#kat arney

[entomoblog]

Harriet Creighton - Strange Stuff And Funky Things

See on Scoop.it - Insect Archive

Voici le second épisode de la nouvelle chronique "Not Just The Wife", [Pas seulement “femme de”] sur Podcast Science. Pour rappel, il s'agit des traductions des épisodes du Dr Kat Arney du Podcast Genetics Unzipped, le podcast de la Société de Génétique du Royaume Uni. Genetics Unzipped est produit par First Create The Media. Retrouvez Kat Arney, Genetics Unzipped et First Create The Media sur twitter (@Kat_Arney @geneticsunzip @FirstCreateMe). La traduction a été réalisée par Élise et Pierre Kerner et son incarnation par la jolie voix d’Élise Kerner. Cette seconde chronique s’intéresse à l’histoire d'Harriet Creighton (Épisode Originel).

  Par taupo, jeudi 9 janvier 2020

À l'époque, de nombreux généticiens sont perplexes face à un phénomène observé pendant la méiose, c’est-à-dire la division cellulaire qui se produit lorsque les cellules sexuelles sont fabriquées - les ovules et les spermatozoïdes chez les animaux ou le pollen et les ovules chez les plantes. Ils observent que des versions particulières de gènes, appelées allèles, semblent parfois passer d'un chromosome à l'autre.

  Ensemble, Creighton et McClintock parviennent à montrer que cela est dû au croisement physique des chromosomes, qui entraîne l'échange de fragments d'ADN entre eux. À Berlin, le généticien travaillant sur les mouches du vinaigre, Curt Stern, avait fait une découverte similaire, mais Barbara et Harriet le devancent de quelques semaines en publiant leur article dans Proceedings of the National Academy of Sciences en août 1931, alors que Stern est en vacances.

Il s’avère qu’un célèbre généticien, Thomas Hunt Morgan, avait eu connaissance des résultats de Creighton et McClintock alors qu’il se trouvait à Cornell pour donner une conférence, et les avait exhortées à publier au plus vite. Il a avoué plus tard qu'il était au courant des résultats concurrents de Stern, mais avait décidé qu'il était peut-être temps que les difficiles expériences réalisées par les deux femmes sur du maïs, plante caractérisée par une croissance lente, méritent la vedette en comparaison avec les recherches exploitant les mouches du vinaigre, dont la reproduction est rapide, et qui récoltaient tous les honneurs en génétique. La carrière scientifique de Creighton atteint un point culminant en 1932, lorsqu'elle participe au sixième congrès annuel de génétique, qui se tenait à Ithaca cette année-là. McClintock donne une conférence sur leurs travaux, et les deux femmes organisent une petite exposition expliquant leur découverte du crossing-over."

(...)

  Streamez l'épisode Harriet Creighton du podcast Strange Stuff And Funky Things - 2020 https://soundcloud.com/taupossaft/harriet-creighton

[wisdomfish]

I Find Meaning in Self-Contradiction

There is a long history of atheists wrestling with the question of the meaning of life, and it usually ends the same way. In 2015 the online periodical BuzzFeed interviewed atheists about how they found meaning. While they uniformly denied that there was any overarching meaning to life or the universe, they insisted that they find meaning and significance in their own personal lives. Many also implied that certain moral positions are objectively better than others, even though they presumably do not believe in objective morality.

One example was the response of the atheistic scientist and journalist Kat Arney. She said her rejection of religion “was an incredibly liberating moment, and made me realise that the true meaning of life is what I make with the people around me – my family, friends, colleagues, and strangers. People tell religious fairy stories to create meaning, but I’d rather face up to what all the evidence suggests is the scientific truth – all we really have is our own humanity. So let’s be gentle to each other and share the joy of simply being alive, here and now. Let’s give it our best shot.”

Arney’s position powerfully illustrates the problem many atheists seem loathe to confront. The “scientific truth” does not tell us to be “gentle to each other.” It doesn’t tell us anything about how we should live (and obviously many people are not gentle to each other, so there is nothing empirical to suggest that being gentle to each other is the way of nature).

But apparently many atheists and non-religious people have a hunger for meaning and a sense of moral rectitude that their worldview cannot satisfy. Sure, they are free to invent their own meaning and morality, but then they should be honest and admit that their meaning and morality has no advantage over the meaning or morality religious people put forward —or for that matter, it has no advantage over the meaning and purpose evil people invent.

