Structural Brain Changes during the Neonatal Period in a Rabbit Model of Intrauterine Growth Restriction.

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.

Concentración de relaxina en pacientes con insuficiencia cardiaca aguda: comportamiento y determinantes clínicos / Relaxin concentrations in acute heart failure patients: kinetics and clinical determinants

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Factor de transcripción TBX1 en el remodelado cardiaco asociado al infarto de miocardio / The TBX1 transcription factor in cardiac remodeling after myocardial infarction

Introducción y objetivos: TBX1 es un factor de transcripción importante en el desarrollo embrionario del corazón. Se desconoce su implicación en el remodelado miocárdico tras infarto agudo de miocardio (IAM) y si es modulable por una terapia con beneficio demostrado como es el bloqueo del receptor mineralocorticoideo. Métodos: Se sometió a IAM a 60 ratas mediante ligadura de la coronaria izquierda: 50 animales fueron aleatorizados a ser sacrificados pasadas 1, 2, 4, 12 o 24 semanas; 10 animales se trataron con eplerenona (100 mg/kg/día) 7 días antes del IAM, hasta su sacrificio (4 semanas después); 8 animales se sometieron a cirugía sin ligadura (control). Se analizó la expresión cardiaca de TBX1, genes fetales y marcadores de fibrosis. Resultados: La expresión génica y proteica de TBX1 se incrementó en el miocardio infartado, con pico de expresión 1 semana tras el IAM (p < 0,01), sin variar en el miocardio no infartado. Los genes fetales y los marcadores de fibrosis también aumentaron, con expresión máxima 4 semanas (p < 0,001) y 1 semana (p < 0,01) tras el IAM respectivamente. La expresión de TBX1 se correlacionó con la de los marcadores de fibrosis (p < 0,01), pero no con los genes fetales. La eplerenona redujo el incremento de TBX1 y la fibrosis inducida tras IAM, que se asociaron con una mejora de función y remodelado ventricular por ecocardiografía. Conclusiones: Estos resultados muestran la reactivación de la expresión de TBX1 e indican su implicación en la fibrosis y el remodelado cardiacos tras el IAM y que puede participar en el beneficio del bloqueo mineralocorticoideo (AU)

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 non-infarcted 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 (AU)

The TBX1 Transcription Factor in Cardiac Remodeling After Myocardial Infarction.

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.

Pressure-tuning of magnetism and linkage isomerism in iron(II) hexacyanochromate.

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.