Visit our http://www.roseznlace.com/ store for unique and affordable items featuring our new United States of America leader President Barack Obama. View the inaugaral speech on a previous post.
Thursday, January 29, 2009
President Obama Memorabilia
Visit our http://www.roseznlace.com/ store for unique and affordable items featuring our new United States of America leader President Barack Obama. View the inaugaral speech on a previous post.
Friday, January 16, 2009
Huntingtons Disease Society of America, a short history of its beginning
Tamara Kopp, 18 yrs Tamara Kopp, 34 yrs
Although Tami showed signs of illness at the age of 18 she was not diagnosed with Huntingtons disease until she was 24 yrs old.
HD Research - Past and Future
There has been an explosion of Huntington's Disease research since the gene was discovered in 1993. The discovery of the gene was the culmination of ten years of work by more than fifty collaborators in six labs and it represents a critical milestone in the effort to understand and treat the disease. As Dr. James Gusella, Coalition for the Cure researcher and member of the gene discovery team, has said, once the gene was found, the research could begin in earnest.
Huntington's Disease is caused by a genetic stutter in a gene that produces a large protein found in animals from yeast to humans. Its functions are not yet fully understood. There is a section of the gene that encodes for glutamine; the code consists of a series of the base pairs cytosine, adenine, and guanine (CAG repeats). In the Huntington's gene, these CAG triplets occur an abnormal number of times, changing the protein in ways that challenge the medium spiny neurons in the brain. Since the discovery of the HD gene, the genes for eight other polyglutamine disorders have been discovered.
Much has been learned about where and how the HD protein causes its damage. The most cell death occurs in the striatum but the cortex is affected too and cortical dysfunction has emerged as a major source of pathology.
The Huntington's Disease protein has been found to affect hundreds of cellular processes and components but several areas appear to be critical, including impaired protein folding and clearance, reduced cellular metabolism, neurotransmission problems, fragmentation of the protein and nuclear aggregation, and dysregulation of gene transcription with some genes being underexpressed and some overexpressed. Two of the affected genes which play a role in HD pathology include Brain Derived Neurotrophic Factor (BDNF) which is down-regulated and P53 which is up-regulated.
Much of what we now know about how Huntington's Disease develops has come about as a result of the development of the transgenic mouse in 1996 by Gillian Bates. Only humans get Huntington's naturally, but Dr. Bates was able to produce this model by inserting a short fragment of the human gene including about 150 CAG repeats.
Today there are various mouse models and each one captures a somewhat different set of Huntington's symptoms. The models include ones in which the entire human HD gene have been inserted (transgenic, full length) and ones in which extra mouse CAG repeats have been added to the mouse's own huntingtin's protein gene (knock-in models).
Various pathogenic processes have been found in the HD mice and other models and confirmed in human HD, adding to our knowledge about the disease. The mice are also used to test potential treatments.
Rigorous research has shown conclusively that the disease can be modified by various treatments in mouse models. This gives rise to the hope that at least some of these drugs, supplements, and interventions will make it through the research pipeline and become available treatments for people with the HD gene within the next few years.
The mouse models and new technologies have made it possible to identify targets for drugs, supplements, and other interventions that might prevent, slow or reverse disease progression. Knowing where to intervene allows researchers to find existing drugs that affect the target and test them as potential treatments. It is also the first step in drug development.
There has been an explosion of Huntington's Disease research since the gene was discovered in 1993. The discovery of the gene was the culmination of ten years of work by more than fifty collaborators in six labs and it represents a critical milestone in the effort to understand and treat the disease. As Dr. James Gusella, Coalition for the Cure researcher and member of the gene discovery team, has said, once the gene was found, the research could begin in earnest.
Huntington's Disease is caused by a genetic stutter in a gene that produces a large protein found in animals from yeast to humans. Its functions are not yet fully understood. There is a section of the gene that encodes for glutamine; the code consists of a series of the base pairs cytosine, adenine, and guanine (CAG repeats). In the Huntington's gene, these CAG triplets occur an abnormal number of times, changing the protein in ways that challenge the medium spiny neurons in the brain. Since the discovery of the HD gene, the genes for eight other polyglutamine disorders have been discovered.
