I found out a few weeks back that samurai were only 5'2-5'3(157cm-160cm). I started checking other groups height and found out literally every group was around 5'5(165cm) or smaller on avg with few exceptions yamnaya steppe who are said to be around 5'10(178cm). I found height increase data in rich countries.

South korea height was reported to be max 5'5/165 cm on avg in 1950s. Now its reported young adults in south korea are close to 5'9(175cm).

European were also at the same level in 17-18 century there avg is 6 ft in some countries.

Whereas poor countries like India have stayed exactly where they were before 5'4-5'5.

Europe seems to have reached its peak height as not much height increase is noticed in new gen in some countries avg is believed to have fallen(due to immigration?). But my question is would korea eventually reach european height as europe has been rich for centuries now.

Or is it european will be few inches taller due to yamnaya steppe ancestory. I saw sardinians are couple inches shorter than north italians is that due to genetics(low yamnaya ancestory)? But its also poorer compared to them.

I uploaded my raw AncestryDNA results into ChatGPT, and it flagged a BRCA1 marker (rs80357914) with a D/D result. Apparently, this marker is associated with a mutation linked to breast and ovarian cancer. I have no family history of either. Does anyone know what this result means or if I should be concerned?

Hi everyone! I’m a final-year B.Sc. Biomedical Sciences student working with my team on an academic bioinformatics project focused on hereditary cancer variants.

We’re developing a research prototype that compares submitted sequences with reference sequences, annotates detected variants, and brings together information from public variant databases. We’re also exploring how to present selected ACMG/AMP evidence criteria transparently, while keeping database classifications separate from our tool’s own evidence assessment.

I’m still learning, and I’d appreciate constructive input from people with experience in variant interpretation or bioinformatics:

How would you design a realistic validation set for an undergraduate project?

What mapping or annotation errors should we specifically test for?

How should we handle conflicting database evidence or unavailable results?

What would make the evidence report useful and scientifically clear?

Are there papers or validation resources you would recommend?

We’ve tested some examples, but we’re still working on systematic validation. This is a research project, not a clinical diagnostic tool.

Since it’s an ongoing team dissertation project, I’m keeping the source code and detailed implementation private for now. I can discuss the general approach and share selected, anonymised examples if helpful.

I’m mainly looking for methodological feedback and suggestions about what we might be overlooking. Thank you!

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Hello!

By the title you can correctly assume I'm not a geneticist, or scientist at all. But I'm a huge science fiction/horror fan. I know that science fiction takes a lot of liberties with how science acts in our world, but there is SOME truth to it and it's interesting to know what's possible and how it can be easily explained.

I am a huge fan of the game series Gears of War. For those who don't know, it takes place on an alternate, earth-like planet called Sera (Earth doesn't exist, humans naturally evolved on Sera). The entire crust of Sera is riddled with a massive tunnel network called the Hollow. One day, a species of reptilian humanoids called the Locust emerged from the Hollow and onto the surface to begin waging a genocidal war against humanity. Their goal was to to colonize the surface world and escape the Hollow because there was an epidemic killing their people called the Lambent. And despite the Locust looking inhuman, their leader (Queen Myrrah) is a regular human.

In the sequel, there is this abandoned genetics lab the soldiers go to because the government declassified it and believes it will have a location on where the Locust are. There's a lot of subtle clues about what this place was, and it includes these monstrous things that look like human AND Locust called Sires. In the fifth game, the characters return to this lab and they get a more detailed explanation.

-----------------

Here it is:

Over a century before the Locust emerged, the people of Sera discovered Imulsion - this golden liquid found in the Hollow that could be used as a nearly-limitless fuel source. It belongs to a single government power called the Coalition of Ordered Governments (COG). Imulsion legitimized the COG as an economic and political superpower on Sera. Other countries without formed the Union of Independent Republics (UIR) to fight them over who gets to control the world's Imulsion supply. While this is happening, Imulsion miners and those who work on refineries were getting sick with a progressive, terminal respiratory disease called Rustlung.

Unknown until a century later, Imulsion is actually a living organism comparable to a parasitic fungus like cordyceps. Imulsion is also mutagenic and teratogenic. It caused horrific mutations akin to John Carpenter's The Thing. It also caused birth defects in the children of Imulsion miners. Knowing the public's reaction to the revelation that Imulsion was toxic would result in the COG losing its economic and political power. Wanting to resolve the issue and cover it up, the COG built the New Hope Research Facility (the genetics lab the game). It was designed to house (hide) the children sick with Rustlung and other birth defects.

