Lifeboat Foundation

New discoveries have raised the possibility of exploring dino genetics, but controversy surrounds the results.

Just like a virus hijacks your cells and forces them to churn out more copies of the virus, this vaccine is expected to automate the production of those particles, which B-cells and T-cells — the biological hunter-seekers of the immune system — can use to ready themselves to fight the real-deal coronavirus.

The main difference between this sort of DNA-based vaccine and a traditional one, Slavcev told Futurism, is that it relies on the person’s cells to create the mock virus instead of merely exposing them to an inert version of the real virus.

“Personal genetics only has to do with how the vaccine is presented,” Slavcev told Futurism, regarding the decision to develop a DNA-based vaccine. “There is some variation between individuals and populations, but in this case the DNA is just to improve immune response and make it mimic a viral infection as closely as possible to stimulate the most effective immune response.”

Via Harvard David A. Sinclair “The coronavirus is part bat & part human virus. A new study says the Frankenstein event happened well before its transmission to humans. Wait, what? Humans first infected bats?

The intermediate Frankenstein coronavirus has part human/part bat versions of the spike protein (the knobs on the outside of the virus & what COVID-19 vaccines target). Coronafrankenstein is formally called RaTG13, the name, rank & serial # of a horseshoe bat sample. If we gave bats coronavirus first, then people, including scientists, should stay away from bats especially if they don’t feel well. That’s why, as much as I like cats, I don’t like how they can catch it from us. It’s a potentially vicious cycle.

The new study says a mutation has changed the spike protein of an Indian strain of coronavirus that likely reduces its ability to transmit, but “raises the alarm that the ongoing vaccine development may become futile in future epidemics” like seasonal flu.”

Monitoring the mutation dynamics of SARS-CoV-2 is critical for the development of effective approaches to contain the pathogen. By analyzing 106 SARS-CoV-2 and 39 SARS genome sequences, we provided direct genetic evidence that SARS-CoV-2 has a much lower mutation rate than SARS. Minimum Evolution phylogeny analysis revealed the putative original status of SARS-CoV-2 and the early-stage spread history. The discrepant phylogenies for the spike protein and its receptor binding domain proved a previously reported structural rearrangement prior to the emergence of SARS-CoV-2. Despite that we found the spike glycoprotein of SARS-CoV-2 is particularly more conserved, we identified a mutation that leads to weaker receptor binding capability, which concerns a SARS-CoV-2 sample collected on 27^th January 2020 from India. This represents the first report of a significant SARS-CoV-2 mutant, and raises the alarm that the ongoing vaccine development may become futile in future epidemic if more mutations were identified.

Humans and all other living things have DNA, which contains hereditary information. The information in your DNA gives your cells instructions for producing proteins. Proteins drive important body functions, like digesting food, building cells, and moving your muscles.

Your DNA is the most unique and identifying factor about you—it helps determine what color your eyes are, how tall you are, and how likely you are to have certain health problems. Even so, over 99% of DNA sequences are the same among all people. It is the remaining 1% that explains much of what makes you, you!

DNA is arranged like two intertwined ropes, in a structure called a double helix (see figure 1). Each strand of DNA is made of four types of molecules, also called bases, attached to a sugar-phosphate backbone. The four bases are adenine (A), guanine (G), cytosine ©, and thymine (T). The bases pair in a specific way across the two strands of the helix: adenine pairs with thymine, and cytosine pairs with guanine.

UC San Francisco researchers have discovered how a mutation in a gene regulator called the TERT promoter—the third most common mutation among all human cancers and the most common mutation in the deadly brain cancer glioblastoma—confers “immortality” on tumor cells, enabling the unchecked cell division that powers their aggressive growth.

The research, published September 10, 2018 in Cancer Cell, found that patient-derived glioblastoma cells with TERT promoter mutations depend on a particular form of a protein called GABP for their survival. GABP is critical to the workings of most cells, but the researchers discovered that the specific component of this protein that activates mutated TERT promoters, a subunit called GABP-ß1L, appears to be dispensable in normal cells: Eliminating this subunit using CRISPR-based gene editing dramatically slowed the growth of the human cancer cells in lab dishes and when they were transplanted into mice, but removing GABP-ß1L from healthy cells had no discernable effect.

