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Ebola–One Plane Away

July 2, 2014

While we fret over childish court rulings, and homeless children dare to cross our borders, the spread of Ebola virus gets buried. For true heroism, nothing beats Doctors Without Borders–for months, the main source of care and treatment in a growing epidemic. So far the disease has struck Guinea, Liberia and Sierra Leone. Most of our Google news feeds relegate the disease below the first screen on our monitors. But experts say it’s just one plane flight away from Paris. Yes, a place that “matters” (sarcasm).

What makes Ebola virus so deadly? An RNA virus, Ebola has a relatively simple structure, just eight genes encoding proteins. The small RNA  is coiled within a flexible tubular protein capsid. The main host cells the virus can infect are white blood cells, liver cells, and endothelial cells–cells that line the blood vessels. That’s quite a deadly combination. By infecting the white blood cells, the Ebola virus disrupts the immune system, avoiding effective defense. Also, the cells carry the virus through the blood, all throughout the body. When the endothelial cells get infected, the blood vessels leak. More from my post in April.


Disco Clam

June 26, 2014

With so much strife in the world, it’s a relief to know that scientists have solved one of nature’s great mysteries: the disco clam. The disco clam, Ctenoides ales, appears to flash lightning bolts within its mouth. Young scientist Lindsey Dougherty at Berkeley has figured out the mechanism of this light display. Note that her research on this project involved “high speed video, transmission electron microscopy, spectrometry, energy dispersive x-ray spectroscopy and computer modeling.” Funded by the National Science Foundation, among several conservation organizations.

So how does it work? Not bioluminescence; that is, there is no biological light organ that emits its own light, like a firefly or the jellyfish Aequorea. Instead, the lip of the clam grows to form a narrow edge that scatters light–only from one side. The edge contains miniature balls of silica (glass) that efficiently reflect and scatter light. So as the lip moves the light appears to flash on and off, like the facets of a disco ball.

Does the clam use this flashing for anything useful? The next stage of research is to figure out if clams use the light signals to communicate. Great possibilities for science fiction.

The Sloths are Coming

June 23, 2014

Appropriately, this story took three years to crawl into my consciousness. The world’s slowest creature, the sloth, turns out to be the cutest.

A fascinating question: What kind of selective pressure favors slowness? Avoiding energy loss? The faster you move, the less efficient you are. We all know that from everyday experience–the faster you try to clear the table, the more likely you drop a dish.

Anyway, these lucky sloths at the Aviarios Sloth Sanctuary in Costa Rica don’t seem to have such problems.

The absolute opposite of Costa Rica’s awesome soccer team.

Bionic Pancreas

June 16, 2014

Our bodies are machines; and one failed part can mean we never wake up. So now we try to replace a failing part with something we design. The classic case is diabetes, in which the pancreas fails to produce insulin on demand. In this case, the father of an insulin-dependent boy designed an artificial insulin regulator.

It’s actually not the whole pancreas, which has many functions besides insulin. But the device monitors blood sugar and readjusts the hormone levels. Blood sugar monitors already exist; what is new about the “bionic pancreas” is that it not only monitors the sugar, it responds by pumping insulin (lowers glucose) or glucagon (raises glucose) as needed.

Will we see more and more of such devices? The current device (still in testing) addresses a life-threatening condition; for an entire lifetime, the patient must monitor their own glucose 24/7, every moment of the day. It will be interesting to see, though, how many such devices begin to augment our bodies, picking up for failing functions–or adding new ones.

Window into Brain Sleep

June 8, 2014


Sleep builds learning and memory. Many studies show this–and we keep telling students that sleep will improve their grades. But how does it work? Here’s an actual window into a mouse brain, watching what might be new memories form.

At the NYU Skirball Institute (as typed, not “Screwball”) researchers Wen-Biao Gan and colleagues tested a mouse genetically modified to express Yellow Fluorescent Protein (YFP) in its brain neurons. This means that one of the mouse’s own genes in the DNA was fused to a DNA sequence encoding the fluorescent YFP; so the mouse’s own cells make the protein. Now, the researchers cut a window into the mouse’s skull, which enables them to put a microscope up to the brain and record photons coming out of YFP. Thus, one can take live pictures of individual mouse brain neurons as they grow.

