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New research shows how it is possible to directly analyze DNA from a member of our own species who lived around 30,000 years ago. (Credit: iStockphoto/Andrey Prokhorov)

ScienceDaily (Jan. 4, 2010) – DNA that is left in the remains of long-dead plants, animals, or humans allows a direct look into the history of evolution. So far, studies of this kind on ancestral members of our own species have been hampered by scientists’ inability to distinguish the ancient DNA from modern-day human DNA contamination. 

Now, research by Svante Pääbo from The Max-Planck Institute for Evolutionary Anthropology in Leipzig, published online on December 31st in Current Biology — a Cell Press publication — overcomes this hurdle and shows how it is possible to directly analyze DNA from a member of our own species who lived around 30,000 years ago. 

DNA — the hereditary material contained in the nuclei and mitochondria of all body cells — is a hardy molecule and can persist, conditions permitting, for several tens of thousands of years. Such ancient DNA provides scientists with unique possibilities to directly glimpse into the genetic make-up of organisms that have long since vanished from the Earth. Using ancient DNA extracted from bones, the biology of extinct animals, such as mammoths, as well as of ancient humans, such as the Neanderthals, has been successfully studied in recent years. 

The ancient DNA approach could not be easily applied to ancient members of our own species. This is because the ancient DNA fragments are multiplied with special molecular probes that target certain DNA sequences. These probes, however, cannot distinguish whether the DNA they recognize comes from the ancient human sample or was introduced much later, for instance by the archaeologists who handled the bones. Thus, conclusions about the genetic make-up of ancient humans of our own species were fraught with uncertainty. 

Using the remains of humans that lived in Russia about 30,000 years ago, Pääbo and his colleagues now make use of the latest DNA sequencing (i.e., reading the sequence of bases that make up the DNA strands) techniques to overcome this problem. These techniques, known as “second-generation sequencing,” enable the researchers to “read” directly from ancient DNA molecules, without having to use probes to multiply the DNA. Moreover, they can read from very short sequence fragments that are typical of DNA ancient remains because over time the DNA strands tend to break up. By contrast, DNA that is younger and only recently came in contact with the sample would consist of much longer fragments. This and other features, such as the chemical damage incurred by ancient as opposed to modern DNA, effectively enabled the researchers to distinguish between genuine ancient DNA molecules and modern contamination. “We can now do what I thought was impossible just a year ago — determine reliable DNA sequences from modern humans — but this is still possible only from very well-preserved specimens,” says Pääbo. 

The application of this technology to the remains of members of our own species that lived tens of thousands of years ago now opens a possibility to address questions about the evolution and prehistory of our own species that were not possible with previous methods, for instance whether the humans living in Europe 30,000 years ago are the direct ancestors of present-day Europeans or whether they were later replaced by immigrants that brought new technology such as farming with them. 

The authors include Johannes Krause, Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany; Adrian Briggs, Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany; Matrin Kircher, Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany; Tomislav Maricic, Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany; Nicolas Zwyns, Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany; Anatoli Derevianko, Russian Academy of Sciences, Novosibirsk, Russia; Svante Paabo, Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany.


Story Source:

Adapted from materials provided by Cell Press

SingularityHub.com, January 2010, by Aaron Saenz  —  If you want to live forever you better start figuring out how your body is doing today. A&D Medical, a San Jose based company, and their Life Source products should allow anyone with a pulse to monitor their health via wireless connections. Their combo kit, which monitors activity, weight, and blood pressure, is now available for under $200 at Amazon! This puts the most basic indicators of health at almost anyone’s disposal.

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Need a better health monitoring system?

Those indicators will be transmitted via wireless connection to be stored and analyzed online. Using software form Life Source, you just log on, and watch how the little graphs change from day to day. There’s even a way for you to share your information with others so that an elderly patient can be observed by their caretakers, or so that weight loss buddies can encourage one another. After all, living forever would be boring if you did it by yourself.

Life Source has a whole host of monitors they sell, and the combo kit has three: a scale, a blood pressure cuff, and a pedometer/motion sensor for determining your daily activity. Other monitors can be cheaper, and some even fit these functions on a single watch. However, Life Source provides a USB wireless connector, allowing your monitors to automatically update online records and keep track of how your doing no matter where you go. That’s pretty cool.

