Wednesday, July 3, 2013

Travelling at the Speed of Light Could Make Your Ass Look Great

Travelling at the Speed of Light Could Make Your Ass Look Great

Next time you're trying to squeeze into your skinny jeans, it might pay to give physics a thought?because depending on how fast you're travelling, you fat frame could look a little different. Randall Munroe explains in the mouse-over text of today's XKCD:

"It's commonly believed that Lorentz contraction makes objects appear flatter along the direction of travel. However, this ignores light travel times. In fact, a fast-moving butt would appear rotated toward the observer but not substantially distorted."

Still, every little helps, right? Now you just need to find a spaceship that can go fast enough to make you look good. [XKCD]

Source: http://gizmodo.com/travelling-at-the-speed-of-light-could-make-your-ass-lo-655333617

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6 Radical Infrastructure Schemes That Almost Changed NYC Forever

6 Radical Infrastructure Schemes That Almost Changed NYC Forever

The East River? Oh, we dammed that thing up and threw a new City Hall on top. The Hudson? Filled it with traffic years ago. New Yorkers have never been prudes about changing the natural landscape of their city, but if you dig into the archives, you'll find dozens of ideas so radical, they make present-day Gotham feel like a nature reserve.

Read more...

    


Source: http://feeds.gawker.com/~r/gizmodo/full/~3/AgzWdVBFXNY/6-radical-infrastructure-schemes-that-almost-changed-ny-636053287

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Tuesday, July 2, 2013

Cancer is a result of a default cellular 'safe mode,' physicist proposes

June 30, 2013 ? With death rates from cancer have remained largely unchanged over the past 60 years, a physicist is trying to shed more light on the disease with a very different theory of its origin that traces cancer back to the dawn of multicellularity more than a billion years ago.

In this month's special issue of Physics World devoted to the "physics of cancer," Paul Davies, principal investigator at Arizona State University's Center for Convergence of Physical Sciences and Cancer Biology, explains his radical new theory.

Davies was brought in to lead the centre in 2009 having almost no experience in cancer research whatsoever. With a background in theoretical physics and cosmology, he was employed to bring fresh, unbiased eyes to the underlying principles of the disease.

He has since raised questions that are rarely asked by oncologists: thinking about why cancer exists at all and what place it holds in the grand story of life on Earth.

His new theory, drawn together with Charles Lineweaver of the Australian National University, suggests that cancer is a throwback to an ancient genetic "sub-routine" where the mechanisms that usually instruct cells when to multiply and die malfunctions, thus forcing the cells to revert back to a default option that was programmed into their ancestors long ago.

"To use a computer analogy, cancer is like Windows defaulting to 'safe mode' after suffering an insult of some sort," Davies writes.

The result of this malfunction is the start of a cascade of events that we identify as cancer -- a runaway proliferation of cells that form a tumour, which eventually becomes mobile itself, spreading to other parts of the body and invading and colonizing.

Orthodox explanations suppose that cancer results from an accumulation of random genetic mutations, with the cancer starting from scratch each time it manifests; however, Davies and Lineweaver believe it is caused by a set of genes that have been passed on from our very early ancestors and are "switched on" in the very early stages of an organism's life as cells differentiate into specialist forms.

The pair suggests that the genes that are involved in the early development of the embryo -- and that are silenced, or switched off, thereafter -- become inappropriately reactivated in the adult as a result of some sort of trigger or damage, such as chemicals, radiation or inflammation.

"Very roughly, the earlier the embryonic stage, the more basic and ancient will be the genes guiding development, and the more carefully conserved and widely distributed they will be among species," Davies writes.

Several research teams around the world are currently providing experimental evidence that shows the similarities between the expression of genes in a tumour and an embryo, adding weight to Davies and Lineweaver's theory.

Davies makes it clear that radical new thinking is needed; however, just like ageing, he states that cancer cannot generally be cured but can be mitigated, which we can only do when we better understand the disease, and its place in the "great sweep of evolutionary history."

Source: http://feeds.sciencedaily.com/~r/sciencedaily/most_popular/~3/p6KiNvaRN-s/130630225413.htm

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Selena Gomez Wardrobe Malfunction: Cover That Thing Up!

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Shut down of cell survival process found to influence fate of lung cancer tumors

July 1, 2013 ? New research from Rutgers Cancer Institute of New Jersey, Princeton University and other collaborators suggests that inactivation of an essential gene responsible for the cell survival process known as autophagy can suppress the growth of non-small-cell lung cancer tumors and render them more benign. The findings suggest a possible role for autophagy blockers in the treatment of this type of lung cancer, which has a five-year survival rate of only 30 to 50 percent for early-stage disease.

Previous research from the laboratories of the senior authors Eileen P. White, PhD, associate director for basic science at the Cancer Institute of New Jersey and Joshua D. Rabinowitz, MD,PhD, professor of chemistry at Princeton University and Cancer Institute of New Jersey member, revealed that autophagy dependence is prevalent in cancers with Ras mutations. These mutations are activated in aggressive cancers with poor outcomes, such as lung. In this current study, published in the latest online and print versions of Genes & Development, Drs. White and Rabinowitz and other investigators used mouse models to examine non-small-cell lung cancer tumors driven by activating mutations in the K-Ras cancer gene.

In order to survive times of stress and grow, cancer cells eat themselves. In blocking this self-preservation mechanism of autophagy, cancer cells are stripped of the self-sustaining energy provided through the powerhouse of the cell -- the mitochondria. Investigators found in this current study that in the absence of autophagy, or when it is defective, dysfunctional mitochondria accumulate and what once was a malignant tumor becomes a rare, predominantly benign tumor known as an oncocytoma.

