#adeno tag

[jennifersbod]

leaving for the hospital 😬

[jackals-ships]

decided yesterday that since im dealing w a Lot of breakthrough symptoms despite being on continuous BC id just take a mini break from it, let my body throw it's lil fit then go back on and

y'all i fear my body heard me talking shit both bc Ow and bc i did not wake up until jus a lil ago at 6pm, despite passing out Early, fuckin hell man

[opalsiren]

we don't talk enough about the bowel problems that come with having arfid so shout out to those of us who experience irregular bowel movements, constipation, abdominal cramps, diarrhoea, and ibs. also shout out to those of us who have to take laxatives, anti diarrhoea, and anti cramping medications too. especially shout out to those of us who have been told by medical professionals to just 'get more fibre in your diet' like it's that simple. we deserve adequate medical care that takes our eating disorder into account, and to be listened to by medical professionals when we share our struggles.

[crackersandjuice]

discover the duck

intro post revamp woooooo

extra info that's not up top: i'm black, aroace, and disabled (triple kill am i right). scoliosis sucks and my uterus hates me (endo and adeno gang wooo).

some tags that i used:

#cj quacks - for general talk. mostly. i can never decide whether to use it or not. #cj honks angrily - for venting and general life complaints maybe i'll add more??? who knows it might not be needed

feel free to interact and ask questions and what not. can't guarantee i'll answer but i'll try my best (social anxiety is a bitch ya know).

If I don’t like you/your blog, I’ll just block and go on with my day.

[pharmaphorumuk]

Zynteglo halt re-ignites viral vector safety concerns; analysts

Bluebird Bio’s decision to hit pause on the launch of Zynteglo for beta thalassaemia after two cases of cancer were seen in a clinical trial could see fears over the safety of viral vectors used to deliver gene therapies resurface. 

That’s the view of analysts at Jefferies, who suggest it could “re-ignite concerns over the use of lentiviral vectors and the risk of secondary (vector-mediated) cancer”.

Cancer is a perennial fear for therapies that involve altering DNA in cells, because of the risk that the viruses used to deliver genes into patient cells could inadvertently lodge in the wrong place on a chromosome, triggering a mutation or disrupting a mechanism that guards against a cell becoming cancerous.

Last week, Bluebird said it was pausing its Zynteglo (betibeglogene autotemcel) programme in Europe after a phase 1/2 trial in patients with sickle cell disease (SCD) – another red blood cell disorder – turned up two cases of blood cancers, one of acute myeloid leukaemia (AML) and another of myelodysplastic syndrome (MDS).

In addition to the pause on new treatments, the phase 1/2 study and another phase 3 trial of Zynteglo in SCD have been suspended as the company investigates whether the cancers could be related to the BB305 lentiviral vector used in the therapy.

If a causal link is shown, it could have “significant ramifications” on the use of lentiviral vectors, a type of self-inactivating virus that underpins both approved cell therapies like Novartis’ CAR-T Kymriah as well as a host of experimental therapies that involve genetic manipulation of cells.

One UK company that could be affected greatly by that is Oxford BioMedica, which has built a business around its LentiVector delivery platform used in Kymriah and other emerging therapies, according to Jefferies.

They note however that so far there have been no reported cases of secondary cancers to date with Kymriah, which has been available commercially for around three years.

Bluebird has said it hopes to have some data within the next few weeks that should explore the possibility of a causal link. That is concentrating on determining where the vector integrated into the chromosomes of the two patients with cancer, and if that has resulted in changes to gene expression in neighbouring areas.

The case comes just weeks after UniQure halted a trial of its haemophilia B gene therapy AMT-061 after an unexpected case of liver cancer. That therapy uses an adeno-associated virus (AAV) as a vector rather than a lentivirus, a vector type that features in approved gene therapies such as Roche’s Luxturna and Novartis’ Zolgensma.

Lentiviral vectors have become a popular alternative for some therapies because they can deliver larger gene sequences into target cells and are less likely to stimulate an immune response in the patient that could affect their safety and efficacy.

News of the pause came as UK cost-effectiveness watchdog NICE rejected Zynteglo for regular NHS use in first draft guidance, despite a confidential discount to its price tag of around €1.57 million in Europe.

The post Zynteglo halt re-ignites viral vector safety concerns; analysts appeared first on .

from https://pharmaphorum.com/news/zynteglo-halt-re-ignites-viral-vector-safety-concerns-analysts/

[jennifersbod]

How did you get your doctor to let you have a hysterectomy? I have endo and they won’t let me saying I could change my mind on having children and it’s so frustrating bc it causes me so much pain

So I’ve been in a similar position as you completely and my whole journey has led up to this so I’m sorry if this is super long. I didn’t get diagnosed with endometriosis till 2019 despite having symptoms for 10+ years before that. I went on everything from pills to three (3!) iuds my body rejected both before and after surgery. My symptoms came back about a year later but I’d had a lot of life stuff happen and moved to my home (less conservative) state. The first specialist I could get into turned out to be one of the most highly regarded on the east coast (Dr. Mansuria at Magee in Pennsylvania in case you’re nearby!), he saw my symptoms and previous ultrasounds, did an exam and immediately knew where my pain was and that it’s most likely adenomyosis causing most of my problems, I’d tried most of the treatments for it (my failed iuds) and the only cure (and official diagnosis) for that is a hysterectomy. They scheduled me for like a month later because I’m turning 26 and losing insurance at the end of this month (thanks, America!). I was absolutely floored, shocked, jaw on the floor because I’d always made it clear fertility is not an issue for me and that I wanted a hysterectomy but no doctor had ever taken that seriously, but this surgeon? I didn’t even bring it up. No follow ups, just straight to surgery a month after my first appointment with him.

tl;dr: it’s all in getting the right doctor that has the right training to know that a hysterectomy is your best option! I know there are some threads on reddit and groups on facebook that have resources for finding a hysterectomy-friendly doctor near you so definitely just research doctors and a good one will listen to you! dm with questions if you have any, I honestly love to help anyone in this position because it’s absolute hell.