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Learn about your vital signs and share them with others with Life Source.

We’ve seen similar approaches to health monitoring before, so none of this is exactly new. There are toilets that analyze blood pressure, and er…fluids. Body Trace also has a scale that will track your weight and send it for online recording/analysis. Toumaz has a high tech networking system that will interface with monitors in homes as well as hospitals. But Life Source is unique in that their system is an all-encompassing package.

Of course, by trying to hit it all, they’ve opened themselves up for some misses. Life Source’s online software (the Wellness Connected application) has the typical problems with allowing multiple instances of the same device on the same profile. Or even handling multiple profiles on the same device. Life Source does allow you to opt into using ActiHealth from Massachusetts based Fit Sense, but you can’t use both Wellness Connected and ActiHealth at the same time.

Whether you use Life Source, or some other monitoring system, knowing more about your health will help you maintain it. As the world continues to age, wellness systems will become more common, and tracking health information more important. I’m interested to see if the US trend of obesity encourages the sell of monitors. Americans might really be encouraged by tracking their fitness. After all, GI Joe said it best: knowing is half the battle.

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Will your child’s umbilical cord be a missed opportunity?

 

SingularityHub.com, January 2010, by Aaron Saenz  —  As if you didn’t have enough to worry about, now you’ve got to figure out if storing your child’s umbilical cord blood might just save his or her life. With the advent of amazing and clinically tested stem cell treatments, today’s expecting parents are faced with the real possibility that their child may one day require a stem cell transplant. Umbilical cords, with a host of hematopoietic (blood-developing) stem cells, may be puffy tubes filled with the equivalent of medical miracles. So, to store or not to store, that is the question. Let’s take a look at the benefits, costs, likely uses, and possible alternatives to freezing the umbilical cord blood of your baby. There’s a video about the collection method itself, after the break.

Here’s a short list of horrible illnesses that your child could develop and that might keep you awake at night: leukemia, lymphoma, aplastic anemia, severe sickle cell anemia, immune deficiencies, and heart disease. Each of these disasters are can be treated with hematopoietic stem cells. While you could get these cells from a bone marrow transplant, an umbilical cord allows a child to provide it’s own donation. So, if you chose to store your child’s cord blood, and he or she gets hit by one of the above disasters, you may be on your way to the ‘most cautious and loving parent award.’

Would you gamble with your baby’s life?

 It really all comes down to numbers. The chances of your child developing any one of these diseases in their youth may be as high as 1 in 5000 or possibly much greater. Some of these diseases, such as types of anemia, may require a donor other than the patient. In these cases, cord blood would be useless unless it belonged to a sibling. Parents who already have a child with a disease will likely store a new baby’s cord blood to help save the first child. As Hollywood loves to remind us, some parents get pregnant with donation in mind.

In most other cases, parents choosing to save the umbilical blood are really just hedging their bets against catastrophe. You could say its a different kind of health insurance. Those who want to take the extra precaution can do so. The rest will just roll the dice and take their chances. It’s that simple, right?

C’mon Singularity Hub reader, you should know that we’re all about helping you beat the odds and cheat death. First, you shouldn’t be relying on dumb luck. Working with a genome sequencing company, like 23andMe, can provide a cheap(ish) method to discovering if you and your mate have genetic markers that indicate an increased risk for certain diseases. With the proper genetic screening, you’ll see if your future baby’s chances are more like 1 in 5 or 1 in 5 million. These tests aren’t free, but they’d certainly help you decide if storing cord blood is worth the costs, and it’s information you may want to know anyway.

How do you collect cord blood? A private bank, Viacord, posted this helpful video on YouTube.

Let’s get down to some more numbers: $1000-$2000 for setting up an account, more than $100 per year for storage, hundreds for collection costs. That’s your minimum bill for storing cord blood. Depending on your financial situation, these prices may seem anything from a bargain to highway robbery. You should expect that storage will last 10-15 years. After that, you may not need the cells anymore.

