On the thermal noise introduced by a resistor in a circuit

Comentari sobre l'article publicat anteriorment pels mateixos autors: Vargas, M; Pallás, R; The seemingly paradoxical noise behaviour some active circuits. IEEE Transactions on Instrumentation and Measurement. 1994, vol. 43, núm. 5, p. 764-767

Disseny d’un circuit analògic reconfigurable

En l’actualitat, l’electrònica digital s’està apoderant de la majoria de camps de desenvolupament, ja que ofereix un gran ventall de possibilitats que permeten fer front a gran quantitat de problemàtiques. Poc a Poc s’ha anat prescindint el màxim possible de l’electrònica analògica i en el seu lloc s’han utilitzat sistemes microprocessats, PLDs o qualsevol altre dispositiu digital, que proporciona beneficis enlluernadors davant la fatigosa tasca d’implementar una solució analògica.Tot i aquesta tendència, és inevitable la utilització de l’electrònica analògica, ja que el mon que ens envolta és l’entorn en el que han de proporcionar servei els diferents dissenys que es realitzen, i aquest entorn no és discret sinó continu. Partint d’aquest punt ben conegut hem de ser conscients que com a mínim els filtres d’entrada i sortida de senyal juntament amb els convertidors D/A A/D mai desapareixeran.Així doncs, aquests circuits analògics, de la mateixa forma que els digitals, han de sercomprovats un cop dissenyats, és en aquest apartat on el nostre projecte desenvoluparà un paper protagonista, ja que serà la eina que ha de permetre obtenir les diferents senyals característiques d’un determinat circuit, per posteriorment realitzar els tests que determinaran si es compleix el rang de correcte funcionament, i en cas de no complir, poder concretar quin paràmetre és el causant del defecte

Six new loci associated with body mass index highlight a neuronal influence on body weight regulation.

Common variants at only two loci, FTO and MC4R, have been reproducibly associated with body mass index (BMI) in humans. To identify additional loci, we conducted meta-analysis of 15 genome-wide association studies for BMI (n > 32,000) and followed up top signals in 14 additional cohorts (n > 59,000). We strongly confirm FTO and MC4R and identify six additional loci (P < 5 x 10(-8)): TMEM18, KCTD15, GNPDA2, SH2B1, MTCH2 and NEGR1 (where a 45-kb deletion polymorphism is a candidate causal variant). Several of the likely causal genes are highly expressed or known to act in the central nervous system (CNS), emphasizing, as in rare monogenic forms of obesity, the role of the CNS in predisposition to obesity.

Triodothyronine enhancement of neuronal differentiation in aggregating fetal rat brain cells cultured in a chemically defined medium.

Triiodothyronine (30 nM) added to serum-free cultures of mechanically dissociated re-aggregating fetal (15-16 days gestation) rat brain cells greatly increased the enzymatic activity of choline acetyltransferase and acetylcholinesterase throughout the entire culture period (33 days), and markedly accelerated the developmental rise of glutamic acid decarboxylase specific activity. The enhancement of choline acetyltransferase and acetylcholinesterase specific activities in the presence of triiodothyronine was even more pronouned in cultures of telencephalic cells. If triiodothyronine treatment was restricted to the first 17 culture days, the level of choline acetyltransferase specific activity at day 33 was 84% of that in chronically treated cultures and 270% of that in cultures receiving triiodothyronine between days 17 and 33, indicating that relatively undifferentiated cells were more responsive to the hormone. Triiodothyronine had no apparent effect on the incorporation of [3H]thymidine at day 5 or on the total DNA content of cultures, suggesting that cellular differentiation, rather than proliferation was affected by the hormone. Our findings in vitro are in good agreement with many observations in vivo, suggesting that rotation-mediated aggregating cell cultures of fetal rat brain provide a useful model to study thyroid hormone action in the developing brain.

