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Relatam-se os resultados de uma investigação em que se fez uma comparação de avaliações em mostras científicas de trabalhos de pesquisa produzidos em escolas profissionalizantes, confrontando a Avaliação Tradicional, feita por uma comissão de especialistas, com a Avaliação Participativa, realizada com envolvimento de alunos expositores e professores orientadores. Foram comparados os resultados dos dois tipos de avaliação, além da coleta e análise de dados junto aos alunos e professores sobre seus sentimentos e percepção de competência em se envolverem em processos desta natureza. Dentre as conclusões se destaca que a Avaliação Participativa de trabalhos em Feiras e Mostras escolares se apresenta como uma forma válida e confiável de avaliação, além de propiciar um grande número de vantagens educativas.

Introduction: Plasma biomarkers for Alzheimer's disease (AD) diagnosis/stratification are a "Holy Grail" of AD research and intensively sought; however, there are no well-established plasma markers. Methods: A hypothesis-led plasma biomarker search was conducted in the context of international multicenter studies. The discovery phase measured 53 inflammatory proteins in elderly control (CTL; 259), mild cognitive impairment (MCI; 199), and AD (262) subjects from AddNeuroMed. Results: Ten analytes showed significant intergroup differences. Logistic regression identified five (FB, FH, sCR1, MCP-1, eotaxin-1) that, age/APOe4 adjusted, optimally differentiated AD and CTL (AUC: 0.79), and three (sCR1, MCP-1, eotaxin-1) that optimally differentiated AD and MCI (AUC: 0.74). These models replicated in an independent cohort (EMIF; AUC 0.81 and 0.67). Two analytes (FB, FH) plus age predicted MCI progression to AD (AUC: 0.71). Discussion: Plasma markers of inflammation and complement dysregulation support diagnosis and outcome prediction in AD and MCI. Further replication is needed before clinical translation. (C) 2019 The Authors. Published by Elsevier Inc. on behalf of the Alzheimer's Association. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

Giovanni Cochetti,1 Francesco Barillaro,1 Emanuele Cottini,1 Francesco D’Amico,1 Alberto Pansadoro,1 Solajd Pohja,1 Andrea Boni,1 Roberto Cirocchi,2 Veronica Grassi,2 Rosa Mancuso,1 Elisa Silvi,1 Katifenia Ioannidou,1 Maria Giulia Egidi,1 Giulia Poli,1 Ettore Mearini1 1Department of Surgical and Biomedical Science, Institute of Urological, Andrological Surgery and Minimally Invasive Techniques, University of Perugia, Terni, Italy; 2Department of Surgical Sciences, University of Perugia, Terni, Italy Abstract: Pneumoscrotum is the term used to describe the presence of air within the scrotum and includes scrotal emphysema as well as pneumatocele. The etiology varies; in some cases, pneumoscrotum may be due to life-threatening disease like pneumothorax or Fournier gangrene. Despite this, pneumoscrotum is a rarely debated issue. We present two different cases of pneumoscrotum and a review of the literature. The first case report is about a 29 year old male patient affected by Duchenne syndrome who showed pneumoscrotum after cardiopulmonary resuscitation that was performed for asphyxic crisis and cardiovascular arrest. We carried out local puncture with an 18-gauge needle, and the pneumoscrotum was successfully solved. The second case report is about a 56 year old male with pneumoscrotum due to Fournier gangrene who underwent radical exeresis of all necrotic tissues and drainage. This is why most of the scrotal skin and all of the penis skin were removed; as a result, the testicles, epididymis, and cavernosa corpora were externalized. On postoperative day one, the patient was feverless and underwent hyperbaric chamber therapy. No postoperative complications occurred. Accurate evaluation of the pneumoscrotum is always needed. Despite the benign course of most of the clinically evident pneumoscrotum cases, this condition should never be underestimated. Keywords: cardiopulmonary resuscitation, Fournier gangrene, pneumoscrotum, spontaneous causes, traumatic causes

Una de las alteraciones patológicas más frecuentes de la columna vertebral se debe al desplazamiento del núcleo pulposo del disco intervertebral produciendo hernias. El objetivo de este trabajo es discutir las evidencias esqueletales dejadas por esta patología (nódulos de Schmorl) y su relación con diversos factores de riesgo, al mismo tiempo que se analizará de manera preliminar su prevalencia en colecciones histórico-contemporáneas. Se examinaron cuatro muestras documentadas pertenecientes a las Universidades de La Plata (Argentina), Coimbra (Portugal), Granada (España) y Valladolid (España). Se observaron las vértebras de 100 individuos adultos de ambos sexos en cada una de ellas. Se procedió a un análisis descriptivo mediante una observación macroscópica y con lupa del material, en búsqueda de oquedades que reflejen la protrusión del núcleo pulposo del disco intervertebral. Para su registro se dividió la cara dorsal y ventral de cada vértebra en tres áreas: centro, canal y periferia, mientras que las lesiones se clasificaron como: pequeñas (Grado 1) o grandes (Grado 2) dependiendo de la profundidad y el área lesionada. Posteriormente se relacionaron las observaciones con factores de riesgo para dicha patología. Los resultados observados mostraron diferencias en las prevalencias totales (27% La Plata; 48% Coimbra; 55% Granada; 51% Valladolid), sin mayores diferencias entre los sexos. La mayor frecuencia de casos se detectó en la zona torácica baja y lumbar alta, sin afectar la zona cervical. El centro de la vértebra fue el área en donde se encontró un mayor número de nódulos de Schmorl. La predisposición genética, el envejecimiento, y en menor medida el stress mecánico serían los principales factores de riesgo para la aparición y desarrollo de las hernias discales. Fil: Desántolo, B. Universidad Nacional de la Plata; Facultad de Ciencias Médicas; Argentina Fil: Plischuk, L. Universidad Nacional de la Plata; Facultad de Ciencias Médicas; CONICET; Argentina Fil: García-Mancuso, R. Universidad Nacional de la Plata; Facultad de Ciencias Médicas; Argentina Fil: Inda, A.M.Universidad Nacional de la Plata; Facultad de Ciencias Médicas;CIC;Argentina