The director of the program was Niles Samson, the most renowned geneticist on Sera. In order to accelerate his findings, he continued to expose the children to Imulsion to see what would happen. Basically, Imulsion's effects lead to intense and immediate cell stress/cellular degradation. But he also found that when exposed to Imulsion's mutagenic effects, other cells underwent point mutations that could be considered beneficial. As he kept pumping the kids full of Imulsion, there was one child that somehow survived the experiments despite having a lethal dose of Imulsion: Myrrah (the future queen of the Locust).

Niles found that Myrrah had been mutated by the Imulsion. Instead of her cells degrading when exposed to Imulsion, they improved. The more she was exposed to Imulsion, the more her body benefitted and improved. Her T-cells became particularly responsive - becoming resistant to ALL disease including Rustlung. She then gained the ability to age at 50% the rate of a normal female child. Niles hoped to replicate Myrrah's results in the other children. One child managed to gain the ability of physical immortality by accelerating his healing process. But other than these two, the rest of the children continued to suffer and die.

Perplexed by this, he went into the Hollow and found a natural wildlife of reptilian animals. Theorizing they also had genetic immunity because of cohabitated with Imulsion, he used Imulsion to introduce Hollow animal DNA into the sick children via transgenesis. This resulted in the children horribly mutating into human-animal chimeras Niles called the Sires. The Sires were distempered, sterile, and genetically unstable. Despite this, Niles saw promise in the Sires and Myrrah. He didn't just see a cure for Rustlung, he saw the possibility to evolve the human race and make super soldiers for the COG army to fight the UIR.

Due to Myrrah's response to Imulsion, Niles used her embryonic stem cells and Sire DNA to create a female hybrid called the Matriarch. Myrrah's genetic immunity to Imulsion complimented Sire DNA and balanced it out to create a healthy hybrid. This hybrid served as the matrilineal most recent common ancestor to the Locust. So that's what they are. The Locust are genetically modified human hybrids using Imulsion (a potent mutagen and teratogen), Hollow creature DNA, and the embryonic stem cells of a woman genetically immune to the ill-effects of Imulsion.

---------

Do you have thoughts on this? It's impossible given how our biology works, but how would this work in the field of genetics?

What exactly are point mutations? Could something like Imulsion be used to create this? In your best possible explanation, how exactly did Niles Samson create the Locust using Myrrah's embryonic stem cells and Sire DNA?

For context, I'm from Europe but I'd imagine most white Americans would be a mix of several white ethnicities and the same would probably go for black Americans with being a mix of a bunch of different African ethnicities

Does this give them a distinct look compared to white Europeans and black Africans? Who are likely mostly just one ethnicity?

Hi everyone!
At the first-trimester genetic screening, the NT measured 3mm and nasal bone hypoplasia was noted.
A week later, we had a CVS procedure done. By then, the NT was 2.9mm and the nasal bone had normalized.
CVS results:
FISH, QF-PCR: negative
Cultured karyotype: negative
SNP array: negative

At the 17-week early anatomy scan, everything was fine (though the nasal bone turned out to be smaller, they said they weren't concerned about that anymore due to the CVS results).

Then, at the 19-week second genetic ultrasound, a smaller nasal bone and borderline NF were noted.
Everything else was fine; at that point, they said these were just constitutional traits, given the negative CVS results.

I was reassured at the time, but now—at 30 weeks—anxiety has set in: what if the CVS result was a false negative?
Does anyone have similar experiences? What do you think?
I'm hoping for the best.

I’m following SKY-0515 and votoplam closely, particularly their potential to slow Huntington’s disease before noticeable symptoms develop.
SKY-0515 has reported up to 69% mutant huntingtin lowering in blood, alongside encouraging preliminary clinical findings.
My question for neuroscientists, biostatisticians, and clinical researchers is:
If future randomized trials demonstrate reduced caudate and putamen atrophy, lower neurofilament light, and slower clinical deterioration, could researchers use those measurements to develop a validated mathematical model predicting 10–30 additional symptom-free years?
Are there existing models that could support such projections, and what evidence would be needed before scientists could estimate the probability of 20+ years of sustained neurological protection?
I’d particularly appreciate links to peer-reviewed studies or research tools. Thank you!

My queries

Question 1

Can anyone, regardless of genetics, get a top 99.99 percentile score in, say, the NEET or JEE (Indian hyper competitive scientific entrance examinations for medicine and engineering)?

Upon objective analysis, I have seen that these examinations impose exceptionally high demands on working memory, executive function, and cognitive fluid intelligence. The examinations require you to function as a human calculator, performing multi step calculations and intense analysis, often 5-6 steps of advanced scientific reasoning and mathematical calculation, without a calculator. NEET is 180 marks, 180 minutes. Each question is 4 marks, negative marking applies- scored out of 720.

