Directrius per a l'accessibilitat al contingut web, versió 1.0

Aquestes directrius expliquen com fer que el contingut web sigui accessible a persones amb discapacitats i s'adrecen a creadors de contingut (autors de pàgines web o dissenyadors de llocs web) i a creadors d'eines d'autor. L'objectiu principal d'aquestes directrius és promoure l'accessibilitat. Tanmateix, l'aplicació de les directrius facilitarà l'accés al contingut a tot tipus d'usuari, sigui quin sigui l'agent d'usuari usat (navegador web, navegador de veu, telèfon mòbil, ordinador de cotxe, etc.) o les condicions de l'entorn de consulta (entorns sorollosos, espais mal il·luminats, entorns en què no es poden usar les mans, etc.). L'aplicació d'aquestes directrius també ajudarà els usuaris a trobar la informació d'una manera més ràpida dins el web. Les directrius no pretenen desincentivar l'ús d'imatges, vídeo, etc., sinó que expliquen com fer que el contingut multimèdia sigui més accessible a una àmplia audiència.Aquest és un document de referència per a uns principis d'accessibilitat i idees de disseny. Algunes de les estratègies comentades tracten d'aspectes relatius a la internacionalització del web i a l'accés des de terminals mòbils. Tanmateix, el document se centra en l'accessibilitat i no tracta exhaustivament dels aspectes relacionats amb altres activitats del W3C. Si voleu més informació sobre aquests temes podeu consultar les pàgines inicials W3C Mobile Access Activity (per a l'accés des de terminals mòbils) i W3C Internationalization Activity (per als aspectes d'internacionalització).Aquest document està pensat per a ser estable en el temps i, per tant, no dóna informació específica sobre si els navegadors funcionen o no amb una determinada tecnologia, ja que aquesta informació varia molt ràpidament. Aquesta informació es pot trobar al web de la Web Accessibility Initiative ,WAI, (Iniciativa d'Accessibilitat Web) [WAI-UA-SUPPORT].Aquest document inclou un annex que organitza tots els punts de verificació ordenats per tema i per prioritat. Els punts de l'annex estan enllaçats a les respectives definicions en el document. Els temes recollits en l'annex inclouen les imatges, el contingut multimèdia, les taules, els marcs, els formularis i els scripts. L'annex es presenta en forma de taula o com a simple llista.Un document a part, amb el títol Techniques for Web Content Accessibility Guidelines 1.0 (Tècniques per a les directrius per a l'accessibilitat al contingut web, versió 1.0) ([TECHNIQUES]) explica com posar a la pràctica els punts citats fins aquí. El document de tècniques explica cada punt amb més detalls i dóna exemples usant el llenguatge d'etiquetatge d'hipertext (HTML), fulls d'estil en cascada (CSS), el llenguatge d'integració multimèdia sincronitzada (SMIL) o el llenguatge d'etiquetatge matemàtic (MathML). Aquest document també inclou tècniques per a provar o validar una pàgina web i un índex dels elements i atributs HTML amb les tècniques que els usen. El document de tècniques està pensat per a seguir de prop els canvis tecnològics i es preveu que s'actualitzi més sovint que les directrius.Nota: Algunes de les característiques descrites en les directrius no estan encara implementades en tots els navegadors o eines multimèdia; en concret pot ser que no es puguin utilitzar funcions noves d'HTML 4.0, de CSS1 o CSS2.Les Directrius per a l'accessibilitat al contingut web, versió 1.0 són part d'una col·lecció de directrius sobre accessibilitat publicades per la Web Accessibility Initiative, WAI (Iniciativa d'Accessibilitat Web). La col·lecció comprèn User Agent Accessibility Guidelines (Directrius d'accessibilitat per a agents d'usuari) [WAI-USERAGENT] i Authoring Tool Accessibility Guidelines (Directrius d'accessibilitat per a eines d'autor [WAI-AUTOOLS].

