http://health.groups.yahoo.com/group/FA_babelFAmily/message/2036 (ITA)

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2057 (ESP)

http://finance.boston.com/boston?GUID=6067499&Page=MediaViewer&ChannelID=3198

SRI International Research Team Identifies Rare Sleep-Activated Neurons in the Cerebral Cortex

Findings May Have Important Implications for Treatment of Sleep Disorders and for Understanding Mood and Memory

MENLO PARK, CA -- (MARKET WIRE) -- 07/21/08 -- SRI International announced today that a research team has identified the first example of neurons that are activated in the cerebral cortex during slow wave sleep (SWS). The research, led by Dmitry Gerashchenko and Thomas Kilduff, will be published in the Proceedings of the National Academy of Sciences (PNAS) in a paper titled "Identification of a Population of Sleep-Active Cerebral Cortex Neurons." The paper is available via the PNAS Web site starting July 21.

The presence of slow waves in the electroencephalogram (EEG) is the distinctive "signature" of SWS and a type of activity that does not normally occur during wakefulness. For years, researchers have hypothesized that 'slow-wave activity' (SWA) is correlated with the recuperative properties of sleep and the brain's ability to learn, in part, because brain cells are relatively quiet during this time. While populations of neurons activated during sleep have been identified in the forebrain and the hypothalamus, up until this point, neurons in the cortex have been seen as dormant. These new results show that a group of rare neurons are active, rather than at rest, during SWS.

"To date, the role of the cortex in SWA has been a mystery since all cortical cells were thought to be quiescent during SWS," said SRI's Dmitry Gerashchenko. "We have discovered that the cortex not only plays a role, but harbors a small population of neurons that is activated during spontaneous and catch-up sleep, which occurs after sleep deprivation."

The authors found that these neurons are active in the cortex of three species (mice, rats and hamsters) during SWS. "Since these neurons also exist in the human brain, they likely 'turn on' while we sleep as well," said SRI's Thomas Kilduff, senior director of Neurobiology at SRI in whose laboratory at SRI the work was conducted. Kilduff is also a consulting professor at Stanford University School of Medicine. "As such, these neurons will be important to study in sleep disorders such as insomnia. Activation of these cells during sleep may have important implications for aspects of our behavior and cognitive activities that depend heavily on sleep, such as our daytime performance, memory and mood."

The research also found that the type of neurons that are "turned on" during sleep are the rarest of all currently known cortical neurons. These cells express the enzyme neuronal nitric oxide synthase (nNOS) and thus make nitric oxide (NO), which regulates blood flow in the brain and periphery.

A notable feature of these results is that the proportion of nNOS neurons that are activated seems to be related to the magnitude of homeostatic sleep drive; that is, the longer animals are kept awake, the more nNOS neurons are activated when the animals finally go to sleep. Additionally, nNOS neurons are the only inhibitory cell type known to have long projections both within and between the two hemispheres of the brain.

"The next step will be to determine whether these neurons are the 'superhighway' that conducts slow waves across the cortex during sleep," Kilduff continued.

The research was conducted by Dmitry Gerashchenko (SRI International), Jonathan P. Wisor (SRI International), Deirdre Burns (SRI International), Rebecca K. Reh (University of Washington), Priyattam J. Shiromani (West Roxbury VA Medical Center and Harvard Medical School), Takeshi Sakurai (Kanazawa University), Horacio O. de la Iglesia (University of Washington), and Thomas S. Kilduff (SRI International and Stanford University School of Medicine).

The research was supported by the National Heart, Lung and Blood Institute, National Institute of Aging, National Institute of Mental Health, and the Sleep Research Society Foundation.

Gerashchenko presented the team's findings at the SLEEP 2008 symposium, "New Developments in Sleep Research: Molecular Genetics, Gene Expression and Systems Neurobiology" on Monday, June 9. For details on the symposium, visit: http://www.sleepmeeting.org/.

About SRI International

Silicon Valley-based SRI International (www.sri.com) is one of the world's leading independent research and technology development organizations. Founded as Stanford Research Institute in 1946, SRI has been meeting the strategic needs of clients and partners for more than 60 years. The nonprofit research institute performs client-sponsored research and development for government agencies, businesses, and foundations. In addition to conducting contract R&D, SRI licenses its technologies, forms strategic partnerships, and creates spin-off companies.

