Course actions define certificate formats and issuing conditions, rules, availability and the order of completing the course lessons.
The Information tab includes a detailed description of the course under several topics (e.g, Objectives, Resources).
Apart from this basic information, the professor can also describe the lesson using several course metadata, that follow the doublin care standard. The professor can override the completion status by hand using the related function next to each user's name (last column).
Through the course rules tab in the Educational and Enterprise editions, we can add rules between different courses and though define the order in which courses can be accessed and completed. The Order tab offers a drag-and-drop interface to change the order of the lessons inside the courses. The Scheduling tab offers an interface for setting the availability for individual lessons inside the course. Each certification has an identification number (certificate key) that is unique and can be used to track its validity. After the expiration and the reset of the course, that is done automatically by the system, the students will have to attend the course again, complete all the course rules and they will be certified again after completing it. Although the course is reset, the system stores the students' grades for all the previous certifications that they have gained, so that their history will be retained. Apart from them, you can design your own template, a process that presupposes basic knowledge of XML. You can preview, edit, rename, clone and delete your own designed templates but only preview and clone the default templates. Furthermore please note that you can use any custom user profile field in your certificate , as well as course properties, ceu and training hours.
When the certificates templates are described in RTF format, the certifications can be exported in DOC and PDF format. Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction.
Lo central de la drogadiccion, a pesar de la importancia de los numerosos factores psicosociales, es que implica un proceso biologico. Malgre l'importance de nombreux facteurs psychosociaux, l'addiction a une drogue repose essentiellement sur un processus biologique: l'etat de dependance se definit par la faculte d'une exposition repetee a une consommation de drogue a provoquer des modifications dans un cerveau vulnerable conduisant a leur recherche et a leur prise compulsive et a la perte du controle de leur utilisation. Drug addiction, which can be defined as the compulsive seeking and taking of drugs despite horrendous consequences or loss of control over drug use, is caused by long-lasting drug-induced changes that occur in certain brain regions.[1] Only some individuals, however, succumb to addiction in the face of repeated drug exposure, while others are capable of using a drug casually and escaping an addiction syndrome.
The knowledge that addicts can remain at increased risk for relapse despite years of abstinence means that addiction involves drug-induced changes in the brain that can be very stable. Stimulant and opiate drugs of abuse activate CREB in several brain regions important for addiction, including prominently in the NAc.[23],[24] CREB is known to be activated in other systems by cAMP, Ca2+, and growth factor pathways,[25] and it is not yet known which of these mediates its activation in NAc by drugs of abuse. Acute exposure to virtually any drug of abuse induces all Fos family transcription factors in NAc and several other brain regions.
In more recent years, studies of transcription have been pushed one step further to epigenetics[44] (see Figure 1), which can be broadly defined as a change in gene expression that occurs in the absence of a change in DNA sequence. Molecular mechanisms underlying cocaine induction of dendritic spines on nucleus accumbens (NAc) medium spiny neurons. While the majority of research involving neurophysiological changes in neurons in drug abuse phenomena, as in learning and memory phenomena, has focused on synaptic plasticity, there is increasing evidence for the importance of whole cell plasticity as well. Working model of chronic morphine-induced adaptations in ventral tegmental area (VTA) dopamine neurons. Increasing evidence, much of it from studies of hippocampal and cerebral cortical neurons, has shown that changes in synaptic plasticity are associated with morphological changes at synapses.
The above narrative underscores the tremendous advances that have been made in understanding the molecular and cellular adaptations that occur in brain reward regions in response to repeated exposure to a drug of abuse, and in relating individual adaptations to certain behavioral features of addiction syndromes in animal models. Amazon acquired online math instruction company, TenMarks, for an undisclosed amount Thursday, as the company moves to push its Kindle Fire tablets into schools. The course export includes all underlying lessons but it does not export users or their progress. If you decide that the certificates will expire after a period of time, you can also define that the system will reset the course for the certified users as soon as the validation time ends or prior the certificate expiration. This information can be found through the administrator's page and the 'Certificate reports'. Also, you can set the time for expiration after certificate will be issued or select no expiration date. The new template default xml code contains the new fields and once defined they will appear in the certificate.
