Improving Signal-Strength Aggregation for Mobile Crowdsourcing Scenarios.

Due to its huge impact on the overall quality of service (QoS) of wireless networks, both academic and industrial research have actively focused on analyzing the received signal strength in areas of particular interest. In this paper, we propose the improvement of signal-strength aggregation with a special focus on Mobile Crowdsourcing scenarios by avoiding common issues related to the mishandling of log-scaled signal values, and by the proposal of a novel aggregation method based on interpolation. Our paper presents two clear contributions. First, we discuss the misuse of log-scaled signal-strength values, which is a persistent problem within the mobile computing community. We present the physical and mathematical formalities on how signal-strength values must be handled in a scientific environment. Second, we present a solution to the difficulties of aggregating signal strength in Mobile Crowdsourcing scenarios, as a low number of measurements and nonuniformity in spatial distribution. Our proposed method obtained consistently lower Root Mean Squared Error (RMSE) values than other commonly used methods at estimating the expected value of signal strength over an area. Both contributions of this paper are important for several recent pieces of research that characterize signal strength for an area of interest.

Termino-terminal Ureteral Laparoscopic Anastomosis in a Case of Deep Infiltrating Endometriosis.

STUDY OBJECTIVE: Laparoscopic termino-terminal ureteral anastomosis has all the advantages of a minimally invasive approach in addition to the treatment of the pathologic condition [1]. Ureteral deep endometriosis can lead to severe consequences, such as hydroureteronephrosis and renal failure [2,3]. The main objective of this video is to present our surgical strategy and technique for cases of ureteral deep infiltrating endometriosis, which could help surgeons to understand and perform this surgery in a safe way in patients. DESIGN: Video demonstration of the technique. SETTING: French university tertiary-care hospital. INTERVENTIONS: This video presents a termino-terminal laparoscopic ureteral anastomosis and shows our team's strategy for surgical treatment in a 42-year-old woman with deep infiltrating ureteral left endometriosis, with consequent stenosis and left hydroureteronephrosis. A full resection of the endometriotic ureteral nodule was performed, followed by a termino-terminal anastomosis of the ureter. The use of intravenous indocyanine green to assess the postanastomotic ureteral perfusion and its risk of leakage or fistula are described in the video [2-5]. CONCLUSION: Ureteral endometriosis can lead to severe consequences, and the surgical treatment can be difficult and, most times, incomplete. This video gives a detailed example of the strategy our team used to perform a termino-terminal ureteral laparoscopic anastomosis in a structured way.

Neuroprotección mediada por BDNF y óxido nítrico frente a excitotoxicidad en neuronas corticales e hipocampales / BDNF and nitric oxide-mediated neuroprotection against excitotoxicity in cortical and hippocampal neurons

En la epilepsia del lóbulo temporal (ELT), el hipocampo y estructuras temporales adyacentes se convierten en foco epiléptico, lo que ocurre después de un insulto cerebral, como una convulsión prolongada (o Status Epilepticus [SE]). Posterior al insulto, en el hipocampo ocurre muerte neuronal por excitotoxicidad, es decir, por sobre estimulación de receptores glutamatérgicos tipo NMDA (R-NMDA) y síntesis de óxido nítrico (NO) por la óxido nítrico sintasa neuronal (nNOS), una enzima dependiente de calcio. Sin embargo, otras estructuras cerebrales, como la corteza cerebral, son más resistentes al daño excitotóxico. Postulamos que esta menor susceptibilidad de la corteza cerebral a la excitotoxicidad, se debería a neuroprotección dependiente de la neurotrofina BDNF, que se sabe estimula la sobrevida neuronal. Se utilizaron cultivos neuronales primarios de hipocampo y corteza cerebral. Para evaluar excitotoxicidad, se agregó NMDA 30 uM. Se utilizaron estrategias farmacológicas para poner a prueba esta hipótesis, como el uso de L-NNA (inhibidor NOS), y TrkB-Fc (atrapador de BDNF). Se evaluó el porcentaje de sobrevida celular mediante el test de exclusión de Azul de Tripán. La viabilidad de los cultivos después de agregar NMDA fueron: corticales 71,2 +/- 2,8 por ciento, hipocampales 24,6 +/- 2,2 por ciento (p<0,01). Al inhibir la NOS, la viabilidad fue: corticales 31 +/- 6,5 por ciento, hipocampales 79,2 +/- 5,4 por ciento (p<0,01). En ausencia de BDNF fue: corticales 28,7+/- 7,9 por ciento, hipocampales 88,9 +/- 3 por ciento (p<0,01). Concluimos que después de un insulto excitotóxico, BDNF/NO son neuroprotectores en neuronas corticales pero no hipocampales. La potenciación de mecanismos neuroprotectores podría ser una alternativa terapéutica en patologías que involucran muerte neuronal por excitotoxicidad.

In temporal-lobe epilepsy (TLE), the hippocampus and adjacent temporal structures become an epileptic focus following a brain insult, such as a prolonged seizure (or Status Epilepticus). After the insult, neuronal death by excitotoxicity ocurrs, this is, by over stimulation of NMDA-type glutamate receptors (R-NMDA) and nitric oxide sinthesis by neuronal nitric oxide synthase (nNOS), a calcium-dependant enzyme. However, other brain structures, such as the cerebral cortex, are much more resistant to an excitotoxic challenge. We propose that the decreased susceptibility of the cerebral cortex could be explained by neuroprotection mediated by the neurotrophin BDNF, which is known to stimulate neuronal survival. Primary hippocampal and cortical neuronalcultures were used. To evaluate excitotoxicity, 30 uM NMDA was added. The signaling pathways to be tested were inhibited by using pharmacological inhibitors: L-NNA (NOS inhibitor), and TrkB-Fc, a BDN-scavenger. Percentages of cellular survival were evaluated using the Trypan Blue exclusion test. The viability of the cultures after adding NMDA was: larger in cortical than in hippocampal cultures, 71,2 +/- 2,8 percent for cortical and 24,6 +/- 2,2 percent hippocampal cells (p<0,01). When inhibiting NOS, the viability was: 31 +/- 6,5 percent for cortical and 79,2 +/- 5,4 percent for hippocampal cells (p<0,01). In absence of BDNF, 28,7 +/- 7,9 percent of the cortical cells survived, while in the hippocampal cultures it was of 88,9 +/- 3 percent (p<0,01). We conclude that after an excitotoxic insult, BDNF/NO are neuroprotective in cortical but not hippocampal neurons. The potentiation of such neuroprotective mecanisms could be used as a therapeutic alternative in pathologies that involve neuronal death by excitotoxicity.