#RNA interference

[science-sculpt]

Exploring RNA Interference

Imagine a molecular switch within your cells, one that can selectively turn off the production of specific proteins. This isn't science fiction; it's the power of RNA interference (RNAi), a groundbreaking biological process that has revolutionized our understanding of gene expression and holds immense potential for medicine and beyond.

The discovery of RNAi, like many scientific breakthroughs, was serendipitous. In the 1990s, Andrew Fire and Craig Mello were studying gene expression in the humble roundworm, Caenorhabditis elegans (a tiny worm). While injecting worms with DNA to study a specific gene, they observed an unexpected silencing effect - not just in the injected cells, but throughout the organism. This puzzling phenomenon, initially named "co-suppression," was later recognized as a universal mechanism: RNAi.

Their groundbreaking work, awarded the Nobel Prize in 2006, sparked a scientific revolution. Researchers delved deeper, unveiling the intricate choreography of RNAi. Double-stranded RNA molecules, the key players, bind to a protein complex called RISC (RNA-induced silencing complex). RISC, equipped with an "Argonaut" enzyme, acts as a molecular matchmaker, pairing the incoming RNA with its target messenger RNA (mRNA) - the blueprint for protein production. This recognition triggers the cleavage of the target mRNA, effectively silencing the corresponding gene.

So, how exactly does RNAi silence genes? Imagine a bustling factory where DNA blueprints are used to build protein machines. RNAi acts like a tiny conductor, wielding double-stranded RNA molecules as batons. These batons bind to specific messenger RNA (mRNA) molecules, the blueprints for proteins. Now comes the clever part: with the mRNA "marked," special molecular machines chop it up, effectively preventing protein production. This targeted silencing allows scientists to turn down the volume of specific genes, observing the resulting effects and understanding their roles in health and disease.

The intricate dance of RNAi involves several key players:dsRNA: The conductor, a long molecule with two complementary strands. Dicer: The technician, an enzyme that chops dsRNA into small interfering RNAs (siRNAs), about 20-25 nucleotides long. RNA-induced silencing complex (RISC): The ensemble, containing Argonaute proteins and the siRNA. Target mRNA: The specific "instrument" to be silenced, carrying the genetic instructions for protein synthesis.

The siRNA within RISC identifies and binds to the complementary sequence on the target mRNA. This binding triggers either:Direct cleavage: Argonaute acts like a molecular scissors, severing the mRNA, preventing protein production. Translation inhibition: RISC recruits other proteins that block ribosomes from translating the mRNA into a protein.

From Labs to Life: The Diverse Applications of RNAi

The ability to silence genes with high specificity unlocks various applications across different fields:

Unlocking Gene Function: Researchers use RNAi to study gene function in various organisms, from model systems like fruit flies to complex human cells. Silencing specific genes reveals their roles in development, disease, and other biological processes.

Therapeutic Potential: RNAi holds immense promise for treating various diseases. siRNA-based drugs are being developed to target genes involved in cancer, viral infections, neurodegenerative diseases, and more. Several clinical trials are underway, showcasing the potential for personalized medicine.

Crop Improvement: In agriculture, RNAi offers sustainable solutions for pest control and crop development. Silencing genes in insects can create pest-resistant crops, while altering plant genes can improve yield, nutritional value, and stress tolerance.

Beyond the Obvious: RNAi applications extend beyond these core areas. It's being explored for gene therapy, stem cell research, and functional genomics, pushing the boundaries of scientific exploration.

Despite its exciting potential, RNAi raises ethical concerns. Off-target effects, unintended silencing of non-target genes, and potential environmental risks need careful consideration. Open and responsible research, coupled with public discourse, is crucial to ensure we harness this powerful tool for good.

RNAi, a testament to biological elegance, has revolutionized our understanding of gene regulation and holds immense potential for transforming various fields. As advancements continue, the future of RNAi seems bright, promising to silence not just genes, but also diseases, food insecurity, and limitations in scientific exploration. The symphony of life, once thought unchangeable, now echoes with the possibility of fine-tuning its notes, thanks to the power of RNA interference.