For example, to insert the course's Training Hours you will type this ###training_hours### . In this section, we will figure out how to draw lines, display pictures, set background image and insert fields within the certificate. After your account is confirmed, go back to your eFront installation and through the administrator's page select the System settings function. Chris Gregoire signed legislation (Engrossed Second Substitute Senate Bill 6696) to help Washington win a $250 million federal Race to the Top (R2T). Here, we review the types of molecular and cellular adaptations that occur in specific brain regions to mediate addiction-associated behavioral abnormalities. Un estado de adiccion se define por la capacidad que tiene la exposicion repetida a una droga de abuso para inducir cambios en un cerebro vulnerable, el impulse a la busqueda compulsiva y la obtencion de drogas, y la perdida de control sobre el uso de estas. Nous analysons ici les types d'adaptation moleculaire et cellulaire qui interviennent dans des regions cerebrales particulieres a l'origine des anomalies du comportement addictif: ce sont des alterations de l'expression genique dues en partie a des mecanismes epigenetiques, a la plasticite du fonctionnement neurophysiologique des neurones et des synapses et l'association d'une plasticite au niveau de la morphologie neuronale et synaptique due en partie a une modification de la transmission du signal des facteurs neurotrophiques. This has led several groups to consider changes in gene expression as an important component of the addiction process (Figure 1). In eukaryotic cells, DNA is organized by wrapping around histone octomers to form nucleosomes, which are then further organized and condensed to form chromosomes (left part).
This induction is rapid but also highly transient, with Fos protein levels reverting to normal within 8 to 12 hours. Epigenetic mechanisms control the packaging of DNA within a cell nucleus via its interactions with histones and many other types of nuclear proteins, which together comprise chromatin.
Chronic exposure to cocaine results in a time-dependent and transient reorganization of ?-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartic acid (NMDA) glutamate receptors at NAc medium spiny neuron (MSN) synapses, as well as structural changes in the spine head of NAc MSNs that correlate with distinct forms of synaptic plasticity.
A) shows cocaine-induced increases in dendritic spine number that can be blocked by viral overexpression of G9a or JunD (an antagonist of AP1 -mediated transcription), or mimicked by viral overexpression of FosB.
Whole cell plasticity, also referred to as homeostatic plasticity,[71] involves changes in the intrinsic excitability of an entire nerve cell in a manner that it is not synapse-specific.
Chronic morphine decreases VTA dopamine (DA) soma size yet increases neuronal excitability, while dopamine transmission to the nucleus accumbens is decreased. Carlezon WA Jr J, Thome J, Olson VG, Lane-Ladd SB, Brodkin ES, Hiroi N, Duman RS, Neve RL, Nestler EJ.

Part of this information is visible to the student through the integrated tooltip, when the student passes over a course on the catalog. This option ensures that all students satisfying the lesson or course criteria, are automatically acknowledged by the system and given the completed status. The administrator can look for the students who have gotten certificate for the course that interests him, in a specific period of time.
They are called, Minimum Decoration, Medium Decoration, Heavy Decoration and Portrait Minimum Decoration. Predefined variables like for example ###3m###, ###1y###, ###10d### can be used in custom fields and will be translated in 3 months, 1 year, 10 days respectively when the certificate is issued, for example. After selecting the desired template, you can set the time for expiration after certificate will be issued or select no expiration date.
Then, select External tools, click on the PHP livedocx tab and supply the username and password of your previously registered LiveDocx account.
These include alterations in gene expression achieved in part via epigenetic mechanisms, plasticity in the neurophysiological functioning of neurons and synapses, and associated plasticity in neuronal and synaptic morphology mediated in part by altered neurotrophic factor signaling.
En este articulo se examinan los tipos de adaptaciones moleculares y celulares que ocurren en regiones especificas del cerebro y que median alteraciones conductuales asociadas con la adiccion. Chacun de ces types de modifications induites par les drogues peut etre vu comme une forme de «memoire cellulaire ou moleculaire». Several types of environmental factors have been implicated in addiction, including psychosocial stresses, but by far the most powerful factor is exposure to a drug of abuse itself. Accordingly, studies of candidate genes or genome-wide investigations involving DNA microarrays and more recently RNA-seq (high-throughput sequencing of expressed RNAs) has identified numerous genes whose expression is altered in a given brain region in rodent and primate models of addiction and in human addicts (eg, refs 10-17). Only by temporarily unraveling compacted chromatin can the DNA of a specific gene be made accessible to the transcriptional machinery.
