Health

In 1960, a young hematologist named Madison Cawein began hearing rumors at the University of Kentucky. People spoke about the blue hill folks of the Cumberland Plateau. There were blue Stacys, Combses, Smiths, and Fugates at that time as a result of inbreeding and the small gene pool from which many of Eastern Kentucky’s families came.

Cawein was an accomplished doctor. He helped isolate the antidote for cholera and helped create a drug for Parkinson’s Disease. He was, however, a hematologist at heart. Cawein said that “blood cells always looked beautiful to me,” so when he began hearing about the blue people, his interest was piqued.

Cawein, along with Ruth Pendergrass, a nurse from the American Heart Association clinic in Hazard, scoured the hollers for blue people. Pendergrass was fascinated with the blue people since she gave a blood test to a woman who identified herself as a blue Combs from Ball Creek. Cawein and Pendergrass went on daily missions to find blue people until they were frustrated and near giving up. After all, Cawein was forced to drive eight hours one way, from Lexington to Hazard, when he wanted to go on a search. Then a pair of siblings, Rachel and Patrick Ritchie, walked into the heart clinic in Hazard. They were blue, and Cawein had found his white (or blue) whale.

This illustrates the growing impact of artificial intelligence (AI) on healthcare delivery and service quality in lower-income regions, from Africa to Southeast Asia. Physicians with limited training or experience are increasingly using their phones to call up AI as a supplementary tool for diagnosis and prescription decisions.

Beyond that, AI is supporting faster screening, improving diagnostic accuracy, and reducing prescription errors. According to a recent study, AI-assisted tuberculosis screening reduced misdiagnosis rates by more than 30 percent and improved predictive forecasting of seasonal disease outbreaks by more than 80 percent.

Zoonotic spillovers of viruses have occurred through the animal trade worldwide. The start of the COVID-19 pandemic was traced epidemiologically to the Huanan Seafood Wholesale Market. Here, we analyze environmental qPCR and sequencing data collected in the Huanan market in early 2020. We demonstrate that market-linked severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) genetic diversity is consistent with market emergence and find increased SARS-CoV-2 positivity near and within a wildlife stall. We identify wildlife DNA in all SARS-CoV-2-positive samples from this stall, including species such as civets, bamboo rats, and raccoon dogs, previously identified as possible intermediate hosts. We also detect animal viruses that infect raccoon dogs, civets, and bamboo rats. Combining metagenomic and phylogenetic approaches, we recover genotypes of market animals and compare them with those from farms and other markets. This analysis provides the genetic basis for a shortlist of potential intermediate hosts of SARS-CoV-2 to prioritize for serological and viral sampling.

Just this past May, the Food and Drug Administration approved a new drug named vepdegestrant (Veppanu) for a subset of patients suffering from metastatic breast cancer. First and foremost, this is a promising development for individuals with oestrogen receptor-positive, HER2-negative breast cancer. However, there is an extra layer of excitement to this news: Veppanu is the first drug of its kind (known as a PROTAC) to ever be approved by the FDA. For the remainder of the article, I will go over exactly what I mean by this and unpack all these science terms.

Let’s break it down into simple concepts: proteins are everywhere in the body. Receptors, enzymes, structural elements—they’re all made up of proteins. Many diseases stem from proteins that aren’t behaving as expected. For example, an overactive protein could lead to cancer, or a misfolded protein could lead to a neurodegenerative disease. Therefore, many existing drugs work by blocking a protein’s function.

PROTACs (which is short for proteolysis-targeting chimera) work in a completely different way. In simple terms, they stick onto a specific protein and bring it to our cell’s natural garbage-disposal system.

What is this “garbage disposal system”? In biology, when a protein needs to be destroyed by the body, this is referred to as “ubiquitination.” A faulty or misfolded protein that needs to be destroyed is first “tagged” with a little flag called an E3 ligase. This flag calls over another protein called ubiquitin, the cell’s garbage man. Basically, ubiquitin’s job is to destroy whatever the E3 is connected to. […]

Medicine is learning not only how to inhibit problematic proteins, but how to remove them. Consider the plethora of diseases caused by protein malfunction: Alzheimer’s, Parkinson’s, Huntington’s, cystic fibrosis—the list goes on. With this in mind, this step forward has promising implications for many diseases that have long been considered non-treatable.