~ Richard Weikart, Study: Atheists Find Meaning In Life By Inventing Fairy Tales

[equine-science]

[E]volution is not a flawless engine, continually driving living things onwards to make better and better versions of themselves in the generations that come after. This misconception comes about as a result of the way that evolution is often described, especially in school. We’re taught that a DNA sequence gets altered, creating some kind of change in the resulting organism. If this is advantageous, then these genetic changes get to stay in the population. If they’re not, they get ditched. Over time the useful variation might even become the only version of that part of the genome in the whole species, like the missing control switch in the hipless lake-dwelling sticklebacks from Chapter 7. Evolutionary biologists refer to this as ‘fixing’ a trait. This process is natural selection at its finest – survival of the fittest and all that. And while this is certainly one way that genes shift and change over time, it’s not the only one. Things aren’t as clear cut as a school biology class might make them out to be. That’s because evolution doesn’t really care whether you’re the bestest, fittest organism you can possibly be. All it cares about is that you get laid and pass your genes on. You could have a genetic variation that makes you 10 times smarter than everyone else, but if you spend all of your time in the library instead of trying to meet someone of the opposite sex and make babies with them, your brilliant genes will die with you. All the time, random changes are happening in our genomes that get passed on to the next generation. Some of them are handy, some of them are positively damaging, while most are just neutral – the genetic equivalent of a Gallic shrug. Bof. Whatever. Due to the vagaries of life and love, the proportion of some of these neutral variations will increase in the population, despite not being actively advantageous, while others fade away. This is known as genetic drift, conjuring up a nice image of a random tide of DNA variations ebbing and flowing through time, with as little purpose or direction as the sea splashing on the shore. This vision of genetics is a stark contrast to the analogies that started to come forward in the 1970s in the wake of the twin revolutions in molecular biology and electronics. Everyone was buzzing with the idea of DNA as a form of computer code or blueprint, with genes forming neat regulatory circuits that could be pulled apart and put back together again. Although this view of genetics-as-electronics was helpful in some ways, time has shown that it was deeply flawed in many others. Real life is a long way from mimicking the tidy precision of a pre-printed circuit board. Our genome was not designed by an engineer, plotting out the most sensible way to make protein X or respond to signal Y. It was bodged and pasted together, not needing to be great, but just good enough to make a human that can pass it on. Probably the thing that has struck me the most is how consistently this process works, despite the fact that it’s driven by essentially stochastic (i.e. chaotic) chemical interactions. As I learned from people like Wendy Bickmore with her baubles and Ben Lehner with his wobbly worms, when you get right down to the level of the writhing DNA and blobby proteins inside a single cell’s nucleus, physics takes over from biology. The interactions between control switches and transcription factors are flaky, and it’s a matter of chance that the right things will come together at the right time. Obviously things have evolved so there’s a pretty good chance that it’ll happen, otherwise we wouldn’t be here, but it’s still a statistical event rather than a guaranteed one. Engineers, mathematicians and religious believers hate this idea, maintaining that a better understanding of the complexities of DNA will explain exactly how it all works (or that we’ll give up and just accept that God did it). But it won’t, in my view. Not completely. We live in a world driven by probabilities, not certainties.2 All too often genetics is sold to the public as solid fact: this gene does this, that gene does that. Yet as I’ve spoken to scientists in the course of my travels, it’s become increasingly clear to me that there’s a huge amount we don’t know about how our genes work. There may well be things we can never know. But the pace of change is accelerating rapidly, and there’s talk of entering a ‘golden age’ of genomics where high-speed, cut-price gene sequencing will finally lay open more of the mysteries in our DNA.

Herding Hemingway's Cats: Understanding How Our Genes Work by Kat Arney

[bpod-bpod]

Bee Brained

Bee-lieve it or not, this image is the brain of a honeybee, with the coloured areas highlighting the parts that are involved in interpreting the signals coming from the insect’s antennae as it smells the world around it. Insects like bees are important subjects in neuroscience research, because they’re small enough to study their entire brains in detail but complex enough to show behaviours like sensing and learning. All around the world, researchers are collecting detailed images and datasets from a wide range of insects, from bees and butterflies to beetles and flies. But because all this information is stored in different places and formats, it’s hard to know what’s out there or make comparisons between different insects. The new InsectBrainDatabase (IBdb) gathers together all these datasets and makes them searchable and shareable, allowing researchers to compare brains of different insect species and gain new insights into how they work.

Written by Kat Arney

Image from work by Stanley Heinze and colleagues

Department of Biology, Lund University, Lund, Sweden

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

Published in eLife, August 2021

You can also follow BPoD on Instagram, Twitter and Facebook

[comedyfan2013]

Revisiting Lee’s stint as curator on ‘Museum of Curiosity’ as his episodes are all now available on BBC Sounds

https://www.bbc.co.uk/sounds/play/b0bqdhwr

[curiositydotcom]

Learn about why cancer is stranger than we think and how scientists have “teleported” the behavior of real fish into robot fish.

