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1.
Environ Sci Pollut Res Int ; 31(35): 48423-48449, 2024 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-39031315

RESUMEN

The effectiveness of an aquaponic system significantly relies on the habitat provided for both the fish and plants. As an integral component of aquaponics, hydroponic cultivation benefits greatly from the controlled environment of a greenhouse. Within this environment, factors such as temperature, carbon dioxide levels, humidity, and light can be carefully adjusted to maximize plant growth and development. This precise regulation ensures an ideal growing environment, fostering the flourishing of plants and contributing to the overall success of the aquaponic ecosystem. This study presented a control approach for an aquaponic greenhouse system. It aims to keep the greenhouse climate parameters (temperature, CO2 concentration, and humidity) at their ideal levels. The proposed control strategy is a two-layered mechanism in which the first layer presents an optimization framework using particle swarm optimization (PSO) algorithm to give the setpoints for the controller, and the second layer demonstrates a constrained discrete model predictive control (CDMPC) strategy to maintain the desired trajectories received from the optimization layer. To validate the results obtained using PSO, this study incorporates genetic algorithms (GA) and assesses their performance in comparison. Given similar computational efficiency and low computational time for both algorithms, the optimal values identified by particle swarm optimization (PSO) are adopted as the setpoints. Two performance criteria, relative average deviation (RAD) and mean relative deviation (MRD), are derived to evaluate the tracking performance of the proposed CDMPC controller under external disturbances. A comparison of the proposed CDMPC with the PI controller is also offered. According to the comparison results, our proposed CDMPC performs better than the PI controller with lower RAD values (temperature, 1.1315; CO2 concentration, 0.9225; humidity, 2.547) and MRD values (temperature, 0.315; CO2 concentration, 0.25; humidity: 1.013). The controller is validated to be efficient by its strong control performance, highlighted by robustness, efficient setpoint tracking, and adequate disturbance rejection. This novel approach might prove to be a useful technique for developing environmental control strategies that can be used for potentially boosting production rates of aquaponic greenhouse systems, maximizing profitability, and reducing labor needs. By maintaining optimal conditions, it can enhance ecosystem health, improve yields, and streamline operations, paving the way for greater system performance and sustainability.


Asunto(s)
Dióxido de Carbono , Modelos Teóricos , Ecosistema , Algoritmos , Temperatura , Hidroponía/métodos
2.
PeerJ Comput Sci ; 9: e1216, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-37346544

RESUMEN

Automatic facial expression recognition (FER) plays a crucial role in human-computer based applications such as psychiatric treatment, classroom assessment, surveillance systems, and many others. However, automatic FER is challenging in real-time environment. The traditional methods used handcrafted methods for FER but mostly failed to produce superior results in the wild environment. In this regard, a deep learning-based FER approach with minimal parameters is proposed, which gives better results for lab-controlled and wild datasets. The method uses features boosting module with skip connections which help to focus on expression-specific features. The proposed approach is applied to FER-2013 (wild dataset), JAFFE (lab-controlled), and CK+ (lab-controlled) datasets which achieve accuracy of 70.21%, 96.16%, and 96.52%. The observed experimental results demonstrate that the proposed method outperforms the other related research concerning accuracy and time.

3.
J Mol Biol ; 434(12): 167618, 2022 06 30.
Artículo en Inglés | MEDLINE | ID: mdl-35500842

RESUMEN

The double-membrane-bound architecture of mitochondria, essential for ATP production, sub-divides the organelle into inter-membrane space (IMS) and matrix. IMS and matrix possess contrasting oxido-reductive environments and discrete protein quality control (PQC) machineries resulting inherent differences in their protein folding environments. To understand the nature of stress response elicited by equivalent proteotoxic stress to these sub-mitochondrial compartments, we took misfolding and aggregation-prone stressor proteins and fused it to well described signal sequences to specifically target and impart stress to yeast mitochondrial IMS or matrix. We show, mitochondrial proteotoxicity leads to growth arrest of yeast cells of varying degrees depending on nature of stressor proteins and the intra-mitochondrial location of stress. Next, by employing transcriptomics and proteomics, we report a comprehensive stress response elicited by stressor proteins specifically targeted to mitochondrial matrix or IMS. A general response to proteotoxic stress by mitochondria-targeted misfolded proteins is mitochondrial fragmentation, and an adaptive abrogation of mitochondrial respiration with concomitant upregulation of glycolysis. Beyond shared stress responses, specific signatures due to stress within mitochondrial sub-compartments are also revealed. We report that stress-imparted by bipartite signal sequence-fused stressor proteins to IMS, leads to specific upregulation of IMS-chaperones and TOM complex components. In contrast, matrix-targeted stressors lead to specific upregulation of matrix-chaperones and cytosolic PQC components. Finally, by systematic genetic interaction using deletion strains of differentially upregulated genes, we found prominent modulatory role of TOM complex components during IMS-stress response. In contrast, VMS1 markedly modulates the stress response originated from matrix.