The authors also found that the processes necessary for autophagy are influenced by the p53 tumor suppressor gene. When researchers disabled the autophagy gene, the tumor suppressing mechanism of p53 was prematurely activated, thus halting cancer growth and spread. When p53 was removed, investigators determined that Ras-driven tumors are dependent on autophagy to preserve mitochondrial and other functions that help maintain cell viability when changes with the external cell environment are present.

"In finding that autophagy can influence the fate of non-small-cell lung cancer tumors, the possibility now exists to target that mechanism in the treatment of this disease," noted White, who is also a professor of molecular biology and biochemistry at Rutgers University.

Along with White, the author team consists of Jessie Yanxiang Guo and Gizem Karsli-Uzunbas, Rutgers Cancer Institute of New Jersey; Robin Mathew, Cancer Institute of New Jersey and Rutgers Robert Wood Johnson Medical School; Seena C. Aisner, Cancer Institute of New Jersey and Rutgers New Jersey Medical School; Jurre J. Kamphorst, Princeton University; Anne M. Strohecker, Cancer Institute of New Jersey and Robert Wood Johnson Medical School; Guanghua Chen and Sandy Price, Cancer Institute of New Jersey; Wenyun Lu and Xin Teng, Princeton University; Eric Snyder, MIT and Brigham and Women's Hospital; Urmila Santanam, Cancer Institute of New Jersey; Robert S. DiPaola, Cancer Institute of New Jersey and Robert Wood Johnson Medical School; and Tyler Jacks, MIT.

The study was supported in part by grants from the National Institutes of Health (R37 CA53370 and RO1 CA 130893 to White, RC1 CA 147961 to White and Rabinowitz), the Department of Defense (W81XWH-09-01-0394 to DiPaola and White) and the Val Skinner Foundation.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/top_health/~3/Azq29JKDGhg/130701080838.htm

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Brain differences seen in depressed preschoolers

July 1, 2013 ? A key brain structure that regulates emotions works differently in preschoolers with depression compared with their healthy peers, according to new research at Washington University School of Medicine in St. Louis.

The differences, measured using functional magnetic resonance imaging (fMRI), provide the earliest evidence yet of changes in brain function in young children with depression. The researchers say the findings could lead to ways to identify and treat depressed children earlier in the course of the illness, potentially preventing problems later in life.

"The findings really hammer home that these kids are suffering from a very real disorder that requires treatment," said lead author Michael S. Gaffrey, PhD. "We believe this study demonstrates that there are differences in the brains of these very young children and that they may mark the beginnings of a lifelong problem."

The study is published in the July issue of the Journal of the American Academy of Child & Adolescent Psychiatry.

Depressed preschoolers had elevated activity in the brain's amygdala, an almond-shaped set of neurons important in processing emotions. Earlier imaging studies identified similar changes in the amygdala region in adults, adolescents and older children with depression, but none had looked at preschoolers with depression.

For the new study, scientists from Washington University's Early Emotional Development Program studied 54 children ages 4 to 6. Before the study began, 23 of those kids had been diagnosed with depression. The other 31 had not. None of the children in the study had taken antidepressant medication.

Although studies using fMRI to measure brain activity by monitoring blood flow have been used for years, this is the first time that such scans have been attempted in children this young with depression. Movements as small as a few millimeters can ruin fMRI data, so Gaffrey and his colleagues had the children participate in mock scans first. After practicing, the children in this study moved less than a millimeter on average during their actual scans.

While they were in the fMRI scanner during the study, the children looked at pictures of people whose facial expressions conveyed particular emotions. There were faces with happy, sad, fearful and neutral expressions.

"The amygdala region showed elevated activity when the depressed children viewed pictures of people's faces," said Gaffrey, an assistant professor of psychiatry. "We saw the same elevated activity, regardless of the type of faces the children were shown. So it wasn't that they reacted only to sad faces or to happy faces, but every face they saw aroused activity in the amygdala."

Looking at pictures of faces often is used in studies of adults and older children with depression to measure activity in the amygdala. But the observations in the depressed preschoolers were somewhat different than those previously seen in adults, where typically the amygdala responds more to negative expressions of emotion, such as sad or fearful faces, than to faces expressing happiness or no emotion.

In the preschoolers with depression, all facial expressions were associated with greater amygdala activity when compared with their healthy peers.

Gaffrey said it's possible depression affects the amygdala mainly by exaggerating what, in other children, is a normal amygdala response to both positive and negative facial expressions of emotion. But more research will be needed to prove that. He does believe, however, that the amygdala's reaction to people's faces can be seen in a larger context.

"Not only did we find elevated amygdala activity during face viewing in children with depression, but that greater activity in the amygdala also was associated with parents reporting more sadness and emotion regulation difficulties in their children," Gaffrey said. "Taken together, that suggests we may be seeing an exaggeration of a normal developmental response in the brain and that, hopefully, with proper prevention or treatment, we may be able to get these kids back on track."

Funding for this study comes from the National Institute of Mental Health (NIMH) of the National Institutes of Health (NIH). It also was supported by the Klingenstein Third Generation Foundation and the Communities Healing Adolescent Depression and Suicide (CHADS) Coalition for Mental Health. NIH Grant number K23 MH098176.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/mind_brain/mental_health/~3/AaeiMK91sSk/130701172022.htm

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QUIZ: Celebrity Yearbook Photos: Guess Who's Who!

Test your skills and see if you can recognize the A-listers from their school days!

Source: http://www.ivillage.com/celebrity-yearbook-photos-1/1-b-380559?dst=iv%3AiVillage%3Acelebrity-yearbook-photos-1-380559

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