Professores iniciantes na educação básica em tempos pandêmicos

This research aims to highlight some difficulties experienced by beginning teachers in Basic Education, specifically, in early childhood, and also considering different realities: the moment of their professional insertion and the the pandemic moment we have experienced in Brazil since 2020. So, the leading question here is: What are the difficulties experienced by beginning teachers working in Basic Education when they are inserted in provide teaching, and facing this pandemic period? We support the theoretical framework from studies of Garcia (1999), Huberman (1987). A qualitative approach was used as methodology base, from a literature revision, and applying an electronic form as data collection instruments. The results and discussions obtained show us that the challenges faced up the teachers, who participated in this research, are countless and diferents. Therefore, we found that these difficulties were intensified by the pandemic scenario in which we live since 2020.Esta pesquisa tem como objetivo evidenciar algumas dificuldades sentidas por professores iniciantes na Educação Básica, especificamente, na educação infantil e nos anos iniciais, considerando dois aspectos: o momento da inserção profissional e o momento pandêmico que vivenciamos, no Brasil, desde 2020. A questão norteadora é assim expressa: quais as dificuldades sentidas pelos docentes iniciantes atuantes na Educação Básica quando inseridos na docência e frente ao cenário da pandemia? O referencial teórico se apoia nos estudos de Garcia (1999), Huberman (1995), Nono (2011), Farias (2020), entre outros. A metodologia que alicerça essa pesquisa é de abordagem qualitativa, sustentada pela revisão de literatura e pela aplicação de um questionário eletrônico. Os resultados e discussões indicaram que os desafios encontrados pelos docentes participantes da pesquisa são inúmeros e distintos e foram intensificados pelo cenário pandêmico no qual nos encontramos desde 2020

Mortalin Inhibition in Experimental Parkinson's Disease

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Neuroinflammation and Dyskinesia: A Possible Causative Relationship?

Levodopa (L-DOPA) treatment represents the gold standard therapy for Parkinson’s disease (PD) patients. L-DOPA therapy shows many side effects, among them, L-DOPA-induced dyskinesias (LIDs) remain the most problematic. Several are the mechanisms underlying these processes: abnormal corticostriatal neurotransmission, pre- and post-synaptic neuronal events, changes in gene expression, and altered plasticity. In recent years, researchers have also suggested non-neuronal mechanisms as a possible cause for LIDs. We reviewed recent clinical and pre-clinical studies on neuroinflammation contribution to LIDs. Microglia and astrocytes seem to play a strategic role in LIDs phenomenon. In particular, their inflammatory response affects neuron-glia communication, synaptic activity and neuroplasticity, contributing to LIDs development. Finally, we describe possible new therapeutic interventions for dyskinesia prevention targeting glia cells

Alpha-Synuclein as a Prominent Actor in the Inflammatory Synaptopathy of Parkinson’s Disease

Parkinson’s disease (PD) is considered the most common disorder of synucleinopathy, which is characterised by intracellular inclusions of aggregated and misfolded α-synuclein (α-syn) protein in various brain regions, and the loss of dopaminergic neurons. During the early prodromal phase of PD, synaptic alterations happen before cell death, which is linked to the synaptic accumulation of toxic α-syn specifically in the presynaptic terminals, affecting neurotransmitter release. The oligomers and protofibrils of α-syn are the most toxic species, and their overexpression impairs the distribution and activation of synaptic proteins, such as the SNARE complex, preventing neurotransmitter exocytosis and neuronal synaptic communication. In the last few years, the role of the immune system in PD has been increasingly considered. Microglial and astrocyte activation, the gene expression of proinflammatory factors, and the infiltration of immune cells from the periphery to the central nervous system (CNS) represent the main features of the inflammatory response. One of the actors of these processes is α-syn accumulation. In light of this, here, we provide a systematic review of PD-related α-syn and inflammation inter-players

Use of the SpineJack direct reduction for treating type A2, A3 and A4 fractures of the thoracolumbar spine: a retrospective case series

Compression injuries of the thoracolumbar spine without neurological impairment are usually treated with minimally invasive procedures. Intravertebral expandable implants represent an alternative strategy in fractures with low fragments' displacement