Please nominate Curiosity Daily for Best Technology & Science Podcast in the 2020 Discover Pods Awards! It's free and only takes a minute. Thanks so much! https://awards.discoverpods.com/nominate/ 

Scientists "teleported" the real-time behavior of a real fish onto a robot fish by Grant Currin

Zebrafish Help Unlock Clues to Human Disease. (2018). Hopkinsmedicine.Org. https://www.hopkinsmedicine.org/research/advancements-in-research/fundamentals/in-depth/zebrafish-help-unlock-clues-to-human-disease 

Zebrafish Behavior: Opportunities and Challenges. (2019). Annual Reviews. https://www.annualreviews.org/doi/full/10.1146/annurev-neuro-071714-033857 

‌Beam me up: Researchers use “behavioral teleporting” to study social interactions. (2020). EurekAlert! https://www.eurekalert.org/pub_releases/2020-08/ntso-bmu082420.php 

‌Karakaya, M., Macrì, S., & Porfiri, M. (2020). Behavioral Teleporting of Individual Ethograms onto Inanimate Robots: Experiments on Social Interactions in Live Zebrafish. IScience, 23(8), 101418. https://doi.org/10.1016/j.isci.2020.101418 

Additional resources from Kat Arney:

Pick up "Rebel Cell: Cancer, Evolution, and the New Science of Life's Oldest Betrayal" on Amazon: https://amzn.to/32zrPqg

Rebel Cell's website: https://www.rebelcellbook.com/

Kat Arney's website: https://katarney.com/

Kat Arney's Twitter: https://twitter.com/Kat_Arney

Genetics Unzipped podcast: https://geneticsunzipped.com/

Subscribe to Curiosity Daily to learn something new every day with Ashley Hamer and Natalia Reagan (filling in for Cody Gough). You can also listen to our podcast as part of your Alexa Flash Briefing; Amazon smart speakers users, click/tap “enable” here: https://www.amazon.com/Curiosity-com-Curiosity-Daily-from/dp/B07CP17DJY

See omnystudio.com/listener for privacy information.

[aflamethatneverdies]

Tagged by @melle93, Thank you friend!!! I always forget to do these things, so doing it now before I forget. ><

rules: tag nine people you want to get to know better.

top 3 ships:

Bahorel/Prouvaire- I need moar of weird hijinks with them always, but more so now because it has been a month and a half of me not feeling and doing so great and I need cheerful distractions.

Spock/Kirk- I didn't know how much I needed them in my life until I saw Star Trek TOS but I always want space husbands and space OT3 Spock/Kirk/Bones

Watson/Holmes- my first fandom and a pairing I always have in my mind somewhere. I just really like them either as queer platonic or a queer couple in Victorian England.

Honourable mention to French Romantics/gothic architecture. In my defence, they shipped themselves with it first and were ridiculous dorks about it -see Elias Wildmanstadius and pretty much anything by French Romantics.

Reading: The Titans by Andre Maurois,The Three Musketeers by Alexandre Dumas, Dracula by Bram Stoker, Herding Hemingway's cats by Kat Arney (non-fiction).

lipstick or chapstick: chapstick or vaseline sometimes.

last song: It was Rachmaninoff's 2nd Piano concerto in C Minor (when I am working, I can only listen to music without lyrics) but usually these days it is Hadestown and I was recently listening to 'We raise our cups to them' sung by Anaïs Mitchell and crying.

last movie: I have no idea...maybe 72 Les Mis with the groupwatch? I am bad at watching movies and listening to podcasts, it's easier watching a tv series or reading books, but I really want to watch a few recent movies.

I don't know 9 people but uh...@pilferingapples @ghostplantss @fixaidea @lizardrosen @bookish-huntress-art if any of you want to do this meme?

If anyone reading this enjoys doing memes feel free to say I tagged you.

[goodtobegeeking]

The Compact Guide: DNA by Kat Arney (book review).

The Compact Guide: DNA by Kat Arney (book review).

There is an old saying that you should never judge a book by its cover. This should also extend to cover the size of a book. Publisher Andre Deutsch is doing a series of small ‘Compact Guides’ and ‘DNA’ by Kat Arney was the closest to our remit. What I didn’t expect was a dense but very readable text giving all the details about deoxyribonucleic acid (DNA) from its discovery to how it is used to…

[nalachew]

"More than 2 metres of DNA is packed into almost every cell in your body, crammed with thousands of genes that need to be turned on and off at the right time and in the right place. Rather than a neatly bound set of recipes, the genome as we understand it today is a dynamic, writhing library, buzzing with biological readers and writers. The text is constantly copied, tweaked and occasionally even torn up altogether. Every volume bulges with annotations and sticky notes, and there are thousands of pages that just seem to be complete nonsense. The cataloguing system would give even the hardiest librarian a nervous breakdown. Yet out of this chaos, we create life.

Right from the start, when a lucky sperm enters an egg, we're built by a complex biological ballet of gene activity enabling us to grow from a single cell into a baby. Intricate structures form: the twisting tubes of a heart, the rippling folds of a brain, the birdlike bones of a tiny skeleton. Along the way, each type of cell develops its own specialism. Skin cells form sturdy, neat layers to keep our insides in and the outside out, while our brains crackle with tiny pores transmitting electrical impulses. All of this is controlled by our genes. But how are they doing it? How do our genes really work?"