Media Contact:
Lindsay Sheppard
SRI International
(650) 859-2491
 

http://www.medicalnewstoday.com/articles/116566.php

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2044 (ITA)

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2058 (ESP)

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2063 (FRA)

Translated by Tom Sathre

Note from babelFAmily:  Daniela is an Italian patient with Friedreich’s ataxia, undergoing treatment with Deferiprone (an iron chelator) and Lokomat (specialized physical therapy).  For more information, go to the following link:

http://health.groups.yahoo.com/group/FA_babelFAmily/message/1508 (ENG)

Message from Daniela to Gian Piero Sommaruga, distributed with Daniela’s approval

From: Daniela

For: “gippi”

Sent on: Wednesday July 23, 2008 9:44 PM

Topic: Greetings

Hi Giampi,

First of all I would like to say hello, because vacation time is approaching, and before long, I’ll be going off;  besides, I wanted to keep you informed about how it’s going for me.

Up to now I have been able to maintain the improvements I made in the hospital, and I also have better truncal and neck posture, together with better movements and coordination.

In some manual movements and some exercises, such as putting pegs in holes and handling the Rubik’s cube, I have been able to do it faster and more correctly.

My muscle mass has increased a little all over my body.

I have improved my standing posture when I am upright with my weight on both legs, and also my voice is clearer.

See you soon and happy vacation!

Dany

http://www.sciencedaily.com/releases/2008/07/080724123241.htm

Key Mechanism Of Cellular Damage In Aging And Disease Discovered

Reactive oxygen species (ROS), which include free radicals, are highly reactive molecules that force change upon many molecules they encounter. The body uses ROS to signal for wound healing and to destroy invaders. Excess amounts, however, damage sensitive cell components, including proteins and DNA, in a process called oxidative stress. ROS are kept in check by the body's natural antioxidants, but when uncontrolled can lead to disease.

These highly reactive molecules are created as a side effect when structures within all human cells, the mitochondria, use oxygen to convert food into energy for life. Researchers once thought that altered mitochondrial function was important only in rare genetic diseases, but recent studies have revealed that oxidative stress plays a role in conditions that afflict many millions of patients. As a result, mitochondrial medicine is gaining momentum as groups like the Mitochondria Interest Group at the National Institutes of Health, professional societies and drug companies push basic science toward drug discovery.

"Our study provides a better glimpse of why a cell under assault by disease makes 10 times as many reactive oxygen species as the same cell when healthy," said Shey-Shing Sheu, Ph.D., professor of Pharmacology and Physiology at the University of Rochester Medical Center, and a study author. "We have discovered a chemical tool for investigating how diseases cause damage, mitochondrion by mitochondrion, which should represent a tremendous advance as both a disease biomarker and for drug discovery."

Meltdown at the Powerhouse

The primary role of mitochondria is to convert food into chemical energy in the form of adenosine triphosphate (ATP), the molecule used by all human cells to store energy. To drive ATP production, electrons are passed along a series of enzymes, but a few "leak" during the process. Leaked electrons react with available oxygen to form the reactive oxygen species, termed superoxide. The emerging theory is that excess superoxide production causes the mitochondria to swell and rupture, resulting in a "cellular energy crisis" that ultimately leads to cell death in the many diseases of oxidative injury.

In the Cell study, researchers used a newly patented, protein-based probe to discover, and make visible, for the first time, fleeting bursts of superoxide production in mitochondria termed "superoxide flashes." The superoxide bursts oxidize cysteine residues in the probe, causing it to emit fluorescent light, which can then be detected and analyzed for patterns. Experiments not only identified superoxide flashes for the first time, but also confirmed that they exhibit a similar size and duration, regardless of the cell type they occur in. This uniform pattern of low-level superoxide production in the mitochondria of healthy cells is normal, perhaps keeping the ROS signaling system ready to fire, researchers said. The one quality of superoxide flashes found to vary was frequency, which dramatically increased during disease.

The research team looked at one kind of oxidative stress in particular: that caused when the oxygen supply to the heart is initially cut off (e.g. during a heart attack or stroke) and then re-established. When heart muscle cells were exposed to a non-oxygen solution for six hours, superoxide flash frequency decreased four-fold, to one event per 100 seconds. Upon re-introduction of oxygen, superoxide production increased eight-fold, confirming past work that re-oxygenation after a heart attack comes with a burst of destructive and uncontrolled superoxide production and oxidative stress.

Existing methods for measuring superoxide production involve chemical indicators or older protein probes, but these previous methods are not specific for superoxide, are damaged by light and provide a limited signal above background noise. The new probe is more sensitive, specific to superoxide, provides a stronger signal than other probes, and is the first to permit reversible measurements of superoxide levels on a millisecond timescale. The research team also created a genetically engineered mouse that expresses the probe within the mitochondria of all of its cells. These "superoxide mice" will enable researchers in the future to quantify the impact of uncontrolled mitochondrial superoxide production across many diseases.

