An update on the Vivaldi browser

The more I use Vivaldi, the more I like it. I have now made it my default browser. When you install, get the full package with Notes and Calendar and the rest. It’s feature-rich, so don’t expect to learn it all at once, but day by day and bit by bit it becomes better and better as you learn more and more how to use it.

Also, important point: it’s free.

It’s Not Just Us: Even American Animals Are Getting Fatter

David Epstein had an interesting article back in October 2013. I came across it this morning. It begins:

Everyone knows Americans are fat and getting fatter, and everyone thinks they know why: more eating and less moving.

But the “big two” factors may not be the whole story. Consider this: Animals have been getting fatter too. The National Pet Obesity Survey recently reported that more than 50 percent of cats and dogs—that’s more than 80 million pets—are overweight or obese. Pets have gotten so plump that there’s now a National Pet Obesity Awareness Day. (It was Wednesday.) Lap dogs and comatose cats aren’t alone in the fat animal kingdom. Animals in strictly controlled research laboratories that have enforced the same diet and lifestyle for decades are also ballooning.

In 2010, an international team of scientists published findings that two dozen animal populations—all cared for by or living near humans—had been rapidly fattening in recent decades. “Canaries in the Coal Mine,” they titled the paper, and the “canaries” most closely genetically related to humans—chimps—showed the most troubling trend. Between 1985 and 2005, the male and female chimps studied experienced 33.2 and 37.2 percent weight gains, respectively. Their odds of obesity increased more than 10-fold.

To be sure, some of the chimp obesity crisis may be caused by the big two. According to Joseph Kemnitz, director of the Wisconsin National Primate Research Center, animal welfare laws passed in recent decades have led caretakers to strive to make animals happier, often employing a method known to any parent of a toddler: plying them with sugary food. “All animals love to eat, and you can make them happy by giving them food,” Kemnitz said. “We have to be careful how much of that kind of enrichment we give them. They might be happier, but not healthier.”

And because they don’t have to forage for the food, non-human primates get less exercise. Orangutans, who Kemnitz says are rather indolent even in their native habitats in Borneo and Sumatra, have in captivity developed the physique of spreading batter.

Still, in “Canaries in the Coal Mine,” the scientists write that, more recently, the chimps studied were “living in highly controlled environments with nearly constant living conditions and diets,” so their continued fattening in stable circumstances was a surprise. The same goes for lab rats, which have been living and eating the same way for thirty years.

The potential causes of animal obesity are legion: ranging from increased rates of certain infections to stress from captivity. Antibiotics might increase obesity by killing off beneficial bacteria. “Some bacteria in our intestines are associated with weight gain,” Kemnitz said. “Others might provide a protective effect.”

But feral rats studied around Baltimore have gotten fatter, and they don’t suffer the stress of captivity, nor have they received antibiotics. Increasingly, scientists are turning their attention toward factors that humans and the wild and captive animals that live around them have in common: air, soil, and water, and the hormone-altering chemicals that pollute them.

Hormones are the body’s chemical messengers, released by a particular gland or organ but capable of affecting cells all over the body. While hormones such as testosterone and estrogen help make men masculine and women feminine, they and other hormones are involved in a vast array of functions. Altering or impeding hormones can cause systemic effects, such as weight gain.

More than a decade ago, Paula Baille-Hamilton, a visiting fellow at Stirling University in Scotland who studies toxicology and human metabolism, started perusing scientific literature for chemicals that might promote obesity. She turned up so many papers containing evidence of chemical-induced obesity in animals (often, she says, passed off by study authors as a fluke in their work) that it took her three years to organize evidence for the aptly titled 2002 review paper: “Chemical Toxins: A Hypothesis to Explain the Global Obesity Epidemic.” “I found evidence of chemicals that affect every aspect of our metabolism,” Baille-Hamilton said. Carbamates, which are used in insecticides and fungicides, can suppress the level of physical activity in mice. Phthalates are used to give flexibility to plastics and are found in a wide array of scented products, from perfume to shampoo. In people, they alter metabolism and have been found in higher concentrations in heavier men and women.

