Effect of Sn on the oxide subscale structure formed on a 3% Si steel

Addition of tin in 3% Si steel is a method to improve magnetic properties since tin in steel is known as an element that segregates at grain boundaries, inhibits grain growth and has a dragging effect on grain boundary movement. However, tin is generally known as an element that has a harmful effect on surface coating properties. The oxide subscale formed on the decarburization annealing of a 3% Si steel containing tin was investigated by SEM, EDS, GDS and FTIR. The forsterite film was evaluated by SEM, EDS and GDS. The higher tin content decreased thickness, oxygen and fayalite/silica ratio in the subscale and resulted into a discontinuous forsterite film with poor oxidation resistance. After secondary coating the samples presented a reddish color due to the formation of iron oxide and poor dielectric property

Storage in the yolk platelets of low MW DNA produced by the regressing follicle cells.

The present work was carried out to clarify the nature and origin of the yolk DNA present in vitellogenic oocytes of the lizard Podarcis sicula. Morphological and biochemical evidences indicate that it has an intrafollicular origin, from the apoptotic bodies resulting from follicle cells regression at the end of previtellogenesis. This conclusion is reinforced by the observation that the oocyte membrane, in in vitro experiments, is unpermeable to exogenous DNA. Biochemical evidences reveal that the yolk DNA has a low (200bp) molecular weight and this suggests that it is produced by the endonucleases typically involved in apoptotic DNA laddering. Indeed, immunocytochemical analyses demonstrate that follicle cells contain significant amounts of DNAse I. In immunoblots, carried out during different periods of the ovarian cycle, the enzyme shows a MW of about 33, 66 or 100 kDa thus indicating that its activity in the follicle of Podarcis is modulated by dimerization and/or binding to regulatory factors

Storage in the yolk platelets of low MW DNA produced by the regressing follicle cells.

The present work was carried out to clarify the nature and origin of the yolk DNA present in vitellogenic oocytes of the lizard Podarcis sicula. Morphological and biochemical evidences indicate that it has an intrafollicular origin, from the apoptotic bodies resulting from follicle cells regression at the end of previtellogenesis. This conclusion is reinforced by the observation that the oocyte membrane, in in vitro experiments, is unpermeable to exogenous DNA. Biochemical evidences reveal that the yolk DNA has a low (200bp) molecular weight and this suggests that it is produced by the endonucleases typically involved in apoptotic DNA laddering. Indeed, immunocytochemical analyses demonstrate that follicle cells contain significant amounts of DNAse I. In immunoblots, carried out during different periods of the ovarian cycle, the enzyme shows a MW of about 33, 66 or 100 kDa thus indicating that its activity in the follicle of Podarcis is modulated by dimerization and/or binding to regulatory factors

Farnesyl transferase inhibitors induce neuroprotection by inhibiting Ha-Ras signalling pathway.

In previous studies we found that the GTPase p21 Harvey-Ras (Ha-Ras) stimulates the production of reactive oxygen species and induces apoptosis by oxidative stress; this effect was reversed by farnesyl transferase inhibitors (FTIs). In this study we investigated whether FTIs reduce rat brain damage induced by an excitotoxic stimulus, and the signalling pathway(s) underlying the neuroprotection by FTIs. In brain tissue, protein levels of Ha-Ras and farnesylation inhibition were assayed by Western blot, and superoxide production was measured by hydroethidine. The excitotoxic lesion was induced by intrastriatal injection of N-methyl-d-aspartate (NMDA). The survival of mouse neuronal cortical cells was assessed by 3-(4,5 dimethylthialzol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). In brain tissue, NMDA increased the protein levels of Ha-Ras, FTIs caused the accumulation of non-prenylated inactive Ras in the cytosolic fraction, and significantly reduced superoxide production and necrotic volume after excitotoxicity. FTIs increased the viability of mouse neuronal cortical cells following oxidative stress. In conclusion, FTIs inhibited Ha-Ras, decreased oxidative stress and reduced necrotic volume by partly acting on neuronal cells. Thus, Ha-Ras inhibition plays a role in the pathology of neuroprotection, suggesting a potential role of FTIs in the treatment of cerebrovascular diseases

Changes in Systolic and Diastolic Function in a Mouse Model Overexpressing Cardiac Angiotensin II AT-1 Receptor

