Podcasts about saido

Kutana na Saido Omar Noor, binti mwenye umri wa miaka 25 mkimbizi kutoka Somalia anayeishi Kakuma kambi kubwa zaidi ya wakimbizi nchini Kenya. Kupitia video ya shirika la Umoja wa Mataifa la kuhudumia wakimbizi UNHCR anasema katika jamii yake ni yeye mwanamke pekee wa Kisomali anayecheza mpira kwa kikapu au basketball. Flora Nducha na taarifa zaidi..

Once regarded as one of the Premier League's brightest young talents, it's safe to say Saido Berahino's career did not go to plan.

En último episodio de la temporada cinco Said Vázquez, El Saido, desde la barrera  comparte en tercera persona desde sus entrañas algunas anécdotas y vivencias que permiten conocer a Said el sociólogo utópico vs Saido el antropólogo indecente. Como dice la canción «Queremos coger a la historia y tirárnosla por detrás, por detrásBum, bum, hay que tirar la puerta.»

In the 2nd installment of Season 3, Mr Era sits down with ex West Brom ace, Saido Berahino. They touch on everything from fleeing his native Burundi as a child to receiving political asylum in Birmingham and all the madness followed. Berahino credits football with helping him integrate into English society and providing a better for him and his family. X: @Total_media_pro Instagram: @totalmedia_productionsSee omnystudio.com/listener for privacy information.

/*! elementor - v3.16.0 - 20-09-2023 */ .elementor-heading-title{padding:0;margin:0;line-height:1}.elementor-widget-heading .elementor-heading-title[class*=elementor-size-]>a{color:inherit;font-size:inherit;line-height:inherit}.elementor-widget-heading .elementor-heading-title.elementor-size-small{font-size:15px}.elementor-widget-heading .elementor-heading-title.elementor-size-medium{font-size:19px}.elementor-widget-heading .elementor-heading-title.elementor-size-large{font-size:29px}.elementor-widget-heading .elementor-heading-title.elementor-size-xl{font-size:39px}.elementor-widget-heading .elementor-heading-title.elementor-size-xxl{font-size:59px}Episode 378: Score Big in Business with These Home Run Strategies /*! elementor - v3.16.0 - 20-09-2023 */ .elementor-widget-image{text-align:center}.elementor-widget-image a{display:inline-block}.elementor-widget-image a img[src$=".svg"]{width:48px}.elementor-widget-image img{vertical-align:middle;display:inline-block} Episode NotesWho doesn't love hitting a home run in business? It's the feeling of pure excitement, accomplishment, and success all rolled into one. Achieving our goals and exceeding expectations is what every entrepreneur dreams of. Let's dive deeper into what it takes to hit that home run and make your business the best it can be.When you hit a home run in business, it opens the floodgates of opportunities. This was the case for one of my clients, who permitted me to share their story with you. The work began in July 2022, when their business was still finding its footing. I then met Mahomud Ali and Saido Ali Jama at an annual MEDA meeting. MEDA is an international economic development organization that creates business solutions to poverty.The First Strategy for hitting home runs in business is to make sure you have someone you trust who has your best interest at heart to talk things through and help you clarify what you want.Before attending the MEDA annual meeting, I discussed things with my husband, Matthew Foli, as usual. To have someone you trust to talk things through and help you clarify what you want is priceless. It takes time to get to the heart of what truly matters to you, and having someone invested in your best interest to witness your journey and provide valuable feedback can empower both of you.I went to the annual MEDA meeting with clear intentions. I first wanted to learn more about how they are helping minority-owned businesses and how the organization is evolving. Additionally, I wanted to meet and mentor at least one business owner and connect with potential guest mentors for my podcast.After the meeting ended, I spoke with a few people before scanning the room one last time. As I was leaving, Mahomud and Saido introduced themselves, and Mahomud mentioned that he needed help with marketing. Though I am not a marketing expert, I have been involved in marketing since 1992 and offered to meet with them to see how I could help them achieve their goals. At the very least, I could provide them with valuable resources.Second Strategy: Understand that the Universe works on our behalf.Even when we feel alone, we are not. There is a spiritual realm of Guardian Angels and spirit guides waiting for us to invite them to help us. The Universe collaborates to bring our dreams into reality when we know what we want. That's why people say, "Be careful what you wish for." Or, more commonly now, "Be mindful of your thoughts and words."Many times, the Universe delivers beyond our wildest dreams in unexpected ways. What we achieve at Midwest Bakery fits my understanding of how the Universe pleasantly surprises us. If this isn't the case for you, refine what you think, say, or what you put out into the Universe. Let go of the outcomes and ensure your intentions are not from a place of fear or avoidance. The Universe keeps giving us the same lessons in different ways until we get the lesson.

