U of R boffins discover wrinkle therapy chem may cure cancer in naked mole rats

The husband and wife team of Seluanov and Gorbunova at the University of Rochester may be one step closer to discovering a practical cancer treatment. They have isolated a specific chemical in the naked mole rat which seems to gird the rodent Lothario’s cells against tumors. And as it turns out, curing wrinkles may have been better for your health than previously thought:

Seluanov and Gorbunova then showed that when HMW-HA was removed, the cells became susceptible to tumors, confirming that the chemical did play a role in making naked mole rats cancer-proof. The Rochester team also identified the gene, named HAS2, responsible for making HMW-HA in the naked mole rat. Surprisingly, the naked mole rat gene was different from HAS2 in all other animals. In addition naked mole rats were very slow at recycling HMW-HA, which contributed to the accumulation of the chemical in the animals’ tissues.

The next step will be to test the effectiveness of HMW-HA in mice. If that test goes well, Seluanov and Gorbunova hope to try the chemical on human cells. “There’s indirect evidence that HMW-HA would work in people,” said Seluanov. “It’s used in anti-wrinkle injections and to relieve pain from arthritis in knee joints, without any adverse effects. Our hope is that it can also induce an anti-cancer response.”

It was this same husband and wife team that, in November of last year, announced that they’d discovered a protein which may prevent run-away cell growth in NMR. Unchecked cell growth is the hallmark of cancer.

HMW-HA is known to help vascular health by maintaining the integrity of Endothelial cells, which line the inside of veins and arteries. It is this property that makes it desirable in wrinkle therapy. Seluanov and Gorbunova discovered the same chemical in a “goop” that seemed to clog up testing equipment while the scientists tested other properties of the NMR.


You could train a baboon to work at a dollar store: U of R and SPZ study

In still more primate news for this week, it now turns out that yet another tenet of human arrogation goes up in a huff of baboon fur. It turns out that, given the choice of more or less treats in a cup, Seneca Park Zoo olive baboons proved they understand numbers just fine.

The baboons were given a choice of two cups, each containing a random selection of one to eight peanuts, to choose from. Based on their snap assessment of which cup had the greater number of treats, the baboons got to keep their booty. And after 54 trials with eight baboons, the research revealed that they were able to come up with the right answer 75% of the time:

Count on it: Baboons ‘know’ numbers

The baboons’ choices clearly relied on the “more than” or “less than” cognitive approach, known as the analog system. The baboons were able to consistently discriminate pairs with numbers larger than three as long as the relative difference between the peanuts in each cup was large.

Research has shown that children who have not yet learned to count also depend on such comparisons to discriminate between number groups, as do human adults when they are required to quickly estimate quantity.

So yeah. The next time you think the clerk at the Dollar General may have gotten the count wrong of your items despite having picked each one up, maybe you realize the reason is that they’re using the same cognitive appraisal technique as babies and your buddies in the new expansion of the SPZ.


A fast-moving needle in a deadly haystack: U of R sensor to spot asteroids before they hit us.

Stars are easy to see. They emit light. Planets – in our own Solar System, anyway – are easy to see, because they move slowly and are reflected by our own Sun’s light. But what about all that other debris hurtling through space? The stuff that created craters on the moon and the Earth alike? They don’t emit their own light and passing at incredible speeds, may not be noticed until it is too late.

Fortunately, however, they do emit infrared light. And they do so at a wavelength that is uncommon enough in interstellar space that a properly-trained camera sensor might just be able to spot them from considerably farther away, where they might still have their courses altered to less devastating trajectories. That is the aim of University of Rochester boffins William J. Forrest, Judith Pipher and Craig McMurtry. And their sensor has just passed a critical test to move on to the next phase of development:

Craig McMurtry, the paper’s lead author, is also a member of the Rochester team. “We were delighted to see in this generation of detectors a factor of 1000 improvement in sensitivity compared with previous generations, while simultaneously raising the operating temperature to one readily attainable in space,” he says.


U of R neuro-boffins create super-smart mice with human brain cells

Because we all needed something new to worry about in our pantries, the University of Rochester neuroscience boffins decided to see what happens when you put human glial cells into prenatal mice. The answer? Mice that can perform calculus.

Well, ok. Not really.

But they did discover that the much more complex and robust human glial cells would operate exactly the same in mice as they do in humans. By grafting “glial progenitor” cells -basically brain-specific stem cells – into mice before they were born, the boffins were able to create mice that used the human glial cells instead of their own. The result seems to have been a major boost to the cognitive abilities of the affected mice:

They found that two important indicators of brain function drastically improved in the mice with human glia. First, when measuring a phenomenon called calcium wave – the speed and distance at which a signal spreads within and among adjoining astrocytes in the brain – the researchers noted that the speed of wave transmission in the transplanted mice was faster than normally observed in mice, and more similar to that of human brain tissue.

