Virtual reality and process mining applied to operator training in complex assembly tasks

One of the proposals of Industry 4.0 is the integration of machines and operators through network connections and information management. One of the challenges that can be addressed following this approach is the management of knowledge in the industry or, in other words, the transmission of knowledge from the expert operators to the new ones. This work has been developed a system that combines Virtual Reality and Process Mining to allow this knowledge transmission in the particular case of assembly tasks. Virtual Reality allows to create work environments that reproduce the real ones and interact with them without detracting resources of other processes or facing the risks of working with real systems. Process Mining allows to acquire the knowledge of experts, store it in models and then transmit it to novices. The developed system has been tested by means of several examples of assemblies with Lego

Sistema de adiestramiento en tareas de ensamblado mediante realidad virtual y minería de procesos

En este trabajo se ha decidido desarrollar y evaluar un sistema de basado en realidad virtual para la formación y entrenamiento de operarios en tareas de ensamblado. Se propone asumir uno de los desafíos de la Industria 4.0: el uso de la Realidad Virtual para mejorar los procesos de adiestramiento del personal; y proporcionar un sistema automatizado e inmersivo de entrenamiento. Pero además el sistema desarrollado va más allá y, mediante la Minería de Procesos, permite la digitalización y recopilación automática de los procesos de ensamblado realizados por el operador, permitiendo su análisis y optimización

Sistema de adiestramiento en tareas de ensamblado mediante realidad virtual y minería de procesos

En este trabajo se ha decidido desarrollar y evaluar un sistema de basado en realidad virtual para la formación y entrenamiento de operarios en tareas de ensamblado. Se propone asumir uno de los desafíos de la Industria 4.0: el uso de la Realidad Virtual para mejorar los procesos de adiestramiento del personal; y proporcionar un sistema automatizado e inmersivo de entrenamiento. Pero además el sistema desarrollado va más allá y, mediante la Minería de Procesos, permite la digitalización y recopilación automática de los procesos de ensamblado realizados por el operador, permitiendo su análisis y optimización

Salivary Glands after Prolonged Aluminum Exposure: Proteomic Approach Underlying Biochemical and Morphological Impairments in Rats

Aluminum (Al) is one of the most abundant elements on Earth, and its high extraction rate and industrial use make human exposure very common. As Al may be a human toxicant, it is important to investigate the effects of Al exposure, mainly at low doses and for prolonged periods, by simulating human exposure. This work aimed to study the effects of low-dose exposure to chloride aluminum (AlCl3) on the oxidative biochemistry, proteomic profile, and morphology of the major salivary glands. Wistar male rats were exposed to 8.3 mg/kg/day of AlCl3 via intragastric gavage for 60 days. Then, the parotid and submandibular glands were subjected to biochemical assays, proteomic evaluation, and histological analysis. Al caused oxidative imbalance in both salivary glands. Dysregulation of protein expression, mainly of those related to cytoarchitecture, energy metabolism and glandular function, was detected in both salivary glands. Al also promoted histological alterations, such as acinar atrophy and an increase in parenchymal tissue. Prolonged exposure to Al, even at low doses, was able to modulate molecular alterations associated with morphological impairments in the salivary glands of rats. From this perspective, prolonged Al exposure may be a risk to exposed populations and their oral health

Oxidative Biochemistry Disbalance and Changes on Proteomic Profile in Salivary Glands of Rats Induced by Chronic Exposure to Methylmercury

Methylmercury (MeHg) is one of the most toxic mercury species, which can cause many systemic damages, but little is known about its effect in the salivary glands. This study aimed to analyze the mercury levels, oxidative stress, and proteomic profile in parotid, submandibular, and sublingual salivary glands of rats, after chronic MeHg intoxication. Two groups of twenty male Wistar rats (90 days of age) were used on the experiment. MeHg group was intoxicated by intragastric gavage with MeHg at a dose of 0.04 mg/kg/day for 60 days, while the control group received only oil. After the period of intoxication, the glands were collected for evaluation of total mercury levels, proteomic profile, and oxidative balance by analyzing the antioxidant capacity against peroxyl radicals (ACAP), lipid peroxidation (LPO), and nitrite levels. Our results have showed that mercury levels were significant in all three glands compared to the respective control. It also showed lower levels of ACAP, as well as higher LPO and nitrite levels. The proteomic profile presented impairments on structural components of cytoskeleton, metabolic pathways, and oxidative biochemistry. Thus, the exposure to MeHg was able to generate oxidative stress that could be associated with changes in the proteomic profile of salivary glands

Fluoride exposure during pregnancy and lactation triggers oxidative stress and molecular changes in hippocampus of offspring rats

