(Source: atomstargazer)

Einstein’s Voice?

Well, listen as Albert Einstein reads you a scientific essay. It’s his voice, in your ears, from 1941, reading his essay ‘The Common Language of Science’.

Click Here : http://is.gd/O4s3F5
More Recordings At: http://is.gd/CMzE1S

Benefits Of Bike Riding

When they invented the bike for the first time, they had no idea that a time will come when it will have all these benefits, otherwise its price would have been too high to afford! — Here is my new infographic on the “Benefits Of Bike Riding”…

➤ Runs on Fat Not Fuel
➤ Reduces Stress
➤ Reduces Risk of Diabetes
➤ Reduces Risk of Blood Pressure
➤ Increases Muscle Tone
➤ Gives You Legs of Steel
➤ Helps You See The World Differently
➤ Unlimited Free Parking
➤ Faster & Easier Than Walking
➤ Zero Emission
➤ No Noise Pollution
➤ It Feels Like Flying
➤ It Carries Your Goodies Home
➤ Whizzes Past Traffic Jams
➤ Puts A Big Fat Smile on Your Face
➤ Bye Bye Spare Tire
➤ Reduces Roadkill & Saves Animals

Enlarge This Graphic : http://is.gd/FSF6R8

(Source: atomstargazer)

These photographs document several of the various types of mould which can be found growing on your average loaf of bread, given enough time and neglect. I am interested in the inherent contradiction of finding aesthetic beauty in something almost universally perceived as disgusting. I was also fascinated by the extraordinary structure and microscopic nature of these life forms, something that those of us not involved in the biological sciences are probably only vaguely aware of.

 

(Source: scienceyoucanlove)

Desert ‘fairy circles’ mystery solved

Termites appear to be feeding on the grass roots to create the characteristic rings, but scientists aren’t sure why termites are eating in circles.

(Source: mothernaturenetwork)

Periodial Cicadas Coming to U.S. East Coast This Spring

Periodical cicadas (Magicicada septendecim), the cousins of katydids and crickets, have a unique breeding schedule, and after 17 years of living underground, a large group of them are preparing to fill the skies along the U.S. East Coast, from North Carolina up to Connecticut.

Normally, periodic cicadas spend their lives in complete darkness underground, sucking the fluid out of the roots of trees and shrubs. At the end of their life, they emerge, breed, and almost instantly die, completing a lifecycle that humans have studied for centuries….

Cicadas are easy to anticipate because of their extremely consistent mating behavior. Every 13 or 17 years, depending on the population, species of periodic cicadas will emerge as part of a specific brood in order to look for a mate.

The group expected this spring, known as Brood 2, are the offspring of cicadas last seen in 1996. If they follow the same tracks as their parents, they’ll emerge in Connecticut, Maryland, North Carolina, New Jersey, New York, Pennsylvania, Virginia, and Washington, D.C.

The genetic mechanism that prompts periodical cicadas to emerge kicks in every 17 years (or every 13 years for other broods) when the ground warms up to 64°F (18°C).

Some researchers think the timing of a brood’s emergence is a defensive mechanism—appearing at infrequent intervals means that it’s harder for would-be predators like birds and squirrels to anticipate when the insects will be available to eat.

Others suggest that the 13- and 17-year cycles, prime numbers in mathematics, help cicadas avoid parasites. A 2004 study from the University of Campinas in Brazil suggested that a cicada with a 17-year cycle and a parasite with a two-year cycle, for example, would meet only twice each century.

But not all cicadas breed on this multiyear cycle. Some, like the tibicen cicadas, work on an annual rotation, leaving them more susceptible to predators like the cicada killer wasp (Sphecius speciosus).

The wasps know exactly when to expect the annual cicadas in late summer or early fall. The wasp lays its eggs on the cicadas, and the larvae slowly kill the cicada and feed off its carcass.

(Read more)

(Source: dendroica)

TSA: *perplexed, talking to another agent*

TSA: “….it’s not a threat” *tilts head*

me: “is that my bag?”

TSA: “yeah, what is that?”

me: “it’s a telescope”

TSA: “a telescope, ohh, it’s the whole thing…”

me: “yeah, just without the tripod”

TSA: “how powerful is that telescope?”

me: *laughs* “it’s only a few mirrors, ma’m”

astrogasmic:

(via wildlydistorted)

The science of how your mind-wandering is robbing you of happiness.

(Source: http, via explore-blog)

New Insights on How Spiral Galaxies Get Their Arms

Spiral galaxies are some of the most beautiful and photogenic residents of the universe. Our own Milky Way is a spiral. Our solar system and Earth reside somewhere near one of its filamentous arms. And nearly 70 percent of the galaxies closest to the Milky Way are spirals.

But despite their common shape, how galaxies like ours get and maintain their characteristic arms has proved to be an enduring puzzle in astrophysics. How do the arms of spiral galaxies arise? Do they change or come and go over time?

Read More.

(Source: christinetheastrophysicist)

New clues about how amyotrophic lateral sclerosis (ALS) develops

Role of cells other than motor neurons much larger than anticipated

Johns Hopkins scientists say they have evidence from animal studies that a type of central nervous system cell other than motor neurons plays a fundamental role in the development of amyotrophic lateral sclerosis (ALS), a fatal degenerative disease. The discovery holds promise, they say, for identifying new targets for interrupting the disease’s progress.