Directrius per a l'accessibilitat al contingut web, versió 1.0. Recomanació de W3C, 5 de maig de 1999

Aquestes directrius expliquen com fer que el contingut web sigui accessible a persones ambdiscapacitats i s'adrecen a creadors de contingut (autors de pàgines web o dissenyadors de llocs web) ia creadors d'eines d'autor. L'objectiu principal d'aquestes directrius és promoure l'accessibilitat.Tanmateix, l'aplicació de les directrius facilitarà l'accés al contingut a tot tipus d'usuari, sigui quin siguil'agent d'usuari usat (navegador web, navegador de veu, telèfon mòbil, ordinador de cotxe, etc.) o les condicions de l'entorn de consulta (entorns sorollosos, espais mal il·luminats, entorns en què no es poden usar lesmans, etc.). L'aplicació d'aquestes directrius també ajudarà els usuaris a trobar la informació d'unamanera més ràpida dins el web. Les directrius no pretenen desincentivar l'ús d'imatges, vídeo, etc., sinóque expliquen com fer que el contingut multimèdia sigui més accessible a una àmplia audiència.Aquest és un document de referència per a uns principis d'accessibilitat i idees de disseny. Algunes deles estratègies comentades tracten d'aspectes relatius a la internacionalització del web i a l'accés desde terminals mòbils. Tanmateix, el document se centra en l'accessibilitat i no tracta exhaustivament delsaspectes relacionats amb altres activitats del W3C. Si voleu més informació sobre aquests temes podeuconsultar les pàgines inicials W3C Mobile Access Activity (per a l'accés des de terminals mòbils) i W3CInternationalization Activity (per als aspectes d'internacionalització). Aquest document està pensat per a ser estable en el temps i, per tant, no dóna informació específica sobre si els navegadors funcionen o no amb una determinada tecnologia, ja que aquesta informació varia molt ràpidament. Aquesta informació es pot trobar al web de la Web Accessibility Initiative ,WAI, (Iniciativa d'Accessibilitat Web) [WAI-UA-SUPPORT].Aquest document inclou un annex que organitza tots els punts de verificació ordenats per tema i perprioritat. Els punts de l'annex estan enllaçats a les respectives definicions en el document. Els temesrecollits en l'annex inclouen les imatges, el contingut multimèdia, les taules, els marcs, els formularis iels scripts. L'annex es presenta en forma de taula o com a simple llista. Un document a part, amb el títol Techniques for Web Content Accessibility Guidelines 1.0 (Tècniques per a les directrius per a l'accessibilitat al contingut web, versió 1.0) ([TECHNIQUES]) explica com posar a la pràctica els punts citats fins aquí. El document de tècniques explica cada punt amb més detalls i dóna exemples usant el llenguatge d'etiquetatge d'hipertext (HTML), fulls d'estil en cascada (CSS), el llenguatge d'integració multimèdia sincronitzada (SMIL) o el llenguatge d'etiquetatge matemàtic (MathML). Aquest document també inclou tècniques per a provar o validar una pàgina web i un índex Directrius per a l'accessibilitat al contingut web, versió 1.0 dels elements i atributs HTML amb les tècniques que els usen. El document de tècniques està pensat per a seguir de prop els canvis tecnològics i es preveu que s'actualitzi més sovint que les directrius.

Botulinum neurotoxin type A blocks the morphological changes induced by chemical stimulation on the presynaptic membrane of Torpedo synaptosomes.