The inside cover picture shows a catalytic cycle, in which an in situ generated bis(2,6-diisopropyl)acenaphthenequinonediimine palladium catalyst is able to divergently convert terminal and internal alkynes into propiolic esters or maleic esters and their derivatives, respectively, with a wide range of alcohols, under oxidative alkoxycarbonylation conditions (4 bar of carbon monoxide, in the presence of benzoquinone as oxidant at 20 °C).

The APRAC-1A diffusion model was developed as a versatile and practical model for computing the concentrations of pollutants at any point within a city. The model calculates pollutant contributions from diffusion on various scales, including: extra-urban diffusion, mainly from sources in upwind cities; intra-urban diffusion from freeway, arterial, and feeder street sources; local diffusion of emissions within a street canyon. The model treats only carbon monoxide (CO), a relatively inert gas in the atmosphere but an important pollutant in terms of health. Motor vehicles are the major source of this gas. (Author/JR)

Frontotemporal dementia (FTD)-causing mutations in the CHMP2B gene lead to the generation of mutant C-terminally truncated CHMP2B. We report that transgenic mice expressing endogenous levels of mutant CHMP2B developed late-onset brain volume loss associated with frank neuronal loss and FTD-like changes in social behaviour. These data are the first to show neurodegeneration in mice expressing mutant CHMP2B and indicate that our mouse model is able to recapitulate neurodegenerative changes observed in FTD. Neuroinflammation has been increasingly implicated in neurodegeneration, including FTD. Therefore, we investigated neuroinflammation in our CHMP2B mutant mice. We observed very early microglial proliferation that develops into a clear pro-inflammatory phenotype at late stages. Importantly, we also observed a similar inflammatory profile in CHMP2B patient frontal cortex. Aberrant microglial function has also been implicated in FTD caused by GRN, MAPT and C9orf72 mutations. The presence of early microglial changes in our CHMP2B mutant mice indicates neuroinflammation may be a contributing factor to the neurodegeneration observed in FTD.

Microglial proliferation and activation is a hallmark of Alzheimer's disease. Olmos-Alonso et al. show that microglial proliferation in Alzheimer's disease tissue correlates with overactivation of the colony-stimulating factor 1 receptor (CSF1R) pathway. CSF1R blockade arrests microglial proliferation and activation in a mouse model of Alzheimer-like pathology and slows disease progression.Microglial proliferation and activation is a hallmark of Alzheimer's disease. Olmos-Alonso et al. show that microglial proliferation in Alzheimer's disease tissue correlates with overactivation of the colony-stimulating factor 1 receptor (CSF1R) pathway. CSF1R blockade arrests microglial proliferation and activation in a mouse model of Alzheimer-like pathology and slows disease progression.The proliferation and activation of microglial cells is a hallmark of several neurodegenerative conditions. This mechanism is regulated by the activation of the colony-stimulating factor 1 receptor (CSF1R), thus providing a target that may prevent the progression of conditions such as Alzheimer's disease. However, the study of microglial proliferation in Alzheimer's disease and validation of the efficacy of CSF1R-inhibiting strategies have not yet been reported. In this study we found increased proliferation of microglial cells in human Alzheimer's disease, in line with an increased upregulation of the CSF1R-dependent pro-mitogenic cascade, correlating with disease severity. Using a transgenic model of Alzheimer's-like pathology (APPswe, PSEN1dE9; APP/PS1 mice) we define a CSF1R-dependent progressive increase in microglial proliferation, in the proximity of amyloid-beta plaques. Prolonged inhibition of CSF1R in APP/PS1 mice by an orally available tyrosine kinase inhibitor (GW2580) resulted in the blockade of microglial proliferation and the shifting of the microglial inflammatory profile to an anti-inflammatory phenotype. Pharmacological targeting of CSF1R in APP/PS1 mice resulted in an improved performance in memory and behavioural tasks and a prevention of synaptic degeneration, although these changes were not correlated with a change in the number of amyloid-beta plaques. Our results provide the first proof of the efficacy of CSF1R inhibition in models of Alzheimer's disease, and validate the application of a therapeutic strategy aimed at modifying CSF1R activation as a promising approach to tackle microglial activation and the progression of Alzheimer's disease.