Not that your child’s risk of severe illness goes down at age fifteen, sadly the opposite is true. No, it’s just that the few ounces of blood in the cord are suitable to developing enough stem cells for a baby or small child. When you’re little bundle of joy hits puberty, size becomes an issue. Of course, in ten or fifteen years scientists may be able to reliably multiply stem cells indefinitely. In that case, you may be storing that cord blood for a long time.

Can anyone give me a straight answer? …Not really, no.

The future won’t just see the possibility of multiplying stem cells, it may see the multiplication of their uses as well. The list of disasters that could be solved by hemapoietic cells could potentially get much longer. The general use of stem cells may expand as well. Stem cell treatments for diabetes, which affects almost 8% of children in the US, have had success. Arteriocyte and other companies are figuring out how to use cord cells to produce enough red blood cells for a traditional blood donation. Dr. Ralf Sodian of the University Hospital of Munich was able to develop completely new heart valves from umbilical cord stem cells in 2008 (that’s amazing!) The list of possible uses goes on and on.

On the other side of the coin, the possible risks of harvesting cord blood are not well understood either. While people have been saving cord blood since the 1970s, no one can say for certain if an infant will be adversely affected by the collection. We know the risks for lower blood volume and anemia aren’t zero, but we can’t predict what future research may reveal about the importance of an infant getting all their cord blood. I should point out that in a non-collection delivery, cords are often cut quickly, so many infants may not normally get their tube of blood anyway.

Public vs. Private Cord Blood Banks 

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Private storage may cost you more than $4000. Up to 50% of publicly donated cord blood is not used to treat patients. In either case, collected cord blood may not contain enough stem cells to be of any use.

Just to make things more complicated, you also have the option of donating your child’s cord blood. Like bone marrow, cord blood has the chance of saving another child’s life. Cord blood donors don’t even have to be a perfect match because the stem cells in the cord are naive (undeveloped). The American Academy of Pediatricians (AAP) doesn’t recommend universal private storage of cord blood because the possibility of autologous use seems small, and as such, they don’t consider it a wise investment. AAP and the National Marrow Donor Program, however, recognize that donating cord blood is a sure way to help treat children who are suffering from leukemia and other diseases in the disaster list. As we mentioned above, some illnesses can’t be treated by your own stem cells. Sharing cord blood, rather than storing it against a rainy day, may be a more useful choice. Certain races and ethnicities are in special need of cord donation because of limited supplies. This is a common problem in all manner of donations.

Many public cord blood banks will cover the collection costs if you choose to donate your child’s cord. They save some money by only having to store the cord for a short time (the need is that high). Many private banks will test and add your child’s cord blood information onto the national database while still storing it for your personal use. In that way, you could keep the cells for your child if he or she needs it, and if they do not need it you can match the blood to a needy recipient.

Donating your child’s cord blood isn’t all about saving lives, however. 50% of all donations are not even stored. Many collected cord blood bags do not contain enough stem cells to adequately serve as a transplant (this affects private storage as well). Others are donated to science for research. Actually, that leads to lives being saved too, but not in the ‘here’s a picture of the child you helped’ sort of way.

Yeah, ask the blogger, I’m sure he knows what to do.

So here’s how I break it down:

  • The chances of your child ever needing his or her cord blood is small right now. You can use genetic testing to help you inform your decision, but at some level it’s going to remain a crapshoot.
  • The costs of storing umbilical blood privately is on the order of $3000-$4000 total (collection fees, initiation fees, storage costs for around ten to fifteen years).
  • The risks of harvesting an umbilical cord are small, but not zero. Undiscovered risks are always a possibility just like undiscovered benefits.
  • Those undiscovered benefits will continue to grow as medical research explores the uses of stem cells. However, there’s no guarantee that umbilical cord cells would be preferred or even necessary in such treatments.
  • There is a current need for cord blood donation. Whether for science or for little kids with leukemia, your child’s blood could make a difference. It could also get tossed in the garbage because it didn’t contain enough stem cells.