This work was supported by Pro-Reitoria ´ de Pesquisa da UFPA (PROPESP, UFPA, Brazil), Brazilian National Council for Scientific and Technological Development (CNPq, Grant n. 435093/2018-5) and Coordenaçao ˜ de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)- Finance Code 001.Federal University of Pará. Institute of Biological Sciences. Laboratory of Functional and Structural Biology. Belém, PA, Brazil.Federal University of Pará. Institute of Biological Sciences. Laboratory of Functional and Structural Biology. Belém, PA, Brazil.Federal University of Pará. Institute of Biological Sciences. Laboratory of Functional and Structural Biology. Belém, PA, Brazil.Federal University of Pará. Institute of Biological Sciences. Laboratory of Functional and Structural Biology. Belém, PA, Brazil.University of São Paulo. Bauru Dental School. Department of Biological Sciences. Bauru, SP, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Laboratório de Cultura Celular e Citogenética. Ananindeua, PA, Brasil.University of São Paulo. Bauru Dental School. Department of Biological Sciences. Bauru, SP, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Laboratório de Cultura Celular e Citogenética. Ananindeua, PA, Brasil.Federal University of Pará. Institute of Biological Sciences. Laboratory of Molecular Pharmacology. Belém, PA, Brazil.Federal University of Pará. Institute of Biological Sciences. Laboratory of Functional and Structural Biology. Belém, PA, Brazil.Long-term exposure to high concentrations of fluoride (F) can damage mineralized and soft tissues such as bones, liver, kidney, intestine, and nervous system of adult rats. The high permeability of the blood–brain barrier and placenta to F during pregnancy and lactation may be critical to neurological development. Therefore, this study aimed to investigate the effects of F exposure during pregnancy and lactation on molecular processes and oxidative biochemistry of offspring rats’ hippocampus. Pregnant Wistar rats were randomly assigned into 3 groups in accordance with the drinking water received: G1 – deionized water (control); G2 – 10 mg/L of F and G3 – 50 mg/L of F. The exposure to fluoridated water began on the first day of pregnancy and lasted until the 21st day of breastfeeding (when the offspring rats were weaned). Blood plasma samples of the offspring rats were collected to determine F levels. Hippocampi samples were collected for oxidative biochemistry analyses through antioxidant capacity against peroxyl (ACAP), lipid peroxidation (LPO), and nitrite (NO2 − ) levels. Also, brainderived neurotrophic factor (BDNF) gene expression (RT-qPCR) and proteomic profile analyses were performed. The results showed that exposure to both F concentrations during pregnancy and lactation increased the F bioavailability, triggered redox imbalance featured by a decrease of ACAP, increase of LPO and NO2 − levels, BDNF overexpression and changes in the hippocampus proteome. These findings raise novel questions regarding potential repercussions on the hippocampus structure and functioning in the different cognitive domains

Chronic methylmercury exposure causes spinal cord impairment: proteomic modulation and oxidative stress

Conselho Nacional de Desenvolvimento Científico e Tecnológico – Brasil (CNPq) and Coordenação de Aperfeiçoamento de Pessoal de Nível Superior Brasil (CAPES) - Finance Code 001; Universidade Federal do Pará (PROPESP, UFPA, Brazil)Federal University of Pará. Institute of Biological Sciences. Laboratory of Functional and Structural Biology. Belém, PA, Brazil.Federal University of Pará. Institute of Biological Sciences. Laboratory of Functional and Structural Biology. Belém, PA, Brazil.Federal University of Pará. Institute of Biological Sciences. Laboratory of Functional and Structural Biology. Belém, PA, Brazil.Federal University of Pará. Institute of Biological Sciences. Laboratory of Functional and Structural Biology. Belém, PA, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Ananindeua, PA, Brasil.Federal University of Pará. Institute of Biological Sciences. Laboratory of Functional and Structural Biology. Belém, PA, Brazil.University of São Paulo. Department of Biological Sciences. Bauru Dental School. Bauru, SP, Brazil.University of São Paulo. Department of Biological Sciences. Bauru Dental School. Bauru, SP, Brazil.Federal University of Pará. Laboratory of Molecular Pharmacology. Belém, PA, Brazil.Federal University of Pará. Institute of Biological Sciences. Laboratory of Functional and Structural Biology. Belém, PA, Brazil.Methylmercury (MeHg) is considered by the World Health Organization (WHO) as one of the chemicals of greatest public health concern. Although central nervous system (CNS) is the main target organ, the effects over the spinal cord are not well understood, especially in chronic exposure at similar doses to those faced by humans. This study aimed to investigate possible changes on global proteomic profile and oxidative biochemistry status of rats spinal cord, related to the maintenance and balance of the organism functioning, mimicking a human daily exposure by diet (chronic and with relatively low levels). For this, 28 adults male Wistar rats were divided into two groups: MeHg group, which was intoxicated by intragastric gavage with MeHg at a dose of 0.04 mg/kg/day for 60 days, and control group, that received only vehicle. After the exposure period, the spinal cords were collected for evaluation of total mercury levels, proteomic profile, with further bioinformatic overrepresentation analysis (ORA), and oxidative biochemistry, by analyzing the antioxidant capacity against peroxyl radicals (ACAP), lipid peroxidation (LPO), nitrite levels, measurement of Trolox Equivalent Antioxidant Capacity (TEAC) and Reduced Glutathione (GSH). The MeHg exposure increased total mercury levels in spinal cord parenchyma, which increased lipid peroxidation and nitrite levels, and reduced antioxidant status. The proteomic analysis showed several proteins related to biological processes, cellular components and molecular functions. Moreover, according to the ORA analysis, the proteins are involved in processes such as mitochondrial activity, stress response, cytoskeleton and apoptosis. Therefore, we concluded that exposure to low doses of MeHg can activate the oxidative stress pathway and thus, modulate the status of regulation of several important proteins

