Science Updates August 2016

Further, the researchers linked an additional enzyme—a uracil-DNA glycosylase inhibitor—to the Cas9-deaminase complex, increasing the efficiency of the complex in creating cytosine-to-thymine substitutions and minimizing the creation of inadvertent deletion mutations in mammalian cell lines.

The modified gene-editing complex also worked well in mammalian cell lines and resulted in relatively few off-target mutations. In yeast, expression of either version of the DNA-editing complex resulted in better growth compared to cells that expressed the standard CRISPR/Cas9 system, suggesting that the new tool is also less toxic.
The so-called Target-AID complex had high specificity, modifying a cytosine within a three to five base pair window within the target gene, the team reported. “We were surprised that the mutation window was so very narrow,” said Nishida.
By comparison, Liu and his colleagues reported variants of their base-editing tool—using a deaminase derived from rats—with windows ranging between three and six nucleotides. “To be maximally useful, the base-editing window needs to be neither too wide nor too narrow so it is helpful that both of these approaches offer researchers more choices, increasing the chance that they can solve their base-editing need,”
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If I understood that correctly, there's a new gene editing tool besides CRISPR?

I don't think this is really thread worthy for Holla Forums.

There is always room for science news on Holla Forums, filthy newfag


Good stuff op… But how does this pertain to space elevator and/or the Imperial Fleet?

The cells, which arrived within the hour, expressed general markers of macrophages, immune cells known for engulfing foreign cells and debris, but their source was unclear. They couldn’t be the liver’s resident macrophages, as those are stationary, and the injury had obliterated local cells. Nor could they be derived from macrophage precursors called monocytes, because that process of recruitment and differentiation takes days.

Rather, the cells expressed GATA6, a marker specific to large macrophages from the peritoneum, the body cavity that surrounds visceral organs such as the liver. The result revealed a job no one had known these cells were performing. “It shows that the peritoneal cavity . . . actually contains macrophages which themselves translocate into damaged tissues and therein actually help drive the repair process,” says Steve Jenkins, who studies the cells at the University of Edinburgh.

When Kubes and his colleagues transferred GFP-labeled peritoneal macrophages into a mouse with liver damage, the glowing green cells flocked to the injury. When the labeled macrophages were injected into the bloodstream, however, they did not reach the wound, indicating that the peritoneal macrophages took a nonvascular path.

Whatever the route, the actions of these peritoneal macrophages are important for healing. Once at the liver, the macrophages dismantled the nuclei of dead cells, releasing DNA into the injured area, which could possibly protect the area from infection by trapping microbes, Kubes says. And the wounded areas in mice whose peritoneal macrophages had been depleted regrew blood vessels more slowly than in mice whose macrophages were intact.

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Good question. By allowing researchers a more versatile gene editing repertoire there are less limitations on what can be done. Each system has peculiarities that can become weaknesses depending on what you want to do.
Enhancing our bodies to survive below -50 temperatures might be a first step to deep space travel. Enhancing our bodies to be capable of actively surviving in a conscious state in these temperatures might be a big step towards colonizing otherwise inhospitable planets.

Many of these techniques have specific targets they are better at getting, or functions they do better than others. Ultimately it comes down to ease of use and cost. You could probably do almost anything with the original method. However depending on what you wanted to do the costs might vary wildly. Other techniques might make something hard much much simpler.

Genetic modificaton is the switch from terrestrial bound civilization and uninhibited expansion. Metabolism can be altered. Mind states. Survival of all types of currently deadly conditions.

Friendly bump. Bring back Space Elevator!

Space Elevator is in all of us.
Scientists at Case Western Reserve University and MIT have demonstrated that the drug candidate phenanthriplatin can work better than an approved drug in vivo, and that a plant virus-based carrier successfully delivers a drug in vivo.
Triple-negative breast cancer tumors of mice treated with the phenanthriplatin-carrying nanoparticles were four times smaller than those treated either with cisplatin or free phenanthriplatin injected intravenously into circulation. Researchers believe this work is a promising step toward clinical trials.

His lab also found that phenanthriplatin is up to 40 times more potent than traditional platins when tested directly against cancer cells of lung, breast, bone, and other tissues. This molecule also appears to avoid defense mechanisms that convey resistance. But when his team injected the drug in mouse models of cancer, it performed no better than standard platins. Dr. Lippard realized phenanthriplatin wasn't reaching its target and that he had a drug-delivery problem.