[techcrunchappcom]

New Post has been published on https://techcrunchapp.com/deal-alert-oneplus-7t-256gb-model-at-an-effective-price-of-rs-32999-on-amazon-check-details/

Deal alert: OnePlus 7T 256GB model at an effective price of Rs 32,999 on Amazon – check details

By: Tech Desk | New Delhi | October 24, 2020 12:27:23 pm

OnePlus 7T is powered by Snapdragon 855+ (Express File Photo)

Even after the launch of the OnePlus 8T 5G, the OnePlus 7T continues to be one of the best smartphones to can get in India in our opinion. OnePlus is leaving no stones unturned to woo consumers in India. For the very same reason, after the launch of the OnePlus 8T, the price of the OnePlus 7T was discounted in the country. The deal now gets even more tempting as Amazon offers a Rs 5,000 instant discount on the OnePlus 7T as a part of the Great Indian Festival sale.

The Amazon offer further brings down the price of the 8GB RAM/256GB storage model of the OnePlus 7T to Rs 32,999. Notably, this is a limited period offer so you must hurry if you have been waiting to get a premium Android smartphone under Rs 35,000.

OnePlus 7T Amazon deal explained

As far as the Amazon offer is concerned, the OnePlus 7T is listed on Amazon with a price tag of Rs 37,999. The e-commerce giant is offering an instant discount of Rs 5,000 on Axis Bank, Citi Bank, and ICICI Bank Cards. The deal gets even more tempting as there’s an exchange offer of up to Rs 16,400 off. The exchange value clearly depends on the old phone you are exchanging to get the new OnePlus 7T.

The OnePlus 7T might be a one-year-old device, but you still get a flagship Qualcomm Snapdragon 855+ SoC for such an affordable price tag. So, you don’t need to worry about the performance here. Its successor OnePlus 8 offers the latest Snapdragon 865 chipset and you will get almost similar performance with the OnePlus 7T. Apart from this, you also get an AMOLED panel, high refresh rate display, 30W fast charging, and a lot more features.

What OnePlus 7T offers

The OnePlus 7T packs a 6.55-inch Fluid AMOLED display, which operates at  FHD+ (2400 x 1080 pixels) resolution. The display also features a 402ppi pixel density, a 20:9 aspect ratio, and 3D corning gorilla glass. The panel even supports a 90Hz refresh rate for smoother transitions. OnePlus has also added support for sRGB, HDR10+, and Display P3 color profiles.

ALSO READ | OnePlus 7T review: A fresh take on a near perfect smartphone

There is a waterdrop style notched display. The Snapdragon 855+ SoC is backed by Adeno 640 GPU, 8GB RAM and up to 256GB UFS 3.0 internal storage. As for the photography sessions, you get a triple rear camera setup. The OnePlus 7T has a great rear camera setup if you consider its price.

It has a 48MP primary camera with a Sony IMX586 sensor with f/1.6 aperture. It supports OIS for images and EIS for video stabilization. There is also a 12-megapixel camera with a telephoto lens and a 16-megapixel sensor with an ultra-wide lens. Compared to the competition, you do get a slightly small battery. However, you get a 30W fast charger, which will help fill up the 3,800mAh battery in about 40-45 minutes. The device runs OxygenOS, which is based on Android 11. The company will roll out the latest Android 11 OS before the end of this year. All-in-all, we believe, the OnePlus 7T is still a great phone and you must not miss the deal.

Express Tech is now on Telegram. Click here to join our channel (@expresstechie) and stay updated with the latest tech news.

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[ladykailolu]

Well thanks for opening the door!

Favorite color: Royal blue

Currently reading: articles on adeno-associate virus vectors lol

Last series: uuuhhh idk I dont really watch TV regularly lol

Last movie: Wicked City (1987)

Last Song: "Today was a good day" --Ice Cube

Sweet, savory, or spicy: sweet :3

Currently working on: a fanfiction 😉

Tags: go ahead and do it if you want to!

Tag game

Rules: Tag nine people you want to get to know better. Thank you for the tag @minniedlucca <33

Favorite color: blue

Currently reading: 妻为上/The Wife is First (although i’m paused on that for now bc too much stuff to do :’))

Last song: 浮生/Floating Life by Yu-Peng Chen! It’s actually the original song he composed that he used for Ayaka’s dance scene but with lyrics and it’s so pretty <333

Last series: Squid Game 👉

Last movie: Shang-Chi and the Legend of the Ten Rings 

Sweet, savory, or spicy: I’d say sweet and savory are tied but never spicy lol i can’t handle spice at all

Currently working on: college bullshit…🙃 (i’d be working on my woh wip if i could but hahaha no time)

Tagging: @ghostjellyfishheart @adangersandwich @void-listens @noisyaliengiantpatrol @punsandcoookies @flipflapyoutwat @spacey-png @rage-youdamnnerd @itadoriiii no pressure if you don’t want to do it!

