Thursday, January 4, 2018 at 7 pm Eastern Time:
James V. Kohl @jvkohl Your Tweets earned 3,525 impressions over the last 24 hours
Please calculate the number of potential victims who might be saved by the information in my tweets. I will sleep better if you know that you may not be among those who survive.
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See: A Mathematical Model Links Quantum Physics to Quantum Souls (2)
See: Viruses exacerbate disease caused by Leishmania parasite
How do parasite viruses worsen parasitic diseases?
It’s important to remember that people are not infected with both a parasite and a virus. Rather, people are infected with a parasite that has a virus hidden inside it. What we think happens is that immune cells kill some invading parasites, releasing the virus. The body then generates an immune response to fight off the virus. But when you’re infected with a parasite, this is the wrong kind of immune response. It doesn’t kill the parasite; it seems to help the parasite make the disease worse.
What makes the disease better? SARCASM ALERT: Could it be the anti-entropic virucidal energy of sunlight that is consistently linked from the food the organisms eat to their biophysically constrained physiology of pheromone-controlled viral latency via the transgenerational epigenetic inheritance of all phenotypes in all living genera?
Alternatively, see: A virus-bacteria coevolutionary ‘arms race’ solves diversity by ‘killing the winner’
Theoretical models of population dynamics have not presented a fully satisfactory explanation for what has come to be known as the diversity paradox.
And so they developed another theoretical model
Goldenfeld and Xue developed a stochastic model that accounts for multiple factors observed in ecosystems, including competition among species and simultaneous predation on the competing species. Using bacteria and their host-specific viruses as an example, the researchers showed that as the bacteria evolve defenses against the virus, the virus population also evolves to combat the bacteria. This “arms race” leads to a diverse population of both and to boom-bust cycles when a particular species dominates the ecosystem then collapses—the so-called “Kill the Winner” phenomenon. This coevolutionary arms race is sufficient to yield a possible solution to the diversity paradox.
Simply put, they advise you to just say no to autophagy, and to ignore the information at Autophagy.pro
For comparison: This was reported in 2005: A universal trend of amino acid gain and loss in protein evolution
We cannot conceive of a global external factor that could cause, during this time, parallel evolution of amino acid compositions of proteins in 15 diverse taxa that represent all three domains of life and span a wide range of lifestyles and environments. Thus, currently, the most plausible hypothesis is that we are observing a universal, intrinsic trend that emerged before the last universal common ancestor of all extant organisms.
The likelihood that the universal, intrinsic trend that emerged before the last universal common ancestor of all extant organisms was ignored again in this report Study of 385-million-year-old shark suggests humans and sharks shared common ancestor 440 million years ago.
Scientists explore mysteries behind diversity of DNA composition among species
The study was published in the journal Nature Ecology and Evolution.
To err is universal
Driving evolution are DNA mutations, errors in the genome that are introduced and passed along to the next generation, so that over time, providing the fuel for the invention of new adaptations or traits.
See for comparison: The Secret to Long Life? It May Lurk in the DNA of the Oldest Among Us and The secret to safe DNA repair
…if you don’t have this enzyme, then this error-free repair is stopped. You can’t do it. If you can’t do the error-free repair, among other things that happen is that you expect these cells to be cancer prone.
Career summary
I often wonder how I found myself in a career as a medical laboratory scientist at a time when some people still believe in mutation-driven evolution. See for comparison: The Darwin Code
Perhaps the most intriguing method of gene swapping in bacteria is the bacteriophage, or bacterial virus. Bacteriophages–phages for short–can either kill large numbers of host bacteria, reproducing rapidly, or lie dormant in the bacterial chromosome until the time is right for expression and release. Lytic phages almost invariably kill their hosts. But these latter types–known as lysogenic phages–can actually transport useful genes between hosts, and not just randomly, but in a targeted fashion. In fact, bacterial pathogens frequently rely on lysogenic phages to spread toxin genes throughout a population. Cholera populations become pathogenic in this fashion. In outbreaks of E. coli that cause illness in humans, lysogenic phages have transported genes from shigella–a related bacterial type–conferring the ability to produce shiga toxin, a potent poison.
See also: The evolution of RNAi as a defence against viruses and transposable elements
RNA interference (RNAi) is an important defence against viruses and transposable elements (TEs). RNAi not only protects against viruses by degrading viral RNA, but hosts and viruses can also use RNAi to manipulate each other’s gene expression, and hosts can encode microRNAs that target viral sequences.
Claims about the evolution of food energy-dependent endogenous RNA interference have been made by biologically uninformed theorists.”Endogenous” is used to indicate that fact that RNA interference is an energy-dependent biophysically constrained example of creation.
See for details: Energy as information and constrained endogenous RNA interference
See for an example: AlmG, responsible for polymyxin resistance in pandemic Vibrio cholerae, is a glycyltransferase distantly related to lipid A late acyltransferases December 22, 2017
Reported as: An unusual form of antibiotic resistance in pandemic cholera
AlmG is structured differently from other lipid A-modifying enzymes, with a different active site responsible for carrying out the modification. In addition, AlmG can add either one or two glycines to the same lipid A molecule, which has also not been observed in other bacteria.
The enzymatic addition of achiral glycine in position 6 of the GnRH decapeptide helps to protect the organized genomes of all vertebrates from the virus-driven degradation of messenger RNA that links mutations to all pathology.
For comparison, antibiotic resistance is driven by ecological adaptations in viruses. The viruses steal the quantized energy that host cells need to use for error free DNA repair of the cell membrane which contains quantized energy as information that is required for species-specific survival. If the availability of food is restricted, the virus-driven degradation of messenger RNA is linked to all species-specific and cell type-specific pathology.
See also: Waiting for the big one: A new flu pandemic is a matter of time (Subscription required)
At least two flu strains are only a few mutations away from developing deadly human-to-human transmission. So how do we minimise the impact?
You minimize the impact by learning how quantized energy-dependent RNA-mediated biophysically constrained cell type differentiation occurs. Then, you stop claiming that different strains of the flu virus evolve.
The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.
The Spanish flu of 1918 remains the worst flu pandemic on record, but there have been several milder ones since (see chart, below). A pandemic is a global epidemic and, in theory, flu does that every year in the northern and southern winters. But with flu, the term is reserved for when an influenza A virus emerges that isn’t just a slightly mutated version of last winter’s flu, but a complete novelty, with surface proteins most people have no immunity to.
Novel viruses are constantly evolving in the birds, pigs and other animals that also carry influenza A, and they can shuffle their genes with human strains, or just adapt to mammals directly. Virologists consider flu pandemics inevitable. The World Bank says a bad one “
How much worse could it be? Spanish flu of 1918 killed 50 million people in a world with a much smaller population size and less ability to quickly travel from one part of the world to another.
12 Monkeys
The movie uses its future world as a home base and launching pad for the central story, which is set in 1990 and 1996, and is about a time traveler trying to save the world from a deadly plague.
… lives with a handful of other human survivors in an underground shelter put together out of scrap parts and a lot of wire mesh. The surface of the planet has been reclaimed by animals, after the death of 5 billion people during a plague in 1996.
Thursday, January 4, 2018 at 7 pm Eastern Time:
James V. Kohl @jvkohl Your Tweets earned 3,525 impressions over the last 24 hours
Please calculate the number of potential victims who might be saved by the information in my tweets. I will sleep better if you know that you may not be among those who survive.
