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#four sketches and eight (ten???) people and not a single brain cell to be found
dxullinkz-blog · 6 years
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                                   Heba Mutou | YGO DM OC
Basics
Name (& pronunciation): Heba (H/Eh/Ba) Mutou. Date of Birth (& age): June 4th, 22. Place of Birth: Domino, Japan. Gender: Male. Species/Racial Origin: Human, Egyptian/Japanese. Social Class/Community Status: Middle Class. Languages: Hieroglyphics, Arabic, Japanese & English. Family/Friends/Pets/Etc: Yugi Mutou (twin), Solomon Mutou (Grandfather). Duel Links ID: 738-665-651
Physical Description
Height: 5” (153cm) Weight: 100 pounds (45kg) Hair: Tri-colored (purple, black, blonde) Eyes: Purple. Limb Dexterity: He's actually fairly decently strong. Detailed Physical Description: Pretty lean in build Heba has stacked on a bit more muscle from walking around Egypt and being in places he shouldn't. Being on the more adventurous side he has pretty decent leg muscle and upper arm strength. Though he is still shorter than the average male (something he detests). Typical Clothing/Equipment: Heba's preferred style of clothing is a black shirt and a pair of form fitting jeans. Though in Egypt he cuts it back to tank tops and cargo pants. If it does happen to get colder he wears a wool cardigan. Shoe wise will always be some form of boot.
Personality/Attributes 
Personality: Heba is a very short tempered person with the mouth of a sailor. Not a word leaves his tongue that isn't some sort of insult or swear word. He can flip on the switch of a dime, go from having a nice polite conversation to a fireball of anger at something that was said. He doesn't have a lick of patience and only typically tolerates people rather than try to form close bonds. That isn't to say he isn't capable of doing that, quite the opposite. Heba makes a much better ally than he does enemy, fiery loyal to the end and would give his life in a second if he thought it would protect someone that he cared about. Though he isn't an overly affectionate person he makes up for that in being bluntly honest and protective of friends and family. He'll never say something he doesn't mean and words of affection, when given out, are rare and few in between. Skills/Talents: Heba can hunt with a bow and arrow, figure out rather difficult puzzles easily and can read and translate Hieroglyphics. Favourites/Likes: Tea, studying and learning new things,  Black Luster Soldier. Most Hated/Dislikes: Anything that requires patience, disgracing ancient tombs, people who he believes has the brain cells of a fish. Goals/Ambitions: His current goal in life is a little difficult to figure out. He's changed his college major a few times bouncing between what he wants to do. So far all he can figure out is that he wants to attend college, just isn't quite sure for what. Strengths: Art (fairly good at sketching), archery, history, deciphering old books, physical exertion. Weaknesses: Math, making choices (good choices), temper, doctors/hospitals/medical professionals, slight drug addiction. Fears: Medical Professionals, relationships (romantic or platonic), his grandmother, actually being diagnosed as crazy. Hobbies/Interests: Heba likes arts and crafts but specifically sketching, Ancient Egypt and Egypt's history, Duel Links. Regular Routine: He gets up in the morning, logs into Duel Links to clean out the standard duelists and keys while having a cup of tea and toast. After he heads off to school for his general education (as he hasn't decided his major) for a few hours of class. About two his lectures will end and he'll swing by the museum for a little piece and quiet. Around four he'll end up back and home for another hour of Duel Links until he makes dinner. Homework is stuffed in between eating, random google searches for entertainment and then after the dishes he'll end up logging back into Duel Links until it's time for bed. Between all of this his alarm on his phone will go off every six hours to take his medication. Philosophy of Life: Fuck it. Attitude Toward Death: At one point he craved it now he simply acknowledges it'll come eventually. Religion/Beliefs: None. Fetishes/Strange Behaviors: If his medication runs off and he doesn't take it he'll end up talking a bit to himself or something else that only he can see. He'll also switch languages a lot more frequently and stare off into space. Most Instructive/Painful/Memorable Experience: Growing up with his grandmother was an entire painful experience. The woman was only ever verbally abusive but the amount of doctors she dragged him to left a horrible impact. Sexual Preference/Experience/Values: Bisexual/had sex a few time. Education/Special Training: High School Diploma, Archery training (hunting wise), in college. Place/Type of Residence: Apartment in Japan near his college. Occupation: None. Place of Work: - Work-related Skills: - Past Occupations: Librarian after school in Egypt.
