sunbeds and carcinogenesis the need for new regulations and restrictions in europe from the euromelanoma perspective

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Early TBI-Induced Cytokine Alterations are Similarly Detected by Two Distinct Methods of Multiplex Assay

Annually, more than a million persons experience traumatic brain injury (TBI) in the US and a substantial proportion of this population develop debilitating neurological disorders, such as, paralysis, cognitive deficits, and epilepsy. Despite the long-standing knowledge of the risks associated with TBI, no effective biomarkers or interventions exist. Recent evidence suggests a role for inflammatory modulators in TBI-induced neurological impairments. Current technological advances allow for the simultaneous analysis of the precise spatial and temporal expression patterns of numerous proteins in single samples which ultimately can lead to the development of novel treatments. Thus, the present study examined 23 different cytokines, including chemokines, in the ipsi and contralateral cerebral cortex of rats at 24 h after a fluid percussion injury (FPI). Furthermore, the estimation of cytokines were performed in a newly developed multiplex assay instrument, MAGPIX (Luminex Corp), and compared with an established instrument, Bio-Plex (Bio-Rad), in order to validate the newly developed instrument. The results show numerous inflammatory changes in the ipsi and contralateral side after FPI that were consistently reported by both technologies

Leukocyte telomere length as potential biomarker of HD progression: A follow-up study

The identification of biomarkers for neurodegenerative disorders such as Huntington's disease (HD) is crucial for monitoring disease progression and therapeutic trial outcomes, especially in the pre-manifest disease stage (pre-HD). In a previous study, we observed that leukocyte telomere length (LTL) was strongly correlated with the estimated time to clinical onset in pre-HD subjects. To validate this hypothesis, we designed a follow-up study in which we analyzed LTL in 45 pre-HD stage subjects at baseline (T0) and then again after clinical onset at follow-up (T1); the follow-up interval was about 3 years, and the CAG range was 39-51 repeats; 90 peripheral blood mononuclear cell samples (PBMCs) were obtained from the Enroll-HD biorepository. In pre-HD subjects at T0, LTL was significantly reduced by 22% compared to the controls and by 14% from T0 at T1. No relationship was observed between the LTL and CAG numbers in subjects carrying different CAG repeats at T0 and at T1, suggesting that LTL reduction occurs independently of CAG number in pre-HD subjects. ROC curve analysis was used to test the validity of LTL as a potential biomarker of HD progression and showed that LTL measurement is extremely accurate in discriminating pre-HD subjects from the controls and even pre-HD from manifest HD, thus yielding a robust prognostic value in pre-HD subjects

Chemokine CCL2 and its receptor CCR2 are increased in the hippocampus following pilocarpine-induced status epilepticus

<p>Abstract</p> <p>Background</p> <p>Neuroinflammation occurs after seizures and is implicated in epileptogenesis. CCR2 is a chemokine receptor for CCL2 and their interaction mediates monocyte infiltration in the neuroinflammatory cascade triggered in different brain pathologies. In this work CCR2 and CCL2 expression were examined following status epilepticus (SE) induced by pilocarpine injection.</p> <p>Methods</p> <p>SE was induced by pilocarpine injection. Control rats were injected with saline instead of pilocarpine. Five days after SE, CCR2 staining in neurons and glial cells was examined using imunohistochemical analyses. The number of CCR2 positive cells was determined using stereology probes in the hippocampus. CCL2 expression in the hippocampus was examined by molecular assay.</p> <p>Results</p> <p>Increased CCR2 was observed in the hippocampus after SE. Seizures also resulted in alterations to the cell types expressing CCR2. Increased numbers of neurons that expressed CCR2 was observed following SE. Microglial cells were more closely apposed to the CCR2-labeled cells in SE rats. In addition, rats that experienced SE exhibited CCR2-labeling in populations of hypertrophied astrocytes, especially in CA1 and dentate gyrus. These CCR2+ astroctytes were not observed in control rats. Examination of CCL2 expression showed that it was elevated in the hippocampus following SE.</p> <p>Conclusion</p> <p>The data show that CCR2 and CCL2 are up-regulated in the hippocampus after pilocarpine-induced SE. Seizures also result in changes to CCR2 receptor expression in neurons and astrocytes. These changes might be involved in detrimental neuroplasticity and neuroinflammatory changes that occur following seizures.</p

