Hear from Carl June at the Gladstone-UCSF Institute of Genomic Immunology Symposium Inbox Gladstone Events Unsubscribe Wed, Oct 20, 12:59 PM (5 days ago) to me Images are not displayed. Display images below - Always display images from events@gladstone.ucsf.edu Forward to a Friend GLADSTONE-UCSF INSTITUTE OF GENOMIC IMMUNOLOGY Innovators in Genomic Immunology November 3, 2021 9am–5pm PDT • Online Join this 1-day symposium to meet the investigators of the Gladstone-UCSF Institute of Genomic Immunology and discover how their labs are using genomic and genome engineering technologies to address key questions in human immunology and repurpose the immune system to fight disease. You’ll also get to hear from invited speaker Carl June, director of the Center for Cellular Immunotherapies, and director of the Parker Institute for Cancer Therapy at the University of Pennsylvania. VIEW THE AGENDA AND REGISTER Know someone who’d like to attend? Forward to a friend. The Gladstone-UCSF Institute of Genomic Immunology was launched in 2020 to bring experts in diverse, rapidly advancing fields together around the shared goal of understanding how to genetically control human immune cells and using this knowledge to develop innovative cell‑based immunotherapies. View in Your Browser © 2021 Gladstone Institutes. All rights reserved. Want to change how you receive these emails? Update your preferences or unsubscribe from this list. Gladstone Institutes 1650 Owens Street San Francisco, CA 94158 Add us to your address book

FREEDOM, SEX AND TERRITORY.

FREEDOM, SEX AND TERRITORY:

Tools to Investigate SARS-CoV-2 Infection

Proteins | Antibodies | Neutralizing Antibodies |ELISA | Molecular Biology Reagents

GENTLE PEOPLE:

 It has been over a year now since the covid-19 virus created an international pandemic of sickness and death. As of this date, Sunday, October 10, we continue to live in fear of the deadly virus but thanks to new and quickly developed and distributed vaccines, millions of us have survived the pandemic.

THE BIG QUESTION NOW IS, ARE WE FINALLY SAFE? 

SADLY, THE ANSWER IS NO! THE VIRUS HAS MUTATED AND WE NEED TO CONTINUE DEVELOPING NEW AND BETTER METHODS TO BLOCK COVID AND OTHER DANGEROUS VIRUS FROM PROLIFERATING...

COVID-19 is caused by the coronavirus SARS CoV-2, previously called 2019-nCoV. It belongs to the Coronaviridae family and is broadly distributed in humans and other mammals. hCoV-229E, OC43, NL63 and HKU1 are some of the known coronaviruses that cause mild respiratory diseases unlike SAR-CoV and MERS that cause severe to fatal respiratory diseases [1].

Why is SARS-CoV-2 spreading faster than its two ancestors? Why is SARS-CoV-2 lethal? Recent publications have shown that there are differences in their genome structure and immunological response to SARS-CoV-2 infection. The key markers involved in these interactions include Spike protein (S), Nucleocapsid (N), ACE-2 receptor, FURIN protease in addition to the cytokines.

Coronavirus with Spike

Spike Protein (S): SARS-CoV2 enters the cells through the Spike mediated interaction with the ECD domain of the ACE2 cell receptor. (A recombinant fusion protein (RBD of Spike protein and ECD of membrane protein) can be a great tool to investigate this interaction.

Learn more about the purified recombinant Spike Protein (S).

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ACE2 and TMPRSS2 in Coronoa virus

Transmembrane Serine Protease 2 (TMPRSS2): This is a serine protease that cleaves and activates the viral spike glycoproteins which facilitates virus-cell membrane fusions. A recent study showed that SARS-CoV-2 needs both ACE2 receptor and serine protease TMPRSS2 for protein priming to enter the cell.[2]

Tools for analyzing TMPRSS2

1. ORF clones
2. Goat and Rabbit Polyclonal Antibodies
3. CRISPR kits
4. Unique controls

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Corona virus structure 

Nucleocapsid: The nucleocapsid phosphoprotein packages the viral genome into a helical ribonucelocapsid, thus playing a crucial role in viral self-assembly.

Tools for analyzing the Nucleocapsid

1. Recombinant SARS-CoV-2 Nucleocapsid Protein
2. Biotinylated recombinant SARS-CoV-2 Nucleocapsid protein
3. SARS-CoV-2 N protein Rabbit Polyclonal Antibody

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ACE-2 Receptor Protein

ACE-2 receptor: ACE-2 is the host cell receptor responsible for mediating infection by SARS-CoV-2.

Tools for analyzing ACE-2 protein

1. Human Recombinant Protein Angiotensin Converting Enzyme (ACE2)
2. ACE-2 specific Mouse Monoclonal Antibody
3. ACE-2 Human ORF clones

Find out more about the additional ACE-2 specific tools here

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ACE-2 Receptor Protein 

Furin: It is a protease present in many human organs that recognizes and activates a specific site on the SARS-CoV-2 Spike protein, thus facilitating a tighter binding to the ACE-2 receptor and might play a role in the higher infection rate [3].

How can you analyze Furin? Learn about the tools for analyzing Furin.