Doing a cost benefit analysis will be easier for some than others. Many simply do not have four grand to spare when starting their families. For those of you with large disposable incomes and a baby on the way, I can see how the choice may be more difficult. Since I have no idea how to make money nor babies I am saved from that dilemma. If you are facing this choice, best of luck and try to keep in mind that some stem cell treatments will certainly be available to all children, cordless or otherwise.

Harvard Medical School, January 5, 2009  —  Your thyroid is a small, butterfly-shaped gland which weighs less than an ounce. When functioning normally, it perches unobtrusively with its wings wrapped around the front of your windpipe (trachea), below your voice box (larynx). Despite its slight size, your thyroid controls the rate at which every cell, tissue, and organ in your body functions, from your muscles, bones, and skin to your digestive tract, brain, heart, and more. It does this primarily by secreting hormones that control how fast and efficiently cells convert nutrients into energy-a chemical activity known as metabolism-so that the cells can perform their functions.

How the thyroid gland works

Just as your car engine can’t run without gasoline, your thyroid needs fuel to produce thyroid hormone. This fuel is iodine. Iodine is found in such foods as iodized table salt, seafood, bread, and milk. When you eat these foods, the iodine passes into your bloodstream. Your thyroid then extracts this necessary ingredient from your blood and uses it to make two kinds of thyroid hormone: thyroxine, called T4 because it contains four iodine atoms, and triiodothyronine, or T3, which contains three iodine atoms. The thyroid’s output consists primarily of T4. Most of the T3 the body needs is created outside the thyroid in organs and tissues that use T3, such as the liver, kidneys, and brain. These tissues convert T4 from the thyroid into T3 by removing an iodine atom.

As the thyroid produces thyroid hormone, it stores it in a vast number of microscopic follicles. When the body needs thyroid hormone, the thyroid secretes it into your bloodstream in quantities needed for the metabolic needs of your cells. The hormone easily slips into cells and attaches to special receptors.

Your car engine burns fuel, but it is you who tells it how hard to work by stepping on the gas pedal. The thyroid also needs to be told what to do. It takes its orders from your pituitary gland, located at the base of your brain. No larger than a pea, the pituitary is sometimes known as the “master” gland, because it controls functions of the thyroid and other glands in the endocrine system. The pituitary gland signals the thyroid to tell it how much hormone to make. The messages come in the form of thyroid-stimulating hormone (TSH). TSH levels in your bloodstream rise or fall depending on whether there is enough thyroid hormone in your system. Higher levels of TSH prompt the thyroid to produce more hormone, until TSH levels come down to a constant level. Conversely, low TSH levels signal the thyroid to slow down production.

 

When things go wrong

Normally, the thyroid doles out just the right amount of hormone to keep your body running smoothly. TSH levels remain fairly constant, yet they respond to the slightest changes in T4 levels, and vice versa.

But even the best network is subject to interference. Outside influences-such as disease or certain medicines-can break down communication. When this happens, the thyroid might not produce enough hormone, slowing down all of your body’s functions, a condition known as hypothyroidism or underactive thyroid. Or your thyroid could produce too much hormone, sending your systems into overdrive, a condition known as hyperthyroidism, or overactive thyroid.

 

Signs and symptoms of hypothyroidism

The symptoms and course of hypothyroidism are quite variable. One person may become hypothyroid quickly over a few months, while another develops symptoms slowly over many years, making the condition even more difficult to detect. Generally speaking, the lower thyroid hormone levels fall, the more pronounced symptoms will be. Still, a person with severe disease might not experience severe symptoms. This is particularly true among older people. Following is a list of classic symptoms.

Constant tiredness
Cold intolerance
Loss of appetite
Weight gain
Slow pulse
Enlarged thyroid gland
Depression
Dry skin
Brittle fingernails
Hair loss
Constipation
Joint pain
Heavier menstrual periods
High cholesterol
Carpal tunnel syndrome
More common in older people:
High cholesterol
Heart failure
Bowel movement changes constipation, or diarrhea
Joint pain or general muscular pain
Depression or psychosis
Dementia
Unsteadiness while walking

 

Signs and symptoms of hyperthyroidism

The symptoms of hyperthyroidism tend to come on slowly and also vary from person to person. It’s not always obvious that symptoms such as excess thirst or increased appetite are an indication that something is wrong. Often, people don’t see a doctor until they experience palpitations or shortness of breath.