[jfleurcannon]

oh fuck. a hysterectomy story.

just so i don't have to go through explaining. please visit links and read up if you are interested, i simplified it AF and wiki'd the source, otherwise, this is legit not the place for you. i talk about things, life, whatnot, and my life is fucking bullshit sometimes.

endometriosis

adenomysosis

fibromyalgia - i'm not even gonna get into this one. because, as the doctor who diagnosed me said, 'not many people believe in this one, so maybe don't say that you have it out loud.' but chalk that guy up for chronic musculoskeletal & joint pain in my wrists, arms, shoulders, back, butt, and knees. but 🤫.

i'm sure y'all know wtf depression and anxiety are, i see those #bellletstalk tags. it's been with me for years, since i guess the chronic pain started. i got my period and wondered why the fuck i was the only one who got sick, like sick. fainting, knocking over a mannequin display at the eddie bauer at fairview mall (you're welcome, sisters), passing out at school and having to be carried out by julie (thank you, sister), missing so many activities and things i wanted to do but couldn't. having 'jenn's always sick anyways' thrown in my face by a childhood friend, being made to feel bad about pain and not wanting to be in the mood, having to cancel plans last minute because of pending pain, side effects from meds i'm taking that make me sick, but not quite as sick as the original problem - so i deal. like i deal with it all. [like a warrior. i have held my pain like the damn death star. my uterus is the death star. except that time i carried and birthed a baby, and then it was fucking AWESOME!] typically it's bottom shelf paper bag internalized. and for years my solution was to therapy it out, or shove the feels down hard so i developed massive GI issues, or maybe that is the endo, who the fuck knows. fast forward years of therapy and a shit ton of medication and three suicide attempts, the final one being in 2007. i was hospitalized for the final attempt at sunnybrook's mental health ward. the F ward, i shit you not. i felt like girl intrurrupted, but there was no winona or angelina. there was a pam and a joan. no padded room, but i couldn't leave to go outside for the first week. that was fucked up.

pain is pain, and although i am a fan of ja-rule, pain has never equaled love to me. it has only left me with an overwhelming hate for parts of my life, that were always plagued by illness, pain, and brewing depressive state. i would get sick for long, long periods of time and there would be no reason for it. had i known then what i had (endo, adeno, fibro, MFGT's) it would have made sense. two of the three are auto-immune diseases. i get a cold, and i really get it. i lose my voice, and it's gone for months.

the only fast thing i've done is labour and delivery. it might seem strange to put the birth of my child in the pain category, however the story will explain why in a mo. i arrived at the hospital at 10am at 2cm dilated, upon exam by a nurse i pushed and my water broke, i was put in a wheelchair and brought to wait for a L&D room, outside the exam room and in the tiny hallway, there my insides tore open, quite literally, nerve damage, and rapid labour. i screamed and screamed and was told to wait while they got things ready. i mean. i thought i was dying. why was this happening so fast? my husband came back up as i was being brought into the room (i think, some details are fuzzy). i was examined by a doctor and was at 10cm. it hadn't been more than 10 minutes since i had arrived. i remember things moving too quickly for me and i was very panicked that something was wrong. i remember being told the boy's heartbeat was becoming compromised and we needed to get him out. options included a C-section, forceps, or the vacuum. all terrified me as i literally was without ANY pain management. we opted for the vacuum and they offered me laughing gas as a super sad knife-in-the-back compromise. i took it, but the hell? AT THAT VERY MOMENT I WANTED THE SWEET, SWEET NECTAR OF THE ALL POWERFUL EPIDURAL! four pushes with the vacuum on and the boy was born, at 10:35am. in 35 minutes i arrived at the hospital had my baby, like whatevs, and held him while being stitched up. naturally there were stitches. i can't even with that pain. OMG. people say you won't remember the labour pain and that 'it'll just go away when you see your perfect baby', you know what? they lied to your face, or they had an epidural, or they didn't experience rapid labour. 2-10 in 5 minutes. they did not teach me that in L&D class. i wanted ice chips, and the tub, and the playlist of music, and maybe a pelvic roll or two on the ball, but no, miles wanted his entrance to be dramatic and fast and it was nothing less than that.

any and all of the things i've battled have stayed with me like wearing a cloak, all day everyday i feel pain, whether it's physical, mental, emotional, or otherwise, i feel it. i can't see it but i fucking feel it. with diagnosis always come the waiting game of endless specialists, tests, interventions by way of oral medication, physical therapy, walking epidurals, suppositories in my ass or vag, chiropractor visits, along with visits to acupuncture, massage, GP, GYNE, and psychologists.

after a thirty year battle, and almost one year of keeping this in my drafts folder, i finally have felt an end to my endometriosis and adenomyosis pain. a hysterectomy and final excision of endo from nerve clusters fused together because of it, i can breathe. i can breathe clearly and without a constant fear of nausea, hot flashes, bizarre mood swings because of the menopausal state the IUD was causing, and chronic pelvic/back/low abdomen/bowel pain. i still have a 44 year old body and permanent nerve damage from rapid labour and negligence from a past surgeon, but holy hot hell it's nice to not want to punch people in the face for asking you how you feel. i know that's not a normal reaction to that question. i get that. however, as someone who has suffered from chronic pain her whole adult life, it is the hardest question to answer honestly. how you feel sometimes is like shit, or crap, or a god damn mess, or you just don't want to talk, especially to that person but you can't say it. so you answer, 'fine', 'great', or 'living the dream'. is the honest answer the best answer? it may not be, but it's the one with the least amount of follow up questions or lengthy conversation to follow. i love things, and flowers, and coffee, and white wine, and my man friend, and my kid, and my family, and a handful of others - but for the most part i would honestly prefer not to talk to anyone about anything. it's all the same conversation anyway. and i'm tired. tired of listening. tired of talking/hearing my own voice. tired of noise. in need of quiet and calm. my one year surgery anniversary is coming up and i'm looking forward to it. i have never looked forward to a post surgery anything because those have always led to more surgeries. but the doctor from brazil with the 'small hands' did the job this time. removed the death star and its accompanying bullshit organs (tubes and cervix) and we are good to go now. she works again, without pain 😉

surgeries for endometriosis & adenomyosis

2006 - laser laparoscopic discovery of endo

2009 - stage IV endo excision via laparoscopy

2015 - laser laparoscopic removal of endo & appendectomy

2016 - endo excision via laparoscopy

2019 - full hysterectomy (minus ovaries) and extensive endo excision on nerve clusters fused together

