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#genetic
ancientorigins · 29 days
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Advances in the study of ancient DNA are making the impossible a reality. The face of a Chinese Emperor, dead for 1,500 years, has been rebuilt using his skull and his genes, revealing what he looked like with startling accuracy.
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kemetic-dreams · 1 year
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African populations today harbor more genetic diversity than any other population in the world, and the genetic diversity found in non-Africans represents only a subset of that found in Africa.
The claim has even been made that East Africans are more genetically different from West Africans than Europeans are from Asians. That diversity has fit well with the fossil evidence that the human species originated in Africa. It is well established that when a new species, be it plant or animal, arises and spreads, genetic differences accumulate more in geographic regions where the species has been present longer. The more distant populations represent only a small subset of the genetic variation that arose nearer the center of origin.
Some of the genetic variants the researchers identified, coding for both light and dark skin pigmentation, were quite ancient, between 300,000 and 1 million years old, meaning that skin color variation seems to have been present since before the emergence of Homo sapiens.
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Tishkoff noted that the work underscores the diversity of African populations and the lack of support for biological notions of race.
WE ARE NOT BLACKS WE ARE AFRICANS WE LITERALLY DEFINE DIVERSITY
“Many of the genes and new genetic variants we identified to be associated with skin color may never have been found outside of Africa because they are not as highly variable,” Tishkoff says. “There is so much diversity in Africa that’s not often appreciated. There’s no such thing as an African race. We show that skin color is extremely variable on the African continent, and that it is still evolving.”
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davidaugust · 2 months
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What could possibly go wrong? 🧬
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diadotcom · 17 days
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okay who wants me to write a sereshaw afl au
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Darkstalkers children would look more icewing than himself even though he partnered with Clearsight(nightwing). (there was a really good post explaining it months ago but I can't find it)
as if a super simple punnett square: Nn(Clear100%) Ni(Dark90%), out of four, two would be pure nightwing, one the same (90/10%) and one 50%
I feel like he probably would've killed that last one, yikes
.
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dk-thrive · 1 month
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In each of my cells Dad and Mom are still doing their jobs. As always, Dad says yes, Mom no. I split the difference and feel deep sympathy for my children.
— Jim Harrison, in Braided Creek, A Conversation in Poetry, with Ted Kooser, Copper Canyon Press, 2003
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glorianasims · 1 year
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https://www.patreon.com/posts/coconot-sweet-83196949
(free) skin :) 
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by  毒瘤
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kota-bee · 2 years
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Ok gang I’m in some dire need of assistance. My chronic pain from my elhers danlos syndrome has reached a height that I never expected it to. My doctors are refusing to help me until i get a genetic test that tells them what type I have. I can’t get any helpful pain medication, braces, or therapies without it. However my insurance refuses to pay for genetic testing.
I can’t get a job to pay for the test either as no one will hire me given my disability. I’m selling art and doing commissions in an effort to make money but it’s not quite fast enough so I need help. Any help is appreciated, even just reblogging or sending it to someone.
This genetic test will change my life and how my doctors treat me
My cash app is also $k0tab33
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wodeworm · 1 year
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Mewtwo 150
Legendary 
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don-lichterman · 2 years
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Genetics and environmental factors contribute to how socioeconomic status shapes the brain architecture
Genetics and environmental factors contribute to how socioeconomic status shapes the brain architecture
Your education, your job, your income, the neighborhood you live in: Together these factors are considered to represent socioeconomic status (SES) and contribute to a variety of health and social outcomes, from physical and mental health to educational achievement and cognitive capacities. The brain acts as an obvious mediator between SES and many of these outcomes. But the mechanism by which it…
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ancientorigins · 4 months
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Unprecedented genetic research with scientists from around the globe, led by Prof. Eske Willerslev, sheds light on the origins of multiple sclerosis. The research team has unraveled the ancient genetic codes, exposing the surprising link between Yamnaya herders, the spread of MS – as well as why northern Europeans are taller!