Curtiu este episódio? Então, bora compartilhar e enviar esse podcast para todos os incendiários que você conhece. Assine o feed para ficar por dentro de tudo que rola por aqui. Me segue no insta (@andrefernandes.ofc) tem novidades todos os dias e um conteúdo irado, que com certeza vai edificar você! incendiarios.com/

Spirits are always with you! And so is this week's episode of Anime Re:Wind. In this episode, there's an odd amount of himbo talk, discussion of Grand Fisher's physique and Saido conspiracy theories. Mist, Shang and Loofie are back with more anime and gacha updates, and Loofie can't seem to say Bleach 8 - 10 correctly until the end of the episode.Timestamps:0:00 - Intro0:40 - Wallet Updates18:01 - Gone Bleaching41:22 - Outro

Neste episódio, os buga buga comentam sobre um anime que foi senasação alguns anos atrás e inspiração por trás de vários memes: Dumbbell Nan Kilo Motteru. A grande tentativa de fazer um milagre: um otaku fazer exercício físico. O PDV Podcast é um podcast (jura?) focado em animes e tópicos relacionados. Junte-se aos nossos dois Hosts: CB e Iida durante as suas discussões, análises e comentários sobre toda uma plenitude de assuntos e produtos de entretenimento, relacionados (ou não) a mangás e animes. Music: https://www.purple-planet.com