While CREB is also activated in several other brain regions by stimulants and opiates,[23],[24] less is known about the behavioral consequences of this effect and the target genes through which they occur. Gene expression is controlled by the state of this packaging through the covalent modification of histones, other proteins, and DNA itself. A role for CREB and ?FosB has been implicated in these phenomena, as well as in associated changes in the morphology of glutamatergic synapses (see below). For example, chronic cocaine induces surface expression of NMDA receptors, silent synapse formation and long-term depression (LTD) at early withdrawal time points.
B) Regulation of AMPA receptor (AMPAR) trafficking and of the actin cytoskeleton (left), as well as regulation of the transcription of glutamate receptors and actin regulatory proteins (eg, as mediated via ?FosB, right) have been shown to play important roles in mediating cocaine's regulation of NAc dendritic spine density. Most of our existing knowledge focuses on the VTA and NAc, with much less information available about other key limbic brain regions that are also crucial for drug addiction. Identification of PSD-95 as a regulator of dopamine-mediated synaptic and behavioral plasticity. Distinctive profiles of gene expression in the human nucleus accumbens associated with cocaine and heroin abuse.
Substance specific and shared transcription and epigenetic changes in the human hippocampus chronically exposed to cocaine and alcohol. Gene coexpression networks in human brain identify epigenetic modifications in alcohol dependence. ELK1 transcription factor linked to dysregulated striatal mu opioid receptor signaling network and OPRM1 polymorphism in human heroin abusers. Induction of a long-lasting AP-1 complex composed of altered Fos-like proteins in brain by chronic cocaine and other chronic treatments. Regional and cellular mapping of CRE-mediated transcription during naltrexone-precipitated morphine withdrawal. CREB activity in the nucleus accumbens shell controls gating of behavioral responses to emotional stimuli. Altered sensitivity to rewarding and aversive drugs in mice with inducible disruption of cAMP response element-binding protein function within the nucleus accumbens. Overexpression of CREB in the nucleus accumbens shell increases cocaine reinforcement in self-administering rats.
FosB mutant mice: Loss of chronic cocaine induction of Fos-related proteins and heightened sensitivity to cocaine's psychomotor and rewarding effects.
Periadolescent mice show enhanced DeltaFosB upregulation in response to cocaine and amphetamine. Molecular mechanism for a gateway drug: epigenetic changes initiated by nicotine prime gene expression by cocaine. Increased impulsivity during withdrawal from cocaine self-administration: role for ?FosB in the orbitofrontal cortex. Integration of long-term-memory-related synaptic plasticity involves bidirectional regulation of gene expression and chromatin structure. Morphine epigenomically regulated behavior through alterations in histone H3 lysine 9 dimethylation in nucleus accumbens.
Drug-evoked synaptic plasticity in addiction: from molecular changes to circuit remodeling.
Long-term depression in the nucleus accumbens: a neural correlate of behavioral sensitization to cocaine.
Different adaptations in AMPA receptor transmission in the nucleus accumbens after short vs long access cocaine self-administration regimens.
CaMKII: a biochemical bridge linking accumbens dopamine and glutamate systems in cocaine seeking.
Rescuing cocaine-induced prefrontal cortex hypoactivity prevents compulsive cocaine seeking. Homeostatic plasticity in neuronal networks: the more things change, the more they stay the same. Elevated basal firing rates and enhanced responses to 8-Br-cAMP in locus coeruleus neurons in brain slices from opiate-dependent rats. CREB (cAMP response element-binding protein) in the locus coeruleus: biochemical, physiological, and behavioral evidence for a role in opiate dependence.
Role of cAMP response element-binding protein in the rat locus ceruleus: regulation of neuronal activity and opiate withdrawal behaviors.
Essential role of the cAMP-cAMP response-element binding protein pathway in opiate-induced homeostatic adaptations of locus coeruleus neurons.
Role for mTOR signaling and neuronal activity in morphine-induced adaptations in ventral tegmental area dopamine neurons.
The addicted synapse: mechanisms of synaptic and structural plasticity in nucleus accumbens. For example Lesson-3 can depend on Lesson-1 *and* Lesson-2; only when both Lesson-1 and Lesson-2 are completed will Lesson-3 become available for the student. First, appear the most recent certifications and below there is a list with all the previous certificates, the date and the student's grade.

