The research could lead to new treatments for millions of people suffering from common forms of blindness, such as retinitis pigmentosa and age-related macular degeneration, says Rachael Pearson, a Royal Society Research Fellow at University College London.The achievement was hailed by biologist Stephen Rose, chief research officer of the Foundation Fighting Blindness, a private nonprofit that raises money for inherited-retinal-disease research. “We are very happy with it,” he says. “We believe that it’s extremely good work.”

In a paper published on earlier this year in Nature, Pearson and her colleagues describe how they injected immature rods—the cells responsible for peripheral vision and the ability to see at night—into the eyes of mice that had been bred without functioning rods.

In these night-blind mice, the thousands of newly transplanted cells linked up with existing nerve cells in the retina, the layer of light-sensitive tissue in the back of the eye. The researchers had previously proved that transplantation could work; this time they greatly increased the number of transferred cells, boosting the number of apparently functional rod cells 20- to 30-fold. Then, they looked for evidence that the mice actually had better night vision.

Pearson and her team examined the transplanted cells to see whether they responded to light. They also measured electrical activity in the visual cortex of the mice, tracked the mice’s head movements to see whether they would react to patterns on a screen, and plopped them in a water tank to see if they’d swim toward a less than obvious exit. Despite the dim light, the transplanted mice were able to find their way out. “The mice who didn’t have the transplant swam around in circles,” Pearson says. “These mice can’t see in dim light, and so they can’t use any visual cues to escape.”

The trick to getting transplanted rods to function, Pearson says, is to harvest cells that are at just the right stage of development from donor mice. In people, it soon may be possible to cultivate a patient’s own stem cells and turn them into rods and cones. Meanwhile, Pearson and her colleagues are still trying to perfect the process of transplanting cones. “We demonstrated proof of principle a couple of years ago, but currently the numbers we can get to integrate are much lower than with the rods,” she says.

Age-related macular degeneration, the leading cause of blindness in people over 50, gradually damages the macula, the part of the retina responsible for central vision. A National Institutes of Health study estimates that nearly three million Americans will be affected by 2020. An additional 100,000 people in the U.S. suffer from retinitis pigmentosa, a group of inherited diseases that cause the retina to deteriorate.

Successful animal research doesn’t always translate into an effective treatment for humans, Rose cautions. “These are very carefully done studies, very well conducted,” he says. “There’s no reason to believe, from what I’ve seen, that it couldn’t work. But the proof of the pudding is the eating thereof.”

UNTIL A FEW WEEKS AGO I didn’t have the slightest interest in mouse urine. But after some study I’ve concluded that it is covertly running and ruining the world, strangling small children, and driving the profits of Big Pharma.

I came to know mouse urine, the molecules of which are known as MUPs (Major Urinary Proteins), and specifically as Mus m 1, because the molecules were stubbornly clinging to the studs of a cabin that I recently bought. Though I didn’t yet know the molecular names or weights of my MUPs, I knew they were there. Mice had burrowed through the cabin’s fiberglass insulation, and it looked like a splendid and huge pink ant farm.

Mice sort their food; there were larders of pasta, lentils, acorns, and blue poison crystals in my walls. Looking at the elaborate networks in the walls, it’s easy to imagine that my new-old (built in 1939) cabin’s erstwhile owner was a rustic prisoner who suffered respiratory ailments. The mice operated a space-age metropolitan economy in the walls around him, communicating through sophisticated molecular signaling.

Once the mice and the insulation were gone, a ghastly smell remained. So I set to googling the hows and whys, until the basic crystalline structure of our problem (specifically) and the scourge of mouse urine (generally) became clear: field mice, especially males, secrete proteins in their urine to signal to other mice their sex, degree of male dominance, age, and genetic makeup.

Turns out, our walls are a giant social network, a Facebook of old mouse news. And just as Facebook has been designed by diabolical engineers, the molecule Mus m 1 has been designed to stick around, blasting out its code for a very long time. A picture of Mus m 1 looks like an exploded cartoon of a clown—colored curls and a helix. It is barrel-shaped so that it can hold volatile, signaling chemicals and release them slowly over time. MUPs are like graffiti spray-paint: lightweight so they’ll stay airborne, and sticky so they’ll remain on the walls.