- Kat Arney, Herding Hemingway's Cats

[vileart]

Dramaturgywould: Sh!t Theatre @ Edfringe 2017

Sh!t Theatre with Show And Tell present

DollyWould

WORLD PREMIERE

Old Lab, Summerhall, 4 - 27 August 2017 (not 21), 21.15 (22:15)

Oh look, it’s 2016 Fringe First winners Sh!t Theatre again following their Fringe First winning sell-out festival hit, Letters to Windsor House. What is it this time? 

Oh, is it unemployment? Is there a crisis? Did the government do something wrong? No, it’s a show about Dolly Parton. Sh!t Theatre f*cking love Dolly Parton. This sharp and hilarious performance takes you on an adventure into the heartland of Tennessee, USA and beyond to explore life

, death, branding and cloning. Enlisting the expertise of the ‘Nigella of science’ genetic scientist Dr Kat Arney, Sh!t Theatre explore the enigma that is Dolly in this rollercoaster ride of a show complete with live music and sing-a-longs. 

What was the inspiration for this performance?

Dolly. The sheep and Parton. The first and original, unique, clone. And the (probably - definitely) queer legendary country and western singer.

Is performance still a good space for the public discussion of ideas? 

Performance is definitely still a good space for the public discussion of ideas - especially if those ideas are 'Isn't Dolly amazing?' ' Isn't Dolly brilliant?' 'She's so talented' 'Wouldn't it be amazing if Dolly never died' 'What is life anyway?' 'Where's Dolly the sheep right now? Oh what?! Just down the road you say!'

How did you become interested in making performance?

One of us got too much love as a child, one not enough.

Is there any particular approach to the making of the show?

All our previous shows were written from a place of anger, this one from a place of love. Our main approach to making this show is spending loads of money on merch and travel.

Does the show fit with your usual productions?

No. This show is our B-side prog-rock concept album. Sh!t Theatre's Kid A. 

What do you hope that the audience will experience?

Love and fear.

What strategies did you consider towards shaping this audience experience?

We always do work-in-progress showings every step along the way as we write a show. There have currently been about 4 different versions of this show. It is shaped in front of an audience. It's a combination of actual feedback and that intangible feeling in the room of 'How's it going?' The show is also about our experience. Are we getting joy from this bit? No? Don't need it then. This show is more about joy and love than a political message or narrative. It's also about mortality though.

from the vileblog http://ift.tt/2tqYECf

[wigmund]

From Biomedical Picture of the Day; April 9, 2017:

Scaly Skin

Ichthyosis – a name derived from the Greek word for fish – is a condition where the skin becomes scaly and hard rather than soft and supple, and it’s often due to inherited gene faults. Over the years, scientists have found many genes implicated in ichthyosis. Several of these were first identified in dogs – including terriers, retrievers and bulldogs – which also suffer from the condition. These images show samples of skin from a German Shepherd dog with ichthyosis (top panels), which have been stained with green fluorescent dyes that highlight two important molecules involved in skin formation, ASPRV1 (left) and fillagrin (right). DNA in the skin cells is stained blue. The patterns are very different in skin from a healthy dog (bottom panels), and genetic analysis reveals that this case of ichthyosis is caused by an unusual fault in ASPRV1. Perhaps this gene could also be involved in some human patients too.

Written by Kat Arney Image from work by Anina Bauer and colleagues; Institute of Genetics, Vetsuisse Faculty, University of Bern, Bern, Switzerland; Image originally published under a Creative Commons Licence (BY 4.0); Published in PLOS Genetics, March 2017

[healthupdatede-blog]

Angelina Jolie-Effekt – Brustkrebsgen nicht tödlich sagen Forscher

Im Juni 2012 veröffentlichte ich ein paar Gedanken über die „prophylaktische Brustamputation von Angelina Jolie“. Zentrale Idee der prophylaktischen Amputation ist ein angeblich genetisch bedingtes erhöhtes Risiko durch das Brustkrebsgen BRCA1 bzw. BRCA2, an Brustkrebs zu erkranken.

Um der Genetik jetzt ein Schnippchen zu schlagen, operiert man das weg, was „die Genetik“ befallen will. Unglücklicherweise ist das Brustkrebsgen nicht nur ein Brustkrebsgen. Es erhöht angeblich auch noch das Risiko für Eierstock- und Dickdarmkrebs.

Meine in dem Artikel etwas ironisch vorgebrachte Aufforderung, sich dann (nur um konsequent zu sein), auch noch die Eierstöcke und den Dickdarm entfernen zu lassen, scheint von der Schauspielerin zumindest teilweise erhört worden zu sein. Aber es geht um mehr, wie wir gleich sehen werden!

In einem Artikel der „DailyMail online“ mit der Überschrift „The Jolie effect: Number of women asking about mastectomies quadruples since actress revealed she had her breasts removed to reduce cancer risk“ kommt die Mitteilung, dass sich „Miss Jolie, die mit Brad Pitt, 49, verheiratet ist, sich einer Totaloperation unterziehen wird, um das Risiko von Eierstockkrebs zu reduzieren.“ Unter einer Totaloperation versteht man eine operative Entfernung von Eierstöcken und Gebärmutter.