[gpstudios]

Celebrating World RNA Day: Exploring the Wonders of Ribonucleic Acid 🌍🔬

Happy World RNA Day! 🌍🔬 Celebrate the incredible world of RNA and its vital role in biology and medicine. Learn about RNA, support research, and promote STEM education. #WorldRNADay #RNAResearch

Introduction Happy World RNA Day! 🌍🔬 Celebrated annually on August 1st, World RNA Day is dedicated to recognizing and appreciating the crucial role of RNA (ribonucleic acid) in biology and medicine. RNA is essential for numerous biological processes, including protein synthesis and gene regulation. Today, we celebrate the scientific discoveries and innovations surrounding RNA and its profound…

[medicomunicare]

Galectina-1: non solo marker ma anche potenziale bersaglio per contrastare il cancro al fegato

Il carcinoma epatico (HCC) o cancro al fegato, è uno dei tumori più comuni al mondo. E i numeri sono in aumento, con tassi di incidenti più che triplicati rispetto agli anni ’80. La malattia può essere anche piuttosto mortale: negli stadi avanzati il tasso di sopravvivenza a cinque anni è inferiore al 20%. I ricercatori del Davis Comprehensive Cancer Center dell’Università della California hanno…

[vivianascarincilibellulalab]

Ecofemminismo della petunia

Del giardino mi piace soprattutto quanto sia vicino all’imponderabile, a quel punto ineffabile in cui natura e cultura, fisica e metafisica, tangibile e simbolico coabitano in un tempo che è dentro e fuori le cose. Un tempo pieno di sorprese. Non ponderabile significa non misurabile ma non per questo inesistente. In passato quando il colore, la luce, il calore, l’elettricità, il magnetismo non…

[soumyafwr]

RNA Interference (RNAi) Drug Delivery Market Share, Overview, Competitive Analysis and Forecast 2031

[literaryvein-reblogs]

Hello! First of all, thank you for the wonderful content! It's a real joy, and an enrichment, food for both the brain and the heart! I was wondering if through your treasures, you could find some writing notes/words/concepts/vocabulary relating to genetic engineering? Like...creating a virus, and a vaccine for it, modifying the virus so it has certain specific effects.... Thank you in advance!

Writing Notes: Virus & Vaccine

References How Viruses Work; Replication Cycle; Mutation, Variants, Strains, Genetically Engineering Viruses; Writing Tips; Creating your Fictional Virus & Vaccine

Virus - an infectious microbe consisting of a segment of nucleic acid (either DNA or RNA) surrounded by a protein coat.

It is a tiny lifeform that is a collection of genes inside a protective shell. Viruses can invade body cells where they multiply, causing illnesses.

It cannot replicate alone; instead, it must infect cells and use components of the host cell to make copies of itself. Often, a virus ends up killing the host cell in the process, causing damage to the host organism.

Well-known examples of viruses causing human disease include AIDS, COVID-19, measles and smallpox. Examples of viruses:

Viruses are even smaller than bacteria and can invade living cells—including bacteria. They may interfere with the host genes, and when they move from host to host, they may take host genes with them.

Bacteriophages (also known as phages)—viruses that infect and kill bacteria.

Size differential between virus and bacterium

Viruses are measured in nanometers (nm).

They lack the cellular structure of bacteria, being just particles of protein and genetic material.

How Viruses Work

Viruses use an organism’s cells to survive and reproduce.

They travel from one organism to another.

Viruses can make themselves into a particle called a virion.

This allows the virus to survive temporarily outside of a host organism. When it enters the host, it attaches to a cell. A virus then takes over the cell’s reproductive mechanisms for its own use and creates more virions.

The virions destroy the cell as they burst out of it to infect more cells.

Viral shedding - when an infected person releases the virus into the environment by coughing, speaking, touching a surface, or shedding skin.

Viruses also can be shed through blood, feces, or bodily fluids.

Virus Replication Cycle

While the replication cycle of viruses can vary from virus to virus, there is a general pattern that can be described, consisting of 5 steps:

Attachment – the virion attaches to the correct host cell.

Penetration or Viral Entry – the virus or viral nucleic acid gains entrance into the cell.

Synthesis – the viral proteins and nucleic acid copies are manufactured by the cells’ machinery.

Assembly – viruses are produced from the viral components.

Release – newly formed virions are released from the cell.

Mutations, Variants, and Strains

Not all mutations cause variants and strains. Below are definitions that explain how mutations, variants, and strains differ.

