Workshop redacción científica

El Departamento de Ingeniería Civil y Ambiental de la Universidad de la Costa, con el fin de fortalecer los procesos académicos, realizó un “Workshop de redacción científica”', dirigido a profesores y estudiantes interesados en la publicación de artículos científicos, desarrollado del 5 al 6 de febrero de 2020, en la Sala de Conferencias 2, ubicada en el bloque 11, jornada matutina y liderado por el Dr. Juciano Gasparotto, profesor titular medio tiempo internacional. El curso se efectuó con una intensidad de 8 horas y su programación temática en módulos. Primer día: Módulo I: El género literario. Módulo II: Títulos, autores y resumen. Módulo III: Introducción. Módulo IV: Resultados, discusión y conclusiones. Segundo día: Módulo V: Precisión y Complejidad. Módulo VI: Acción verbal, flujo de texto. Módulo VII: Inglés simple, escritura en inglés. Módulo VIII: Párrafos, cartas de presentación y proceso editorial.Departamento de Ingeniería Civil y Ambiental; Universidad de la Cost

Mitochondrial bioenergetics deregulation caused by long-chain 3-hydroxy fatty acids accumulating in LCHAD and MTP deficiencies in rat brain: A possible role of mPTP opening as a pathomechanism in these disorders?

AbstractLong-chain 3-hydroxylated fatty acids (LCHFA) accumulate in long-chain 3-hydroxy-acyl-CoA dehydrogenase (LCHAD) and mitochondrial trifunctional protein (MTP) deficiencies. Affected patients usually present severe neonatal symptoms involving cardiac and hepatic functions, although long-term neurological abnormalities are also commonly observed. Since the underlying mechanisms of brain damage are practically unknown and have not been properly investigated, we studied the effects of LCHFA on important parameters of mitochondrial homeostasis in isolated mitochondria from cerebral cortex of developing rats. 3-Hydroxytetradecanoic acid (3 HTA) reduced mitochondrial membrane potential, NAD(P)H levels, Ca2+ retention capacity and ATP content, besides inducing swelling, cytochrome c release and H2O2 production in Ca2+-loaded mitochondrial preparations. We also found that cyclosporine A plus ADP, as well as ruthenium red, a Ca2+ uptake blocker, prevented these effects, suggesting the involvement of the mitochondrial permeability transition pore (mPTP) and an important role for Ca2+, respectively. 3-Hydroxydodecanoic and 3-hydroxypalmitic acids, that also accumulate in LCHAD and MTP deficiencies, similarly induced mitochondrial swelling and decreased ATP content, but to a variable degree pending on the size of their carbon chain. It is proposed that mPTP opening induced by LCHFA disrupts brain bioenergetics and may contribute at least partly to explain the neurologic dysfunction observed in patients affected by LCHAD and MTP deficiencies

Obesity associated with coal ash inhalation triggers systemic inflammation and oxidative damage in the hippocampus of rats

People with large amounts of adipose tissue are more vulnerable and more likely to develop diseases where oxidative stress and inflammation play a pivotal role, than persons with a healthy weight. Atmospheric contamination is a reality to which a large part of the worldwide population is exposed. Half of today's global electrical energy is derived from coal. Each organism, in its complexity, responds in different ways to dietary compounds and air pollution. The objective of this study was to investigate the effects of obesity and coal ash inhalation within the parameters of oxidative damage and inflammation in different regions of the brain of rats. A diet containing high-fat concentration was administered chronically to rats, along with exposure to coal ash, simulating the contamination that occurs daily throughout human life. High-resolution transmission electron microscopy was performed to identify the particles present in coal ash samples. Our results demonstrated that obese rats exposed to coal ash inhalation were more affected by oxidative damage with subsequent systemic inflammation in the hippocampus. Since there is an inflammatory predisposition caused by obesity, the inhalation of nanoparticles increases the levels of free radicals, resulting in systemic inflammation and oxidative damage, which can lead to chronic neurodegeneration

Nanoparticles in fossil and mineral fuel sectors and their impact on environment and human health: A review and perspective