The long, thin TMV nanoparticles are naturals for delivering the drug candidate into tumors, said Dr. Steinmetz. The virus particles, which won't infect humans, are hollow with a central tube about 4 nanometers (nm) in diameter that runs the length of the shell; the tube’s lining carries a negative charge.
The phenanthriplatin molecule is about 1 nm across and, when treated with silver nitrate, has a strong positive charge. Thus, it readily enters and binds to the central lining of the TMV nanoparticle. Because of its elongated shape, the TMV nanoparticle causes tumbling along the margins of blood vessels, remaining unnoticed by immune cells, passing through the leaky vasculature of tumors, and accumulating inside. Little healthy tissue is exposed to the toxic drug.
Inside tumors, the nanoparticles gather inside the lysosomal compartments of cancer cells, where they are, in essence, digested. Because the pH is much lower than in the circulating blood, explained Dr. Steinmetz, the nanoparticle shell deteriorates and releases phenanthriplatin.
The shell is broken down into proteins and cleared through metabolic or natural cellular processes within a day while the drug candidate starts blocking transcription. The result is greater amounts of cell death via apoptosis than occurs with cross-linking platins.
The researchers say delivery of the phenanthriplatin into the tumor has led to its improved performance over cisplatin or free phenanthriplatin.
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With the latest success of immunotherapy drugs for a variety of oncology patients, researchers have turned their focus toward methods that may positively influence outcomes of the administered therapies. Previous work has shown that even classical chemotherapeutic compounds, like cyclophosphamide, are affected by depletions of the microbiome due to the recent exposure of the patient to antibiotics, compromising the drug regimen. Moreover, data has begun to pile up suggesting that fluctuation in the microbial diversity within the gut influence new checkpoint blockade drugs such as anti-PD-L1 and anti-CTLA-4 immunotherapies.
In a recent study published in Science—“Anticancer immunotherapy by CTLA-4 blockade relies on the gut microbiota”—investigators found that the antitumor activity of Ipilimumab, a fully human monoclonal antibody directed against CTLA-4, a key negative regulator of T-cell activation, was dependent on a distinct species of Bacteroides bacteria (B. thetaiotamicron or B. fragilis). This study found that tumors in antibiotic or germ-free mice did not respond to CTLA-4 blockade treatment, but could be overcome through the exogenous addition of Bacteroides. This is one of the numerous examples of the immunostimulatory effects of microbiota on various cancer therapies.
“The biggest challenge is the difficulty in studying [these links] in humans with their tremendous genetic and environmental heterogeneity, and the cost of performing long-term longitudinal studies,” Dr. Mayer stated.
Yet, strong mechanistic evidence is beginning to emerge that should firmly establish the microbiomes interactions with the brain and what the importance will be for both disease and daily metabolic functions.
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...

up

I don't think you pay respects to the techno god.

EVERY FUCKING Holla ForumsACK NEEDS TO MAKE SURE THAT HUMAN ALTERATION COMES AS SOON AS POSSIBLE AND THAT IT IS FREELY AND WIDELY AVAILABLE WHEN IT DOES

This is the only way to preserve K-type genes at this point, not to mention what it can do for you and your children.

THE (((ELITES))) WILL ONLY CONTROL GENETIC MODIFICATION TECHNOLOGY IF YOU LET THEM

Very true user.

Fuck off newfag we need space elevator back, it will do wonders for our sanity.

Seconded, the (((elites))) will ruin us if we can't spread this type of technology evenly amongst the population.

Quite true. Remember that the computers were designed and meant to be used by ((( businesses ))) only. But it went mainstream anyway. Gene-editing MUST take the same path.

It's a modification of CRISPR-Cas9 such that it allows for single nucleotide editing. CRISPR is a fucking versatile tool.

There are movements in the field of genetic engineering that encourages the public to play with such technology. The Addgene and Biobricks repository are good places to procure parts from other researchers worldwide.

en.wikipedia.org/wiki/Do-it-yourself_biology

Have fun and be responsible :^)

This is extremely important.

We must create the master race.

Have these people done anything besides make their own shitty PCR machines? It takes millions of dollars to establish and maintain your average university biology department. Ultracentrifuges, chromatography equipment, autoclaves, and fluorescent microscopes all cost tens of thousands of dollars, not to mention the operation and repair costs involved. Atop that, you have to pay for all these expensive biochemical reagents. Unless you have millions of dollars of disposable income, the only meaningful Biology you could do yourself is field work (i.e., capturing and tagging meadowlarks, or something equally boring) or bioinformatics (which is really biology-themed computer science).

So, any new weed strains?

From what I have read they are just doing simple molecular biology stuff, with the equipment and reagents already provided by the centers themselves. Setting up your own lab is not a simple task, but it seems like for some places the lab has already been set up fo public use.