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.28.534515v1?rss=1 Authors: Jiang, L., Roberts, R., Wong, M., Zhang, L., Webber, C. J., Kilci, A., Jenkins, M., Rashad, S., Sun, J., Dedon, P., Daley, S. A., Xia, W., Ortiz, A. R., Dorrian, L., Sado, T. C., Saido, T., Wolozin, B. Abstract: The study for the pathophysiology study of Alzheimers disease (AD) has been hampered by lack animal models that recapitulate the major AD pathologies, including extracellular {beta}-amyloid (A{beta}) deposition, intracellular aggregation of microtubule associated protein tau (MAPT), inflammation and neurodegeneration. We now report on a double transgenic APPNL-G-F MAPTP301S mouse that at 6 months of age exhibits robust A{beta} plaque accumulation, intense MAPT pathology, strong inflammation and extensive neurodegeneration. The presence of A{beta} pathology potentiated the other major pathologies, including MAPT pathology, inflammation and neurodegeneration. However, MAPT pathology neither changed levels of amyloid precursor protein nor potentiated A{beta} accumulation. The APPNL-G-F/MAPTP301S mouse model also showed strong accumulation of N6-methyladenosine (m6A), which was recently shown to be elevated in the AD brain. M6A primarily accumulated in neuronal soma, but also co-localized with a subset of astrocytes and microglia. The accumulation of m6A corresponded with increases in METTL3 and decreases in ALKBH5, which are enzymes that add or remove m6A from mRNA, respectively. Thus, the APPNL- G-F/MAPTP301S mouse recapitulates many features of AD pathology beginning at 6 months of aging. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.11.18.516922v1?rss=1 Authors: Daniels, M. J. D., Lefevre, L., Drake, A., Szymkowiak, S., McCulloch, L., Tzioras, M., Barrington, J., Dando, O. R., He, X., Mohammad, M., Sasaguri, H., Saito, T., Saido, T. C., Spires-Jones, T. L., McColl, B. W. Abstract: Microglial endolysosomal (dys)function is strongly implicated in neurodegeneration. Transcriptomic studies show that a microglial state characterised by a set of genes involved in endolysosomal function is induced in both mouse Alzheimers Disease (AD) models and in human AD brain and that the onset of this state is emphasized in females. Cst7 (encoding protein Cystatin F) is among the most highly upregulated genes in these microglia. However, despite such striking and robust upregulation, the sex-specific function of Cst7 in neurodegenerative disease is not understood. Here, we crossed Cst7-/- mice with the AppNL-G-F mouse to test the role of Cst7 in a model of amyloid-driven AD. Surprisingly, we found that Cst7 plays a sexually dimorphic role regulating microglia in this model. In females, Cst7-deficient microglia had greater endolysosomal gene expression, lysosomal burden, and amyloid beta (A{beta}) burden in vivo and were more phagocytic in vitro. However, in males, Cst7-deficient microglia were less inflammatory and had a reduction in lysosomal burden but had no change in A{beta} burden. This study has important implications for AD research, confirming the functional role of a gene which is commonly upregulated in disease models, but also raising crucial questions on sexual dimorphism in neurodegenerative disease and the interplay between endolysosomal and inflammatory pathways in AD pathology. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.11.07.515410v1?rss=1 Authors: Yang, Y., Zhang, W., Murzin, A. G., Schweighauser, M., Huang, M., Lovestam, S., Peak-Chew, S. Y., Saito, T., Saido, T. C., McDonald, J., Lavenir, I., Ghetti, B., Graff, C., Kumar, A., Nordberg, A., Goedert, M., Scheres, S. H. Abstract: The Arctic mutation, encoding E693G in the amyloid precursor protein (APP) gene [E22G in amyloid-beta] (Abeta)], causes dominantly inherited Alzheimer's disease. Here we report the high-resolution cryo-EM structures of A beta filaments from the frontal cortex of a previously described case (A beta PParc1) with the Arctic mutation. Most filaments consist of two pairs of non-identical protofilaments that comprise residues V12-V40 (human Arctic fold A) and E11-G37 (human Arctic fold B). They have a substructure (residues F20-G37) in common with the folds of type I and type II Abeta42. When compared to the structures of wild-type Abeta42 filaments, there are subtle conformational changes in the human Arctic folds, because of the lack of a side chain at G22, which may strengthen hydrogen bonding between mutant Abeta molecules and promote filament formation. A minority of Abeta42 filaments of type II was also present, as were tau paired helical filaments. In addition, we report the cryo-EM structures of Abeta filaments with the Arctic mutation from mouse knock-in line App NL-G-F. Most filaments are made of two identical mutant protofilaments that extend from D1-G37 (murine Arctic fold). In a minority of filaments, two dimeric folds pack against each other in an anti-parallel fashion. The murine Arctic fold differs from the human Arctic folds, but shares some substructure. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Episode 335: Fantastic Client News and How to Sustain Your Focus Fantastic Client News! Mohamud Ali and Saido Jama founded Midwest Bakery & Café in 2019. I have been working with them to get their Halal whole wheat and white loaves of bread and whole wheat hoagie buns into Cub Foods on 28th and Lake Street in Minneapolis to test the market. Guess what? We did it! Midwest Bakery & Café is now in its first Cub Foods grocery store. (For those of you outside of the midwest. Cub Foods is a supermarket chain of 45 stores.) Congratulations to Mohamud and Saido and their family! On the first day, we sold out and rushed to refill the order. The two bottom shelves are now bread. The detergent was replaced. We moved so fast that I didn't get a picture of Saido and their adult children working to fill the orders. They have expanded their customer base from restaurants and daycare centers to Cub Foods customers. The demand for their loaves of bread and hoagie buns is growing. I am thrilled to collaborate with them to expand their bakery and evolve their businesses. They also own Midwest Auto Repairs. I'll have them on the podcast soon so you can hear them describe their multi-venture entrepreneurial journey. Among the many things I appreciate about Mohamud and Saido is that they reached out for mentoring so I could help them cross this particular finish line and set the next big goal. They knew they needed help getting their six types of loaves of bread and hoagies buns on the shelves at Cub Foods. I knew I could deliver. In under a week, they have passed the market test. Now, we can work steadily to evolve with the needs of their customers and set new processes and systems in place to maintain efficiency as the demand continues to grow and the offerings expand to other locations.  You can purchase their loaves of bread and hoagie buns at 28th and Lake Street. I just had one for lunch after helping them fill orders; it was so good. The picture is Mohamud delivering their first order last week. With fast growth, sustaining focus under pressure is critical. Today's podcast meditation will help you sustain your focus with the pressures you are under. How to Sustain Your Focus Can you focus on the right things at the right time, most of the time? If so, you are practicing the first of four aspects connected with one mind skill: FOCUS. To start focusing, we need to direct our attention to what we want to think about. We then sustain attention as long as we need and want to, controlling impulses and noticing when our attention wanders and redirecting our mind back to its focal point. Once the task is complete, we can relax our attention, resting our minds for a few minutes before directing our attention to a new task. Sounds easy, right? We resist so often what is good for us, especially when it comes to our minds. Sitting down for a few minutes to calm our thoughts and let go is difficult. Sometimes, I find it challenging to sit with myself, especially if I feel anxious or have nervous energy. This means something big lurks underneath all that nervousness, and I don't know if I want to know what it is just yet. Giving myself permission to sit and see what happens takes the pressure off. Last week we practiced Directing Focus. Today is the complimentary 6-minute meditation; How to Sustain Your Focus. I first aired this episode on March 7, 2022. Both meditations give your mind something to do while you sit. You can return to your focal point whenever you get distracted, or your thoughts drift. Where does focus fit in the grand scheme of building a healthy mind? According to The Center for Healthy Minds, it is connected to awareness. The first place we start when we make a behavior change, we become self-aware and shift our focus. The four areas below are what a regular meditation practice helps us do after we open our eyes. Awareness: means practicing presence, focus, and self-awareness. Connection: means practicing appreciation,