By default, the XML section is filled up with the XML schema of the Minimum Decoration (Unicode) template.
Moreover variables like ###training_hours###, ###ceu###  and any custom user profile field could also be used in the same way.
Each of these types of drug-induced modifications can be viewed as a form of “cellular or molecular memory.” Moreover, it is striking that most addiction-related forms of plasticity are very similar to the types of plasticity that have been associated with more classic forms of “behavioral memory,” perhaps reflecting the finite repertoire of adaptive mechanisms available to neurons when faced with environmental challenges. Estas adaptaciones incluyen alteraciones en la expresion genica, producidas en parte por mecanismos epigeneticos, en la plasticidad del funcionamiento neurofisiologico de neuronas y sinapsis, y en la plasticidad asociada con la morfologia neuronal y sinaptica mediada en parte por las senales alteradas del factor neurotrofico, Cada uno de estos tipos de modificaciones inducidos por drogas se puede considerar como una forma de “memoria celular o molecular”.
De plus, il est frappant de voir que la plupart des formes de plasticite liees a l'addiction sont tres semblables aux types de plasticite associes aux formes plus classiques de «memoire comportementale» refletant peut-etre le caractere limite du repertoire des mecanismes adaptatifs disponibles pour les neurones lorsqu'ils font face aux defis environnementaux.
Examples of such genes are discussed in subsequent sections of this review.Likewise, many types of transcription factors—proteins that bind to regulatory regions of genes and thereby increase or decrease the transcription of those genes—have been implicated in mediating the long-term effects of drug of abuse on gene expression in the brain.
Drugs of abuse act through synaptic targets such as reuptake mechanisms, ion channels, and neurotransmitter (NT) receptors to alter intracellular signaling cascades (right part).
As just some examples, acetylation of histones tends to promote gene activation, methylation of histones can either promote gene activation or repression depending on the Lys residue undergoing this modification, and methylation of DNA is generally associated with gene repression although certain variant forms of methylation (eg, 5-hydroxymethylation) may be associated with gene activation.Epigenetics is an appealing mechanism because, in other systems, for example, developmental and cancer biology, certain epigenetic modifications can be permanent. During more prolonged withdrawal (wd), these synaptic changes reverse with the result being increased expression of surface AMPA receptors, a consolidation of the synapse into a mushroom-shaped spine and long-term potentiation (LTP).
Downregulation of IRS2-AKT signaling in VTA mediates the effects of chronic morphine on soma size and electrical excitability; the effect on excitability is mediated via decreased ?-aminobutyric acid (GABA)A currents and suppression of K' channel expression.
In addition, all experimental demonstrations of the causal role of a molecular-cellular adaptation in a drug-related behavior have manipulated individual adaptations one at a time.
The first three templates follow the landscape page orientation and last one follows the portrait page orientation. Finally, addiction-related molecular and cellular adaptations involve most of the same brain regions that mediate more classic forms of memory, consistent with the view that abnormal memories are important drivers of addiction syndromes. Sin embargo, llama la atencion que la mayoria de las formas de plasticidad relacionadas con la adiccion son muy similares a los tipos de plasticidad que se han asociado con las formas mas clasicas de “memoria conductual”, lo que refleja tal vez el repertorio limitado de los mecanismos de adaptacion de que disponen las neuronas cuando se enfrentan con las exigencias del medioambiente. Finalement, les adaptations moleculaires et cellulaires liees a l'addiction concernent la plupart des memes regions cerebrales impliquees dans les formes plus classiques de memoire, ce qui conforte l'idee que des souvenirs anormaux sont d'importants vecteurs de syndromes de dependance.
This leads to the activation or inhibition of transcription factors (TFs) and of many other nuclear targets, including chromatin-regulatory proteins (shown by thick arrows); the detailed mechanisms involved in the synaptic regulation of chromatin-regulatory proteins remain poorly understood. For this reason, epigenetics has been pursued both in learning and memory models (eg, refs 45-48) as well as in addiction;[44],[49] in both systems profound changes have been reported in histone acetylation and methylation and in DNA methylation. These effects rapidly revert back again upon exposure to a challenge dose of cocaine leading to restructuring of the spine into thin spines and a depression of synaptic strength.
