Acting out as criminal impulse. History, Definitions, Forensic aspects / Sobre el pasaje al acto criminal. Historia, definiciones, aspectos forenses.

The present article aims to conduct a comprehensive review of the existing scientific literature on this human behavioral modality, impulsive and transient, which escapes the conscious control of the subject, from a psychopathological and forensic approach. To achieve this, historical points about the different nuances of the topic will be made, supplying a panoramic and critical overview of it. It can be said that these are implicit memories about past traumatic situations that, because of a present reenactment of the unpleasant event through a dissociative mechanism, generate in the individual an impulsive aggressive reaction, over which the person has no control or awareness. This type of behavior opens the debate, within the framework of Forensic Psychology and Psychiatry, about the defendants' ability, under these circumstances, to understand the criminality of the act and direct their actions, posing a controversial challenge to the criteria of different courts. Similarly, it is necessary to understand these behaviors, develop more proper prevention strategies, propose new therapeutic approaches to psychological trauma, and intervene in these criminal behaviors that endanger society's safety and well-being.

El presente artículo se propone llevar a cabo una revisión exhaustiva de la literatura científica existente sobre esta modalidad conductual humana particular, impulsiva y transitoria, que escapa al control consciente del sujeto, desde un enfoque psicopatológico y forense. Para ello, se realizarán puntualizaciones históricas de los diferentes matices de la temática, proporcionando una visión panorámica y crítica de la misma. Se puede decir que se trata de memorias implícitas acerca de situaciones traumáticas pasadas que, a raíz de una reedición presente del evento displacentero mediante un mecanismo disociativo, generan en el individuo una reacción impulsiva agresiva, sobre la cual la persona no dispone de control ni conciencia. Este tipo de comportamiento abre el debate, en el marco de la Psicología y Psiquiatría Forense, sobre la  capacidad que tienen los acusados de un crimen, de comprender la criminalidad del acto y dirigir sus acciones, presentando un desafío controversial para los tribunales de diferentes países. Así mismo, es menester poder entender estas conductas, desarrollar estrategias de prevención más adecuadas, plantear los nuevos abordajes terapéuticos frente al trauma psicológico e intervenir en estas conductas delictivas que ponen en peligro la seguridad, así como el bienestar de la sociedad.

Neuroinflammation and gliosis in the injured and contralateral retinas after unilateral optic nerve crush.

The main purpose of this study is to analyze the effects of unilateral optic nerve crush in the gene expression of pro- and anti-inflammatory mediators, and gliosis markers in injured and contralateral retinas. Retinas from intact, unilaterally optic nerve injured or sham-operated C57BL/6J mice were analyzed 1, 3, 9 and 30 days after the surgery (n = 5/group and time point) and the relative expression of TGF-ß1, IL-1ß, TNF-α, Iba1, AQP4, GFAP, MHCII, and TSPO was analyzed in injured and contralateral using qPCR. The results indicated that compared with intact retinas, sham-operated animals showed an early (day 1) upregulation of IL-1ß, TNF-α and TSPO and a late (day 30) upregulation of TNF-α. In sham-contralateral retinas, TNF-α and TSPO mRNA expression were upregulated and day 30 while GFAP, Iba1, AQP4 and MHCII downregulated at day 9. Compared with sham-operated animals, in retinas affected by optic nerve crush GFAP and TSPO upregulated at day 1 and TNF-α, Iba1, AQP4 and MHCII at day 3. In the crushed-contralateral retinas, TGF-ß1, TNF-α, Iba1 and MHCII were upregulated at day 1. TSPO was upregulated up to day 30 whereas TGF-ß1 and Iba1 downregulated after day 9. In conclusion, both sham surgery and optic nerve crush changed the profile of inflammatory and gliosis markers in the injured and contralateral retinas, changes that were more pronounced for optic nerve crush when compared to sham.

Comparative Analysis of Retinal Organotypic Cultures and In Vivo Axotomized Retinas.