Angiotensin II (Ang II) is involved in various pathophysiological processes throughthe activation of angiotensin II AT-1 receptors. The purpose of this study was toassess in vivo and in vitro systolic and diastolic ventricular function in mice overexpressingthe cardiac-specific Ang II AT-1 receptor (AT1R). A second objective was todetermine whether ventricular function changes could be reversed with acute andchronic ATIR blockade.Mice were divided into four experimental groups. The first group included nontransgenicanimals (NTG, n=10), the second group consisted of transgenic mice (TG,n=7) with cardiac-specific AT1R overexpression and the third and fourth groupswere TG animals treated with losartan (L) for 7 (TG L7, n=9) and 30 days (TG L30,n=7), respectively. Transgenic animals exhibited left ventricular hypertrophy (LVH)which was only regressed with losartan treatment for 30 days. They also presented asignificant decrease in shortening fraction from 47.1±2.3% to 32.3±1.3% (p <0.05)and of +dP/dtmax from 7073 ± 674 to 3897.5 ± 209.7 mmHg/sec (p< 0.05). Systolicdysfunction recovered both with losartan treatment for 7 and 30 days.Isovolumic relaxation time and t1/2 were 24.1±1.3 and 5.1±0.5ms, respectively, inthe NTG group. These indexes increased to 33.1±2.2 and 8.4±0.4 ms, respectively,in TG mice (p<0.05). Diastolic dysfunction was completely reversed by losartantreatment for 7 and 30 days. In vitro ventricular function with controlled variablesconfirmed in vivo findings.In conclusion, cardiac-specific AT1R overexpression induces systolic and diastolicventricular dysfunction which is completely reversed by AT1R blockade. This beneficialeffect is independent of left ventricular mass changes.La angiotensina II (Ang II) está involucrada en diferentes procesos fisiopatológicos, particularmente actuando sobre los receptores AT-1 de Ang II (AT1R). El objetivo de este trabajo fue evaluar la función ventricular sistólica y diastólica in vivo e in vitro en ratones con sobreexpresión cardíaca específica del receptor AT-1 de Ang II (AT1R). Un segundo objetivo fue determinar si el bloqueo agudo y crónico del AT1R revierte los cambios en la función ventricular.Se estudiaron ratones divididos en cuatro grupos experimentales. El primer grupo incluyó animales no transgénicos (NTG, n = 10), el segundo grupo ratones transgénicos (TG, n = 7) que sobreexpresan el AT1R solo a nivel cardíaco y el tercero y el cuarto grupos, animales TG tratados con losartán (L) durante 7 días (TG L7, n = 9) y 30 días (TG L30, n = 7), respectivamente. Los ratones TG presentaron hipertrofia ventricular izquierda (HVI). El tratamiento con losartán por 7 días no revirtió la HVI, lo que sí sucede cuando se extiende por 30 días. Los animales TG presentan una disminución significativa de la fracción de acortamiento, desde un valor de 47,1% ± 2,3% hasta 32,3% ± 1,3% (p < 0,05), y de la +dP/dtmáx, que se reduce desde un valor de 7.073 ± 674 mm Hg hasta 3.897,5 ± 209,7 mm Hg/seg (p < 0,05). El tratamiento con losartán por 7 y 30 días revierte esta disfunción sistólica.El tiempo de relajación isovolúmica y el t1/2 fueron de 24,1 ± 1,3 mseg y de 6,1 ± 0,5 mseg, respectivamente, en los NTG. Estos índices se incrementaron a 33,1 ± 2,2 mseg y a 8,4 ± 0,4 mseg, respectivamente, en los ratones TG (p < 0,05). Esta alteración de la función diastólica fue revertida por completo con el tratamiento con losartán por 7 y 30 días. El análisis de la función ventricular in vitro con control de variables corroboró los hallazgos realizados in vivo.La sobreexpresión cardíaca de los AT1R induce una disfunción ventricular sistólica y diastólica que es revertida completamente por el bloqueo del AT1R. Este efecto beneficioso es independiente de modificaciones en la masa ventricular izquierda

Current Evidence and Theories in Understanding the Relationship between Cognition and Depression in Childhood and Adolescence: A Narrative Review

The present narrative review has covered the current evidence regarding the role of cognitive impairments during the early phase of major depressive disorder (MDD), attempting to describe the cognitive features in childhood, adolescence and in at-risk individuals. These issues were analyzed considering the trait, scar and state hypotheses of MDD by examining the cold and hot dimensions, the latter explained in relation to the current psychological theoretical models of MDD. This search was performed on several electronic databases up to August 2022. Although the present review is the first to have analyzed both cold and hot cognitive impairments considering the trait, scar and state hypotheses, we found that current evidence did not allow to exclusively confirm the validity of one specific hypothesis since several equivocal and discordant results have been proposed in childhood and adolescence samples. Further studies are needed to better characterize possible cognitive dysfunctions assessing more systematically the impairments of cold, hot and social cognition domains and their possible interaction in a developmental perspective. An increased knowledge on these topics will improve the definition of clinical endophenotypes of enhanced risk to progression to MDD and, to hypothesize preventive and therapeutic strategies to reduce negative influences on psychosocial functioning and well-being