Mutation - errors in the replication of the virus’s genetic code; can be beneficial to the virus, deleterious to the virus, or neutral

Variants - viruses with these mutations are called variants; the Delta and Omicron variants are examples of coronavirus mutations that cause different symptoms from the original infection

Strains - variants that have different physical properties are called strains; these strains may have different behaviors or mechanisms for infection or reproduction

Genetically Engineering Viruses

Using reverse genetics, the sequence of a viral genome can be identified, including that of its different strains and variants.

This enables scientists to identify sequences of the virus that enable it to bind to a receptor, as well as those regions that cause it to be so virulent.

Vaccine - a special preparation of substances that stimulate an immune response, used for inoculation

Vaccines & Fighting Viruses with Viruses

Common pathogenic viruses can be genetically modified to make them less pathogenic, such that their virulent properties are diminished but can still be recognized by the immune system to produce a robust immune response against. They are described as live attenuated.

This is the basis of many successful vaccines and is a better alternative than traditional vaccine development which typically includes heat-mediated disabling of viruses that tend to be poorer in terms of immunogenicity.

Viruses can also be genetically modified to ‘fight viruses’ by boosting immune cells to make more effective antibodies, especially where vaccines fail. Where vaccines fail, it is often due to the impaired antibody production by B-cells, even though antibodies can be raised against such viruses – including HIV, EBV, RSV & cold-viruses.

Related Articles: Modified virus used to kill cancer cells ⚜ Genetic Engineering ⚜ Engineering Bacterial Viruses ⚜ Benefits of Viruses

A Few Writing Tips

As more writers look to incorporate infectious diseases into their work, there are quite a few things writers should keep in mind:

Don’t anthropomorphize. Really easy to do, but scientifically wrong. Viruses don’t want to kill you; bacteria don’t want to infect you; parasites don’t want to make your blood curdle. None of these things are big enough to be sentient to want to do anything. They just do it (or don’t do it).

Personal protective equipment. This includes wearing gloves, lab coats, safety glasses, and tying your hair back if it’s long. It is the same as Edna Mode’s “no capes.” Flowing hair looks cool all the way to the explosive ball of flames that engulfs someone’s head.

Viruses are small. You can’t see viruses down a normal microscope—they need a special microscope called an electron microscope. These are highly specialized and take a long time to make the preparations to be able to see the virus. Normally viruses are detected by inference—measuring part of them using an assay that can amplify tiny amounts of material, for example PCR.

Viruses don’t really cause zombie apocalypses. 

Vaccines work. But they take time. The best vaccine in the world will still only prevent infections two weeks after it is given. Drugs are quicker, but still take some time. But the good news is an infection is not going to kill you (or turn you into a zombie) quickly, so they both have time to work.

Scientists use viruses as a vector to introduce healthy genes into a patient’s cells:

Your Fictional Virus & Vaccine

When creating your own fictional virus, research further on the topic and consider choosing a specific one as your basis/inspiration.

Here's one resource. For some of them, you'll need a subscription to access, but those that are available give you a good overview of the virus, as well as treatment options.

You can do the same for creating your fictional vaccine:

Here's one resource. And here's one on vaccine developments.

Sources: 1 2 3 4 5 6 7 8 9 10 11 12 13 ⚜ Writing Notes & References

Lastly, here's an interesting article on how science fiction can be a valuable tool to communicate widely around pandemic, whilst also acting as a creative space in which to anticipate how we may handle similar future events.

Thanks so much for your kind words, you're so lovely! Hope this helps with your writing. Would love to read your work if it does :)

[wachinyeya]

New Safer RNA Insecticide Can Target Only the Devastating Potato Beetles and No Other Bugs https://www.goodnewsnetwork.org/new-safer-rna-insecticide-can-target-only-the-devastating-potato-beetles-and-no-other-bugs/

[cleverwordsandotherstuffilike]

Medical innovations and scientific advances at Harvard Medical School through the decades (Part 2 of 2)