Much has been learned about where and how the HD protein causes its damage. The most cell death occurs in the striatum but the cortex is affected too and cortical dysfunction has emerged as a major source of pathology.
The Huntington's Disease protein has been found to affect hundreds of cellular processes and components but several areas appear to be critical, including impaired protein folding and clearance, reduced cellular metabolism, neurotransmission problems, fragmentation of the protein and nuclear aggregation, and dysregulation of gene transcription with some genes being underexpressed and some overexpressed. Two of the affected genes which play a role in HD pathology include Brain Derived Neurotrophic Factor (BDNF) which is down-regulated and P53 which is up-regulated.
Much of what we now know about how Huntington's Disease develops has come about as a result of the development of the transgenic mouse in 1996 by Gillian Bates. Only humans get Huntington's naturally, but Dr. Bates was able to produce this model by inserting a short fragment of the human gene including about 150 CAG repeats.
Today there are various mouse models and each one captures a somewhat different set of Huntington's symptoms. The models include ones in which the entire human HD gene have been inserted (transgenic, full length) and ones in which extra mouse CAG repeats have been added to the mouse's own huntingtin's protein gene (knock-in models).
Various pathogenic processes have been found in the HD mice and other models and confirmed in human HD, adding to our knowledge about the disease. The mice are also used to test potential treatments.
Rigorous research has shown conclusively that the disease can be modified by various treatments in mouse models. This gives rise to the hope that at least some of these drugs, supplements, and interventions will make it through the research pipeline and become available treatments for people with the HD gene within the next few years.
The mouse models and new technologies have made it possible to identify targets for drugs, supplements, and other interventions that might prevent, slow or reverse disease progression. Knowing where to intervene allows researchers to find existing drugs that affect the target and test them as potential treatments. It is also the first step in drug development.
Woody Guthri was a storyteller who used music to tell his stories. His work ranged from social commentaries about the working conditions of migrant workers and the urban poor to ballads and children’s songs. In 1967, Woody Guthrie, lost his battle with HD. He was just 55 years old. During the more than 15 years that the disease affected him, he struggled to continue to communicate his conviction that every man, woman and child has within them the power to make a difference.Soon after his death, his widow Marjorie vowed to do something about this silent killer. At the time, little was known about the disease. Marjorie placed a small ad in a New York City newspaper and slowly gathered a determined handful of volunteers and HD families from across the United States. From that first moment, when Marjorie Guthrie reached out to other HD families, a worldwide movement began that would change the lives of those living with HD and bring hope to families.Dynamic and compelling, Marjorie Guthrie convinced then President Jimmy Carter to form a Presidential Commission to study neurological diseases, including HD. The recommendations that resulted from that 1977 report have served as the cornerstone of HDSA’s commitment to the care and cure of HD. In 1983, HDSA Coalition for the Cure investigator, Jim Gusella, found the very first marker for the disease and, after a ten year search that involved collaboration among the top HD researchers worldwide, the gene was located on the short arm of chromosome 4. Since that time, research has progressed rapidly and, in 2004, HDSA formed a pipeline for drug discovery that begins in the laboratory with basic science (HDSA Grants & Fellows program and the prestigious HDSA Coalition for the Cure) progresses to applied/transitional research (HDSA partner CHDI) and then moves to patient’s bedside in the form of human clinical trials that test the most promising compounds often at HDSA Centers of Excellence. Today the question our families ask is not “if” there will be a treatment or cure, but “when.”In the area of care, HDSA has created a national network of resources and referrals that are unmatched by any other HD organization. HDSA Centers of Excellence provide medical and social services to those affected by HD and their families while a toll free helpline and extensive national web site (www.hdsa.org) help to provide access to services. HDSA chapters, affiliates, regions, social workers, and support groups work in tandem with the Centers of Excellence to increase awareness about HD and raise funds for research, education and family services.Marjorie Guthrie died just a few months before the marker was found in 1983. But in the 16 years that she worked to bring this disease out of the family closet, she brought empathy and hope – a hope for a future free of HD- to those affected by this devastating disease. Her work resulted in what is today the Huntington’s Disease Society of America http://www.hdsa.org/. HDSA is dedicated to completing the work that this courageous woman started.