DNA damage and proteomic profile changes in rat salivary glands after chronic exposure to inorganic mercury

This study was financed in part by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior–Brasil (CAPES)–Financing Code 001.Federal University of Pará. Institute of Biological Sciences. Laboratory of Functional and Structural Biology. Belém, PA, Brazil.Federal University of Pará. Institute of Biological Sciences. Laboratory of Functional and Structural Biology. Belém, PA, Brazil.Federal University of Pará. Institute of Biological Sciences. Laboratory of Functional and Structural Biology. Belém, PA, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Ananindeua, PA, BrasilMinistério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Laboratório de Cultura Celular e Citogenética. Ananindeua, PA, BrasilUniversity of São Paulo. Bauru School of Dentistry. Department of Biological Sciences. Bauru, SP, BrazilUniversity of São Paulo. Bauru School of Dentistry. Department of Biological Sciences. Bauru, SP, BrazilMinistério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Laboratório de Cultura Celular e Citogenética. Ananindeua, PA, BrasilFederal University of Pará. Institute of Biological Sciences. Laboratory of Molecular Pharmacology. Belém, PA, BrazilFederal University of Pará. Institute of Biological Sciences. Laboratory of Functional and Structural Biology. Belém, PA, BrazilMercury (Hg) is a toxic metal that became a public health problem due to environmental contamination caused by anthropogenic activity. In this sense, oral homeostasis can undergo changes due to the toxic effects of metal on the salivary glands. Therefore, our objective was to investigate the proteomic and genotoxic changes in salivary glands after exposure to inorganic mercury (IHg). Forty Wistar rats that were divided into a control group, which received distilled water, and an exposed group, which received 0.375 mg/kg of mercury chloride for 45 days via orogastric gavage. After that, the animals were euthanized, and the parotid and submandibular glands were collected for analysis of the genotoxic effects, using the comet assay and proteome global profile assessment. The results showed that IHg promoted damage to cellular DNA associated with proteomic changes that showed events such as oxidative stress, mitochondrial dysfunction, changes in the cytoskeleton, and apoptosis. Therefore, these findings show a profile of molecular changes due to the interactions of IHg with several proteins and mechanisms inherent to the cell, which consequently may result in dysfunction of the salivary glands and impaired homeostasis of the oral cavity

Long-Term Lead Exposure Since Adolescence Causes Proteomic and Morphological Alterations in the Cerebellum Associated with Motor Deficits in Adult Rats

Lead (Pb) is an environmental contaminant that presents a high risk for human health. We aimed to investigate the possible alterations triggered by the exposure to Pb acetate for a long period in motor performance and the possible relationship with biochemical, proteomic and morphological alterations in the cerebellum of rats. Male Wistar rats were exposed for 55 days, at 50 mg/Kg of Pb acetate, and the control animals received distilled water. Open field (OF) and rotarod tests; biochemistry parameters (MDA and nitrite); staining/immunostaining of Purkinje cells (PC), mature neurons (MN), myelin sheath (MS) and synaptic vesicles (SYN) and proteomic profile were analyzed. Pb deposition on the cerebellum area and this study drove to exploratory and locomotion deficits and a decrease in the number of PC, MN, SYN and MS staining/immunostaining. The levels of MDA and nitrite remained unchanged. The proteomic profile showed alterations in proteins responsible for neurotransmitters release, as well as receptor function and second messengers signaling, and also proteins involved in the process of apoptosis. Thus, we conclude that the long-term exposure to low Pb dose promoted locomotion and histological tracings, associated with alterations in the process of cell signaling, as well as death by apoptosis

Deciphering the Global Proteomic Profile Involved in Methylmercury-Induced Cerebellar Neurodegeneration and Motor Dysfunction in Adult Rats

Mercury is a ubiquitous pollutant in the environment with potential neurotoxic effects. Several populations are susceptible to mercurial exposure, especially methylmercury (MeHg) at low doses for long periods through food consumption. Given this, the present work aimed to assess the effects of long-term MeHg exposure on the cerebellum of rats from a translational perspective using a representative dose, assessing molecular, biochemical, morphological, and behavioral parameters. The model was produced by administering 40 µg/kg of MeHg for 60 days to adult male Wistar rats by oral gavage. As a result of this exposure, the animals presented motor deficits in open field and rotarod tests which were associated with an increase in total mercury content in cerebellar parenchyma, a reduction in antioxidant competence against peroxyl radicals, and increased nitrite and lipid peroxidation levels. The proteomic approach showed 317 modulated proteins. Such findings were associated with reductions in mature neuron and Purkinje cell densities and glial fibrillary acidic protein immunostained areas and increased microglial density. In addition, decreases in myelin basic protein and synaptophysin immunostaining were also observed. The results thus provided new evidence of the mechanisms underlying complex MeHg-induced neurodegeneration, especially the proteins underlying the biochemical and morphological features associated with motor dysfunction