[phgq]

Cebuano News: WHO: Moderna labing mahal, AstraZeneca labing barato nga bakuna

#PHinfo: Cebuano News: WHO: Moderna labing mahal, AstraZeneca labing barato nga bakuna

TAGBILARAN CITY, Bohol, Jan. 19 (PIA) -- Kon presyo ang hisgutan, ang Moderna, ang bakuna batok sa coronavirus disease (COVID-19), maoy may labing mahal sa unom ka mga nag-una nga bakuna nga mahimong magamit sa mga katawhan.

Segun sa mga kasayuran nga gikan sa World Health Organization, mga ahensya nga nagtutok sa bakuna ug mismo nga mga kompanya sa bakuna, napakita nga ang Moderna (USA) nga mugna nga bakuna gamit ang messenger Ribonucleic Acid (MRNA) mapalit sa tag $33 ang matag tupok.

Ang bakuna nga Moderna nga nakalabang na sa tulo ka medical trials may 95% nga ka epektibo, gikinahanglang nga itupok sa makaduha nga higayon o $66 alang sa usa ka tawo, katumbas na sa P3,300. 

Sunod sa labing mahal nga bakuna mao ang sa Pfizer-BioNtech (USA-Germany), nga sama sa Moderna, migamit sa binag-ong teknolohiya nga gitawag og MRNA.

Bakuna nga miangkon nga 95% usab ka epektibo, ang bakuna sa Pfizer mapalit sa tag $20 matag tupok ug nangnahanglan og duha  ka tupok arom moepekto mao nga kini may local nga bili nga anaa sa P2,000 matag tawo nga tupokan.

Ang bakuna nga ginama sa Russia nga Gamaleya Institute maoy ikatulo sa labing mahal. 

Ang Sputnik V may gikataho nga 91.4% ka epektibo padayon pang gihimoan sa ika tulong hugna sa medical trials ug migamit sa adenoviral-vector-based platform, aron makabuntog sa COVID-19.

Ang Sputnik V gipresyohan na nga anaa sa tag $10 ang matag tupok sa tag duha  ka tupok o P1,000 ang kinatibuk-an nga dosage.

Ang bakuna migamit sa adenovirus, o usa  ka matang sa kagaw nga maoy magdala sa mandu sa  mga sundawo sa lawas sa paghimo og dugang mas gamhanan nga sundawo batok sa SARS-CoV-2 aron kon sa higayon nga may COVID nga kagaw nga mosulod sa lawas, dali ra kining tapuk-an ug buntogon.

Ika-upat sa labing mahal ang Sinovac, nga gikan sa China, nga anaa sa $5 ang matag tupok sa duha   ka tupokan, naa na sa $10 o P500. 

Ang Sinovac migamit sa patay na nga kagaw (inactivated) sa COVID nga itupok sa lawas aron makasuway ang lawas sa pag-ila sa mosulod unya nga kagaw sa COVID. 

Sa laing bahin, ika-upat usab ang Johnson and Johnson gipaabut pa nga mopagawas sa unsa  ka epektibo sa ilang bakuna kay nagpadayon pa ang ilang katapusang hugna sa clinical trials, mibutyag na nga mapalit ang ilang bakuna sa tag $10 apan magkinahanglan lamang kini ug usa  ka tupokan, o P500 lamang.

Ang Johnson and Johnson (USA) migamit sa kagaw sa sip-on aron maoy magdala sa mandu ngadto sa mga sundawo sa lawas sa paghimog mga protina nga makigbungo sa kagaw sa COVID nga mosulod unya.

Labing barato sa unom ka mga ag-una nga bakuna karon mao ang Oxford University ug sa AstraZeneca (Britain-Sweden) nga may kaepektibo nga naa sa 62-90 porsyento, nga gibaligya lamang sa $4 matag tupok ug itupok sa maka duha, o anaa ra sa tag P400.

Ang bakuna sa AstraZeneca migamit sa susamang teknolohiya sa Sputnik nga adeno-viral vector nga us aka genetically modified virus, nga maoy magtunol sa mandu ngadto sa mga sundawo sa lawas sa paghimo og mga makabuntog sa kagaw sa COVID.

Ang AstraZeneca gikataho nga una na nga misaad nga dili sila magpaginansya sa ilang bakuna isip ilang halad alang sa kalibutan nga naapektohan sa COVID.  (rahc/PIA-7/Bohol)

***

References:

* Philippine Information Agency. "Cebuano News: WHO: Moderna labing mahal, AstraZeneca labing barato nga bakuna." Philippine Information Agency. https://pia.gov.ph/news/articles/1064422 (accessed January 22, 2021 at 09:42AM UTC+08).

* Philippine Infornation Agency. "Cebuano News: WHO: Moderna labing mahal, AstraZeneca labing barato nga bakuna." Archive Today. https://archive.ph/?run=1&url=https://pia.gov.ph/news/articles/1064422 (archived).

