Search

The SLS additive manufacturing industry enables the development of products for diverse applications with distinct properties due to its excellent surface finish and ability to create varied part geometries, but it consumes high-performance materials with high acquisition costs. An extensive quarrying of stone leads to the accumulation of mineral residues, posing environmental hazards by contaminating soil and water when disposed of in landfills. The primary objective of the study was to incorporate mineral waste into the SLS technique and investigate the influence of its addition, along with a silane-based chemical treatment, on the mechanical performance of polymer-mineral composites (PA12-slate). Additionally, the feasibility of producing a highly loaded printed prototype, employing 50 wt% of mineral waste, was examined. Samples of PA12, PA12 blended with 50 wt% slate waste, and slate waste treated with silane underwent fabrication via selective laser sintering (SLS) and subsequent mechanical characterization, including tensile, flexural, and compressive tests. Additionally, the samples underwent accelerated aging using a QUV weathering tester, followed by mechanical characterization. The geometric accuracy, stability, and processing feasibility of these formulations were evaluated through SLS-printed composite prototypes utilizing PA12_50Sla_Si. It was found that the addition of 50% of slate to the PA12 presented mechanical properties decreasing compared to the printed PA12 only. However, an increase was verified when using silane-induced mineral bonding. The incorporation of mineral agents and silane enhanced the resistance of PA12 to aging. However, after aging, both tensile and flexural strength decreased across all printed samples. Nonetheless, this study showcased the feasibility of producing complex PA12-slate waste specimens containing up to 50 wt% of mineral waste using the SLS printing technique. Therefore, SLS presents itself as a viable means of adding value to this mineral waste. [ABSTRACT FROM AUTHOR]

This systematic review explored the neurobiological mechanisms underlying the clinical time course of cancer-related cognitive impairment (CRCI) in breast cancer patients through the review of longitudinal neuroimaging studies. Before chemotherapy, results reported no evidence for neuropsychological, structural (gray matter) and brain perfusion changes. However, functional brain alterations were evident and revealed a frontoparietal hyperactivation during working memory tasks. Fatigue and number of days since surgery were the two suggested confounding factors. Acutely after chemotherapy, this review found no evidence for neuropsychological changes while suggesting a pattern of frontal structural, perfusion and functional brain abnormalities. These findings seemed to be dependent on age, menopausal status at baseline, and fMRI task performed. Years after chemotherapy, results revealed evidence of partial neuropsychological, structural, and functional brain recovery. Regarding brain abnormality, this review suggested that it may begin quite early in the disease course, be more prominent shortly after chemotherapy and partially recover over time. Several hypotheses underlying these changes were discussed. The present review also provided important information for developing a time-specific treatment and prevention strategies and for the consideration of functional neuroimaging as a relevant tool for CRCI diagnosis, clinical monitoring, and intervention studies. The findings also suggested the need to implement studies with longitudinal designs, including a pre-treatment assessment, since cross-sectional studies were not able to detect this pattern of recovery over time, supporting only the theory of brain abnormalities, in breast cancer survivors. [ABSTRACT FROM AUTHOR]

The continuous generation of new neurons and glial cells in the adult hippocampal dentate gyrus (DG) represents an important form of adult neuroplasticity, involved in normal brain function and behavior but also associated with the etiopathogenesis and treatment of psychiatric disorders. Despite the large number of studies addressing cell genesis along the septotemporal axis, data on the anatomical gradients of cytogenesis along the DG transverse axis is scarce, especially after exposure to stress. As such, in this study we characterized both basal proliferation and survival of adult-born neural cells along the transverse axis of the rat dorsal DG, and after stress exposure. In basal conditions, both proliferating cells and newborn neurons and glial cells were preferentially located at the subgranular zone and suprapyramidal blade. Exposure to chronic stress induced an overall decrease in the generation of adult-born neural cells and, more specifically, produced a regional-specific decrease in the survival of adult-born neurons at the suprapyramidal blade. No particular region-specific alterations were observed on surviving adult-born glial cells. This work reveals, for the first time, a distinct survival profile of adult-born neural cells, neurons and glial cells, among the transverse axis of the DG, in both basal and stress conditions. Our results unveil that adult-born neurons are preferentially located in the suprapyramidal blade and suggest a regional-specific impact of chronic stress in this blade with potential repercussions for its functional significance. [ABSTRACT FROM AUTHOR]

Major depression is a highly prevalent, multidimensional disorder. Although several classes of antidepressants (ADs) are currently available, treatment efficacy is limited, and relapse rates are high; thus, there is a need to find better therapeutic strategies. Neuroplastic changes in brain regions such as the hippocampal dentate gyrus (DG) accompany depression and its amelioration with ADs. In this study, the unpredictable chronic mild stress (uCMS) rat model of depression was used to determine the molecular mediators of chronic stress and the targets of four ADs with different pharmacological profiles (fluoxetine, imipramine, tianeptine, and agomelatine) in the hippocampal DG. All ADs, except agomelatine, reversed the depression-like behavior and neuroplastic changes produced by uCMS. Chronic stress induced significant molecular changes that were generally reversed by fluoxetine, imipramine, and tianeptine. Fluoxetine primarily acted on neurons to reduce the expression of pro-inflammatory response genes and increased a set of genes involved in cell metabolism. Similarities were found between the molecular actions and targets of imipramine and tianeptine that activated pathways related to cellular protection. Agomelatine presented a unique profile, with pronounced effects on genes related to Rho-GTPase-related pathways in oligodendrocytes and neurons. These differential molecular signatures of ADs studied contribute to our understanding of the processes implicated in the onset and treatment of depression-like symptoms. [ABSTRACT FROM AUTHOR]