You might think that mouse urine is more my problem than yours. Ha! Eighty-two percent of American homes have mups floating about in them. In the inner cities of the Northeast and Midwest, the majority of all homes have mouse-urine proteins, but some of them have concentrations a thousandfold higher than homes in the suburbs. In the Northeast and Midwest we all live in a house made of mice. And that’s a big—very big—problem: mouse-urine proteins can trigger allergies and asthma. (Mouse-urine proteins are clever; they look like other allergens such as ragweed, which, according to the authors of a recent study, may be a trick that has arisen through convergent evolution.)

Dr. Elizabeth Matsui, a pediatrician and an associate professor at Johns Hopkins Children’s Center, started studying mouse urine a decade ago, when she was trying to figure out why a quarter of the kids in some low-income Baltimore neighborhoods have severe asthma. (The national rate is closer to 6 percent.) “If you live in public housing or Section 8 housing or anywhere … you can’t control mice, cockroaches, or other pollutants,” Matsui says. She found that higher exposure to mouse-urine proteins led kids to develop more problematic asthma.

Mice are obviously not the only trigger for asthma—auto pollution, dust, pets, and cockroaches are also on the list—but about half of Matsui’s asthmatic subjects were allergic to mice. (But the immune system is a hairball: Matsui also came across a curious paradoxical effect. Not everyone exposed to high levels of mups becomes allergic; some become immune. High exposure to mouse urine can, in other words, work a bit like allergy-immunotherapy shots, by reshaping the body’s immune response.)

In 2005, kids under 15 made 679,000 visits to emergency rooms for asthma. Currently, our medical remedy focuses on getting kids into long-term treatment with anti-asthma drugs of various sorts, but the mouse urine remains. Which brings me to the mouse-pharmaceutical complex. We currently spend about $50 billion a year in the U.S. on health care costs for asthma, and this is bound to rise as children grow older.

But we aren’t giving kids mouse-free houses.

Without a coordinated public-health response, Matsui says, trying to bring down asthma rates, or even asthma attacks in individual kids, is like playing Whac-A-Mole.

The shaking is a 20-minute session of whole-body vibration developed by the Soviet Union’s space program to prevent muscle and bone loss during long periods of weightlessness. Its reception since has been mixed: Biomechanical stimulation has since been linked to a number of positive effects, such as improved strength and reduced bone loss, even as studies have questioned those claims of improved strength and reduced bone loss. A quick Google search of the term “whole-body vibration” suggests a dab of skepticism might be warranted, with ads shilling machines offering to take the sweat out of fitness far outnumbering, say, analyses from the Mayo Clinic.

The researchers in Georgia were looking at a way to “leverage” the dawning realization that bones are endocrine organs, not to sell exercise gadgets. Dr. Yu, a craniofacial surgeon who heads the plastic and reconstructive surgery section at his university’s medical college,  suggests that the vibration mimics the motion bones get during exercise, and so the body responds as if muscles were busy beavering away. Among those responses to bending bones is the production of a bone-building protein that also tells the pancreas that a meal is likely inbound. The vibration-sponsored bone bending also produced a vast improvement in the mice’s ability to handle inflammation.

Researchers joining Yu found that eight weeks of daily sessions in the mouse-shaker did more to reduce one indicator of glucose levels in the blood than did prescription drugs. In fact, just four days of treatment saw the mice better handling a sugar-surge after a big meal (the mice were, by the way, genetically designed to overeat). Keep in mind that the inability to handle glucose levels properly is essentially shorthand for diabetes. Adding to the general feeling that the experiment might be onto something, diabetes symptoms, such as excessive thirst and diluted urine, were reduced in the lab animals.

The vibrations, however, only worked their magic on young mice—but that’s OK.

“This is our model: the average American teenager who eats too much,” said Yu in a release from Georgia Health Sciences University. The next step for the researchers is to try out whole-body vibration on human adolescents.

There shouldn’t be too much trouble finding human subjects. Besides the epidemic of teen obesity—more than 37 percent in Georgia, for example—creating lots of roly-poly kids, Yu reports his subjects seemed to enjoy being vibrated.