El circuit comercial de Barcino: reflexions al voltant de les marques amfòriques

Barcino és encara avui una ciutat romana poc coneguda de la província Tarraconense, que segons la majoria d’especialistes fou fundada per raons polítiques. Malgrat això, una anàlisi detallada de les característiques econòmiques suggereixen que es va crear com a resultat de necessitats comercials, ja que es localitzava en una de les millors zones portuàries del NE de la península. L’article present pretén reconstruir tot el circuit comercial de Barcino a partir de les nombroses estampilles d’àmfores trobades en les excavacions. Aquestes marques comercials no solament evidencien una pròspera producció de vi en l’àrea, sinó també la corresponent demanda externa.

Réouverture [du circuit automobile] de Brooklands, Miss Ivy Cummings et son père [Sydney] : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 58772

Réouverture [du circuit automobile] de Brooklands : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 58773

Neuroligin-1 links neuronal activity to sleep-wake regulation.

Maintaining wakefulness is associated with a progressive increase in the need for sleep. This phenomenon has been linked to changes in synaptic function. The synaptic adhesion molecule Neuroligin-1 (NLG1) controls the activity and synaptic localization of N-methyl-d-aspartate receptors, which activity is impaired by prolonged wakefulness. We here highlight that this pathway may underlie both the adverse effects of sleep loss on cognition and the subsequent changes in cortical synchrony. We found that the expression of specific Nlg1 transcript variants is changed by sleep deprivation in three mouse strains. These observations were associated with strain-specific changes in synaptic NLG1 protein content. Importantly, we showed that Nlg1 knockout mice are not able to sustain wakefulness and spend more time in nonrapid eye movement sleep than wild-type mice. These changes occurred with modifications in waking quality as exemplified by low theta/alpha activity during wakefulness and poor preference for social novelty, as well as altered delta synchrony during sleep. Finally, we identified a transcriptional pathway that could underlie the sleep/wake-dependent changes in Nlg1 expression and that involves clock transcription factors. We thus suggest that NLG1 is an element that contributes to the coupling of neuronal activity to sleep/wake regulation.

Transfer entropy reconstruction and labeling of neuronal connections from simulated calcium imaging

Neuronal dynamics are fundamentally constrained by the underlying structural network architecture, yet much of the details of this synaptic connectivity are still unknown even in neuronal cultures in vitro. Here we extend a previous approach based on information theory, the Generalized Transfer Entropy, to the reconstruction of connectivity of simulated neuronal networks of both excitatory and inhibitory neurons. We show that, due to the model-free nature of the developed measure, both kinds of connections can be reliably inferred if the average firing rate between synchronous burst events exceeds a small minimum frequency. Furthermore, we suggest, based on systematic simulations, that even lower spontaneous inter-burst rates could be raised to meet the requirements of our reconstruction algorithm by applying a weak spatially homogeneous stimulation to the entire network. By combining multiple recordings of the same in silico network before and after pharmacologically blocking inhibitory synaptic transmission, we show then how it becomes possible to infer with high confidence the excitatory or inhibitory nature of each individual neuron.

Neuronal survival induced by neurotrophins requires calmodulin

It has been reported that phosphoinositide 3-kinase (PI 3-kinase) and its downstream target, protein kinase B (PKB), play a central role in the signaling of cell survival triggered by neurotrophins (NTs). In this report, we have analyzed the involvement of Ca2+ and calmodulin (CaM) in the activation of the PKB induced by NTs. We have found that reduction of intracellular Ca2+ concentration or functional blockade of CaM abolished NGF-induced activation of PKB in PC12 cells. Similar results were obtained in cultures of chicken spinal cord motoneurons treated with brain-derived neurotrophic factor (BDNF). Moreover, CaM inhibition prevented the cell survival triggered by NGF or BDNF. This effect was counteracted by the transient expression of constitutive active forms of the PKB, indicating that CaM regulates NT-induced cell survival through the activation of the PKB. We have investigated the mechanisms whereby CaM regulates the activation of the PKB, and we have found that CaM was necessary for the proper generation and/or accumulation of the products of the PI 3-kinase in intact cells.