1995 Triple-organ transplant; kidney disease blood glucose levels

1996 How cells sense oxygen; Alzheimer's treatments; immune system advances

1997 p73 gene; aspirin

1998 Adult live-donor liver transplant

1999 Fluorescent molecular probes

2000 Brain abnormalities associated with abuse and neglect

2001 Circadian clock

2002 Rheumatoid arthritis pathway; C-reactive protein

2003 Multi-drug-resistant tuberculosis treatment; source of pre-eclampsia

2004 Blood stem cells; protein transfer

2005 Prenatal nutrition; herpes vaccine candidate

2006 Cholesterol mechanism; DNA sequencing techniques

2007 Cellular switch; rheumatoid arthritis gene; brown-fat cell switch

2008 RIPKI inhibitors; metastatic melanoma remission

2009 LIN28 protein; RNA interference; cancer cells' starvation; brown fat

2010 Enhancer transcription

2011 Kidney failure markers; cancer cell vulnerability; global health care budget models

2012 Tumour suppressor gene p53; ancient migration; infectious disease diagnostics

2013 Cardiac hypertrophy reversal; cathepsin k pathways

2014 Hematopoietic stem cells; pancreatic stem cells

2015 Bioartificial replacement limb; PD-1 pathway; The Lancet Commission on Global Surgery; pseudogene; damaged protein disposal; multiple sclerosis; somatic mutations; deafness gene therapies

2016 Sigma-1 receptor structure; Zika vaccine candidate; circadian rhythm-bipolar disorder link; microbiome

2017 Unlocking the blood-brain barrier; deciphering the structure of a scissor like enzyme

2018 The 'graying' of T cells; From one cell, a detailed road map

2019 Finding herpes' Achilles' heel; viral peptides critical to natural HIV control

2020 How COVID causes loss of smell; obesity fuels tumour growth; heart muscle dysfunction

2021 SARS-CoV-2 vaccine; immune evasion; AI gene interpretation; radiation vulnerability

2022 Fruit fly cell atlas; viral infection on video; boot camp for immune cells

2023 How the brain senses infection; new origin of breast cancer; the microbiome and cancer immunotherapy

[bpod-bpod]

Stopping Sprouts

Like roads in a city, veins in your body need careful mapping. When they don’t stick to the plan, sporadic vascular malformation – malformed veins – occur, causing pain and disfigurement. These veins form lesions containing genetically faulty cells (mutants). Currently, lesions often recur after treatment. Researchers now search for new therapeutics by growing mutant endothelial cells (ECs), collected from the veins of patients, in dishes. RNA sequencing revealed mutant ECs produced the signalling molecule TGFa. Fluorescence microscopy revealed when supporting cells from lesions (stromal cells) were grown alongside normal ECs, they triggered more EC sprouting (pictured, middle, right) compared with non-lesion stromal cells (left). Next, by grafting mutant ECs into mice, they found EC-produced TGFa triggered stromal cells to release the signalling molecule VEGFA. This caused EC sprouting and malformed veins. Treating mice with afatinib, a drug that interferes with VEGF signalling, decreased lesions, suggesting it may be a useful therapeutic.

Written by Lux Fatimathas

Image from work by Suvi Jauhiainen and Henna Ilmonen, and colleagues

A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in eLife, May 2023

You can also follow BPoD on Instagram, Twitter and Facebook

[farcillesbian]

I love talking to non biologists about my research because I get to think of fun and creative ways to explain oxidative stress or RNA interference or freeze tolerance and usually I'm pretty successful at conveying it and that make me feel good :) a couple weeks ago a sociologist asked me what a model organism is and then why we would want to work with something that isn't a model organism and that was a fun brain exercise too

[falseandrealultravival]

Japan's 30-year recession and innovation (Essay)

Professor Kaliko (m-RNA vaccine inventor)

Since the bubble economy collapsed in the 1990s, Japan has been stuck in a 30-year recession. Workers' wages are shrinking, and Japan is the only developed country in the world to experience subsidence. There are various reasons for this phenomenon, but it is probably due to the government's wrong policies (the Liberal Democratic Party).

What is most troubling to the population is the ultra-low interest rate policy introduced after Abenomics, launched by the exiled politician Shinzo Abe. However, the underlying cause is much deeper. The real culprit is Prime Minister Junichiro Koizumi. This man believed in neoliberalism and applied this false economics to the world of education. -- ``Selection and concentration,'' placing fixed rankings on universities, sparing research funding, and only allowing research that would produce immediate results. Researchers atrophied, and original research faded into obscurity. There are almost no Japanese Nobel Prize winners in science anymore.

This hindered innovation, and Japan no longer developed novel science and technology. Look, isn't the USA, with its active innovation, currently leading the world? The interference of science and technology amateurs in this field is the cause of Japan's current stagnation. Junichiro Koizumi's sin is serious.