“These findings suggest that the ß1L subunit is a promising new drug target for aggressive glioblastoma and potentially the many other cancers with TERT promoter mutations,” said study senior author Joseph Costello, Ph.D., a leading UCSF neuro-oncology researcher.

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Networks are at the heart of everything from communications systems to pandemics. Now researchers have found that a unique type of network also underlies the structures of critical cellular compartments known as membraneless organelles. These findings may provide key insights into the role of these structures in both disease and cellular operations.

“Prior to this study, we knew the basic physical principle by which these protein-rich compartments form — they condense from the cytoplasm into liquid droplets like dew on a blade of grass,” said David Sanders, a post-doctoral researcher in Chemical and Biological Engineering at Princeton University. “But unlike dew drops, which are composed of a single component (water), cellular droplets are intimidatingly complex. Our work uncovers surprisingly simple principles that we think are universal to the assembly of liquid organelles, and opens new frontiers into studying their role in health and disease.”

Sanders is the lead author in an article in the journal Cell describing a blueprint for the assembly of these liquid structures, also called condensates. The researchers looked closely at two types of condensates, stress granules and processing bodies (“P-bodies”). In the Cell paper, researchers directed by Clifford Brangwynne, a professor of Chemical and Biological Engineering at Princeton and the Howard Hughes Medical Institute, combined genetic engineering and live cell microscopy approaches to reveal the rules underlying the assembly and structure of stress granules, and why they remain distinct from their close relatives, P-bodies.

The National Aeronautics and Space Administration, NASA, aims to send human missions to Mars in the 2030s. But scientists are still trying to learn more about the potential cancer risks for astronauts due to radiation exposure. Cancer risk from galactic cosmic radiation exposure is considered a potential “showstopper” for a manned mission to Mars.

A team led by researchers at Colorado State University used a novel approach to test assumptions in a model used by NASA to predict these health risks. The NASA model predicts that astronauts will have more than a three percent risk of dying of cancer from the radiation exposures they will receive on a Mars mission. That level of risk exceeds what is considered acceptable.

The study, “Genomic mapping in outbred mice reveals overlap in genetic susceptibility for HZE ion- and gamma-ray-induced tumors,” was published April 15 in Science Advances.

It is an engineer’s dream to build a robot as competent as an insect at locomotion, directed action, navigation, and survival in complex conditions. But as well as studying insects to improve robotics, in parallel, robot implementations have played a useful role in evaluating mechanistic explanations of insect behavior, testing hypotheses by embedding them in real-world machines. The wealth and depth of data coming from insect neuroscience hold the tantalizing possibility of building complete insect brain models. Robotics has a role to play in maintaining a focus on functional understanding—what do the neural circuits need to compute to support successful behavior?

Insect brains have been described as “minute structures controlling complex behaviors” (1): Compare the number of neurons in the fruit fly brain (∼135,000) to that in the mouse (70 million) or human (86 billion). Insect brain structures and circuits evolved independently to solve many of the same problems faced by vertebrate brains (or a robot’s control program). Despite the vast range of insect body types, behaviors, habitats, and lifestyles, there are many surprising consistencies across species in brain organization, suggesting that these might be effective, efficient, and general-purpose solutions.

Unraveling these circuits combines many disciplines, including painstaking neuroanatomical and neurophysiological analysis of the components and their connectivity. An important recent advance is the development of neurogenetic methods that provide precise control over the activity of individual neurons in freely behaving animals. However, the ultimate test of mechanistic understanding is the ability to build a machine that replicates the function. Computer models let researchers copy the brain’s processes, and robots allow these models to be tested in real bodies interacting with real environments (2). The following examples illustrate how this approach is being used to explore increasingly sophisticated control problems, including predictive tracking, body coordination, navigation, and learning.