Satellites witness lowest Arctic ice coverage in history
The area covered by sea ice in the Arctic has shrunk to its lowest level this week since satellite measurements began nearly 30 years ago, opening up the Northwest Passage – a long-sought short cut between Europe and Asia that has been historically impassable.
2007 Envisat mosaic of Arctic Ocean
In the mosaic image above, created from nearly 200 images acquired in early September 2007 by the Advanced Synthetic Aperture Radar (ASAR) instrument aboard ESA's Envisat satellite, the dark gray colour represents the ice-free areas while green represents areas with sea ice.
Leif Toudal Pedersen from the Danish National Space Centre said: "We have seen the ice-covered area drop to just around 3 million sq km which is about 1 million sq km less than the previous minima of 2005 and 2006. There has been a reduction of the ice cover over the last 10 years of about 100 000 sq km per year on average, so a drop of 1 million sq km in just one year is extreme.
"The strong reduction in just one year certainly raises flags that the ice (in summer) may disappear much sooner than expected and that we urgently need to understand better the processes involved."
Arctic sea ice naturally extends its surface coverage each northern winter and recedes each northern summer, but the rate of overall loss since 1978 when satellite records began has accelerated.
Mosaics of Arctic Ocean for 2005, 2006, 2007
The most direct route of the Northwest Passage (highlighted in the top mosaic by an orange line) across northern Canada is shown fully navigable, while the Northeast Passage (blue line) along the Siberian coast remains only partially blocked. To date, the Northwest Passage has been predicted to remain closed even during reduced ice cover by multi-year ice pack – sea ice that survives one or more summers. However, according to Pedersen, this year's extreme event has shown the passage may well open sooner than expected.
The previous record low was in 2005 when the Arctic area covered by sea ice was just 4 million sq km. Even then, the most direct Northwest Passage did not fully open.
A 2007 ice-free portion of the Northwest Passage
The Polar Regions are very sensitive indicators of climate change. The UN's Intergovernmental Panel on Climate Change showed these regions are highly vulnerable to rising temperatures and predicted the Arctic would be virtually ice free by the summer of 2070. Still other scientists predict it could become ice free as early as 2040 due to rising temperatures and sea ice decline.
Because sea ice has a bright surface, the majority of solar energy that hits it is reflected back into space. When sea ice melts, the dark-coloured ocean surface is exposed. Solar energy is then absorbed rather than reflected, so the oceans get warmer and temperatures rise, making it difficult for new ice to form.
The Arctic is one of Earth's most inaccessible areas, so obtaining measurements of sea ice was difficult before the advent of satellites. For more than 20 years, ESA has been providing satellite data to the cryosphere communities. Currently, ESA is contributing to the International Polar Year (IPY) – a large worldwide science programme focused on the Arctic and Antarctic.
Since 2006, ESA has supported Polar View, a satellite remote-sensing programme funded through the Earthwatch GMES Service Element (GSE) that focuses on the Arctic and the Antarctic.
In 2009, ESA will make another significant contribution to cryosphere research with the launch of CryoSat-2. The observations made over the three-year lifetime of the mission will provide conclusive evidence on the rates at which ice cover is diminishing.
September 15, 2007 Posted by FMS Global News | Global Health Vision, Global News, RSS Feed, Science, Washington DC City Feed, Weather Anomolies, World Health Organisation, World News	| Leave a comment
Research links genetic mutations to lupus
WINSTON-SALEM, N.C. – A gene discovered by scientists at Wake Forest University School of Medicine has been linked to lupus and related autoimmune diseases. The finding, reported in the current issue of Nature Genetics, is the latest in a series of revelations that shed new light on what goes wrong in human cells to cause the diseases.
"This research is a huge leap toward understanding the cause of lupus and related autoimmune diseases," said Fred Perrino, Ph.D., a co-author on the paper and a professor of biochemistry at Wake Forest. "There had been few clues before now."
Perrino, who discovered the gene in 1998, said he suspected it was involved in human disease, but it took a group of researchers from around the world collaborating to put the puzzle together.
"We've known that lupus was a complex disease, but now we have a specific protein and a particular cellular process that appears to be one of the causes," said Perrino. "We're connecting the dots to understand the biology of what's going on with the disease."