Asunto(s)
Mitocondrias , Proteínas del Complejo de Importación de Proteínas Precursoras Mitocondriales , Chaperonas Moleculares , Proteínas de Saccharomyces cerevisiae , Saccharomyces cerevisiae , Estrés Fisiológico , Proteínas Portadoras/metabolismo , Mitocondrias/metabolismo , Membranas Mitocondriales/metabolismo , Proteínas del Complejo de Importación de Proteínas Precursoras Mitocondriales/metabolismo , Chaperonas Moleculares/metabolismo , Pliegue de Proteína , Saccharomyces cerevisiae/genética , Saccharomyces cerevisiae/metabolismo , Proteínas de Saccharomyces cerevisiae/genética , Proteínas de Saccharomyces cerevisiae/metabolismo
4.
Stat Med ; 41(14): 2542-2556, 2022 06 30.
Artículo en Inglés | MEDLINE | ID: mdl-35441378

RESUMEN

Cluster/group randomized controlled trials (CRTs) have a long history in the study of health sciences. CRT is a special type of intervention trial in which a complete group is randomly assigned to a study condition (or intervention). It is typically performed when individual randomization is difficult/impossible without substantial risk of contamination across study arms or prohibitive from the cost or group dynamics point of view. In this article, the aim is to design and analyze four-level longitudinal cluster randomized trials. The main interest here is to study the difference between treatment groups over time for such a four-level hierarchical data structure. This work is motivated by a real-life study for education based HIV prevention. Such trials are not only popular for administrative convenience, ethical considerations, subject compliance, but also help to reduce contamination bias. A random intercept mixed effects linear regression including a time by intervention interaction is used for modeling. Closed form expression of the power function to detect the interaction effect is determined. Sample size equations depend on correlation among schools but not on correlations among classes or students while, the power function depends on the product of number of units at different levels. Optimal allocation of units under a fixed cost by minimizing the expected standardized variance is also determined and are shown to be independent of correlations among units in any level. Results of detailed simulation studies find the theoretical power estimates based on the derived formulae close to the empirical estimates.


Asunto(s)
Proyectos de Investigación , Análisis por Conglomerados , Simulación por Computador , Humanos , Ensayos Clínicos Controlados Aleatorios como Asunto , Tamaño de la Muestra
5.
PeerJ Comput Sci ; 7: e453, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-33954237

RESUMEN

In this work, a novel fuzzy decision making technique namely trapezoidal fuzzy Best-Worst method (fuzzy BWM) is developed which is based on Best-Worst method (BWM) and Trapezoidal fuzzy number. The real motive behind our work is to take a broad view of the existing fuzzy BWM based on triangular fuzzy number by trapezoidal fuzzy number. Also, we have presented a new hybrid MCDM technique called as Trapezoidal fuzzy Best Worst Analytic Hierarchy based on proposed trapezoidal fuzzy BWM and existing trapezoidal fuzzy Analytic Hierarchy Process (AHP). BWM approach is employed in evaluating the PV of considering criteria and trapezoidal fuzzy AHP is used to assess the local priority vale (PV) of considering alternatives (or indicators) of a decision problem. Moreover it used to identify the most significant alternative which is responsible for performance efficiency of a hydro power plant under climatic scenario. From the result, it is undoubtedly found that hydraulic had is most responsible indicator. Further, the CR (consistency ratio) value which is determined by our proposed trapezoidal fuzzy BWM is less than that of existing BWM and fuzzy BWM techniques. Finally, we have validated our result by comparative study, scenario analysis and sensitivity analysis.