But too often, people suffering from anxiety disorders fail to respond to the all-clear signal. This leaves them in an ongoing state of heightened tension, which—if it lasts long enough, or gets triggered often enough—can take a severe physical and mental toll. Why are some of us able to relax, while others stay on guard long after any danger has passed?

An answer that could point the way toward breakthrough therapies is emerging from complementary studies of humans and mice. But Ahmad Hariri, a neurobiologist at Duke University, crystallizes the idea with a different animal altogether. He refers to the amygdala, which has been called “the fear center of the brain,” as a sort of watchdog. “A watchdog responds reflexively to threat,” he notes. It’s up to its owner to say ‘That’s enough. I heard you bark. I checked it out. It’s okay.’”

In getting our hearts racing, the amygdala is simply doing its job. For sufferers of PTSD and other anxiety disorders, the dysfunction evidently occurs in another part of the brain altogether: the prefrontal cortex, the region that processes sensory information. In Hariri’s view, the prefrontal cortex is the owner entrusted with comforting the agitated watchdog—the amygdala. This process occurs through the release of endocannabinoids, chemicals that occur naturally in the brain and act in essentially the same manner as marijuana: they help us chill.

A research group at the National Institute on Alcohol Abuse and Alcoholism led by Andrew Holmes found that when a specific brain enzyme (fatty acid amide hydrolase, or FAAH) in mice was inhibited, the mice spent less time in a fear state. Taught to associate a distinctive tone with an electrical shock, they quite naturally froze in fear when they heard it. But when they were subsequently exposed to the tone minus the shock, the enzyme-inhibited rodents shrugged off the formerly frightening sound far more quickly than their still-frozen-in-place peers.

Hariri conducted a similar study with middle-aged humans, using brain scans to measure amygdala activity as they looked at a series of faces with threatening expressions. Among participants who carried a specific version of the FAAH gene, brain activity decreased rapidly as the test proceeded, with scowls viewed later in the experiment triggering minimal reaction. This suggests that, for at least some people suffering from anxiety disorders, a drug that blocks the FAAH enzyme “could bring you back to a middle-of-the-road response,” Hariri says. “That’s certainly what we’re working toward.” Many of us will be waiting anxiously.

Two years ago, researchers at Dana-Farber created a hybrid molecule that was able to inhibit BRD4, a cancer-causing gene. Soon the researchers learned that the molecule, named JQ1, also inhibits another protein, BRDT, which is crucial for the development of mature sperm.

“We wondered, could the JQ1 molecule, intended initially for cancer, have activity as a male contraceptive agent?” said Dr. James Bradner, the lead author of a study in the August 17^th issue of Cell.

Martin Matzuk of Baylor College of Medicine, injected mice with Bradner’s JQ1. The mice treated with the compound had lower sperm counts and less mobile sperm, rendering them infertile. Crucially, when the mice stopped receiving JQ1 their sperm count rebounded and they were able to produce healthy offspring.

“These findings suggest that a reversible, oral male contraceptive may be possible,” Bradner said in a release. “While we will be conducting more research to see if we can build on our current findings, JQ1 shows initial promise as a lead compound for male contraception.”

Female birth control pills have come with a laundry list of side effects, from nausea to decreased libido to melasma. So far JQ1 has shown no negative consequences on the animals’ testosterone levels, behavior, or future offspring. In the future, maybe it will be men checking their watches, discreetly popping a pill at the same time each day.

Dr. Hugh Taylor was curious when he read a report saying mothers of kids with behavioral problems seem to spend a lot of time on cell phones. Did the moms’ chatty habits affect the children’s behavior, he wondered, or could cell phones themselves somehow cause the kid’s attention deficit disorders?

Taylor, a Yale School of Medicine professor who studies fetal development, decided to find out. So he got cell phones for 33 expecting mice.

The professor suspended the phones a few inches above the rodents’ feeding bottles. Then he left them on an active, though silent, call for the mice’s 19-day gestation period, steadily emitted radiation. “We’re in-network, so we didn’t get charged for the minutes,” Taylor assured us. Meanwhile, as a control, 42 other pregnant mice lived under the same conditions, except the phones above their bottles were deactivated.

Once born, the radiation-exposed baby mice were found to be hyperactive, and to have impaired memory compared to the control group. The exposed group’s little brains also betrayed signs of weakened function in the prefrontal cortex, which helps maintain focus.