Biography:
Heba was born to the Mutou family in Domino Japan. He had one twin brother that he never got to know. As far as he is aware he was raised in the house until he was one before a custody battle was fought between his grandmother (their fathers mother) and Heba's own. The Game Shop at that point didn't bring in much money and their mother was a bit flaky in staying home. An old man raising two kids on such a small salary, according to Child Protective Services, wasn't the best home situation for what was going on. As a result they decided the best case scenario for the children was to split them. Yugi would stay in Japan with Solomon and Heba would be raised by the grandmother Amara in Egypt.
Perhaps, in some way, she did have the best interest of the children at heart but that didn't in any means make her an over caring woman. She was hard in the way she raised him, showed affection only when need be and lectured him constantly on the proper way he should be. Any child would look at her like she was the devil drilling him like a soldier but it only ever got worse when he started to have his little slips.
He was eight the first time it happened, Heba could barely even remember it now, but he started to hear this voice. It sounded amazingly like his own and yet different at the same time, the language was certainly one he wasn't familiar with though the similarity to Arabic was undeniable. From what he thought he had sat there for a while, just listening to it, but when he blinked his way back into reality he found himself in a completely different room with his grandmother staring at him like he was some sort of monster.
One event out of several more that happened.
Sometimes he'd find himself dreaming, thinking a little two hard on what he saw in his head. He'd lose himself in whatever it was and when he'd finally come back around he'd found he'd done something he probably shouldn't have. His grandmother said he'd scream sometimes, shout words that didn't make sense, even break things and that last one would always end him in incredible trouble—Amara either making him work to pay for it or forbidding him from leaving his room for anything.
It was hard to imagine what other people saw, or even to believe them, since it was apparently his own body doing it. He couldn't deny the lapses in memory, the odd little 'visions' and 'voices' he heard. Doing it in public at school apparently seemed to be the breaking point for it all though. At that point he had turned ten, scared an entire room of elementary students and was sent home with a clear order to find some sort of help for himself.
The amount of doctors between ten and sixteen and they finally put him on an experimental drug was intense... enough to even drive a person insane which ended up being the 'diagnoses' they came up with.
The first few doctors put him up anti-psychotics, another drugged him with psychosis pills, there was some liquid things thrown in there that made his skin feel like it was boiling from underneath. Being poked, prodded and drugged so many times lead to a fear so intense that his grandmother needed to have someone sedate him before they could do anything. He was sure it was mostly because he had stabbed a nurse with her own needle when she tried to inject something into him.
Heba, at sixteen, ended up in a medical ward where they started him on this experimental drug that didn't even have a name. His bottle was a series of letters and numbers that made no sense to him but whatever it was they drugged him with seemed to work. For an entire year he didn't have a lapse in memory, didn't have an outburst (aside from his usual ones) and didn't hear or see things.
They declared him cured and released him.
The pill bottle's recommended dosage was one every six hours but it also said to take as needed. As he focused on finishing school online he slowly started to find he was either developing a tolerance toward it or whatever was wrong with him was getting worse. So he slowly started taking more, and more, until it was one almost every three hours.
He found if he took them in close proximity he got a bit woozy and light headed so he tried to make it low. He wasn't addicted to them, he just didn't want Black Luster Soldier talking to him from the corner of the room again.
Never once did he tell his grandmother any of this though and when he turned eighteen he decided to head 'home' or what the home on his birth certificate said he was. Heba had long since learned of Yugi's existence, his grandmothers favorite insult was “maybe I should have left you with Solomon”, it didn't take a genius to look them up.
Yugi was impressive from what he noticed, a Duel Masters god according to the internet, and most of all sane. That last part was the most interesting one for him, apparently between twins sanity wasn't biological. Though he was curious he never reached out, never made a point to contact, he figured if Yugi wanted to know about him all he had to do was look at his own birth certificate and see the little check that wasn't single.
That didn't stop him from attending a college in Japan, from moving to Domino. Though he told himself he didn't care that was apparently far from the truth. But he wouldn't approach because that made a burden.
His college degree between eighteen and twenty-two changed from Teaching to Archaeologist to Egyptian Historian, to art until he finally just settled on getting a general education until he could decide. His grandmother had money, she didn't care so long as he took his meds and was a good boy.