How does the experiment work? First, mice are trained to learn a new task, how to climb upon a rotating bar. After learning this challenging task, the mice take a nap. That is, they are allowed to sleep as they wish for 8 hours, or else sleep-deprived for 8 hours. How the mice were sleep-deprived is described as “gentle handling” — not sure what that means. I would think 8 hours of hiphop music and fending off drunk bros would work better.

The bottom line is that:

  • After training, the microscope at the brain window detects neurons forming new “dendritic spines,” that is, branches on the nerve dendrites that may form new connections with other neurons–part of learning and stabilizing a new task or memory.
  • Mice that get to sleep form  more dendritic spines than mice that are sleep-deprived. Presumably, the well-rested mice learn their tasks better.

Much food for thought when planning your schedule next fall.


Amazon versus Hachette

May 29, 2014


Anyone living outside a box has heard by now of the megabattle between Amazon and Hachette over who gets to pocket more of the readers’ money. As the NY Times (to which I quaintly subscribe) so aptly put it, Amazon “promises a world where books are cheap, where anyone can publish anything,” whereas Hachette “is holding fast to the traditional publishing system that underpins modern culture.” So there.

Put that way, the choice could not be more stark–between good, and, well, something else good. It’s Godzilla versus MUTO–but who is which? And what about those two little people running underneath–Writer and Reader?

Ultraphyte has no real answers, but some thoughts.

  • Publishers do a lot for authors; more than most realize. Blockbusters make up for the myriad titles that never pay back their advance. Good editors help some authors reach the bar of professional communication. And good marketers promote works that would not otherwise get noticed.
  • Does the publisher’s work merit more than half the cover price? Even for ebooks? Do authors really want overpriced ebooks–or are we better off with lower price, larger volume?
  • Does the “added value” of a “traditional publisher” really merit the current backlog, approaching two years at my publisher? When anyone  could post it overnight on a website?
  • Lower price, larger volume, quicker publication all favor Amazon. But what happens when they’re the only game in town? Do we really expect them to just win and go home like Godzilla?

Personally, I’ve cheered Amazon for years as the place where all my “out of print” books could be found forever, and where I could find anything else out there. If selling kitchen and hardware stuff subsidizes books (one of the claims) so be it.

But I’d also like to see more competition. So, for the moment at least, I’ve switched my book links (at right) to Barnes and Noble.

Tell me what you think.



Microbial News at ASM

May 24, 2014

So what did we all learn at ASM, the American Society for Microbiology meeting 2014?

  • Bacteria you eat may prevent osteoporosis (bone thinning). Don’t all go out and buy probiotics, because health foods are unregulated and make outrageous claims. However, Lactobacillus reuteri makes a hormone-like molecule that does prevent bone thinning in mice. We saw slides of bones with and without. Furthermore, the bone-protective molecule inhibits development of cells that eat bone (osteoclasts). The doctors think that if post-menopausal women consume L. reuteri in some form, it may maintain bone density with fewer side effects than estrogen treatments.
  • Bacteria have a sense of touch. Before they make biofilms (multicellular communities), bacteria can “feel” the surface they touch using touch-sensitive proteins. How the touch transduction works, we still don’t understand.
  • Bacteria tell eukaryotic microbes to become multicellular bodies. Much evidence shows how bacteria and viruses activate key steps of embryonic development and immune system maturation. Now, a case has been shown in which marine bacteria tell unicelled eukaryotes called choanoflagellates to join together in rosettes.

The choanoflagellates then eat the bacteria–or do they? Do some of the bacteria take up residence?
Leading to the hypothesis that bacteria invented multicellular life to provide them a home.

  • More evidence for the bacterial home hypothesis: Human placenta contains specific bacteria. A few percent of the placental mass consist of normal bacteria, related to those of our mouths. These normal placental bacteria are actually needed for normal birth.
  • Even the deadly fungus Cryptococcus can provide a way to treat brain diseases. Cryptococcus makes an enzyme (a metal-containing protease) that can sneak its way across the blood-brain barrier. We may be able to use this enzyme to help us get therapeutic drugs into the brain.
  • Some bacteria may signal the gut via cannabinoid receptors. Getting ahead of my science fiction story, where the alien invaders take over Earth by spreading cannabinoids.

Alas, though, the “don’t floss” suggestion from previous post turned out to be a joke. Yes, keep flossing, despite the researchers who adore the dental bacteria they study.


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