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The CDC recommends the flu vaccine for nearly everyone over the age of 6 months (Photo Credit: James Gathany, Centers for Disease Control and Prevention)

Should you get vaccinated for the flu this year? Yes, says the Centers for Disease Control and Prevention, and they have fewer qualifiers than usual for that recommendation.

Until now, the CDC has recommended the vaccine only for people in specific “high-risk” groups (such as children, the elderly and those with compromised immune systems) and those who may come in contact with high-risk individuals (such as doctors and nurses). If you were, say, 30 and healthy and didn’t come into contact with kids, you could be vaccinated but weren’t urged to do so.

This year, however, the CDC is urging everyone over the age of 6 months to be vaccinated (with exceptions for people who may be allergic to the vaccine or have had a bad reaction to one in the past).

The change comes, in part, because the H1N1 flu virus hit younger adults particularly hard last year, and that group was unlikely to be vaccinated against flu in previous years. Also, it was sometimes difficult for people to know if they fell into a high-risk group; it’s easier just to tell everyone to get the vaccine.

This year’s vaccine has been engineered to protect against the flu strains most likely to be troublesome this season: H1N1, H3N2 (a type of influenza A) and an influenza B strain. Even if people were vaccinated against H1N1 and/or last year’s seasonal flu, they’ll still need to get this year’s vaccine.

“In an average year, there are more than 200,000 hospitalizations and more than 35,000 deaths from flu. Many of those would be preventable by simply getting the flu shot,” said David Weber, a medical professor at the University of North Carolina Chapel Hill. “Flu shots are far and away the best way for preventing flu.”

Grrlscientist posted this video, of a mercury fountain that can be found at the Fundació Joan Miró museum in Barcelona, last week and said “I think this is supposed to be art, but it’s kinda scary art, if you ask me.”

Humans have long been fascinated by this liquid metal, but it wasn’t until 1866 that it was first identified as being toxic to humans when two lab techs died of dimethyl mercury posioning. But the danger wasn’t truly recognized until after the mid-1950s. That’s when people around Minamata Bay in Japan began to act strangely. Some would stumble as they walked or have uncontrollable tremors. Others had difficulty writing or swallowing. Twenty people died. Medical researchers eventually identified mercury-contaminated fish and shellfish as the cause. The bay was laced with decades of mercury released by a nearby plastics plant.

Today mercury is heavily regulated, so how could a mercury fountain exist? Well, you can’t see it in the video, but a glass wall protects people from the art. And the employee who cleans the exhibit wears what the security guard calls an “astronaut suit.”

This hasn’t always been the setup, however. The mercury fountain was created by American artist Alexander Calder in 1937 for the Spanish pavilion at the Paris World’s Fair (Exposition Internationale des Arts et Techniques dans la Vie Moderne). Spain wanted to highlight the town of Almadén, home to the world’s oldest and largest mercury mine and displayed the fountain prominently in the pavilion near Pablo Picasso’s Guernica.

A newborn Kihansi spray toad sits on the back of a female (Credit: Julie Larsen Maher/Wildlife Conservation Society)

The Kihansi spray toad (Nectophrynoides asperginis) is a fairly new species to science, discovered only in 1996. There were once as many as 21,000 of the toads living in a five-acre region around Kihansi Falls in the Udzungwa Mountains of eastern Tanzania. They could be found nowhere else in the world and are particularly special because the females give birth to fully formed baby toads, bypassing the tadpole stage.

About a decade ago, a dam built upstream cut off 90 percent of the flow of water to the region. Artificial sprinklers were set up to mimic the natural spray of the falls, but they were unreliable. This may have made the toads more susceptible to the chytrid fungus, which was detected in dead Kihansi spray toads in 2003. The sprinklers failed that year and a brief opening of the dam’s floodgates released water tainted with pesticides at high enough levels to potentially kill the toads. The Kihansi spray toad population crashed. In January 2004, just three toads could be found, and none have been seen since an unconfirmed sighting in 2005. The IUCN now lists the species as Extinct in the Wild.

Two populations of the toads now live in zoos: 5,000 at the Toledo Zoo and 1,500 at the Bronx Zoo. A third population was established just this week at a facility in Dar Es Salaam, Tanzania, as part of a program established by the two U.S. zoos, the Tanzanian government and the World Bank. One hundred toads were transferred to the Tanzanian facility in the hopes that they soon may be reintroduced to their previous home territory.

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Though we may call catnip “kitty crack,” the herb is non-addictive and isn’t even a drug (so it’s perfectly safe to give to your kitty, big or small). But how does it work? And why doesn’t it have any effect on humans?