Enlarged thyroid gland
Heat intolerance
Exhaustion
Emotional changes (insomnia, anxiety that is sometimes mixed with depression)
Nervousness
Excessive perspiration
Excessive thirst
Excessive hunger
Weight loss
Racing and irregular heartbeat
Fast pulse
Hand tremors
Muscle weakness
Diarrhea
Eye problems
Lighter menstrual periods
Infertility
Generalized itching (with or without hives)

 

More common in older people

Depression
Heart failure
Irregular heartbeat

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Peter Dazeley/Getty Images

 

The New York Times, January 5, 2009, by Gretchen Reynolds  —   For years, cardiologists were aware that heart attacks are more common during the winter months than in any other season. Most assumed that the cause was cold weather. But then researchers in California examined death certificates in Los Angeles County, an area not known for its inclement winters, and found that, even there, fatal heart attacks spiked during the winter months. More specifically, they started rising around Thanksgiving, climbed inexorably through Christmas and peaked on New Year’s Day. A subsequent study of death certificates nationwide, published in Circulation in 2004, confirmed the association between the two holidays and heart-attack deaths. It was accompanied by a cheery editorial headlined “The ‘Merry Christmas Coronary’ and ‘Happy New Year Heart Attack’ Phenomenon.”

Why the number of heart-attack deaths should surge so significantly during the holidays still is not clear, although cardiologists have some well-founded guesses. “We suspect there is often an inappropriate delay in seeking medical attention” at this time of year, says Dr. Robert A. Kloner, a professor of medicine at the University of Southern California, a cardiologist at Good Samaritan Hospital and the lead author of both the 2004 study of deaths in Los Angeles County and the accompanying editorial. “People ignore the pain in their chest,” perhaps because they don’t wish to disrupt the festivities or they misinterpret the ache as overindulgence, Dr. Kloner says. By the time they get to an emergency room, it’s too late to save them. Stress and tension likely play a role, too. “Spending time with family members can be trying,” he says. “And there are often concerns about financial issues, buying presents and so on.” Even a wood-burning fireplace, a romantic symbol of wintry, holiday evenings, could be a contributing factor, because particulate matter in the air has been connected to an increase in the risk of heart attacks, Dr. Kloner says.

A provocative new study published this year in the journal Heart and Circulatory Physiology suggests, however, that there may be a novel way to test at least one element of your heart’s health right in your own living room, right in the middle of the holidays. Sit on the floor with your legs stretched straight out in front of you, toes pointing up. Reach forward from the hips. Are you flexible enough to touch your toes? If so, then your cardiac arteries probably are also flexible.

In the study’s experiment, scientists from the University of North Texas and several Japanese universities recruited 526 healthy adults between the ages of 20 and 83 and had them perform the basic sit-and-reach test described above, although their extensions were measured precisely with digital devices. Taking into account age and gender, researchers then sorted the subjects into either the high-flexibility group or the poor-flexibility group.

Next, using blood-pressure cuffs at each person’s ankles and arms, researchers estimated how flexible their arteries were. Cardiac artery flexibility is one of the less familiar elements of heart health. Supple arterial walls allow the blood to move freely through the body. Stiff arteries require the heart to work much harder to force blood through the unyielding vessels and over time could, according to Kenta Yamamoto, a researcher at North Texas and lead author of the study, contribute to a greater risk for heart attack and stroke.

What the researchers found was a clear correlation between inflexible bodies and inflexible arteries in subjects older than 40. Adults with poor results on the sit-and-reach test also tended to have relatively high readings of arterial stiffness. In short, the study concluded that “a less flexible body indicates arterial stiffening, especially in middle-aged and older adults.” No such correlation was found in those under 40, even when gender and fitness were considered as factors.

These results do not mean, of course, that people in the inflexible group were in imminent danger of a heart attack on Christmas Day. Arterial stiffening does not indicate or inevitably lead to arterial disease, Mr. Yamamoto emphasizes. In fact, some degree of arterial stiffening is inevitable with age. But the stiffer your arteries are, the less efficient your heart.

