MDOnly Report - Part 2

Protecting Against Radiation

Posted by admin on March 27th, 2011

Three basic concepts apply to all types of ionizing radiation. When we develop regulations or standards that limit how much radiation a person can receive in a particular situation, we consider how these concepts might affect a person’s exposure.

The 3 Basic Concepts of Radiation Protection revolve around: time, distance, shielding

Time
The amount of radiation exposure increases and decreases with the time people spend near the source of radiation.

In general, we think of the exposure time as how long a person is near radioactive material. It’s easy to understand how to minimize the time for external (direct) exposure. Gamma and x-rays are the primary concern for external exposure.

However, if radioactive material gets inside your body, you can’t move away from it. You have to wait until it decays or until your body can eliminate it. When this happens, the biological half-life of the radionuclide controls the time of exposure. Biological half-life is the amount of time it takes the body to eliminate one half of the radionuclide initially present. Alpha and beta particles are the main concern for internal exposure.

How does EPA use the concept of time in radiation protection?

When we set a radiation standard that assumes an exposure over a certain period, we are applying the concept of time. For example, we often express exposures in terms of a committed dose. A committed dose is one that accounts for continuing exposures over long periods of time (such as 30, 50, or 70 years). It refers to the exposure received from radioactive material that enters and remains in the body for many years.

When we assess the potential for exposure in a situation, we consider the amount of time a person is likely to spend in the area of contamination. For example, in assessing the potential exposure from radon in a home, we estimate how much time people are likely to spend in the basement.

Distance
The farther away people are from a radiation source, the less their exposure.

How close to a source of radiation can you be without getting a high exposure? It depends on the energy of the radiation and the size (or activity) of the source. Distance is a prime concern when dealing with gamma rays, because they can travel long distances. Alpha and beta particles don’t have enough energy to travel very far.

As a rule, if you double the distance, you reduce the exposure by a factor of four. Halving the distance, increases the exposure by a factor of four.

Why does exposure change more rapidly than the distance?

The area of the circle depends on the distance from the center to the edge of the circle (radius). It is proportional to the square of the radius. As a result, if the radius doubles, the area increases four times.

Think of the radiation source as a bare light bulb. The bulb gives off light equally in every direction, in a circle. The energy from the light is distributed evenly over the whole area of the circle. When the radius doubles, the radiation is spread out over four times as much area, so the dose is only one fourth as much. (In addition, as the distance from the source increases so does the likelihood that some gamma rays will lose their energy.

The exposure of an individual sitting 4 feet from a radiation source will be 1/4 the exposure of an individual sitting 2 feet from the same source

How does EPA use the concept of distance in radiation protection?

We also consider distance in analyzing potential exposures from a source. If a person is at a contaminated site, or working around radioactive material, we assess how the exposures vary if the person is closer to, or farther away from, the source of radiation.

Shielding
The greater the shielding around a radiation source, the smaller the exposure.

Shielding simply means having something that will absorb radiation between you and the source of the radiation (but using another person to absorb the radiation doesn’t count as shielding). The amount of shielding required to protect against different kinds of radiation depends on how much energy they have.

(Alpha)
A thin piece of light material, such as paper, or even the dead cells in the outer layer of human skin provides adequate shielding because alpha particles can’t penetrate it. However, living tissue inside body, offers no protection against inhaled or ingested alpha emitters.

(Beta)
Additional covering, for example heavy clothing, is necessary to protect against beta-emitters. Some beta particles can penetrate and burn the skin.

(Gamma)
Thick, dense shielding, such as lead, is necessary to protect against gamma rays. The higher the energy of the gamma ray, the thicker the lead must be. X-rays pose a similar challenge, so x-ray technicians often give patients receiving medical or dental X-rays a lead apron to cover other parts of their body.

How does EPA use the concept of shielding in radiation protection?

We take into account the type of shielding that might be provided by soil when we assess sites that have been contaminated or used for disposal of radioactive material. We also account for the shielding provided by buildings for a person working or living at a site that has been cleaned up.

Radiation Exposure Health Effects

Posted by admin on March 27th, 2011

What kinds of health effects does exposure to radiation cause?

