Efecto de un programa lúdico de actividad física general de corta duración y moderada intensidad sobre las cifras de presión arterial y otros factores de riesgo cardiovascular en hipertensos mayores de 50 años / Effects of a recreational general physical activity program with short term and moderate intensity of blood pressure and other cardiovascular risk factors in hypertensive patients over 50 years old

Objetivo: Evaluar los efectos de un programa recreativo de actividad física general, de intensidad moderada y corta duración, sobre las cifras de hipertensión arterial y otros factores de riesgo cardiovascular (FRCV) en hipertensos mayores de 50 años. Diseño: Estudio cuasi-experimental no aleatorizado con diseño pre-post. Emplazamiento: Íllora (Granada). Participantes: Sesenta sujetos sedentarios de 50-75 años pertenecientes al programa de hipertensos del Centro de Salud. Intervención: Programa lúdico de actividad física general donde predomina la capacidad aeróbica, 3días/semana, durante 4 semanas, y una intensidad del 45-55% de la FC Reserva. Mediciones principales: PAS, PAD, FC, IMC, colesterol total, HDL, LDL, TG y glucosa. Resultados y conclusiones: Disminuciones estadísticamente significativas (p < 0,05) en el IMC (-0,51%; IC95%: 30,26-31,93 unid), la FC (-5,57 lat/min; IC95%: 68,76-71,73 lat/min), la PAS (-14,82 mmHg; IC95%: 131,57-137,52 mmHg), la PAD (-5,33 mmHg; IC95%: 78,94-83,68 mmHg), la glucosa (-7,63 mg/dl; IC95%: 125,06-153,73 mg/dl) y el riesgo REGICOR (-20,46%; IC95%: 5,45-6,90%). Aumentos estadísticamente significativos en el HDL (+2,82mg/dl; IC95%: 46,78-52,11 mg/dl) y los TG (+8,27 mg/dl; IC95% 133,89-152,60 mg/dl). Según el sexo, los hombres presentaron la mayor variación en la FC y la PAD, y las mujeres en la PAS (p < 0,05). Sujetos con valores iniciales de PAS≥160mmHg experimentaron mayores descensos de FC, PAS, PAD, glucosa y TG (-(-10,67lat/min, -31mmHg, -8,27mmHg, -10,86mg/dl y 34,66mg/dl, respectivamente) que aquellos con PAS inicial < 160 mmHg, donde aumentó el HDL y disminuyó el LDL. Tras este programa se obtuvieron mejoras en la presión arterial y otros FRCV en sujetos hipertensos mayores de 50 años (AU)

Objectives: To evaluate the effects of a recreational general physical activity program with moderate intensity and short duration on blood pressure and other cardiovascular risk factors (BMI, cholesterol, Rest Heart Rate, HDL, LDL, Triglycerides) in hypertensive patients older than 50 years. Design: Non-randomised pre-post design, quasi-experimental study. Location: Íllora, Granada, Spain. Participants: A total of 60 subjects aged 50-75 years taking part in the Health Hypertensive Program in the Medical Centre were selected. Intervention: A recreational general physical activity program, mainly aerobic capacity, of 4weeks duration, 3days/week, and an intensity of 45-55% HR Reserve. Main measurements: SBP, DBP, HR, BMI, total cholesterol, HDL, LDL, TG, and Glucose. Results and conclusions: Statistically significant decreases (P < .05) were observed in BMI (-0.51%; 95%CI: 30.26 to 31.93 units), HR (-5.57 beats/min; 95% CI: 68.76 to 71.73 beats/min), SBP (-14.82 mmHg; 95%CI: 131.57 to 137.52 mmHg), DBP (-5.33 mmHg; 95%CI: 78.94 to 83.68 mmHg), Glucose (-7.63 mg/dL; 95%CI: 125.06 to 153.73 mg/dL) and REGICOR risk (-20.46%; 95%CI: 5.45 to 6.90%). Statistically significant increases were observed in HDL (+2.82 mg/dl; 95%CI: 46.78 to 52.11 mmHg), and TG (+8.27 mg/dl; 95%CI: 133.89 to 152.60 mg/dL). Men had a wider variation in HR and DBP, and women in SBP (P<.05). Subjects with baseline SBP≥160 mmHg experienced greater declines in HR, SBP, DBP, Glucose and TG (-10.67 beats/min, -31 mmHg, -8.27 mmHg, -10.86mg/dL, and 34.66mg/dL, respectively) than those with an initial SBP<160 mmHg, where there was an increase in HDL and a decrease in LDL. After this program, improvements in BP and other cardiovascular risk factors were obtained in hypertensive subjects over 50 years (AU)