How it is that stiff muscles in the back and legs are linked to stiff tissues near the heart is an issue that hasn’t been fully elucidated, Mr. Yamamoto says, although arterial walls are composed of the same kinds of elastic tissues as muscles elsewhere in the body. So it’s likely, he says, that alterations in the composition of muscle tissues in the lower back (including aging-related alterations in the amount of collagen within the muscles) could be occurring in the arterial walls at the same time.

What is surprising are some early indications that increasing your flexibility might somehow loosen up your arteries, too. That was the accidental and, as yet unreplicated finding of a small 2008 study at the University of Texas at Austin. The study was designed to examine whether weight lifting increased arterial stiffness. (It didn’t, at least on this occasion.) The control group consisted of people who stretched. They were not expected to show any change in cardiac function, but over the course of 13 weeks they in fact increased the pliability of their arteries by more than 20 percent.

Mr. Yamamoto and his colleagues are currently conducting an ambitious study to determine just how and whether stretching directly affects the arteries. The results won’t be available for some time. Until then, Mr. Yamamoto says, it’s best to consider your flexibility (or lack thereof) as a marker of your probable arterial elasticity. “If you can touch your toes in the sit-and-reach test, your flexibility is good,” he says. If you can’t, you might consider talking to your cardiologist – although, remember, as Mr. Yamamoto points out, that tight arteries are not necessarily diseased arteries. They’re just less than ideally fit.

As for avoiding the “Merry Christmas Coronary,” Dr. Kloner’s advice is succinct: “Don’t ignore symptoms,” he says. Avoid overimbibing, too, and tamp down stress. If this requires turning down an invitation from a wheedling relative, you could always try explaining that your cardiologist would say that it’s for the best.

 

Abstract

Poor trunk flexibility is associated with arterial stiffening

Am J Physiol Heart Circ Physiol. 2009 Oct;297(4):H1314-8. Epub 2009 Aug 7.

Yamamoto K, Kawano H, Gando Y, Iemitsu M, Murakami H, Sanada K, Tanimoto M, Ohmori Y, Higuchi M, Tabata I, Miyachi M.

Health Promotion and Exercise Program, National Institute of Health and Nutrition, Tokyo, Japan. kyamamot@hsc.unt.edu

Flexibility is one of the components of physical fitness as well as cardiorespiratory fitness and muscular strength and endurance. Flexibility has long been considered a major component in the preventive treatment of musculotendinous strains. The present study investigated a new aspect of flexibility. Using a cross-sectional study design, we tested the hypothesis that a less flexible body would have arterial stiffening. A total of 526 adults, 20 to 39 yr of age (young), 40 to 59 yr of age (middle-aged), and 60 to 83 yr of age (older), participated in this study. Subjects in each age category were divided into either poor- or high-flexibility groups on the basis of a sit-and-reach test. Arterial stiffness was assessed by brachial-ankle pulse wave velocity (baPWV). Two-way ANOVA indicated a significant interaction between age and flexibility in determining baPWV (P < 0.01). In middle-aged and older subjects, baPWV was higher in poor-flexibility than in high-flexibility groups (middle-aged, 1,260 +/- 141 vs. 1,200 +/- 124 cm/s, P < 0.01; and older, 1,485 +/- 224 vs. 1,384 +/- 199 cm/s, P < 0.01). In young subjects, there was no significant difference between the two flexibility groups. A stepwise multiple-regression analysis (n = 316) revealed that among the components of fitness (cardiorespiratory fitness, muscular strength, and flexibility) and age, all components and age were independent correlates of baPWV. These findings suggest that flexibility may be a predictor of arterial stiffening, independent of other components of fitness.

PMID: 19666849 [PubMed – indexed for MEDLINE]

Johns Hopkins School of Medicine, January 5, 2010  –  By combining a research technique that dates back 136 years with modern molecular genetics, a Johns Hopkins neuroscientist has been able to see how a mammal’s brain shrewdly revisits and reuses the same molecular cues to control the complex design of its circuits.