That was the state of computers in the 60s. Most real progress doesn't have any instant gratification.

Oy vey! Now we Jews can incest to our hearts content!

No more Tay Sachs or other genetic consequences for incest with our cousins!

I'm gonna marry my niece right now and arrange 1st cousin marriages!

That would be one use of it…

MacArthur and colleagues pooled exome data contributed by researchers from more than two dozen disease-specific projects, creating a list of more than 7.4 million genetic variants from 60,706 individuals—10-fold larger than any prior exome database. The information took up almost a petabyte of storage (an aggregate of 4,000 laptops worth of raw data, according to MacArthur).
“Many of these projects were directly studying common human diseases but had variable success which points to the fact that data can have uses besides its intended purpose,” Shendure told The Scientist.
The team, led by Monkol Lek, a research fellow in the MacArthur lab, found variants spaced around every eight base pairs, on average, within regions of the genome that are particularly prone to variation. The researchers often captured the same variant over and over, suggesting that the dataset is large enough that variants within these regions were becoming saturated. While the dataset is not large enough to see every possible genetic variant, at these particular sites, the team was able to capture about 63 percent of all possible synonymous variants. “I find that exciting, as it previews what is in store in the long future trajectory of this field as we sequence millions of human genomes,” said Shendure.
The large number of exomes allowed the researchers to find that 183 of 192 allelic variants previously categorized as pathogenic (but found at a relatively high frequency in the ExAC database) are likely benign.
The team also identified 3,230 genes that are particularly intolerant to mutation even when the second copy of the gene is wild-type. Seventy-two percent of these genes have not been linked to any known disease, demonstrating the ability of data from apparently healthy individuals to reveal genes that—when mutated—may contribute to disease.

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You can get a DIY Crispr lab going for about a $1,000.

the-odin.com/gene-engineering-kits/

This was one of the acknowledged perks of Crispr.

In both the lab and the lake, cyanobacteria's genetic makeup changed in response to increasing CO2 concentrations. 'It's a textbook example of natural selection', says lead author Giovanni Sandrini. 'Cyanobacteria absorb CO2 during photosynthesis to produce their biomass, and we observed that the strain best equipped to absorb dissolved CO2 eventually gains the upper hand.'

Some Microcystis strains have a slow but efficient carbon uptake system that enables them to squeeze out the last bit of CO2 from the water even at very low concentrations. Those strains become dominant in low CO2 conditions. By contrast, other strains have a fast uptake system that allows them to take up dissolved CO2 at very high rates when in high concentrations. 'We discovered that these high-speed strains enjoy a major selective advantage in CO2-rich water', Sandrini continues. 'Given the rising atmospheric CO2 values, these strains are poised to thrive.'

Bathing and drinking water

Cyanobacteria's adaptation to rising CO2 is cause for concern. That's because Microcystis can produce microcystin, a toxin that causes liver damage in birds and mammals. In high concentrations, cyanobacteria also disrupt freshwater ecosystems, killing fish and aquatic plants. In the Netherlands, blue-green algal blooms regularly put swimming areas off limits.
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Among the various microbial platforms, E. coli remains dominant. And E. coli protein expression in inclusion bodies (IBs) continues to dominate manufacturing, with about 85–90% capacity. More microbial users are seeking to avoid the refolding problems and lower purification yields associated with IBs, and are adopting newer E. coli soluble expression systems. Currently, soluble E. coli expression systems involve protein excretion into the cell cytoplasm. Likely, 10 years out, the vast majority of E. coli new processes will be secretory.
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The E. coli plasmid, called lncX4, which the researchers recovered from the patient was 99.9 percent similar in sequence to a Klebsiella pneumonia plasmid taken from a person in China and to an E. coli plasmid collected from a pig slurry in Estonia.
“What is surprising is the fact that the IncX4 plasmids bearing mcr-1 obtained from different bacterial species, belonging to different [sequence types], isolated in different clinical contexts and found in different continents are highly similar in the plasmid backbone sequences,” the authors wrote. “This strongly suggests that self-transmissible IncX4-type plasmids may represent promiscuous plasmids contributing to the intercontinental spread of the mcr-1 gene.”
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ftfy

B-b-b-but, user! The Genetic sciences are an invention of the jew that seeks to steer us away from the jewish messiah uh I mean savior of the white race Jeesus and his 5 star sky hotel. If we play god with the help of science we won't go to there and be reunited with out brothers and sisters in the Abrahamic religions.

will this be able to cure my shitskin eyes?

here's your reply

Thank you.

