Densitometria da vértebra dorsal, osso pleural e osso neural em tartarugas verdes hígidas por tomografia computadorizada quantitativa Densitometry of dorsal vertebrae, pleural bone and neural bone in healthy green sea turtles by quantitative computed tomography

A tomografia computadorizada quantitativa (TCQ) é uma técnica com alta sensibilidade, aplicabilidade e precisão no diagnóstico de perda de massa óssea, entretanto a falta de valores de normalidade para animais silvestres limita a sua aplicação clínica. O presente estudo objetiva estabelecer valores médios de radiodensidade do osso trabecular das vértebras dorsais, osso pleural e osso neural de tartarugas marinhas juvenis hígidas utilizando a TCQ. Para isso, utilizou-se um grupo experimental de cinco animais que foram submetidos a exames de tomografia computadorizada helicoidal, sendo as mensurações da radiodensidade óssea realizadas ao nível da terceira, quarta e quinta vértebras dorsais. Os valores médios de radiodensidade do osso trabecular das vértebras dorsais, osso pleural e osso neural foram, respectivamente, de 287,4±39,1, 1093,74±100,4 e 1089,6±86,5 unidades Hounsfield (HU). Estudos complementares devem ser realizados em diferentes espécies e faixas etárias de quelônios para favorecer a aplicação clínica desta técnica.<br>Quantitative computed tomography (QCT) is a technique with high sensitivity, applicability and accuracy in the diagnosis of bone loss; however the lack of normal values for wild animals limits their clinical application. This study aims to establish medium values radiodensity trabecular bone of the dorsal vertebrae, bone pleural and neural bone in healthy juvenile sea turtles using the QTC. For this we used an experimental group of five animals that underwent helical computed tomography, and measurements of bone radiodensity conducted at the level of the third, fourth and fifth dorsal vertebrae. The medium values of radiodensity trabecular bone of the dorsal vertebrae, pleural bone, and neural bone were respectively 287.4±39.1, 1093.74±100.4, and 1089.6±86.5 Hounsfield units (HU). Further studies should be performed in different species and ages of turtles to encourage the clinical application of this technique

Tumour necrosis factor - alpha mediated mechanisms of cognitive dysfunction

Background: Tumour necrosis factor - alpha (TNF-α) is a pro-inflammatory cytokine that combines a plethora of activities in the early stages of an immune response. TNF-α has gained increasing importance given TNF-α upregulation in multiple brain pathologies like neuropsychiatric conditions such as depression, schizophrenia, as well as neuroinflammatory disorder like multiple sclerosis (MS).\ud \ud Aim: The aim of this review is to critically analyse neurobiological, immunological and molecular mechanisms through which TNF-α influences the development of cognitive dysfunction.\ud \ud Principal findings/results: The review presents several lines of original research showing that the immunological properties of TNF-α exacerbate inflammatory responses in the central nervous system such as microglial and endothelial activation, lymphocytic and monocytic infiltration and the expression of downstream pro-inflammatory cytokines and apoptotic factors. Depression, schizophrenia, and MS all manifest symptoms of activated immune response along with cognitive dysfunction, with TNF-α overexpression as a central clinical feature common to these disorders. Furthermore, TNF-α acts negatively on neuroplasticity and the molecular mechanisms of memory and learning (i.e., long-term potentiation and long-term depression). TNF-α also exerts influence over the production of neurotrophins (i.e., nerve growth factor and brain-derived neurotrophic factor), neurogenesis, and dendritic branching.\ud \ud Conclusions/significance: This review outlines that TNF-α and its receptors have a substantial yet underappreciated influence on the development and progression of neuropsychiatric symptoms across several disease entities. An improved understanding of these underlying mechanisms may help develop novel therapeutic targets in the form of drugs specifically targeting downstream products of TNF-α activation within the central nervous system