Ja, und was ist dann mit dem Darm und seinem Krebsrisiko? Und was ist, wenn wir ein Gen für ein erhöhtes Risiko für Hirntumore entdecken? Müssen wir uns dann das Hirn wegoperieren lassen? Bei dieser Operationswut rund um ein Gen und seinem möglichen Risiko liegt die Vermutung nahe, dass ein solches oder ähnliches Gen schon aktiv geworden sein muss und die Hirne aller Beteiligen für eine OP hat reif werden lassen. Ja, ich weiß, jetzt geht mir der Zynismus-Gaul durch. Aber was sich hier abspielt, ist in Sachen Zynismus schwer zu schlagen.

Der Artikel jubelt, ähnlich wie der bereits im Juni-Artikel erwähnte Spiegelbeitrag, dass das Bewusstsein für diese Problematik Dank der Hollywood-Größen erwacht sei. Denn immerhin kommen heute viermal so viele Anfragen bei Cancer Research UK und ähnlichen Organisationen an als zuvor.

Viermal (400 Prozent!) – das klingt gewaltig. Wenn man den Artikel aber etwas genauer liest, dann stößt man etwas weiter unten auf die „absoluten“ Zahlen. Bei Cancer Research UK riefen im April 13 Leute an. Im Mai waren es 88. Der Unterschied von 75 Leuten bei einer Bevölkerung von über 60 Millionen Briten – ist das wirklich „der Hammer“?

Auch die Webseite von Cancer Research UK sprang von 3.659 im Vormonat auf 4.796 am Vortag der Ankündigung auf 15.920 Klicks danach. Interessant hier, wie auf den Klick genau die Zeitung die Angaben wiedergibt. Aber 16.000 Klicks oder Besuche auf einer Webseite halte ich nicht für besonders beachtenswert. Andere Webseiten haben mehrere Hunderttausend an einem Tag.

Nachdem der Daily-Artikel aus ein paar Klicks und Anrufen mehr bei einer krebsforschenden Organisation eine beeindruckende Vervierfachung gezaubert hat, geht es nahtlos weiter mit den Ratschlägen rund um dieses Thema. Denn es sollen ja nicht nur Schauspieler zu Wort kommen, sondern man will die Gunst der Stunde nutzen, um sich selbst mit auf die Hollywood-Bühne zu hieven.

So kommt eine Dr. Kat Arney von Cancer Research UK zu Wort, die eine Operation voll und ganz befürwortet. Denn immerhin soll die Operation das Risiko in einem signifikanten Maß reduzieren.

Brustkrebsgen nicht tödlich sagen Forscher

So ist die Gefahr an Brustkrebs zu erkranken bei den genetischen Varianten um das Vierfache erhöht. Das Risiko an den Tumoren zu sterben ist allerdings genauso hoch wie bei Frauen, die die genetische Abweichung nicht in sich tragen. Das ergab eine groß angelegte Studie der Universität Southampton.

Die Forscher verfolgten 10 Jahre lang das Schicksal Tausender Brustkrebs-Patientinnen. Darunter waren auch Frauen, die von der Genmutation betroffen waren. Auch nach 10 Jahren lag die Wahrscheinlichkeit eines letalen Verlaufes der Krankheit nicht über dem Durchschnitt. Sogar die Frauen mit stattgehabter doppelter Mastektomie hatten insgesamt keine höhere Lebenserwartung. Die Forscher vermuten nun, dass die fehlerhaften Gene BRCA1 und BRCA2 den Verlauf der Krankheit sogar mildern können (Quelle: Lancet Oncology, 2018; thelancet.com/pdfs/journals/lanonc/PIIS1470-2045(17)30891-4.pdf).

Zumindest für die ersten 2 Jahre könnte dies der Fall sein. Die Southamptoner Ärzte geben daher Entwarnung. Nach ihrer Ansicht sollten Frauen die Brustamputationen nicht unbedingt vornehmen lassen. Direkt abraten wollen sie aber auch nicht. Meine Meinung: Die fürchten starken Gegenwind aus den eigenen Reihen der Ärzteschaft! Denn wie sagte es der berühmte Chirurg Prof. Dr. Julius Hackethal seinerzeit: „Die Heldenchirurgen warten überall!“.

Von solchen Relativierungen will Kat Arney nichts wissen. Statt dessen hat sie andere Vorschläge für diejenigen Frauen, die sich ihre Brüste absolut nicht abschneiden lassen wollen. Fast so, als sollten die ungehorsamen eitlen Damen dafür büßen und den Ärzten trotzdem irgendwie Geld in die Kassen spülen…

Die Antwort der Schulmediziner: Screening

Screening wäre eine gute Alternative, heißt es. Wie gut diese Alternative wirklich ist, habe ich im Beitrag Mammografie-Untersuchungen fragwürdig näher untersucht. Und da kann man nur den Kopf schütteln, wie die Reihen-Mommografie-Untersuchung in Deutschland weiter propagiert wird! Und warum wohl? Na, da fragen Sie einfach mal, wer der größte Hersteller der Geräte ist!