Listening to the statements made by the Japanese government, the central bank (Bank of Japan), politicians, and the Japan Federation of Economic Organizations (Keidanren), I find that while they mention money redistribution, they rarely say anything about innovation in science and technology. Today, Japan is dominated by people with liberal arts backgrounds, not science and engineers. Because they are ignorant of science and technology, they have no idea that innovation determines a country's rise and fall. Japan is on the path to becoming a second-rate country. The Bank of Japan now (Head: Kazuo Ueda) is a group of idiots. No matter how much they twist finance, it will not lead to innovation.

Rei Morishita

日本の３０年不況とイノベーション

１９９０年代にバブル経済が破綻して以降、日本は３０年にわたる不況から抜け出せない。労働者の賃金は目減りし、先進国では唯一地盤沈下している。この現象の要因は、いろいろ言われるが、もとは政府＝自民党の誤った諸政策に起因するであろう。

もっ��も人口に膾炙しているのは、亡国政治家安倍晋三が始めたアベノミクス以降の超低金利性政策だが、深層はもっと根深い。ずばり、真犯人は小泉純一郎首相である。この男は新自由主義の信奉者で、教育の世界にも、この誤った経済学を適用した。――「選択と集中」、大学に固定した順位をつけ、研究費を出し惜しみして、すぐに結果のでる研究しか認めなかった。研究者は委縮し、独創的な研究は影を潜めた。もう、科学におけるノーベル賞受賞者は、日本人からはほとんどでないだろう。

これはイノベーションを阻害し、日本には斬新な科学技術は生まれなくなった。見よ、現在世界をリードしているのはイノベーションが活発なUSAではないか。科学技術の素人がこの分野に口を出したことが今の日本の停滞の元凶なのである。小泉純一郎の罪は重い。

日本の政府、中央銀行（日本銀行）、政治家、経団連の発言を聞いていると、お金の再配分のことは言及しても、科学技術のイノベーションについての発言はほとんどない。今の日本を支配しているのは、理系の科学技術者ではなく、文科系の出身者ばかりである。彼らは科学技術に無知であるから、国の興亡を左右するのがイノベーションであることが全く理解できない。日本は２流国への道をまっしぐらである。日本銀行もバカ集団だ。金融をいくらこねくりまわしても、イノベーションにはつながらない。

[soumyafwr]

RNA Interference (RNAi) Drug Delivery Market Share, Overview, Competitive Analysis and Forecast 2031

[krishgen]

Exploring the Role and Applications of dsRNA J2 Antibody in Research and Diagnostics

The dsRNA J2 antibody is a vital tool in the fields of virology, immunology, and molecular biology. This antibody specifically targets double-stranded RNA (dsRNA), a molecular pattern recognized by the immune system as a sign of viral infection. Researchers employ dsRNA J2 antibodies to study viral infections, cellular immune responses, and the mechanisms of gene expression. In this article, we’ll explore the importance, applications, and benefits of the dsRNA J2 antibody in scientific research and diagnostics.

What Is dsRNA J2 Antibody?

The DsRNA J2 Antibody is a monoclonal antibody that binds specifically to double-stranded RNA, which is often generated during viral replication. B ecause many viruses produce dsRNA as part of their life cycle, the presence of dsRNA in cells often indicates a viral infection. By using the dsRNA J2 antibody, researchers can detect and visualize dsRNA within cells, making it easier to study viral infection pathways and cellular immune responses.

Key Applications of dsRNA J2 Antibody

Virus Detection and Research One of the primary applications of the dsRNA J2 antibody is in the detection of viral infections. Researchers use it to identify viral replication sites within infected cells, helping to pinpoint where the virus is active. This is essential for understanding how viruses, like influenza, hepatitis, or coronaviruses, replicate and spread within the host.

Immunology Studies The immune system recognizes dsRNA as a "danger signal," triggering a response to eliminate the infection. The dsRNA J2 antibody allows researchers to study these immune pathways in detail, examining how cells detect dsRNA and how they respond to viral presence. This is crucial in developing treatments that can strengthen or regulate the immune response.

Gene Silencing and RNA Interference (RNAi) In gene silencing studies, dsRNA plays a significant role. RNA interference, a natural cellular process, uses dsRNA to silence specific genes. The dsRNA J2 antibody helps researchers track the activity of dsRNA within cells, aiding in studies of gene function and expression.

