Life begins at 40 (Home)

Using infrared cameras, surgically implanted electrocardiograms, and radio transmitters, Barnes and his team monitored hibernating black bears (Ursus americanus) for three years. Think of it as CBS’s Big Brother—except someone actually cared about the bear feeds. Their research showed that bears can drop their heart rate from 55 to 9 beats per minute and reduce their metabolism by an incredible 53 percent. They accomplish this without compromising much on body temperature, a crucial fact that allows bears to be more alert than true hibernators. (Those fancy squirrels can require hours to thaw out.)

Higher body temperatures also allow hibernating bears to keep newborn cubs warm. During a period when most animals are locked in hand-to-hand combat with the bony fists of Death, bears perform the miracle of Life. Bear reproduction is actually sort of a boring story though, so let’s move on to …

I’m kidding, of course. Bear reproduction is all kinds of curious. The coitus occurs in spring or summer, when many animals are already giving birth. The male is aided by a penis bone called a baculum, which is not attached to the rest of the skeleton. (Baculi are rather common among mammals, from walruses and chimps to cats and bats. Because the Internet is a wonderful, horrible place, you can purchase baculi online, where they are marketed improbably as Mountain Man Toothpicks. Humans do not have penis bones, alas. Just the euphemism.)

After bears rock it in the usual way, the reproductive process takes a hard left from everything you learned in that sex-ed class taught by the school gym teacher. Following fertilization, the baby bears stop growing after becoming multicelled blastocysts. For a few months, they just float around in a state of arrested development known as delayed implantation. Should the female bear fail to fatten up enough over the course of the year, her body can put the kibosh on pregnancy in an act of self-preservation. Conversely, if times are good, her body will allow more blastocysts to develop and implant in her womb—adjusting the number of cubs created based on fat stores.

Even though the deed is done months ahead of time, active gestation is surprisingly short—just 60 days in polar bears—and this results in helpless, underdeveloped cubs that are usually born between November and February, depending on the species and climate. Super-rich milk ensures that by the time spring comes, the cubs are ready to hit the ground running in a life-or-death race to rotundness. Polar bear milk contains up to 46 percent fat and tastes like the chalky cream of a fishy cow. And how do we know what it tastes like? Well, because polar bear scientists like Andrew Derocher are absurdly dedicated dudes. (click through to read the whole thing)

Photo by Kaisa Siren/AFP/Getty Images(via Do bears hibernate: Polar bear, black bear, grizzly bear sex and torpor. - Slate Magazine)

a-a-a-a-a-a-a-a-a:

(Photo from Scientific American, click through to read the story)

From Scientific American, an article about a real life Bones and MacArthur genius grant recipient- Mercedes Doretti. An Argentinian anthropologist who got her start in forensic anthropology following the collapse of the Argentinian dictatorship in 1982, she’s now working to find answers for families of migrants who have disappeared. In her words:

What we are trying to do with the Missing Migrants program that we started in 2009 is improve the search of missing migrants among unidentified remains by creating a regional exchange system. 

(Source: aa-teeth)

Amanda, I think the circular areas in the kidney pancake were meant to represent the medulla, which has a somewhat triangular/pyramidal shape in the human kidney.

This 2 hour special about the periodic table and the elements is airing tonight on PBS (9 p.m EDT).

A SHOUT OUT TO -periodic-meltdowns- ESPECIALLY!

(via NOVA | Hunting the Elements)

mabelmoments:

Photograph: Courtesy of Emiko Paul and Quade Paul/ Echo Medical Media; Ron Gamble/UAB Insight/Science. 2011 International Science & Engineering Visual Challenge

Tumour death-cell receptors on breast cancer cell (Illustration – Honorable Mention). This artist’s illustration shows a monoclonal antibody (green) developed by scientists at the University of Alabama binding to a ‘death cell receptor’ on a cancer cell (top left). This triggers the cell’s inbuilt suicide program (apoptosis).

It looks like a setting for a sci-fi movie.

(I wish those monoclonal antibodies were as super specific as the researchers would like them to be. They seem to end up hitting receptors on cells you don’t want taken out.)

