Podcasts about ebna

Obec Paseka se nachází na rozhraní údolí Hornomoravského úvalu a prvních kopců Nízkého Jeseníku. Dnes je to vesnice známá také díky zdejšímu léčebnému ústavu, jehož kořeny sahají do počátku 20. století, kdy ještě populaci kosila zákeřná hrozba v podobě tuberkulózy.Všechny díly podcastu Od Pradědu na Hanou můžete pohodlně poslouchat v mobilní aplikaci mujRozhlas pro Android a iOS nebo na webu mujRozhlas.cz.

Kvalitní vzdělávání v 21. století často vyžaduje přístup k elektřině a internetu. Dostat je do nejodlehlejších míst teď už nemusí být nákladné, říká britsko-finská podnikatelka Yesika Aguilerová. Spolu s týmem dalších mladých lidí vyvinula například přenosnou multimediální učebnu s vlastní elektrárnou. Obojí se dá doslova sbalit na cesty letadlem nebo pěšky divočinou. Svoje vize představila tento týden na konferenci mladých inovátorů v Praze.Všechny díly podcastu Magazín Experiment můžete pohodlně poslouchat v mobilní aplikaci mujRozhlas pro Android a iOS nebo na webu mujRozhlas.cz.

Hostem Hovorů s rodokmenem je Zuzana Pavlík-Šimonková. Studovala dějiny umění, ale poté, co rodina v restitucích získala zpět rodinné dědictví, lesy a polnosti, přešla na Českou zemědělskou univerzitu. „Můj prapradědeček byl jedním z posledních, komu habsburský císař Karel I. udělil šlechtický titul za zásluhy v průmyslu, byl totiž mužem číslo jedna ve Škodových závodech. Pro mě je to dnes spíš úsměvná rodinná historka,“ říká.

Hostem Hovorů s rodokmenem je Zuzana Pavlík-Šimonková. Studovala dějiny umění, ale poté, co rodina v restitucích získala zpět rodinné dědictví, lesy a polnosti, přešla na Českou zemědělskou univerzitu. „Můj prapradědeček byl jedním z posledních, komu habsburský císař Karel I. udělil šlechtický titul za zásluhy v průmyslu, byl totiž mužem číslo jedna ve Škodových závodech. Pro mě je to dnes spíš úsměvná rodinná historka,“ říká.Všechny díly podcastu Hovory můžete pohodlně poslouchat v mobilní aplikaci mujRozhlas pro Android a iOS nebo na webu mujRozhlas.cz.

Rekonstrukce budovy druhého stupně královéhradecké Základní školy Úprkova je hotová. Stavební práce trvaly rok a vyšly město na víc než 75 milionů korun. Zahrnovaly mimo jiné výstavbu nového podlaží, výtahu nebo venkovní učebny. Učitelé už se v opravené budově připravují na začátek školního roku.

Brát děti co nejvíce do přírody a učit se podle ní, tím se řídí učitelka Kateřina Čiháková, která se dostala mezi letošní finalisty ceny pro inspirativní pedagogy. Žáky základní školy Světice ve Středočeském kraji hodiny s Kačkou, jak své učitelce říkají, baví. Poslechněte si, co se naučili na cyklovýletě.Všechny díly podcastu Seriál Radiožurnálu můžete pohodlně poslouchat v mobilní aplikaci mujRozhlas pro Android a iOS nebo na webu mujRozhlas.cz.