 

Details of the observation in lab mice, published Dec. 24 in Nature, reveal that semaphorin, a protein found in the developing nervous system that guides filament-like processes, called axons, from nerve cells to their appropriate targets during embryonic life, apparently assumes an entirely different role later on, once axons reach their targets. In postnatal development and adulthood, semaphorins appear to be regulating the creation of synapses — those connections that chemically link nerve cells.

 

“With this discovery we’re able to understand how semaphorins regulate the number of synapses and their distribution in the part of the brain involved in conscious thought,” says David Ginty, Ph.D., a professor in the neuroscience department at the Johns Hopkins University School of Medicine and a Howard Hughes Medical Institute investigator. “It’s a major step forward, we believe, in our understanding of the assembly of neural circuits that underlie behavior.”

 

Because the brain’s activity is determined by how and where these connections form, Ginty says that semaphorin’s newly defined role could have an impact on how scientists think about the early origins of autism, schizophrenia, epilepsy and other neurological disorders.

 

The discovery came as a surprise finding in studies by the Johns Hopkins team to figure out how nerve cells develop axons, which project information from the cells, as well as dendrites, which essentially bring information in. Because earlier work from the Johns Hopkins labs of Ginty and Alex Kolodkin, Ph.D., showed that semaphorins affect axon trajectory and growth, they suspected that perhaps these guidance molecules might have some involvement with dendrites.

 

Kolodkin, a professor in the neuroscience department at Johns Hopkins and a Howard Hughes Medical Institute investigator, discovered and cloned the first semaphorin gene in the grasshopper when he was a postdoctoral fellow. Over the past 15 years, numerous animal models, including strains of genetically engineered mice, have been created to study this family of molecules.

 

Using two lines of mice — one missing semaphorin and another missing neuropilin, its receptor — postdoctoral fellow Tracy Tran used a classic staining method called the Golgi technique to look at the anatomy of nerve cells from mouse brains. (The Golgi technique involves soaking nerve tissue in silver chromate to make cells’ inner structures visible under the light microscope; it allowed neuroanatomists in 1891 to determine that the nervous system is interconnected by discrete cells called neurons.)

 

Tran saw unusually pronounced “spines” sprouting willy-nilly in peculiar places and in greater numbers on the dendrites in the neurons of semaphorin-lacking and neuropilin-lacking mice compared to the normal wild-type animals. It’s at the tips of these specialized spines that a lot of synapses occur and neuron-to-neuron communication happens, so Tran suspected there might be more synapses and more electrical activity in the neurons of the mutant mice.

 

The researchers tested this hypothesis by examining even thinner brain slices under an electron microscope.

 

The spines of both semaphorin-lacking and neuropilin-lacking mice were dramatically enlarged, compared to those of the smaller, spherical-looking spines in the wild-type mice. In wild types, Tran generally noted a single site of connection per spine. In the mutants, the site of connection between two neurons was often split.

 

Next, the team recorded the electrical output of mutant and wild-type neurons and found that the mutants, with more spines and larger spines, also had about a 2.5-times increase in the frequency of electrical activity, suggesting that this abnormal synaptic transmission is due to an increase in the number of synapses.

 

What causes synapses to form or not form in appropriate or inappropriate places is an extremely important and poorly understood process in the development of the nervous system, Kolodkin says, explaining that the neurons his team studies can have up to 10,000 synaptic connections with other neurons. If connections between neurons are not being formed how and where they’re supposed to, then miscommunication occurs and circuits malfunction; as a result, any number of diseases or disorders might develop.

 

“Seizures can be interpreted as an uncontrolled rapid-firing of certain neural circuits,” Kolodkin asserts. “Clearly there’s a deficit in these animals that has a human corollary with respect to epilepsy. It’s also thought that schizophrenia and autism spectrum disorders have developmental origins of one sort or another. There likely are aspects to the formation of synapses — if they’re not in the correct location and in the correct number — that lead to certain types of defects. The spine deficits in these mice that are lacking semaphorin or its receptor appear very similar to those that are found in Fragile X, for instance.”

 

This work was supported by the National Institutes of Health, National Science Foundation, and the Howard Hughes Medical Institute.

