Showing posts with label BIO5. Show all posts
Showing posts with label BIO5. Show all posts
Thursday, February 5, 2009
RECOMB: The 13th Annual International Conference on Research in Computational Molecular Biology May 17-21
Registration is now open for the RECOMB 2009, the 13th Annual International Conference on Research in Computational Molecular Biology. The conference is hosted by the BIO5 Institute and will be held in Tucson. Keynote presenters scheduled to date include: Carlos Bustamante, Cornell University; Eran Halperin, Navigenics; Michael Hammer, The University of Arizona; Joanna Mountain, 23andMe; Stephen Quake, Stanford University; Pardis Sabeti, Harvard University; and Michael Snyder, Yale University. RECOMB is a well-established scientific conference bridging the computational, mathematical, and biological sciences. More information: http://www.bio5.org/recomb2009/
Arizona Board of Regents approves new cancer prevention company
The Arizona Board of Regents gave approval for a UA researcher to take on part ownership of the new Tucson company Cancer Prevention Pharmaceuticals (CPP). CPP's work may one day help prevent colon cancer in those at high risk for the disease. UA Professor of Cell Biology and Anatomy Eugene Gerner will run CPP with his colleague Frank L. Meyskens, Jr., Professor of Medicine and Director of the Chao Family Comprehensive Cancer Center at the University of California in Irvine. Gerner is a member of UA's BIO5 Institute and the Arizona Cancer Center. (Read More)
Renowned researcher Dr. Fernando Martinez to lead UA’s BIO5 Institute
One of the most highly regarded researchers worldwide in childhood lung diseases, Fernando Martinez, has accepted the position of interim director for the BIO5 Institute at The University of Arizona (UA) beginning February 9, 2009. Dr. Martinez is the Swift-McNear Professor of Pediatrics, the director of the UA College of Medicine's Arizona Respiratory Center, and a long time BIO5 faculty member. (Read More)
Tuesday, December 23, 2008
UA losing major bioscience researcher
[Source: Aaron Mackey, ARizona Daily Star] - The leader of the UA's top research institute — whom colleagues hail as a key architect of the region's burgeoning bioscience industry — is leaving to head a San Francisco-based non-profit's scientific endeavors, the university announced Monday.
Vicki Chandler, director of the University of Arizona's Bio5 Institute, played a critical role in establishing the collaborative research center, which has brought tens of millions of grant dollars to the UA, including a $50 million award thought to be the largest grant in Arizona history.
The second high-profile professor with ties to Bio5 to leave the UA this year, Chandler will become chief program officer for the Gordon and Betty Moore Foundation's science efforts in February.
In July, Bio5 founder Thomas Baldwin left the UA to become dean of UC-Riverside's College of Natural and Agricultural Sciences. Baldwin founded the program, which at the time was known as the Institute for Biomedical Science and Biotechnology, in 2001.
Besides being one of the UA's premier scientists, Chandler has become a regional ambassador for bioscience research, lobbying for state money to build research facilities while striving to tell the public about the importance of the work.
"She had a vision for Bio5 that was about much more than just scientific research," said Leslie Tolbert, the UA's vice president for research. "She has an enthusiasm for outreach and the role a university can play in community development."
Taking over Bio5 in 2002, Chandler led several efforts that culminated in the UA's landing a $50 million grant in January to establish the iPlant Collaborative, a research program aimed at unlocking the secrets of plant biology. That alone accounted for roughly 10 percent of the UA's overall $500 million research budget.
The project, co-led by Chandler, was seeded by state support in research funding and new buildings — both of which Chandler lobbied for, Tolbert said.
Chandler "has been a strong spokesperson with the Legislature and with private donors as well," Tolbert said. "She gets them to see that it isn't just about the institute in the abstract, but the people doing the science and getting results."
The Bio5 Institute is the UA's most prominent interdisciplinary research center, blending researchers from five fields —agriculture, medicine, pharmacy, basic science and engineering — with industry leaders to find solutions to common problems, such as disease.