The creation of the world's largest ancient gene bank has provided astonishing insights into the origins of diseases and the migration of genes across Western Europe and Asia over 34,000 years!
How did ancient farmers' advantage against infections lead to a higher risk of MS today? The past has never been so relevant to our present health!
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kemetic-dreams · 1 year
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jcmarchi · 1 month
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A protein found in human sweat may protect against Lyme disease
New Post has been published on https://thedigitalinsider.com/a-protein-found-in-human-sweat-may-protect-against-lyme-disease/
A protein found in human sweat may protect against Lyme disease
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Lyme disease, a bacterial infection transmitted by ticks, affects nearly half a million people in the United States every year. In most cases, antibiotics effectively clear the infection, but for some patients, symptoms linger for months or years.
Researchers at MIT and the University of Helsinki have now discovered that human sweat contains a protein that can protect against Lyme disease. They also found that about one-third of the population carries a genetic variant of this protein that is associated with Lyme disease in genome-wide association studies.
It’s unknown exactly how the protein inhibits the growth of the bacteria that cause Lyme disease, but the researchers hope to harness the protein’s protective abilities to create skin creams that could help prevent the disease, or to treat infections that don’t respond to antibiotics.
“This protein may provide some protection from Lyme disease, and we think there are real implications here for a preventative and possibly a therapeutic based on this protein,” says Michal Caspi Tal, a principal research scientist in MIT’s Department of Biological Engineering and one of the senior authors of the new study.
Hanna Ollila, a senior researcher at the Institute for Molecular Medicine at the University of Helsinki and a researcher at the Broad Institute of MIT and Harvard, is also a senior author of the paper, which appears today in Nature Communications. The paper’s lead author is Satu Strausz, a postdoc at the Institute for Molecular Medicine at the University of Helsinki.
A surprising link
Lyme disease is most often caused by a bacterium called Borrelia burgdorferi. In the United States, this bacterium is spread by ticks that are carried by mice, deer, and other animals. Symptoms include fever, headache, fatigue, and a distinctive bulls-eye rash.
Most patients receive doxycycline, an antibiotic that usually clears up the infection. In some patients, however, symptoms such as fatigue, memory problems, sleep disruption, and body aches can persist for months or years.
Tal and Ollila, who were postdocs together at Stanford University, began this study a few years ago in hopes of finding genetic markers of susceptibility to Lyme disease. To that end, they decided to run a genome-wide association study (GWAS) on a Finnish dataset that contains genome sequences for 410,000 people, along with detailed information on their medical histories.
This dataset includes about 7,000 people who had been diagnosed with Lyme disease, allowing the researchers to look for genetic variants that were more frequently found in people who had had Lyme disease, compared with those who hadn’t.
This analysis revealed three hits, including two found in immune molecules that had been previously linked with Lyme disease. However, their third hit was a complete surprise — a secretoglobin called SCGB1D2.
Secretoglobins are a family of proteins found in tissues that line the lungs and other organs, where they play a role in immune responses to infection. The researchers discovered that this particular secretoglobin is produced primarily by cells in the sweat glands.
To find out how this protein might influence Lyme disease, the researchers created normal and mutated versions of SCGB1D2 and exposed them to Borrelia burgdorferi grown in the lab. They found that the normal version of the protein significantly inhibited the growth of Borrelia burgdorferi. However, when they exposed bacteria to the mutated version, twice as much protein was required to suppress bacterial growth.
The researchers then exposed bacteria to either the normal or mutated variant of SCGB1D2 and injected them into mice. Mice injected with the bacteria exposed to the mutant protein became infected with Lyme disease, but mice injected with bacteria exposed to the normal version of SCGB1D2 did not.
“In the paper we show they stayed healthy until day 10, but we followed the mice for over a month, and they never got infected. This wasn’t a delay, this was a full stop. That was really exciting,” Tal says.