Sexualidade no interior conservador brasileiro: uma experiência de educação para a diversidade sexual e de gênero em Foz do Iguaçu

Assistimos em nível internacional ao auge de políticas e movimentos conservadores com ênfase na exaltação dos papéis dos gêneros tradicionais e no combate à assim chamada “ideologia de gênero” ao mesmo tempo em que parece ganhar força o chamado à defesa das identidades nacionais e das fronteiras, das famílias tradicionais, e da vida do nascituro em contra do aborto. Este artigo trata da experiência de extensão, pesquisa e educação sobre gênero e sexualidade, desenvolvida por uma universidade federal brasileira em uma cidade do interior do Paraná, localizada na tríplice fronteira do Brasil com Argentina e Paraguai. É importante notar que o Paraná é um estado considerado como extremamente conservador. Consideramos que iniciativas que incidem diretamente nas comunidades escolares, como as descritas neste artigo, se configuram como espaços pedagógicos de resistência, onde são trilhados caminhos possíveis para contribuir na criação de  espaços educativos onde preconceito e discriminações por razões de gênero e sexualidade sejam problematizados e eliminados. Consideramos, além disso, que especialmente nesses tempos atuais de ataques globais aos direitos das mulheres, lésbicas, gays, pessoas trans e aos direitos humanos, é fundamental que, em nível local, continuem existindo e resistindo espaços de promoção a reflexão e à desconstrução de estruturas opressoras

Isolamento de um fragmento do gene de lipase de staphylococcus xylosus U5 e AD1.

Projeto/Plano de Ação: 03.08.06.009-02

NGF steers microglia toward a neuroprotective phenotype

Microglia are the sentinels of the brain but a clear understanding of the factors that modulate their activation in physiological and pathological conditions is still lacking. Here we demonstrate that Nerve Growth Factor (NGF) acts on microglia by steering them toward a neuroprotective and anti-inflammatory phenotype. We show that microglial cells express functional NGF receptors in vitro and ex vivo. Our transcriptomic analysis reveals how, in primary microglia, NGF treatment leads to a modulation of motility, phagocytosis and degradation pathways. At the functional level, NGF induces an increase in membrane dynamics and macropinocytosis and, in vivo, it activates an outward rectifying current that appears to modulate glutamatergic neurotransmission in nearby neurons. Since microglia are supposed to be a major player in Aβ peptide clearance in the brain, we tested the effects of NGF on its phagocytosis. NGF was shown to promote TrkA-mediated engulfment of Aβ by microglia, and to enhance its degradation. Additionally, the proinflammatory activation induced by Aβ treatment is counteracted by the concomitant administration of NGF. Moreover, by acting specifically on microglia, NGF protects neurons from the Aβ-induced loss of dendritic spines and inhibition of long term potentiation. Finally, in an ex-vivo setup of acute brain slices, we observed a similar increase in Aβ engulfment by microglial cells under the influence of NGF. Our work substantiates a role for NGF in the regulation of microglial homeostatic activities and points toward this neurotrophin as a neuroprotective agent in Aβ accumulation pathologies, via its anti-inflammatory activity on microglia

Primer development for detection of Phaseolus vulgaris and Olathe transgenic bean.

Several strategies have been employed for genetically engineering resistance to viruses in transgenic plants. The bean golden mosaic virus (BGMV) is responsible for causing the gold mosaic of common bean (Phaseolus vulgaris L.) and causes severe yield losses due to yellow-green mosaic of leaves, stunted growth and distorted pods. Olathe transgenic bean (Olathe 5.1) was successfully produced by EMBRAPA using the RNA interference (RNAi) concept to silence the rep viral gene in common bean to generate transgenic lines with strong resistance to BGMV. In this work, real time PCR (RT-PCR) method with SYBR Green was developed to detect this newly genetically modified (GM) plant