármacos , Oximas/farmacologia , Animais , Animais Recém-Nascidos , Antracenos/farmacologia , Western Blotting/métodos , Células Cultivadas , Relação Dose-Resposta a Droga , Interações Medicamentosas , Inibidores Enzimáticos/farmacologia , Proteínas Quinases JNK Ativadas por Mitógeno/antagonistas & inibidores , Neurônios/enzimologia , Fosforilação/efeitos dos fármacos , Potássio/toxicidade , Ratos
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