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1.
J Healthc Eng ; 2021: 9937904, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-34804462

RESUMEN

With the advancement in imaging technology, many commercial systems have been developed for performing motion analysis in mice. However, available commercial systems are expensive and use proprietary software. In this paper, we describe a low-cost, camera-based design of an autonomous gait acquisition and analysis system for inspecting gait deficits in C57BL/6 mice. Our system includes video acquisition, autonomous gait-event detection, gait-parameter extraction, and result visualization. We provide a simple, user-friendly, step-by-step detailed methodology to apply well-known image processing techniques for detecting mice footfalls and calculating various gait parameters for analyzing gait abnormalities in healthy and neurotraumatic mice. The system was used in a live animal study for assessing recovery in a mouse model of Parkinson's disease. Using the videos acquired in the study, we validate the performance of our system with receiver operating characteristic (ROC) and Hit : Miss : False (H : M : F) detection analyses. Our system correctly detected the mice footfalls with an average H : M : F score of 92.1 : 2.3 : 5.6. The values for the area under an ROC curve for all the ROC plots are above 0.95, which indicates an almost perfect detection model. The ROC and H : M : F analyses show that our system produces accurate gait detection. The results observed from the gait assessment study are in agreement with the known literature. This demonstrates the practical viability of our system as a gait analysis tool.


Asunto(s)
Análisis de la Marcha , Marcha , Animales , Análisis de la Marcha/métodos , Humanos , Procesamiento de Imagen Asistido por Computador , Ratones , Ratones Endogámicos C57BL , Programas Informáticos
2.
Sensors (Basel) ; 21(7)2021 Apr 05.
Artículo en Inglés | MEDLINE | ID: mdl-33916439

RESUMEN

In this paper, we explore the performance of the distance-weighting probabilistic data association (DWPDA) approach in conjunction with the loopy sum-product algorithm (LSPA) for tracking multiple objects in clutter. First, we discuss the problem of data association (DA), which is to infer the correspondence between targets and measurements. DA plays an important role when tracking multiple targets using measurements of uncertain origin. Second, we describe three methods of data association: probabilistic data association (PDA), joint probabilistic data association (JPDA), and LSPA. We then apply these three DA methods for tracking multiple crossing targets in cluttered environments, e.g., radar detection with false alarms and missed detections. We are interested in two performance metrics: tracking accuracy and computation time. LSPA is known to be superior to PDA in terms of the former and to dominate JPDA in terms of the latter. Last, we consider an additional DA method that is a modification of PDA by incorporating a weighting scheme based on distances between position estimates and measurements. This distance-weighting approach, when combined with PDA, has been shown to enhance the tracking accuracy of PDA without significant change in the computation burden. Since PDA constitutes a crucial building block of LSPA, we hypothesize that DWPDA, when integrated with LSPA, would perform better under the two performance metrics above. Contrary to expectations, the distance-weighting approach does not enhance the performance of LSPA, whether in terms of tracking accuracy or computation time.

3.
Toxicol Sci ; 177(2): 506-520, 2020 10 01.
Artículo en Inglés | MEDLINE | ID: mdl-32692843

RESUMEN

Chronic exposure to manganese (Mn) is associated with neuroinflammation and extrapyramidal motor deficits resembling features of Parkinson's disease. Activation of astrocytes and microglia is implicated in neuronal injury from Mn but it is not known whether early life exposure to Mn may predispose glia to more severe inflammatory responses during aging. We therefore examined astrocyte nuclear factor kappa B (NF-κB) signaling in mediating innate immune inflammatory responses during multiple neurotoxic exposures spanning juvenile development into adulthood. MnCl2 was given in drinking water for 30-day postweaning to both wildtype mice and astrocyte-specific knockout (KO) mice lacking I kappa B kinase 2, the central upstream activator of NF-κB. Following juvenile exposure to Mn, mice were subsequently administered 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) at 4 months of age. Animals were evaluated for behavioral alterations and brain tissue was analyzed for catecholamine neurotransmitters. Stereological analysis of neuronal and glial cell counts from multiple brain regions indicated that juvenile exposure to Mn amplified glial activation and neuronal loss from MPTP exposure in the caudate-putamen and globus pallidus, as well as increased the severity of neurobehavioral deficits in open field activity assays. These alterations were prevented in astrocyte-specific I kappa B kinase 2 KO mice. Juvenile exposure to Mn increased the number of neurotoxic A1 astrocytes expressing C3 as well as the number of activated microglia in adult mice following MPTP challenge, both of which were inhibited in KO mice. These results demonstrate that exposure to Mn during juvenile development heightens the innate immune inflammatory response in glia during a subsequent neurotoxic challenge through NF-κB signaling in astrocytes.