Discover our day at Tokyo Tokyo Delicious Museum food festival: 5 surprises, Michelin Stars, Japanese & world food (✔ vegan ✔ Muslim), influencer's tasks & thoughts, organization (✔ wheelchair ✔ kids), tips for next time… Host: Sébastien Duval Guest: Mehdi Fliss, influencer in Japan, Instagram @sugoiijapan. With voices from: Australia (Anna Yoshida), China (Ushin Cho), Germany (Maria Neumann), Japan (Kota Hasegawa). Online highlights: [OFFICIAL] https://tokyotokyo-delicious-museum.jp [SAIDO] https://edition.cnn.com/videos/travel/2020/02/21/saido-vegan-restaurant-tokyo.cnn/video/playlists/destination-tokyo/ Sound effects obtained from https://zapsplat.com.

An introspective of Saido Berahino's career up to date. Experience his rise and eventual missteps that led to a fall out at WBA and the steps he has took to change his path and become The Redeemed Footballer. A 2 Baggies 1 Lightbulb Production. Produced by Maximiliano Palermo. Contributors: @YesWeCrann @louisbent_ @baggiesbulletin

No Liam this week but James and GIles were joined by Patreon member Tom, to wax lyrical about the likes of Berahino, Bannan and Byers for a full 90 minutes after an emphatic 6-0 win against Cambridge United. What a performance. What a result. What a team. Enjoy.Once again, thank you for listening and if you enjoyed it then leave a rating.Make sure you hit subscribe so you're notified about all the new episodes as soon as they go live.Follow us over on Twitter, Facebook and Instagram by searching for @WTIDPOD.The TerracePatreonThe Wednesday Way Facebook GroupYouTube See acast.com/privacy for privacy and opt-out information.

Setiap perkembangan jaman pasti banyak banget perubahan yg terjadi, salah satunya soal cara nyari uang, kira-kira seperti apa ya? mendingan yuk langsung aja dengerin

Welcome to our podcast your destination for all things West Bromwich Albion. On this weeks episode we have plenty of stuff to chat about even though were on an international break including; Valerien Ismael's job being under pressure,  The Saido Berahino interview and whether we should sign him again. We also take a look at Jake Livermore's performances and whether he should remain as captain. We have our Huddersfield preview & as always our trivia! Boing Boing! Music Credit: Kovan & Electro-Light - Skyline [NCS Release]

