Podcasts about cntf

Host Chris Adams is joined by Max Schulze from the SDIA (The Sustainable Digital Alliance) and they discuss three stories from the worlds of IaaS, PaaS and Saas! While these three acronyms are more than likely ever present in most digital people's lives, we might not know about the environmental impact that they have. Chris and Max cover stories from the CNCF, Google, CIODive and OpenJS as well as upcoming events in the Green Software community.

We discuss clinical trials using CNTF to treat MacTel Type 2 with Dr. John Pollack, Chief Medical Officer of Neurotech Pharmaceuticals.

Au Congo-Brazzaville, l'État a vendu à un particulier le site du Chantier naval et transports fluviaux (CNTF), une société liquidée depuis 2013. Au moins 350 ex-agents de cette entreprise exigent de l'État le paiement intégral de leurs droits avant de libérer ce site. C'est la grande saison sèche. Sur le site du chantier naval, les eaux ont visiblement baissé. Dans un bateau à quai, on peut entendre des coups de marteau. Des ouvriers font des réparations. Mais ils seront déguerpis dans un proche avenir, car le site a été vendu par les autorités à un particulier qui va y ériger un grand centre commercial. Un membre du gouvernement est descendu sur les lieux donner l'information aux ex-travailleurs du Chantier naval et transports fluviaux. « L'État a depuis toujours procédé à des ventes. La dernière en date est celle du chantier naval et des transports fluviaux qui a eu lieu début juin. L'État a vendu le site à 100 milliards de FCFA (152 millions d'euros) », a affirmé Vincent Edgard Boura, président du syndicat des anciens agents.  Les anciens travailleurs ne s'opposent nullement à cette vente. Mais ils exigent le paiement intégral de leurs droits avant de libérer le site. « Les travailleurs attendent toujours d'être payés pour un montant de plus de 7 milliards de FCFA (plus de 10 millions d'euros) pour les droits de licenciement et 6 milliards environ (plus de 9 millions d'euros) pour les arriérés de salaires ; soit une somme d'environ 15 milliards de FCFA (plus de 22 millions d'euros). À ce jour, nous attendons que ces sommes nous soient payées en totalité. En tout cas le même jour où nous serons payés tous, nous évacuerons et libérerons ce site », a promis M. Boura.  Par l'entremise d'Antoine Okonolingui, ils brandissent une décision de justice qui fait obligation à l'État d'utiliser les fonds qui résulteraient de la vente du chantier au règlement de leurs arriérés de salaires et autres droits de licenciement collectif. « Les fonds résultant de la réalisation des actifs et du recouvrement des créances sont destinés au règlement du passif non transféré au portefeuille de l'État, et prioritairement au paiement des droits des travailleurs », stipule la décision de justice lue par M.Okonolingui.  Journaliste et analyste des transports fluviaux Alexis Mélemon, dit de la Rivière, juge cette vente inopportune. « Le chantier naval vendu est une triste nouvelle pour moi parce que ce chantier a été construit en 1925 par les sociétés concessionnaires qu'on désignait  par les messageries fluviales du Congo », se lamente-t-il.   Sans chantier naval, que deviendra le transport sur le fleuve, s'interroge-t-il. « Puisqu'on n'a plus de chantier naval, donc il n'y aura plus de bateaux. Donc, on ne pourra plus reconquérir cette vocation perdue de pays de transit », analyse Alexis Mélemon.   Le chantier naval et transports fluviaux (CNTF) était une entité résiduelle née de la dislocation l'ancienne Agence transcongolaise de communication (ATC).