Is the narrative that anyone - regardless of genetics- can obtain an exceptionally high score (e.g. 650+/720, a score range that admits you into top medical school programs like AIIMS) with focused, intense practice, dedication and hard work, focused practice, 10 thousand hours, scientifically defensible or indefensible?

Other similar achievements include

Gaining at least 5+ Grade 9’s in the 9-1 GCSE examinations, including GCSE Maths, GCSE English, GCSE Triple Sciences. Grade 9 requires answering highly complex, multi step questions which impose demands similar to those high demand questions in NEET and JEE. A question might give you a complex question and solve for the novel answer, or give you data and information and ask you to analyse it.

Please decide on one answer.

Societally, there is a very common narrative that goes like this

“Genetics is irrelevant. Anyone can develop high executive function. Anyone can develop high WM. Anyone can develop high levels of fluid intelligence, with focused practice and training.”

Is this defensible or not?

Question 2

Can anyone, regardless of genetics, learn to be exceptionally high in affective or cognitive empathy, can anyone learn to be really kind, compassionate, empathetic, emotionally connected, with practice or training? Genetics does not matter- is this scientifically defensible or indefensible?

Please decide on one answer.

Kindly provide studies and official scientific quotations and citations to support your answer.

Please do not include social optics in your answer.

Provide answers directly, no matter the implications of said answers.

I just watched the old movie Star Trek Into Darkness with Chris Pine and Benedict Cumberbatch. The villain Khan is a genetically engineered superhuman who is smarter, stronger and faster than almost every normal human. Benedict does a great job playing a very smug and arrogant bad guy too. I'm just wondering how close we are to that kind of genetic engineering where we can make people smarter, stronger and faster? Or at least use it to do things like giving people stronger immune systems and stronger bones for better health? Or is that still very far off?

I know there's a lot of moral and ethical red lines here. Even if it's possible, playing God with the genetic code would raise all sorts of moral and ethical questions. It could only be done with consenting volunteers under strict controls and monitoring.

My dad has a job where he's upper middle class in salary writing on equipment in filmmaking. My parents met in the film industry. My grandfather was the famous statistician. I went to a college prep school and struggled academically throughout my highschool years. I often plaigarized in my essays and relied on my mom to do large amounts of my assignments in ELA and history. I was given ritalin in 10th grade for potential ADD and had minimal results from it. 11th grade was COVID lockdown and I did virtual school. At this point I completely phoned in my classes and have no idea how to do algebra II (or college algebra) or any math surpassing that. I got accepted into a college with a 96% acceptance rate with my grades from my first two years of HS. I only lived there for a year then commuted afterwards. Now I'm 23 and live with my parents. I've never had an IQ test or diagnosis of a mental disorder, though I had a counselor in HS suggest I'm on the autism spectrum because of social awkwardness and analytic thinking. I've gotten into nootropics hoping that a mix of creatine, nootropic supplements, and full dose of effexor could treat depression and brain fog and I've had so so results from over 7 months of it. I've considered drug use being the only way to numb my depression and suicidality from my hopeless situation.

I can't understand how if my parents are smart and functional how did I become essentially a mental vegtable. And why has no friend, family member, or therapist been able to give an explanation or antidote to my mental problems. Would an IQ test be helpful for what job is realistic for me given my mental capacities? What best explanation is there for my intelligence and what other advice could you give me in my situation?

This year I was diagnosed with the KIF1A genetic mutation which can manifest in terms of cognitive impairment. on my physical evaluation from a doctor, he says I meet the physical symptoms that align with this mutation. Although many with this mutation are physically disabled I am concerned how this rare mutation effects my cognitive deficits. I had my blood drawn for research. Aug 19 I will get an MRI scan for further investigation.

Last, Here's what I've found on how it KIF1A effects neurology:

KIF1A-Associated Neurological Disorder (KAND) fundamentally affects how neurons function, Developmental delay occurs in about 90% of affected individuals and cognitive function ranges from normal to profound intellectual disability. Speech/language impairment is also very common. Autism and ADHD occur in a substantial minority.

But there is a major caveat: not every KIF1A variant causes KIF1A-NDD. KIF1A has several different associated phenotypes. Some people with KIF1A-associated disease have predominantly motor or peripheral neurological problems and normal cognition. The particular molecular variant and its mechanism matter considerably. That means the single most useful piece of information you haven’t given me is the exact KIF1A variant. For example, something written as c.XXXG>A (p.XXX) plus its classification as pathogenic, likely pathogenic or VUS would allow a much more meaningful assessment. GeneReviews specifically notes substantial genotype–phenotype differences between individual KIF1A variants.