“This is the first study showing that cell phones can cause neural problems, albeit in a mouse,” Taylor says. “It at least warrants further investigation.”

Cell phone radiation isn’t strong enough to kill or mutate cells, Taylor says, but it can do more subtle things, like raise tissue temperature and affect cell membranes in a fetus’s brain. “Those effects could cause the brain to be wired differently,” he says. And that could set the stage for behavioral problems like attention deficit hyperactivity disorder.

There are, however, big differences between human and mouse babies, such as skull thickness, volume of amniotic fluid and the sizes of their mothers, so human babies might not be affected in the same way. “I don’t want to say we have definitely shown that cell phones can be dangerous to humans in pregnancy,” he adds. But he does suggest that pregnant women might want to keep their phones away from their bellies.

Could an apple a day help keep obesity away? In a new study, researchers at the University of Iowa found that ursolic acid, a compound found in the waxy skin of apples, increased muscle mass and reduced total body weight.

The researchers put two groups of mice on high-fat diets where 55% of their calories came from fat. But for one of the groups, researchers added an ursolic acid supplement to their diet. The mice that had the supplement developed more muscle mass, were able to exercise longer and had an increase in brown fat—a type of tissue that burns large amounts of calories to maintain body temperature—than the mice without the supplement. Turns out, the ursolic acid led a multi-pronged, calorie burning assault on the high-fat diet of the mice. Not only that, but it reduced glucose intolerance and fatty-liver disease, common ailments for obese people.

The results suggest that ursolic acid is “a potential therapeutic approach for obesity and obesity-related illness,” the researchers write. More muscle, more energy, more calories burned? Maybe that’s why Eve ate the apple.

Move over, “Madagascar 3”: Now we can see mice brains … in 3-D
—Cold Spring Harbor Laboratory via Pop Sci

Might skin cells be transformed into stem cells to treat Alzheimer’s?
—Cell Stem Cell via ABC News

Targeting the brain’s appetite control switch suggests we could flip it to ‘off’
—Cell via ABC News

Decades-old antidepressant found to slow colon cancer growth
—PLOS One via Focus Taiwan

“Rogue” stem cells now blamed for hardening arteries
—Nature Communications via International Business Times

“Fungi Gone Awry in Gut May Contribute to Intestinal Diseases”
—Science via San Francisco Chronicle

Researchers in Hong Kong report chronic exposure to smoky air apparently affected the brains of rats. “These changes might serve as evidence of early phases of neurodegeneration,” they write in the online journal PLoS ONE, “and may explain why smoking can predispose brains to Alzheimer’s Disease and dementia.”

Echoing the conclusions of a 2008 study from England, a 2010 paper published in the American Journal of Epidemiology reported a link between lifetime exposure to secondhand smoke and an increased risk of dementia, at least in certain elderly individuals. A research team led by Yuen-Shan Ho of the University of Hong Kong’s Laboratory of Neurodegenerative Diseases used male Sprague-Dawley rats to try to determine the medical reasons underlying this linkage.

The researchers conducted an experiment using nine rats, each of which spent one hour per day for 56 days in a specially ventilated chamber. For five of the rodents, the air in the chamber had a smoke concentration of 4 percent. This mimicked “the situation of humans in restaurants or bars were cigarette smoking is permitted,” the researchers write.

Compared to the rodents who breathed clean air, “Many abnormalities were observed in the hippocampus in the smoking-exposed rats,” they report. “These changes collectively may have an impact in normal cellular function.”

“Our data suggested that daily exposure to cigarette smoke could accelerate the aging of the brain,” the researchers write. Specifically, they report that ongoing exposure to smoke appeared to alter the proteins that allow proper functioning of the synaptic system, which plays an essential role in our ability to form and hold onto memories.

“Our study demonstrated that exposure to cigarette smoke could induce pathological changes in the brain,” they conclude, “and these changes might make us more susceptible to the development of cognitive impairment, or even Alzheimer’s disease, late in life.”

So while that job as a bartender or cocktail waitress at a smoke-filled establishment may be temptingly lucrative, the long-term price you pay could be enormous—even if you don’t get cancer.