This episode of The Baggies Podcast sees us welcome former West Bromwich Albion player Saido Berahino onto the show. We chat about Saido's time at the club, including joining the academy, a top goalscoring season, his exit from WBA, Jeremy Peace + much more! ⬇ Comment your memories of Saido below! ⬇ thebaggiespodcast@gmail.com Be sure to subscribe and leave a like if you've enjoyed the episode! ⬇LINKS TO ALL OTHER PLATFORMS⬇ https://linktr.ee/thebaggiespodcast #WBA #Albion #WestBrom #Baggies

Chris and Adrian assess Albion's new players after a creditable 1-1 draw against Manchester United.  Plus Saido Berahino re-assessed and Roy Hodgson remembered.BUY OUR MERCH HERE

In episode 4 of The Sit Down, Max and Dom are joined by the most polarising player in West Bromwich Albion's recent history. Saido Berahino. Saido offers incredible insight on his career past and present, sharing his side to the story that unfolded in the media and before us all.

Olivia 'Liv' Layton, your Dungeon Master is joined by her lovely wife Yayna Layton in the start of this campaign for Ones Aren't Fun. A One Piece inspired D&D Campaign, the pair will take four characters down a funnel session where one will become the very first member of the Crew. Samuel, Havlock, Saido, and Marina have all reached Welcon Isle, after hearing rumors of a particular item stolen from the Marines in the area being on said island. The four encounter "The Wire" a tiefling who says she will share her information with them if, and only if they help her out of a seemingly simple situation. --- Support this podcast: https://anchor.fm/onesarentfun/support