Advantages of Using dsRNA J2 Antibody

The dsRNA J2 antibody is a precise and reliable tool in research. It offers high specificity, reducing background noise in assays and ensuring that results are accurate. Additionally, it is compatible with various laboratory techniques, including immunofluorescence and Western blotting.

Conclusion

The dsRNA J2 antibody is invaluable in virology, immunology, and gene expression research, making it easier to detect viral infections, study immune responses, and understand gene-silencing mechanisms. Its specificity and versatility have made it a trusted tool in laboratories worldwide, advancing our understanding of cellular responses to infection and disease.

[lifeblender]

I spent some time reading the original paper yesterday. My take on it is that there's a pathway in the body's response to viruses that hasn't been talked about much, and this mechanism leverages it.

Essentially within each cell there's a process that will generate some bits of RNA or protein, I'm not sure which, that interfere with the specific RNA of the virus as it's being replicated, on its way to spew out a bunch of copies and spread.

But, as far as I can tell from what I've read the viruses have a counter for this, and it's a supressor protein for that RNA interference bit. So viruses usually don't get blocked.

The vaccine method is to ship a virus that's been mutated so that it doesn't have the suppressor and also maybe doesn't have some other bits that make it really effective.

Apparently, this results in the body producing good amounts of the interference bits for a really long time, like ten years, and also clamps down on the virus spread enough that's it's not dangerous at all. The modified virus might be live in the person's body all that time, I'm not sure.

We have tools to do a really good job of editing virus genomes, so we can be accurate about removing the intended bits.

Obviously, there could be people out there without the ability to make those suppressors, but they'd probably die from other diseases right after birth. That's probably why this is considered as something that would be safe for infants.

All in all it feels like pulling a rabbit out of a hat, like they just invented this extra pathway and decided they could target it. But it's been successful in mice, so we'll work our way up to people eventually. We'll see.

Here's hoping.

“Scientists at UC Riverside have demonstrated a new, RNA-based vaccine strategy that is effective against any strain of a virus and can be used safely even by babies or the immunocompromised. Their flu vaccine will also likely be delivered in the form of a spray, as many people have an aversion to needles. “Respiratory infections move through the nose, so a spray might be an easier delivery system,” Hai said. Additionally, the researchers say there is little chance of a virus mutating to avoid this vaccination strategy. “Viruses may mutate in regions not targeted by traditional vaccines. However, we are targeting their whole genome with thousands of small RNAs. They cannot escape this,” Hai said. Ultimately, the researchers believe they can ‘cut and paste’ this strategy to make a one-and-done vaccine for any number of viruses. “There are several well-known human pathogens; dengue, SARS, COVID. They all have similar viral functions,” Ding said. “This should be applicable to these viruses in an easy transfer of knowledge.””

—

Vaccine breakthrough means no more chasing strains

This is HUGE. This will fundamentally change how we get inoculated.

[bpod-bpod]

All Knees

It’s tough, it’s rubbery, it’s your cartilage. Your joints contain two types: articular cartilage, which covers the ends of your bones, and growth-plate cartilage, which forms the ends of long bones. Both comprise cells called chondrocytes. How these types of cartilage develop isn’t clear. Researchers now investigate in mice genetically engineered with fluorescently-tagged NFATc1 – a protein which when inactivated interferes with cartilage development. Using fluorescent microscopy of developing mouse knee joints, they found NFATc1-containing cells (progenitors) matured into articular chondrocytes but not growth-plate chondrocytes. NFATc1-containing progenitors also matured into cells that contribute to the joint lining, ligaments and developing kneecap (pictured, green). Analysing the RNA of articular chondrocytes revealed that NFATc1 levels dropped as the cells matured. Reducing NFATc1 levels in progenitors triggered articular cartilage formation while increasing levels blocked this from happening. NFATc1 is therefore vital for articular — but not growth-plate — cartilage development.

Written by Lux Fatimathas

Image from work by Fan Zhang and Yuanyuan Wang, and colleagues

Xuanwu Hospital, Capital Medical University, China; National Clinical Research Center for Geriatric Diseases, China

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in eLife, February 2023

You can also follow BPoD on Instagram, Twitter and Facebook