Autonomous video compression system for environmental monitoring

[EN] The monitoring of natural environments is becoming a very controversial topic because people are more and more concerned about preserving and monitoring these natural spaces. The monitoring tasks are usually complemented with a network infrastructure composed by cameras and network devices that make easy the remote visualization of the monitored environments. This work presents the design, implementation and test of an autonomous video compression system for environmental monitoring. The system is based on a server in charge of collecting the videos and analyzing the network constraints. As a function of the measured parameters and the predominant color of the requested video, the system determines the best compression codec for transmitting the video through the network. Additionally, the server should run an algorithm developed in Python and MATLAB(c) in charge of analyzing the RED-GREEN-BLUE (RGB) components of the video and performing the transcoding tasks. The system has been tested with different videos and the results of Quality of Service (QoS) and Quality of Experience (QoE) shows that H264 is a good option when the predominant color of videos are black or white while XVID is one the codecs that offer interesting results when colors as red, green or blue are predominant in the video.This work has been supported by the Programa para la Formación de Personal Investigador (FPI-2015-S2-884) by the Universitat Politecnica de Valencia . The research leading to these results has received funding from la Caixa Foundation and Triptolemos FoundationMateos-Cañas, I.; Sendra, S.; Lloret, J.; Jimenez, JM. (2017). Autonomous video compression system for environmental monitoring. Network Protocols and Algorithms. 9(1-2):48-70. https://doi.org/10.5296/npa.v9i1-2.12386S487091-

Immune response after experimental allergic encephalomyelitis in rats subjected to calorie restriction

Male Lewis rats (6 weeks-old) were submitted to a calorie restriction equivalent to 33% or 66% of food restriction. Fifteen days later, groups of 7 animals were injected with complete Freund's adjuvant plus spinal cord homogenate (SCH) to induce experimental allergic encephalomyelitis (EAE) or with complete Freund's adjuvant alone. EAE was defined solely on clinical grounds. Rats were assessed daily for clinical signs of EAE and were killed on day 15 after immunization. Both diet and SCH injection diminished body weight significantly. In contrast to rats receiving a normal diet or a 33% calorie-restricted diet, rats subjected to severe calorie restriction did not exhibit clinical signs of EAE. Concomitantly with the lack of disease manifestation, 66% of calorie-restricted rats injected with SCH showed significantly less splenic and lymph node mitogenic response to concanavalin A (Con A) and a higher splenic response to lipopolysaccharide. Fewer splenic, lymph node and thymic CD4(+ )cells, greater numbers of splenic and lymph node CD8(+ )and CD4(+)- CD8(+ )cells, and fewer splenic T, B and T-B cells, and lymph node and thymic B and T-B cells were observed. There was impaired interferon (IFN)-γ production occurred in the three examined tissues. The results are compatible with the view that the acute phase of EAE can be curtailed by severe calorie restriction, presumably through impaired IFN-γ production

De-repression of myelin-regulating gene expression after status epilepticus in mice lacking the C/EBP homologous protein CHOP.

The C/EBP homologous protein CHOP is normally present at low levels in cells but increases rapidly after insults such as DNA damage or endoplasmatic reticulum stress where it contributes to cellular homeostasis and apoptosis. By forming heterodimers with other transcription factors, CHOP can either act as a dominant-negative regulator of gene expression or to induce the expression of target genes. Recent work demonstrated that seizure-induced hippocampal damage is significantly worse in mice lacking CHOP and these animals go on to develop an aggravated epileptic phenotype. To identify novel CHOP-controlled target genes which potentially influence the epileptic phenotype, we performed a bioinformatics analysis of tissue microarrays from chop-deficient mice after prolonged seizures. GO analysis revealed genes associated with biological membranes were prominent among those in the chop-deficient array dataset and we identified myelin-associated genes to be particularly de-repressed. These data suggest CHOP might act as an inhibitor of myelin-associated processes in the brain and could be targeted to influence axonal regeneration or reorganisation

Ultrasonography Assessment Based on Muscle Thickness and Echo Intensity in Post-Polio Patients

There is no specific designed diagnostic test for post-poliomyelitis syndrome. The most important symptoms of this syndrome are new loss of muscle strength and more fatigue. Previous studies have investigated muscle ultrasound parameters to distinguish neuromuscular disease patients from healthy controls. The aim of this study was to investigate if muscle thickness and echo intensity measured by ultrasound can discriminate post-poliomyelitis syndrome patients from healthy controls. A total of 29 post-polio patients and 27 healthy controls participated in this cross-sectional study. Anthropometric measures, muscle thickness, echo intensity using B-mode ultrasound in rectus femoris and biceps brachii muscles, and muscle strength test data were collected. Muscle thickness in rectus femoris was significantly lower in post-poliomyelitis patients than in healthy controls, but not in biceps brachii. Echo intensity in rectus femoris and biceps brachii was higher in post-poliomyelitis syndrome patients than in healthy controls. Correlations were found between muscle thickness and strength in the upper and lower limbs. The results of the present study showed that muscle thickness in rectus femoris and echo intensity in rectus femoris and biceps brachii can discriminate post-poliomyelitis syndrome patients from healthy controls. A better assessment is possible because it can observe differences and relevant parameters in this clinical populationThe study has been co-funded under the OTRI research contract nº 806/87.5076 between the Universidad de Málaga and the Asociación Malagueña de Afectados Polio y Postpolio (AMAPyP). Partial funding for open access charge: Universidad de Málag

Transgenic overexpression of 14-3-3 zeta protects hippocampus against endoplasmic reticulum stress and status epilepticus in vivo.

14-3-3 proteins are ubiquitous molecular chaperones that are abundantly expressed in the brain where they regulate cell functions including metabolism, the cell cycle and apoptosis. Brain levels of several 14-3-3 isoforms are altered in diseases of the nervous system, including epilepsy. The 14-3-3 zeta (ζ) isoform has been linked to endoplasmic reticulum (ER) function in neurons, with reduced levels provoking ER stress and increasing vulnerability to excitotoxic injury. Here we report that transgenic overexpression of 14-3-3ζ in mice results in selective changes to the unfolded protein response pathway in the hippocampus, including down-regulation of glucose-regulated proteins 78 and 94, activating transcription factors 4 and 6, and Xbp1 splicing. No differences were found between wild-type mice and transgenic mice for levels of other 14-3-3 isoforms or various other 14-3-3 binding proteins. 14-3-3ζ overexpressing mice were potently protected against cell death caused by intracerebroventricular injection of the ER stressor tunicamycin. 14-3-3ζ overexpressing mice were also potently protected against neuronal death caused by prolonged seizures. These studies demonstrate that increased 14-3-3ζ levels protect against ER stress and seizure-damage despite down-regulation of the unfolded protein response. Delivery of 14-3-3ζ may protect against pathologic changes resulting from prolonged or repeated seizures or where injuries provoke ER stress

Virtual Laboratory Methodologies in Electrical Engineering

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