In a study described online in Nature Neuroscience, the researchers found that, in mice bred with a gene mutation that causes human ALS, dramatic changes occurred in oligodendrocytes—cells that create insulation for the nerves of the central nervous system—long before the first physical symptoms of the disease appeared. Oligodendrocytes located near motor neurons—cells that govern movement—died off at very high rates, and new ones regenerated in their place were inferior and unhealthy.

The researchers also found, to their surprise, that suppressing an ALS-causing gene in oligodendrocytes of mice bred with the disease—while still allowing the gene to remain in the motor neurons—profoundly delayed the onset of ALS. It also prolonged survival of these mice by more than three months, a long time in the life span of a mouse. These observations suggest that oligodendrocytes play a very significant role in the early stage of the disease.

“The abnormalities in oligodendrocytes appear to be having a negative impact on the survival of motor neurons,” says Dwight E. Bergles, Ph.D., a co-author and a professor of neuroscience at the Johns Hopkins University School of Medicine. “The motor neurons seem to be dependent on healthy oligodendrocytes for survival, something we didn’t appreciate before.”

“These findings teach us that cells we never thought had a role in ALS not only are involved but also clearly contribute to the onset of the disease,” says co-author Jeffrey D. Rothstein, M.D., Ph.D., a professor of neurology at Johns Hopkins and director of the Johns Hopkins Medicine Brain Science Institute.

Scientists have long believed that oligodendrocytes functioned only as structural elements of the central nervous system. They wrap around nerves, making up the myelin sheath that provides the “insulation” that allows nerve signals to be transmitted rapidly and efficiently. However, Rothstein and others recently discovered that oligodendrocytes also deliver essential nutrients to neurons, and that most neurons need this support to survive.

The Johns Hopkins team of Bergles and Rothstein published a paper in 2010 that described in mice with ALS an unexpected massive proliferation of oligodendrocyte progenitor cells in the spinal cord’s motor neurons, and that these progenitors were being mobilized to make new oligodendrocytes. The researchers believed that these cells were multiplying because of an injury to oligodendrocytes, but they weren’t sure what was happening. Using a genetic method of tracking the fate of oligodendrocytes, in the new study, the researchers found that cells present in young mice with ALS were dying off at an increasing rate in concert with advancing disease. Moreover, the development of the newly formed oligodendrocytes was stalled and they were not able to provide motor neurons with a needed source of cell nutrients.

To determine whether the changes to the oligodendrocytes were just a side effect of the death of motor neurons, the scientists used a poison to kill motor neurons in the ALS mice and found no response from the progenitors, suggesting, says Rothstein, that it is the mutant ALS gene that is damaging oligodendrocytes directly.

Meanwhile, in separate experiments, the researchers found similar changes in samples of tissues from the brains of 35 people who died of ALS. Rothstein says it may be possible to see those changes early on in the disease and use MRI technology to follow progression.

“If our research is confirmed, perhaps we can start looking at ALS patients in a different way, looking for damage to oligodendrocytes as a marker for disease progression,” Rothstein says. “This could not only lead to new treatment targets but also help us to monitor whether the treatments we offer are actually working.”

ALS, also known as Lou Gehrig’s disease, named for the Yankee baseball great who died from it, affects nerve cells in the brain and spinal cord that control voluntary muscle movement. The nerve cells waste away or die, and can no longer send messages to muscles, eventually leading to muscle weakening, twitching and an inability to move the arms, legs and body. Onset is typically around age 50 and death often occurs within three to five years of diagnosis. Some 10 percent of cases are hereditary.

There is no cure for ALS and there is only one FDA-approved drug treatment, which has just a small effect in slowing disease progression and increasing survival. 

Even though myelin loss has not previously been thought to occur in the gray matter, a region in the brain where neurons process information, the researchers in the new study found in ALS patients a significant loss of myelin in one of every three samples of human tissue taken from the brain’s gray matter, suggesting that the oligodendrocytes were abnormal. It isn’t clear if the oligodendrocytes that form this myelin in the gray matter play a different role than in white matter—the region in the brain where signals are relayed.

The findings further suggest that clues to the treatment of other diseases long believed to be focused in the brain’s gray matter—such as Alzheimer’s disease, Huntington’s disease and Parkinson’s disease—may be informed by studies of diseases of the white matter, such as multiple sclerosis (MS). Bergles says ALS and MS researchers never really thought their diseases had much in common before.

Oligodendrocytes have been under intense scrutiny in MS, Bergles says. In MS, the disease over time can transform from a remitting-relapsing form—in which myelin is attacked but then is regenerated when existing progenitors create new oligodendrocytes to re-form myelin—to a more chronic stage in which oligodendrocytes are no longer regenerated. MS researchers are working to identify new ways to induce the creation of new oligodendrocytes and improve their survival. “It’s possible that we may be able to dovetail with some of the same therapeutics to slow the progression of ALS,” Bergles says.

Renowned scientist Stephen Hawking suffers from amyotrophic lateral sclerosis (ALS). 

(Source: neuromorphogenesis)

ScienceCasts: Collision Course? A Comet Heads for Mars
A comet is heading for Mars, and there is a chance that it might hit the Red Planet in October 2014. An impact wouldn’t necessarily mean the end of NASA’s Mars program. But it would transform the program along with Mars itself.

via ScienceAtNASA

“A sense of wonder is not our only starting point. It can also be our destination.”

Sharman Apt Russell | Anatomy of A Rose: Exploring the Secret Life of Flowers