Efforts to develop antioxidant drugs (e.g. vitamin E) to treat diseases of increased oxidative stress have met with limited success to date because they tried to eliminate ROS, rather than maintain the right amount, Sheu said. He established the Mitochondrial Research & Innovation Group (MRIG) at the Medical Center in 2002 with the goal of designing therapies to deliver precise amounts of antioxidants to the mitochondria of diseased cells only. MRIG teams are, for example, screening through compounds to confirm that oxidative stress can be reversed by mitochondria-specific drugs. The new superoxide flash probe will provide a powerful tool for determining the effectiveness of new classes of antioxidant drugs in reducing superoxide production at the right place and time.

The "birthday" for superoxide flashes came in June of 2003 in the lab of Robert Dirksen, Ph.D., associate professor of Pharmacology and Physiology at the Medical Center, when Linda Groom observed spontaneous bursts of fluorescent light using the newly developed protein-based superoxide indicator.

The current paper's lead author was Wang Wang, Ph.D. formerly a postdoctoral fellow at the National Institute on Aging at the National Institutes of Health. Aiwu Cheng, Jinhu Yin, Weidong Wang, Edward Lakatta and Mark Mattson also contributed from the NIH, as did Joseph Kao from the University of Maryland. Also contributing from Peking University in Beijing were Huaqiang Fang, Wanrui Zhang, Jie Liu, Xianhua Wang, Kaitao Li, Peidong Han, Ming Zheng, and Heping Cheng, the corresponding author.

"One co-author on the current paper, Dr. Cheng of Peking University, 15 years ago published a seminal study regarding local calcium release events, or calcium sparks," Dirksen said. "This study has been cited more than 900 times and has provided a major contribution to our understanding how the heart beats and why it fails. We believe that our serendipitous discovery of local mitochondrial superoxide flash events could be even more important because superoxide flash frequency may provide an accurate, real-time picture of how uncontrolled oxidative stress contributes to the progression of several, debilitating cardiovascular and neurological diseases."

Adapted from materials provided by University of Rochester Medical Center, via EurekAlert!, a service of AAAS.

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2050 (ITA)

http://www.medicalnewstoday.com/articles/115773.php

MIT Identifies Cells For Spinal-Cord Repair - Could Lead To Non-Surgical Treatment For Injuries

Article Date: 23 Jul 2008 - 0:00 PDT

A researcher at MIT's Picower Institute for Learning and Memory has pinpointed stem cells within the spinal cord that, if persuaded to differentiate into more healing cells and fewer scarring cells following an injury, may lead to a new, non-surgical treatment for debilitating spinal-cord injuries.

The work, reported in the July issue of the journal PLoS (Public Library of Science) Biology, is by Konstantinos Meletis, a postdoctoral fellow at the Picower Institute, and colleagues at the Karolinska Institute in Sweden. Their results could lead to drugs that might restore some degree of mobility to the 30,000 people worldwide afflicted each year with spinal-cord injuries.

In a developing embryo, stem cells differentiate into all the specialized tissues of the body. In adults, stem cells act as a repair system, replenishing specialized cells, but also maintaining the normal turnover of regenerative organs such as blood, skin or intestinal tissues.

The tiny number of stem cells in the adult spinal cord proliferate slowly or rarely, and fail to promote regeneration on their own. But recent experiments show that these same cells, grown in the lab and returned to the injury site, can restore some function in paralyzed rodents and primates.

The researchers at MIT and the Karolinska Institute found that neural stem cells in the adult spinal cord are limited to a layer of cube- or column-shaped, cilia-covered cells called ependymal cells. These cells make up the thin membrane lining the inner-brain ventricles and the connecting central column of the spinal cord.

"We have been able to genetically mark this neural stem cell population and then follow their behavior," Meletis said. "We find that these cells proliferate upon spinal cord injury, migrate toward the injury site and differentiate over several months."

The study uncovers the molecular mechanism underlying the tantalizing results of the rodent and primate and goes one step further: By identifying for the first time where this subpopulation of cells is found, they pave a path toward manipulating them with drugs to boost their inborn ability to repair damaged nerve cells.

"The ependymal cells' ability to turn into several different cell types upon injury makes them very interesting from an intervention aspect: Imagine if we could regulate the behavior of this stem cell population to repair damaged nerve cells," Meletis said.

Upon injury, ependymal cells proliferate and migrate to the injured area, producing a mass of scar-forming cells, plus fewer cells called oligodendrocytes. The oligodendrocytes restore the myelin, or coating, on nerve cells' long, slender, electrical impulse-carrying projections called axons. Myelin is like the layer of plastic insulation on an electrical wire; without it, nerve cells don't function properly.

"The limited functional recovery typically associated with central nervous system injuries is in part due to the failure of severed axons to regrow and reconnect with their target cells in the peripheral nervous system that extends to our arms, hands, legs and feet," Meletis said. "The function of axons that remain intact after injury in humans is often compromised without insulating sheaths of myelin."

If scientists could genetically manipulate ependymal cells to produce more myelin and less scar tissue after a spinal cord injury, they could potentially avoid or reverse many of the debilitating effects of this type of injury, the researchers said.

