Swine Flu Shot Safety Concerns
Why the H1N1 Pandemic Influenza Vaccine Is Not Safe
© Johneen Manning
Nov 6, 2009
Sunday, November 8, 2009
Schizophrenia risk rises with father’s age
Schizophrenia risk rises with father’s age
Sunday, November 08, 2009
Children fathered by older men have an increased risk of schizophrenia in later life, possibly because of mutations in their father’s DNA, according to a new study from Sweden.
A link between paternal age and schizophrenia has been reported before but scientists were not sure whether this was due to increasing mutations with advancing age or the result of inherited personality traits.
To find out, researchers at the University of Wales College of Medicine in Cardiff and Gothenburg University in Sweden examined the medical records of 50,087 Swedish army conscripts recruited between 1969 and 1970.
Their findings, reported in the British Journal of Psychiatry, show that 362 of the former soldiers had been diagnosed with schizophrenia by 1996.
Their fathers’ ages varied between 19 and 65. In a control group of men without schizophrenia, the fathers’ ages ranged from 15 to 75.
The study found that the odds of developing schizophrenia increased by 30 percent for each 10-year increase in paternal age.
Adjusting for poor social integration had only a minimal effect on the findings, suggesting personality traits were not a major factor.
“This supports the hypothesis that accumulating germ cell mutations may lead to an increase in genetic liability to schizophrenia in the offspring,” Dr Stanley Zammit, from the University of Wales, said.
Extra copies of gene may cause Parkinson’s: Certain patients with Parkinson’s disease carry extra copies of a gene that may clog their brains with excess proteins — a finding that may lead to better treatments and perhaps a way to stop the disease, scientists said.
They found members of a family plagued by Parkinson’s carried additional copies of a gene called alpha synuclein. A buildup of the protein the gene controls is believed to cause the Parkinson’s symptoms.
The findings, reported in Friday’s issue of the journal Science, might shed light on all cases of Parkinson’s and perhaps other brain diseases, the researchers said.
The four patients each have not only an extra copy of the gene, but also of an entire region of the chromosome that carries it, said Andrew Singleton of the National Institute on Aging’s Laboratory of Neurogenetics, who led the study.
“It’s amazingly rare,” Singelton said in a telephone interview. “It includes 16 other genes that flank synuclein.”
His team is now checking whether these patients have extra high levels of the protein synuclein, controlled by the gene, as suggested by other studies of Parkinson’s patients.
“This study is an exciting step forward in our understanding of this disease,” Singelton said.
“It contributes to the growing body of evidence suggesting that genetic variations in alpha-synuclein contribute to Parkinson’s disease. It suggests that in Parkinson’s disease, both mutated and normal alpha-synuclein behave in a way that is quantitatively different from the way the protein functions in people without Parkinson’s disease.”
Parkinson’s is the second most common neurodegenerative disease after Alzheimer’s. Incurable and always fatal, Parkinson’s affects an estimated 500,000 Americans. It is caused by the death of brain cells that produce dopamine, a neurotransmitter or message-carrying chemical important to muscle movement. Patients develop tremors and gradually become paralyzed.
Singleton and colleagues were studying the “Iowa kindred,” a family in which many relatives developed Parkinson’s or related neurological diseases at an average age of 34. They found four family members had two extra versions of the gene.
“We hope that this type of basic research will yield new understandings that will ultimately allow us to go beyond just treating the symptoms of Parkinson’s disease to one day halting the disease’s progression,” said Matthew Farrer of the Mayo Clinic in Rochester, Minnesota, who worked on the study.
The symptoms in this family are similar to those in other Parkinson’s patients, the researchers noted. Insights into many diseases have been provided by families carrying a rare genetic mutation that points doctors in the right direction for finding broader causes of illness.
They could also help in other diseases, such as Alzheimer’s disease in Down syndrome patients. Down syndrome is caused by an extra copy of chromosome 21, which in turn causes overproduction of certain proteins.
Cambridge, Massachusetts-based Alnylam Pharmaceuticals said it had signed an agreement with the Mayo Clinic to try to develop a drug that will work against the synuclein gene.
Alnylam was founded by biotechnology researchers seeking to start a new field of drug research called RNA interference. The idea is to interfere with the output of faulty genes.
Sunday, November 08, 2009
Children fathered by older men have an increased risk of schizophrenia in later life, possibly because of mutations in their father’s DNA, according to a new study from Sweden.
A link between paternal age and schizophrenia has been reported before but scientists were not sure whether this was due to increasing mutations with advancing age or the result of inherited personality traits.