Episode Highlights With JimIs Vitamin D harmful?Most of the work done on Vitamin D has been associative dataThe difference between D3 (intermediate molecule) vs storage form vs active formDifferent forms of Vitamin D we can test for and why these aren't always accurateIs there actually accurate testing for Vitamin D?How to actually test the active form of Vitamin D in the bodyWhy he doesn't recommend taking an isolated pill of vitamin DThe reason he says you don't actually need vitamin K to absorb Vitamin DGenetic components of Vitamin D receptors and useMany genetic mutations are meant to be an advantage Why you aren't going to get over 60 on a vitamin D test naturallyOne snip that is important for vitamin DMisconceptions about Vitamin D during pregnancyThe difference between getting Vitamin D as a supplement vs making it from sun exposureWe make a sulfated form of D3 from sun exposure7-Dehydrocholesterol from the sun (not present in supplements)Why the most important molecule from sun exposure can't be obtained from a supplementHow PUFA molecules interact with the sun equation and his take on PUFASHow viruses like Epstein-barr can interfere with the vitamin D process in the bodyWhat to do if you've taken a lot of oral Vitamin D and think it might have caused an issueHow vitamin K can actually be helpful and why magnesium is important tooCan sun exposure actually help avoid cancerThe problems with sunscreenWhat to know for healthy sun exposure and what it means when we look pink for a few minutes after sun exposureThe importance of not wearing sunglasses in the sun because it makes your more likely to burnResources We MentionJim Stephenson - Facebook GroupJim Stephenson - SubstackAIDS: The crime Beyond Belief by William L. C. ScottBenefits of Sunlight: A Bright Spot for Human HealthAbsence of Seasonal Variation in Serum Concentrations of 1,25-Dihydroxyvitamin D Despite a Rise in 25-Hydroxyvitamin D in SummerUVB Light Prevents Atherosclerosis By Reducing InflammationThe "D" Vitamins by Jack DeRuiterA human skin equivalent model that mimics the photoproduction of vitamin D3 in human skinEpstein-Barr virus encoded EBNA-3 binds to vitamin D receptor and blocks activation of its target genesThanks to Our Sponsors:Hiya Children's Vitamins - A clean line of children's vitamins that provides growing kids with all the essential nutrients that might be missing from their dietBON CHARGE - A holistic wellness brand with a huge range of evidence-based products to optimize your life, such as blue light glasses, EMF protection products and circadian friendly lighting. Use code wellnessmama to save.

Učebna osnova je veľmi dvoležita, ale, keď nemáte ten správny náboj, ako nato tak aj to najlepšie náradie vám nepomôže docieliť želaneho účinku. Balanc je nevyhnutný stejne ako je jing a jang.

Jak může ve válce přežít nemocnice pro psychicky a mentálně nemocné pacienty zjišťovalo v reportáži Rádio Svobodná Evropa. Poslechněte si svědectví zaměstnanců léčebny z ukrajinského města Borodianka nedaleko Kyjeva. Když Rusko v únoru napadlo Ukrajinu, byla nemocnice domovem pro 350 padesát lidí, přičemž mnozí z pacientů potřebovali neustálou péči. Z 250 zaměstnanců jich v zařízení zůstalo jen deset. Na kritickou situaci vzpomíná ředitelka nemocnice Marina Ganitskajová.Všechny díly podcastu Svět ve 20 minutách můžete pohodlně poslouchat v mobilní aplikaci mujRozhlas pro Android a iOS nebo na webu mujRozhlas.cz.

Maria Cecilia Guerra, Sottosegretaria MEF ; Dario Bruni, EBNA ; Dario Stevanato, Univ. Trieste ; Stefano Marcucci, Gr .

Maria Cecilia Guerra, Sottosegretaria MEF ; Dario Bruni, EBNA ; Dario Stevanato, Univ. Trieste ; Stefano Marcucci, Gr .

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MisHa @ Techno Live Stream - Zkušebna MNV | 19.2.2021 by Perpetuum Klub

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Zdravotnické muzeum je v Pardubickém kraji jediné. Prohlédnout si mohou nejen klienti Hamzovy léčebny v Luži-Košumberku, ale také veřejnost, v době, kdy je areál přístupný.

Bezpečněji by se měli cítit lidé v okolí autobusového a vlakového nádraží v Přerově. Díky nové policejní služebně, která sídlí od pondělí v budově železniční výpravní budovy v Husově ulici. Tedy v části města, která je nechvalně proslulá vysokou kriminalitou. Sloužit v ní budou na čtyři desítky policistů. Policie za rekonstrukci a vybavení prostor zaplatila 3 miliony korun.