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IL2 Pathway

Cytokines: Studies have shown a strong correlation between severity of the disease and concentrations of IL2, IL7, IL10, GCSF, MCP1 and TNF alpha [1].

Tools to analyze the 6 cytokines associated Cytokine Storm:
IL2 | IL7 | IL10 | GCSF | MCP1 | TNF alpha

References:

1. https://link.springer.com/article/10.1007/s12098-020-03263-6
2. https://science.sciencemag.org/content/367/6483/1260
3. https://science.sciencemag.org/content/367/6483/1260

 

ATTENTION WORLD GOVERNMENT LEADERS!

 YOUR SCHOOLS ARE CURRENTLY TRAINING CHILDREN TO WORK FOR BIG BUSINESS. THIS MUST STOP! CHILDREN NEED TO CHANGE AND GREEN THE ECONOMY TO HELP PRESERVE NATURE. WE NEED AN ECONOMY BASED ON NATURE AND NOT AN ECONOMY BASED ON OIL AND GAS AND POLLUTING INDUSTRY.

 EVERY SCHOOL MUST HAVE : TREES, VEGETABLES, AND FLOWER GARDENS, WITH CHILDREN LEARNING ABOUT AND CARING FOR PLANTS. WHY? BECAUSE WITHOUT NATURE LIFE CEASES TO EXIST AND TODAY NATURE IS BARELY SUSTAINING THE LIFE OUR POLLUTING INDUSTRIAL ECONOMY IS DESTROYING!  THIS IS NOT AN OPINION OR A THEORY, IT IS A FACT.

WE NEED PEOPLE WHO HAVE LEARNED IN CHILDHOOD AS MUCH BOTANY AND BIOLOGY AND  WAYS TO PROTECT THE ENVIRONMENT AS IS HUMANLY POSSIBLE AND WHO ARE NOT AFRAID TO TAKE ACTION.  IT BEGINS BY CHANGING THE SCHOOL ENVIRONMENT AND IT ENDS WITH THE CREATION OF A BEAUTIFUL NATURAL ENVIRONMENT WE CAN ALL BE PROUD OF.

N.J.R.

THE FOLLOWING ARE MORALLY WRONG AND ETHICALLY EVIL...

1. THE MURDER OF  AIR BREATHING FRIENDLY DOLPHINS AND WHALES FOR THEIR MEAT AND OIL.

2. THE POLLUTION OF AIR AND WATER WITH OIL AND PLASTIC AND GAS.

3. GENETICALLY CONVERTED SEEDS THAT RESIST POLLUTION AND PESTICIDES AND ALLOW FARMERS THE USE OF DANGEROUS PESTICIDES WHICH CONSEQUENTLY KILL SONG BIRDS AND BEES.

OH TO BE A TREE!

OH TO BE A TREE

STANDING QUIET AND TALL

IN ELEGANT SIMPLICITY...

TALL AND QUIET AND MAJESTIC

IN A FOREST OF MAGNIFICENT TREES....

BUT A TREE NEVER SO PROUD

AS TO HUMBLE THOSE AROUND ME

AND NEVER SO HUMBLE AS TO BE SHADOWED

UNDER THEIR CANOPY.

N.J. RAGLIONE . JAN 2013

if it works against the h.i.v. virus, Why can't "adaptive transmissible therapies" be adopted and activated by world governments and their giant pharmaceutical companies, to stop the spread of the covid-19 variant pandemic?

======================

ADAPTIVE TRANSMISSIBLE THERAPIES: A NEW CONCEPT FOR DISEASE CONTROL

Existing measures for infectious disease control face three ‘universal’ barriers:

(i)  Deployment (e.g. reaching the highest-risk, infectious ‘superspreaders’ who drive disease circulation)

(ii)  Pathogen persistence & behavioral barriers (e.g. adherence)

(iii)  Evolution (e.g. resistance and escape)

These barriers exist because pathogens are dynamic—they mutate and transmit—while existing therapies are static, neither mutating nor transmitting.  To surmount these barriers, we have proposed a radical shift in therapeutic paradigm toward developing adaptive, dynamic therapies (Metzger et al. 2011).  Building off data-driven epidemiological models, we show that engineered molecular parasites, designed to piggyback on HIV-1, could circumvent each barrier and dramatically lower HIV/AIDS in sub-Saharan Africa as compared to established interventions. 

Above: A representative model for how a small 'core groups' of high-risk 'superspreaders' (e.g. commercial sex workers and their clients) drove the HIV-1 

epidemic in sub-Saharan Africa along the trans-Africa highway in the 1980s.  These hard-to-reach groups--often stigmatized and disenfranchised--disproportionately drive disease spread and can be described by the Pareto '80/20' rule - where 80% of new infections are driven by 20% of the population.

Above: Theoretical model of how Therapeutic Interfering Particles (TIPs) would act to reduce the burden of HIV on a population-wide scale. Small blue "pools" of infection represent a local reduction in HIV by the TIP, and are rapidly spread by a "superspreader population".

