The contribution of initial concussive forces and resulting acrolein surge to ß-amyloid accumulation and functional alterations in neuronal networks using a TBI-on-a-chip model.

Trauma-induced Alzheimer's disease (AD) is rapidly emerging as a major consequence of traumatic brain injuries (TBI), with devastating social and economic impacts. Unfortunately, few treatment options are currently available due to a limited understanding of the underlying mechanisms. A clinically-relevant, in vitro experimental model that emulates in vivo scenarios with high levels of spatial and temporal resolution is critical for demystifying the pathways of post-TBI AD. Using a unique, recently established "TBI-on-a-chip" system with murine cortical networks, we demonstrate the correlative elevation of oxidative stress (acrolein), inflammation (TNF-α), and Aß42 aggregation, with concomitant reduction of neuronal network electrical activity post-concussive impact. These findings confirm that TBI-on-a-chip could provide a novel paradigm to supplement in vivo studies of trauma, while simultaneously validating the interaction of these alleged, key-pathological factors in post-TBI AD development. Specifically, we have shown that acrolein, acting as a diffusive factor of secondary injury, is both critical and sufficient in promoting inflammation (TNF-α) and Aß42 aggregation, two known contributors of AD pathogenesis. Furthermore, using a cell-free preparation with TBI-on-a-chip, we have confirmed that both force and acrolein can independently and directly stimulate the aggregation of purified Aß42, highlighting the key capabilities of primary and secondary injury mechanisms towards inducing Aß42 aggregation, independently and synergistically. In addition to morphological and biochemical assessment, we also demonstrate parallel monitoring of neuronal network activity, further validating the chief pathological role of acrolein in not only inflicting biochemical abnormalities, but also functional deficits in neuronal networks. In conclusion, through this line of investigations, we have shown that by recapitulating clinically-relevant events, the TBI-on-a-chip device is capable of quantitatively characterizing parallel force-dependent increases in oxidative stress, inflammation, protein aggregation, and network activity, offering a unique platform for mechanistic investigations of post-TBI AD, and trauma-induced neuronal injury in general. It is expected that this model could provide crucial insights into pathological mechanisms which will be critical in developing novel, effective diagnostics and treatment strategies that significantly benefit TBI victims.

Síndrome de transfusión fetofetal / Twin-twin transfusion síndrome

Introducción: el síndrome de transfusión feto fetal es una complicación mayor presente en el 10 a 15% de los embarazos monocorialesbiamnióticos, se conoce que parte de su fisiopatología corresponde a la presencia de anastomosis placentarias entre los dos fetos que conllevan a presentar una clínica aguda y de urgente intervención en presencia de anemia, restricción de crecimiento intrauterino, oliguria y oligohidramnios en el gemelo donante, mientras que el receptor se torna pletórico, poliúrico, presentando cardiomegalia, falla cardiaca congestiva y polihidramnios. Objetivo: presentar una revisión de tema acerca del síndrome de transfusión feto fetal, características clínicas, complicaciones y su tratamiento. Metodología: se utilizaron bases de datos como Pubmed y ScienceDirect para la búsqueda de la información, encontrándose 186 artículos de los cuales 41 fueron seleccionados según los criterios de inclusión. Resultados: se encontraron 41 artículos con información actualizada, se revisó su fisiopatología, clasificación y tratamiento, destacando el papel del sistema renina angiotensina aldosterona, la presencia de anastomosis placentarias, la implicación de los niveles de vasopresina y su actual tratamiento. Conclusiones: el síndrome de trasfusión feto fetal es una de las más severas complicaciones de las gestaciones monocoriales-biamnióticas con una alta tasa de morbimortalidad fetal y perinatal. Su patología es causada por desbalance de flujos entre las anastomosis placentarias, alteraciones en el eje renina angiotensina aldosterona, cambios en los niveles de vasopresina, entre otros factores. El tratamiento actual es la terapia de ablación láser de las anastomosis placentarias, con una sobrevida del 70% y una disminución de secuelas neurológicas. Se reitera la importancia de conocer esta patología para realizar un diagnóstico asertivo y un tratamiento inmediato, invitándose a investigarla.

Introduction: twin twin transfusion syndrome is one further complication in the 10-15% of all monochorionic-biamniotic pregnancies, it is known that part of its pathophysiology corresponds to the presence of placental anastomosis between two fetuses that lead to present an acute clinic and urgent intervention for anemia, restriction of intrauterine growth, oliguria and olgohydramnios in the donor twin, while the receiver becomes plethoric, polyuric, cardiomegaly, congestive heart failure and polyhydramnios appear. Objective: present a review about twin-twin transfusion syndrome, clinical features, complications and its treatment. Methodology: databases such as Pubmed and ScienceDirect were used to search for the information. Results: we found 41 articles with updated information, reviewing its pathophysiology, classification and treatment, highlighting the role of the renin angiotensin aldosterone system, the presence of placental anastomosis, the involvement of vasopressin levels and its present treatment. Conclusions: twin-twin transfusion syndrome is one of the most severe complications of the monochorionic-biamniotic pregnancies with a high rate of fetal and perinatal morbidity and mortality. It’s pathology is caused due to imbalance of flows between placental anastomoses, alterations in the axis renin angiotensin aldosterone, changes in the levels of vasopressin, among other factors. The current treatment is the therapy of laser ablation of placental anastomoses with a survival of 70% and a decrease of neurologic sequelae. We reiterate the importance of understanding this disease to make an assertive diagnosis and immediate treatment, inviting you to investigate it.

Rinoporidiosis conjuntival (oculosporidiosis) / Conjuntival rhinosporidiosi (oculosporidiosis): report of a case

Se presenta un caso de rinosporidiosis localizada en la conjuntiva; la paciente tenía 15 años, residía en Nechí, Antioquia, y su lesión fue diagnosticada inicialmente como hemangioma. El diagnóstico de rinosporidiosis se hizo por el estudio histológico.

A case of localized conjunctival rhinosporidiosis (oculosporidiosis) of the left eye in a fifteen year old woman is presented. The patient lived in Nechl, Antioquia, Colombia, and the Initial diagnosis was a hemangioma. The correct diagnosis was established by means of histological examination of the excised lesion