Carbon will still be carbon in 30 years. It can be reclaimed, reused or recycled then.

Pollution from coal plants is killing people, right now.

that could create waste problems in the future unless swift action is taken to make it ready for recycling and reuse.

Air pollution from coal-fired power plants is linked with asthma, cancer, heart and lung ailments, neurological problems, acid rain, global warming, and other severe environmental and public health impacts.

This air pollution includes:

Mercury: Coal plants are responsible for 42 percent of US mercury emissions, a toxic heavy metal that can damage the nervous, digestive, and immune systems, and is a serious threat to the child development. Just 1/70th of a teaspoon of mercury deposited on a 25-acre lake can make the fish unsafe to eat. According to the Environmental Protection Agency’s (EPA) National Emissions Inventory, US coal power plants emitted 45,676 pounds of mercury in 2014 (the latest year data is available).

Sulfur dioxide (SO2): Produced when the sulfur in coal reacts with oxygen, SO2 combines with other molecules in the atmosphere to form small, acidic particulates that can penetrate human lungs. It’s linked with asthma, bronchitis, smog, and acid rain, which damages crops and other ecosystems, and acidifies lakes and streams. US coal power plants emitted more than 3.1 million tons of SO2 in 2014.

Nitrogen oxides (NOx): Nitrous oxides are visible as smog and irritate lung tissue, exacerbate asthma, and make people more susceptible to chronic respiratory diseases like pneumonia and influenza. In 2014, US coal power plants emitted more than 1.5 million tons.

Particulate matter: Better known as “soot,” this is the ashy grey substance in coal smoke, and is linked with chronic bronchitis, aggravated asthma, cardiovascular effects like heart attacks, and premature death. US coal power plants emitted 197,286 tons of small airborne particles (measured as 10 micrometers or less in diameter) in 2014..

Other harmful pollutants emitted in 2014 by the US coal power fleet include:

41.2 tons of lead, 9,332 pounds of cadmium, and other toxic heavy metals.
576,185 tons of carbon monoxide, which causes headaches and places additional stress on people with heart disease.
22,124 tons of volatile organic compounds (VOC), which form ozone.
77,108 pounds of arsenic. For scale, arsenic causes cancer in one out of 100 people who drink water containing 50 parts per billion.

But there is another, equally important argument for transitioning to clean fuels. Tens of thousands of Americans die every year from old-fashioned air pollution, generated by electric power plants that burn fossil fuels. Estimates vary, but between 7,500 and 52,000 people in the United States meet early deaths because of small particles resulting from power plant emissions. That’s huge. It is roughly comparable to the 40,000 people that died in car crashes in 2016.

Goodbye Aberration: Physicist Solves 2,000-Year-Old Optical Problem



When you look through your viewfinder and things seem a little bit blurry or lacking definition, it’s probably because you are using an “el cheapo” lens. So you read reviews and buy a much more expensive lens, and what do you do next?

You don’t go out to learn about composition and lighting to make better pictures. No. If you are a conscious and professional photographer, you start pixel-peeping to rationalize your expensive purchase.

And what do you find then?

The problem is still there. Right there, in the corners. They’re soft. The center is OK, but the corners are still soft. So you read more reviews and buy a better lens.

Lather, rinse, repeat.

But it’s not the manufacturer’s fault, nor yours for not having enough money to buy a perfect lens. Blame Greek mathematician Diocles, who formulated the problem over two thousand years ago in his book Burning Mirrors.

The Problem

You see, lenses are made from spherical surfaces. The problem arises when light rays outside the center of the lens or hitting at an angle can’t be focused at the desired distance in a point because of differences in refraction.

Which makes the center of the image sharper than the corners. Which leads to countless YouTube reviews on lenses. And countless hours of watch time. And makes advertisers and YouTubers happy.