[dorcasrempel]

Experimental peptide targets Covid-19

The research described in this article has been published on a preprint server but has not yet been peer-reviewed by scientific or medical experts.

Using computational models of protein interactions, researchers at the MIT Media Lab and Center for Bits and Atoms have designed a peptide that can bind to coronavirus proteins and shuttle them into a cellular pathway that breaks them down.

This type of peptide could hold potential as a treatment that would prevent the SARS-CoV-2 virus from reproducing itself within infected cells, the researchers say.

“Our idea was to use computational techniques to engineer a peptide that could be a therapeutic for Covid-19. Once the peptide gets in the cell, it can simply tag and degrade the virus,” says Pranam Chatterjee, a recent MIT PhD recipient and the lead author of the study.

The researchers have tested the peptide in human cells, and they are now planning additional cell and animal studies to further evaluate its efficacy. They reported their initial findings in a preprint posted on bioRxiv, an online preprint server, on June 1, and have also submitted it to a peer-reviewed journal. Graduate student Manvitha Ponnapati and Joseph Jacobson, an associate professor in the MIT Media Lab, co-authored the study.

Modeling peptides

Scientists are pursuing many different strategies to develop new therapeutics against SARS-CoV-2. One area of interest is developing antibodies that bind to and inactivate viral proteins such as the spike protein, which coronaviruses use to enter human cells. A related approach uses small protein fragments called peptides instead of antibodies.

The MIT team set out to engineer peptides that could strongly bind to the spike protein inside cells, and to use these peptides to trigger the cells to break down the viral proteins. Their idea was to have their peptides recruit naturally occurring proteins called E3 ubiquitin ligases, which can mark proteins for destruction when cells no longer need them.

To generate their spike-protein-binding peptides, the researchers used a computational model of protein interactions that they had previously trained to optimize binding strength between two proteins. Chatterjee and others recently used similar computational methods to design improved versions of enzymes used for the genome-editing technique known as CRISPR. Their new CRISPR-Cas9 enzymes, together, can target more than 70 percent of DNA sequences, while the most commonly used form of CRISPR-Cas9 reaches only about 10 percent.

In this case, the researchers used as their starting point the human ACE2 protein, which is found on the surface of certain types of human cells and binds to the coronavirus spike protein.

They used their model to break ACE2 into many small fragments and then computationally predict how the fragments would interact with the spike protein. They instructed the model to optimize three features: First, they engineered peptides to have strong binding affinity to the spike protein. Second, they established that the peptides could bind well to other coronavirus spike proteins, in hopes that it could work against past and future strains of coronaviruses. Third, they ensured that the peptides would not bind strongly to human proteins called integrins, which are the proteins that normally bind to the ACE2 receptor in the body.

This process generated about 25 candidate peptides, which the researchers fused to an E3 ubiquitin ligase and tested in human cells that expressed a fragment of the spike protein known as the receptor-binding domain (RBD).

The best of these candidates, a 23-amino-acid peptide, broke down about 20 percent of the RBD proteins in the cells. However, this peptide did not work as well as the original ACE2 protein, which broke down about 30 percent of the RBD proteins. To improve the peptide’s performance, the researchers used their model to simulate how its RBD-binding would be affected if they substituted different amino acids at each of its 23 positions. That optimization process yielded a mutant peptide that improved the degradation rate to over 50 percent.

Tagged for destruction

One key advantage of this peptide is its small size — even when fused to the E3 ubiquitin ligase, the entire chain is only around 200 amino acids in length. The researchers envision that RNA or DNA encoding the peptides could be delivered by harmless viruses called adeno-associated viruses.

Another possibility would be to deliver the peptide on its own, allowing it to bind to the coronavirus spike protein outside of cells and be carried into cells with the virus. In that case, the virus would then be tagged for destruction as soon as it enters the cell, Chatterjee says.

The researchers are now planning to test the peptide in human cells infected with the SARS-CoV-2 virus, which will occur at specialized biosafety labs outside MIT. If those tests are successful, the researchers hope to test the peptide in animal models. They are also working on further improving the peptide so that it can bind the spike protein more strongly.

This work was supported by the consortium of sponsors of the MIT Media Lab, the MIT Center for Bits and Atoms, and Jeremy and Joyce Wertheimer.

Experimental peptide targets Covid-19 syndicated from https://osmowaterfilters.blogspot.com/

[abbkine]

New Post has been published on Abbkine - Antibodies, proteins, biochemicals, assay kits for life science research

Hard work, Do not forget your initiative mind-—Abbkine Breaks 1400 citations

Since Abbkine document collection began, as of December 31, 2019, the number of English articles published by google using Abbkine products has exceeded 1400, with an impact factor exceeding 5400 points.

Thank you for your trust and support to Abbkine. We will continuously stimulate our internal creativity, provide competitive biomedical products and services, and continuously create maximum value for our customers. With a view to becoming a respected and world-class provider of biomedical products and services.

Figure 1: Number of English Articles Published Using Abbkine Products from 2017 to 2019

In December 2019, Abbkine added 200+ citations. Some high-score citations are as below.

