Indeed, as Gizmodo’s report highlights, many experts believe that these researchers have not actually found evidence of dinosaur DNA. They told the news outlet, for example, that—even under the best circumstances—DNA couldn’t last more than three million years. Let alone more than 100 million. And that the chemicals may have been staining inorganic matter that only looks cellular in nature.
As of now, the most ancient DNA that scientists have been able to sequence was that of a million-year-old woolly mammoth. And the youngest dinosaurs are at least 65 million years old. But if future experiments do confirm this evidence as real, then that really changes things. At least in our fantasies, where reanimated dinosaurs and Ian Malcolms abound.
Residents of Abusir el-Meleq, an ancient Egyptian city south of Cairo, the men died between 1,380 B.C.E. and 450 C.E. A team from Parabon NanoLabs presented the trio’s facial reconstructions at the International Symposium on Human Identification in September.
“[T]his is the first time comprehensive DNA phenotyping has been performed on human DNA of this age,” says Parabon, a Virginia-based company that typically uses genetic analysis to help solve cold cases, in a statement.
To approximate the men’s faces, researchers used DNA phenotyping, which predicts individuals’ physical appearance based on genetic markers. (Phenotyping can suggest subjects’ skin, hair and eye color, but as Caitlin Curtis and James Hereward wrote for the Conversationin 2,018 the process has its limitations.) The team determined the mummies’ other characteristics through examination of their physical remains, reports Hannah Sparks for the New York Post.
Today, the conjunction of climate change, the advent of artificial intelligence and the capacity to import human purposiveness into evolution through the reading and rewriting of our own genome are, like the first leaps in technology and their consequences, stirring a search for the sacred that frames both the limits and potentialities of what it means to be human. As the Polish thinker Leszek Kołakowski sagely put it, without a sense of the sacred, culture loses all sense.
For this reason, he posited in a conversation some years ago at All Souls College in Oxford, that “mankind can never get rid of the need for religious self-identification. … Who am I, where did I come from, where do I fit in, why am I responsible, what does my life mean, how will I face death? Religion is a paramount aspect of human culture. Religious need cannot be excommunicated from culture by rationalist incantation.”
In this, Rees agrees. Far from consigning faith to the past, science fiction plumbs its future. Where technology and its consequences go, the religious imagination will follow.
When Dr. Robert Murphy first started researching biochemistry anddrug development in the late 1970s, creating a pharmaceutical compound that was effective and safe to market followed a strict experimental pipeline that was beginning to be enhanced by large-scale data collection and analysis on a computer.
Now head of the Murphy Lab for computational biology at Carnegie Mellon University (CMU), Murphy has watched over the years as data collection and artificial intelligence have revolutionized this process, making the drug creation pipeline faster, more efficient, and more effective.
Recently, that’s been thanks to theapplication of machine learning—computer systems that learn and adapt by using algorithms and statistical models to analyze patterns in datasets—to the drug development process. This has been notably key to reducing the presence of side effects, Murphy says.
The timeframe for reinfection is fundamental to numerous aspects of public health decision making. As the COVID-19 pandemic continues, reinfection is likely to become increasingly common. Maintaining public health measures that curb transmission—including among individuals who were previously infected with SARS-CoV-2—coupled with persistent efforts to accelerate vaccination worldwide is critical to the prevention of COVID-19 morbidity and mortality.
And, depending on how further studies progress, it could be implemented via gene therapy.
Early-stage pancreatic cancer has a ‘reset button’
“These findings open up the possibility of designing a new gene therapy or drug because now we can convert cancerous cells back into their normal state,” said Professor Bumsoo Han of Purdue’s mechanical engineering, who is also the program leader for the university’s Center for Cancer Research, in a blog post shared on the university’s official website. Han has also received a courtesy appointment in biomedical engineering, according to the post. The new time machine (speaking figuratively) from Han’s lab is a lifelike reproduction of a specific structure of the pancreas, called the acinus, which secretes and produces digestive enzymes into the small intestine. When pancreatic cancer strikes, it typically comes from chronic inflammation, which is caused by a mutation that tricks the digestive enzymes to begin digesting the pancreas itself. This is bad.
Brains aren’t the easiest of organs to study, what with their delicate wiring and subtle whispering of neurotransmitter messages. Now, this research could be made a little easier, as we’ve learned we can swap some critical chemical systems with the host animal being none the wiser.
In a proof-of-concept study run by a team of US researchers, the microscopic worm Caenorhabditis elegans was genetically gifted pieces of a nervous system taken from a radically different creature – a curious freshwater organism known as Hydra.
The swap wasn’t unlike teaching a specific brain circuit a foreign language, and finding it performs its job just as well as before.
Genetic information can be messy. Mapping proteins could offer a clearer view of what’s driving cancer.
Scientists have unveiled new maps of the protein networks underlying different types of cancer, offering a potentially clearer way to see what’s driving the disease and to find therapeutic targets.
Sequencing the genetic information of tumors can provide a trove of data about the mutations contained in those cancer cells. Some of those mutations help doctors figure out the best way to treat a patient, but others remain more of a mystery than a clear instruction manual. Many are exceedingly rare, or there are so many mutations it’s not clear what’s fueling the cancer.
A new resource profiles gene expression and the accessibility of DNA in single cells across the developing human cerebral cortex and may help scientists decipher the effects of noncoding mutations linked to autism.
Developing drugs for a range of tauopathies — dr leticia toledo-sherman, senior director, drug discovery, tau consortium, rainwater charitable foundation.
Dr. Leticia Toledo-Sherman is Senior Director of Drug Discovery of the Tau Consortium (https://tauconsortium.org/) for The Rainwater Charitable Foundation (https://rainwatercharitablefoundation.org/medical-research) and also holds an appointment as Adjunct Assistant Professor of Neurology at UCLA.
Dr. Toledo-Sherman leads drug discovery activities for an international network of scientists working to develop therapies for Tauopathies, a group of neurodegenerative disorders characterized by the deposition of abnormal Tau protein in the brain.
Previously, Dr. Toledo-Sherman was Director of Medicinal Chemistry and Computer-Aided Drug Design at the CHDI Foundation, leading drug discovery programs for therapeutic development in Huntington’s Disease (HD). At CHDI, she also led a structural biology initiative critical to the understanding of the relationship between structure and biological function of huntingtin, the protein that when mutated causes HD.
Prior to joining CHDI, Dr. Toledo-Sherman was Executive Director of Chemistry at Lymphosign (now part of Pharmascience Inc), a privately held biotechnology company that applied rational design principles to the development of therapeutics for blood cancers. From 2000 to 2,004 she led a multi-site, multidisciplinary team using chemical proteomics and bioinformatics to discover therapeutic targets and to investigate the mechanism of action of drugs.
Dr. Toledo-Sherman started her professional career as a leading scientist at Kinetix Pharmaceuticals (acquired by Amgen), where she implemented an in-silico platform aimed at rational drug design of kinase inhibitors targeting multiple therapeutic areas.
Besides her work in discovery and development of therapies for neurodegenerative diseases, Dr. Toledo-Sherman is interested in the field of Chemical Biology. She has been involved in several initiatives and expert panels on the use of sharp proof-of-concept chemical probes to validate targets and interrogate biological mechanisms. She is also an advocate for open science at the pre-competitive drug discovery stage.
Dr. Toledo-Sherman received a PhD in Organic Chemistry from The State University of New York at Stony Brook and did postdoctoral research at the Massachusetts Institute of Technology and The Skaggs Institute for Chemical Biology at The Scripps Research Institute in La Jolla, California.