[Effects of a recreational general physical activity program with short term and moderate intensity of blood pressure and other cardiovascular risk factors in hypertensive patients over 50 years old]. / Efecto de un programa lúdico de actividad física general de corta duración y moderada intensidad sobre las cifras de presión arterial y otros factores de riesgo cardiovascular en hipertensos mayores de 50 años.

OBJECTIVES: To evaluate the effects of a recreational general physical activity program with moderate intensity and short duration on blood pressure and other cardiovascular risk factors (BMI, cholesterol, Rest Heart Rate, HDL, LDL, Triglycerides) in hypertensive patients older than 50years. DESIGN: Non-randomised pre-post design, quasi-experimental study. LOCATION: Íllora, Granada, Spain. PARTICIPANTS: A total of 60 subjects aged 50-75years taking part in the Health Hypertensive Program in the Medical Centre were selected. INTERVENTION: A recreational general physical activity program, mainly aerobic capacity, of 4weeks duration, 3days/week, and an intensity of 45-55% HR Reserve. MAIN MEASUREMENTS: SBP, DBP, HR, BMI, total cholesterol, HDL, LDL, TG, and Glucose. RESULTS AND CONCLUSIONS: Statistically significant decreases (P<.05) were observed in BMI (-0.51%; 95%CI: 30.26 to 31.93units), HR (-5.57beats/min; 95%CI: 68.76 to 71.73beats/min), SBP (-14.82mmHg; 95%CI: 131.57 to 137.52mmHg), DBP (-5.33mmHg; 95%CI: 78.94 to 83.68mmHg), Glucose (-7.63mg/dL; 95%CI: 125.06 to 153.73mg/dL) and REGICOR risk (-20.46%; 95%CI: 5.45 to 6.90%). Statistically significant increases were observed in HDL (+2.82mg/dl; 95%CI: 46.78 to 52.11mmHg), and TG (+8.27mg/dl; 95%CI: 133.89 to 152.60mg/dL). Men had a wider variation in HR and DBP, and women in SBP (P<.05). Subjects with baseline SBP≥160mmHg experienced greater declines in HR, SBP, DBP, Glucose and TG (-10.67beats/min, -31mmHg, -8.27mmHg, -10.86mg/dL, and 34.66mg/dL, respectively) than those with an initial SBP<160mmHg, where there was an increase in HDL and a decrease in LDL. After this program, improvements in BP and other cardiovascular risk factors were obtained in hypertensive subjects over 50years.

Background subtraction based on color and depth using active sensors.

Depth information has been used in computer vision for a wide variety of tasks. Since active range sensors are currently available at low cost, high-quality depth maps can be used as relevant input for many applications. Background subtraction and video segmentation algorithms can be improved by fusing depth and color inputs, which are complementary and allow one to solve many classic color segmentation issues. In this paper, we describe one fusion method to combine color and depth based on an advanced color-based algorithm. This technique has been evaluated by means of a complete dataset recorded with Microsoft Kinect, which enables comparison with the original method. The proposed method outperforms the others in almost every test, showing more robustness to illumination changes, shadows, reflections and camouflage.

A novel dominant hyperekplexia mutation Y705C alters trafficking and biochemical properties of the presynaptic glycine transporter GlyT2.