6.
Adv Exp Med Biol ; 1352: 125-147, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-35132598

RESUMEN

INTRODUCTION: The recent outbreak of coronavirus infection by SARS-CoV-2 that started from the Wuhan Province of China in 2019 has spread to most parts of the world infecting millions of people. Although the case fatality rate of SARS-CoV-2 infection is less than the previous epidemics by other closely related coronaviruses, due to its high infectivity, the total number of SARS-CoV-2 infection-associated disease, called Covid-19, is a matter of global concern. Despite drastic preventive measures, the number of Covid-19 cases are steadily increasing, and the future course of this pandemic is highly unpredictable. The most concerning fact about Covid-19 is the absence of specific and effective preventive or therapeutic agents against the disease. Finding an immediate intervention against Covid-19 is the need of the hour. In this chapter, we have discussed the role of different branches of the cellular proteostasis network, represented by Hsp70-Hsp40 chaperone system, Ubiquitin-Proteasome System (UPS), autophagy, and endoplasmic reticulum-Unfolded Protein Response (ER-UPR) pathway in the pathogenesis of coronavirus infections and in the host antiviral defense mechanisms. RESULTS: Based on scientific literature, we present that pharmacological manipulation of proteostasis network can alter the fate of coronavirus infections and may help to prevent the resulting pathologies like Covid-19.


Asunto(s)
COVID-19 , Humanos , Pandemias , Proteostasis , SARS-CoV-2 , Respuesta de Proteína Desplegada
7.
Mitochondrion ; 57: 37-46, 2021 03.
Artículo en Inglés | MEDLINE | ID: mdl-33340711

RESUMEN

BACKGROUND: Biogenesis and function of mitochondria is profoundly dependent on cytosolic translation of mitochondrial pre-proteins and its subsequent translocation and folding inside the organelle. Continuous exposure of non-native precursor proteins, exposure to damaging by-products of oxidative phosphorylation, load of mis-targeted or misfolded proteins from neighbouring compartments and unremitting demand of communication between mitochondrial and nuclear genomes, continuously pose proteotoxic threats to the organelle. Our knowledge of cellular mechanisms to cope up with such impending threat of proteotoxicity to mitochondria, is currently evolving. In recent years, several unique response and survival pathways have been discovered shedding light on cellular strategies to cope with stressed and dysfunctional mitochondria. As mitochondria compulsorily communicate with nucleus, cytosol and endoplasmic reticulum (ER) for its own biogenesis and function and in turn maintain critical cellular processes for survival, any impairment in communication by stressed or dysfunctional mitochondria may end up with fatal consequences. DISCUSSION AND IMPLICATION: In this review, we have discussed about possible sources of mitochondrial proteotoxicity and the recent developments regarding cellular strategies to counter such stress to overcome dysfunctions of the organelle. Mitochondrial communication with neighbouring subcellular compartments like ER and cytosol during proteotoxic stress have been explored. In the context of mitochondrial proteotoxicity, alterations of crucial inter-organelle connections like ER-mitochondria contact sites and its implication on mitochondrial signaling activity like Ca2+ signaling have been dissected. Furthermore, an overview of pathological conditions, mainly neurodegenerative disorders that are known to be associated with mitochondrial proteotoxicity and Ca2+ dysregulation has been presented.


Asunto(s)
Mitocondrias/metabolismo , Proteínas Mitocondriales/química , Proteínas Mitocondriales/metabolismo , Animales , Señalización del Calcio , Retículo Endoplásmico/metabolismo , Humanos , Fosforilación Oxidativa , Pliegue de Proteína , Transporte de Proteínas
8.
Traffic ; 20(12): 943-960, 2019 12.
Artículo en Inglés | MEDLINE | ID: mdl-31472037

RESUMEN

Presence of cytosolic protein aggregates and membrane damage are two common attributes of neurodegenerative diseases. These aggregates delay degradation of non-translocated protein precursors leading to their persistence and accumulation in the cytosol. Here, we find that cells with intracellular protein aggregates (of cytosolic prion protein or huntingtin) destabilize the endoplasmic reticulum (ER) morphology and dynamics when non-translocated protein load is high. This affects trafficking of proteins out from the ER, relative distribution of the rough and smooth ER and three-way junctions that are essential for the structural integrity of the membrane network. The changes in ER membranes may be due to high aggregation tendency of the ER structural proteins-reticulons, and altered distribution of those associated with the three-way ER junctions-Lunapark. Reticulon4 is seen to be enriched in the aggregate fractions in presence of non-translocated protein precursors. This could be mitigated by improving signal sequence efficiencies of the proteins targeted to the ER. These were observed using PrP variants and the seven-pass transmembrane protein (CRFR1) with different signal sequences that led to diverse translocation efficiencies. This identifies a previously unappreciated consequence of cytosolic aggregates on non-translocated precursor proteins-their persistent presence affects ER morphology and dynamics. This may be one of the ways in which cytosolic aggregates can affect endomembranes during neurodegenerative disease.