In Nature Genetics, lead author Min Ae Lee-Kirsch, M.D., from the Technische Universität Dresden in Dresden, Germany, and colleagues report finding variations of the TREX1 gene discovered by Perrino in patients with systemic lupus erythematosus. The study involved 417 lupus patients from the United Kingdom and Germany. Mutations were found in nine patients with lupus and were absent in 1,712 people without lupus.
"Our data identify a stronger risk for developing lupus in patients that carry variants of the gene," said Lee-Kirsch.
In recent years, the gene was also linked to Aicardi-Goutieres syndrome, a rare neurological disease that causes death in infants, and to chilblain lupus, an inherited disease associated with painful bluish-red skin lesions that occur during cold weather and usually improve in summer. The current research also links it to Sjogren's syndrome, a form of lupus.
The diseases are all autoimmuine diseases, which means that the body makes antibodies against itself. In lupus, these antibodies cause pain and inflammation in various parts of the body, including the skin, joints, heart, lungs, blood, kidneys and brain. The disease is characterized by pain, heat, redness, swelling and loss of function.
Perrino began studying the protein made by the gene more than 14 years ago.
"We basically cracked open cells to locate the protein and find the gene," said Perrino. "In the 14 years since, we've learned a lot about the protein and how it functions."
The gene manufactures a protein, also known as TREX1, whose function is to "disassemble" or "unravel" DNA, the strand of genetic material that controls processes within cells. The "unraveling" occurs during the natural process of cells dying and being replaced by new cells. If a cell's DNA isn't degraded or unraveled during cell death, the body develops antibodies against it.
"If the TREX1 protein isn't working to disassemble the DNA, you make antibodies to your own DNA and can end up with a disease like lupus," said Perrino.
Perrino and colleagues at Wake Forest have been studying the gene and its protein since 1993. Thomas Hollis, Ph.D., an assistant professor of biochemistry at Wake Forest, is credited with solving the structure of both TREX1 and a similar protein, TREX2. Perrino has also developed a way to measure the function of the proteins.
In a study reported in April in the Journal of Biological Chemistry, Hollis and Perrino found that three variations of the gene reduced the activity of the protein by four- to 35,000-fold.
"Now that we have the structure, we can understand how it disassembles DNA and how mutations in the gene may affect that process," said Hollis.
The researchers hope that understanding more about the gene's mutations and the structure of the protein may lead to drug treatments to help ensure that mutant copies of the gene are inactive.
Media Contacts: Karen Richardson, krchrdsn@wfubmc.edu; Shannon Koontz, shkoontz@wfubmc.edu; at 336-716-4587.
Wake Forest University Baptist Medical Center is an academic health system comprised of North Carolina Baptist Hospital and Wake Forest University Health Sciences, which operates the university's School of Medicine. U.S. News & World Report ranks Wake Forest University School of Medicine 18th in primary care and 44th in research among the nation's medical schools. It ranks 35th in research funding by the National Institutes of Health. Almost 150 members of the medical school faculty are listed in Best Doctors in America.
Contact: Karen Richardson
krchrdsn@wfubmc.edu
Fibromyalgia Support
July 29, 2007 Posted by FMS Global News | Alberta, Baltimore, Barcelona, Bethesda, Biological Sciences, Calgary, Canada, Clinical Trials, France, Genes, Genetic, Genetic Link, Genetic Marker C allele of rs10505477, Genetics, Genome, Genomic, Global, Global Health Vision, Global News, Health Canada, Human Genome, Italy, Japan, Lupus, Nature Genetics, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, NIH, Nova Scotia, Nunavut, Osaka, Ottawa, Prince Edward Island, Public Health, Quebec, Research, RSS, RSS Feed, Slovakia, Spain, Toronto, UK, US, Virginia, Wake Forest University Baptist Medical Center, WASHINGTON, Washington DC, Washington DC City Feed, World Health Organisation, World News	| 1 Comment
New research provides hope for childhood cancer sufferers
Dr Richard Lock, Head of the Leukaemia Biology Program at the Children's Cancer Institute Australia for Medical Research, Sydney, along with collaborators from the Childrens Hospital Los Angeles and University of Southern California, USA, recently published their findings in the prestigious scientific journal Blood.
