RESUMO
BACKGROUND: Intrauterine growth restriction (IUGR) is associated with abnormal neurodevelopment, but the associated structural brain changes are poorly documented. The aim of this study was to describe in an animal model the brain changes at the cellular level in the gray and white matter induced by IUGR during the neonatal period. METHODS: The IUGR model was surgically induced in pregnant rabbits by ligating 40-50% of the uteroplacental vessels in 1 horn, whereas the uteroplacental vessels of the contralateral horn were not ligated. After 5 days, IUGR animals from the ligated horn and controls from the nonligated were delivered. On the day of delivery, perinatal data and placentas were collected. On postnatal day 1, functional changes were first evaluated, and thereafter, neuronal arborization in the frontal cortex and density of pre-oligodendrocytes, astrocytes, and microglia in the corpus callosum were evaluated. RESULTS: Higher stillbirth in IUGR fetuses together with a reduced birth weight as compared to controls was evidenced. IUGR animals showed poorer functional results, an altered neuronal arborization pattern, and a decrease in the pre-oligodendrocytes, with no differences in microglia and astrocyte densities. CONCLUSIONS: Overall, in the rabbit model used, IUGR is related to functional and brain changes evidenced already at birth, including changes in the neuronal arborization and abnormal oligodendrocyte maturation.
Assuntos
Encéfalo/patologia , Retardo do Crescimento Fetal/patologia , Animais , Animais Recém-Nascidos , Modelos Animais de Doenças , Feminino , Gravidez , CoelhosRESUMO
INTRODUCTION AND OBJECTIVES: The transcription factor TBX1 plays an important role in the embryonic development of the heart. Nothing is known about its involvement in myocardial remodeling after acute myocardial infarction (AMI) and whether its expression can be modulated by a treatment with proven benefit such as mineralocorticoid receptor blockade. METHODS: Acute myocardial infarction was induced in 60 rats via left coronary artery ligation: 50 animals were randomized to be euthanized after 1, 2, 4, 12, or 24 weeks; 10 animals were treated with eplerenone (100 mg/kg/days) 7 days before the AMI until their euthanasia (4 weeks later); 8 additional animals underwent surgery without ligation (control). We analyzed the cardiac expression of TBX1, fetal genes, and fibrosis markers. RESULTS: The gene and protein expression of TBX1 was increased in the infarcted myocardium, peaking 1 week after AMI (P < .01), without changes in the noninfarcted myocardium. Levels of the fetal genes and fibrosis markers also increased, peaking 4 weeks (P < .001) and 1 week (P < .01) after AMI, respectively. The TBX1 expression was correlated with that of the fibrosis markers (P < .01) but not the fetal genes. Eplerenone reduced the TBX1 increase and fibrosis induced by AMI, with an association improvement in ventricular function and remodeling in echocardiography. CONCLUSIONS: These results show the reactivated expression of TBX1 and indicate its involvement in cardiac fibrosis and remodeling after AMI and its participation in the benefit from mineralocorticoid receptor blockade.
Assuntos
Infarto do Miocárdio/genética , Miocárdio/patologia , RNA Mensageiro/metabolismo , Proteínas com Domínio T/genética , Remodelação Ventricular/genética , Actinina/genética , Actinina/metabolismo , Animais , Fator Natriurético Atrial/genética , Fator Natriurético Atrial/metabolismo , Western Blotting , Eplerenona , Fibrose , Regulação da Expressão Gênica no Desenvolvimento , Coração/efeitos dos fármacos , Antagonistas de Receptores de Mineralocorticoides/farmacologia , Miocárdio/metabolismo , Cadeias Pesadas de Miosina/genética , Cadeias Pesadas de Miosina/metabolismo , Peptídeo Natriurético Encefálico/genética , Peptídeo Natriurético Encefálico/metabolismo , RNA Mensageiro/efeitos dos fármacos , Ratos , Reação em Cadeia da Polimerase em Tempo Real , Espironolactona/análogos & derivados , Espironolactona/farmacologia , Proteínas com Domínio T/efeitos dos fármacos , Proteínas com Domínio T/metabolismo , Remodelação Ventricular/efeitos dos fármacosAssuntos
Insuficiência Cardíaca/sangue , Relaxina/sangue , Doença Aguda , Idoso , Idoso de 80 Anos ou mais , Progressão da Doença , Ecocardiografia , Serviço Hospitalar de Emergência , Ensaio de Imunoadsorção Enzimática , Feminino , Insuficiência Cardíaca/diagnóstico por imagem , Insuficiência Cardíaca/fisiopatologia , Humanos , Cinética , Masculino , Pessoa de Meia-Idade , Peptídeo Natriurético Encefálico/sangue , Fragmentos de Peptídeos/sangue , Volume SistólicoRESUMO
A pressure-induced linkage isomerization of the cyanide anion has been observed in single crystals of a chromium(III)-iron(II) Prussian blue analogue of formula K0.4Fe4[Cr(CN)6]2.8 square1.2.16H2O (1). Upon application of pressure in the 0-1200 MPa range, the cyanide ligand rotates and becomes C-bonded to the iron(II) cations, leading to a stabilization of their diamagnetic low-spin states. The result is a decrease of magnetization and magnetic ordering temperatures from TC = 19 K at ambient pressure to 13 K at 1200 MPa. The initial magnetic properties can be restored on pressure release. The reversible movement of cyanide in the solid state can be exploited as a switch of the magnetic interaction at the molecular level.