The action of botulinum neurotoxin on acetylcholine release, and on the structural changes at the presynaptic membrane associated with the transmitter release,was studied by using a subcellular fraction of cholinergic nerve terminals (synaptosomes) isolated from the Torpedo electric organ. Acetylcholine and ATP release were continuously monitored by chemiluminescent methods.To catch the membrane morphological changes, the quick-freezing method was applied. Our results show that botulinum neurotoxin inhibits the release of acetylcholine from these isolated nerve terminals in a dose-dependent manner, whereas ATP release is not affected. The maximal inhibition (70%) is achieved at neurotoxin concentrations as low as 125 pM with an incubation time of 6 min. This effect is not linked to an alteration of the integrity of the synaptosomes since, after poisoning by botulinum neurotoxin type A, they show a nonmodified occluded lactate dehydrogenase activity. Moreover, membrane potential is not altered by the toxin with respect to the control, either in resting condition or after potassium depolarization. In addition to acetylcholine release inhibition, botulinum neurotoxin blocks the rearrangement of the presynaptic intramembrane particles induced by potassium stimulation. The action of botulinum neurotoxin suggests that the intramembrane particle rearrangement is related to the acetylcholine secretion induced by potassium stimulation in synaptosomes isolated from the electric organ of Torpedo marmorata.

VGLUT1 is Present in Cortical, Hippocampal and Striatal Astrocytes

The last decade has presented studies providing evidence for astrocytic exocytosis of glutamate potentiating nerve signals. To make further investigations into this astrocytic attribute we investigated the localization of the vesicular glutamate transporter 1 (VGLUT1) in small processes of astrocytes close to glutamatergic terminals in frontal cortex, striatum, molecular layer of hippocampus and stratum radiatum of hippocampus. According to the importance of VGLUT1 in glutamate exocytosis the presence of VGLUT1 in astrocytic processes indicates the ability to exocytose glutamate. METHODS: For qualitative analysis we used immunoflourescence histochemistry. Sections from rat frontal cortex, striatum, molecular layer of hippocampus and stratum radiatum of hippocampus were labeled with antibodies against glutamine synthetase (an astrocytic marker) and VGLUT1. Z-stacks of 4.5-5 lm obtained by confocal microscopy from each section were deconvolved and 3D reconstructed in Amira. Small astrocytic processes were analysed for the presence of VGLUT1 inside the processes. The quantitative analysis was done by immunogold labeling. Ultrathin sections from each brain region were labeled for GLT (an astrocytic marker) and VGLUT1. Pictures obtained by electron microscopy were analysed and the point density (gold particles/nm2) for VGLUT1 in astrocytic processes was measured. RESULTS: Using confocal 3D reconstructions we were qualitatively able to identify VGLUT1 within small processes of astrocytes in all four brain regions. Reflecting our qualitative findings the electron microscopical immunogold quantifications showed a significant density of gold particles signaling VGLUT1 in astrocytic processes in all four brain regions. CONCLUSION: We extend the results of previous studies on glutamate release from astrocytes, which have focused on the hippocampus, proposing that astrocytic exocytosis of glutamate is a global phenomenon in the brain.

Spatial, temporal and subcellular localization of islet-brain 1 (IB1), a homologue of JIP-1, in mouse brain.

Islet-brain 1 (IB1) was recently identified as a DNA-binding protein of the GLUT2 gene promoter. The mouse IB1 is the rat and human homologue of the Jun-interacting protein 1 (JIP-1) which has been recognized as a key player in the regulation of c-Jun amino-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) pathways. JIP-1 is involved in the control of apoptosis and may play a role in brain development and aging. Here, IB1 was studied in adult and developing mouse brain tissue by in situ hybridization, Northern and Western blot analysis at cellular and subcellular levels, as well as by immunocytochemistry in brain sections and cell cultures. IB1 expression was localized in the synaptic regions of the olfactory bulb, retina, cerebral and cerebellar cortex and hippocampus in the adult mouse brain. IB1 was also detected in a restricted number of axons, as in the mossy fibres from dentate gyrus in the hippocampus, and was found in soma, dendrites and axons of cerebellar Purkinje cells. After birth, IB1 expression peaks at postnatal day 15. IB1 was located in axonal and dendritic growth cones in primary telencephalon cells. By biochemical and subcellular fractionation of neuronal cells, IB1 was detected both in the cytosolic and membrane fractions. Taken together with previous data, the restricted neuronal expression of IB1 in developing and adult brain and its prominent localization in synapses suggest that the protein may be critical for cell signalling in developing and mature nerve terminals.