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naivelocus · 7 years
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The trickiest family tree in biology
Illustration by Jasiek Krzysztofiak/Nature
For 18 months in the early 1980s, John Sulston spent his days watching worms grow. Working in twin 4-hour shifts each day, Sulston would train a light microscope on a single Caenorhabditis elegans embryo and sketch what he saw at 5-minute intervals, as a fertilized egg morphed into two cells, then four, eight and so on. He worked alone and in silence in a tiny room at the Medical Research Council Laboratory of Molecular Biology in Cambridge, UK, solving a Rubik's cube between turns at the microscope. “I did find myself little distractions,” the retired Nobel prize-winning biologist once recalled.
His hundreds of drawings revealed the rigid choreography of early worm development, encompassing the births of precisely 671 cells, and the deaths of 111 (or 113, depending on the worm’s sex). Every cell could be traced to its immediate forebear and then to the one before that in a series of invariant steps. From these maps and others, Sulston and his collaborators were able to draw up the first, and so far the only, complete ‘cell-lineage tree’ of a multicellular organism1.
Although the desire to record an organism’s development in such exquisite detail preceded Sulston by at least a century, the ability to do so in more-complex animals has been limited. No one could ever track the fates of billions of cells in a mouse or a human with just a microscope and a Rubik’s cube to pass the time. But there are other ways. Revolutions in biologists’ ability to edit genomes and sequence them at the level of a single cell have sparked a renaissance in cell-lineage tracing.
The effort is attracting not just developmental biologists, but also geneticists and technology developers, who are convinced that understanding a cell’s history — where it came from and even what has happened to it — is one of biology’s next great frontiers. The results so far serve up some tantalizing clues to how humans are put together. Individual cells from an organ such as the brain could be related more closely to cells in other organs than to their surrounding tissue, for example. And unlike the undeviating developmental dance of C. elegans, more-complex organisms invoke quite a bit of improvisation and chance, which will undoubtedly complicate efforts to unpick the choreography.
But even incomplete cellular ancestries could be informative. Sulston’s maps paved the way for discoveries surrounding programmed cell death and small, regulatory RNA molecules. New maps could elucidate the role of stem cells in tissue regeneration or help combat cancer — a disease of unharnessed lineage expansion. “There’s a real feeling of a new era,” says Alexander Schier, a developmental biologist at Harvard University in Cambridge, Massachusetts, who is using genome editing to trace the cell-lineage history of zebrafish and other animals.
Reconstructing history
A cell’s history is written in its genome: every mutation acquired that gets passed on to daughter cells serves as a record. In 2005, the computer scientist Ehud Shapiro at the Weizmann Institute of Science in Rehovot, Israel, calculated that researchers could use the natural mutations in individual human cells to piece together how they are related2. He conceived of a corollary (in concept at least) to the C. elegans cell map, which he called the Human Cell Lineage Project. But the field, he says, wasn’t ready. “When we offered this vision, neither the field nor the name of single-cell genomics existed.”
Fast forward a decade, and researchers have developed a suite of powerful tools to probe the biology of lone cells, from their RNA molecules and proteins to their individual and unique genomes. Now, he envisions a way of capturing the developmental course of a human, frame by frame, from fertilized egg to adult. “You want the whole movie with 3D frames from beginning to end,” he says. To make such a film, it’s not even necessary to look at the entire genome. Shapiro’s team is focusing on repetitive stretches of DNA peppered across the genome called microsatellites. These sequences tend to mutate more frequently than other bits of the genome, and his team is working on sequencing tens of thousands of them across the genomes of hundreds of individual human cells to determine how they relate.
“We’re beginning to see the rules of development in normal human beings.”
Christopher Walsh, a neuroscientist and developmental biologist at Boston Childrens Hospital and Harvard Medical School, doubts that researchers will ever reconstruct a complete human cell-lineage map to match that of C. elegans, but even a less than complete tree will pay dividends, he says. “I’ve been studying cell lineage in the cortex for 25 years, and the idea of studying it directly in the human brain was an inconceivable dream. Now it’s a reality.”
In experiments described in 2015, Walsh’s team sequenced the complete genomes of 36 cortical neurons from 3 healthy people who had died and donated their brains to research3. Reconstructing the relationship between the brain cells in an individual revealed that closely related cells can be spread across the cortex, whereas local areas can contain multiple distinct lineages. Successive generations of cells seem to venture far from their ancestral homes. One cortical neuron, for instance, was more closely related to a heart cell from the same person than to three-quarters of the surrounding neurons. “We were not expecting to find that,” Walsh says.