Cellular gene regulation depends on fundamental epigenetic mechanisms, but epigenetic modifications also govern the regulation of the life cycle of Epstein-Barr virus (EBV). Promoter usage during latency depends on DNA methylation of the viral genome and CpG-methylation of certain promoters with meZREs is an indispensable prerequisite to switch from the latent to the lytic phase. In my thesis, I wanted to assess the underlying epigenetic principles of EBV’s gene regulation during the establishment of latency and upon lytic reactivation. My results suggested a new classification of viral promoters and phases of gene regulation that depend on the epigenetic state of the viral chromatin. According to this new model, EBV’s infectious cycle consists of an initial abortive lytic, a latent, and a productive lytic phase, and the viral promoters can be classified into default-on, poised-on, and poised-off promoters. Default-on promoters are immediately active upon infection of primary B cells leading to the so-called abortive lytic phase of an EBV infection. Default-on promoters encounter the cell in an environment that supports binding of the basal transcription machinery to activate viral gene transcription. Default-on promoters include the promoters of BALF1, BHRF1, BZLF1, BRLF1, BNLF2a, BCRF1, and Wp. The protein products are indispensible for the permanent establishment of EBV’s genome in latently infected cells supporting growth transformation, immune evasion, and anti-apoptotic cellular pathways. Default-on promoters are epigenetically silenced upon occupancy of EBV’s DNA with nucleosomes very early after infection and a switch to poised-on promoters is initiated. Poised-on promoters embody an epigenetically active state upon infection, but their activation requires an additional, virus-encoded factor to allow initiation of transcription. Wp-induced expression of EBNA1 promotes the switch to the poised-on promoter Cp to sustain long-term EBNA expression. Other poised-on genes including the viral structural proteins are not provided with their cofactor initially. During latency, these promoters are repressed through compaction of chromatin by high nucleosome occupancy, trimethylation of H3K27, and a stable transmission of repressive modifications by Polycomb-mediated long-term silencing. The establishment of a defined DNA methylation pattern on EBV’s DNA further represses poised-on promoters. DNA methylation is a prerequisite for the activation of a third promoter class, termed default-off promoters. Default-off promoters are bound and transactivated by BZLF1 in a methylation-dependent manner. Upon infection of primary B cells, EBV’s DNA is completely unmethylated, impeding an early expression of default-off genes. Only two to three weeks post infection the viral genome has acquired a proper epigenetic configuration that supports transcription of default-off genes. Binding of BZLF1 alone does not suffice to recruit the cellular transcription machinery including RNA polymerase II, but the chromatin requires remodeling, including a loss of nucleosomes and repressive modifications at default-off promoter sites. Default-off genes encode the viral lytic DNA replication machinery. The newly synthesized DNA templates lack epigenetic modifications because lytic DNA amplification is uncoupled from cellular DNA replication, eliminating the epigenetic maintenance mechanisms during the synthesis of viral progeny. As a consequence, default-on promoters and silenced poised-on promoters, which rely on unmethylated, epigenetically naïve templates, become also activated in the onset of the lytic phase. Silenced poised-on promoters require additionally a viral cofactor for their activation. This so-far unknown factor is probably provided upon lytic DNA amplification allowing the transcription of genes encoding for structural proteins that are necessary for the packaging of viral progeny. The released EBV progeny is epigenetically unmodified and ready to infect other cells. In essence, the regulation of EBV’s life cycle by epigenetic mechanisms is a paradigm for viral coevolution with its host. Repressive epigenetic modifications are common cellular defense mechanism to fight invading pathogens. EBV has hijacked this system for the regulation of promoter usage during its own life cycle, which has become a key principle of EBV’s success in infecting and persisting in its host.