The institute has been a pipeline for grants and also has proved successful at creating a number of spin-off companies that use technologies developed in UA laboratories.
Managing the complex relationships between business leaders and researchers, Chandler was integral in convincing several bioscience companies to either expand in or move to Tucson, said Joe Snell, president and CEO of Tucson Regional Economic Opportunities Inc.
"Her leadership has been incredibly valuable in helping to position Tucson as the next bioscience hub," he said.
"I don't think we would be where we're at or where we're going without her efforts."
Chandler also has helped build interest in science among high school students and UA undergraduates. She holds summer programs that get high schoolers in laboratories with researchers and often touts how half the Bio5 researchers are undergrads.
She also has narrated the UA-produced PBS show "WaveLengths," which provides a 30-minute snapshot of some of the research produced on campus.
On top of that, Chandler maintains a full-time lab and conducts field research as a Regents Professor in both the plant science and molecular and cellular biology departments. She also holds the Weiler Endowed Chair for Excellence in Agriculture and Life Sciences.
Chandler, who has been at the UA since 1997, said she has mixed emotions about her new role.
"It's always exciting to take on a new challenge, but I poured my heart and soul into the University of Arizona and really care deeply for it," she said.
The move will take her back to her roots. She grew up in Northern California and studied at the University of California-Berkeley and UC-San Francisco while later working at Stanford after earning her Ph.D.
The foundation she is joining invests $300 million each year in projects, including science and environmental conservation research around San Francisco.
Even with her new job, Chandler will be in Tucson often. She plans to retain her endowed chair and conduct research as part of the iPlant Collaborative, a process she says will take up about 20 percent of her time.
"The university has been incredibly gracious to allow me to continue to research," she said. "By keeping my feet squarely planted in science, it will hopefully help me in my new position."
The UA will name an interim director of Bio5 early next year and plans to conduct a national search for a permanent replacement, Tolbert said.
Vicki Chandler, director of the University of Arizona's Bio5 Institute, played a critical role in establishing the collaborative research center, which has brought tens of millions of grant dollars to the UA, including a $50 million award thought to be the largest grant in Arizona history.
The second high-profile professor with ties to Bio5 to leave the UA this year, Chandler will become chief program officer for the Gordon and Betty Moore Foundation's science efforts in February.
In July, Bio5 founder Thomas Baldwin left the UA to become dean of UC-Riverside's College of Natural and Agricultural Sciences. Baldwin founded the program, which at the time was known as the Institute for Biomedical Science and Biotechnology, in 2001.
Besides being one of the UA's premier scientists, Chandler has become a regional ambassador for bioscience research, lobbying for state money to build research facilities while striving to tell the public about the importance of the work.
"She had a vision for Bio5 that was about much more than just scientific research," said Leslie Tolbert, the UA's vice president for research. "She has an enthusiasm for outreach and the role a university can play in community development."
Taking over Bio5 in 2002, Chandler led several efforts that culminated in the UA's landing a $50 million grant in January to establish the iPlant Collaborative, a research program aimed at unlocking the secrets of plant biology. That alone accounted for roughly 10 percent of the UA's overall $500 million research budget.
The project, co-led by Chandler, was seeded by state support in research funding and new buildings — both of which Chandler lobbied for, Tolbert said.
Chandler "has been a strong spokesperson with the Legislature and with private donors as well," Tolbert said. "She gets them to see that it isn't just about the institute in the abstract, but the people doing the science and getting results."
The Bio5 Institute is the UA's most prominent interdisciplinary research center, blending researchers from five fields —agriculture, medicine, pharmacy, basic science and engineering — with industry leaders to find solutions to common problems, such as disease.
The institute has been a pipeline for grants and also has proved successful at creating a number of spin-off companies that use technologies developed in UA laboratories.
Managing the complex relationships between business leaders and researchers, Chandler was integral in convincing several bioscience companies to either expand in or move to Tucson, said Joe Snell, president and CEO of Tucson Regional Economic Opportunities Inc.