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.10.07.329318v1?rss=1 Authors: Watamura, N., Kakiya, N., Nilsson, P., Tsubuki, S., Kamano, N., Takahashi, M., Hashimoto, S., Sasaguri, H., Saito, T., Saido, T. Abstract: The neuropeptide somatostatin (SST) regulates amyloid {beta} peptide (A{beta}) catabolism by enhancing neprilysin (NEP)-catalyzed proteolytic degradation. However, the mechanism by which SST regulates NEP activity remains unclear. Here we report the identification by differential proteomics of -endosulfine (ENSA), an endogenous ligand of the ATP-sensitive potassium (KATP) channel, as a negative regulator of NEP activity downstream of SST signaling. Genetic deficiency of ENSA resulted in enhanced NEP activity and decreased A{beta} deposition in the brains of wild-type and Alzheimer's disease (AD) model mice. Pharmacological intervention to increase the probability of KATP channel opening reduced A{beta} deposition in AD model mice. Our findings provide new insights into possible mechanisms to prevent AD. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.09.22.308015v1?rss=1 Authors: Clayton, K. A., Delpech, J. C., Herron, S., Iwahara, N., Saito, T., Saido, T., Ikezu, S., Ikezu, T. Abstract: Microglia have an emerging role in development of tau pathology after amyloid plaque deposition in Alzheimers disease, although it has not been definitively shown. We hypothesize that plaque-associated activated microglia accelerate tau propagation via enhanced phagocytosis and secretion of tau. Here we show that the injection of adeno-associated virus expressing P301L tau mutant into the medial entorhinal cortex (MEC) in humanized APPNL-G-F knock-in mice induces exacerbated tau propagation in the dentate gyrus compared to wild type mice. Depletion of microglia dramatically reduces accumulation of phosphorylated tau (pTau) in the dentate gyrus as well as an extracellular vesicle (EV) marker, Tumor susceptibility gene 101, co-localized in microglia. Mac2+ activated microglia secrete significantly more EVs compared to Mac2- microglia in APPNL-G-F mice in vivo when injected with lentivirus expressing EV reporter gene mEmerald-CD9, suggesting enhanced EV secretion by microglial activation. Our findings indicate that amyloid plaque-mediated acceleration of tau propagation is dependent on activated microglia, which show enhanced EV secretion in vivo. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.09.13.295642v1?rss=1 Authors: Hata, S., Kikuchi, K., Kano, K., Saito, H., Sobu, Y., Kinoshita, S., Saito, T., Saido, T. C., Sano, Y., Taru, H., Aoki, J., Komano, H., Tomita, T., Natori, S., Suzuki, T. Abstract: Conjugated linoleic acid (CLA) comprises several geometric and positional isomers of the parental linoleic acid (LA). Two of the isomers, cis-9, trans-11 CLA (c9,t11 CLA) and trans-10, cis-12 CLA (t10,c12 CLA) exert various biological activities. However, the effect of CLA on generation of neurotoxic amyloid-{beta} (A{beta}) protein remains unclear. We found that c9,t11CLA significantly suppressed generation of A{beta} in primary cultures of mouse neurons. CLA treatment did not affect the levels of {beta}-site APP-cleaving enzyme 1 (BACE1), a component of active {gamma}-secretase complex presenilin 1 amino-terminal fragment (PS1 NTF), or A{beta} protein precursor (APP) in cultured neurons. BACE1 activity in lysate of neurons treated with c9,t11 CLA, but not t10,c12 CLA, decreased slightly, although c9,t11 CLA did not directly affect the activity of recombinant BACE1. Interestingly, localization of BACE1 and APP in early endosomes increased in neurons treated with c9,t11 CLA; concomitantly, the localization of both proteins was reduced in late endosomes, where APP is predominantly cleaved by BACE1. c9,t11 CLA and t10,c12 CLA appeared to be incorporated into membrane phospholipids, as the level of CLA-containing lysophosphatidylcholine (CLA-LPC) increased dramatically in neurons incubated with CLA. Taken together, our findings indicate that accumulation of c9,t11 CLA-LPC, but not t10,c12 CLA-LPC, in neuronal membranes suppresses amyloidogenic cleavage of APP, thereby contributing to preservation of brain neurons by suppressing neurotoxic A{beta} production in aged subjects. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.24.264259v1?rss=1 Authors: Sato, K., Sasaguri, H., Kumita, W., Inoue, T., Kurosaki, Y., Nagata, K., Mihira, N., Sato, K., Sakuma, T., Yamamoto, T., Tagami, M., Manabe, R.-i., Ozaki, K., Okazaki, Y., Saido, T. C., Sasaki, E. Abstract: Alzheimer's disease (AD) is a major cause of dementia, with the number of patients with this condition anticipated to exceed 50 million worldwide in the near future. Despite extensive research efforts, no effective measures are available to facilitate the prevention or treatment of AD, which is due in part to a lack of animal models able to closely replicate a human-like disease state. Here, we describe the generation of three mutant marmoset individuals in which exon 9 of PSEN1 gene product has been deleted (PSEN1-DeltaE9). Such DeltaE9 mutations have been reported to cause early on-set familial AD (references 1-5). We used Transcription Activator-Like Effector Nuclease (TALEN) to destroy the 3' splice site of exon 9 in the marmoset PSEN1 gene. To this end, TALEN exhibits high genome-editing efficacy, generates few off-target effects, and produces minimal mosaicism. Indeed, whole genome sequencing and other analyses illustrated an absence of off-target effects and an apparent absence of mosaicism. Fibroblasts obtained from newborn marmosets exhibited uncleaved full-length presenilin 1 protein (PS1) caused by the perturbation of PS1 endoproteolysis as well as an increased ratio of Abeta42/Abeta40 production, a signature of familial AD pathogenesis. To our knowledge, this is the first non-human primate model of familial AD. We intend to make our marmoset model available to the research community to facilitate the global fight against AD. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.25.220707v1?rss=1 Authors: Vandenabeele, M., Veys, L., Lemmens, S., Hadoux, X., Gelders, G., Masin, L., Serneels, L., Theunis, J., Saito, T., Saido, T., Jayapala, M., De Boever, P., De Strooper, B., Stalmans, I., van Wijngaarden, P., Moons, L., De Groef, L. Abstract: In this study, we report the results of a comprehensive phenotyping of the retina of the AppNL-G-F mouse. We demonstrate that soluble A{beta} accumulation is present in the retina of these mice early in life and progresses to A{beta} plaque formation by midlife. This rising A{beta} burden coincides with local microglia reactivity, astrogliosis, and abnormalities in retinal vein morphology. Electrophysiological recordings reveal signs of neuronal dysfunction yet no neurodegeneration was observed and visual performance outcomes were unaffected in the AppNL-G-F mouse. Furthermore, we show that hyperspectral imaging can be used to quantify retinal A{beta}, underscoring its potential as a biomarker for AD diagnosis and monitoring. These findings suggest that the AppNL-G-F retina mimics the early, preclinical stages of AD, and, together with retinal imaging techniques, offers unique opportunities for drug discovery and fundamental research into preclinical AD. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.22.215418v1?rss=1 Authors: Tachida, Y., Miura, S., Imamaki, R., Ogasawara, N., Takuwa, H., Sahara, N., Shindo, A., Matsuba, Y., Saito, T., Taniguchi, N., Kawaguchi, Y., Tomimoto, H., Saido, T., Kitazume, S. Abstract: The deposition of amyloid {beta} (A {beta}) in blood vessels of the brain, known as cerebral amyloid angiopathy (CAA), is observed in more than 90% of Alzheimer disease (AD) patients. The presence of such CAA pathology is not as evident, however, in most mouse models of AD, thereby making it difficult to examine the contribution of CAA to the pathogenesis of AD. Since blood levels of soluble amyloid precursor protein (sAPP) in rodents are less than 1% of those in humans, we hypothesized that endothelial APP expression would be markedly lower in rodents, thus providing a reason for the poorly expressed CAA pathology. Here we generated mice that specifically express human APP770 in endothelial cells. These mice exhibited an age-dependent robust deposition of A {beta} in brain blood vessels but not in the parenchyma. Crossing these animals with APP knock-in mice led to an expanded CAA pathology as evidenced by increased amounts of amyloid accumulated in the cortical blood vessels. These results show that both neuronal and endothelial APP contribute cooperatively to vascular A {beta} deposition, and suggest that this mouse model will be useful for studying disease mechanisms underlying CAA and for developing novel AD therapeutics. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.05.09.085795v1?rss=1 Authors: Nilsson, P., Sorgjerd, K., Kakiya, N., Sasaguri, H., Shimozawa, M., Tsubuki, S., Takamura, R., Zhou, Z., Loera-Valencia, R., Sekiguchi, M., Petrish, A., Schulz, S., Saito, T., Winblad, B., Saido, T. Abstract: Alzheimer's disease (AD) brains are characterized by increased levels of the pathogenic amyloid beta (Abeta) peptide, which accumulates into extracellular plaques. Finding a way to lower Abeta levels is fundamental for the prevention and treatment of AD. Neprilysin is the major Abeta-degrading enzyme which is regulated by the neuropeptide somatostatin. Here we used a combination of in vitro and in vivo approaches to identify the subtype specificity of the five somatostatin receptors (SSTs) expressed in the brain, involved in the regulation of neprilysin. Using a battery of Sst double knockout (dKO) mice we show that neprilysin is regulated by SST1 and SST4 in a redundant manner. Sst1 and Sst4 dKO mice exhibit a specific decrease of presynaptic neprilysin in the Lacunosum molecular layer. Moreover, a genetic deficiency of Sst1 and Sst4 in amyloid beta precursor protein (App) knock-in mice, an AD mouse model, aggravates the Abeta pathology in the hippocampus. As a first proof of concept towards an Abeta-lowering strategy involving neprilysin, we demonstrate that treatment with an agonist selective for SST1 and SST4 ameliorates the Abeta pathology and improves cognition in the App knock-in AD mouse model. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.04.27.062729v1?rss=1 Authors: Tanaka, T., Hirai, S., Hosokawa, M., Saito, T., Sakuma, H., Saido, T., Hasegawa, M., Okado, H. Abstract: Alzheimer's disease (AD), a progressive neurodegenerative disorder, is a serious social problem. Recently, several early-life factors have been associated with an increased risk of a clinical diagnosis of AD. In the present study, we investigated the involvement of early-life stress in AD pathogenesis using heterozygous APP mutant mice (AppNL-G-F/wt) and wild-type (Appwt/wt) mice. Maternal separation was used as an animal paradigm for early-life stress. We found that stressed Appwt/wt mice showed narrowing of vessels and decreased pericyte coverage of capillaries in prefrontal cortex, while stressed AppNL-G-F/wt mice showed impairment of place memory, and earlier formation of A{beta} plaques and disruption of the blood-brain barrier than non-stressed AppNL-G-F/wt mice. We detected severe activation of microglia in the stressed AppNL-G-F/wt mice and stressed Appwt/wt mice. In the earlier stage, we detected morphological change and functional change in microglia in the stressed AppNL-G-F/wt mice and stressed Appwt/wt mice, and also detected morphological change in the microglia in the non-stressed AppNL-G-F/wt mice. Therefore, we hypothesize that activated microglia induced by the combination of maternal separation and APP mutation impairs the vascular system, leading to AD progression. These findings therefore suggest that maternal separation causes early induction of AD pathology. Copy rights belong to original authors. Visit the link for more info