I had an EEG and MRI and found nothing significant going on.

Since all of this I've been diagnosed FOX-P4 genetic mutation, another rare genetic mutation. I also found some useful information on this mutation:

There is published evidence that particular heterozygous loss-of-function FOXP4 variants can cause a neurodevelopmental disorder involving developmental delay and particularly speech/language difficulties. However, the original clinical series was extremely small: eight individuals were identified and detailed phenotype information was available for six. Of those six, two had mild intellectual disability while three did not have intellectual disability. The researchers also found considerable variability between variants.

I want to ask if anyone is familiar with animal genetics and the relation of using it to sex fish specifically Diodon holocanthus. Thank you.
https://www.ncbi.nlm.nih.gov/datasets/genome/GCA_984586875.1/.
https://portal.atlasea.fr/organism/diodon-holocanthus/

Hi guys im 21 (F) and my bf is 26 and he is completely normal while i have beta thalseemia trait ...we are 3 siblings out of us only i got it and i got it from my dad...my dad found out at around the age of 50 that he has this.

Dad got it from my grandmother but we all are asymptomatic and live a normal life...my dad is 54 now , im 21 and grandma died at almost 100 so its fine with all of us but my future partner is a bit concerned.

Any person here who can tell me what exactly to expect if we have kids?will they have thal minor too ?(remember i am beta thal minor trait and he doesnt have anything like this )will they live a normal life like all of us?

Any guidance in this regard will be highly appreciated.

My task is to identify the chromosomes in these images… i’m trying but i have no one to ask so i don’t know if im doing it right. If y’all could help me with even just one of these images i would be very grateful. If you can, write the number of the chromosomes above them in the pictures so i can see if i’m doing it right.

If you can’t help directly, I’d really appreciate any similar practice images: metaphase spreads with numbered chromosomes and an answer key. I don’t need to practice arranging the karyotype, but identifying each chromosome directly from the metaphase image, which is what I have to do for my test next week. I’ve struggled to find exercises like these online, especially with solutions

We have a project... due in 2 days. We need TWO people to interview regarding their views on gene therapy/editing. Ti**mezone: UTC +8

We ask for your profession and full name. If you consent to be interviewed, we must also ask your consent to record the meeting through Meet or Zoom. We will NOT post any media gathered from the interview on any platform, and all that is said will only be used for educational purposes

Thank you!!!

Hi, I recently graduated with a BSc in biochem, and am interested in pursuing a career related to genetics down the road. Currently considering a couple masters and advanced certificate programs, but I would do these later as I’m planning to work for a couple years before returning to school full time.

I’m wondering if there are any other programs/courses that I can do on the side that would be helpful for grad school applications/just to increase my knowledge. I am in Vancouver, Canada, but am open to online options as well. Thank you!

Christie's catalog notes for auction Oct. 13, Lot 81 Fine Printed Books, Manuscripts and Science

MENDEL, Johann Gregor (1822-1884). "Versuche uber Pflanzen-Hybriden." Offprint from: Verhandlungen des naturforschenden Vereines in Brunn. Vol. IV (1865). pp. [3]-47. Brno: Georg Gastl for the Naturforschenden Verein, 1866."One of the most important papers in the history of biology, and the foundation of modern genetics" (DSB).

Extremely rare offprint issue and in very fine condition. Sold for $640,000; high presale estimate was $350,000 (lot 81)

The son of Moravian peasants, Mendel was an academically gifted child. He was determined not to follow the family tradition of farming, and instead entered the Augustinian monastery at Brunn (now Brno) in 1843. The monastery itself was dedicated to teaching, and was filled with an array of academic monks, one of whom, Fr Aurelius Thaler (1796-1843), established an experimental garden.

In 1851 Mendel enrolled at Vienna University, where he was exposed to a wide range of scientific courses including plant physiology. Here, he learned that plants were composed of cells, and was introduced to hybridization by artificial fertilization. Upon his return to the monastery, Mendel used the experimental plot and a new green-house to explore the effects of cross-fertilization in plants.

His paper "reports the results of ten years of experimental work on artificial plant hybridization, during which he followed a program designed to test his working hypothesis that hereditary matter is discrete and particulate. Mendel bred and cultivated nearly thirty thousand pea plants, performing careful statistical analyses of the distribution of seven pairs of mutually exclusive seed and plant characteristics -- a manageable number that allowed him to observe all possible combinations of traits" (Grolier Medicine).