Nicotine: From Discovery to Biological Effects

: Nicotine, the primary psychoactive agent in tobacco leaves, has led to the widespread use of tobacco, with over one billion smokers globally. This article provides a historical overview of tobacco and discusses tobacco dependence, as well as the biological effects induced by nicotine on mammalian cells. Nicotine induces various biological effects, such as neoangiogenesis, cell division, and proliferation, and it affects neural and non-neural cells through specific pathways downstream of nicotinic receptors (nAChRs). Specific effects mediated by α7 nAChRs are highlighted. Nicotine is highly addictive and hazardous. Public health initiatives should prioritize combating smoking and its associated risks. Understanding nicotine's complex biological effects is essential for comprehensive research and informed health policies. While potential links between nicotine and COVID-19 severity warrant further investigation, smoking remains a significant cause of morbidity and mortality globally. Effective public health strategies are vital to promote healthier lifestyles

Nicotine upregulates ACE2 expression and increases competence for SARS-CoV-2 in human pneumocytes

The coronavirus disease 2019 (COVID-19) pandemic has a variable degree of severity according to underlying comorbidities and life-style. Several research groups have reported an association between cigarette smoking and increased severity of COVID-19. The exact mechanism of action is largely unclear.We exposed low angiotensin-converting enzyme 2 (ACE2)-expressing human pulmonary adenocarcinoma A549 epithelial cells to nicotine and assessed ACE2 expression at different times. We further used the nicotine-exposed cells in a virus neutralisation assay.Nicotine exposure induces rapid and long-lasting increases in gene and protein expression of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) receptor ACE2, which in turn translates into increased competence for SARS-CoV-2 replication and cytopathic effect.These findings show that nicotine worsens SARS-CoV-2 pulmonary infection and have implications for public health policies

Synaptic mechanisms underlying onset and progression of memory deficits caused by hippocampal and midbrain synucleinopathy.

Cognitive deficits, including working memory, and visuospatial deficits are common and debilitating in Parkinson’s disease. α-synucleinopathy in the hippocampus and cortex is considered as the major risk factor. However, little is known about the progression and specific synaptic mechanisms underlying the memory deficits induced by α-synucleinopathy. Here, we tested the hypothesis that pathologic α-Synuclein (α-Syn), initiated in different brain regions, leads to distinct onset and progression of the pathology. We report that overexpression of human α-Syn in the murine mesencephalon leads to late onset memory impairment and sensorimotor deficits accompanied by reduced dopamine D1 expression in the hippocampus. In contrast, human α-Syn overexpression in the hippocampus leads to early memory impairment, altered synaptic transmission and plasticity, and decreased expression of GluA1 AMPA-type glutamate receptors. These findings identify the synaptic mechanisms leading to memory impairment induced by hippocampal α-synucleinopathy and provide functional evidence of the major neuronal networks involved in disease progression

Effect of Cigarette Smoking on Clinical and Molecular Endpoints in COPD Patients

Cigarette smoking is a primary contributor to mortality risks and is associated with various diseases. Among these, COPD represents a significant contributor to global mortality and disability. The objective of this study is to investigate the effect of smoking on a selected battery of variables, with an emphasis on DNA damage. A total of 87 elderly patients diagnosed with COPD, divided into three groups based on their smoking history (current, former, never-smokers), were evaluated using a cross-sectional approach. Clinical features including mortality and inflammatory/oxidative parameters (Lymphocytes/Monocytes, Neutrophils/Lymphocytes, Platelets/Lymphocytes ratio), SII, MDA, 8-Oxo-dG, and IL6 (ELISA assay), as well as DNA damage (comet assay), were investigated. Virus infection, i.e., influenza A virus subtype H1N1, JC polyomavirus (JCPyV), BK polyomavirus (BKPyV), and Torquetenovirus (TTV), was also tested. Current smokers exhibit higher levels of comorbidity (CIRS; p p p p p < 0.0017). This study showed a clear interaction between events which are relevant to the oxidative pathway and cigarette smoking. A category of particular interest is represented by former smokers, especially for lower survival, possibly due to the presence of more health problems. Our findings raise also the attention to other parameters which are significantly affected by smoking and are useful to monitor COPD patients starting a program of pulmonary rehabilitation (DNA damage, inflammation parameters, and selected viral infections)