Disseny de circuit de proves de traçabilitat amb rfid

ITENE és un institut tecnològic de recerca situat a Paterna (València). Té una plantapilot especialitzada en logística on les empreses que ho vulguin (mitjançant convenis,en règim de lloguer, etc.), poden utilitzar les instal•lacions (magatzem intel•ligent,aplicacions RFID, etc.), per provar els seus productes i simular processos de logística itraçabilitat.En aquesta planta s'ha detectat la necessitat de poder provar nous productes cometiquetes, detectors i processadors equipats amb tecnologia RFID (Identificació perRadiofreqüència). Aquesta tecnologia consisteix en passar informació que conté unaetiqueta “intel•ligent” cap a un terminal (PC) mitjançant uns detectors que, perproximitat, poden llegir la informació. Per exemple, quan un camió ple de mercaderiesprèviament etiquetades, passa per un pòrtic amb detectors RFID, es genera unainformació que passa directament a un terminal. Al moment es pot saber què porta elcamió, quantitat, color, mides, etc. Si això es combina amb un ERP, es pot descomptarde l'estoc en temps real. De fet s'utilitza per moltes aplicacions logística, control deprocessos de fabricació, traçabilitat de productes, etc.Per aquest motiu, ITENE, mitjançant el contacte de AIFOS SOLUTIONS S.L (empresaespecialitzada en RFID) ha encarregat un sistema de transportadors de banda per provarnoves solucions.L'objecte del present projecte consisteix en el disseny i automatització d'un sistema de 4cintes transportadores 2 elevadors per tal de fer un circuit tancat per moure caixes en un“bucle” de forma automàtica. L'objectiu és “llençar” caixes plenes de productes (etiquetats amb RFID) mitjançant untransportador equipat amb un pòrtic que té instal•lats diversos detectors de radiofreqüència,i poder-ne provar la correcta detecció a diferents velocitats. Un “buffer” s'encarrega desubministrar les caixes d'una en una que, un cop acabat el circuit, tornen al lloc d'on hansortit. Per donar un producte per bo, es realitzen tests de diverses hores i se n'obté unaestadística de lectures bones/dolentes. Si la ràtio és la desitjada es dóna per bo elproducte.Per aconseguir un disseny correcte s'ha utilitzat diferents eines CAD per dimensionar elsistema de transportadors i els seus elements. Tota l'aplicació està realitzada en 3Dmitjançant el software AutoCAD 3D. L'abast d'aquest projecte inclourà la solució mecànica i pneumàtica del sistema, aixícom el seu muntatge i tot el referent a les normes de seguretat per tal que el sistemacompleixi la normativa referida a la seguretat de màquines

Lack of GDAP1 induces neuronal calcium and mitochondrial defects in a knockout mouse model of charcot-marie-tooth neuropathy.

Mutations in GDAP1, which encodes protein located in the mitochondrial outer membrane, cause axonal recessive (AR-CMT2), axonal dominant (CMT2K) and demyelinating recessive (CMT4A) forms of Charcot-Marie-Tooth (CMT) neuropathy. Loss of function recessive mutations in GDAP1 are associated with decreased mitochondrial fission activity, while dominant mutations result in impairment of mitochondrial fusion with increased production of reactive oxygen species and susceptibility to apoptotic stimuli. GDAP1 silencing in vitro reduces Ca2+ inflow through store-operated Ca2+ entry (SOCE) upon mobilization of endoplasmic reticulum (ER) Ca2+, likely in association with an abnormal distribution of the mitochondrial network. To investigate the functional consequences of lack of GDAP1 in vivo, we generated a Gdap1 knockout mouse. The affected animals presented abnormal motor behavior starting at the age of 3 months. Electrophysiological and biochemical studies confirmed the axonal nature of the neuropathy whereas histopathological studies over time showed progressive loss of motor neurons (MNs) in the anterior horn of the spinal cord and defects in neuromuscular junctions. Analyses of cultured embryonic MNs and adult dorsal root ganglia neurons from affected animals demonstrated large and defective mitochondria, changes in the ER cisternae, reduced acetylation of cytoskeletal α-tubulin and increased autophagy vesicles. Importantly, MNs showed reduced cytosolic calcium and SOCE response. The development and characterization of the GDAP1 neuropathy mice model thus revealed that some of the pathophysiological changes present in axonal recessive form of the GDAP1-related CMT might be the consequence of changes in the mitochondrial network biology and mitochondria-endoplasmic reticulum interaction leading to abnormalities in calcium homeostasis.