Second, the researchers also looked at long-term potentiation (LTP), a process that measures how long the neurons in the brain are affected by a brief electrical stimulation. LTP is considered one of the central molecular mechanism underlying learning and memory.   In this test as well, the researchers found that the transplanted mice developed more rapid and sustained LTP, suggesting their improved learning capability.

So the mice with the human glial cells (chimeras, as they’re referred to in the study) are able to send signals across the brain faster and remember learned responses better. All of which adds up to a much smarter mouse.

Glial cells are a suite of different types of brain cells, sometimes referred to as “white matter,” that perform regulation and maintenance functions in the brain. U of R researchers have been studying glial cells, trying to understand the much more complex role they play in the brain than previously thought. Some research may lead to cures for Alzheimer’s disease or MS.

And some research may lead to empty mouse traps and a lot less pancake batter mix in your house than you thought you’d bought. Science is full of such trade-offs.


Stony Brook researchers build on U of R Alzheimer’s research

In August of last year, we reported on the recent discovery of a “Glymphatic Pathway,” which is essentially a waste-disposal system for the brain. This system, discovered by Jeffrey Iliff and Maiken Nedergaard of the University of Rochester, mirrors the role of the lymphatic system in other organs of the body. The system removes waste proteins from the brain and the effective running of this system, scientists believe, is the difference between a healthy brain and one with Alzheimer’s Disease.

Building on that research, boffins at the University of Stony Brook used tracing elements and MRI scanning to trace the entire glymphatic system, from the back of the brain to the nasal cavity, to better understand the pathway and what a damaged one might look like:

This advanced imaging technique has the potential to be used as a way to monitor the human brain to map brain waste clearance and access (sic) disease susceptibility. Theoretically, if clinicians were able to capture a defect in the glymphatic system where certain channels are malfunctioning, plaque formation would likely accelerate, Benveniste says.

This plaque buildup may be an early sign of disease susceptibility before evidence of any cognitive changes. Though there is no known way to repair malfunctions in the glymphatic system, the research team is investigating ways to repair or open malfunctioning channels.

Mapping out this system is part of a wider effort to understand “white matter” in the neurological system.


Is Big Bird really teaching kids?

Is television really the brain rot your parents used to tell you it was? Well, the jury is still out about that, but one thing University of Rochester neurology researchers seem to have discovered is that the brain activity of a kid watching Big Bird generally mirrors that of adults. That is: the parts of the brain which are active in an adult watching Sesame Street and those of a child are similar, and also map to specific cognitive aptitudes in both groups.

The study conducted on 27 children and 20 adults used fMRI imaging to watch the brain activity of test subjects as they watched Sesame Street. The purpose of the experiment was to see if doing more natural tasks such as watching television would reveal more clues as to how the brain functions. Previous tests using simplified tasks failed to predict which parts of the brain governed which types of cognitive ability. However, when subjects watched The Bird:

Children whose neural maps more closely resembled the neural maps of adults scored higher on standardized math and verbal tests. In other words, the brain’s neural structure, like other parts of the body, develops along predictable pathways as we mature.

The study also confirmed where in the brain these developing abilities are located. For verbal tasks, adult-like neural patterns in the Broca area, which is involved in speech and language, predicted higher verbal test scores in children. For math, better scores were linked to more mature patterns in the intraparietal sulcus (IPS), a region of the brain known to be involved in the processing of numbers.

On the issue of whether watching television actually teaches children, well, the researchers are quick to point out that they’re not actually endorsing television as an educational tool. Heaven forfend. But the findings of the study do seem at minimum to suggest that the correct neural pathways are getting teased by the content of Sesame Street episodes.

Whether this is because kids are learning from television or simply responding to information they already understand based on some other means of learning is not clear. It is also entirely possible that, just as the simple task-based studies failed to reveal correlations, the current set of studies might be revealing genuine correlations that are not actually tied to the same cause.

But knowing that a correlation does exist opens up entirely new neurological pathways for the continued research of learning and learning disability. With more research and corroborating evidence from other disciplines, this could be a whole new suite of tools to get the best out of kids.


Radiation may make a trip to Mars the most forgettable adventure in a lifetime.

News out of the University of Rochester this week that a research paper, printed in PLOS ONE, will show evidence that certain types of cosmic radiation may speed the onset of Alzheimer’s disease in astronauts. Research was done at NASA’s Space Radiation Laboratories and analyzed by researchers at the U of R.