In general, the amount and duration of radiation exposure affects the severity or type of health effect. There are two broad categories of health effects: stochastic and non-stochastic.

Stochastic Health Effects

Stochastic effects are associated with long-term, low-level (chronic) exposure to radiation. (“Stochastic” refers to the likelihood that something will happen.) Increased levels of exposure make these health effects more likely to occur, but do not influence the type or severity of the effect.

Cancer is considered by most people the primary health effect from radiation exposure. Simply put, cancer is the uncontrolled growth of cells. Ordinarily, natural processes control the rate at which cells grow and replace themselves. They also control the body’s processes for repairing or replacing damaged tissue. Damage occurring at the cellular or molecular level, can disrupt the control processes, permitting the uncontrolled growth of cells–cancer. This is why ionizing radiation’s ability to break chemical bonds in atoms and molecules makes it such a potent carcinogen.

Other stochastic effects also occur. Radiation can cause changes in DNA, the “blueprints” that ensure cell repair and replacement produces a perfect copy of the original cell. Changes in DNA are called mutations.

Sometimes the body fails to repair these mutations or even creates mutations during repair. The mutations can be teratogenic or genetic. Teratogenic mutations are caused by exposure of the fetus in the uterus and affect only the individual who was exposed. Genetic mutations are passed on to offspring.

Non-Stochastic Health Effects

Non-stochastic effects appear in cases of exposure to high levels of radiation, and become more severe as the exposure increases. Short-term, high-level exposure is referred to as ‘acute’ exposure.

Many non-cancerous health effects of radiation are non-stochastic. Unlike cancer, health effects from ‘acute’ exposure to radiation usually appear quickly. Acute health effects include burns and radiation sickness. Radiation sickness is also called ‘radiation poisoning.’ It can cause premature aging or even death. If the dose is fatal, death usually occurs within two months. The symptoms of radiation sickness include: nausea, weakness, hair loss, skin burns or diminished organ function.

Medical patients receiving radiation treatments often experience acute effects, because they are receiving relatively high “bursts” of radiation during treatment.

Brain Selectively Stores Most Useful Memories During Sleep

Posted by admin on February 7th, 2011

After a good night’s sleep, people remember information better when they know it will be useful in the future, according to a new study in the Feb. 2 issue of The Journal of Neuroscience. The findings suggest that the brain evaluates memories during sleep and preferentially retains the ones that are most relevant.

Humans take in large amounts of information every day. Most is encoded into memories by the brain and initially stored, but the majority of information is quickly forgotten. In this study, a team of researchers led by Jan Born, PhD, of the University of Lübeck in Germany set out to determine how the brain decides what to keep and what to forget.

“Our results show that memory consolidation during sleep indeed involves a basic selection process that determines which of the many pieces of the day’s information is sent to long-term storage,” Born said. “Our findings also indicate that information relevant for future demands is selected foremost for storage.”

The researchers set up two experiments to test memory retrieval in a total of 191 volunteers. In the first experiment, people were asked to learn 40 pairs of words. Participants in the second experiment played a card game where they matched pictures of animals and objects — similar to the game Concentration — and also practiced sequences of finger taps.

In both groups, half the volunteers were told immediately following the tasks that they would be tested in 10 hours. In fact, all participants were later tested on how well they recalled their tasks.

Some, but not all, of the volunteers were allowed to sleep between the time they learned the tasks and the tests. As the authors expected, the people who slept performed better than those who didn’t. But more importantly, only the people who slept and knew a test was coming had substantially improved memory recall.

The researchers also recorded electroencephalograms (EEG) from the individuals who were allowed to sleep. They found an increase in brain activity during deep or “slow wave” sleep when the volunteers knew they would be tested for memory recall.

“The more slow wave activity the sleeping participants had, the better their memory was during the recall test 10 hours later,” Born said. Scientists have long thought that sleep is important in memory consolidation. The authors suggest that the brain’s prefrontal cortex “tags” memories deemed relevant while awake and the hippocampus consolidates these memories during sleep.