Hyperekplexia or startle disease is characterized by an exaggerated startle response, evoked by tactile or auditory stimuli, producing hypertonia and apnea episodes. Although rare, this orphan disorder can have serious consequences, including sudden infant death. Dominant and recessive mutations in the human glycine receptor (GlyR) α1 gene (GLRA1) are the major cause of this disorder. However, recessive mutations in the presynaptic Na(+)/Cl(-)-dependent glycine transporter GlyT2 gene (SLC6A5) are rapidly emerging as a second major cause of startle disease. In this study, systematic DNA sequencing of SLC6A5 revealed a new dominant GlyT2 mutation: pY705C (c.2114A→G) in transmembrane domain 11, in eight individuals from Spain and the United Kingdom. Curiously, individuals harboring this mutation show significant variation in clinical presentation. In addition to classical hyperekplexia symptoms, some individuals had abnormal respiration, facial dysmorphism, delayed motor development, or intellectual disability. We functionally characterized this mutation using molecular modeling, electrophysiology, [(3)H]glycine transport, cell surface expression, and cysteine labeling assays. We found that the introduced cysteine interacts with the cysteine pair Cys-311-Cys-320 in the second external loop of GlyT2. This interaction impairs transporter maturation through the secretory pathway, reduces surface expression, and inhibits transport function. Additionally, Y705C presents altered H(+) and Zn(2+) dependence of glycine transport that may affect the function of glycinergic neurotransmission in vivo.

Protein kinase C (PKC)-promoted endocytosis of glutamate transporter GLT-1 requires ubiquitin ligase Nedd4-2-dependent ubiquitination but not phosphorylation.

Glutamate transporter-1 (GLT-1) is the main glutamate transporter in the central nervous system, and its concentration severely decreases in neurodegenerative diseases. The number of transporters in the plasma membrane reflects the balance between their insertion and removal, and it has been reported that the regulated endocytosis of GLT-1 depends on its ubiquitination triggered by protein kinase C (PKC) activation. Here, we identified serine 520 of GLT-1 as the primary target for PKC-dependent phosphorylation, although elimination of this serine did not impair either GLT-1 ubiquitination or endocytosis in response to phorbol esters. In fact, we present evidence indicating that the ubiquitin ligase Nedd4-2 mediates the PKC-dependent ubiquitination and down-regulation of GLT-1. Overexpression of Nedd4-2 increased the ubiquitination of the transporter and promoted its degradation. Moreover, phorbol myristate acetate enhanced Nedd4-2 phosphorylation and the formation of GLT-1·Nedd4-2 complexes, whereas siRNA knockdown of Nedd4-2 prevented ubiquitination, endocytosis, and the concomitant decrease in GLT-1 activity triggered by PKC activation. These results indicate that GLT-1 endocytosis is independent of its phosphorylation and that Nedd4-2 mediates PKC-dependent down-regulation of the transporter.

FPGA implementation for real-time background subtraction based on Horprasert model.

Background subtraction is considered the first processing stage in video surveillance systems, and consists of determining objects in movement in a scene captured by a static camera. It is an intensive task with a high computational cost. This work proposes an embedded novel architecture on FPGA which is able to extract the background on resource-limited environments and offers low degradation (produced because of the hardware-friendly model modification). In addition, the original model is extended in order to detect shadows and improve the quality of the segmentation of the moving objects. We have analyzed the resource consumption and performance in Spartan3 Xilinx FPGAs and compared to others works available on the literature, showing that the current architecture is a good trade-off in terms of accuracy, performance and resources utilization. With less than a 65% of the resources utilization of a XC3SD3400 Spartan-3A low-cost family FPGA, the system achieves a frequency of 66.5 MHz reaching 32.8 fps with resolution 1,024 × 1,024 pixels, and an estimated power consumption of 5.76 W.

Intraperiaqueductal gray glycine and D-serine exert dual effects on rostral ventromedial medulla ON- and OFF-cell activity and thermoceptive threshold in the rat.