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These molecular parasites essentially steal replication and packaging resources from HIV within infected cells thereby generating Therapeutic Interfering Particles (TIPs)[1] which deprive HIV of critical replication machinery thereby reducing viremia.  The fundamental departure from conventional therapies is that TIPs are under strong evolutionary selection to maintain parasitism with HIV and will thus co-evolve with HIV, establishing a co-evolutionary ‘arms race’ (Rouzine and Weinberger, 2013).

Like Oral Polio Vaccine, (OPV)—currently used for the W.H.O. worldwide polio-eradication effort—TIPs could also transmit between individuals, a recognized benefit for OPV.  TIP transmission would occur along HIV-transmission routes (via identical risk factors), thereby overcoming behavioral issues and automatically reaching high-risk populations to limit HIV transmission even in resource-poor settings. 

For review:  Notton et al. Current Opinion in Biotechnology 2014.

HIV TIPs Executive Summary

Papers of note: Metzger, Lloyd-Smith, and Weinberger. PLoS Computational Biology 2011 (videos above) and Rouzine and Weinberger. Journal of Virology 2013 (Linked above).

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[1] TIPs are a distinct form of defective interfering particles (DIPs) engineered to have a basic reproductive ratio (R0) > 1.

How to write great News Letters.

Anna from Revue <anna@getrevue.co> Unsubscribe Sep 12, 2021, 12:16 AM (9 days ago) to me Hi there, Welcome to the Revue Email Academy! Thank you for enrolling in this five-day course. I’m delighted you chose to join me for  what I hope will be a helpful journey that results in your newsletter’s success. I’ll talk a lot over the next few days about how to make the most of the tools in Revue to make the  creation process a breeze, as well as how to promote and monetize your newsletter, but I wanted to  start with addressing something a bit broader: how do you build a newsletter creation habit in the  first place? It’s no exaggeration to say that every writer deals with this problem, so you’re in  great company. Let’s dive in. Find your niche First, we need to pin down the value you bring to your reader (Already know that?  Awesome — you can skip to the next section!). If you’re just getting started with your newsletter, now is not the time to worry about  your subscriber count. We’re used to seeing huge numbers on social media. 10,000 followers on Twitter?  1 million views on TikTok? Standard. But it’s good to realise at this point that most  newsletter audiences don’t look like that. And you don’t need them to. 1,000 engaged readers is much better than 10,000 who  never open your emails. Here’s why: They’ll be more likely to offer feedback to help you reach your target audience  better They’ll be more likely to pay for your content They’ll be more likely to spread the word With the promotion tips we’ll provide later in this course, you’ll have a great head-start  on building your subscriber base organically — but at this point, right at the  beginning, the best advice we can give you is to focus on finding something you’re  passionate about and putting it in your newsletters on a regular basis.  Even better: find your niche. You can choose any topic under the sun, but I’d  encourage you to think about the specific value you can bring to your audience.  Do you read lots of articles about a particular topic? Are you on top of the latest  trends and news? Do your friends come to you for music tips? Recipes?  Your impeccable taste in old movies? Channel that into your newsletter — and keep  tweaking until you find the right fit.  Set a rhythm One thing we know from the experience of tens of thousands of creators on Revue is  that subscribers reward consistency. If you publish, say, every Friday morning for a  few months, opening your email will become a habit for your most engaged readers. They’ll learn to expect, and eagerly anticipate, your next issue. Sure, you can throw in a bonus issue here and there when it fits your schedule (and subscribers won’t mind if you need to take a holiday once in a while!) — but it’s best to develop a rhythm. Here’s why: It’s more reader-friendly. If you send one newsletter on Monday lunchtime and the next on Friday evening, it’s harder for your readers to build a habit around opening your newsletter.  It’s more you-friendly. By committing to this structure, you’re encouraging yourself to be productive. The more you produce and share, the more you’ll learn about what resonates with your audience, and your newsletter will get even better.  You’ll be able to compare stats more effectively. If you start with a baseline send time (eg. Friday at 9am), you reduce the variables that could be affecting your engagement stats.  Find a time of day, or a day in the week, that works best for you. Grab a hot drink (or a glass of wine, don’t let us hold you back), turn off distractions, and dedicate some time to your newsletter draft.  Start writing If you take away one piece of advice from this email, I’d want it to be this: Don’t wait for the perfect conditions to get started.  You’ll learn far more by trying things out and iterating than by spending lots of time getting your ducks in a row. An added bonus to this approach is that your readers will come along with you on your journey, and you’ll build a feeling of loyalty among those who have been with you from the start, before you honed your perfect newsletter machine. Email is a personal medium, so it’s great to get comfortable addressing your subscribers as friends — and even asking them for help along the way.  And on top of that, pressing ‘Send’ becomes much less daunting the more you do it.  I’ll be back in touch tomorrow with some practical tips on making the most of Revue’s tools. In the meantime, don’t hesitate to reach out if you have any questions. Just reply to this email and a member of our team will get back to you as soon as possible.  I’ll see you tomorrow! All the best, Anna If you’d like to unsubscribe from the rest of the Revue Email Academy, you can do so here. We'll keep the emailing to a minimum, promise. If you still want to opt out, you can unsubscribe here.