Background: Epidemiological studies have suggested that long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with a reduced incidence of Alzheimer's disease (AD). Several mechanisms have been proposed to explain these findings including increased shedding of the soluble ectodomain of the amyloid precursor protein (sAPP), which functions as a neurotrophic and neuroprotective factor in vitro and in vivo. Objective: To clarify whether NSAIDs consistently stimulate sAPP secretion. Methods: 293-EBNA cells with stable overexpression of an APP-alkaline phosphatase fusion protein (APP-AP), SH-SY5Y and PC12 cells or primary telencephalic chicken neurons were treated with ibuprofen or indomethacin. APP shedding was then determined by measuring AP activity in conditioned media, Western blot analysis with antibodies against total sAPP or specific for sAPP-alpha, or in a pulse-chase paradigm. Results: AP activity in conditioned media was not increased after NSAID treatment of 293-EBNA cells whereas it was elevated by phorbol ester. Surprisingly, ibuprofen or indomethacin treatment of SH-SY5Y and PC12 cells expressing endogenous APP did not cause changes in sAPP or sAPP-alpha secretion or downregulation of cellular APP. These findings were further corroborated in primary chicken neuronal cultures. Conclusions: Using various experimental settings, we were unable to confirm sAPP or sAPP-alpha stimulation with the NSAIDs ibuprofen and indomethacin in transfected and nontransfected cells of neuronal and nonneuronal origin. Importantly, these findings seem to rule out chronic sAPP stimulation as an alternative mechanism of NSAID action in AD. Copyright (C) 2008 S. Karger AG, Basel

Zusammenfassung Das Epstein-Barr Virus nukleäre Antigen 2 (EBNA-2) ist ein Schlüsselprotein bei der Initiation und der Aufrechterhaltung der B-Zelltransformation nach einer EBV-Infektion. EBNA-2 reguliert die Genexpression von viralen und zellulären Genen und induziert so das physiologische Proliferationsprogramm der B-Zelle. Die DNA-Bindung erfolgt indirekt durch eine Interaktion mit zellulären Adapterproteinen, zu denen das CBF1 (C-promoter binding factor 1) Protein zählt. Mit dieser Arbeit sollte ein Beitrag zum Verständnis der bisher wenig untersuchten molekularen Mechanismen, über die EBNA-2 zelluläre Zielgene transaktiviert, geleistet werden. Die drei zellulären EBNA-2-Zielgene SLAMF1, DNASE1L3 und CCL3 wurden in dieser Arbeit exemplarisch untersucht. Die EBNA-2-Transaktivierung der drei Gene ist CBF1 abhängig. In allen drei Genen konnte erstmals eine EBNA-2-Bindung am Transkriptionsstart nachgewiesen werden. Erstmalig ist auch der Nachweis gelungen, dass EBNA-2 an intronständige CBF1-Bindestellen rekrutiert wird. Eine EBNA-2-Aktivierung führte in allen untersuchten Genen zur Rekrutierung der an Serin 5 phosphorylierten Polymerase II an den Transkriptionsstart, sowie auch zu CBF1-Bindestellen in Regionen, die distal zum Transkriptionsstart lokalisiert sind. Die Aktivierung der Genexpression korreliert in allen Fällen mit einer erhöhten Acetylierung der Histone H3 und H4, die nicht auf den Bereich des Transkriptionsstarts beschränkt war. Eine detaillierte Analyse des CCL3-Gens erwies, dass die DNA-Bindung von CBF1 durch EBNA-2 unterstützt wird. Des Weiteren zeigte sich, dass eine nahe dem Transkriptionsstart gelegene Region entscheidend zur EBNA-2 vermittelten Transaktivierung beiträgt und vermutlich nicht durch CBF1 vermittelt wird. Möglicherweise reguliert EBNA-2 nicht nur über eine Bindung an CBF1 die Transaktivierung eines Genes, sondern noch über einen zweiten Mechanismus, bei dem EBNA-2 direkt oder indirekt an den Transkriptionsstart oder in dessen unmittelbarer Nähe bindet. Zur Identifikation von Proteinen, die direkt an dem molekularen Mechanismus der EBNA-2-Transaktivierung beteiligt sind, wurde die „Tandem Affinity Purification“ (TAP-Reinigung) zur Aufreinigung nativer EBNA-2-Komplexe in B-Zellen etabliert. Durch eine anschließende massenspektrometrische Analyse konnten potentielle EBNA-2-Interaktionspartner identifiziert werden. Für das interessante Kandidatenprotein TFE3, ein Transkriptionsfaktor des Immunglobulinlokus, konnte bereits eine spezifische Anreicherung über EBNA-2 nachgewiesen werden.