Asunto(s)
Retículo Endoplásmico/metabolismo , Agregado de Proteínas , Retículo Endoplásmico/ultraestructura , Aparato de Golgi/metabolismo , Células HeLa , Humanos , Proteínas de la Membrana/metabolismo , Proteínas Nogo/metabolismo , Proteínas Priónicas/química , Proteínas Priónicas/metabolismo , Unión Proteica , Precursores de Proteínas/química , Precursores de Proteínas/metabolismo , Señales de Clasificación de Proteína , Transporte de Proteínas , Receptores de Hormona Liberadora de Corticotropina/química , Receptores de Hormona Liberadora de Corticotropina/metabolismo
9.
Mol Neurobiol ; 55(3): 2631-2644, 2018 03.
Artículo en Inglés | MEDLINE | ID: mdl-28421536

RESUMEN

Prion diseases are transmissible, familial or sporadic. The prion protein (PrP), a normal cell surface glycoprotein, is ubiquitously expressed throughout the body. While loss of function of PrP does not elicit apparent phenotypes, generation of misfolded forms of the protein or its aberrant metabolic isoforms has been implicated in a number of neurodegenerative disorders such as scrapie, kuru, Creutzfeldt-Jakob disease, fatal familial insomnia, Gerstmann-Sträussler-Scheinker and bovine spongiform encephalopathy. These diseases are all phenotypically characterised by spongiform vacuolation of the adult brain, hence collectively termed as late-onset spongiform neurodegeneration. Misfolded form of PrP (PrPSc) and one of its abnormal metabolic isoforms (the transmembrane CtmPrP) are known to be disease-causing agents that lead to progressive loss of structure or function of neurons culminating in neuronal death. The aberrant forms of PrP utilise and manipulate the various intracellular quality control mechanisms during pathogenesis of these diseases. Amongst these, the lysosomal quality control machinery emerges as one of the primary targets exploited by the disease-causing isoforms of PrP. The autophagosomal-lysosomal degradation pathway is adversely affected in multiple ways in prion diseases and may hence be regarded as an important modulator of neurodegeneration. Some of the ESCRT pathway proteins have also been shown to be involved in the manifestation of disease phenotype. This review discusses the significance of the lysosomal quality control pathway in affecting transmissible and familial types of prion diseases.


Asunto(s)
Lisosomas/metabolismo , Enfermedades por Prión/metabolismo , Priones/metabolismo , Animales , Encéfalo/metabolismo , Encéfalo/patología , Humanos , Lisosomas/genética , Lisosomas/patología , Enfermedades por Prión/genética , Enfermedades por Prión/patología , Priones/genética , Control de Calidad , Transducción de Señal/fisiología
10.
Traffic ; 18(12): 791-807, 2017 12.
Artículo en Inglés | MEDLINE | ID: mdl-28902452

RESUMEN

MGRN1-mediated ubiquitination of α-tubulin regulates microtubule stability and mitotic spindle positioning in mitotic cells. This study elucidates the effect of MGRN1-mediated ubiquitination of α-tubulin in interphase cells. Here, we show that MGRN1-mediated ubiquitination regulates dynamics of EB1-labeled plus ends of microtubules. Intracellular transport of mitochondria and endosomes are affected in cultured cells where functional MGRN1 is depleted. Defects in microtubule-dependent organellar transport are evident in cells where noncanonical K6-mediated ubiquitination of α-tubulin by MGRN1 is compromised. Loss of MGRN1 has been previously correlated with late-onset spongiform neurodegeneration. Mislocalised cytosolically exposed PrP (Ctm PrP) interacts with MGRN1 leading to its loss of function. Expression of Ctm PrP generating mutants of PrP[PrP(A117V) and PrP(KHII)] lead to decrease in MGRN1-mediated ubiquitination of α-tubulin and intracellular transport defects. Brain lysates from PrP(A117V) transgenic mice also indicate loss of tubulin polymerization as compared to non-transgenic controls. Depletion of MGRN1 activity may hamper physiologically important processes like mitochondrial movement in neuronal processes and intracellular transport of ligands through the endosomal pathway thereby contributing to the pathogenesis of neurodegeneration in certain types of prion diseases.


Asunto(s)
Transporte Biológico/fisiología , Tubulina (Proteína)/metabolismo , Ubiquitina-Proteína Ligasas/metabolismo , Ubiquitinación/fisiología , Proteínas de Unión al ADN/metabolismo , Complejos de Clasificación Endosomal Requeridos para el Transporte/metabolismo , Células HeLa , Humanos , Microtúbulos/metabolismo , Mitocondrias/metabolismo , Ubiquitina-Proteína Ligasas/genética
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