A group of scientists and economists has devised a simple, tunable strategy for achieving exponential decrease in the number of new cases of Covid-19 while partially reopening the economy — or so it seems to me. The simplest form of the strategy is to alternate between consecutive days of work and consecutive days of lockdown. Although I am reluctant to add to the cacophony of inexpert opinions on how to deal with the pandemic, I will say that the strategy obviously works in an epidemiologic sense if the number of workdays per two-week cycle is sufficiently small. Furthermore, it is obvious that the number of workdays can be adjusted in response to the number of new cases. However, it is not obvious that can be set sufficiently high for the strategy to work in an economic sense. Modeling reported in the preprint “Cyclic Exit Strategies to Suppress COVID-19 and Allow Economic Activity” indicates that is likely to be sufficiently small. In other words, it seems that people might work half-time ( hours per two-week period) while driving the number of new cases toward zero. I am not qualified to judge epidemiological models, but will note that the results make sense if it is indeed the case that there is a “three-day delay on average between the time a person is infected and the time he or she can infect others.”
To be perfectly clear, I have not become a true believer in a strategy addressed in a preprint. I am saying that we should reject the notion that the pandemic will end only with herd immunity. It is not irrational to say that there may be, in the absence of an effective vaccination program, practicable methods of preventing most people from being infected, and that we should keep looking for them.
This past Friday, I bumped into Dr. Michael Behe, and again on Saturday, along with Drs. Brian Miller (DI), Research Coordinator CSC, and Robert Larmer (UNB), currently President of the Canadian Society of (Evangelical) Christian Philosophers. Venue: local apologetics conference (https://www.diganddelve.ca/). The topic of the event “Science vs. Atheism: Is Modern Science Making Atheism Improbable?” makes it relevant here at TSZ, where there are more atheists & agnostics among ‘skeptics’ than average.
On the positive side, I would encourage folks who visit this site to go to such events for learning/teaching purposes. Whether for the ID speakers or not; good conversations are available among people honestly wrestling with and questioning the relationship between science, philosophy and theology/worldview, including on issues related to evolution, creation, and intelligence in the universe or on Earth. Don’t go to such events expecting miracles for your personal worldview in conversation with others, credibility in scientific publications or in the classroom, if you are using ‘science’ as a worldview weapon against ‘religion’ or ‘theology’. That argument just won’t fly anymore and the Discovery Institute, to their credit, has played a role, of whatever size may still be difficult to tell, in making this shift happen.
A question arises: what would be the first question you would ask or thing you would say to Michael Behe if you bumped into him on the street?
The prevailing paradigm is that cancer is a genetic disease caused by somatic mutations occurring in the course of cell division. However, it has been know for many years, ever since Otto Warburg’s effect has been discovered, that cancer cells favor a less efficient metabolism via glycolysis rather than the much more efficient oxidative phosphorylation pathway even in the presence of sufficient oxygen.
The alternative theory to somatic mutations as the culprit of cancer is that most cancers are metabolic diseases caused by dysfunctional mitochondria and mutations occurring in nucleus are the effect of metabolic instability of the cell. It follows that cell machineries in charge of normal cell growth suffer mutations leading to proliferation rather than the other way around.
The following experimental evidence points to conclusions that the many genetic mutations associated with cancers (over 11.000 mutations have been associated with colon cancer alone) have almost no effect on cancer as long as fully functional mitochondria (s) are present in the cell…
Dr. Sabine Hossenfelder has a PhD in physics from the University of Frankfurt. Since 2006 she has written the popular weblog Backreaction as well a the book “Lost in Math: How Beauty Leads Physics Astray”. She has a very interesting OP on cognitive biases that apparently explains what influences our the decision making…
The OP is also linked to a presentation on How to Reduce Biases in Decision-Making. I found Dr. Hossenfelder blog and the OP really intriguing because I could never understand why so many people would support ideologies that were pure nonsense or against scientific facts or logic…
Now I find it easier to understand those biases, although I still have a very hard time understanding why someone would deceive himself into believing something because of his or her preconceived ideas…
It really makes my day whenever I read “scientific theories” that don’t fit the main paradigm or predictions of evolutionary theory. The evolution of homosexuality is one of my favorite paradoxes, maybe with the exception of gender evolution/sexual reproduction, that I’m going to save for another OP.
It doesn’t take Einstein to notice that the evolution of homosexuality is not only a paradox but it totally contradicts the driving force of evolution, which is supposed to be reproduction. Since homosexuals can’t reproduce, not in homosexual relations, a problem for evolutionary theory arises. Why would homosexuality evolve in the first place? But more so, why would natural selection preserve homosexuality?
However, as it is with many, many other evolutionary paradoxes the theories to explain them abound… Check out this one of the evolution of homosexuality:
Very nice. Congratulations! But where is the “directed evolution” oxymoron in this story?The process used is simple organism breeding as done by mankind for thousands of years, in this case sped up by advanced technologies. “Random mutations” are not entirely random as the mutations desired had to converge towards a clear, specified target. Random generator devices also generate within specific ranges, say 0 to 9, rejecting outright any “randomness” outside that range (‘a’, ‘#’, ‘21’ will all be rejected). “Natural selection” is also missing as the selection has been clearly done by qualified researches pursuing a specific goal. At best this would be called “artificial selection”, but even that is misleading since organism breeding is a human activity that goes well beyond simple ‘selection’.
