Implementation of AMI Systems in CFE-Distribution, Mexico

The Smart Grid concept has been conceived as the integration of the electrical grid (generation, transmission and distribution) and the communications network of an electric utility. Although, traditional communications interfaces, protocols and standards has been used in the electrical grid in an isolated manner, modern communications networks are considered as the fundamental enabling technologies within a Smart Grid environment. Emerging communications technologies, protocol architectures and standards can help to build a common communications network infrastructure for data transport between customer premises, power substations, power distribution systems, utility control centers and utility data centers. The Smart Grid will support traditional applications such as supervisory control and data acquisition (SCADA), distribution automation (DA), energy management systems (EMS), demand site management (DSM) and automated meter reading (AMR), etc., as well as new applications like advanced metering infrastructure (AMI), substation automation (SA), microgrids, distributed generation (DG), grid monitoring and control, data storage and analysis, among others. To make this possible, the Smart Grid requires a two-way wide area communications network between different dispersed areas, from generation to consumer premises. An AMI system uses communication technologies for smart meter reading several times a day to get data consumption of electricity, as well as sending outage alarm information and meter tampering almost in real time, from the meter to the control center. Currently, there are various communication technologies to implement AMI systems. This paper presents an overview of the most relevant communications technologies that can be used to implement AMI communications infrastructure such as neighborhood area networks (NAN), field area networks (FAN) and wide area networks (WAN) using different transmission media such as fiber optics, spread spectrum radio frequency, microwave, WiMax, Wi-Fi, ZigBee, cellular, and power line carrier. In addition, a review of the current state of various AMI projects around the world, including the progress in the implementation of AMI systems in Mexico, besides the evaluation performance of CFE´s AMI networks

Size, Age, and Spatial-Temporal Distribution of Shortfin Mako in the Mexican Pacific Ocean

Abstract Basic population parameters such as age, size, and distribution have been poorly evaluated for the Shortfin Mako Isurus oxyrinchus in the Mexican Pacific Ocean. According to data collected by scientific observers on board medium-size fishing vessels during the period of 2006–2013, size as TL was obtained for 5,740 individual sharks. The range of TL was 70–362 cm for females and 71–296 cm for males. Weight (W), measured randomly from 1,409 individuals, ranged from 2 to 90 kg for females and from 2 to 80 kg for males. The weight-to-TL ratio was best fitted by the equation W = 4 × 10−5(TL)2.59 (r2 = 0.6532). No sex-specific difference was found in the weight-to-TL relationship between males and females, nor in W or TL separately. By using the inverse von Bertalanffy equation and parameters described by other authors for the same study area, we determined the age range for individuals captured on the basis of their TL. The age ranged from 0 to 39 years in females and from 0 to 21 years in males. Using a logistic model, the mean length at sexual maturity was obtained for 2,532 males (TL = 190 cm). The quarterly distribution of young of the year and 1-year-old juveniles showed that there is a tendency for these sharks to mov

Identification of causative and susceptibility variants in the neurexin-neuroligin pathway in patients with Alzheimer's disease. The role of a truncating mutation in Neuroligin 1

Póster presentado en el 16th National Congress of the Spanish Society of Neuroscience (SENC 2015), celebrado el Granada del 23 al 25 de septiembre de 2015.Neurexins (NRXN) and neuroligins (NLGN) are synaptic cell-adhesion proteins involved in neurodevelopmental disorders, as autism and intellectual disability. Previously, we have postulated a role of NRNX-NLGN in Alzheimer's disease (AD). Here, we present genetic and functional approaches to identify variants of the NRNX-NLGN pathway in AD patients. Using next-generation sequencing, we have studied a panel of 36 genes of the NRNX-NLGN synaptic pathway in 192 AD patients. Potential causal variants were studied by in silico analysis and validated by Sanger sequencing. Susceptibility variants were analyzed by manual inspection in IGV (Integrative Genomics Viewer). Functional studies of selected variants were performed in N2A and COS cells and cultured hipocampal neurons. To identify susceptibility alleles, we selected SNPs whose allelic frequency differed among the genotyped AD patients and the control databases. These SNPs were then genotyped in a geographically-matched control population. On the other hand, potential causative mutations were selected among novel variants with a predicted pathogenic effect. We present a two base-pair insertion in NLGN1 (p.Thr271fs) in a patient with familial history of AD. The frameshift mutation in NLGN1 predicts a premature STOP codon that truncates the extracellular domain. We generated expression vectors for the p.Thr271fs mutation. In western blot experiments we detected a band of ~130 kD corresponding to wild type NLGN1. In contrast, the p.Thr271fs mutation resulted in truncated proteins of ~30 kDa. Localization studies in COS cells showed that p.Thr271fs NLGN1 failed to reach the plasma membrane and accumulated in the ER. In neurons, NLGN1 induces the formation of glutamatergic synapses. We showed that p.Thr271fs NLGN1 failed to induce the formation of glutamatergic synapses and accumulated in the soma of transfected neurons. Thus, the synaptic activity of NLGN1 was abolished by the AD-associated p.Thr271fs mutation. Our data report the first inactivating mutation in the NLGN1 gene in AD patients and support a role for the NRXN-NLGN pathway in the etiology of AD.Peer Reviewe

A truncating mutation in Alzheimer's disease inactivates neuroligin-1 synaptic function

Neuroligins (NLs) are cell-adhesion proteins that regulate synapse formation and function. Neuroligin 1 (NL1) promotes the formation of glutamatergic synapses and mediates long-term potentiation in mouse models. Thus, altered NL1 function could mediate the synaptic and memory deficits associated with Alzheimer's disease (AD). Here, we describe a frameshift mutation, c.875_876insTT, in the neuroligin 1 gene (NLGN1) in a patient with AD and familial history of AD. The insertion generates a premature stop codon in the extracellular domain of NL1 (p.Thr271fs). Expression of mutant NL1 shows accumulation of truncated NL1 proteins in the endoplasmic reticulum. In hippocampal neurons, the p.Thr271fs mutation abolishes the ability of NL1 to promote the formation of glutamatergic synapses. Our data support a role for inactivating mutations in NLGN1 in AD. Previous studies have reported rare mutations in X-linked NLGNL3 and NLGNL4 genes in patients with autism, which result in the inactivation of the mutant alleles. Therefore, together with a role in neurodevelopmental disorders, altered NL function could underlie the molecular mechanisms associated with brain diseases in the elderly.This work was funded by grants from Junta de Andalucía (P11-CVI-7599) and Instituto de Salud Carlos III (PI11/1058).Peer Reviewe

Polygala reinii Franch. et Savat.

原著和名: カキノハグサ科名: ヒメハギ科 = Polygalaceae採集地: 静岡県 引佐郡 引佐町 渋川 (遠江 引佐郡 引佐町 渋川)採集日: 1966/6/4採集者: 萩庭丈壽整理番号: JH036052国立科学博物館整理番号: TNS-VS-98605