The findings hinge on research done by exposing mice to radiation at levels scientists predict are similar to that encountered in space, where our fragile eggshell minds must survive without Earth’s natural radiation shield. The research focused on high-mass radiation particles like iron, as shielding astronauts from such particles poses significant engineering problems. Basically, we can’t right now. And if we’re going to put humans into space for the anticipated three-year journey to Mars, we’re probably going to want to work on that:

The brains of the mice also showed signs of vascular alterations and a greater than normal accumulation of beta amyloid, the protein “plaque” that accumulates in the brain and is one of the hallmarks of [Alzheimer’s] disease.

“These findings clearly suggest that exposure to radiation in space has the potential to accelerate the development of Alzheimer’s disease,” said O’Banion. “This is yet another factor that NASA, which is clearly concerned about the health risks to its astronauts, will need to take into account as it plans future missions.”

Mind you: even without any ill effects to your noggin, low-level, constant bombardment by radiation for the next three years would certainly take its toll. The threat of Alzheimer’s is just one more bit of the puzzle, and one that may need to be addressed.

The article leaves me wondering, though. How do they know that the plaque buildup is irreversible? Other studies at the U of R have shown that the loss of “white matter” in the brain, which is essentially the repair and maintenance crew, also may lead to Alzheimer’s. If the white matter stays intact and the plaque build up occurs, might the brain’s natural defenses right the wrongs done by space travel?

I’ve got a call in to see if I can get some clarification on all this. I’ll report back when I find out.

Rochester Science

Need cash? Sneeze on a boffin. It pays!

It’s that time of year again: the season in which the University of Rochester exchanges quick cash (for you and your whole family!) in exchange for research into why you feel so shitty. It’s a sweet deal, if you can stand going to a hospital four times in the next month.

The U of R has released a presser announcing that anyone who comes down with a flu virus who qualifies can get $25 cash money for showing up to the hospital to let a boffin poke them. If anyone else in your household is also sick, they want them too! Same deal, $25 per visit.

The research is part of a collaborative effort from the awesomely-named New York Influenze Center of Excellence, made up of researchers from the U of R, Cornell and quite inexplicably, the University of Tennessee.


the research is part of the NYICE’s broader mandate to analyze the pathogenesis of flu viruses. This means the route by which infection happens and the life-cycle of the flu while it is in an infected host.

Bonus Excellence:  The NYICE website also links to an article interviewing a “metaphysical healer” named Louise L. Hay who suggests that, if you’d like to avoid sneezing on boffins, your best defense is a positive attitude. I have no idea how this gets linked to from that website. But there you have it.

Health Rochester Science

Does quitting smoking ease back pain? U of R study

Scientists are often fond of saying “correlation does not prove causality.” That meaning: just because two things happen at the same time or in sequence in no way implies that one caused the other. They may simply have coincidentally happened in an order tantalizing us to make hasty assumptions.

I cannot say for certain that the study the University of Rochester released today does or does not display that false sense of causality. But my sense is that much more research is probably necessary. This study followed about 5,000 respondents to a questionnaire about pain after treatment for back issues. The results pretty conclusively correlated less back pain with those who either quit smoking years ago or never smoked, compared to those who currently smoked. However:

Of the 5,333 people, those who had never smoked or had quit some time ago reported less pain than smokers or those who had just quit. By the end of the follow-up period, the people who had recently quit or who quit during treatment showed significant improvements in pain. People who continued to smoke during treatment had no improvement in pain on all scales.

Behrend noted that younger people tended to comprise the group of current smokers and those who only decided to quit during treatment; this is consistent with other studies showing that smoking is associated with degenerative spine disease at a younger age. Older patients tended to comprise the group who had never smoked or quit long ago.

The trouble here is that we’re dealing with two hugely divergent groups of people. To simply say that the fact that they smoke or don’t smoke is one correlated item is to completely under cut all the other vastly significant differences between these two groups. For example: those who continue to smoke into old age are probably also making a great deal many more decisions which are not beneficial to their health. And those who quit smoking while still young are probably eager to move on.

When I quit smoking six years or so ago, I swore I’d never be what I always referred to as a “Born Again Non-Smoker.” It is easy, when smoking is such a great scapegoat and straw man, to blame the habit for all the ills of any individual and claim the Holy Grail of health benefits every time something seems to prove a socially agreed-upon conclusion. But this report leaves a whole lot to be desired in the facts department.


U of R engineers join the hunt for dark matter

Space. All those stars and shit. What holds it all together?

The generally-assumed answer is gravity, and that is true, but physicists know there is more to the answer. Many a simulation has been run using the properties we understand gravity to have and enough matter to create, say, a small galaxy. And the numbers never really add up: every time, scientists find their virtual galaxies spinning off into ether, rather than curling into the elegant spirals and clusters we’re so accustomed to seeing. Why is that?

The answer, as inferred by scientists, is a type of matter called “dark matter.” Dark matter neither emits nor radiates light and is electrically neutral, and is thus far undetectable by any instruments science has developed. “Dark,” get it? But when dark matter is added into the boffin’s equation for a working galaxy, lo and behold, the galaxy stays together the way we expect it to.