Auch der nächste Vorschlag reißt mich vom Hocker: Bestimmte Medikamente, prophylaktisch genommen, reduzieren das Risiko. Um welche Medikamente handelt es sich hier? Um alte Bekannte! Tamoxifen wird hier genannt, ein als „Wunderdroge“ angepriesenes rezeptpflichtiges Medikament. Es soll die Östrogenwirkung hemmen, die für die Tumorbildung und das Tumorwachstum verantwortlich ist. Wie günstig die Wirksamkeit und das Sicherheitsprofil von dieser Substanz ist, habe ich unter Die besten Medikamente zum Krankwerden? beschrieben: Auf einen hypothetischen Fall (= 1!) von Brustkrebsverhinderung kommt ein Fall von lebensbedrohlichen Blutgerinnseln, Schlaganfällen und Gebärmutterkrebs! Ist das jetzt eine „Alternative“ oder blanker schulmedizinischer Zynismus? Da definiert die Schulmedizin (=Allopathie) die „Alternativmedizin“ doch mal auf ihre ganz eigene Art.

Und zum Happy-End der schulmedizinischen Krebsrisiko-Diskussion kommt dann wieder die Schauspielerin und Patientin zu Wort. Sie gibt Zeugnis von der heilsamen Macht der erbärmlichen…  – äh nein, der barmherzigen „Mutter Schulmedizin“. Denn die Operation, habe sie in ihrer gesundheitlichen Krise näher an ihren Mann gebracht. Ich weiß jetzt nicht, wie weit der von ihr weg war. Und ich weiß auch nichts von einer gesundheitlichen Krise, ging es doch ausschließlich um eine Risikobewertung für sie. Oder sind Diskussionen über ein Krebsrisiko schon mit einer handfesten gesundheitlichen Krise gleichzusetzen?

Wer das noch nicht einmal auseinander halten kann, der kann auch keine qualifizierten Aussagen zu dem viel komplexeren Risikothema machen. Hollywood lässt grüßen. Warum fragen die eigentlich nicht Supermann, der das Gen mit seiner Krypton-Laser-Kanone ganz leicht ausschalten könnte? Das würde Cancer Research UK bestimmt in eine Telefonzentrale verwandeln

Dieser Beitrag wurde erstmalig im November 2013 erstellt und letztmalig am 19.1.2018 aktualisiert.

Dieser Beitrag Angelina Jolie-Effekt – Brustkrebsgen nicht tödlich sagen Forscher wurde erstmalig von Heilpraktiker René Gräber auf NaturHeilt.com Blog veröffentlicht.

Quelle: NaturHeilt.com Blog https://naturheilt.com/blog/der-angelina-jolie-effekt-hollywood-verstaerker-fuer-medizinisches-schauspiel/ via IFTTT

[equine-science]

It’s not just fish hips and cat thumbs that are the result of small changes in genetic control switches. David Kingsley has also discovered a few human traits that work in the same way, with the most immediately obvious being skin and hair colour. A few years back, he and his team discovered that the DNA around a gene called Kitlg, found in many animals including both sticklebacks and humans, seemed to be chock-full of control switches. The protein encoded by Kitlg (known as Kit ligand) is a biological multi-tasker, helping to make blood, sperm and cells packed full of the dark pigment melanin. It’s this molecule that determines your coloration. More melanin and you’ll be darker, less and you’ll be lighter. Kingsley and his team discovered that playing with these switches in sticklebacks changed their coloration, making them darker or lighter depending on which ones were missing. So they took the same DNA region from humans and broke it down into pieces, testing each one to find out when and where it was active. Sure enough, they tracked down one specific control switch that could turn on the gene only in skin and hair. Then when they looked at the DNA sequence of this switch in West Africans and white Europeans, they noticed a consistent difference in a region more than 300,000 letters (300 kilobases) away from Kitlg. Not as far as the distance between Sonic Hedgehog and its limb control switch, but still a long way off. One single letter was switched: an A in the Africans, a G in Europeans. Just one. Next, they tested whether this change affected how well the switch could turn on Kitlg, by looking at the two different versions in skin cells grown in the lab. They discovered that it wasn’t as simple as an on/off (or rather, black/white) switch. Instead, the version in Europeans wasn’t quite as effective at activating the gene as the African version was. A quick calculation in their paper suggests that having two copies of Kitlg with the European switch makes a person’s skin around six or seven shades lighter than someone with two West African versions. Because you have two copies of every gene – one from Mum and one from Dad – the effects of the switches will be more apparent if they are both the same, while having one of each will give a colour somewhere in the middle. However, there are around 30 shades between a typical Nigerian’s dark skin and a pale European complexion, so the difference in the Kitlg switch only explains part of our skin colour, rather than the whole thing. David suspects that there are probably other similar genes and switches out there that add up to give each person their particular hue. But even so, just a single letter can make a big difference to what you look like. This is true of hair colour as well as skin. In 2014 Kingsley and his team published another paper showing that European blondes have a single letter difference in a control switch around 350,000 DNA letters (350 kilobases) away from the Kitlg gene, compared to dark-haired people. Again, it’s a tiny change miles away from the gene, but it has a big impact. This subtle alteration in blondes means that a transcription factor protein called Lef can’t stick quite as well to the DNA of the control switch, so it’s not as effective at turning on Kitlg activity. It’s not on/off, but it’s enough to significantly cut down the melanin production in hair cells, and make them fair. Growing up in the 1980s, I would often hear jokes about blondes being stupid – and as a brunette (to my shame) I would often repeat them. I now know better, but many people apparently don’t. In a news article about his hair colour research, Kingsley attacked this long-held stereotype, saying, ‘It’s clear that this hair colour change is occurring through a regulatory mechanism that operates only in the hair. This isn’t something that also affects other traits, like intelligence or personality. The change that causes blonde hair is, literally, only skin deep.’ Blonde jokes aside, his work on coloration has more profound implications. As I’m writing this chapter, the United States is fracturing under the stress of racial tension following several high-profile incidents of white police officers killing unarmed black people, and a horrific racist shooting in a church. Countless numbers have been unfairly judged, oppressed or killed throughout history because of the colour of their skin, yet it boils down to little more than a handful of DNA letters in a few genetic switches. For a species named after our intelligence – Homo sapiens translates as ‘man who knows’ – we really are very stupid at times."