2009 Iowa’s Rail System Background Prepared by the Office of Systems Planning December 2010

Iowa’s Rail Environment Iowa’s rail transportation system provides both freight and passenger service. Rail serves a variety of trips, including those within Iowa and those to other states as well as to foreign markets. While rail competes with other modes, it also cooperates with those modes to provide intermodal services to Iowans. In 2009 Iowa’s rail transportation system could be described as follows: Freight Iowa’s 130,000-mile freight transportation system includes an extensive railroad network, a well-developed highway system, two bordering navigable waterways, and a pipeline network as well as air cargo facilities. While rail accounts for only 3 percent of the freight network, it carries 43 percent of Iowa’s freight tonnage. A great variety of commodities ranging from fresh fish to textiles to optical products are moved by rail. However, most of the Iowa rail shipments consist of bulk commodities, including grain, grain products, coal, ethanol, and fertilizers. The railroad network performs an important role in moving bulk commodities produced and consumed in the state to local processors, livestock feeders, river terminals and ports for foreign export. The railroad’s ability to haul large volumes, long distances at low costs will continue to be a major factor in moving freight and improving the economy of Iowa. Key 2008 Facts • 3,945 miles of track • 18 railroads • 49.5 million tons shipped • 39.7 million tons received • 2 Amtrak routes • 6 Amtrak stations • 66,286 rail passenger rides Key Rail Trends • slightly fewer miles being operated; • railroads serving Iowa has remained the same; • more rail freight traffic; • more tons hauled per car; • higher average rail rates per ton-mile since 2002; • more car and tons hauled per locomotive; and • more ton miles per gallon of fuel consumed. Iowa’s rail system and service has been evolving over time relative to its size, financial conditions, and competition from other modes.

Astrocytes contain a vesicular compartment that is competent for regulated exocytosis of glutamate.

Astrocytes establish rapid cell-to-cell communication through the release of chemical transmitters. The underlying mechanisms and functional significance of this release are, however, not well understood. Here we identify an astrocytic vesicular compartment that is competent for glutamate exocytosis. Using postembedding immunogold labeling of the rat hippocampus, we show that vesicular glutamate transporters (VGLUT1/2) and the vesicular SNARE protein, cellubrevin, are both expressed in small vesicular organelles that resemble synaptic vesicles of glutamatergic terminals. Astrocytic vesicles, which are not as densely packed as their neuronal counterparts, can be observed in small groups at sites adjacent to neuronal structures bearing glutamate receptors. Fluorescently tagged VGLUT-containing vesicles were studied dynamically in living astrocytes by total internal reflection fluorescence (TIRF) microscopy. After activation of metabotropic glutamate receptors, astrocytic vesicles underwent rapid (milliseconds) Ca(2+)- and SNARE-dependent exocytic fusion that was accompanied by glutamate release. These data document the existence of a Ca(2+)-dependent quantal glutamate release activity in glia that was previously considered to be specific to synapses.

Large scale purification of presynaptic plasma membranes from Torpedo marmorata electric organ

The presynaptic plasma membrane (PSPM) of cholinergic nerve terminals was purified from Torpedo electric organ using a large-scale procedure. Up to 500 g of frozen electric organ were fractioned in a single run, leading to the isolation of greater than 100 mg of PSPM proteins. The purity of the fraction is similar to that of the synaptosomal plasma membrane obtained after subfractionation of Torpedo synaptosomes as judged by its membrane-bound acetylcholinesterase activity, the number of Glycera convoluta neurotoxin binding sites, and the binding of two monoclonal antibodies directed against PSPM. The specificity of these antibodies for the PSPM is demonstrated by immunofluorescence microscopy.