At the University of Toronto, Tony Lam and his assistant Danna Breen performed “duodenal-jejunal” bypass surgery — taking out most of the rats’ upper intestine and part of the middle section. The jejunum is below the duodenum (but less commonly-known, despite having a way better name .) Without a duodenum or a proximal jejunum, the rats’ digestion skipped the upper intestine, which appeared to trigger a response that targeted the rats’ blood sugar.

According to the resulting study published in the journal Nature Medicine, when doctors Lam and Breen removed the top or “proximal” half of the jejunum, the latter or distal jejunum revealed it “could sense glucose” and “signal to the brain to let the liver know that it must lower glucose production.”

Lowering the amount of glucose pumped out by the liver allowed the diabetic rats’ bodies to regulate their blood sugar better.

Doctors Lam and Breen claim this to be the first time surgery has successfully caused a rapid drop in glucose production, at least among “non-obese type 1 uncontrolled diabetic rats.” Which is a roundabout way of saying, all other things being equal, the surgery helped ease the diabetes.

But that pint of Ben and Jerry’s could cost you. A new study from the University of California, Los Angeles suggests that an unhealthful diet of too few omega-3 fatty acids and too much high fructose corn syrup might do real damage to the brain’s ability to learn and recall information.

It’s long understood that eating too much sugary food can be a surefire path to diabetes and heart disease. But UCLA’s Rahul Agrawal and Fernando Gomez-Pinilla wanted to know what effect it might have on the brain. To find out, they trained two dozen rats to do a simple Barnes maze, requiring them to find a hidden escape chamber. For five days the rats slowly got faster. Then the researchers serated the rats into two groups, and deprived one group of dietary omega-3s while allowing them to binge on fructose-sweetened water. Six weeks later, they ran the maze again. Rats who’d been given plenty of omega-3s and no sugar had a relatively easy time recalling how to escape. But rats that were omega-3 deficient and hopped-up on sugar took five times as long to do so.

In post-mortems, the researchers found that the gluttonous rats had elevated levels of insulin resistance (the same condition responsible for America’s diabetes epidemic). Agrawal and Gomez-Pinalla hypothesize that insulin resistance may be linked to cognitive impairment, a decrease in brain plasticity, and perhaps even mental illness—theories that, if borne out, could have serious implications for the more than 60 percent of overweight Americans.

One bright spot, however: a regular diet of omega-3s ameliorated some of the sugar’s deleterious effects on insulin resistance and learning. So if a pack of Ding Dongs is the only thing getting you through that Chaucer cram session, do your body—and your GPA—a favor and wash it down with a little fish oil.

Investigators led by Satchidananda Panda at the Salk Institute for Biological Studies offered the same high fat diet to two groups of mice. The first group could access the food only eight hours a day, while mice in the other group could hit the rodent buffet whenever they wanted.

The study, reported in the journal Cell Metabolism, found the mice on the time-restricted diet consumed just as much food as those with “ad lib” food access, yet had lower rates of obesity, excessive insulin, excessive fats in the liver, and inflammation, as well as improved motor coordination.

When we restrict eating to a schedule, organs like the liver “turn on” to process new chemicals from food, then “turn off” afterwards, entering a metabolic trough. In theory, the study argues, the mice that ate eight hours each day allowed their organs to process nutrition more efficiently. Mice who snacked whenever they wanted — like modern humans often do — prevented the body from establishing a proper metabolic rhythm.

“The focus has been on what people eat,” said Panda, in the team’s announcement of the study. “We don’t collect data on when people eat.”

The study’s authors compared diet to sleep. If you sleep eight hours, but in fits and starts throughout the day, you never feel rested. Similarly, even an apple may bring less benefit at 3 a.m. than it would at noon.

It sounds like an ancient proverb from some rodent-infested culture. But it’s the unspoken mantra of a group of computer security researchers who have refined an innovative method of combatting identity theft.

In a newly published paper, a research team led by Clint Feher of Israel’s Ben-Gurion University introduces a novel way of verifying a computer is being operated by its rightful user. Its method, described in the journal Information Sciences, “continuously verifies users according to characteristics of their interaction with the mouse.”

How we manipulate our mice is, if not as unique as a fingerprint or DNA, surprisingly specific.

The idea of user verification through mouse monitoring is not new. As the researchers note, “a major threat to organizations is identity thefts that are committed by internal users who belong to the organization.”