To find out, researchers at the University of Wales College of Medicine in Cardiff and Gothenburg University in Sweden examined the medical records of 50,087 Swedish army conscripts recruited between 1969 and 1970.
Their findings, reported in the British Journal of Psychiatry, show that 362 of the former soldiers had been diagnosed with schizophrenia by 1996.
Their fathers’ ages varied between 19 and 65. In a control group of men without schizophrenia, the fathers’ ages ranged from 15 to 75.
The study found that the odds of developing schizophrenia increased by 30 percent for each 10-year increase in paternal age.
Adjusting for poor social integration had only a minimal effect on the findings, suggesting personality traits were not a major factor.
“This supports the hypothesis that accumulating germ cell mutations may lead to an increase in genetic liability to schizophrenia in the offspring,” Dr Stanley Zammit, from the University of Wales, said.
Extra copies of gene may cause Parkinson’s: Certain patients with Parkinson’s disease carry extra copies of a gene that may clog their brains with excess proteins — a finding that may lead to better treatments and perhaps a way to stop the disease, scientists said.
They found members of a family plagued by Parkinson’s carried additional copies of a gene called alpha synuclein. A buildup of the protein the gene controls is believed to cause the Parkinson’s symptoms.
The findings, reported in Friday’s issue of the journal Science, might shed light on all cases of Parkinson’s and perhaps other brain diseases, the researchers said.
The four patients each have not only an extra copy of the gene, but also of an entire region of the chromosome that carries it, said Andrew Singleton of the National Institute on Aging’s Laboratory of Neurogenetics, who led the study.
“It’s amazingly rare,” Singelton said in a telephone interview. “It includes 16 other genes that flank synuclein.”
His team is now checking whether these patients have extra high levels of the protein synuclein, controlled by the gene, as suggested by other studies of Parkinson’s patients.
“This study is an exciting step forward in our understanding of this disease,” Singelton said.
“It contributes to the growing body of evidence suggesting that genetic variations in alpha-synuclein contribute to Parkinson’s disease. It suggests that in Parkinson’s disease, both mutated and normal alpha-synuclein behave in a way that is quantitatively different from the way the protein functions in people without Parkinson’s disease.”
Parkinson’s is the second most common neurodegenerative disease after Alzheimer’s. Incurable and always fatal, Parkinson’s affects an estimated 500,000 Americans. It is caused by the death of brain cells that produce dopamine, a neurotransmitter or message-carrying chemical important to muscle movement. Patients develop tremors and gradually become paralyzed.
Singleton and colleagues were studying the “Iowa kindred,” a family in which many relatives developed Parkinson’s or related neurological diseases at an average age of 34. They found four family members had two extra versions of the gene.
“We hope that this type of basic research will yield new understandings that will ultimately allow us to go beyond just treating the symptoms of Parkinson’s disease to one day halting the disease’s progression,” said Matthew Farrer of the Mayo Clinic in Rochester, Minnesota, who worked on the study.
The symptoms in this family are similar to those in other Parkinson’s patients, the researchers noted. Insights into many diseases have been provided by families carrying a rare genetic mutation that points doctors in the right direction for finding broader causes of illness.
They could also help in other diseases, such as Alzheimer’s disease in Down syndrome patients. Down syndrome is caused by an extra copy of chromosome 21, which in turn causes overproduction of certain proteins.
Cambridge, Massachusetts-based Alnylam Pharmaceuticals said it had signed an agreement with the Mayo Clinic to try to develop a drug that will work against the synuclein gene.
Alnylam was founded by biotechnology researchers seeking to start a new field of drug research called RNA interference. The idea is to interfere with the output of faulty genes.
Friday, November 6, 2009
Spraying on Skin Cells to Heal Burns
Spraying on Skin Cells to Heal Burns
A new technique in burn treatment provides an alternative to skin grafts in the operating room.
By Lauren Gravitz
Thursday, November 05, 2009
Traditionally, treatment for severe second-degree burns consists of adding insult to injury: cutting a swath of skin from another site on the same patient in order to graft it over the burn. The process works, but causes more pain for the burn victim and doubles the area in need of healing. Now a relatively new technology has the potential to heal burns in a way that's much less invasive than skin grafts. With just a small skin biopsy and a ready-made kit, surgeons can create a suspension of the skin's basal cells--the stem cells of the epidermis--and spray the solution directly onto the burn with results comparable to those from skin grafts.
Spray-on skin: In a unique treatment for second-degree burns, surgeons harvest a small number of skin cells through a skin biopsy, suspend them in solution, and then spray the resulting mixture onto a burn wound. Once in place, skin stem cells, called basal cells, proliferate to create a new layer of skin.