"Her leadership has been incredibly valuable in helping to position Tucson as the next bioscience hub," he said.
"I don't think we would be where we're at or where we're going without her efforts."
Chandler also has helped build interest in science among high school students and UA undergraduates. She holds summer programs that get high schoolers in laboratories with researchers and often touts how half the Bio5 researchers are undergrads.
She also has narrated the UA-produced PBS show "WaveLengths," which provides a 30-minute snapshot of some of the research produced on campus.
On top of that, Chandler maintains a full-time lab and conducts field research as a Regents Professor in both the plant science and molecular and cellular biology departments. She also holds the Weiler Endowed Chair for Excellence in Agriculture and Life Sciences.
Chandler, who has been at the UA since 1997, said she has mixed emotions about her new role.
"It's always exciting to take on a new challenge, but I poured my heart and soul into the University of Arizona and really care deeply for it," she said.
The move will take her back to her roots. She grew up in Northern California and studied at the University of California-Berkeley and UC-San Francisco while later working at Stanford after earning her Ph.D.
The foundation she is joining invests $300 million each year in projects, including science and environmental conservation research around San Francisco.
Even with her new job, Chandler will be in Tucson often. She plans to retain her endowed chair and conduct research as part of the iPlant Collaborative, a process she says will take up about 20 percent of her time.
"The university has been incredibly gracious to allow me to continue to research," she said. "By keeping my feet squarely planted in science, it will hopefully help me in my new position."
The UA will name an interim director of Bio5 early next year and plans to conduct a national search for a permanent replacement, Tolbert said.
Thursday, December 4, 2008
Keeping Chromosomes From Cuddling Up
[Source: Mari N. Jensen, UA College of Science] - If chromosomes snuggle up too closely at the wrong times, the results can be genetic disaster.
Now University of Arizona researchers have found the molecular machines in fruit flies that yank chromosomes, the DNA-carrying structures, apart when necessary.
The machines, proteins called condensin II, separate chromosomes by twisting them into supercoils that kink up and therefore can no longer touch.
Scientists had known of condensin II but did not know how it functioned inside cells.
Keeping specific parts of chromosomes from touching can change how the instructions carried in the DNA are read, said BIO5 member Giovanni Bosco, a UA assistant professor of molecular and cellular biology.
"It's like picking up your favorite book and, depending on what chair you chose to sit in, it turned into a different story -- even though the printed words in the book never changed," research team leader Bosco wrote in an e-mail.
"This now changes the way we think about genetic information. Taking a literal reading of it is not what actually happens," he wrote. "Instead, context matters."
The team also found that condensin II plays a key role in making sure that fruit fly sperm cells each receive the proper number of chromosomes -- not too many, not too few.
Bosco suspects that condensin II plays the same role in the formation of human sperm and eggs.
Having too many or too few chromosomes in egg or sperm cells is the source of several important genetic disorders, including Down syndrome.
Abnormalities in chromosome number is also the cause of some miscarriages of early-term fetuses in humans.
The research is published in two separate papers. "Chromosome Alignment and Transvection are Antagonized by Condensin II," by Tom A. Hartl and Helen F. Smith, UA doctoral students, and Bosco is in the Nov. 28 issue of the journal Science.
Hartl, Sarah J. Sweeney, Peter J. Knepler and Bosco published their paper, "Condensin II Resolves Chromosomal Associations to Enable Anaphase I Segregation in Drosophila Male Meiosis," in the October 2008 issue of PLoS Genetics. Sweeney and Knepler, now doing research at UA, were UA undergraduates when they conducted the research.
The National Institutes of Health and the National Science Foundation funded the research.
Learning how cells control chromosomes and how DNA is transcribed will lead to better understanding of how an organism's DNA affects the organism's final form.
Scientists have known for about 50 years that when chromosomes are in direct contact, the transcription machinery can choose to transcribe either the gene from the mother or the gene from the father.