To combat this, some organizations turn “physiological biometrics” to verify the identity of a computer user. But these techniques, such as fingerprint sensors or retina scanners, “are expensive and not always available,” the researchers write.

An alternative approach is the use of “behavioral biometrics.” Such a system compiles biometric data such as “characteristics of the interaction between the user and input devices such as the mouse and keyboard” and constructs a “unique user signature.”

As you might imagine, this is a tricky process, as the precise way we utilize our mouse or tap the keys of our computer can vary for all sorts of reasons, including the time of day, whether we are sitting or moving about, or how much caffeine we’ve ingested. Feher and his colleagues addressed these concerns by devising “a novel method that continuously verifies users … based on the classification results of each individual mouse action, in contrast to methods which aggregate mouse actions.”

These individual actions include the time it takes the click the mouse (with separate stats for the right and left sides), “the distance traveled between the mouse-down and mouse-up events of the first click,” “the time interval between the first click and the second click,” and many, many more.

This approach “outperforms current state-of-the-art methods by achieving higher verification accuracy while reducing the response time of the system,” they report.

Things like “lint clogging the moving parts of mechanical mice” could throw off their equations, the researchers admit. They also concede that a person “using a laptop in two different places may use the touch pad in one place and an external mouse in another,” which complicates verification.

Nevertheless, their work appears to represent an important advance in this arena, and one that could give them an appreciative following. As that other proverb goes, build a better mouse-based identity protection system, and the world will beat a path to your door.

The research nutritionist had seen studies that connected fatty diets and prostate cancer. And he knew federal guidelines recommend we limit our fat intake to less than 30 percent of our calorie intake. But, he says, he’s also “convinced, given the epidemiological evidence, that the Mediterranean diet, which is high in nuts and high in fat, is one of the best ones around.” He was confounded by the disconnect.

So he took mice that had been genetically engineered to develop the disease and divided them into three groups. One batch ate a high-fat diet that included 155 grams per day of ground walnuts. Another group was fed a comparable amount of fat in the form of soybean oil; while a third received a low-fat diet that also included soybean oil. All other nutrients were identical.

The mice were killed at 9, 18, and 24 weeks; upon examination, researchers found that prostate tumors in the walnut-fed mice were smaller, and tumor growth rate was much slower, than in the other two groups. The walnut-fed mice also had lower levels of “insulin-like hormone growth factor 1,” which has been linked to cancer.

The finding, reported in January in the British Journal of Nutrition, is the first to spell out the effects of walnuts on prostate cancer in animals. The benefits are not due to a particular chemical compound in walnuts, he adds. “It’s a combination of effects” from a whole piece of food.

“It’s not the magic bullet,” he says, “but it’s part of the magic fusillade.”

Add to that, mice who drink caffeine-laced water and spend time on their running wheel see less tissue inflammation (always a handy measure of general unhealthiness), according to Yao-Ping Lu, a Rutgers University researcher who presented his study at the American Association for Cancer Research annual meeting in Chicago.

Following up on other studies that suggest caffeine protects against skin cancer — whether ingested or rubbed on the skin — Lu took 160 mice that were genetically predisposed to develop the disease and exposed them to ultraviolet-B rays (like those found in sunlight). The exposure usually causes these mice to grow tumors.

Lu divided the critters into four groups, who all ate the same food: he gave one bunch caffeine; another had access to the running wheel; a third set got both caffeine and exercise. The fourth was the control group — they only got water.

The caffeinated mice that got plenty of exercise had 62 percent fewer skin tumors, and the size of their tumors decreased by 85 percent compared with the control mice. The caffeine-only mice had 27 percent fewer tumors (and tumors were 61 percent smaller). The exercise-only mice had a 35 percent fewer tumors (with a 70 percent smaller tumors).

Meanwhile, even on a high-calorie diet, the skin of UV-exposed mice that exercise and consume caffeine has a 90 percent reduction in inflammation-causing molecules called cytokines — and their skin has less fat in it, allowing it to do a better job of eliminating sun-damaged cells than the control mice, Lu says.

Still, “this is a long-term regimen,” Lu warns. “You can’t just drink coffee and get a little exercise. You still need sunscreen and other protective measures.”