In his 1690 book, Treatise on Light, astronomer Christiaan Huygens points out that both Isaac Newton (the greatest scientist of all time) and Gottfried Leibniz (the last universal genius) tried to solve the problem, but couldn’t:

As has in fact occurred to two prominent Geometricians, Messieurs Newton and Leibnitz, with respect to the problem of the figure of glasses for collecting rays when one of the surfaces is given.

. . .

To this day, when you see that your lens has aspherical elements to correct for optical aberrations and give you sharper images wide open, you can thank Wasserman-Wolf.

. .

After months of working on solving the problem, Rafael González recalls, “I remember one morning I was making myself a slice of bread with Nutella, when suddenly, I said out loud: Mothers! It is there!”

(Note: “Madres” is a Spanish word that means, of course, many moms. But in this context it is equivalent to the expression “Holy sh*t!” in English, or, to a lesser extent, “Eureka!” in Greek.)

He then ran to his computer and started programming the idea. When he executed the solution and saw that it worked, he says he jumped all over the place. It is unclear whether he finished eating the Nutella bread.

Afterwards, the duo ran a simulation and calculated the efficacy with 500 rays, and the resulting average satisfaction for all examples was 99.9999999999%. Which, of course, is great news for gear reviewers on YouTube, as they will still be able to argue about the 0.0000000001% of sharpness difference among lens brands.

Their findings were published in the article General Formula for Bi-Aspheric Singlet Lens Design Free of Spherical Aberration, in the journal Applied Optics.

How many people die annually because they live near clean, quiet power sources?

yet they still die.

But not because of the clean, quiet power. It's not like wind turbines lead to obesity or opioid overdose.

Give it 30 years and they will find it causes something.

I'm in a snarky mode

Researchers discover that the rate of telomere shortening predicts species lifespan

A flamingo lives 40 years and a human being lives 90 years; a mouse lives two years and an elephant lives 60. Why? What determines the lifespan of a species? After analyzing nine species of mammals and birds, researchers at the Spanish National Cancer Research Center (CNIO) found a very clear relationship between the lifespan of these species and the shortening rate of their telomeres, the structures that protect the chromosomes and the genes they contain. The relationship is expressed as a mathematical equation, a formula that can accurately predict the longevity of the species. The study was done in collaboration with the Madrid Zoo Aquarium and the University of Barcelona.

"The telomere shortening rate is a powerful predictor of species lifespan," the authors write in the prestigious journal Proceedings of the National Academy of Sciences (PNAS).

The study compares the telomeres of mice, goats, dolphins, gulls, reindeer, vultures, flamingos, elephants and humans, and reveals that species whose telomeres shorten faster have shorter lives.

The relationship can be fitted to a certain type of mathematical curve—a power law curve—which, the authors explain in PNAS, is also used to describe other processes such as population growth, city sizes, species extinction, body mass, and individual income.

To Maria Blasco, Head of the Telomeres and Telomerase Group of the CNIO and director of the study, the fact that there is such a clear relationship between the rate of telomere shortening and lifespan suggests that "we have found a universal pattern, a biological phenomenon that explains the lifespan of the species, and that warrants more research."

What counts is not their length, but the rate at which they shorten

In the case of the relationship between telomere shortening and species longevity, the curve found by the CNIO researchers fits the data very well. In fact, "the equation can be used to predict the lifespan of the species solely based on the rate of telomere shortening," the authors write. The fit is better when using the average lifespan of the species—79 years in the case of humans—rather than the maximum lifespan, the 122 documented years lived by the Frenchwoman Jeanne Calment.

Evolutionary gene loss may help explain why only humans are prone to heart attacks

Summary:
Scientists say the loss of a single gene two to three million years ago in our ancestors may have resulted in a heightened risk of cardiovascular disease in all humans as a species, while also setting up a further risk for red meat-eating humans.

. . .