EBNA-2 is a multifunctional viral oncogene involved in the immortalisation of B-cells by EBV. EBNA-2 regulates transcription of viral and cellular genes in the proliferative phase of the viral life cycle, which in vitro results in the outgrowth of EBV positive B-cells into lymphoblastoid cell lines (LCLs). EBNA-2 transcriptional signalling is mediated by cellular DNA-binding proteins, such as RBP-J and PU.1, since EBNA-2 does not contain its own DNA-binding domain. In order to better characterise EBNA-2 signalling we conducted a mutational analysis of the viral LMP-1 promoter that is strongly induced by EBNA-2 in the EBV-immortalised B-cells. Our mutational analysis of the LMP-1 promoter confirmed that the PU.1 binding site is important for transactivation of the LMP-1 promoter by EBNA-2, whereas RBP-J binding to the LMP-1 promoter leads to repression and EBNA-2 binding to RBP-J is not required for transactivation. These results imply that EBNA-2 transactivates the LMP-1 promoter preferentially by an RBP-J independent mechanism. We further characterised EBNA-2 signalling by dissection of promoter targeting domains in the EBNA-2 protein. Two EBNA-2 mutants, the CR4del and WW mutant, preferentially activated RBP-J dependent and independent signalling indicating that EBNA-2 uses at least two separate signalling pathways. We introduced the characterised EBNA-2 mutants into the EBV genome and produced recombinant viruses carrying specific mutations in the EBNA-2 genes. Primary B-cells were infected with increasing titres of recombinant EBVs lacking the EBNA-2 ORF or carrying the WW or CR4del mutant. Viruses lacking the EBNA-2 ORF or carrying the WW mutant were not able to immortalise primary B-cells even at high viral titres. The CR4 region of EBNA-2 strongly influenced B-cell immortalisation efficiency and growth rate of the immortalised B-cells. These results indicate that EBNA-2 and the RBP-J signalling of EBNA-2 are absolutely essential for B-cell immortalisation by EBV. In contrast, the CR4 EBNA-2 region mediating RBP-J independent signalling is critical, but not absolutely essential for the process of EBV immortalisation.

Background: Bacterial artificial chromosomes ( BACs) have been used extensively for sequencing the human and mouse genomes and are thus readily available for most genes. The large size of BACs means that they can generally carry intact genes with all the long range controlling elements that drive full levels of tissue-specific expression. For gene expression studies and gene therapy applications it is useful to be able to retrofit the BACs with selectable genes such as G418 resistance, reporter genes such as luciferase, and oriP/EBNA-1 from Epstein Barr virus which allows long term episomal maintenance in mammalian cells. Results: We describe a series of retrofitting plasmids and a protocol for in vivo loxP/Cre recombination. The vector pRetroNeo carries a G418 resistance cassette, pRetroNeoLuc carries G418 resistance and a luciferase expression cassette, pRetroNeoLucOE carries G418 resistance, luciferase and an oriP/EBNA-1 cassette and pRetroNeoOE carries G418 resistance and oriP/EBNA-1. These vectors can be efficiently retrofitted onto BACs without rearrangement of the BAC clone. The luciferase cassette is expressed efficiently from the retrofitting plasmids and from retrofitted BACs after transient transfection of B16F10 cells in tissue culture and after electroporation into muscles of BALB/c mice in vivo. We also show that a BAC carrying GFP, oriP and EBNA-1 can be transfected into B16F10 cells with Lipofectamine 2000 and can be rescued intact after 5 weeks. Conclusion: The pRetro vectors allow efficient retrofitting of BACs with G418 resistance, luciferase and/or oriP/EBNA-1 using in vivo expression of Cre. The luciferase reporter gene is expressed after transient transfection of retrofitted BACs into cells in tissue culture and after electroporation into mouse muscle in vivo. OriP/EBNA-1 allows stable maintenance of a 150-kb BAC without rearrangement for at least 5 weeks.