Walsh’s team is trying to understand how mosaicism in the brain — in which some cells harbour different gene variants — affects health. They have identified, for example, forms of epilepsy that occur even when just a small percentage of cells in a tiny brain region carry a disease-causing mutation. And they have found that individual neurons from healthy individuals can bear mutations that would cause seizures and schizophrenia if present more widely. It seems from this work that it matters which cells end up with a mutation. “The lineage basically determines what diseases are possible,” Walsh says.
Other scientists are uncovering records of life’s earliest events in the genomes of adult cells. In experiments published this year4, Michael Stratton, a geneticist at the Wellcome Trust Sanger Institute in Hinxton, UK, and his team sequenced white blood cells from 241 women with breast cancer and looked for mutations found in only a subset of their blood cells. The study revealed mutations that occurred very early in development, perhaps as far back as the two-cell embryo. And they noted that the descendants of these cells do not contribute equally to the blood system of adults. This could be because one cell multiplies more efficiently than the other; or it could, as Stratton suspects, be that by chance one ends up contributing more to a developing fetus than to a placenta or other supporting tissues.
Future studies, Stratton says, will look for bottlenecks in development that limit the contribution of some cell lineages. “We’re beginning to see the rules of development in normal human beings,” he says.
From blobs to barcodes
Jay Shendure, a geneticist at the University of Washington in Seattle, still remembers the day he became fascinated with cellular histories. As a 14-year-old with an interest in biology and computers, he wrote a program that modelled a mass of multiplying cells to impress his uncle, a reconstructive surgeon visiting from India. “He said, ‘This is amazing. One day you’ll do the same thing, and instead of a blob it will be a whole baby,’ ” Shendure recalls.
Nearly a decade later, Shendure was a first-year graduate student working for the Harvard geneticist George Church. Church presented a list of ideas (“all of which, at the time, seemed totally absurd”, Shendure says); one of them was to reconstruct the lineages of many cells at once, in a single experiment. Shendure toiled for six months trying to use DNA-flipping enzymes called recombinases to create a readable record in the genomes of bacteria as they divide. Rather than relying on naturally acquired mutations in the genome, the system would essentially create variants to keep track of.
Shendure eventually switched projects, but he revived the idea a few years ago when graduate students Aaron McKenna and Greg Findlay joined his laboratory in Seattle. They realized that the popular genome-editing tool CRISPR–Cas9 would be ideal for introducing traceable mutations to whatever part of the genome they wanted (see ‘The lines of succession’). Teaming up with Schier’s lab, they unleashed CRISPR–Cas9 in two single-cell zebrafish embryos and instructed it to edit DNA ‘barcode’ sequences that had been engineered into their genomes. They then sequenced these barcodes in cells of an adult animal and used the mutations in them to piece together their lineage5.
The trees they produced show that a small number of early-forming embryonic lineages give rise to the majority of cells in a given organ. More than 98% of one fish’s blood cells, for instance, came from just 5 of the more than 1,000 cell lineages that the team traced. And although these five contributed to other tissues, they did so in much lower proportions. They were almost entirely absent from the muscle cells in the heart, for example, which was mostly built from its own small number of precursors. “It was profoundly surprising to me,” says Shendure. His colleague Schier says he is still trying to make sense of the data.
Jan Philipp Junker, a quantitative developmental biologist at the Max Delbrück Center for Molecular Medicine in Berlin, says that the cell-lineage trees of early embryos probably vary greatly between individuals, and that the dominance of particular lineages observed by Shendure and Schier’s team could be the result of chance events. The cells of an early embryo move around, and only a fraction of them contribute to the final organism, for example. It would be more revealing, he adds, to track later developmental events, such as the formation of the three germ layers that give rise to different organs, because these events are less governed by luck.
Junker and others have developed a bevy of other CRISPR-based techniques for piecing together developmental histories. He and Alexander van Oudenaarden, a systems biologist at Utrecht University in the Netherlands, applied such an approach to track the regeneration of a damaged fin in zebrafish. Regeneration, they discovered, occurred in the same kind of way as development: few of the cell lineages that gave rise to the original fin were lost when it was remade from stem cells. The finding confirmed previous studies, but the CRISPR-based methods allowed the team to trace lineages of thousands of cells in a single experiment6.