Credit: ReCell
The cell spray is intended to treat severe second-degree burns, in which the top two layers of skin are damaged but the subcutaneous tissue is left intact. Third-degree burns, which are more severe, still require a skin graft. The spray, already approved for use in some countries, has garnered interest from the United States Army, whose Armed Forces Institute of Regenerative Medicine is funding a trial, slated to begin before the end of this year, of more than 100 patients.
The technology, developed by Australian surgeon Fiona Wood, relies on cells, such as skin progenitor cells and the color-imparting melanocytes, that are most concentrated at the junction between the skin's top two layers. With a small step-by-step kit dubbed ReCell, surgeons can harvest, process and apply these cells to treat a burn as large as 10.5 square feet. The kit, marketed by Avita Medical, a United Kingdom-based regenerative-medicine company, is a tiny, self-contained lab about the size and shape of a large sunglasses case.
After removing a small swatch of skin near the burn site (the closer the biopsy, the better for precise matching of color and texture), the surgeon places it in the kit's tiny incubator along with an enzyme solution. The enzyme loosens the critical cells at the skin's dermal-epidermal junction, and the surgeon harvests them by scraping them off the epidermal and dermal layers and suspending them in solution. The resulting mixture is then sprayed onto the wound, repopulating the burn site with basal cells from the biopsy site.
A new technique in burn treatment provides an alternative to skin grafts in the operating room.
By Lauren Gravitz
Thursday, November 05, 2009
Traditionally, treatment for severe second-degree burns consists of adding insult to injury: cutting a swath of skin from another site on the same patient in order to graft it over the burn. The process works, but causes more pain for the burn victim and doubles the area in need of healing. Now a relatively new technology has the potential to heal burns in a way that's much less invasive than skin grafts. With just a small skin biopsy and a ready-made kit, surgeons can create a suspension of the skin's basal cells--the stem cells of the epidermis--and spray the solution directly onto the burn with results comparable to those from skin grafts.
Spray-on skin: In a unique treatment for second-degree burns, surgeons harvest a small number of skin cells through a skin biopsy, suspend them in solution, and then spray the resulting mixture onto a burn wound. Once in place, skin stem cells, called basal cells, proliferate to create a new layer of skin.
Credit: ReCell
The cell spray is intended to treat severe second-degree burns, in which the top two layers of skin are damaged but the subcutaneous tissue is left intact. Third-degree burns, which are more severe, still require a skin graft. The spray, already approved for use in some countries, has garnered interest from the United States Army, whose Armed Forces Institute of Regenerative Medicine is funding a trial, slated to begin before the end of this year, of more than 100 patients.
The technology, developed by Australian surgeon Fiona Wood, relies on cells, such as skin progenitor cells and the color-imparting melanocytes, that are most concentrated at the junction between the skin's top two layers. With a small step-by-step kit dubbed ReCell, surgeons can harvest, process and apply these cells to treat a burn as large as 10.5 square feet. The kit, marketed by Avita Medical, a United Kingdom-based regenerative-medicine company, is a tiny, self-contained lab about the size and shape of a large sunglasses case.
After removing a small swatch of skin near the burn site (the closer the biopsy, the better for precise matching of color and texture), the surgeon places it in the kit's tiny incubator along with an enzyme solution. The enzyme loosens the critical cells at the skin's dermal-epidermal junction, and the surgeon harvests them by scraping them off the epidermal and dermal layers and suspending them in solution. The resulting mixture is then sprayed onto the wound, repopulating the burn site with basal cells from the biopsy site.
Human x-ray machines: Coming soon to an airport near you
November 6th, 2009
Human x-ray machines: Coming soon to an airport near you
Posted by Doug Hanchard @ November 6, 2009 @ 5:00 AM
Human x-ray machines: Coming soon to an airport near you
Posted by Doug Hanchard @ November 6, 2009 @ 5:00 AM
Thursday, November 5, 2009
Schoolboy campaigner backs vitamin D summit
November 4, 2009
Schoolboy campaigner backs vitamin D summit
(Ashley Coombes/Epicscotland)
Ryan McLaughlin with his mum Kirsten who is suffering from MS
Melanie Reid
2 Comments
Recommend?
A major international summit on the links between multiple sclerosis and vitamin D deficiency, supported by the Scottish government, is to take place in Scotland early next year thanks to the efforts of a campaigning schoolboy.
Ryan McLaughlin, 14, whose mother suffers from the disease, said yesterday he was delighted that that Ministers were backing an opportunity to explore the growing evidence that lack of the vitamin could be implicated in the high incidence of the disease.