No on to the topic at hand. While integration is successful with CRISPR it suffers the drawback of every single other method of integration and replacement of genes. It does it where ever it feels like. Once we can direct integration exactly where we want it it will be a massive leap in scientific progress.

bump

Every fucking time.

I bet when genetic modification and designer babies come into place, everyone will modify skin colors to be lighter. It will probably be a bastardized version of genes of a mix of white and a mix of negro.

Or make themselves immune to every possible disease from the past and present
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“Going down from 64 to 57 codons is a dramatic departure from what exists in nature,” says Farren Isaacs, a synthetic biologist at Yale University in New Haven, Connecticut, who worked with Church on previous recoding studies but was not involved in this project. “It‘s an important step forward for demonstrating the malleability of the genetic code and how entirely new types of biological functions and properties can be extracted from organisms through genomes that have been recoded.”

Church’s lab and others have previously shown2 that it is possible to recode single amino acids in E. coli so that the bacterium can incorporate amino acids not found in nature. Such reprogrammed organisms are highly resistant to viral infection, because they no longer contain the genetic machinery common to all natural organisms that viruses exploit to survive. They can also be made entirely dependent on synthetic amino acids in their diets, to allay the fear that recoded bacteria could escape from a lab and wreak havoc in the wild.

As part of a large phylogenetic study, researchers at the US Department of Energy’s Joint Genome Institute (JGI) in Walnut Creek, California, and their colleagues studied the alignment of predicted proteins in 700 orthologous genes from 29 different yeasts in an effort to identify conserved amino acids and determine which codons they came from. “It’s sort of a footprint of what the organism is using that codon for,” study coauthor Robert Riley, a bioinformatician at the JGI, told The Scientist.
For most species studied, CUG coded for conserved leucine between 70 percent and 86 percent of the time, but for P. tannophilus the standard coding occurred only 7 percent of the time, instead aligning 25 percent with alanine, the researchers reported.
To determine which amino acid was actually present in the proteins, Riley and colleagues extracted peptides from P. tannophilus grown in culture and analyzed them using liquid chromatography mass spectrometry (LC-MS). They found 178 identifiable peptides that mapped to coding sequences containing CUGs; 90 percent of them had LC-MS peaks indicating alanine and only 9 percent of the spectrum implied leucine. When they transformed P. tannophilus with either a wild-type or CUG-replaced, hygromycin–resistance gene, only the yeasts with the altered selection gene grew on antibiotic plates.
Codon modification may be required for researchers using yeast to express novel proteins in P. tannophilus and other yeast species, such as the workhorse Saccharomyces cerevisiae, Riley noted.
Beyond its potential effects on this and other biotech applications, CUG alanine coding might change the way scientists consider codon and transfer RNA (tRNA) evolution.
archive.is/Bcblm


Soon to begin trialing a new CRISPR-based immunotherapy in 10 patients with non-small cell lung cancer that has metastasized and is not responding to treatment. They will remove T cells from patients’ blood, then use the CRISPR-Cas9 system to delete the PD-1 gene, eliminating the surface receptor that binds tumor-produced ligands and tells the immune cells not to fight the cancer. The edited T cells would then be expanded in culture and those that are missing only their PD-1 gene will be infused back into patients. The trial is slated to include a total of 10 patients, but the researchers plan to start with just one, and slowly increase to three different dosage regimens in the remaining patients.
“It’s an exciting step forward,” UPenn’s Carl June, an immunotherapy pioneer and a scientific adviser on the proposed US trial, told Nature. (The US trial would similarly knock out the PD-1 gene, but would also make two other genetic alterations in the cells before they are infused into the patients.)
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Injecting the bacteria expressing the immune-activating gene directly into the tumor was the most effective in deterring malignant growth in a colorectal cancer mouse model, the researchers found.
Next, Hasty and colleagues orally administered a mixture of all three bacterial strains to mice with colorectal tumor metastases, and simultaneously treated the animals with the chemotherapy drug 5-fluorouracil (5-FU). The team found that this combination increased overall survival of the mice compared to either chemotherapy or the bacterial strains alone.
The researchers found that the population of bacteria cycled within the mice for 18 days. While the orally injected bacteria are spread systemically, the anaerobic bacteria are likely able to infiltrate and grow within the anaerobic tumor where standard drug penetration is poor, according to Hasty.
One major question, according to Elowitz, is how to reliably get the synthetic bacteria to efficiently home to the diseased tissue or organ while not harming healthy tissue.
Hasty’s team is now working to develop a modified strain that, rather than cycling through growth and lysis phases on its own, can be killed and mopped by the delivery of a subsequent dose of the bacteria.
archive.is/KKh60

Fuck Transhumanism.