Asunto(s)
1-Metil-4-fenil-1,2,3,6-Tetrahidropiridina , Astrocitos , Encefalitis , Animales , Astrocitos/efectos de los fármacos , Manganeso/toxicidad , Ratones , Ratones Endogámicos C57BL , FN-kappa B/metabolismo
4.
J Pharmacol Exp Ther ; 365(3): 636-651, 2018 06.
Artículo en Inglés | MEDLINE | ID: mdl-29626009

RESUMEN

The orphan nuclear receptor Nurr1 (also called nuclear receptor-4A2) regulates inflammatory gene expression in glial cells, as well as genes associated with homeostatic and trophic function in dopaminergic neurons. Despite these known functions of Nurr1, an endogenous ligand has not been discovered. We postulated that the activation of Nurr1 would suppress the activation of glia and thereby protect against loss of dopamine (DA) neurons after subacute lesioning with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Our previous studies have shown that a synthetic Nurr1 ligand, 1,1-bis(3'-indolyl)-1-(p-chlorophenyl)methane (C-DIM12), suppresses inflammatory gene expression in primary astrocytes and induces a dopaminergic phenotype in neurons. Pharmacokinetic analysis of C-DIM12 in mice by liquid chromatography-mass spectrometry demonstrated that approximately three times more compound concentrated in the brain than in plasma. Mice treated with four doses of MPTP + probenecid over 14 days were monitored for neurobehavioral function, loss of dopaminergic neurons, and glial activation. C-DIM12 protected against the loss of DA neurons in the substantia nigra pars compacta and DA terminals in the striatum, maintained a ramified phenotype in microglia, and suppressed activation of astrocytes. In vitro reporter assays demonstrated that C-DIM12 was an effective activator of Nurr1 transcription in neuronal cell lines. Computational modeling of C-DIM12 binding to the three-dimensional structure of human Nurr1 identified a high-affinity binding interaction with Nurr1 at the coactivator domain. Taken together, these data suggest that C-DIM12 is an activator of Nurr1 that suppresses glial activation and neuronal loss in vivo after treatment with MPTP, and that this receptor could be an efficacious target for disease modification in individuals with Parkinson's disease and related disorders.


Asunto(s)
1-Metil-4-fenil-1,2,3,6-Tetrahidropiridina/farmacología , Indoles/metabolismo , Indoles/farmacología , Neuroglía/efectos de los fármacos , Miembro 2 del Grupo A de la Subfamilia 4 de Receptores Nucleares/metabolismo , Trastornos Parkinsonianos/inducido químicamente , Trastornos Parkinsonianos/tratamiento farmacológico , Transporte Activo de Núcleo Celular/efectos de los fármacos , Animales , Encéfalo/efectos de los fármacos , Encéfalo/metabolismo , Encéfalo/patología , Recuento de Células , Núcleo Celular/efectos de los fármacos , Núcleo Celular/metabolismo , Neuronas Dopaminérgicas/efectos de los fármacos , Neuronas Dopaminérgicas/metabolismo , Neuronas Dopaminérgicas/patología , Regulación de la Expresión Génica/efectos de los fármacos , Indoles/farmacocinética , Indoles/uso terapéutico , Ligandos , Masculino , Ratones , Ratones Endogámicos C57BL , FN-kappa B/metabolismo , Neuroglía/patología , Fármacos Neuroprotectores/metabolismo , Fármacos Neuroprotectores/farmacocinética , Fármacos Neuroprotectores/farmacología , Fármacos Neuroprotectores/uso terapéutico , Trastornos Parkinsonianos/metabolismo , Trastornos Parkinsonianos/patología , Fenotipo , Transducción de Señal/efectos de los fármacos , Distribución Tisular
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