Many researchers investigated how the specific genes were brought close together so that process, known as transvection, could happen.
Bosco wondered, what if the chromosomes stayed stuck together?
To find something that separated chromosomes, he looked for female fruit flies that were sterile because chromosomes in their eggs had stuck together.
Once he had those fruit flies, Hartl isolated the gene that kept the chromosomes from coming apart. He found that the gene coded for condensin II, indicating that the sterile flies couldn't make condensin II.
To be able to watch how condensin II affects chromosomes, the researchers used the salivary glands from normal Drosophila melanogaster fruit flies. Fruit fly salivary glands are unusual, because they have many copies of the same chromosome coiled together like a rope.
Hartl said, "You can actually see chromosomes, because the cells are so huge and the chromosomes are so huge."
The team inserted an additional gene into the chromosomes that would turn the condensin II-producing gene off at 77 F (21 C) and on at 95 F (35 C). The researchers also marked one gene on the chromosomes with green fluorescent protein, or GFP, to be able to see changes in the chromosomes' positions.
The scientists then looked at the salivary glands at the two temperatures to see what happened when condensin II was present and when it was absent.
Bosco said, "Simply turning the condensin gene on or off, we could watch the chromosomes move right before our eyes, demonstrating that condensin was mostly likely the tiny machine that was ripping the chromosomes apart."
He said these findings are significant because more and more genetic tests to sequence people's DNA are becoming available, but the DNA sequence alone does not completely determine what diseases the person will have.
Even if it's in the genes, it might not show, he said. "It's what your cells are doing with your genes that's important."
To pull the chromosomes apart, condensin II changes its shape. Smith said the team's next step is figuring out how condensin II proteins are recruited to the chromosomes and how the condensin II proteins use the cellular energy packets known as ATP to change shape.
Now University of Arizona researchers have found the molecular machines in fruit flies that yank chromosomes, the DNA-carrying structures, apart when necessary.
The machines, proteins called condensin II, separate chromosomes by twisting them into supercoils that kink up and therefore can no longer touch.
Scientists had known of condensin II but did not know how it functioned inside cells.
Keeping specific parts of chromosomes from touching can change how the instructions carried in the DNA are read, said BIO5 member Giovanni Bosco, a UA assistant professor of molecular and cellular biology.
"It's like picking up your favorite book and, depending on what chair you chose to sit in, it turned into a different story -- even though the printed words in the book never changed," research team leader Bosco wrote in an e-mail.
"This now changes the way we think about genetic information. Taking a literal reading of it is not what actually happens," he wrote. "Instead, context matters."
The team also found that condensin II plays a key role in making sure that fruit fly sperm cells each receive the proper number of chromosomes -- not too many, not too few.
Bosco suspects that condensin II plays the same role in the formation of human sperm and eggs.
Having too many or too few chromosomes in egg or sperm cells is the source of several important genetic disorders, including Down syndrome.
Abnormalities in chromosome number is also the cause of some miscarriages of early-term fetuses in humans.
The research is published in two separate papers. "Chromosome Alignment and Transvection are Antagonized by Condensin II," by Tom A. Hartl and Helen F. Smith, UA doctoral students, and Bosco is in the Nov. 28 issue of the journal Science.
Hartl, Sarah J. Sweeney, Peter J. Knepler and Bosco published their paper, "Condensin II Resolves Chromosomal Associations to Enable Anaphase I Segregation in Drosophila Male Meiosis," in the October 2008 issue of PLoS Genetics. Sweeney and Knepler, now doing research at UA, were UA undergraduates when they conducted the research.
The National Institutes of Health and the National Science Foundation funded the research.
Learning how cells control chromosomes and how DNA is transcribed will lead to better understanding of how an organism's DNA affects the organism's final form.
Scientists have known for about 50 years that when chromosomes are in direct contact, the transcription machinery can choose to transcribe either the gene from the mother or the gene from the father.