In men, phthalates interfere with the normal action of testosterone, an important hormone for maintaining healthy body composition. Phthalate exposure in males has been associated with a suite of traits symptomatic of low testosterone, from lower sperm count to greater heft. (Interference with testosterone may also explain why baby boys of mothers with higher phthalate levels have shorter anogenital distances, that is, the distance between the rectum and the scrotum. Call it what you want, fellas, but if you have a ruler handy and find that your AGD is shorter than two inches, you probably have a smaller penis volume and a markedly higher risk of infertility.)

Baille-Hamilton’s work highlights evidence that weight gain can be influenced by endocrine disruptors, chemicals that mimic and can interfere with the natural hormone system.

A variety of flame retardants have been implicated in endocrine disruption, and one chemical originally developed as a flame retardant—brominated vegetable oil, or BVO—is banned in Europe and Japan but is prevalent in citrusy soft drinks in the U.S. Earlier this year, Gatorade ditched BVO, but it’s still in Mountain Dew and other drinks made by Gatorade’s parent company, PepsiCo. (Many doctors would argue that for weight gain, the sugar in those drinks is the primary concern.) PepsiCo did not respond to a request for comment, but shortly after the Gatorade decision was made a company spokeswoman said it was because “some consumers have a negative perception of BVO in Gatorade.”

And then there are the newly found zombie chemicals, which share a nasty habit—rising from the dead at night—with their eponymous horror flick villains. The anabolic steroid trenbolone acetate is used as a growth promoter in cattle in the U.S., and its endocrine disrupting metabolites—which wind up in agricultural run-off water—were thought to degrade quickly upon exposure to sunlight. Until last month, when researchers published results in Science showing that the metabolites reconstitute themselves in the dark. . .

Continue reading. Endocrine disruptors — for example, the microscopic plastic particles now commonly found in seafood — are very bad because their effect is amplified by natural bodily processes: a tiny amount can have a large effect.

Giant Viruses and the Tree of Life

Patrick Forterre writes in Inference:

SCIENTISTS HAVE ALWAYS thought viruses much smaller than bacteria. And with good reason. Most bacteriophages are 100 times smaller than the bacteria that they infect. Bacteria can be viewed under an optical microscope; but an electron microscope is required in order to see a viral particle. When giant viruses were discovered in 2003, they came as a surprise. The giant mimivirus, for example, had actually been discovered in 1992, but misidentified as a bacterium—Bradfordcoccus.¹ The confusion was understandable. Mimivirus particles are 750 nanometers long—easily visible with an optical microscope; and, what is more, the dye used to reveal bacterial cell walls also stained mimivirus particles.

A number of other monster viruses have been discovered in the last decade.² Most of them have been isolated and described by Didier Raoult and Jean-Michel Claverie in Marseille. If Marseille is now the Mecca of giant virus research, Vancouver is something of a mini Mecca. It is there that Curtis Suttle and his team isolated and described both Cafeteria roenbergensis and Bodo saltans.³ Most giant viruses observed in the laboratory have been studied in amoebae,⁴ but giant viruses are found in extraordinarily diverse terrestrial and aquatic environments.⁵ Some infect algae, and there is some suspicion that the mimivirus infects human cells as well.⁶ All giant viruses infect eukaryotes.

Viruses closely related to the mimivirus have been grouped into the family Mimiviridae. The other giant viruses have been classified into three families: Molliviridae, Pandoraviridae, and Pithoviridae.

Mimiviridae and Molliviridae produce virions, or viral particles, with a characteristically icosahedral shape. Pandoraviridae and Pithoviridae produce strange ovoid particles that have often been confused for intracellular protists.⁷ One of the most unusual of the giant viruses is a member of Mimiviridae. Discovered in Brazil, the Tupanvirus contains a virion featuring a gigantic head and an equally gigantic membranous tail. Such a shape is without precedent in the viral world.