Church says his team has used CRISPR to study mouse development and has managed to record the embryonic cell divisions that give rise to the three major germ layers, which form all the body’s organs7. “I don’t think we’re that far away from doing a complete lineage,” he says.
Some researchers strive to know not just how an organism’s cells relate to one another, but what happened to them along the way. Michael Elowitz and Long Cai, both at the California Institute of Technology in Pasadena, have developed a lineage tracer that creates fluorescent probes to help them observe the histories of cells as they develop8. Their method can track whether certain developmental genes have been turned on in the past for a given lineage. On 5 July, Elowitz, along with Shendure and Schier, were awarded a 4-year, US$10 million grant from the Paul G. Allen Frontiers Group to combine their technologies. The trio plan to develop synthetic chromosomes that act as tape recorders for cell-lineage history and molecular events.
Such recordings might allow scientists to tinker with a cell’s development in more delicate ways than current cell-reprogramming techniques allow, says Tim Liu, a synthetic biologist at the Massachusetts Institute of Technology in Cambridge who is also working on a technology to record a cell’s history9. “You might see some version of these recorders being inserted into the cell therapies of the future,” although it won’t be for a while, he cautions. “I’m not going to go and inject my CRISPR recorder into a patient.”
Lineages for life
Cancer is where new lineage-tracing methods are likely to make waves first. “Cancer is a disease of lineage — it’s a disease of stem cells,” says Walsh. One question that researchers are starting to tackle is the origin of metastatic cells, which emerge from the primary tumour and invade sometimes distant organs. They tend to be the hardest tumour cells to vanquish and the ones most likely to kill patients.
A team led by cancer geneticist Nick Navin at the University of Texas MD Anderson Cancer Center in Houston published lineage maps of two colon cancers in May10. The results showed that liver-invading metastatic cells shared many DNA mutations with the primary tumours they came from, suggesting that the metastasis had emerged at a late stage and hadn’t needed a bunch of new mutations to spread. Lineage mapping could also show whether tumours really develop from single cells, as geneticists have argued, or whether they originate from multiple cells, as some imaging studies have suggested. Navin suspects that similar work could be used to direct treatment. His team and others are tracing cancer-cell lineages in patients as they begin taking drugs. They hope these studies can spot resistant lineages, allowing doctors to pick better treatments and switch medicines in time to make a difference.
“Cancer is a disease of lineage — it’s a disease of stem cells.”
At the moment, however, promise in the field far exceeds the reality. And Sulston’s lineage maps of C. elegans still loom large over current efforts. Stephen Quake, a bioengineer at Stanford University in California, devised his own method for tracking cellular ancestry through CRISPR and decided to test it in the worm11. “It’s nice to have a gold standard,” Quake says. He and his team sequenced the cells of a mature animal after CRISPR had mutated its genome during development. The efforts took much less time than the year and a half that Sulston spent with his microscope. But Quake says that the picture they developed was also less than complete. Yes, it captured a key transition in roundworm development — the segregation of cells bound for the intestine and those that give rise to the rest of the body — but it lacked the exquisite detail Sulston observed with his eyes. “I’ll be perfectly blunt. I’m not very impressed with my results,” says Quake, who hadn’t even planned to publish the work until he saw the rush of other papers using similar techniques. “No one has really got it licked yet,” he says.
There is an argument to be made that Sulston set the bar too high with C. elegans. “This whole concept of a lineage tree is very much influenced by this classic work,” says Junker. And that may deserve a rethink.
In fish, mice and humans, no two individuals’ cell lineage trees are likely to look exactly the same, and each probably changes throughout the individual’s lifetime, as tissues repair and regenerate themselves. Junker and others hope that the new techniques will allow biologists to ask questions about the variability in lineage trees — between individuals, between their organs and as they age. As Schier puts it: “We don’t know how many ways there are to make a heart.”
It is that vast unknown that could make such work transformative, says Elowitz: “It would change the kinds of questions you could ask.” Sulston’s map led biologists into uncharted territory, says Schier, and this could do the same. “We can’t tell you what exactly we’re going to find, but there is a sense that we’re going to find some new continents out there.”
— Nature - Issue - nature.com scie...
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