Many researchers investigated how the specific genes were brought close together so that process, known as transvection, could happen.
Bosco wondered, what if the chromosomes stayed stuck together?
To find something that separated chromosomes, he looked for female fruit flies that were sterile because chromosomes in their eggs had stuck together.
Once he had those fruit flies, Hartl isolated the gene that kept the chromosomes from coming apart. He found that the gene coded for condensin II, indicating that the sterile flies couldn't make condensin II.
To be able to watch how condensin II affects chromosomes, the researchers used the salivary glands from normal Drosophila melanogaster fruit flies. Fruit fly salivary glands are unusual, because they have many copies of the same chromosome coiled together like a rope.
Hartl said, "You can actually see chromosomes, because the cells are so huge and the chromosomes are so huge."
The team inserted an additional gene into the chromosomes that would turn the condensin II-producing gene off at 77 F (21 C) and on at 95 F (35 C). The researchers also marked one gene on the chromosomes with green fluorescent protein, or GFP, to be able to see changes in the chromosomes' positions.
The scientists then looked at the salivary glands at the two temperatures to see what happened when condensin II was present and when it was absent.
Bosco said, "Simply turning the condensin gene on or off, we could watch the chromosomes move right before our eyes, demonstrating that condensin was mostly likely the tiny machine that was ripping the chromosomes apart."
He said these findings are significant because more and more genetic tests to sequence people's DNA are becoming available, but the DNA sequence alone does not completely determine what diseases the person will have.
Even if it's in the genes, it might not show, he said. "It's what your cells are doing with your genes that's important."
To pull the chromosomes apart, condensin II changes its shape. Smith said the team's next step is figuring out how condensin II proteins are recruited to the chromosomes and how the condensin II proteins use the cellular energy packets known as ATP to change shape.
Monday, November 3, 2008
New Arizona Company Seeks Valley Fever Cure
[Source: University of Arizona Communications] - A University of Arizona-supported company is working to cure valley fever, a lung disease that affects as many as 150,000 people in the southwest U.S. every year, yet is virtually unknown in the rest of the country.
Valley Fever Solutions Inc. is backed by a broad coalition that includes the UA, the BIO5 Institute, C-Path, a New York-based foundation and private donors. The company is testing nikkomycin Z (nik Z), the first of a new class of drugs that could potentially kill the fungus that causes valley fever.
While other treatments inhibit the valley fever's growth and encourage the immune system to keep it in check, none of them destroy the fungus entirely. For most patients this isn't an issue as valley fever's flu-like symptoms are so mild for them that they don't even seek medical attention.
Occasionally, more severe cases of valley fever can lead to pneumonia, osteomyelitis and meningitis, sometimes with fatal results. Those with weakened immune systems often are most at risk.
"If we can eradicate this disease, then the severe complications won't happen," said Dr. John Galgiani, chief medical officer for VF Solutions, director of the UA's Valley Fever Center for Excellence in the College of Medicine and a BIO5 member. "If you treat a thousand valley fever infections you might, for example, prevent three cases of meningitis." Gagliani said. Even mild infections have an impact because they result in days lost from work and other activities.
Sixty percent of all U.S. valley fever cases occur in Phoenix, Tucson and the corridor along Interstate 10 that connects the two cities. "We have the expertise to do clinical trials in Arizona because this is a very important and common disease here," Galgiani said. "Valley fever is our problem, and we need to look to ourselves to solve it."
Nik Z is now in phase I drug safety trials sponsored by the UA. VF Solutions aims to move the drug from the laboratory to the marketplace. "You can't have a new therapy unless you create a commercial product. With the formation of VF Solutions we can interest investors and write small business grants," Galgiani said.
The company has already obtained a Science and Translational Technology Research grant from the National Institutes of Health to fund pharmacology studies that will help design future clinical trials. The first phase of the grant is worth more than $100,000, with the potential for an additional $700,000.
