Science Ain't So Bad

THE NOTORIOUS BULLS EYE

TICKS

Dear Mister SASB, I live out in the woods with three dogs. I get a lot of ticks on me. No Lyme disease yet but it’s just a matter of time!!! Is there anything I should do? – WoodyLane5

Image credits” Yersinia Pestis. 
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A WORLD OF THEIR OWN

Some people’s senses are “crossed”. One sets off another. The F key on the piano is baby blue in color. Chanel Number Five perfume sounds like a waterfall. Your smelly pooch?

Not going there.

It’s called synesthesia. People with this “problem” live in a special, often delightful, world  where a person’s senses  interact with each other in strange ways, turning life into a symphony/smorgasbord that others can only try to imagine. Intriguing scents  mix with visual cues, sounds with the sensation of touch. Sometimes just two senses combine, sometimes more. Taste and sight. Sound and sight and smell and touch. And, since adding colors or sounds or tastes or smells to a word does make the word (or number) more memorable, synesthetes have amazing memories. Very creative, too.

Degas, Mozart, Stevie Wonder, Duke Ellington, Tessler, Sibelius. Even Richard Feynman and Marilyn Monroe were synesth…

synesth..

whatever!

In case you’re wondering, most synesthetes don’t think it’s so bad. Many don’t realize they’re different  unless someone points it out. And the memory/creativity thing is a nice plus.  A gift, some of them say.

So.

So Dr Devin Terhune and Dr Roi Cohen Kadosh(Current Biology) were curious. They wondered why some people have this “gift” and others have to read about it.  They studied one of the most common forms – the one where words or numbers combine with colors.

Working with volunteers, the two scientists used magnetic or electrical stimulation to control the excitability of the visual cortex  - the part of the brain most associated with vision. They adjusted things just to the point where their subjects started to see light flashes. What the study showed, is that the visual cortex of a synesthete is more easily excited.

Much more easily.

Apparently, this shows that synesthete brains are in a sort of hyper excited state. A clue, perhaps.

This is boutique science. Five subjects. All synesthetes. Maybe that’s not enough to justify sweeping conclusions.  Since there’s no clamor for a pill to cure synesthesia there isn’t much money but, Terhune and Kadosh did good. This is interesting stuff and it does teach something about the brain. Change the excitability and  the colors disappear.

Could this technique be used in reverse ? Could it turn Mister ScienceAintSoBad into a synesthete ? Wouldn’t that be fun? For a little while?

ScienceAintSoBadRating = 7.

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NO SUCH THING AS PEOPLE POX!

Mr. and Mrs. ScienceAintSoBad are off on a trip to see relatives but, first, a short article.

I’ll try to make it good.

CHICKENPOX AND SUNLIGHT

Dr. Phil Rice (University of London) looked at the results of 25 studies from different parts of the world about chickenpox. Do some regions have more chickenpox than other, he wondered?  And, if so, does it depend on humidity? Does it depend on temperature?

The amount of chickens?

Nothing,nothing and nothing.

Could it have something to do with the amount of sunlight?

Bingo! The more sunlight there is, the less chickenpox.

This isn’t news to people who are experts in this field. They figured this might be true. After all, UV light is used to sterilize stuff, right? But this is actual evidence. Science is an evidence game. Now it’s okay to say that chickenpox doesn’t like sunlight. And people who live where it’s sunny may escape the disease and its zitzs.

So?

So Dr. Rice didn’t exactly fall all over himself being specific but he does say there must be some way that this could lead to new methods for reducing the spread of chickenpox.

I hear the motor running. I’ll see you next time.

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Image credits to Hikingartist.comFrits Ahlefeldt-Laurvig and flickr.

This work is licensed under a Creative Commons Attribution-NoDerivs 3.0 Unported License.

GERMS

Nobody has anything good to say about plagues so it’s probably good that antibiotics came along with their ability to knock off bacteria. Viruses are a whole other deal, though. They’re so small that bacteria couldn’t see them without a microscope.