In the new study, the Varkis, and Philip Gordts, PhD, assistant professor of medicine, and others report that mice modified to be deficient (like humans) in a sialic acid sugar molecule called Neu5Gc showed a significant increase in atherogenesis compared to control mice, who retain the CMAH gene that produces Neu5Gc.

The researchers -- members of the Glycobiology Research and Training Center and/or the Center for Academic Research and Training in Anthropogeny at UC San Diego -- believe a mutation that inactivated the CMAH gene occurred a few million years ago in hominin ancestors, an event possibly linked to a malarial parasite that recognized Neu5Gc.

In their findings, the research team said human-like elimination of CMAH and Neu5Gc in mice caused an almost 2-fold increase in severity of atherosclerosis compared to unmodified mice.

"The increased risk appears to be driven by multiple factors, including hyperactive white cells and a tendency to diabetes in the human-like mice," said Ajit Varki. "This may help explain why even vegetarian humans without any other obvious cardiovascular risk factors are still very prone to heart attacks and strokes, while other evolutionary relatives are not."

But in consuming red meat, humans are also repeatedly exposed to Neu5Gc, which researchers said prompts an immune response and chronic inflammation they call "xenosialitis." In their tests, human-like mice modified to lack the CMAH gene were fed a Neu5Gc-rich, high-fat diet and subsequently suffered a further 2.4-fold increase in atherosclerosis, which could not be explained by changes in blood fats or sugars.

Doctors and scientists mystified by spread of Candida auris superbug

The emergence of a partially drug-resistant fungal infection in Canadian hospitals and elsewhere has doctors and scientists scrambling to understand the pathogen and stop its spread.

Candida auris was virtually unknown until 2009, but the past decade has seen outbreaks of infection in hospitals and long-term care facilities around the world, predominantly among patients with weakened immune systems, such as people receiving chemotherapy or surgery and those who receive medication through large intravenous lines.

So far C. auris remains relatively rare, said Dr. Isaac Bogoch, an infectious disease physician at Toronto General Hospital. But the fungus, which can cause infections, including of the blood, of wounds and ears, has three main features that make it worrisome to health-care professionals:

It's tricky for some laboratories to identify.
It can be hard to treat successfully when it invades the bloodstream.
It's frequently resistant to one or more classes of antifungal medications that doctors turn to first.

"It poses a bit of challenge to treat, and the reason is there can be delays in diagnosis: conventional labs might not be able to detect that it's Candida auris right away," said Bogoch.

"With the delayed diagnosis, that can often delay appropriate treatment — and if we delay treatment for fungal infection, especially when they're in the blood, people can get very sick, very quickly."

. . .

Why C. auris started spreading widely after it was first spotted a decade ago in the ear of a patient in Japan remains a mystery. (Auris means ear.)

Dr. Tom Chiller, chief of the CDC's Mycotics Diseases Branch, and his colleagues set out to understand its origins, and documented their findings in a commentary published earlier this month in the Journal of Fungi.

To find some clues, Chiller's team peered into the genome of C. auris and related species, and mapped where its been detected in hospitals globally.

. . .

Our normal body temperature of 37 C prevents most fungal species from replicating. But C. auris's genome showed that it has adapted to higher temperatures, said Casadevall, chair of molecular microbiology and immunology at Johns Hopkins Bloomberg School of Public Health in Baltimore. That heat tolerance could contribute to its emergence as a fungal disease in humans.

Casadevall and his colleagues at the University of Texas in Houston and Westerdijk Fungal Biodiversity Institute in Utrecht, Netherlands, suspected the world's warming climate could be contributing.

They brainstormed for a common denominator to explain C. auris's "mystifying" appearance in three very different regions of the world with distinct flora and geographic conditions: South Africa, South America and India.

Not even trying to be funny here but reading the article about C-Auris I kind of harkened back to when AIDS first started going around. Symptoms way different but started off small and bang next thing you knew it was huge and all over the world. I hope we are not looking at the same thing happening here. C-Auris sounds scary as hell.