Catnip comes from plants of the Nepeta genus. These plants are a type of mint and produce a host of volatile oils and other chemicals. To us, they just smell a little sweet, but most cats have a different reaction. They roll around, rub their heads and bodies on whatever you’ve stuffed with the herb, and often act as if they’ve been smoking some kind of illegal substance. Veterinarian Ramona Turner explained how catnip elicits these reactions a few years ago in Scientific American:

Many cats, big and little, react to catnip (photo by Sarah Zielinski)

Nepetalactone, one of catnip’s volatile oils, enters the cat’s nasal tissue, where it is believed to bind to protein receptors that stimulate sensory neurons. These cells, in turn, provoke a response in neurons in the olfactory bulb, which project to several brain regions including the amygdala (two neuronal clusters in the midbrain that mediate emotional responses to stimuli) and the hypothalamus, the brain’s “master gland” that plays a role in regulating everything from hunger to emotions.

The amygdala integrates the information flow from the olfactory bulb cells and projects to areas governing behavior responses. The hypothalamus regulates neuroendocrine responses through the pituitary gland, creating a “sexual response.” That is, the cat essentially reacts to an artificial cat pheromone.

This reaction lasts for about 5 to 15 minutes and then a cat is immune for an hour or so. Kitties don’t react to the stuff until they’re about six months old, when they reach sexual maturity. And not all cats are affected—sensitivity to catnip is an inherited trait, and only about 70 to 80 percent of house cats will react. (I couldn’t find statistics for big cat species, but we can see in the video above, from Big Cat Rescue, that it works on at least some individuals.)

Humans don’t react in the same way because our brains are different. In us, nepetalactone acts more like valepotriates, the compounds in the herb valerian that are a mild sedative in most people. So if you can’t sleep, you can try drinking catnip tea, if you can keep from laughing at your kitty rolling crazily across the floor.

Snow's map led him to the source of a London cholera outbreak in 1854 (via wikimedia commons)

I started reading about cholera over the weekend after hearing that health officials had confirmed several cases of the disease among victims of the recent Pakistani floods. Cholera is a bacterial disease that produces diarrhea and vomiting; people with the disease can die within hours if they don’t get treatment. About 3 million to 5 million people suffer from cholera each year, mostly in developing countries, and 100,000 die from it, according to the World Health Organization.

This led me to the history of cholera and John Snow. Snow is credited with the discovery that cholera is transmitted through sewage-tainted water. His map of London’s Soho region (right) is often reproduced in biology textbooks with the story of how he made his discovery. Snow mapped out the cases of cholera during an 1854 outbreak and determined where each of the infected families obtained their water. He would later write:

I found that nearly all the deaths had taken place within a short distance of the [Broad Street] pump. There were only ten deaths in houses situated decidedly nearer to another street-pump. In five of these cases the families of the deceased persons informed me that they always sent to the pump in Broad Street, as they preferred the water to that of the pumps which were nearer. In three other cases, the deceased were children who went to school near the pump in Broad Street…

With regard to the deaths occurring in the locality belonging to the pump, there were 61 instances in which I was informed that the deceased persons used to drink the pump water from Broad Street, either constantly or occasionally…

The result of the inquiry, then, is, that there has been no particular outbreak or prevalence of cholera in this part of London except among the persons who were in the habit of drinking the water of the above-mentioned pump well.

The Broad Street well, Snow concluded, was contaminated with cholera (it was later found to have been built near an old cesspit). The well’s pump handle was removed and the cholera outbreak ended. This is where most textbooks end. But there’s a second part to the story—Snow’s Grand Experiment.

There were parts of London that received their water from two distinct sources, the Southwark-Vauxhall Company and the Lambeth Waterworks Company. This was an ideal set-up for Snow for an experiment. Both companies drew water from the Thames, but Lambeth’s intake was farther upriver—and thus less likely to be contaminated with the city’s sewage—than Southwark-Vauxhall’s.

Snow compiled data on the two sets of London households and found that during an 1854 epidemic there were 315 deaths from cholera per 10,000 homes among those supplied by Southwark-Vauxhall but only 37 deaths per 10,000 Lambeth homes.

That would seem to be a slam dunk in the research world, but Snow had gotten his numbers not from an extensive house-to-house search, which would have been too much work for even a team of men, but from a less-precise parliamentary report. Neither Snow nor many of his detractors believed his results were strong enough to make the case that cholera was related to water supply.

A few years ago, Thomas Koch and Kenneth Denike, of the University of British Columbia, re-evaluated the Grand Experiment and found even more problems with his methods and statistics. “The grand experiment … was a failure,” Kock recently told The Scientist.

The irony, of course, is that Snow was right. As cities cleaned up their water supplies over the subsequent decades, cholera ceased being such a problem. But with more than a billion people worldwide lacking access to clean drinking water, the disease will remain with us for years to come.