“The most common daytime symptom of sleep apnea is tiredness or fatigue,” reiterates Dr. Brooke Judd, MD, the Section Chief of Sleep Medicine at Dartmouth Health. “Sometimes this is severe sleepiness to the point that someone may unintentionally fall asleep during a conversation or while driving, but it doesn’t have to be that obvious.”

Imagine a healthcare system made up of multiple AI agents: one that manages symptom assessment, another scheduling, a third insurance, and a fourth pharmacy.

Each is an expert in its domain. But they all have their own distinct knowledge and objectives. Today they can exchange data, but they are not yet able to actually coordinate patient care without a human making the decisions.

“The intelligence is already there. What is missing is the connective tissue that turns four strangers into one team,” explains Vijoy Pandey, senior vice president and general manager of Outshift by Cisco.

This “connective tissue” comes from adding a semantic layer—what Outshift calls the “Internet of Cognition”—that enables agents across domains to work together and, critically, “think” together through shared intent, context, and reasoning.

Hundreds of clinical trials now show that exercise can significantly reduce symptoms of depression. For mild to moderate cases, its effects are generally comparable to medication or therapy. When exercise is combined with medications or therapy, the effects may even be additive. On a population level, even achieving just half the recommended amount of physical activity is linked to an 18% lower risk of developing depression.

Researchers who followed patients for 10 years after they received either the actual procedure, arthroscopic knee surgery to trim degenerative cartilage tears, or merely “sham surgery” — a skin incision — for knee pain, found that the surgery provided little or no benefit and was, in fact, associated with accelerated osteoarthritis and higher rates of reoperation. That generally meant a total knee replacement.

“I don’t know how I would defend this procedure at all,” said one of the study’s authors, Teppo Järvinen, an orthopedist and head of the Finnish Centre for Evidence-Based Orthopaedics.

Consider one of the most repeated tropes about psychopaths, that they are incapable of mirroring or reading other peoples’ emotions: they lack empathy. The problem with this view is that science tells a radically different story. When people diagnosed with psychopathy participate in empathy experiments, their performance is entirely indistinguishable from normal controls.

The most compelling evidence comes from a recent systematic review of empathy research my team conducted, which included a total of 66 studies involving 5,711 persons clinically assessed for psychopathy. We found that the results were ‘overwhelmingly null findings’ (89.11 per cent of all tests). That is, statistical analyses cannot tell the difference in performance between psychopathic vs non-psychopathic persons. We also found that high-quality studies – those using more rigid statistical methods – had an even higher null-ratio of a whopping 94.77 per cent. In behavioural scientific experiments, where datasets are presumed to be rife with false positives, this is arguably as close as you get to proving a negative: people diagnosed with psychopathy do not have empathy deficits.

Consider another well-trodden claim that psychopaths lack emotions. This claim is as old as the idea of psychopathy itself, however it was the psychiatrist Hervey Cleckley who popularised it through his book The Mask of Sanity (1941). Cleckley hypothesised that psychopathy was essentially a neurological disorder of the affective system, causing abnormally shallow emotions. What made psychopathy peculiar was that those who were affected by the disorder could hide or mask their disability, coming across as if they were normal. But, to Cleckley, this is just a façade covering up a barren inner emotional life. In many ways, the Chigurh character effectively captures this aspect of Cleckley’s conception of psychopathy.

However, most researchers have long given up on this idea too, rendering it little more than a myth. There has never been any clear evidence to support it. A person clinically diagnosed with psychopathy might appear as if they are lacking emotions, but once these patients are subjected to careful analysis using technology capable of measuring physiological markers correlated with emotional reactions – like skin conductance, heart rate, brain activity, etc – the data tell a different story.