Legislative Information, January 25, 2012

The Legislative Information Office (LIO) provides information concerning the Iowa General Assembly. As part of the nonpartisan Legislative Services Agency (LSA), the Legislature’s legal, fiscal, and computer services agency, the LIO has access to the most current information on the actions and procedures of the Iowa Legislature. The LIO responds to inquiries from the general public, private and public agencies, and business interests with nonpartisan information about the Iowa General Assembly. The office includes two public access computer terminals, for any member of the public to access legislative information using the Iowa General Assembly web site: www.legis.iowa.gov

Astrocytic αVβ3 integrin inhibits neurite outgrowth and promotes retraction of neuronal processes by clustering Thy-1.

Thy-1 is a membrane glycoprotein suggested to stabilize or inhibit growth of neuronal processes. However, its precise function has remained obscure, because its endogenous ligand is unknown. We previously showed that Thy-1 binds directly to α(V)β(3) integrin in trans eliciting responses in astrocytes. Nonetheless, whether α(V)β(3) integrin might also serve as a Thy-1-ligand triggering a neuronal response has not been explored. Thus, utilizing primary neurons and a neuron-derived cell line CAD, Thy-1-mediated effects of α(V)β(3) integrin on growth and retraction of neuronal processes were tested. In astrocyte-neuron co-cultures, endogenous α(V)β(3) integrin restricted neurite outgrowth. Likewise, α(V)β(3)-Fc was sufficient to suppress neurite extension in Thy-1(+), but not in Thy-1(-) CAD cells. In differentiating primary neurons exposed to α(V)β(3)-Fc, fewer and shorter dendrites were detected. This effect was abolished by cleavage of Thy-1 from the neuronal surface using phosphoinositide-specific phospholipase C (PI-PLC). Moreover, α(V)β(3)-Fc also induced retraction of already extended Thy-1(+)-axon-like neurites in differentiated CAD cells as well as of axonal terminals in differentiated primary neurons. Axonal retraction occurred when redistribution and clustering of Thy-1 molecules in the plasma membrane was induced by α(V)β(3) integrin. Binding of α(V)β(3)-Fc was detected in Thy-1 clusters during axon retraction of primary neurons. Moreover, α(V)β(3)-Fc-induced Thy-1 clustering correlated in time and space with redistribution and inactivation of Src kinase. Thus, our data indicates that α(V)β(3) integrin is a ligand for Thy-1 that upon binding not only restricts the growth of neurites, but also induces retraction of already existing processes by inducing Thy-1 clustering. We propose that these events participate in bi-directional astrocyte-neuron communication relevant to axonal repair after neuronal damage.

Controversies metodològiques de la investigació

En aquest article es plantegen noves formes d'abordar les dues grans crisis generades a causa de l'escisió metodològica que va tenir lloc en els anys seixanta: la de legitimació i la de representació, crisis que són la base de les actuals controvèrsies metodològiques. Superar la dicotomía subjecte-objecte, transformar el concepte de validesa pel de fidelitat, entendre que la investigació es impensable desvinculada del context social i acceptar que la naturalesa més íntima del coneixement es troba en la multiperspectivitat d'aquest, constitueixen els elements clau proposts per a reduïr i tractar de superar la crisi. Per assolir-lo, aquest treball postula la necessitat de no continuar desvinculant la ciència de la filosofia, i de crear espais interactius entre ciència, tecnologia i societat.

SDF 1-alpha (CXCL12) triggers glutamate exocytosis from astrocytes on a millisecond time scale: Imaging analysis at the single-vesicle level with TIRF microscopy