LECT2, a Ligand for Tie1, Plays a Crucial Role in Liver Fibrogenesis.

https://doi.org/10.1016/j.cell.2019.07.021

Magazine: Cell

Impact: 24.38

Abstract: Liver fibrosis is a very common condition seen in millions of patients with various liver diseases, and yet no effective treatments are available owing to poorly characterized molecular pathogenesis. Here, we show that leukocyte cell-derived chemotaxin 2 (LECT2) is a functional ligand of Tie1, a poorly characterized endothelial cell (EC)-specific orphan receptor. Upon binding to Tie1, LECT2 interrupts Tie1/Tie2 heterodimerization, facilitates Tie2/Tie2 homodimerization, activates PPAR signaling, and inhibits the migration and tube formations of EC. In vivo studies showed that LECT2 overexpression inhibits portal angiogenesis, promotes sinusoid capillarization, and worsens fibrosis, whereas these changes were reversed in Lect2-KO mice. Adeno-associated viral vector serotype 9 (AAV9)-LECT2 small hairpin RNA (shRNA) treatment significantly attenuates fibrosis. Upregulation of LECT2 is associated with advanced human liver fibrosis staging. We concluded that targeting LECT2/Tie1 signaling may represent a potential therapeutic target for liver fibrosis, and serum LECT2 level may be a potential biomarker for the screening and diagnosis of liver fibrosis.

Products using from Abbkine:

IPKine™ HRP, Goat Anti-Mouse IgG HCS (CAT#: A25112)

IPKine™ HRP, Goat Anti-Mouse IgG LCS (CAT#: A25012)

2. EMS1 and BRI1 control separate biological processes via extracellular domain diversity and intracellular domain conservation.

https://www.nature.com/articles/s41467-019-12112-w

Magazine: Nature Communications volume

Impact: 12.19

Abstract: In flowering plants, EMS1 (Excess Microsporocytes 1) perceives TPD1 (Tapetum Determinant 1) to specify tapeta, the last somatic cell layer nurturing pollen development. However, the signaling components downstream of EMS1 are relatively unknown. Here, we use a molecular complementation approach to investigate the downstream components in EMS1 signaling. We show that the EMS1 intracellular domain is functionally interchangeable with that of the brassinosteroid receptor BRI1 (Brassinosteroid Insensitive 1). Furthermore, expressing EMS1 together with TPD1 in the BRI1 expression domain could partially rescue bri1 phenotypes, and led to the dephosphorylation of BES1, a hallmark of active BRI1 signaling. Conversely, expressing BRI1 in the EMS1 expression domain could partially rescue ems1 phenotypes. We further show that PpEMS1 and PpTPD1 from the early land plant Physcomitrella patens could completely rescue ems1 and tpd1 phenotypes, respectively. We propose that EMS1 and BRI1 have evolved distinct extracellular domains to control different biological processes but can act via a common intracellular signaling pathway.

Products using from Abbkine:

Anti-Plant Actin Mouse Monoclonal Antibody (3T3) (CAT#: A01050)

3. PLK4 deubiquitination by Spata2‐CYLD suppresses NEK7‐mediated NLRP3 inflammasome activation at the centrosome.

https://www.embopress.org/doi/abs/10.15252/embj.2019102201

Magazine: EMBO JOURNAL

Impact: 10.55

Abstract: The innate immune sensor NLRP3 assembles an inflammasome complex with NEK7 and ASC to activate caspase‐1 and drive the maturation of proinflammatory cytokines IL‐1β and IL‐18. NLRP3 inflammasome activity must be tightly controlled, as its over‐activation is involved in the pathogenesis of inflammatory diseases. Here, we show that NLRP3 inflammasome activation is suppressed by a centrosomal protein Spata2. Spata2 deficiency enhances NLRP3 inflammasome activity both in the macrophages and in an animal model of peritonitis. Mechanistically, Spata2 recruits the deubiquitinase CYLD to the centrosome for deubiquitination of polo‐like kinase 4 (PLK4), the master regulator of centrosome duplication. Deubiquitination of PLK4 facilitates its binding to and phosphorylation of NEK7 at Ser204. NEK7 phosphorylation in turn attenuates NEK7 and NLRP3 interaction, which is required for NLRP3 inflammasome activation. Pharmacological or shRNA‐mediated inhibition of PLK4, or mutation of the NEK7 Ser204 phosphorylation site, augments NEK7 interaction with NLRP3 and causes increased NLRP3 inflammasome activation. Our study unravels a novel centrosomal regulatory pathway of inflammasome activation and may provide new therapeutic targets for the treatment of NLRP3‐associated inflammatory diseases.

Products using from Abbkine:

IFKine™ Green Donkey Anti-Mouse IgG (CAT#: A24211)

4. Cross-Microbial Protection via Priming a Conserved Immune Co-Receptor through Juxtamembrane Phosphorylation in Plants

https://doi.org/10.1016/j.chom.2019.10.010

Magazine: Cell Host & Microbe

Impact: 10.5

Abstract: Living organisms can be primed for potentiated responses to recurring stresses based on prior experience. However, the molecular basis of immune priming remains elusive in plants that lack adaptive immunity. Here, we report that bacterial challenges can prepare plants for fungal attacks by inducing juxtamembrane phosphorylation of CERK1, the co-receptor indispensable for signaling in response to the fungal elicitor chitin. This phosphorylation is mediated by BAK1, a co-receptor for signaling in response to multiple elicitors. BAK1 interacts with CERK1, and loss of BAK1 reduces priming phosphorylation of CERK1. Juxtamembrane phosphomimetic mutations of CERK1 confer accelerated chitin responses and fortified fungal resistance without triggering constitutive immunity, whereas juxtamembrane phosphodeficient mutations diminish bacteria-induced protection against fungal infection. These findings reveal that crosstalk between cell-surface immune co-receptors can prime defense and demonstrate that juxtamembrane phosphorylation of plant receptor-like kinases can occur independent of kinase activation to place the protein into a prime state.