Gilles Einstein, PhD, an expert in memory at Furman University, said the new findings help explain why you are more likely to remember a conversation about impending road construction than chitchat about yesterday’s weather. “These results suggest that sleep is critical to this memory enhancement,” said Einstein, who was unaffiliated with the study. “This benefit extends to both declarative memories (memory for a road detour) and procedural memories (memory for a new dance step).”

The research was supported by the German Research Foundation.

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Article adapted by MD Only from original press release.

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Provided by Society for Neuroscience

An afternoon nap dramatically boosts the brain’s learning capacity

Posted by admin on February 6th, 2011

If you see a student dozing in the library or a co-worker catching 40 winks in her cubicle, don’t roll your eyes. New research from the University of California, Berkeley, shows that an hour’s nap can dramatically boost and restore your brain power. Indeed, the findings suggest that a biphasic sleep schedule not only refreshes the mind, but can make you smarter.

Conversely, the more hours we spend awake, the more sluggish our minds become, according to the findings. The results support previous data from the same research team that pulling an all-nighter — a common practice at college during midterms and finals — decreases the ability to cram in new facts by nearly 40 percent, due to a shutdown of brain regions during sleep deprivation.

“Sleep not only rights the wrong of prolonged wakefulness but, at a neurocognitive level, it moves you beyond where you were before you took a nap,” said Matthew Walker, an assistant professor of psychology at UC Berkeley and the lead investigator of these studies.

In the recent UC Berkeley sleep study, 39 healthy young adults were divided into two groups — nap and no-nap. At noon, all the participants were subjected to a rigorous learning task intended to tax the hippocampus, a region of the brain that helps store fact-based memories. Both groups performed at comparable levels.

Diagram about students who napped.

Students who napped (green column) did markedly better in memorizing tests than their no-nap counterparts. Matthew Walker, assistant psychology professor, image above shows how that a nap clears the brain to absorb new information.

At 2 p.m., the nap group took a 90-minute siesta while the no-nap group stayed awake. Later that day, at 6 p.m., participants performed a new round of learning exercises. Those who remained awake throughout the day became worse at learning. In contrast, those who napped did markedly better and actually improved in their capacity to learn

These findings reinforce the researchers’ hypothesis that sleep is needed to clear the brain’s short-term memory storage and make room for new information, said Walker, who presented his preliminary findings on Sunday, Feb. 21, at the annual meeting of the American Association of the Advancement of Science (AAAS) in San Diego, Calif.

Since 2007, Walker and other sleep researchers have established that fact-based memories are temporarily stored in the hippocampus before being sent to the brain’s prefrontal cortex, which may have more storage space.

“It’s as though the e-mail inbox in your hippocampus is full and, until you sleep and clear out those fact e-mails, you’re not going to receive any more mail. It’s just going to bounce until you sleep and move it into another folder,” Walker said.

In the latest study, Walker and his team have broken new ground in discovering that this memory-refreshing process occurs when nappers are engaged in a specific stage of sleep. Electroencephalogram tests, which measure electrical activity in the brain, indicated that this refreshing of memory capacity is related to Stage 2 non-REM sleep, which takes place between deep sleep (non-REM) and the dream state known as Rapid Eye Movement (REM). Previously, the purpose of this stage was unclear, but the new results offer evidence as to why humans spend at least half their sleeping hours in Stage 2, non-REM, Walker said.

“I can’t imagine Mother Nature would have us spend 50 percent of the night going from one sleep stage to another for no reason,” Walker said. “Sleep is sophisticated. It acts locally to give us what we need.”

Walker and his team will go on to investigate whether the reduction of sleep experienced by people as they get older is related to the documented decrease in our ability to learn as we age. Finding that link may be helpful in understanding such neurodegenerative conditions as Alzheimer’s disease, Walker said.

In addition to Walker, co-investigators of these new findings are UC Berkeley post-doctoral fellow Bryce A. Mander and psychology undergraduate Sangeetha Santhanam.

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Article adapted by MD Only from original press release.