Morphine-induced downregulation of mTORC2 activity in VTA is crucial for these morphine-induced morphological and physiological adaptations as well as for reward tolerance. To manipulate numerous adaptations at the same time is clearly far more difficult, but it is also essential, since we know that drugs produce a large number of disparate types of changes even within individual neurons, which likely summate in complicated ways to influence behavior.
The goal of these studies which aim to explicate the molecular and cellular basis of drug addiction is to eventually develop biologically based diagnostic tests, as well as more effective treatments for addiction disorders. Por ultimo, las adaptaciones moleculares y celulares relacionadas con las adicciones incluyen la mayor parte de las mismas regiones del cerebro que median las formas mas clasicas de la memoria, lo que resulta consistente con la opinion de que las memorias anormales son importantes impulsoras de los sindromes adictivos.
Le but de ces etudes, qui expliquent les bases moleculaires et cellulaires de la dependance a une drogue, est finalement de developper des tests diagnostiques biologiques, ainsi que des traitements plus efficaces pour les troubles addictifs. Second, it is interesting that many, perhaps most, of the types of changes that have been associated with a state of addiction (eg, altered gene transcription, epigenetics, synaptic and whole cell plasticity, and neuronal morphology and neurotrophic mechanisms) are also implicated in traditional forms of “behavioral memory” such as spatial memory, fear conditioning, and operant conditioning, among others.
This progress is illustrated by consideration of CREB and ?FosB, which are the best studied transcription factors in addiction models. These processes ultimately result in the induction or repression of particular genes, including those for noncoding RNAs such as microRNAs; altered expression of some of these genes can in turn further regulate gene transcription.
Reproduced from ref 82: Russo SJ, Dietz DM, Dumitriu D, Morrison JH, Malenka RC, Nestler EJ. Such a systems biology approach will be crucial to ultimately cracking the biological underpinnings of addiction.
El proposito de estos estudios que buscan explicar las bases moleculares y celulares de la adiccion a drogas es, eventualmente, poder desarrollar pruebas diagnosticas con bases biologicas, como tambien contar con terapias mas efectivas para los trastornos adictivos.
Third, among the brain regions affected by drugs of abuse are those that are key neural substrates for behavioral memory, including hippocampus, amygdala, and PFC. It is proposed that some of these drug-induced changes at the chromatin level are extremely stable and thereby underlie the long-lasting behaviours that define addiction. G9a catalyzes the dimethylation of Lys9 of histone H3 (H3K9me2), a major mediator of gene repression.
This phenomenon is, however, surprising, given that CREB and ?FosB are induced by both stimulants and opiates and are both implicated in stimulant-mediated induction of NAc dendritic spine density.
Finally, efforts to understand the molecular-cellular mechanisms of memories related to addiction find themselves at the point at which all other efforts to understand the biological basis of behavioral memory now struggle: our ability to relate biological phenomena to complex behavioral memory remains extremely difficult. These small, noncoding RNAs bind to complementary regions of mRNAs and thereby suppress their translation or induce their degradation. Considerable evidence now indicates that this reduction in cell soma size is mediated by opiate suppression of brain-derived neurotrophic factor (BDNF) expression within these neurons. Deletion of Argonaut, a protein crucial for the processing of miRNAs, alters behavioral responses to cocaine, with distinct effects observed for D1- versus D2-type medium spiny neurons.[54] Several specific miRNAs have likewise been shown to be regulated by drug exposure and, in turn, to influence behavioral responses to the drugs (eg, refs 55,56).
It will be exciting in future studies to identify the mRNA targets of these miRNAs and characterize how they affect the addiction process.
This control over cell excitability involves suppression of K+ channels and of GABAA current in these neurons.This role for BDNF in controlling morphine responses at the level of the VTA contrasts with its very different involvement in the actions of cocaine and other stimulants. You can either display the default logo of your eFront installation or an external image, by supplying its URL.
RTF Certificate templatesCourse actions are settings that Professors can perform on their courses, described as a coherent object on top of contained lessons. Also, the heavy.png file corresponds to the background image of the Heavy Decoration template. Course actions are visible on the Professor's homepage (a set of actions next to each Course). Apart from these background images you can display an external image, by supplying its URL.
Administrators can also access these settings directly from the course list on their interface.

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