Products using from Abbkine:

Anti-GST Tag Mouse Monoclonal Antibody (2A8) (CAT#: A02030)

5. Extracellular vesicles of carcinoma-associated fibroblasts creates a pre-metastatic niche in the lung through activating fibroblasts

https://molecular-cancer.biomedcentral.com/articles/10.1186/s12943-019-1101-4

Magazine: Molecular Cancer

Impact: 9.17

Abstract: Carcinoma-associated fibroblasts (CAFs) have been known to promote cancer progression by modifying the primary tumor microenvironment. We aimed to elucidate the intercellular communication between CAFs and secondary organs in salivary adenoid cystic carcinoma (SACC) metastasis.

Products using from Abbkine:

FITC, Goat Anti-Rabbit IgG (CAT#: A22120)

Dylight 488, Goat Anti-Rabbit IgG (CAT#: A23220)

Dylight 549, Goat Anti-Rabbit IgG (CAT#: A23320) Please learn more details from https://www.abbkine.com/publications/ .

[vinahealth]

Viêm họng cấp là bệnh thường gặp, xảy ra ở mọi lứa tuổi, rất dễ mắc trong điều kiện thời tiết chuyển mùa. Nếu không điều trị kịp thời, bệnh sẽ chuyển thành mạn tính, thậm chí gây biến chứng.

Viêm họng cấp là bệnh thường gặp, xảy ra ở mọi lứa tuổi, rất dễ mắc trong điều kiện thời tiết chuyển mùa.

Viêm họng cấp là bệnh thường gặp, xảy ra ở mọi lứa tuổi, rất dễ mắc trong điều kiện thời tiết chuyển mùa. Nếu không điều trị kịp thời, bệnh sẽ chuyển thành mạn tính, thậm chí gây biến chứng.

Viêm họng cấp là tình trạng viêm niêm mạc họng xảy, ra một cách đột ngột bởi vi sinh vật (vi khuẩn, virut, ký sinh trùng) và do một số yếu tố liên quan.

Với virut có thể là virut cúm, virut sởi, virut Adeno. Vi khuẩn gây bệnh viêm họng cấp thường do vi khuẩn phế cầu, tụ cầu, liên cầu, Hemophillus influenzae.

Nguy hiểm hơn cả là liên cầu khuẩn nhóm A (S. pyogenes) bởi vì nó là thủ phạm gây viêm họng dẫn đến biến chứng viêm khớp cấp, tổn thương van tim (dược gọi là thấp tim tiến triển) hoặc biến chứng viêm cầu thận cấp, nếu không phát hiện sớm sẽ dẫn đến suy thận.

Ngoài các nguyên nhân đó phải kể đến các yếu tố nguy cơ như thay đổi thời tiết (nóng, lạnh đột ngột), ẩm ướt, độ ẩm cao, bụi bẩn (bụi công nghiệp, bụi bẩn), khói (thuốc lá, thuốc lào, khói bếp than, củi, rơm rạ).

Những triệu chứng ban đầu

Bắt đầu sốt cao, đột ngột (39 – 400C), tuy nhiên, có một số trường hợp (trẻ còi xương, suy dinh dưỡng nặng, người cao tuổi sức yếu) có thể sốt không cao, thậm chí không sốt.

Các triệu chứng ớn lạnh kèm theo nhức đầu, nuốt đau, đau mỏi thân mình, ăn, ngủ kém thường xuất hiện. Một số trường hợp có hạch cổ sưng và đau.

Người bệnh ở giai đoạn đầu có cảm giác khô nóng trong họng, khát nước, dần dần cảm giác đau rát tăng lên khi nuốt (ăn, uống, nuốt nước bọt) và khi nói, đau lan lên tai.

Có thể có nghẹt mũi (một hoặc hai bên), chảy mũi nước và ho. Vài ba ngày sau, nếu không được phát hiện và điều trị có thể có khàn tiếng.

Toàn bộ niêm mạc họng đỏ rực. Màn hầu, trụ trước, trụ sau và thành sau họng phù nề, đỏ, xuất tiết, xuất huyết thành sau họng (nếu do virut). Ở người còn amidal sẽ sưng to, nếu viêm tái phát, amidal thường có hốc, có thể có mủ hoặc bựa trắng như nước cháo phủ trên bề mặt hoặc miệng các hốc amidal.

Bệnh dễ chuyển thành viêm tai, viêm mũi xoang khi sức đề kháng yếu

Bệnh viêm họng cấp thường diễn ra trong vòng 3 – 4 ngày, nếu sức đề kháng tốt hoặc được điều trị đúng, bệnh sẽ lui dần, các triệu chứng trên sẽ mất đi rất nhanh.

Nhưng khi sức đề kháng yếu (trẻ em, người cao tuổi), không được chữa trị kịp thời, bệnh diễn biến phức tạp hơn, nặng hơn và có thể gây biến chứng như viêm tai, viêm mũi, viêm thanh quản, viêm phế quản, viêm xoang hoặc nhiễm khuẩn huyết hoặc viêm phổi nặng hoặc trở thành viêm họng mạn tính. Trong trường hợp viêm họng do vi khuẩn liên cầu nhóm A, có thể gây nên bệnh thấp tim tiến triển hoặc viêm cầu thận cấp.

Chẩn đoán viêm họng cấp, ngoài khám lâm sàng, xét nghiệm công thức máu sẽ thấy bạch cầu tăng cao, tốc độ máu lắng tăng, chỉ số CRP (C Reaction Protein) dương tính. Xét nghiệm nhày họng bằng phương pháp nhuộm đơn thấy nhiều tế bào bạch cầu, vi khuẩn (trực khuẩn hoặc cầu khuẩn).