 

Johns Hopkins authors of this paper are Tracy S. Tran, Alex L. Kolodkin, David D. Ginty, Richard L. Huganir, Roger L. Clem, and Dontais Johnson. Other authors are Maria E. Rubio of the University of Connecticut; and Lauren Case and Marc Tessier-Lavigne, of Stanford University.


Story Source:

Adapted from materials provided by Johns Hopkins Medical Institutions

January 5, 2010, By Patrick Cox, Breakthrough Technology Alert

Marco Island, Florida

 

2010 may be the most incredible year in history for medical technology stocks. A handful of truly amazing technologies-in-development are likely to make headlines this coming year…and these headlines could produce huge gains in the share prices of selected medical technology companies…

 

You know that our bodies are incredibly complex. All throughout human history, we’ve fought to understand more about how our bodies work. For millennia, progress was slow. We made our breakthroughs in fits and starts.

 

Complex medical procedures – such as the groundbreaking heart surgery of 1944, was just the beginning. After that, vaccine technology took off with the development of the Polio vaccine in 1952. Soon thereafter, imaging technology began to allow doctors and scientists to take the next step and peer deeper into our bodies.

 

The trend continues today.

 

With the benefit of ultra-advanced microscopes and what’s called “molecularly precise” manufacturing, scientists are figuring out how to use our own cells to help repair vital organs like the heart. “Patients will receive injections containing… their own cells… extracted and multiplied,” BBC News explains, “[to] generate new tissue [and] repair damaged regions.”

 

So rather than relying on some outside treatment, the future of medicine will be in figuring out how to make your body heal itself and rejuvenate itself. No surgery. No invasive procedure of any kind. It’s this kind of promise that makes me believe 2010 will be the dawning of an amazing age of medical marvels.

 

Here’s another example: Vaccines that cure diseases AFTER infection.

 

The way doctors treat viruses now is fairly straightforward. If there’s a vaccine available, the doctor gives it to you ahead of time so you don’t get sick. In other words, getting the “cure” ahead of time is the only way to treat a virus.

 

This model works. Sometimes.

 

But new flu strains emerge all the time. These strains change, become stronger. So imagine the profit potential of a process that could kill the flu – or nearly any other virus – AFTER you contracted it. Now imagine this virus cure coming in the form of a simple skin patch.

 

You get the flu. You put on a patch the size of a band-aid. The flu goes away. Voila. It’s that simple. I am monitoring a company that is trying to develop just such a technology. It is one of my “6 Companies Ready to Change the World in 2010.”

 

Another company I’m monitoring is exploring a revolutionary process for repairing spinal cords. Their work could someday mean precisely this: If someone suffers a spinal cord injury and the paralysis that comes with it, this company’s technology could repair the spinal cord. Just like new.

 

“Cells from the nose may help spinal injury victims walk again,” Fox News explains. “It’s a relatively simple procedure to take them from the patient, grow more of them in the laboratory and then insert them back into the same person.”

 

This revolutionary little firm finally gained media and analyst awareness in 2009 due to its ongoing tests. And this company isn’t just interested in spinal repair – it has groundbreaking cancer treatments and life-extension research and tests currently underway as well. Their blueprint is simple: Save the life of the cell and you live longer…or at least better.

 

Lastly, imagine a simple, fast procedure that gives you a rebuilt heart functionally the same as the clean-beating heart of a 29-year-old person. That’s the full promise here. How big do you think this market could be?

 

Now here’s some background. In May, the CEO of the company that might offer these cures this year made an announcement about his work at an exclusive conference…

 

What did he announce? Cells he’s working on show the potential to re- grow cartilage. Just think for a second what that could mean for folks with arthritis. All that pain and suffering, simply going away. Now imagine the same technology applied to heart cells. That’s exactly what this researcher and his team are working on.

 

2010 will be, I predict, the year it all comes together.

 

The profits of the past 12 months that some folks have booked are nothing compared to what’s in store for the years ahead. Because it’s not just heart treatments and virus cures that could soon be available.

 

I’m talking about a Golden Age of Medical Marvels.