A new way to cleanly separate out cancer cells from a blood sample enables comprehensive genetic profiling of the cancer cells, which could help doctors target tumors and monitor treatments more effectively.
It is a dramatic improvement over current approaches because it also encompasses the variation among cancer cells within a single patient.
“This could be a whole different ball game,” said Max Wicha, the Madeline and Sidney Forbes Professor of Oncology at the University of Michigan and senior physician on the study in Nature Communications.
Imperial medical students have helped to devise a new type of ‘decoy’ drug to tackle infections that are resistant to antibiotics.
In lab tests on bacterial cultures, the new drug successfully killed a strain of drug-resistant bacteria. It works by delivering two antibiotics, one of which is effectively hidden. When the bacteria fight against the first ‘decoy’ antibiotic, this action opens up the drug, triggering the second antibiotic into action.
This enables the second antibiotic to be delivered in a targeted way, only being released where it encounters drug-resistant bacteria. The findings could help prolong the life of existing antibiotics by slowing the rate at which bacteria become resistant to them.
These days, scientists can collect a few skin or blood cells, wipe out their identities, and reprogram them to become virtually any other kind of cell in the human body, from neurons to heart cells.
The journey from skin cell to another type of functional cell involves converting them into induced pluripotent stem cells (iPSCs), which are similar to the developmentally immature stem cells found in embryos, and then coaxing them to mature into something different.
But the process runs on an invisible clock, one in which scientists are interested in speeding up so adult-like cells are available when needed, whether for testing drugs for precision medicine, transplanting to repair injury or defect, or better understanding basic biology. It involves an FDA-approved compound called polyinosine-polycytidylic acid, or pIC, a double-stranded RNA molecule that activates a cell’s innate defense system. The compound is commonly used to boost vaccines and chemotherapy. The researchers found that when added to induced pluripotent stem cells undergoing the process of transitioning into cardiac muscle cells, pIC accelerated cellular maturation.
A team of researchers affiliated with several institutions in China has developed a hydrogel that can stop bleeding from a punctured artery. In their paper published in the journal Nature Communications, the group describes how the hydrogel was made and how well it worked on test animals.
Uncontrolled bleeding is a very serious situation, both during surgical procedures and as a result of trauma. In most cases, it is the result of damage to a major artery or an organ like the liver. In all cases, immediate action must be taken or the victim will die. Currently, treatment for such wounds involves clamping the artery and then using sutures to close the wound. In the past, researchers have attempted to create a type of glue to stem such wounds, but thus far, none of them has worked as hoped—they were either made of toxic materials or were not strong enough to stand up to the high liquid pressure in the bloodstream. In this new effort, the researchers have developed a new type of hydrogel that solves both problems.
The researchers report that the hydrogel is made of water, gelatin and a mix of proteins and other chemicals. It was designed to be as close as possible in structure to human connective tissues. When UV light shines on the gel, it thickens and solidifies, adhering to the wound, preventing blood from flowing out. And it does so in just 20 to 30 seconds. The researchers note that it could also stand up to 290-mmHg blood pressure—much higher than normal.
American researchers have recently published a study in the scientific journal Nature, showing promising results using steroid eye drops for shrinking down and dissolving cataracts.
At the moment cataracts is the leading cause of blindness, and can only be removed through surgery. The surgical procedure, while simple and safe, is unpleasant for the patient and often prohibitively expensive.
A ccording to the Fred Hollows Foundation, approximately 32.4 million people around the world are blind, with more than half of the cases being caused by cataracts. In the United States alone, nearly 22 million Americans who are over age 40 have cataracts, according to the American Academy of Ophthalmology.
Substantially earlier than indicated by most DNA-based estimates, according to new research by a UCL academic.
The research, published in Science Advances, analysed dental evolutionary rates across different homininspecies, focusing on early Neanderthals. It shows that the teeth of hominins from Sima de los Huesos, Spain—ancestors of the Neanderthals—diverged from the modern human lineage earlier than previously assumed.
Sima de los Huesos is a cave site in Atapuerca Mountains, Spain, where archaeologists have recovered fossils of almost 30 people. Previous studies date the site to around 430,000 years ago (Middle Pleistocene), making it one of the oldest and largest collections of human remains discovered to date.
The world recently acknowledged the power of alternative cancer treatments by awarding the 2018 Nobel Prize in Medicine to Dr. James P. Allison and Dr. Tasuku Honjo for their work in immunotherapy. More specifically on checkpoint inhibitor therapies.
Until recently many in the scientific community had dismissed immunotherapy as a viable cancer treatment. Nevertheless, Allison and Honjo persevered and their breakthrough has allowed for the classification of new drugs and treatments that may help patients have run out of options.
Ironically, while many in the mainstream are barely learning of immunotherapy, a hospital in Mexico, CHIPSA Hospital, has been working with these treatments for over 38 year and often under fire from public ridicule that their treatments are strange and ineffective.
Nicola Bagalà and Michael Nuschke take a look at the future of pensions and how the possible defeat of age-related diseases will affect them.
If you work in social security, it’s possible that your nightmares are full of undying elderly people who keep knocking on your door for pensions that you have no way of paying out. Tossing and turning in your bed, you beg for mercy, explaining that there’s just too many old people who need pensions and not enough young people who could cover for it with their contributions; the money’s just not there to sustain a social security system that, when it was conceived in the mid-1930s, didn’t expect that many people would ever make it into their 80s and 90s. Your oneiric persecutors won’t listen: they gave the country the best years of their lives, and now it’s time for the country to pay them their due.
When you wake up, you’re relieved to realize that there can’t be any such thing as people who have ever-worsening degenerative diseases yet never die from them, but that doesn’t make your problem all that better; you still have quite a few old people, living longer than the pension system had anticipated, to pay pensions to, and the bad news is that in as little as about 30 years, the number of 65+ people worldwide will skyrocket to around 2.1 billion, growing faster than all younger groups put together [1]. Where in the world is your institution going to find the budget?