Stoke lose again, but we're so used to it by now we're just chilling as we board the Champion ship. There's praise for a much better Stoke display, chat on xG (eeeuurgh), Diouf, Saido, your correspondence, and breaking news on SJW becoming an SJW.

The tall man does it again for Stoke, as Peter Crouch nets a potential goal of the season candidate as the Potters beat the Saints 2-1 at the Bet365. But, is it a deserved win for Stoke, and what do we do about Saido? Dave, Chris, and a returning Tom Thrower discuss all the talking points from the Saturday fixture, including a love-in for Zouma and Shaq, and a serious pondering over the likes of Berahino and Wimmer. Theme by @DIVENIREUK www.wizardsofdrivel.com patreon.com/wizardsofdrivel

"I've got a sense of impending doom, but I am excited about the new season" pretty much encaspulates the spirit of the podcast as we try to balance the positive of some encouraging pre-season displays and the negative that is the transfer uncertainty. We also talk about our link-up with our new radical punk mates FC St. Pauli, and get a perspective from over in Hamburg thanks to St. Pauli pod MillernTon (@MillernTon). In addition, Ben gets an exclusive transfer story regarding one of our young players, and we discuss Saido, Arnie, Zouma, Bruno, Fletcher, the youth as well as what grounds we're looking forward to visiting in 17/18. @wizardsofdrivel || facebook.com/wizardsofdrivel || patreon.com/wizardsofdrivel || wizardsofdrivel.com

The Wizards go slightly insane in the absence of a Stoke game. So there is chat on: Ireland v Wales, Shaq's mysteriously healing hammy, In-ger-lund, filling the bet365, the sesh with Saido, holidays with Stoke players, Giannelli Imbula and The Temple of Doom, roughly an hour of Lord of the Rings chat, a quiz and a vague attempt at a Leicester preview. ALSO: Listen out for a chance to WIN BEER!

REVIEW THE FRONT 3 ON ITUNES! ► http://getpodcast.reviews/id/734032291 Back with a brand new attack, it's the Front 3 podcast on a Sunday night. Kris leads things tonight as a false 9 host, and kicks things off with a look at Saturday's games and Liverpool against Swansea. The Swans took a swipe at Liverpool's title hopes, but can this be the first of many wins for Paul Clement? Then there's Manchester City against Tottenham and a meeting of two shrewd tactical minds. Laurence explains why jus because you're not attacking doesn't mean you're defending, and Dave reaffirms his appreciation for Hugo Lloris. In the second installment we assess big Sam Allardyce, and whether Palace fans should be worried about how their gaffer is performing. We talk Memphis moving to Lyon, Saido moving to Stoke, as well as a brief round-up of the other Saturday games. Then to take you home we cover Chelsea breaching Marco Silva's hull, and Alexis' late game heroics, all before we have a quick dip into Europe and see... See acast.com/privacy for privacy and opt-out information.

Stoke suffer last-gasp heartbreak as Rooney breaks a little-discussed record to level for Man United. Dave, Ben and Tom discuss our approach to a hard-fought point. There's some disagreement about our performance, but plenty of praise dished out. We look at Mark Clattenburg's game and wonder who got the best of his decisions. Also, there's the Roving RePotters, a reaction to Saido signing and stay tuned for news of History week. In the second part of the pod, Dave chats to club journalist Jon Sidaway about how transfers happen from his point of view, being a Baggie in charge of Stoke's twitter and blocking an entire nation on Facebook.