Preventing infection
After the MIT and University of Helsinki researchers posted their initial findings on a preprint server, researchers in Estonia replicated the results of the genome-wide association study, using data from the Estonian Biobank. These data, from about 210,000 people, including 18,000 with Lyme disease, were later added to the final Nature Communications study.
The researchers aren’t sure yet how SCGB1D2 inhibits bacterial growth, or why the variant is less effective. However, they did find that the variant causes a shift from the amino acid proline to leucine, which may interfere with the formation of a helix found in the normal version.
They now plan to investigate whether applying the protein to the skin of mice, which do not naturally produce SCGB1D2, could prevent them from being infected by Borrelia burgdorferi. They also plan to explore the protein’s potential as a treatment for infections that don’t respond to antibiotics.
“We have fantastic antibiotics that work for 90 percent of people, but in the 40 years we’ve known about Lyme disease, we have not budged that,” Tal says. “Ten percent of people don’t recover after having antibiotics, and there’s no treatment for them.”
“This finding opens the door to a completely new approach to preventing Lyme disease in the first place, and it will be interesting to see if it could be useful for preventing other types of skin infections too,” says Kara Spiller, a professor of biomedical innovation in the School of Biomedical Engineering at Drexel University, who was not involved in the study.
The researchers note that people who have the protective version of SCGB1D2 can still develop Lyme disease, and they should not assume that they won’t. One factor that may play a role is whether the person happens to be sweating when they’re bitten by a tick carrying Borrelia burgdorferi.
SCGB1D2 is just one of 11 secretoglobin proteins produced by the human body, and Tal also plans to study what some of those other secretoglobins may be doing in the body, especially in the lungs, where many of them are found.
“The thing I’m most excited about is this idea that secretoglobins might be a class of antimicrobial proteins that we haven’t thought about. As immunologists, we talk nonstop about immunoglobulins, but I had never heard of a secretoglobin before this popped up in our GWAS study. This is why it’s so fun for me now. I want to know what they all do,” she says.
The research was funded, in part, by Emily and Malcolm Fairbairn, the Instrumentarium Science Foundation, the Academy of Finland, the Finnish Medical Foundation, the Younger Family, and the Bay Area Lyme Foundation.
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heretic-child · 1 year
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''Other genetic studies based on Y-Chr in Kurds from Turkey, Georgia and Iran identify the dominant presence of haplogroups originated in Middle East (Anatolia or Mesopotamia) that show a close association with Jews, Lebanese and Turkish genes. Also, Iranian populations are close to Kurds. This again shows that languages and genes do not correlate because languages may be imposed by a genetic (but powerful) minority. This is the case of Turks: Anatolian people were settled down there since ancient prehistoric times, but a minority of people (Turks) coming from Central Asia imposed language in historical times.''
''In summary, it seems that Turks, Kurds and Armenians are very close genetically and all of them seem to have been living in the area for many millennia, because typical Asian HLA genes are not found. Probably, small different ‘‘elite’’ invaders imposed different languages on these three different groups who originally spoke a similar pre-Indo European language. Armenians (Urartu 900 B.C.) and Kurds (’’Kurti‘‘) probably were initially splits of Hurrian groups (2nd millennium – 1st millennium B.C.), the Kurds remaining mainly at the mountains. Thus, the postulated Asian invasion (1200 B.C.) is not noticed on genetic studies.''
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dk-thrive · 2 months
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habit passing for happiness
Maybe it’s because we could pass along science. You wrote a fact in a book and there it sat until someone born five hundred years later improved it. Refined it, implemented it more usefully. Easy. You couldn’t do that with soul-learning. We all started from zero. From less than zero, actually. We started whiny, without grace. Obsessed only with our own needing. And the dead couldn’t teach us anything about that. No facts or tables or proofs. You just had to live and suffer and then teach your kids to do the same. From a distance, habit passing for happiness.
— Kaveh Akbar, Martyr!: A Novel (Knopf, January 23, 2024)
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