The Ancient Search for Peace
Heather Pringle is a freelance science journalist who has been writing about archaeology for more than 20 years. She is the author of Master Plan: Himmler's Scholars and the Holocaust and The Mummy Congress: Science, Obsession, and the Everlasting Dead. For more about Heather, see our interview or visit www.heatherpringle.com
The Ancient Search for Peace
Hardly a day seems to go by when I don’t read a news story about a group of desperate migrants risking their lives to flee a war zone in search of more peaceful and prosperous lives. I find it wrenching to read about refugees from Afghanistan cramming into small boats and sailing all the way to Australia in search of security, or the 200,000 people from Darfur who are now crowded into tent camps in Chad. Given a choice, people will vote with their feet every time, abandoning all that is familiar in order to make a better future for kith and kin.
Two articles I’ve just read on prehistoric migrations shed some fascinating new light on this phenomenon. In the December 18th issue of Nature, two experts on cultural evolution–Peter J. Richerson from the University of California, Davis, and Robert Boyd from the University of California, Los Angeles–write about the powerful effect that migrants have always had on human societies. “People move to societies that provide a more attractive way of life and if all other things being equal, this process spreads ideas and institutions that promote economic efficiency, social order and equality,” note the pair.
In other words, given the slightest opportunity—even a leaky, overcrowded boat in typhoon-ridden seas—people will always try to flee oppressive, impoverished regimes in favor of those that offer a better chance at prosperity, happiness and justice. And as both history and archaeology shows us, this has had a major impact on political landscapes. Empires that offered prosperity, security and rule of law for their citizens, such as the Roman Empire, grew by attracting migrants and assimilating border peoples. These empires were long-lived. But those that conquered and exploited many of their subjects, such as the Mongol Empire or the old Soviet Union, fell apart relatively quickly. Often their subjects wanted little to do with them: when they saw an opportunity to escape, they packed their bags and headed for the door. “As long as they vote with their feet and hearts,” write Richerson and Boyd, “immigrants are a more powerful engine for social change than armies.” I find this a very intriguing thought.
And it’s possible that this mechanism could be far older than anyone previously suspected. In the new issue of Nature Genetics, Harvard Medical School geneticist Alon Keinan and three colleagues have published a study of differences in the human genetic codes found in populations of Africans, Asians and northern Europeans. The team’s ingenious technique—which focused on variations in both the X chromosome and the non-gender chromosomes—allowed them to calculate the sex ratio of the Out-of-Africa migrants. According to the findings, more men than women took part in that early migration, and this evidence, says Keinan, fits with many anthropological studies. In hunter-gatherer societies, long-distance migration tends to be a male affair.
It is certainly possible, as Keinan has suggests, that our ancient male ancestors weren’t above raiding other bands and carrying off a few women along the way as they journeyed to a new land. But I can imagine another possibility. What if our ancient African ancestors were actually the victims of raiding parties in a time of environmental stress, losing some of their precious women? And what if they, like many migrants today, just wanted to find somewhere else to live in peace? Could that have been an incentive to pull up stakes in Africa and set off to new lands in Asia?
Maybe migration is one of the most powerful instincts that we have inherited from our wandering ancestors.
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"Tales from a Civil War Prison"
Experience the gory chaos of battle, the chilling moment of capture, and the reality of prison life. Feel the reverberations of the Civil War echoing in the lives of prisoners and their families after the war, stretching to the present. Even in two of the modern signatures below, we can trace pride in family names.
Lieutenant William B. Hardy,Private John Hardy, andPrivate Andrew Hardy War Stories The Enemy Comes to Dinner A Messmate Remembers
Lieutenant Elisha Miller Robinson The Stories They Told
Lieutenant Colonel John W. Inzer The Making of a Statesman Prison Life
Reverend Doctor James Durham West No Words A Good Fighter and A Good Loser The Capture
Edward W. Brown,Theodore Z. Brown, andThomas W. Brown I Won't Sign the Oath Poor Ed
Captain Charles Norvell They Ate Rats and Horses A Mother Prays Baskets of Delicacies
Lieutenant Charles Henry Burks andSergeant James Armstrong Burks A Tale of Two Brothers The Benchmarks of War
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