Nanoscience and technology have enabled better insights into the environmental and health impacts arising from the mining, production and use of fossil and mineral fuels. Here we provide an overview of the nanoscience-based applications and discoveries concerning coal and mineral fuel (i.e., uranium-containing minerals) mining, refining/production, use, and disposal of wastes. These processes result in massive nanoparticle release and secondary nanoparticle generation which have highly significant environmental implications and human health consequences on local, regional, and even global levels. Until recently, very little was known about nanoparticle fractions. Recent advancements and sophistications enable us to detect, collect and study these materials which are roughly 1 nm (0.001 µm) up to several tens of nanometers in size. These materials are known to behave differently (chemically, electrically, and mechanically), relative to their macroscopic equivalents. This is what makes nanoscience fascinating and difficult to predict, underscoring the importance of this emerging new field. For example, nanoparticles associated with coal and mineral fuel influence the release, uptake, and transportation of hazardous elements associated with mining, processing, and waste storage in the surrounding areas. This includes long distance transport down streams, rivers, and eventually to oceans such as from coal and uranium mine drainages. In terms of human health, in all phases of mining, production/refining, use, and waste disposal, the associated nanoparticles can be acquired through oral ingestion, inhalation, and dermal absorption. Inhalation has been shown to be particularly damaging, where lung, heart, kidney, and brain diseases are prevalent. Relative to all other fields of science and engineering associated with coal and mineral fuel mining, production, use, and clean-up efforts, nanoscience, although a much newer field then the rest by comparison, is still greatly under-represented and under-utilized. There is also a continuing gap between what we so far know about the behavior of nanoparticles, and what remains to be discovered

A review on the environmental impact of phosphogypsum and potential health impacts through the release of nanoparticles

Many industrial by-products have been disposed along coastlines, generating profound marine changes. Phosphogypsum (PG) is a solid by-product generated in the production of phosphoric acid (PA) using conventional synthesis methods. The raw material, about 50 times more radioactive as compared to unperturbed soils, is dissolved in diluted sulfuric acid (70%) forming PG and PA. The majority of both, reactive hazardous elements and natural radionuclides, remain bound to the PG. A nonnegligible fraction of PG occurs as nanoparticles (<0.1 μm). When PG are used for e.g., agriculture or construction purposes, nanoparticles (NPs) can be re-suspended by Aeolian and fluvial processes. Here we provide an overview and evaluation of the geochemical and radiological hazardous risks associated with the different uses of PG. In this review, we show that NPs are important residues in both raw and waste materials originating from the uses of phosphate rock. Different industrial processes in the phosphate fertilizer industries are discussed in the context of the chemical and mineralogical composition as well as size and reactivity of the released NP. We also review how incidental NPs of PG impact the global environment, especially with respect to the distribution of rare earth elements (REEs), toxic elements such as As, Se, and Pb, and natural radionuclides. We also propose the application of advanced techniques and methods to better understand formation and transport of NPs containing elements of high scientific, economic, and environmental importance

Hypoxia-inducible factor-1α (HIF-1α) inhibition impairs retinoic acid-induced differentiation in SH-SY5Y neuroblastoma cells, leading to reduced neurite length and diminished gene expression related to cell differentiation

Neuroblastoma is the most common extracranial solid tumour in childhood, originated from cells of the neural crest during the development of the Sympathetic Nervous System. Retinoids are vitamin-A derived differentiating agents utilised to avoid disease resurgence in high-risk neuroblastoma treatment. Several studies indicate that hypoxia—a common feature of the tumoural environment—is a key player in cell differentiation and proliferation. Hypoxia leads to the accumulation of the hypoxia-inducible factor-1α (HIF-1α). This work aims to investigate the effects of the selective inhibition of HIF-1α on the differentiation induced by retinoic acid in human neuroblastoma cells from the SH-SY5Y lineage to clarify its role in cell differentiation. Our results indicate that HIF-1α inhibition impairs RA-induced differentiation by reducing neuron-like phenotype and diminished immunolabeling and expression of differentiation markers

Retinoic acid downregulates thiol antioxidant defences and homologous recombination while promotes A549 cells sensitization to cisplatin

Recent studies have investigated the use of retinoic acid (RA) molecule in combined chemotherapies to cancer cells as an attempt to increase treatment efficiency and circumvent cell resistance. Positive results were obtained in clinical trials from lung cancer patients treated with RA and cisplatin. Meanwhile, the signalling process that results from the interaction of both molecules remains unclear. One of the pathways that RA is able to modulate is the activity of NRF2 transcription factor, which is highly associated with tumour progression and resistance. Therefore, the aim of this work was to investigate molecular mechanism of RA and cisplatin co-treatment in A549 cells, focusing in NRF2 pathway. To this end, we investigated NRF2 and NRF2-target genes expression, cellular redox status, cisplatin-induced apoptosis, autophagy and DNA repair through homologous recombination. RA demonstrated to have an inhibitory effect over NRF2 activation, which regulates the expression of thiol antioxidants enzymes. Moreover, RA increased reactive species production associated with increased oxidation of thiol groups within the cells. The expression of proteins associated with DNA repair through homologous recombination was also suppressed by RA pre-treatment. All combined, these effects appear to create a more sensitive cellular environment to cisplatin treatment, increasing apoptosis frequency. Interestingly, autophagy was also increased by combination therapy, suggesting a resistance mechanism by A549 cells. In conclusion, these results provided new information about molecular mechanisms of RA and cisplatin treatment contributing to chemotherapy optimization