Giant viruses contain linear or double-stranded DNA that encode for 500 to 2,500 proteins. The Pandoravirus encodes 2,000 genes, which is only 10 times fewer than a human cell, and, at roughly 2.5 million base pairs, its genome is the largest of any known virus. The mimivirus genome encodes about half that number. Produced by a Pithovirus, the largest known virion is an ovoid particle with a length of 1.5 micrometers and a width of 0.5 micrometers. The size of a virion and the size of its genome are not necessarily correlated. They are no good guide to the threshold beyond which a virus is counted giant.⁸

Five years after giant viruses were discovered, researchers learned that giant viruses can themselves become infected by smaller viruses.⁹ The virophages that infect them have genomes that code for only about twenty genes. These virophages, unable to infect amoebae by themselves, are transported inside amoebae by their giant virus hosts.¹⁰ Once inside, the virophages transcribe and replicate their genes using the machinery of the giant virus, the giant virus then using the amoeba’s machinery to transcribe and replicate its own genes.¹¹ The three known virophages—Mavirus, Sputnik, and Zamilon—happen to infect members of the Mimiviridae family, but virophages targeting other giant viruses are likely to be identified.

Frankenlike

THE DISCOVERY OF giant viruses and their virophages immediately reopened an old question: are viruses alive? Viruses had been excluded from the tree of life because they lacked the machinery needed either to reproduce or to synthesize proteins. A virus must hijack a cell before it can do either. But when scientists realized that viruses are more complex than originally presumed—encoding several thousand genes and becoming infected by other viruses—they began to suspect that viruses might be alive after all. When a virophage infects a Mimiviridae, it seems to become ill, its virions manifesting an abnormal morphology.

How can something be ill if it is not alive?¹²

Viruses had been excluded from living systems for another reason. They did not seem to share proteins that are universal across the three cellular domains: Archaea, Bacteria, and Eukarya. Yet many giant viruses do encode universal proteins, including RNA polymerase, some aminoacyl tRNA synthetases, and a few proteins involved in protein synthesis or DNA replication. Some phylogenetic analysts now place giant viruses in a fourth monophyletic group somewhere between Archaea and Eukarya.¹³ For all that, the fact remains that giant viruses lack the capacity to synthesize their own proteins without parasitizing a cell. Purificación López-García and David Moreira have thus disputed the phylogenetic analysis behind the phylogenetic analysts, arguing that the giant viruses are nothing more than genetic pickpockets, their genes acquired from a cellular origin in yet another triumph of theft over honest toil.¹⁴

Chantal Abergel and Claverie have also argued for the cellular origin of viral genes. But they have noticed, in addition, that most of the genes that giant viruses encode lack homologues in both modern cellular organisms and giant viruses from other families. Giant viruses, they suggest, might have arisen by regressive evolution—features lost instead of gained—from cellular lineages that diverged from modern cellular organisms before the advent of the last universal common ancestor of Archaea, Bacteria, and Eukarya. Claverie predicts that, as new giants are discovered, the distinction between viruses and cells will blur even further.¹⁵

Virus, Virion, and Virocell

WHEN IN DOUBT, define. The existence of giant viruses prompted virologists to search for a definition that could encompass the whole range of viruses, from the smallest, with genomes encoding two genes, to the largest, encoding thousands. All viruses produce virions—a viral particle consisting of a core of nucleic acid surrounded by a capsid protein shell.¹⁶ It is the capsid that distinguishes viruses from other mobile genetic elements, such as plasmids. The smallest virus and the smallest plasmid both have one gene coding for a replication protein. The virus has an additional gene that codes for a capsid.¹⁷

All virions have at least one capsid. For this reason, Raoult and I initially suggested defining viruses as capsid-encoding organisms.¹⁸ Some small virions are formed by one or more DNA- or RNA-binding proteins; others, by several capsid proteins, with a lipid membrane inside or outside the shell. The virions of giant viruses are elaborate structures involving hundreds of proteins and a lipid membrane that is often decorated with polysaccharide extensions. Virions and viruses are not the same thing. Confusion between the two is pervasive. The confusion is easy to understand. Virions can be easily isolated, they are infectious, and they can be photographed.

But they are not viruses.