What is learning and memory? Is amnesia really a loss of stored memories or something more? In this interview, we will discuss where memory goes and if there is a way to retrieve them after trauma. Recent studies have shown that spatial memories are encoded as sparse populations of cells that are activated during learning and are necessary for the retrieval of specific memories. We refer to these cells as "memory engram cells" and the focus of Tomás J Ryan and his team is to understand how engram cells are able to store specific memories as information. Here is a quick summary/breakdown of the video above. The old storage theory of amnesia is WRONG. The problem is the ability to retrieve the memory. Short term memory lasts a few hours. It is very disruptable (long term is not). Long term memory lasts your entire lifetime. It requires transcription and translation of many different genes. We have many different genes that regulate memory. They are different for short term and long term - playing roles at different stages. Most popular was CREB (turns on other genes). Engrams cells are structures in the brain where memories are stored. R They used optigenetics to prove engram cells were important for memory. Engram cells only account for 4-6% of the brain cells in the hippocampus (of mice). V Consolidation idea - a short term memory (unstable) forms into a long term memory (stable), thus stabilizing the engram. Optogenetics - let's us express photoactivatable opsins in whatever region of the brain we want. The brain is electrically active. They put certain opsins into brain cells and then stimulate them with light. These opsins can conduct ions - putting positively charged cations from the external environment of the cell into the neuron. This depolarizes the cell, which results in an action potential (creating neuronal activity). What they did at MIT was integrate optogenetics and memory engram cells. They tested parts of the brain using a transgenetics - they took immediate/early genes (genes that show activity as a function of neuronal spike) and used opsins to only activate those genes. Amnesia and Memory Learning is the enhancement of synaptic connections. Memory is a stable thing in the brain and can last for your entire life. Learning and recall are not "things", they are activities. Learning = process of making a memory. Recall = process of retrieving a memory. So the problem is not memory itself. Amnesic engram cells have a loss of synaptic strength. Increasing the synaptic strength helps get the memory (which is commonly seen in Alzheimer's (AD), Huntington's (HD)). If you increase the synaptic potentiation (increasing the dendritic spine density), esp. of the amnesic engram cells, you can get natural access to those memories. Neurotrophic factors (BDNF, NGF, CNTF, GDNF) do this, but are not localized nor memory specific. Learning something new (about something you are amnesic about) will train your brain to those particular engram cells. Once you activate the engram cells (with optogenetics), you can restore access to old information and add new information on those amnesic memories. Without dealing with the cause, you probably won't be able to really restore memories (in diseases like AD, HD, etc.) In late stages of neurodegeneration, you may actually lose memories. Actions to take for prevention Stay mentally active Engage in physical exercise Actions to take for amnesia (acute memory loss) Do everything to remind yourself of those experiences Retrain on the "forgotten" pieces We briefly discussed gene expression and histone acetylation to enhance memory. https://mybiohack.com/blog/tomas-j-ryan-debunking-amnesia-and-stabilizing-engram-cells

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) accompanied by demyelination and axonal loss. Only a minority of the demyelinated MS lesions gets remyelinated. In animal models, however, remyelination is the default program following immune-mediated or toxic demyelination. This thesis aims to find factors regulating remyelination in MS. The starting point was autoptic tissue from MS patients. First, different types of MS lesions were macrodissected namely, chronic inactive demyelinated lesions that had failed to remyelinate, lesions undergoing active demyelination and remyelinated lesions. Healthy white matter was used as control tissue. Gene expression profiles of these lesions were established using quantitative PCR low density arrays. Thereby the focus was on the extracellular matrix (ECM) and on factors known to regulate the biology of oligodendrocytes. ECM components can regulate oligodendrocyte differentiation and modify immune reactions in multiple ways, e.g., by sequestering or displaying growth factors and by directly interacting with immune cells and glial cells. The expression of 50 ECM components and 34 ECM degrading enzymes was measured by qPCR. COL1A1, COL3A1, COL5A1 and COL5A2 chains were strongly induced in active lesions and even more in chronic inactive lesions. These collagen polypeptide chains interact to form collagen types I, III and V, which are grouped as fibrillar collagens. Furthermore, two Small Leucine Rich Proteoglycans (SLRPs), biglycan and decorin, which can decorate fibrillar collagens, were also strongly induced. Immunostaining localized the fibrillar collagens, biglycan, and decorin around blood vessels. These ECM molecules were largely seen in the perivascular space closely associated with infiltrating immune cells forming a mesh between the endothelium and the astrocytic glia limitans. In active lesions collagen V was also seen in the heavily infiltrated brain parenchyma. Since these ECM molecules were found largely in the perivascular space close to immune cells and hardly in the surrounding parenchyma where oligodendrocyte differentiation takes place, the interaction of these ECM components with immune cells was further analysed. In vitro experiments revealed that the fibrillar collagens I and III inhibited the monocytic production of CCL2 (MCP-1), an inflammatory chemokine thought to be involved in the recruitment of immune cells to the inflamed brain. This suggests that the induced fibrillar collagens may contribute to the limitation of MS lesions expansion by inhibition of the CCL2 production by monocytes. The second set of analysed genes comprised 32 factors regulating survival, proliferation and/or differentiation of oligodendrocytes and 18 receptors of these genes. The key factors for oligodendrocyte differentiation (IGF1, IGF2 and CNTF) and oligodendrocyte proliferation (FGF2 and PDGFAA) were still present in demyelinated lesions, although their expression ratio was altered. The most striking result was the up-regulation of FGF9 in a subset of chronically demyelinated lesions, but in none of the remyelinated shadow plaques. The potential functional role of this observation was investigated by treating myelinating rat central nervous system cultures with exogenous FGF9. In this experimental setting, FGF9 inhibited the ability of mature oligodendrocytes to myelinate and ensheath axons. All these data suggests that the induction of FGF9 in some chronic MS lesions is one of the inhibitory mechanisms accounting for the failure of remyelination. Together, this thesis has two main findings: A) Fibrillar collagens, biglycan and decorin form a perivascular fibrosis and the fibrillar collagens I and III inhibit production of CCL2 by monocytes. Inhibition of CCL2 production by fibrillar collagens might contribute to lesion confinement. B) Expression profiles of remyelinated MS lesions were established for the first time and thereby, up-regulation of FGF9 in demyelinated, but not in remyelinated lesions was revealed. The inhibition of myelination in vitro by FGF9 suggests that this is one potential mechanism to explain why demyelinated lesions expressing higher FGF9 level fail to remyelinate.