Retinal organotypic cultures (ROCs) are used as an in vivo surrogate to study retinal ganglion cell (RGC) loss and neuroprotection. In vivo, the gold standard to study RGC degeneration and neuroprotection is optic nerve lesion. We propose here to compare the course of RGC death and glial activation between both models. The left optic nerve of C57BL/6 male mice was crushed, and retinas analyzed from 1 to 9 days after the injury. ROCs were analyzed at the same time points. As a control, intact retinas were used. Retinas were studied anatomically to assess RGC survival, microglial, and macroglial activation. Macroglial and microglial cells showed different morphological activation between models and were activated earlier in ROCs. Furthermore, microglial cell density in the ganglion cell layer was always lower in ROCs than in vivo. RGC loss after axotomy and in vitro followed the same trend up to 5 days. Thereafter, there was an abrupt decrease in viable RGCs in ROCs. However, RGC somas were still immuno-identified by several molecular markers. ROCs are useful for proof-of-concept studies on neuroprotection, but long-term experiments should be carried out in vivo. Importantly, the differential glial activation observed between models and the concomitant death of photoreceptors that occurs in vitro may alter the efficacy of RGC neuroprotective therapies when tested in in vivo models of optic nerve injury.

Axonal Injuries Cast Long Shadows: Long Term Glial Activation in Injured and Contralateral Retinas after Unilateral Axotomy.

BACKGROUND: To analyze the course of microglial and macroglial activation in injured and contralateral retinas after unilateral optic nerve crush (ONC). METHODS: The left optic nerve of adult pigmented C57Bl/6 female mice was intraorbitally crushed and injured, and contralateral retinas were analyzed from 1 to 45 days post-lesion (dpl) in cross-sections and flat mounts. As controls, intact retinas were studied. Iba1+ microglial cells (MCs), activated phagocytic CD68+MCs and M2 CD206+MCs were quantified. Macroglial cell changes were analyzed by GFAP and vimentin signal intensity. RESULTS: After ONC, MC density increased significantly from 5 to 21 dpl in the inner layers of injured retinas, remaining within intact values in the contralateral ones. However, in both retinas there was a significant and long-lasting increase of CD68+MCs. Constitutive CD206+MCs were rare and mostly found in the ciliary body and around the optic-nerve head. While in the injured retinas their number increased in the retina and ciliary body, in the contralateral retinas decreased. Astrocytes and Müller cells transiently hypertrophied in the injured retinas and to a lesser extent in the contralateral ones. CONCLUSIONS: Unilateral ONC triggers a bilateral and persistent activation of MCs and an opposed response of M2 MCs between both retinas. Macroglial hypertrophy is transient.

Ly6c as a New Marker of Mouse Blood Vessels: Qualitative and Quantitative Analyses on Intact and Ischemic Retinas.

Ly6c is an antigen commonly used to differentiate between classical and non-classical monocytes/macrophages. Here we show its potential as a marker of the mouse vasculature, particularly of the retinal vascular plexuses. Ly6c was immunodetected in several tissues of C57BL/6 mice using isolectin IB4 as the control of vasculature staining. In the retina, Ly6c expression was analyzed qualitatively and quantitatively in intact, ischemic, and contralateral retinas from 0 to 30 days after the insult. Ly6c expression was observed in all organs and tissues tested, with a brighter signal and more homogeneous staining than the IB4. In the retinas, Ly6c was well expressed, allowing a detailed study of their anatomy. The three retinal plexuses were morphologically different, and from the superficial to the deep one occupied 15 ± 2, 24 ± 7, and 38 ± 1.4 percent of the retinal surface, respectively. In the injured retinas, there was extravasation of the classically activated monocyte/macrophages (Ly6chigh) and the formation of new vessels in the superficial plexus, increasing the area occupied by it to 25 ± 1%. In the contralateral retinas, the superficial plexus area decreased gradually, reaching significance at 30 days, and Ly6c expression progressively disappeared in the intermediate and deep plexuses. Although the role of Ly6c in vascular endothelial cell function is still not completely understood, we demonstrate here that Ly6c can be used as a new specific marker of the mouse vasculature and to assess, qualitatively and quantitatively, vascular changes in health and disease.

Disfunción tiroidea y trastornos del ánimo: revisión del estado del arte / Thyroid dysfunction and mood disorders: review of the state of the art