Ohno’s 1984 Proceedings of the National Academy of Science paper put forward the hypothesis that frameshift mutations can create novel proteins and illustrated his claim with the supposed evolution of nylon eating bacteria. Several researchers cite Ohno’s 1984 paper favorably including Dennis Venema, Ken Miller and our very own Arlin Stoltzfus of TSZ. Unfortunately, Ohno’s 1984 hypothesis, as far as nylon eating bacteria, is dead wrong.
Here is another paper that also cited Ohno’s 1984 hypothesis favorably. This paper may or may not hold promise as it claims to have found 470 frameshift translations in the human genome.
Dr. Winston Ewert put forward his module hypothesis, but I put forward an alternate module hypothesis at the domain and motif level of proteins. It is based actually on papers by evolutionists who have pointed out that the problem of “Promiscuous Domains” remains an unsolved problem in evolutionary biology.
When I put Promiscuous Domains on the table in the Common Design vs. Common Descent thread, the TSZ Darwinists ignored the problem and then declared victory. I viewed their non-response as evidence they didn’t understand the problem and/or preferred to ignore it.
Perhaps pictures are worth ten thousand words. From the NIH, that great source inspiration for the Intelligent Design community, we have the CDART database viewer.
From the CDART viewer, I provide a few of the thousands of diagrams that show the promiscuity of protein domains. The diagrams below show the classical zinc finger ZF-C2H2 “ZF” domain and the Plextrin Homology “PH” domains. Note how the location of domains is “shuffled” to different locations in different proteins. It’s as if proteins are made by different lego-like parts in different order and position. My preliminary look into small 4-amino acid motifs that are the target of phosphorylating kinases suggests the the problem of promiscuity goes all the way down to small motif levels.
Such promiscuity is more consistent with common design than common descent. Continue reading →
Bill Basener (a participant here) co-authored a paper with John Sanford. He was given the honor of delivering a KEYNOTE ADDRESS at an international SECULAR biology conference. A video of his presentation is available in a link inside my write up of his presentation below. He alluded to some of the helpful input from his critics at TheSkepticalZone in his talk:
John Sanford is sort of the “Papa John” of creationist genetics. It is customary for the leader of a research group to be listed as the last author in a publication. That convention is seen in a variety of papers and books such as Rupe & Sanford; Basener & Sanford; Carter, Lee & Sanford; Montanyez, Fernandez, Marks & Sanford; and let’s not forget the Legendary High Velocity Team of Klein, Wolf, Wu & Sanford that permanently ensured the infusion of intelligently designed genes into a sizable fraction of Genetically Modified Organisms on planet Earth.
And perhaps one day in the distant future there will be a paper, “Cordova & Sanford”! 🙂
Below is a link of a paper from Papa John’s team about Adam and Eve which will be presented this week, July 29,2018 – August 1, 2018 at the 8th International Conference on Creationism
In the link below are the abstracts with links to the papers presented at the International Conference on Creationism 2018 in Pittsburgh, PA July 29-August 1, 2018. Those presenting are professors at Christian colleges, professors already expelled from secular colleges, or professors at secular colleges who (by God’s grace) can’t be expelled. 🙂
A topic I will raise among the population geneticists there (John C. Sanford, Rob Carter, Nathaniel Jeanson, and others) is the issue of heteroplasmy in mtDNA as they are presenting on these topics.
Mature human cells have 100,000 to 600,000 mitochondrion. So how can a cell be mostly homoplasmic yet have mtDNA mutations that are reflected in lineages whereby an individual has a mostly homoplasmic mtDNA that enable us to identify the 7 daughters of Eve (to quote Oxford Geneticist Bryan Sykes). Continue reading →
Jonathan Wells, who is an embryologist and an ID advocate, has a very interesting paper and video on the issue of ontogeny (embryo development) and the origins of information needed in the process of cell differentiation…
Wells thinks that a major piece of information needed in the process of embryo development can’t be explained by DNA, and therefore may require an intervention of an outside source of information, such as ID/God…
If you don’t want to watch the whole video, starting at about 40 min mark is just as good but especially at 43 min.
Death has been on everyone’s mind at one time or another… It’s unavoidable…
Some are fascinated by death; mainly the possibility of better afterlife. Some, or the great majority of people, are frightened by it. It seems the unknown of after-death is one of the main factors causing many to tremble…
However, it turns out that Craig Venter, the pioneer of the human genome project and the supposed creator of artificial life, turned his attention and efforts toward decoding death… here
It seems obvious Venter believes that death is be caused by genetics; some genetic mutations that could be fixed and we could live forever, otherwise he wouldn’t be digging in the genome looking to fix the death code…