Herding Hemingway's Cats: Understanding How Our Genes Work by Kat Arney

[bpod-bpod]

Ancient and Modern

We often think of cancer as a recent disease, perhaps brought about by modern, industrialised living. In fact, its grim history stretches a lot further back. Evidence of tumours has been found in fossilised dinosaur bones, as well as in human remains from many thousands of years ago in sites all over the world. Even so, the disease was thought to be rare in ancient times. Now a new study using X-ray and CT scanners to analyse bones from skeletons in medieval graveyards ranging from the 6th to the 16th century has revealed previously hidden evidence of cancer in many remains. Here, we see a hole in the right-hand side of an excavated vertebral bone which was caused by cancer cells growing in the spine. The researchers calculate that between 9% and 14% of medieval adults had cancer at the time of their death – around ten times higher than previously thought.

Find out more about the history of cancer in Kat’s recent book, Rebel Cell: Cancer, evolution and the science of life

Written by Kat Arney

Image from work by Piers D. Mitchell MD and colleagues

Department of Archaeology, University of Cambridge, Cambridge, UK

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

Published in Cancer, May 2021

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[curiositydotcom]

Learn about the impressive memories of goldfish. Plus, hear from Dr. Kat Arney about why an evolutionary perspective may be the key to fighting cancer.

Please nominate Curiosity Daily for Best Technology & Science Podcast in the 2020 Discover Pods Awards! It's free and only takes a minute. Thanks so much! https://awards.discoverpods.com/nominate/

Goldfish Have Great Memories, Thank You Very Much by Anna Todd

Brown, C. (2001). Familiarity with the test environment improves escape responses in the crimson spotted rainbowfish, Melanotaenia duboulayi. Animal Cognition, 4(2), 109–113. https://doi.org/10.1007/s100710100105 

‌Gee, P., Stephenson, D., & Wright, D. E. (1994). TEMPORAL DISCRIMINATION LEARNING OF OPERANT FEEDING IN GOLDFISH  (CARASSIUS AURATUS). Journal of the Experimental Analysis of Behavior, 62(1), 1–13. https://doi.org/10.1901/jeab.1994.62-1 

‌Yap, S. (2011). Unbelievable Goldfish Plays Fetch [YouTube Video]. In YouTube. https://www.youtube.com/watch?v=-kuXdYx87s4

Additional resources from Dr. Kat Arney:

Pick up "Rebel Cell: Cancer, Evolution, and the New Science of Life's Oldest Betrayal" on Amazon: https://amzn.to/32zrPqg

Rebel Cell's website: https://www.rebelcellbook.com/

Kat Arney's website: https://katarney.com/

Kat Arney's Twitter: https://twitter.com/Kat_Arney

Genetics Unzipped podcast: https://geneticsunzipped.com/

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[makingscipub]

The GM/gene drive communication confusion

The other day, I was at the airport waiting for a plane back to the UK, when I noticed on twitter that there was some kerfuffle going on about a field trial in Brazil intended to eliminate disease carrying mosquitoes, which had had, it seems, some unintended consequences (see study).

Here is a short summary: “A field experiment in Brazil that deployed genetically modified mosquitoes to control wild populations of the pest may be having unintended consequences. According to a genetic analysis of mosquitoes in the area, it appears the engineered stock has bred with wild mosquitoes and created viable, hybrid insects, scientists reported in Scientific Reports last week (September 10).”

Reading various tweets about the matter (especially this one), I immediately thought of ‘gene drive’ (a topic that I have covered before on this blog).