Das Glioblastoma multiforme ist ein maligner hirneigener Tumor mit einer bislang infausten Prognose. Humane mesenchymale Progenitorzellen des Knochenmarks (hMSC) zeigen in-vitro und in-vivo einen ausgeprägten glioblastom¬induzierten Tropismus. Sie sind einfach in der Handhabung, weil sie leicht zu gewinnen, in Kultur zu vervielfältigen und anschließend autolog zu transplantieren sind. Diese Eigenschaften machen hMSC zu vielversprechenden Kandidaten für eine zellbasierte Gentherapie des Glioblastoms. Die molekularen Mechanismen, welche zu der gerichteten Migration der hMSC hin zu den Glioblastomzellen führen und die biologischen Wechselwirkungen zwischen Stammzellen und Tumorzellen sind bisher kaum verstanden. Um erste Einblicke in diese Wechselwirkungen zu erlangen, wurden im Rahmen des vorliegenden Promotionsvorhabens in-vitro Untersuchungen zu den Grundlagen des glioblastominduzierten Tropismus von hMSC durchgeführt. Die Fragestellung befasste sich insbesondere damit, welche Chemokine an der Vermittlung der glioblastomgerichteten Migration von hMSC beteiligt sind. Hierzu wurden Migrationsversuche mit einer modifizierten Boyden Kammer durchgeführt, wobei zunächst einige bekannte glioblastomassoziierte Chemokin-kandidaten (IL-8, NT-3, TGF-ß1, EGF, CNTF, GDNF, PDGF und BDNF) getestet wurden. Eine signifikante chemotaktische Eigenschaft auf hMSC wurde hierbei für IL-8, TGF-ß1 und NT-3 beobachtet. Die promigratorische Wirkung dieser drei Chemokine erwies sich hierbei als konzentrationsabhängig. Im Weiteren wurde nachgewiesen, dass die bekannte chemotaktische Wirkung von glioblastom-konditioniertem Medium auf hMSC durch die Zugabe von IL-8, TGF-ß, beziehungs¬weise NT-3 neutralisierenden Antikörpern signifikant reduziert wird. Somit konnte funktionell nachgewiesen werden, dass diese Chemokine tatsächlich eine Rolle beim glioblastominduziertem Tropismus der hMSC spielen. Ergänzend wurde mittels Immunfluoreszenzfärbung die Expression der entsprechenden Chemokin¬rezeptoren auf den hMSC nachgewiesen und die Sekretion der Chemokine durch die Glioblastomzellen mittels ELISA quantifiziert. Aus Vorarbeiten unserer Arbeitsgruppe ist bekannt, dass auch VEGF-A eine chemotaktische Wirkung auf hMSC besitzt. Wie VEGF-A werden auch IL-8, TGF-ß1 und NT-3 von Glioblastomen überexprimiert. Zudem wird über diese Chemokine die Neoangiogenese jener Tumore vermittelt. Dies führt zu der Hypo-these, dass Glioblastome die Migration der hMSC aus dem peripheren Blut in das Tumorgebiet über angiogenetische Signalwege vermitteln. Damit könnten hMSC an dem Prozess der Angiogenese des Glioblastoms beteiligt sein. Ein genaues Verständnis des möglichen Beitrages von hMSC zum Glioblastomwachstum ist eine unabdingbare Voraussetzung für ihre mögliche klinische Anwendung als gentherapeutische Vektoren beim Menschen. Deshalb müssen zukünftig neben weiteren in-vitro vor allem in-vivo Studien mit Langzeit-beobachtungen im Tiermodell durchgeführt werden. In diesen Studien sollten die Auswirkungen einer Transplantation nativer hMSC einerseits und genetisch modifizierter therapeutischer hMSC andererseits auf das Glioblastomwachstum untersucht werden. Die vielversprechenden Ergebnisse der bisher vorliegenden Arbeiten lassen hoffen, dass in nicht allzu ferner Zukunft eine bessere Therapie für Patienten mit Glioblastom gefunden werden kann.