Desertmar asked about the big spider trees and the reduction of malaria. I’m filching the nice caption explaining the life cycle of the organisms that cause malaria, Plasmodium spp. Plasmodium is a protozoa that requires mosquitoes to be vectors to spread the organism and needs them (as well as the human) to go through the life cycle and multiply.  Mosquito nets can be extremely helpful in areas with malaria to reduce exposure to mosquitoes.  I also remember when we learned about sickle cell anemia in various classes in vet school that sickle cell anemia is prevalent in people who live in areas (or have ancestry) where malaria is prevalent.  The Plasmodium organism can’t live in a sickled red blood cell and I remember hearing about it being an adaptation (albeit not a good adaptation) to the disease.  That kind of not so great adaptation is thought to be behind cystic fibrosis which is a mutation of a chloride channel in the cell (and is prevalent in people who live or have ancestry in places where cholera is/was endemic). I could say more but then I’ll never publish this post and instead frantically keep trying to edit the draft and then finally give up.

Here’s lots of info about malaria at the CDC website.

(I can’t really help with the spider thing - *shudder*)

The P.vivax life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host (1). Sporozoites infect liver cells (2) and either enter a dormant hypnozoite state or mature into schizonts (3), which rupture and release merozoites (4). After this initial replication in the liver (exo-erythrocytic schizogony A), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony B). Merozoites infect red blood cells (5). The ring stage trophozoites mature into schizonts, which rupture releasing merozoites (6). Some parasites differentiate into sexual erythrocytic stages (gametocytes) (7). Blood stage parasites are responsible for the clinical manifestations of the disease.

The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal (8). The parasites’ multiplication in the mosquito is known as the sporogonic cycle (C). While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes (9). The zygotes in turn become motile and elongated (ookinetes) (10) which invade the midgut wall of the mosquito where they develop into oocysts (11). The oocysts grow, rupture, and release sporozoites (12), which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites (1) into a new human host perpetuates the malaria life cycle. (via Plasmodium vivax)

mabelmoments:

Toxoplasma gondii requires the cat digestive system for reproduction, so it hitches a ride in a rat (photo: flickr user cobalt123)

The Parasite That Makes a Rat Love a Cat

The life cycle of the parasite Toxoplasma gondii goes like this: Toxoplasma reproduces inside the intestine of a cat, which sheds the parasite in its feces. Rats then ingest the parasite when they consume food or water contaminated with cat feces. The parasite takes up residence in the rat’s brain and, once the rat gets eaten by a cat, it starts the cycle all over again.

Researchers have known for a few years that a rat infected with Toxoplasma loses its natural response to cat urine and no longer fears the smell. And they know that the parasite settles in the rat’s amygdala, the part of the brain that processes fear and emotions. Now a new study in the journal PLoS ONE adds another bizarre piece to the tale: When male rats infected with Toxoplasma smell cat urine, they have altered activity in the fear part of the brain as well as increased activity in the part of the brain that is responsible for sexual behavior and normally activates after exposure to a female rat.

The double messages of “you smell a cat but he’s not dangerous” and “that cat is a potential mate” lure the rat into the kitty’s deadly territory, just what the parasite needs to reproduce. Scientists still don’t know how the parasite works to alter the brain, though there apparently is a link to production of dopamine, an important neurotransmitter in the systems for decision-making and reward.

That’s fascinating.

mabelmoments:

These are skeletons of victims of the Black Death from East Smithfield, London. Scientists have extracted fragments of bubonic plague DNA from their teeth. Fragments of 700-year-old DNA from the bug responsible for the Black Death have been pulled from the teeth of four plague victims buried in east London. Scientists used the degraded strands to reconstruct the entire genetic code of the deadly bacterium. It is the first time experts have succeeded in drafting the genome of an ancient pathogen, or disease-causing agent. The researchers found that a specific strain of the plague bug Yersinia pestis caused the pandemic that killed 100 million Europeans - between 30% and 50% of the total population - in just five years between 1347 and 1351. Picture: Museum of London Archaeology /PA

It’s amazing that the DNA isn’t completely degraded after all that time.  It would be interesting to know what virulence factors were in that particular strain.