It turned out I was wrong, and if I had read the title of the study that people were tweeting about, I might have realised that, as it contains the word ‘transgenic’. Once back home and reading stuff properly, I started to think about why I got confused (jumped to conclusions) and why this might be important for science communication/gene drive communication. But first some background.

Diseases and mosquitoes

At the moment nearly 700 million people get a mosquito-borne illness each year resulting in over one million deaths. Mosquito-borne illnesses are diseases caused by bacteria, viruses or parasites transmitted by mosquitoes. Diseases transmitted by mosquitoes include malaria, dengue, West Nile virus, chikungunya, yellow fever, Zika and much more (Wikipedia). In the past, mosquitoes, and the diseases they spread, were confined to specific regions of our planet. However, international travel and global warming contribute to mosquitos, people and diseases globally.

Many efforts are being made to reduce the population of mosquitoes and to protect human populations from their bites.

Dealing with mosquitoes through genetic modification

Measures to deal with this health threat include sprays, nets but also genetically modifying mosquitoes. This can be done in two ways:

“The first is ‘population replacement’ in which a mosquito population biologically able to transmit pathogens is ‘replaced’ by one that is unable to transmit pathogens. This approach generally relies on a concept known as ‘gene drive’ to spread the anti-pathogen genes. In gene drive, a genetic trait – a gene or group of genes – relies on a quirk on inheritance to spread to more than half of a mosquito’s offspring, boosting the frequency of the trait in the population.

The second approach is called ‘population suppression’. This strategy reduces mosquito populations so that there are fewer mosquitoes to pass on the pathogen.”

(A good definition of gene drive can be found here Weiss, 2019; and more info here)

Unintended consequences

What about the genetic modification used in the case I read about at the airport? The insects created by the firm Oxitec and released in Jacobina, Brazil, are genetically modified to be sterile, but do not contain a gene-drive – so we are dealing, it seems, with population suppression. I had been wrong to jump to the gene drive conclusion (population replacement) when I first read about this case at the airport. As one article points out:

“Oxitec, a UK-based biotechnology company, has been testing whether genetically modified (GM) mosquitoes can suppress a population of non-modified mosquitoes since 2009. The strategy: deploy (non-biting) sterile male Aedes aegypti mosquitoes bearing a lethal gene that is passed onto the offspring and, as a result, will see the population plummet.”

The word ‘lethal’ is important here, and seems to be important to Oxitec, too. They used it prominently on a webpage in 2016 (now defunct) (see Nerlich and McLeod, 2016). On that webpage cells were metaphorically framed as machines. And…machines can be controlled! This means the ‘lethal’ (gene) can control the ‘deadly’ (diseases). In theory.

However, the study I read about seems to have shown that there were some problems (unintended consequences) with this ‘control’, namely that the transgenic or genetically modified mosquitoes transferred genes into the natural population – it seems. A widely reported article had the headline: “Failed GM mosquito control experiment may have strengthened wild bugs”.

This caused quite a lot of disquiet and started a conversation about risks relating to the release of GM mosquitoes, be they modified in conventional ways or through gene drive. As Kat Arney said in a twitter exchange about this experiment and gene drive: “yes, not a gene drive but a dominant lethal gene. interesting to ponder whether a gene drive would have behaved in the same way…”.

Lessons for science communication?

I won’t go into the disputes and discussions following the publication of the study, which are really interesting and deserve a separate and more thorough study. However, as somebody interested in how people communicate about gene drive, I think there are some lessons to be learned from this episode and some questions that need to be asked in terms of science communication.

Before I come to these lessons, let me just say that I don’t know whether the paper published in Nature Scientific Reports is overhyped or not. It may be. It has inevitably led to some overhyped headlines, talking for example about a mosquito apocalypse, about super-mosquitoes and mutants. That’s to be expected, however dangerous it may be.

When reading such reports, I came to realise how little I actually know about GM and gene drive mosquitoes. The question is: Would that matter if I was confronted with a choice of having mosquitoes in my locality managed using GM and/or gene drive methods?

And if I knew more, would I prefer one method over the other? The straight GM one, modifying genes and genomes, or the gene drive one, modifying ways of genetic inheritance (and one leading to suppression of insect populations and the other to replacement?). And what about the word ‘lethal’ used in communicating the first?

Beyond that, is it important to make clear that all gene drives are genetic engineering/modification but that not all genetic engineering/modification is gene drive? It is certainly important to point out that ‘gene drives’ are not the same as ‘genetically modified mosquitoes’, despite the fact that some genetically modified mosquitoes have been genetically modified using gene drive technology.

And finally, what would be the impact of such knowledge or lack of knowledge be on conversations about risk and about rejecting or accepting such technologies of insect and disease control in particular circumstances?

(I would like to thank Aleksandra Stelmach for her helpful comments on this post)

Image: Mosquitoes, Pixabay

  The post The GM/gene drive communication confusion appeared first on Making Science Public.

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