The summit will bring together government health advisers as well as researchers from Britain and countries such as Canada, where much work has been done on MS, and where supplementation of vitamin D is officially advocated in the general population
Schoolboy campaigner backs vitamin D summit
(Ashley Coombes/Epicscotland)
Ryan McLaughlin with his mum Kirsten who is suffering from MS
Melanie Reid
2 Comments
Recommend?
A major international summit on the links between multiple sclerosis and vitamin D deficiency, supported by the Scottish government, is to take place in Scotland early next year thanks to the efforts of a campaigning schoolboy.
Ryan McLaughlin, 14, whose mother suffers from the disease, said yesterday he was delighted that that Ministers were backing an opportunity to explore the growing evidence that lack of the vitamin could be implicated in the high incidence of the disease.
The summit will bring together government health advisers as well as researchers from Britain and countries such as Canada, where much work has been done on MS, and where supplementation of vitamin D is officially advocated in the general population
New mechanism for nano damage?
New mechanism for nano damage?Posted by Jef Akst
[Entry posted at 5th November 2009 06:00 PM GMT]
Comment on this news story
Nanoparticles can damage DNA even in cells that are not directly exposed to them, according to an in vitro study published online today (November 5) in Nature Nanotechnology -- raising further questions about the safety of nanomaterials used in clinical therapies.
Image: Wikimedia commons,
Jerome Walker,Dennis Myts
"DNA damage due to nanoparticles has been described for many types of nanoparticles, but that's done in a primary or direct sense," said Andre Nel, chief of NanoMedicine at the University of California, Los Angeles, who was not involved in the study. "Indirect DNA damage to hazardous nanoparticles is not something that I have seen described before."
Scientists are using nanotechnology to develop delivery systems for drugs and imaging agents, but some studies have suggested these particles may be toxic. Researchers have linked inhalation of nanoparticles or nanotubes to cardoirespiratory disease, for example. Additionally, nanoparticle debris from implants, such as cobalt-chromium (CoCr) alloy particles which can be released from metal-on-metal orthopedic joint replacements, are known to damage human cells in culture.
To further explore the toxicity of CoCr nanoparticles, Charles Patrick Case of the University of Bristol, UK, and his colleagues examined human fibroblast cells that were exposed either directly to the particles or through a cellular barrier. (In a living organism, such a barrier might be the placenta or the lining of the lungs.) They constructed the barrier by growing a thick layer of BeWo cells -- a human cell line often used as a model barrier -- in a porous plastic insert, which they placed above a fibroblast culture. After 24 hours of exposure, the researchers measured the amount of DNA damage in the fibroblasts and found that all cells -- those protected by the BeWo barrier and those directly exposed to the CoCr -- had sustained a significant amount of damage. Parallel experiments with micron-sized particles showed a similar effect.
[Entry posted at 5th November 2009 06:00 PM GMT]
Comment on this news story
Nanoparticles can damage DNA even in cells that are not directly exposed to them, according to an in vitro study published online today (November 5) in Nature Nanotechnology -- raising further questions about the safety of nanomaterials used in clinical therapies.
Image: Wikimedia commons,
Jerome Walker,Dennis Myts
"DNA damage due to nanoparticles has been described for many types of nanoparticles, but that's done in a primary or direct sense," said Andre Nel, chief of NanoMedicine at the University of California, Los Angeles, who was not involved in the study. "Indirect DNA damage to hazardous nanoparticles is not something that I have seen described before."
Scientists are using nanotechnology to develop delivery systems for drugs and imaging agents, but some studies have suggested these particles may be toxic. Researchers have linked inhalation of nanoparticles or nanotubes to cardoirespiratory disease, for example. Additionally, nanoparticle debris from implants, such as cobalt-chromium (CoCr) alloy particles which can be released from metal-on-metal orthopedic joint replacements, are known to damage human cells in culture.
To further explore the toxicity of CoCr nanoparticles, Charles Patrick Case of the University of Bristol, UK, and his colleagues examined human fibroblast cells that were exposed either directly to the particles or through a cellular barrier. (In a living organism, such a barrier might be the placenta or the lining of the lungs.) They constructed the barrier by growing a thick layer of BeWo cells -- a human cell line often used as a model barrier -- in a porous plastic insert, which they placed above a fibroblast culture. After 24 hours of exposure, the researchers measured the amount of DNA damage in the fibroblasts and found that all cells -- those protected by the BeWo barrier and those directly exposed to the CoCr -- had sustained a significant amount of damage. Parallel experiments with micron-sized particles showed a similar effect.
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