So now science has a pretty good idea that there’s something out there that we can’t detect. Now how do we detect it?

Engineers from the University of Rochester are helping to try to answer just that question in South Dakota. In a project called the Large Underground Xenon experiment, or LUX, the team led by Dr. Frank Wolfs has installed “trigger” mechanisms that make the determination whether data coming to the instrument is worthy of further study, or is simply noise.

The LUX experiment is an exercise in super-tightly controlled recording. The LUX is shielded from most distracting inputs by a 70,000 gallon pool of water, buried 4,850 feet below the surface of the Earth. Setting the LUX up in this way keeps it from getting confused by solar and ambient radiation. Additionally, the whole system is surrounded by super-sensitive photomultiplier tubes (PMTs) capable of detecting and filtering out even a single photon. All things must remain silent if they’re to find the one signal that proves the existence of the illusive dark matter particle.

Inside the detector, xenon gas cooled to -160 degrees Fahrenheit is monitored by still more PMTs. These tubes will look for the small flashes of light that will hypothetically be produced when a dark matter particle (Weakly Interacting Massive Particle, or WIMP) collides with a xenon atom. A second, stronger flash is caused when a strong magnetic field inside the detector draws the electrons released in the collision upward towards another layer of gaseous xeon.

It is in comparing these two flashes that the University of Rochester’s engineering team comes in. Their trigger must determine whether or not there were two flashes and whether the two flashes are related before passing that data on to researchers.

So if the LUX works out and the mystery particle that makes up 82% of our universe’s mass is laid bare, it will be the U of R that will actually hand the data off. Bitchin.


U of R boffins isolate the “suicide protein” that may be the key to curing cancer.

The cure for cancer may be closer than we know.

At least that is what University of Rochester Professor Vera Gorbunova and Assistant Professor Andrei Seluanov think.

The blind mole rat was known to be one of two mammals that never develop cancer. It was only until recently that University of Rochester scientists found out how the blind mole rat had developed such an immunity.

For their test, the two professors isolated blind mole rat cells and forced them to grow at an accelerated rate. During this process, the scientists witnessed the rapidly growing cells rearrange themselves and secrete a “suicide protein” that halted the abnormal growth. They also found that the adjacent cells that were at at risk for developing cancer were also killed off, stopping any potential for cancer.

Gorbunova said that the next step in their research is to find out why the protein is released in the first place. Once this final secret is discovered, it could be the final piece of the puzzle that will allow scientists to prompt human cells to release a similar “suicide protein” that would allow people to be able to fight off some cancers.

Despite the excitement among the University of Rochester scientists, Jerry Shay, who studies cellular aging at University Texas, does not hold the same optimistic opinion. Shay says that the protein may not actually be what prevents cancer in blind mole rats. He suggests that researchers have simply not found a way to keep the test cells alive for a long enough time.

Even if scientists have not figured out how blind mole rats have managed to prevent cancer to grow, it still does not take away from the fact that they are mammals and that they are immune to it. This means that humans still have a future of becoming resistant to cancer for good as well.


U of R researchers’ myelin breakthrough may have gotten us one step closer to a cure for MS, Alzheimer’s.

So who has actually heard anything about stem cell research lately? I know that there was a ton of controversy around the moral aspect of it a few years ago, but has anybody really been bringing it up? Really. I would like to know.

At any rate, no matter what one’s moral views are (or were, since not many still actively have an opinion), there’s really no arguing the fact that myelin-based stem cell research is probably one of the largest potentially disease-curing gold mines in the medical community.

The key to finding out the true benefit of stem cell research, however, is a safe & stable amount of healthy cells to utilize, which has been hard to come by until very recently.

A study conducted by the University of Rochester Medical Center focuses on cells called “glial progenitor cells,” or GPCs. GPCs are stem cells that are found in the white matter of the brain, and, long story short, yield two crucial body cells, both of which are necessary for a functional central nervous system.

If it’s a disease that’s rooted in myelin deficiency, you’ve probably heard of it; multiple sclerosis and cerebral palsy are just two on the list, and have probably affected whoever is reading this article at one point or another.

Alzheimer’s disease victims and their families are also among the many who would benefit from this. Stem cell research is key in finding a cure for Alzheimer’s, and with this new breakthrough, the process that is used is going to be a much more reliable one. This discovery could lead to something remarkable.

So yes, to put it simply, this is a big breakthrough. The thing to keep your eye on is exactly where doctors are going to be able to go with it. A cure for MS? Fantastic. Ridding the world of cerebral palsy? Magnificent. Hopefully we can knock Alzheimer’s out in the future.

We’ll see what happens. Miracle cures definitely don’t happen over night, but right now, we can see the start of something significant, right here in Rochester.