Chemokines are small chemotactic molecules widely expressed throughout the central nervous system. A number of papers, during the past few years, have suggested that they have physiological functions in addition to their roles in neuroinflammatory diseases. In this context, the best evidence concerns the CXC-chemokine stromal cell-derived factor (SDF-1alpha or CXCL12) and its receptor CXCR4, whose signalling cascade is also implicated in the glutamate release process from astrocytes. Recently, astrocytic synaptic like microvesicles (SLMVs) that express vesicular glutamate transporters (VGLUTs) and are able to release glutamate by Ca(2+)-dependent regulated exocytosis, have been described both in tissue and in cultured astrocytes. Here, in order to elucidate whether SDF-1alpha/CXCR4 system can participate to the brain fast communication systems, we investigated whether the activation of CXCR4 receptor triggers glutamate exocytosis in astrocytes. By using total internal reflection (TIRF) microscopy and the membrane-fluorescent styryl dye FM4-64, we adapted an imaging methodology recently developed to measure exocytosis and recycling in synaptic terminals, and monitored the CXCR4-mediated exocytosis of SLMVs in astrocytes. We analyzed the co-localization of VGLUT with the FM dye at single-vesicle level, and observed the kinetics of the FM dye release during single fusion events. We found that the activation of CXCR4 receptors triggered a burst of exocytosis on a millisecond time scale that involved the release of Ca(2+) from internal stores. These results support the idea that astrocytes can respond to external stimuli and communicate with the neighboring cells via fast release of glutamate.

Inhibitory effect of neuropeptide Y on stimulated renin secretion of awake rats.

1. (1-36)-NPY is a vasoconstrictor peptide widely distributed in sympathetic nerve terminals. This peptide exerts an inhibitory action on renin release induced by various stimuli. Post-synaptic neuropeptide Y (NPY) receptors show a high affinity for (1-36)-NPY as well as for the agonist (Pro34)-NPY, while presynaptic receptors bind preferentially (13-36)-NPY. 2. This study was undertaken to assess whether the NPY induced renin suppression in awake normotensive rats infused with the beta-adrenoceptor stimulant isoproterenol is mediated by activation of pre- or post-synaptic receptors. 3. Non-pressor doses of (1-36)-NPY and (Pro34)-NPY markedly attenuated the renin secretion triggered by isoproterenol whereas (13-36)-NPY had no effect. This suggests that the effect of NPY on renin release is due to the stimulation of post-synaptic receptors. However it remains unknown whether NPY acts directly on juxtaglomerular cells or indirectly by modifying intraglomerular haemodynamics.

PSD-95 promotes synaptogenesis and multiinnervated spine formation through nitric oxide signaling

Postsynaptic density 95 (PSD-95) is an important regulator of synaptic structure and plasticity. However, its contribution to synapse formation and organization remains unclear. Using a combined electron microscopic, genetic, and pharmacological approach, we uncover a new mechanism through which PSD-95 regulates synaptogenesis. We find that PSD-95 overexpression affected spine morphology but also promoted the formation of multiinnervated spines (MISs) contacted by up to seven presynaptic terminals. The formation of multiple contacts was specifically prevented by deletion of the PDZ(2) domain of PSD-95, which interacts with nitric oxide (NO) synthase (NOS). Similarly, PSD-95 overexpression combined with small interfering RNA-mediated down-regulation or the pharmacological blockade of NOS prevented axon differentiation into varicosities and multisynapse formation. Conversely, treatment of hippocampal slices with an NO donor or cyclic guanosine monophosphate analogue induced MISs. NOS blockade also reduced spine and synapse density in developing hippocampal cultures. These results indicate that the postsynaptic site, through an NOS-PSD-95 interaction and NO signaling, promotes synapse formation with nearby axons.

Competències i avaluació d'activitats per a l'aprenentatge de didàctica de la llengua i la literatura

L'experiència d'innovació que es presenta en aquest article tracta del disseny i l'aplicació a l'aulad'activitats d'aprenentatge, implicades en l'ensenyament d'assignatures de didàctica de la llengua i laliteratura, en el marc de l'avaluació de competències pròpies de l'àrea. S'analitza i es reflexiona sobrediversos models d'avaluació i en alguns formats interactius en línia que presenta la plataforma virtual Moodle, amb l'objectiu d'afavorir l'autoregulació dels aprenentatges.