The surprising result of Mendel's years of methodical research and systematic statistical analysis was his discovery of the 'Mendelian ratios,' a mathematical expression of the pattern of dominant and recessive hereditary traits, possibly "the most significant single achievement in the history of genetics" (Garrison-Morton).

Related to this discovery was Mendel's recognition of the independence of each set of traits in a hybrid from all other differences in the two parental plants (later known as Mendel's law of independent assortment).

There are only 16 or 17 known extant offprints, of which eight are in institutions. Although Mendel's paper was distributed, in journal form, to 134 scientific institutions in various countries, and the offprint of 40 copies circulated to colleagues and correspondents at the author's discretion, it was not taken note of and fell into obscurity.

In 1900, within a two-month period, there appeared three independent reports by Hugo de Vries, Carl Correns, and Erich von Tschermak which reached the same conclusions almost simultaneously, each acknowledging that they had been preceded by a virtually unknown monk several decades before.

Subsequent work in the 1930s established that Mendel's laws provided the necessary solution - unknown to Darwin - to understand the mechanism by which evolution by natural selection could work.

Dibner Heralds of Science 35; Garrison-Morton 222; Grolier/Horblit 73a; Grolier Medicine 74; PMM 356a; Stafleu 5818; Norman 1489. For census of copies, see F. Weiling, "Funf weitere sonderdrucke der 'Versuche uber Pflanzen-Hybriden' J.G. Mendels Aufgetaucht" in Folia Mendeliana, 19:257-263, 1984 (identifying 13 copies).

Octavo (228 x 147 mm). 47pp. (Insignificant marginal stain to title-page and second leaf, faint creasing at top corner at end.) Contemporary plain yellow paper wrappers over grey-paper backstrip (tiny spot and insignificant marginal stain at lower edge to upper wrapper, mild rubbing to backstrip); green clamshell box.

Provenance: Christie's, 13 July 2016, lot 177

Acquired at that auction by the current owner

Heyy, so basically I just need help with something simple, what is the law of Independent assortment in a dihybrid cross? And how is that important in a dihybrid cross?

And why is sample size important? Is it because from my understanding so far, it reduces random chance, which in turn , having a larger sample size means that you get more reliable and accurate results?

Highlights

•Total of 37,063 structural variant-human trait associations in 467,152 UK Biobank genomes

•Rare structural variants show a strong effect on human phenotypes and plasma proteins

•Overall, 34.9% of the trait-associated SVs overlap functional genomic regions

•Multi-ancestry meta-analysis identifies SVs associated with disease across ancestries

Summary

Structural variants (SVs) are large (>50 base pairs) genomic rearrangements that can significantly influence human phenotypes, yet their contribution to health and disease remains undercharacterized. We conducted a phenome-wide association study (PheWAS) of 1.6 million SVs identified in whole-genome sequencing data from 467,152 UK Biobank participants, across 13,322 binary, 2,018 quantitative, and 2,923 plasma protein traits. Of these, 82.25% of SVs were outside the detectable range of prior copy-number variant studies. Protein quantitative trait loci analysis linked 3,467 SVs to 1,690 proteins, with effects dependent on SV type and location. In SV-PheWAS, we detected 28,184 associations with human health outcomes. Notably, we uncovered rare SVs with strong phenotypic effects. Furthermore, we show that at known genome-wide association study loci, 32.21% of associated SVs overlapped functional genomic regions. This study underscores the underestimated role of SVs in human genetics and their potential to advance understanding of human biology and drug discovery.

Why do modern Central Italians have only 2%-3% WHG while ancient Romans had over 10% ? Does this mean ancient Italics are only 20% - 25% of the ancestry of Central Italians ? And why do Central Italians have about as much steppe ancestry as ancient Italics at the same time ? What source could have raised it after it decreased in Imperial Rome age, whithout adding some WHG ?

Italic farmers repopulating the cities from the rural areas after the germanic invaders destroyed them does not work because Italic farmers would have been close to ancient Italics and would have over 10% WHG while having under 30% steppe ancestry. Germanic invaders had no genetic impact southward of Tuscany, they do have pretty high WHG, and they are the reason North Italians are at 5% - 9% WHG and Tuscans themselves have still a bit higher than 3%.

It looks like WHG genes were selected out of the pool naturally like Neanderthals genes over the millennia, or alternatively were diluited by Imperial Age new comers from Middle East, and then arrived in Italy some unknown steppe source with no WHG.

At the end, ancient Italics resemble more modern Iberians than Italians by ancestry, because of their higher WHG. In Italy only Sardinians have equally high WHG, but obviously they lack the 20% - 30% steppe ancestry ancient Italics had.