This study was supported by grants from the Swedish Research Council, the Swedish Cancer Society, the Foundation for Strategic Research, the Karolinska Institute, EuroStemCell and the Christopher and Dana Reeve Foundation.

Source: Deborah Halber http://www.mit.edu

http://www.aduc.it/dyn/salute/noti.php?id=227760

AMERICHE - USA
Studio: cellule staminali per riparare lesioni al midollo spinale

24 Luglio 2008

Ricercatori del MIT Picower Institute for Learning and Memory di Cambridge, Massachusetts, e del Karolinska Institute di Stoccolma rivelano che potrebbe essere possibile migliorare le lesioni alla spina dorsale usando le cellule staminali, e senza ricorrere ai bisturi. Gli scienziati hanno dichiarato, infatti, che potrebbe essere prodotto, nel futuro, un medicinale in grado di migliorare le possibilita' che hanno le cellule staminali di riparare i danni al sistema nervoso.
Il midollo spinale di un adulto contiene solo un piccolo numero di cellule staminali, che si riproducono lentamente, sono molto rare e non si riproducono facilmente, ma la ricerca ha dimostrato che le cellule staminali del midollo possono riprodursi in laboratorio e inserendole nella lesione e' possibile ripristinare le funzioni paralizzate. L'esperimento e' stato testato su cavie e primati.
Gli scienziati hanno scoperto che le cellule staminali neurali del midollo sono posizionate su cellule denominate ependimali. "Siamo stati in grado di marcare geneticamente queste cellule staminali neurali e di seguirne il comportamento. Abbiamo cosi' scoperto che si riproducono sulle lesioni al midollo spinale, migrano attraverso tutta la lesione e si "differenziano" nei mesi seguenti. L'abilita' delle cellule ependimali di trasformarsi in diverse cellule le rende interessanti. Immaginiamo, se si potesse controllarne il comportamento, di riparare cosi' i danni alle cellule nervose", ha dichiarato Konstantinos Meletis del MIT.

http://www.dailystar.com.lb/article.asp?edition_id=1&categ_id=1&article_id=94419

AUB adopts accommodating attitude toward students with disabilities

Daily Star staff
Thursday, July 24, 2008

BEIRUT: For Fawzi Yassin, who graduated this year with a degree in computer science, academic standards were not his only motivation for choosing to study at the American University of Beirut (AUB) - an accommodating attitude was a high priority.

Fawzi is one of at least a dozen disabled students who graduated from AUB over the past decade. But he was the only one this year who rolled on his wheelchair to receive his degree from then-President John Waterbury during the June commencement exercises.

Stricken with a debilitating genetic disease - Friedreich's ataxia - that damages the nervous system and leaves its victims with impaired mobility as well as other symptoms, Fawzi needed a university that could provide him with easy access to classes. While AUB's 150-year-old, hilly campus is not ideal to a wheel-chair-bound individual, the university's administration was eager to accommodate its prospective student.

So when Fawzi applied in 2005, the Faculty of Arts and Sciences promised to reschedule any classes that proved inaccessible to him. A year later, the Protection Office bought a wheel-chair accessible car to transport disabled students along with their wheel chairs across campus, and particularly from upper to lower campus and vice versa.

While AUB does not receive many disabled students every year, it has a policy to equip all new buildings with ramps and disabled-friendly bathrooms. As for the old buildings, they are gradually being provided with disabled access. "We are very keen to make our disabled student population feel comfortable and at home," said Dean of Student Affairs Maroun Kisirwani.

Disabled students who wish to study at AUB may also benefit from the Women's League Scholarship Fund for Handicapped Students, which was established in 1999. Several disabled students were awarded financial assistance from this scholarship fund. During the academic year 2005-06, the recipient was Fawzi Yassin.

The Red Cross Youth club at AUB also offers services to students with special needs, helping them around campus and with their studies through the 25-year-old Room for Visually-Challenged Students, which is jointly run with the Office of Student Affairs. The room offers a variety of services, such as turning books into audio tracks, through a computer software or student volunteers, and an archive of taped university text books. "Our volunteers also read for visually-impaired students and help them with their online and library searches," said Rayya Fallis, the president of the Red Cross AUB Youth Club.

Fawzi's experience at AUB changed his perspective on life. Before joining the university, he saw his world as confined to his parents' home, with no prospects for a future. Now, he plans to enroll in a master's program at AUB and work part-time.

"Before joining AUB, I did not think of going to work, and thought I would live at home forever. Now I have lots of hope for the future," he said. "AUB built my personality and allowed me to make lots of friends. I am so thankful for that opportunity and would like to tell people: Never to lose hope. Always keep your eye on the goal and don't think it's impossible." - The Daily Star