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Contact: Yasmin Anwar
University of California, Berkley

Stem cell inactivation may be reason for male pattern balding says new Penn study

Posted by admin on January 5th, 2011

In a study published in the Journal of Clinical Investigation, a team led by Virginia M.-Y. Lee, PhD, director of Penn’s Center for Neurodegenerative Disease Research, describes the first direct evidence of how mutated TDP-43 can cause neurons to die. Although normally found in the nucleus where it regulates gene expression, TDP-43 was first discovered in 2006 to be the major disease protein in ALS and FTLD by the Penn team led by Lee andJohn Q. Trojanowski, MD, PhD, director of the Institute on Aging at Penn. This discovery has transformed research on ALS and FTLD by linking them to the same disease protein.

Caption: Top panels show progenitor cells marked in green (left) and brown (right) in cross section of a hair follicle. Bottom panel shows side view of hair follicle with stem-cell- and progenitor-cell-rich areas.

Credit: George Cotsarelis, MD, University of Pennsylvania School of Medicine

“The discovery of TDP-43 as the pathological link between mechanisms of nervous system degeneration in both ALS and FTLD opened up new opportunities for drug discovery as well as biomarker development for these disorders,” says Lee. “An animal model of TDP-43-mediated disease similar to ALS and FTLD will accelerate these efforts.”

In the case of TDP-43, neurons could die for two reasons: One, the clumps themselves are toxic to neurons or, two, when TDP-43 is bound up in clumps outside the nucleus, it depletes the cell of normally functioning TDP-43. Normally a cell regulates the exact amount of TDP-43 in itself — too much is bad and too little is also bad. The loss of function of TDP-43 is important in regulating disease because it regulates gene expression.

To determine the effects of misplaced TDP-43 on the viability of neurons, the researchers made transgenic mice expressing human mutated TDP-43 in the cytoplasm and compared them to mice expressing normal human TDP-43 in the nucleus of nerve cells. Expression of either human TDP-43 led to neuron loss in vulnerable forebrain regions; degeneration of part of the spinal cord tract; and muscle spasms in the mice. These effects recapitulate key aspects of FTLD and a subtype of ALS known as primary lateral sclerosis.

The JCI study showed that a dramatic loss of function causes nerve-cell death because normal mouse TDP-43 is eliminated when human mutated TDP-43 genes are put into the mice. Since cells regulate the exact amount of TDP-43, over-expression of the human TDP-43 protein prevents the mouse TDP-43 from functioning normally. Lee and colleagues think this effect leads to neuron death rather than clumps of TDP-43 because these clumps were rare in the mouse cells observed in this study. Lee says that it is not yet clear why clumps were rare in this mouse model when they are so prevalent in human post-mortem brain tissue of ALS and FTLD patients.

Neurodegeneration in the mouse neurons expressing TDP-43 — both the normal and mutated human versions — was accompanied by a dramatic downregulation of the TDP-43 protein mice are born with. What’s more, mice expressing the mutated human TDP-43 exhibited profound changes in gene expression in neurons of the brain’s cortex.

The findings suggest that disturbing the normal TDP-43 in the cell nucleus results in loss of normal TDP-43 function and gene regulatory pathways, culminating in degeneration of affected neurons.

Next steps, say the researchers, will be to look for the specific genes that are regulated by TDP-43 and how mRNA splicing is involved so that the abnormal regulation of these genes can be corrected.

At the same time, notes Lee, “We soon will launch studies of novel strategies to prevent TDP-43-mediated nervous system degeneration using this mouse model of ALS and FTLD.”

The study was funded in part by funds from the National Institutes of Health.

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Article adapted by MD Only from original press release.

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Contact: Karen Kreeger
University of Pennsylvania School of Medicine

Protecting Against Radiation

Radiation Exposure Health Effects

Brain Selectively Stores Most Useful Memories During Sleep

An afternoon nap dramatically boosts the brain’s learning capacity

Stem cell inactivation may be reason for male pattern balding says new Penn study

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Protecting Against Radiation

Radiation Exposure Health Effects

Brain Selectively Stores Most Useful Memories During Sleep

An afternoon nap dramatically boosts the brain’s learning capacity

Stem cell inactivation may be reason for male pattern balding says new Penn study

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Twitter: mdonly

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