La relación entre función tiroidea y trastornos del ánimo se ha observado desde hace más de 50 años. Las hormonas tiroideas, actúan en el cerebro modulando génicamente proteínas asociadas a la fisiopatología de los trastornos del ánimo y potenciando los sistemas de neurotransmisión serotoninérgica y noradrenérgica. En el tratamiento de un episodio depresivo, la normalización de hormonas tiroideas es fundamental, y debe realizarse en todo paciente con sintomatología anímica, especialmente en aquellos con respuestas insuficientes a tratamiento, que requieren niveles de hormonas más estrictos que lo recomendado para población general. En pacientes eutiroideos, la potenciación con triyodotironina ha sido probada, pero también se ha utilizado T4 en altas dosis en casos resistentes, en que se postula que pudiese existir un estado de resistencia a hormonas tiroideas, no reflejado en los niveles hormonales periféricos evaluados rutinariamente. Las enzimas deiodasas, el receptor de hormona tiroidea, y el transportador de hormona tiroidea en la barrera hematoencefálica son blancos a investigar. Los objetivos de la presente revisión son ofrecer orientaciones respecto del uso de hormonas tiroideas en pacientes con trastornos del ánimo, una puesta al día sobre la relación entre hormonas tiroídeas y sistema nervioso central, y las interacciones entre psicofármacos y función tiroidea.

The relationship between thyroid function and mood disorders has been observed for more than 50 years. Thyroid hormones act in the brain genetically modulating proteins associated with the pathophysiology of mood disorders and potentiating the serotonergic and noradrenergic neurotransmission systems. In the treatment of a depressive episode, the normalization of thyroid hormones is essential, and should be performed in all patients with mood symptoms, especially in those with insufficient responses to treatment, which require more stringent hormone levels than recommended for the general population. In euthyroid patients, potentiation with triiodothyronine has been proven, but T4 has also been used in high doses in resistant cases, in which it is postulated that there might be a state of resistance to thyroid hormones, not reflected in the peripheral hormonal levels evaluated routinely. The enzymes deiodasas, the thyroid hormone receptor, and the thyroid hormone transporter in the blood brain barrier are white to investigate. The objectives of this review are to provide guidance regarding the use of thyroid hormones in patients with mood disorders, an update on the relationship between thyroid hormones and central nervous system, and the interactions between psychoactive drugs and thyroid function.

Water and Physiological Saline to Prevent the Formation of P-Chloroaniline / Agua y Suero Fisiológico para Prevenir la Formación de Paracloroanilina

This study determined if p-chloroaniline (PCA) can be minimized by using distilled water and physiological saline solution following sodium hypochlorite but before chlorhexidine. Hypochlorite 5%, 0.5%, 0.05%, 0.005% and 0.0005% dissolved in 0.9% NaCl and in distilled water were mixed with 2% chlorhexidine for the formation of PCA. The PCA was determined using UV-VISIBLE spectrometry, with spectral curve was determined the wavelength of maximum absorption of PCA. Formed PCA absorbance was measured between 0.025%, 0.02%, 0.015%, 0.01%, 0.005% and 0.0025% hypochlorite and 2% chlorhexidine. 2% chlorhexidine and hypochlorite with physiological saline form a white precipitate which prevents the measurement of PCA. Colored PCA is formed with 0.05%, 0.005% hypochlorite aqueous dilutions and 2% chlorhexidine. The lwavelength of maximum absorption obtained was 470 nm and absorbance of PCA showed a linear decrease. 0.005% NaClO produces the least amount of PCA. The best solvent to prevent the formation of PCA during the interaction of sodium hypochlorite with chlorhexidine is distilled water.

Este estudio determinó si la p-cloroanilina (PCA) puede ser minimizada mediante el uso de agua destilada y solución salina fisiológica seguido de la aplicación de hipoclorito de sodio, previo a la aplicación de clorhexidina. Hipoclorito al 5%, 0,5%, 0,05%, 0,005% y 0,0005% fue disuelto en 0,9% de NaCl y en agua destilada se mezcló con 2% de clorhexidina para la formación de PCA. El PCA se determinó mediante espectrometría UV-Visible, y con curva espectral se determinó la longitud de onda máxima del PCA. La absorbancia del PCA formado se midió con 0,025%, 0,02%, 0,015%, 0,01%, 0,005% y 0,0025% de hipoclorito y 2% de clorhexidina. La combinación de 2% de clorhexidina e hipoclorito en solución salina fisiológica forman un precipitado blanco que impide la medición del PCA. El PCA coloreado es formado con 0,05%, 0,005% diluciones acuosas de hipoclorito y 2% de clorhexidina. La longitud de onda máxima obtenida fue de 470 nm y la absorbancia del PCA mostró una disminución lineal. NaClO al 0,005% produce menor cantidad de PCA. El mejor disolvente para evitar la formación de PCA durante la interacción de hipoclorito de sodio con clorhexidina es agua destilada.