Lifeboat Foundation

A new model, vetted by experiments on lung cancer cells, may help to explain how cancer and other diseases accumulate drug-resistance mutations that can compromise the effectiveness of treatments.

During the past 50 years, researchers have accumulated a massive arsenal in our war on cancer. Well over 500 drugs have been approved to treat tumors, but cancer remains the second leading cause of death in the United States. The problem is partly due to drug resistance—the emergence of treatment-resistant mutants of the original disease. Now a study led by Jeff Maltas of Cleveland Clinic and Case Western Reserve University, both in Ohio, puts forward a model explaining why drug resistance is so common, vetting the model with experiments on lung cancer cells [1]. This model indicates that treatment-resistant mutants can be present in larger-than-expected numbers before treatment begins. The conclusion implies that we cannot understand cancer evolution by looking at individual mutations in isolation; instead, we should consider each tumor as an interacting ecosystem.

They calculated stellar populations without and with the presence of dark matter. With dark matter, more massive stars experienced a lower dark matter density, and hydrogen in their core fused more slowly and their evolution was slowed down. But stars in a higher dark matter density region were changed significantly—they maintained equilibrium through dark matter burning with less fusion or no fusion, which led to a new stellar population in an HR region above the main sequence.

“Our simulations show that stars can survive on dark matter as a fuel alone,” said lead co-author Isabelle John from Stockholm University, “and because there is an extremely large amount of dark matter near the Galactic Center, these stars become immortal,” staying forever young, occupying a new, distinct, observable region of the HR diagram.

Their dark matter model may be able to explain more of the known mysteries. “For lighter stars, we see in our simulations that they become very puffy and might even lose parts of their outer layers,” said John. She noted that “something similar to this might be observed at the Galactic Center: the so-called G-objects, which might be star-like, but with a gas cloud around them.”

Chapters: 0:00 Colin Wright Highlights 0:48 Colin Wright: A Horrible Person, A Transphobe? 3:43 Did This Piss Colin Off? 6:03 Humans Will Always Do Magical Thinking 8:32 If We Stand Up Together… 9:48 The Fundamental Misunderstanding / Fish 12:48 What Activists Get Wrong (Secondary Characteristics) 15:48 The ‘True’ Hermaphrodite 17:48 Is There A Male or Female Brain? 21:48 Judith Butler’s Contradiction 24:48 Individual Liberty 27:48 Young Girls & Older Men 30:48 Cross-Dressers Getting Aroused 34:18 How Sex Is Determined In Nature 37:38 Why Do Men Have Nipples? 38:58 Why Don’t Testicles Have Rib Cages? 40:18 Creationism vs Evolution (Joe Rogan) 44:18 Alex Jones & Gay Frogs 45:08 What Does ‘Theory’ of Evolution Mean? 48:08 Other Competing Theories? 51:28 Faith vs Science 53:48 Danger of Reality Denial 57:43 A Heretic Colin Admires.

Researchers from the University of Oxford have developed a new small molecule that can suppress the evolution of antibiotic resistance in bacteria and make resistant bacteria more susceptible to antibiotics. The paper, “Development of an inhibitor of the mutagenic SOS response that suppresses the evolution of quinolone antibiotic resistance,” has been published in the journal Chemical Science.

System charts the evolution of complex quantum states.

The human genome is massive, and it contains many highly repetitive sequences that confounded researchers for years. Many of these repeats were simply written off as junk DNA that had no function. However, new research is revealing that many of these regions are much more important than we thought. Some of the repetitive portions of the genome are known to be human endogenous retroviruses (HERVs). These sequences originated from viruses that infected human germ cells millions of years ago and affected our evolution. About eight percent of our genome is thought to be made up of HERVs. These HERVs have also been associated with a variety of psychiatric disorders, although the connection is unclear.

A new study reported in Nature Communications has suggested that HERVs are making a significant but unappreciated contribution to the development of psychiatric disorders, and that they may help explain a genetic component of these disorders that is thought to exist but has not yet been identified.

“If you frame it as an either/or question, it’s too simplistic,” says Utah State University evolutionary biologist Zachariah Gompert. “The answer isn’t ‘completely random’ or ‘completely deterministic and predictable.’ And yet, examining short time scales, we can find predictable, repeatable evolutionary patterns.”

Gompert and colleagues report evidence of repeatable evolution in populations of stick insects in the May 24, 2024, online edition of the American Association for the Advancement of Science’s journal Science Advances. Collaborating authors on the paper include Gompert’s long-time collaborator Patrik Nosil and other researchers from France’s University of Montpelier, Brazil’s Federal University of São Paulo, the University of Nevada, Reno and Notre Dame University. The research is supported by the National Science Foundation and the European Research Council.

The team examined three decades of data on the frequency of cryptic color-pattern morphs in the stick insect species Timema cristinae in ten naturally replicate populations in California. T. cristinae is polymorphic in regard to its body color and pattern. Some insects are green, which allows the wingless, plant-feeding insect to blend in with California lilac (Ceanothus spinosus) shrubs. In contrast, green striped morphs disappear against chamise (Adenostoma fasciculatum) shrubs.

Big black holes in little galaxies, rogue black holes and other behemoths could offer clues to cosmic evolution.

A new study unexpectedly reveals that cells thrive on chaos.