Claverie was the first to emphasize the distinction.¹⁹ Within the cytoplasm of an infected cell, the mimivirus produces a large compartment called a viral factory, where the viral DNA, while being transcribed and replicated, is shielded from the cell’s defense mechanisms. Many RNA and DNA viruses produce viral factories.²⁰ But in the mimivirus, the factory is huge—the size of the infected amoeba’s nucleus. Claverie suggested that the viral factory is the actual virus, and that virions are the equivalent of the spores or gametes of cellular organisms.²¹

After Claverie published this argument, I observed that bacterial and archaeal viruses do not produce an isolated viral factory inside the cytoplasm of the infected cell: they transform the entire cell into a factory.²² I suggested calling the infected cell a virocell.²³ Adopting Claverie’s idea, I argued that . . .

Continue reading. There’s more.

eVTOL aircraft makes little noise

Loz Blain reports in New Atlas on an interesting electric plane:

Lilium’s eVTOL is vastly different to anything else in the air taxi world, using 36 small ducted fans in place of larger open rotors. This has advantages and disadvantages, which we’ve discussed in detail before. Essentially, smaller fans make for vastly lower hover efficiency, but the company says they create less drag than large rotors in forward flight, improving efficiency over longer range flights.

Lilium also says they’ll make these aircraft much easier to scale up to 15 seats and beyond without losing the ability to land on standard helipads.

And it also says that with cutting-edge acoustic treatment they should have a significantly lower noise signature than large-rotor competitors, which will make them much more friendly to people living under the flight path or close to a vertiport.

Now, the company has released a pair of videos showing its 5th-generation tech demonstrator prototype – an older 5-seat model first flown in 2019 – in flight with the sound included, one of which handily gives a measure of distance as the aircraft approaches. It’s more a measure of the quality of the sound than the quantity; there’s no decibel readout, and really nothing to compare the volume against. Take a look: . .

Continue reading. There’s more, including more videos.

A great shave and a shaving cream finding

Yesterday’s shave was a disappointment in the lather department. I thought one possibility was that I had used insufficient cream, since the bead of cream from that tube was thin, but I thought I should do a comparison. D.R. Harris shaving products are excellent, so I brought out this tube of D.R. Harris Rose — and it, too, produced a thin bead of cream, so I could match the amount to what I used yesterday. And I also used a small brush today, just as I did yesterday.

The amount and brush a match, but not the lather. The D.R. Harris lather was thick, plentiful, and fragrant. I have discarded yesterday’s shaving cream: great package, poor performance.

Well-lathered and already feeling good about the shave, I set to work with my Above the Tie R (now called R1), and three passes later applied a good splash of D.R. Harris Pink After Shave. A good way to start the day.

Airless tires: Getting closer

Loz Blain reports in NewAtlas:

We’ve been reporting on Michelin’s airless tire technology for more than 16 years now. Indeed, the first time we wrote about the “Tweel” back in 2005, it quickly became the most popular story ever for what was then called gizmag.com.

The advantages are pretty clear: firstly, you can never be brought to a stop by a puncture or blowout – Michelin says about 200 million tires every year hit scrapyards early thanks to these. Secondly, you don’t have to look after your tire pressures; that doesn’t just save you time, it also eliminates all early wear caused by underinflation.

Their internal spokes are hugely tunable to meet desired performance characteristics. You can individually tune their stiffness under acceleration, braking, cornering and bump handling forces. The bump handling characteristics can even be tuned to eliminate the need for separate suspension in some types of vehicles.

You can poke holes right through the tread to let water escape, potentially creating much better resistance to aquaplaning. They take less raw material and less energy to make, making them better for the environment, and Michelin has estimated they’ll last up to three times as long as a regular ol’ hoop.

They have obviously not been easy to commercialize, though; 16 years and counting is a long and difficult birth for a product people are clearly interested in. The Tweel, which replaces the entire wheel assembly, has been available for some time for various off-road vehicles, but it’s still yet to make it to the road.

Michelin has teamed up with GM to design and start selling an airless tire for street use on passenger cars. Called Uptis, this product is a full-wheel solution requiring specialized rims. Michelin says it will withstand much greater impacts than a regular tire and wheel, and will have a “dramatically” longer lifespan, while adding no extra rolling resistance, not feeling any different to the driver and adding only around seven percent to the weight of the wheel – less than existing run-flat tires do.

GM will begin offering Uptis as an option on . . .

Continue reading.