If bacteria had eyes.

Viruses drift around acting dead which, I guess, they are since they don’t eat, excrete, make babies, and wriggle around like living things (such as bacteria) do. But they’re not quite as dead as you might like. They have a very obnoxious trick. If  the right virus happens to come into contact with a  cell, it can use its shape to fool the cell into opening up its protective membrane and letting it in. Which is the mistake of a lifetime for that cell since the virus quickly winds up in charge. The cell loses its right to vote. Even worse,  the virus starts making  copies of itself, using the cell’s equipment. If this happens to your cells, you “have” a virus. This is how people wind up with HIV, for example. (Please don’t tell me they have to take their clothes off first; I happen know that.)

VIRUSES VS BACTERIA

There are many antibiotics that work against bacteria. Researchers keep trying to invent new ones. It’s a cat and mouse thing. We get a great antibiotic going and the bacteria figure a way to fool it.  It is true that there’s a  fear that we’re losing our edge over bacteria; some think that the miseries of ancient times will return but MISTER ScienceAintSoBad thinks that won’t happen.

Bacteria, however,  are old news. The new frontier is viruses; they have been a harder nut to crack. Only in the the last few years have there been any drugs at all. How do you get at the virus to kill it? After all, it’s living in your cells; you don’t want to kill THEM do you?

See the problem?

Todd Rider  (MIT’s Lincoln Laboratory) has a new approach. His drug, DRACO, goes after a type of RNA that’s only present in virus infected cells. DRACO would be a “broad spectrum” antiviral drug, meaning it would (or should) work against pretty much any virus. Which could mean the end of the common cold as well as the end of the common HIV infection and the end of herpes in all of its rotten forms and many, many other great, great things. Early results are exciting. With  luck,  licensing and human trials will follow.

How do we feel about this potentially fantastic development? ScienceAintSoBadRating = 10.

We’re wishin’ on your star, Todd Rider.

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Credits for the above image? Mister ScienceAintSoBad created that work of art. My vision of a pink germ.

MAKING SICKLE CELL GO AWAY

Mice. You can’t live with’em.  And you can’t get pissed off every time they get cured.

What is it THIS time? Well, it sounds pretty great, actually. Stuart Orking  of Harvard Medical School has been working with mice that have sickle cell disease which is a wretched, painful disease that can cause back pain, abdominal pain, skin ulcers, and a long list of other stuff including organ failure (yes, that’s fatal).  Dr. Orking’s mice (like humans with sickle cell)  make the wrong kind of hemoglobin -hemoglobin s – which causes red blood cells to become sickle shaped (sickle cell, get it?).

Isn’t this WHY we invented science? To DO something about bad things? Knowing just to know is nice. But doing good trumps just knowing over here at ScienceAintSoBad. I hope you understand.

So.

CURE

Oh yes! That’s what I said. Cure. Just for mice. But this is one that WILL lead to practical therapies. Here’s how it works.

Fetuses don’t get sickle cell. It’s only when they switch over to adult type hemoglobin (few months old)  that they – the babies with the bad gene –  start making  the wrong kind of hemoglobin. If they had stuck with fetal hemoglobin, they would have been fine. Fetal hemoglobin doesn’t lump up;  and it  moves oxygen around the body just like its grown up version does.

This is where Stuart Orking comes into the  the picture. Orking, also of Children’s Hospital Boston and Dana Farber (I wouldn’t want to leave anybody out), figured out how to get a protein called BCL11A to shut up. Once he silenced the protein, fetal hemoglobin reemerged and the mice were, basically, cured of their sickle cell disease. There’s no reason this shouldn’t work on humans. Now Orking has to figure out how to do this in a practical way – some type of drug, I imagine, – and do it on beings that have better health plans than mice.

IN THE MEANTIME

No need to despair. There are, currently, drugs that can help sickle cell disease. Not a cure. But, for many people, they do a lot of good. Take good care of yourself. Better days are coming.

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Credit for the above image? Moi.