Nhuộm bằng phương pháp gram có thể thấy cầu khuẩn gram dương hoặc âm hoặc thấy cả xoắn khuẩn Vincent. Nếu có điều kiện nuôi cấy chất nhày họng sẽ xác định được loại vi khuẩn gì gây viêm họng cấp, trên cơ sở đó thực hiện kháng sinh đồ để chọn kháng sinh thích hợp cho việc điều trị.

Nguyên tắc điều trị và phòng bệnh

Khi nghi ngờ bị viêm họng cấp, cần được khám, tốt nhất là khám chuyên khoa Tai mũi họng. Người bệnh cần tuân theo đơn của bác sĩ khám bệnh, mua đúng thuốc và uống thuốc đủ liều, không tự động mua thuốc để chữa bệnh cho mình và người nhà khi chưa có ý kiến của bác sĩ.

Cần bù nước và chất điện giải do sốt cao gây ra. Tốt nhất là uống dung dịch oresol (ORS), có thể dùng ORS cam loại 5,63g/gói cho cả người lớn và trẻ em, pha 1 gói vào 200ml nước (đun sôi, để nguội).

Thông thường, sử dụng ORS như sau: trẻ nhũ nhi dùng 50ml/lần x 2-3 lần/ngày; trẻ từ 2 – 6 tuổi dùng 100ml/lần x 2 -3 lần/ngày; trẻ từ 6 – 12 tuổi dùng 150ml/lần x 2-3 lần. Với người lớn, dùng theo nhu cầu.

Ngoài ra, nên uống thêm các loại nước trái cây (cam, chanh, dưa hấu…). Thức ăn nên dùng loại mềm, nhuyễn, lỏng, dễ nuốt. Cần phải nghỉ ngơi, giữ ấm cơ thể, nhất là cổ, ngực, gan bàn chân. Nên tắm, rửa bằng nước ấm trong phòng kín gió, tắm xong phải lau người thật khô rồi mặc quần áo sạch.

Cần vệ sinh họng, miệng hằng ngày như đánh răng sau khi ăn, trước và sau khi ngủ dậy. Nên súc họng bằng nước muối nhạt hàng ngày, tốt nhất là nước muối sinh lý 9%o.

Khi đi ra ngoài đường, nên đeo khẩu trang để tránh bụi. Nhà ở phải thoáng mát, tránh ẩm thấp. Không nên hút thuốc lá, lào và không nên uống nước lạnh, nước có đá…

Tags: giao mùa, nuốt đau, ớn lạnh kèm theo nhức đầu, triệu chứng, viêm họng cấp, đau mỏi thân mình, điều trị

[neurogenpapers]

p62 Pathology Model in the Rat Substantia Nigra with Filamentous Inclusions and Progressive Neurodegeneration.

PubMed: p62 Pathology Model in the Rat Substantia Nigra with Filamentous Inclusions and Progressive Neurodegeneration.: p62 Pathology Model in the Rat Substantia Nigra with Filamentous Inclusions and Progressive Neurodegeneration. PLoS One. 2017;12(1):e0169291 Authors: Jackson KL, Lin WL, Miriyala S, Dayton RD, Panchatcharam M, McCarthy KJ, Castanedes-Casey M, Dickson DW, Klein RL Abstract One of the proteins most frequently found in neuropathological lesions is the ubiquitin binding protein p62 (sequestosome 1). Post-mortem analysis of p62 is a defining diagnostic marker in several neurodegenerative diseases including amyotrophic lateral sclerosis and inclusion body myositis. Since p62 functions in protein degradation pathways including autophagy, the build-up of p62-positive inclusions suggests defects in protein clearance. p62 was expressed unilaterally in the rat substantia nigra with an adeno-associated virus vector (AAV9) in order to study p62 neuropathology. Inclusions formed within neurons from several days to several weeks after gene transfer. By electron microscopy, the inclusions were found to contain packed 10 nm thick filaments, and mitochondria cristae structure was disrupted, resulting in the formation of empty spaces. In corollary cell culture transfections, p62 clearly impaired mitochondrial function. To probe for potential effects on macroautophagy, we co-expressed p62 with a double fluorescent tagged reporter for the autophagosome protein LC3 in the rat. p62 induced a dramatic and specific dissociation of the two tags. By 12 weeks, a rotational behavior phenotype manifested, consistent with a significant loss of dopaminergic neurons analyzed post-mortem. p62 overexpression resulted in a progressive and robust pathology model with neuronal inclusions and neurodegeneration. p62 gene transfer could be a novel methodological probe to disrupt mitochondrial function or autophagy in the brain and other tissues in vivo. PMID: 28076378 [PubMed - in process] http://dlvr.it/N5Q0zw

[ladykailolu]

Well thanks for opening the door!

Favorite color: Royal blue

Currently reading: articles on adeno-associate virus vectors lol

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Tags: go ahead and do it if you want to!

Tag game

Rules: Tag nine people you want to get to know better. Thank you for the tag @minniedlucca <33

Favorite color: blue

Currently reading: 妻为上/The Wife is First (although i’m paused on that for now bc too much stuff to do :’))

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Sweet, savory, or spicy: I’d say sweet and savory are tied but never spicy lol i can’t handle spice at all

Currently working on: college bullshit…🙃 (i’d be working on my woh wip if i could but hahaha no time)

Tagging: @ghostjellyfishheart @adangersandwich @void-listens @noisyaliengiantpatrol @punsandcoookies @flipflapyoutwat @spacey-png @rage-youdamnnerd @itadoriiii no pressure if you don’t want to do it!