We have studied the involvement of the N-methyl-D-aspartate receptor (NMDAR) glycine site and the strychnine-sensitive glycine receptor (GlyR) in the ventrolateral periaqueductal gray (VL-PAG) on nociceptive behavior (tail flick) and pain-related changes on neuronal activity in the rostral ventromedial medulla (RVM). Glycine or D-serine increased the tail-flick latency, reduced OFF-cell pause, and delayed its onset and increased the time between the onset of the OFF-cell pause and the tail withdrawal. Conversely, they decreased the ongoing activity of the ON cell, the tail-flick-induced ON-cell firing, whereas they delayed the onset of increased tail-flick-induced ON-cell firing. Also, glycine or D-serine reduced the interval between the onset of the increased ON-cell firing and tail withdrawal. Whereas 7-Cl-kynurenic acid (7-Cl-KYN) prevented such effects, strychnine did not do so. A higher dose of 7-Cl-KYN or strychnine was per se able to reduce or increase tail-flick latency and increase or reduce ON-cell activities, respectively. A higher dose of glycine was hyperalgesic in the presence of 7-Cl-KYN, whereas such an effect was prevented by strychnine. These data suggest 1) a dual role of glycine in producing hyperalgesia or analgesia by stimulating the GlyR or the NMDARs within the VL-PAG, respectively; 2) consistently that RVM ON and OFF cells display opposite firing patterns to the stimulation of the VL-PAG NMDAR glycine site and GlyR activation; and 3) a tonic role of these receptors within the VL-PAG-RVM antinociceptive descending pathway.

Constitutive and regulated endocytosis of the glycine transporter GLYT1b is controlled by ubiquitination.

The glycine transporter GLYT1 regulates both glycinergic and glutamatergic neurotransmission by controlling the reuptake of glycine at synapses. Trafficking of GLYT1 to and from the cell surface is critical for its function. Activation of PKC down-regulates the activity of GLYT1 through a mechanism that has so far remained uncharacterized. Here we show that GLYT1b undergoes fast constitutive endocytosis that is accelerated by phorbol esters. Both constitutive and regulated endocytosis occur through a dynamin 2- and clathrin-dependent pathway, accumulating in the transporter in transferrin-containing endosomes. A chimera with the extracellular and transmembrane domains of the nerve growth factor receptor and the COOH-terminal tail of GLYT1 was efficiently internalized through this clathrin pathway, suggesting the presence of molecular determinants for GLYT1b endocytosis in its COOH-terminal tail. Extensive site-directed mutagenesis in this region of the chimera highlighted the involvement of lysine residues in its internalization. In the context of the full-length transporter, lysine 619 played a prominent role in both the constitutive and phorbol 12-myristate 13-acetate-induced endocytosis of GLYT1b, suggesting the involvement of ubiquitin modification of GLYT1b during the internalization process. Indeed, we show that GLYT1b undergoes ubiquitination and that this process is stimulated by phorbol 12-myristate 13-acetate. In addition, this endocytosis is impaired in an ubiquitination-deficient cell line, further evidence that constitutive and regulated endocytosis of GLYT1b is ubiquitin-dependent. It remains to be determined whether GLYT1b recycling might be affected in pathologies involving alterations to the ubiquitin system, thereby interfering with its influence on inhibitory and excitatory neurotransmission.

Mechanisms of endoplasmic-reticulum export of glycine transporter-1 (GLYT1).

The GLYT1 (glycine transporter-1) regulates both glycinergic and glutamatergic neurotransmission by controlling the reuptake of glycine at synapses. Trafficking to the cell surface of GLYT1 is critical for its function. In the present paper, by using mutational analysis of the GLYT1 C-terminal domain, we identified the evolutionarily conserved motif R(575)L(576)(X(8))D(585) as being necessary for ER (endoplasmic reticulum) export. This is probably due to its capacity to bind Sec24D, a component of the COPII (coatomer coat protein II) complex. This ER export motif was active when introduced into the related GLYT2 transporter but not in the unrelated VSVG (vesicular-stomatitis virus glycoprotein)-GLYT1 protein in which this motif was mutated but was not transported to the plasma membrane, although this effect was rescued by co-expressing these mutants with wild-type GLYT1. This behaviour suggests that GLYT1 might form oligomers along the trafficking pathway. Cross-linking assays performed in rat brain synaptosomes and FRET (fluorescence resonance energy transfer) microscopy in living cells confirmed the existence of GLYT1 oligomers. In summary, we have identified a motif involved in the ER exit of GLYT1 and, in analysing the influence of this motif, we have found evidence that oligomerization is important for the trafficking of GLYT1 to the cell surface. Because this motif is conserved in the NSS (sodium- and chloride-dependent neurotransmitter transporter) family, it is possible that this finding could be extrapolated to other related transporters.