ALL is the most common form of childhood cancer. Over the years, improvements in primary therapy have increased the cure rate to approximately 80 percent. However, for the 20 percent of patients who relapse, the majority will die.
"When used in combination with common drugs administered in ALL therapy, ABT-737 has the ability to enhance the combined toxicity of these drugs against the leukaemia cells with minimal effects on the normal cells of the body," said Dr Lock.
Resistance to common therapeutic drugs is associated with poor long-term outcomes in leukaemia patients. In the study, the effects of ABT-737 in combination with three common chemotherapeutic agents: L-Asparaginase, vincristine and dexamethasone, were tested on a number of ALL cell lines under conditions which were considered clinically relevant for the disease.
ABT-737, developed by Abbott Laboratories, acts by inhibiting the Bcl-2 family of proteins. These proteins are expressed in ALL and inhibit the mechanisms responsible for destroying leukaemia cells. High levels of expression of Bcl-2 is linked with chemoresistance in a variety of cancers.
"There is a critical need for new drugs with novel mechanisms of action that might improve the outcome for relapsed ALL patients," said Dr Lock.
The manuscript is available online at http://bloodjournal.hematologylibrary.org/papbyrecent.dtl Children's Cancer Institute Australia for Medical Research is associated with the University of NSW and Sydney Children's Hospital.
July 20, 2007 Posted by FMS Global News | acute lymphoblastic leukemia, Canada, Cancer, Cancer Biology, Cancer Biology and Therapy, Chemotherapy, Childhood Lukemia, Children's Cancer Institute Australia, Childrens Hospital Los Angeles, Germany, Global, Global Health Vision, Global News, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, Oncology, Ottawa, Quebec, RSS, RSS Feed, Sydney Children's Hospital, Toronto, University New South Wales, USC, Washington DC, Washington DC City Feed, World Health Organisation, World News	| Leave a comment
WHO data confirms low level of resistance to Tamiflu
Contact: Lucy Rispin
lucy.rispin@ketchum.com
New data published by the World Health Organisation (WHO) has confirmed a low frequency of resistance to Tamiflu (oseltamivir) over 3 influenza seasons (2003 – 2006)1.
The information, published by the Neuraminidase Inhibitor Susceptibility Network in the WHO's Weekly Epidemiological Record, has shown that resistance of around 0.3% to oseltamivir was seen during the influenza seasons in which there had been substantial Tamiflu use in Japan (35 million patients), the highest use in any market. This level of resistance is extremely low compared to rates of 65% seen in Japan with another antiviral, amantadine2.
"These results confirm that the potential for the development of resistance to Tamiflu is very low, even when used extensively in the management of seasonal influenza," commented Dr. David Reddy, Pandemic Task Force Leader, Roche. "This provides reassurance to the scientific community that since the introduction of Tamiflu in 1999, the levels of resistance have remained similar to those seen in the clinical development programme. Roche and the NISN continue to maintain high vigilance to keep on top of the evolving virus. "
Information gathering and results
As with any antiviral medication, there is a theoretical risk that a virus may emerge with decreased sensitivity to a drug. The Neuraminidase Inhibitor Susceptibility Network undertook screening for susceptibility to oseltamivir of influenza viruses randomly submitted to the national WHO Collaborating Centre for Reference and Research on Influenza and other Respiratory Diseases in Tokyo, Japan. Influenza virus isolates collected were tested by neuraminidase inhibition assay (IC50 or sequence analysis) to detect mutations associated with drug-resistance.
Influenza Season in Japan No of Influenza A isolates tested Resistance No of Influenza B isolates tested Resistance
2003/2004 1180 3 (0.3%) 171 0
2004/2005 618 0 252 1(0.4%)
2005/2006 429 4 (0.9%) 163 0
Total 2227 7 (0.32%) 586 1 (0.17%)
These preliminary findings indicate that a low frequency of oseltamivir resistance was present in community isolates during influenza seasons in which there had been substantial oseltamivir use in Japan.
May 9, 2007 Posted by FMS Global News | Global, Global Health Vision, Global News, World Health Organisation	| Leave a comment