Objective: This comparative in vitro study examined the effects of all known gp130 cytokines on murine corticotroph AtT-20 cell function. Methods: Cytokines were tested at equimolar concentrations from 0.078 to 10 nM. Tyrosine phosphorylation of the signal transducer and activator of transcription ( STAT) 3 and STAT1, the STAT-dependent suppressor of cytokine signaling (SOCS)-3 promoter activity, SOCS-3 gene expression, STAT-dependent POMC promoter activity and adrenocorticotropic hormone ( ACTH) secretion were determined. Results: Leukemia inhibitory factor (LIF), human oncostatin M (OSM) and cardiotrophin (CT)-1 (LIFR/gp130 ligands), as well as ciliary neurotrophic factor ( CNTF) and novel neurotrophin1/B-cell stimulating factor-3 (CNTFRalpha/LIFR/gp130 ligands) are potent stimuli of corticotroph cells in vitro. In comparison, interleukin (IL)-6 (IL-6R/gp130 ligand) and IL-11 (IL-11R/gp130 ligand) exhibited only modest direct effects on corticotrophs, while murine OSM (OSMR/gp130 ligand) showed no effect. Conclusion: (i) CNTFR complex ligands are potent stimuli of corticotroph function, comparable to LIFR complex ligands; (ii) IL-6 and IL-11 are relatively weak direct stimuli of corticotroph function; (iii) differential effects of human and murine OSM suggest that LIFR/gp130 (OSMR type I) but not OSMR/gp130 (OSMR type II) are involved in corticotroph signaling. (iv) CT-1 has the hitherto unknown ability to stimulate corticotroph function, and (v) despite redundant immuno-neuroendocrine effects of different gp130 cytokines, corticotroph cells are preferably activated through the LIFR and CNTFR complexes. Copyright (C) 2004 S. Karger AG, Basel.

The structure of the rat ciliary neurotrophic factor (CNTF) gene and the regulation of CNTF mRNA levels in cultured glial cells were investigated. The rat mRNA is encoded by a simple two-exon transcription unit. Sequence analysis of the region upstream of the transcription start-site did not reveal a typical TATA-box consensus sequence. Low levels of CNTF mRNA were detected in cultured Schwann cells, and CNTF mRNA was not increased by a variety of treatments. Three-week-old astrocyte-enriched cell cultures from new-born rat brain contained easily detectable CNTF mRNA. In astrocyte-enriched cultures, upregulation of CNTF mRNA levels was observed after treatment with IFN-. CNTF mRNA levels were down-regulated in these cells by treatments that elevate intracellular cyclic AMP and by members of the fibroblast growth factor (FGF) family. The implications of these results for potential in vivo functions of CNTF are discussed

Little is known about the signal transduction mechanisms involved in the response to neurotrophins and other neurotrophic factors in neurons, beyond the activation of the tyrosine kinase activity of the neurotrophin receptors belonging to the trk family. We have previously shown that the introduction of the oncogene product ras p21 into the cytoplasm of chick embryonic neurons can reproduce the survival and neurite-outgrowth promoting effects of the neurotrophins nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), and of ciliary neurotrophic factor (CNTF). To assess the potential signal- transducing role of endogenous ras p21, we introduced function-blocking anti-ras antibodies or their Fab fragments into cultured chick embryonic neurons. The BDNF-induced neurite outgrowth in E12 nodose ganglion neurons was reduced to below control levels, and the NGF- induced survival of E9 dorsal root ganglion (DRG) neurons was inhibited in a specific and dose-dependent fashion. Both effects could be reversed by saturating the epitope-binding sites with biologically inactive ras p21 before microinjection. Surprisingly, ras p21 did not promote the survival of NGF-dependent E12 chick sympathetic neurons, and the NGF-induced survival in these cells was not inhibited by the Fab-fragments. The survival effect of CNTF on ras-responsive ciliary neurons could not be blocked by anti-ras Fab fragments. These results indicate an involvement of ras p21 in the signal transduction of neurotrophic factors in sensory, but not sympathetic or ciliary neurons, pointing to the existence of different signaling pathways not only in CNTF-responsive, but also in neurotrophin-responsive neuronal populations.