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Can we objectively tell how fast we are aging? With a good measure, scientists might be able to change our rate of aging to live longer and healthier lives. Researchers know that some people age faster than others and have been trying to concisely measure the internal physiological changes that lead to deteriorating health with age.

For years, researchers have been using clinical factors normally collected at physicals, like hypertension, cholesterol and weight, as indicators to predict aging. The idea was that these measures could determine whether someone is a fast or slow ager at any point in their . But more recently, researchers have theorized that there are other biological markers that reflect aging at the molecular and cellular level. This includes modifications to a person’s genetic material itself, or epigenetics.

While each person has a that largely does not change over their lifetime, to their genetic material that occur throughout life can change which genes are turned on or off and lead to more rapid aging. These changes typically involve the addition of methyl groups to DNA and are influenced by social and environmental exposures, such as , smoking, pollution and depression.

The fungal pathogen that wipes out much of humanity in HBO’s latest series The Last of Us is real, but can the cordyceps fungus actually turn humans into zombies one day?

“It’s highly unlikely because these are organisms that have become really well adapted to infecting ants,” Rebecca Shapiro, assistant professor at University of Guelph’s department of molecular and cellular biology, told Craig Norris, host of CBC Kitchener-Waterloo’s The Morning Edition.

In the television series, the fungus infects the brain of humans and turns them into zombies. In real life, it can only infect ants and other insects in this manner.

The outer layer of the brain, known as the cortex, is made of different types of neurons. Neuroscience studies suggest that these different neuron types have distinct functions, yet for a long time this was difficult to ascertain, due to the inability to examine and manipulate them in the brains of living beings.

In recent years, opened new possibilities for studying cells and their functions. Using some of these techniques, researchers at Forschungszentrum Jülich, RWTH Aachen University, Cold Spring Harbor Laboratory and other institutes in the United States closely examined the functions of different pyramidal cells, which are commonly found in the human cortex.

Their findings, published in Nature Neuroscience, suggest that distinct types of pyramidal cells drive patterns of cortical activity associated with different functions. The team’s study builds on some of their previous works focusing on in the cortex.

Synchron’s BCI is inserted through the blood vessels, which Oxley calls the “natural highways” into the brain. Synchron’s stent, called the Stentrode, is fitted with tiny sensors and is delivered to the large vein that sits next to the motor cortex. The Stentrode is connected to an antenna that sits under the skin in the chest and collects raw brain data that it sends out of the body to external devices.

Peter Yoo, senior director of neuroscience at Synchron, said since the device is not inserted directly into the brain tissue, the quality of the brain signal isn’t perfect. But the brain doesn’t like being touched by foreign objects, Yoo said, and the less invasive nature of the procedure makes it more accessible.

“There’s roughly about 2,000 interventionalists who can perform these procedures,” Yoo told CNBC. “It’s a little bit more scalable, compared to, say, open-brain surgery or burr holes, which only neurosurgeons can perform.”

Early critiques pointed out that proving a network was near the critical point required improved statistical tests. The field responded constructively, and this type of objection is rarely heard these days. More recently, some work has shown that what was previously considered a signature of criticality might also be the result of random processes. Researchers are still investigating that possibility, but many of them have already proposed new criteria for distinguishing between the apparent criticality of random noise and the true criticality of collective interactions among neurons.

Meanwhile, over the past 20 years, research in this area has steadily become more visible. The breadth of methods being used to assess it has also grown. The biggest questions now focus on how operating near the critical point affects cognition, and how external inputs can drive a network to move around the critical point. Ideas about criticality have also begun to spread beyond neuroscience. Citing some of the original papers on criticality in living neural networks, engineers have shown that self-organized networks of atomic switches can be made to operate near the critical point so that they compute many functions optimally. The deep learning community has also begun to study whether operating near the critical point improves artificial neural networks.

The critical brain hypothesis may yet prove to be wrong, or incomplete, although current evidence does support it. Either way, the understanding it provides is generating an avalanche of questions and answers that tell us much more about the brain — and computing generally — than we knew before.

A research team from LKS Faculty of Medicine, the University of Hong Kong (HKUMed) has developed thyroid hormone (TH)–encapsulated nanoparticles modified with an adipose-homing peptide, which selectively transports TH to adipose tissues. This will advance the treatment of obesity-related medical complications with TH by overcoming the severe adverse effects caused by systemic administration. The new findings are now published in Nature Communications.

Obesity is a major risk factor for multiple life-threatening such as diabetes and cardiovascular and neurodegenerative disorders. TH is an ancient hormone with therapeutic potential for obesity and its related medical complications by promoting energy expenditure. However, despite enormous research efforts in the past decades, have failed to demonstrate obvious clinical benefits of chronic systemic administration of TH on in obese individuals.

Furthermore, due to widespread expression of TH receptors, systemic administration of TH often leads to serious deleterious effects on multiple organs, including tachycardia, , muscle wasting, and osteoporosis. Skeletal muscle and adipose tissues are thought to be the two major target organs where TH exerts its stimulatory actions on metabolic rate and energy expenditure. However, whether selective delivery of TH to adipose tissues is sufficient to induce weight loss remains unclear.