VF Solutions CEO David Larwood is now working on his fourth startup company, two of which were taken public. The company also draws expertise from the UA chemistry, biochemistry and pharmacy faculty, as well as other experts and clinicians. Some of them have been working to develop a valley fever drug before the company was formed.
In 2006 the Food and Drug Administration awarded Orphan Drug Status for the project and in 2007 funded the first nik Z clinical trials that are now under way.
Having nik Z's development and possible manufacture in Arizona also brings dollars to the state. "This response to a local problem could become part of the growing Arizona biotechnology initiative," Galgiani said.
Valley Fever Awareness Week is Nov 10-16. The public is invited to a public forum, titled "Learn About Valley Fever: Ask the Doctors your Questions" on Sunday, Nov. 16, from 1 to 4 p.m. at DuVal Auditorium, University Medical Center, 1501 N. Campbell Ave. in Tucson.
Featured UA doctors include Neil Ampel, John Galgiani, Susan Hoover and David Nix.
Valley Fever Solutions Inc. is backed by a broad coalition that includes the UA, the BIO5 Institute, C-Path, a New York-based foundation and private donors. The company is testing nikkomycin Z (nik Z), the first of a new class of drugs that could potentially kill the fungus that causes valley fever.
While other treatments inhibit the valley fever's growth and encourage the immune system to keep it in check, none of them destroy the fungus entirely. For most patients this isn't an issue as valley fever's flu-like symptoms are so mild for them that they don't even seek medical attention.
Occasionally, more severe cases of valley fever can lead to pneumonia, osteomyelitis and meningitis, sometimes with fatal results. Those with weakened immune systems often are most at risk.
"If we can eradicate this disease, then the severe complications won't happen," said Dr. John Galgiani, chief medical officer for VF Solutions, director of the UA's Valley Fever Center for Excellence in the College of Medicine and a BIO5 member. "If you treat a thousand valley fever infections you might, for example, prevent three cases of meningitis." Gagliani said. Even mild infections have an impact because they result in days lost from work and other activities.
Sixty percent of all U.S. valley fever cases occur in Phoenix, Tucson and the corridor along Interstate 10 that connects the two cities. "We have the expertise to do clinical trials in Arizona because this is a very important and common disease here," Galgiani said. "Valley fever is our problem, and we need to look to ourselves to solve it."
Nik Z is now in phase I drug safety trials sponsored by the UA. VF Solutions aims to move the drug from the laboratory to the marketplace. "You can't have a new therapy unless you create a commercial product. With the formation of VF Solutions we can interest investors and write small business grants," Galgiani said.
The company has already obtained a Science and Translational Technology Research grant from the National Institutes of Health to fund pharmacology studies that will help design future clinical trials. The first phase of the grant is worth more than $100,000, with the potential for an additional $700,000.
VF Solutions CEO David Larwood is now working on his fourth startup company, two of which were taken public. The company also draws expertise from the UA chemistry, biochemistry and pharmacy faculty, as well as other experts and clinicians. Some of them have been working to develop a valley fever drug before the company was formed.
In 2006 the Food and Drug Administration awarded Orphan Drug Status for the project and in 2007 funded the first nik Z clinical trials that are now under way.
Having nik Z's development and possible manufacture in Arizona also brings dollars to the state. "This response to a local problem could become part of the growing Arizona biotechnology initiative," Galgiani said.
Valley Fever Awareness Week is Nov 10-16. The public is invited to a public forum, titled "Learn About Valley Fever: Ask the Doctors your Questions" on Sunday, Nov. 16, from 1 to 4 p.m. at DuVal Auditorium, University Medical Center, 1501 N. Campbell Ave. in Tucson.
Featured UA doctors include Neil Ampel, John Galgiani, Susan Hoover and David Nix.
Proposal to centralize UA information technology functions meets opposition
[Source: RENÉE SCHAFER HORTON, Tucson Citizen] - The message to University of Arizona President Robert N. Shelton and Provost Meredith Hay is loud and clear on the Transformation Plan Web site: Don't centralize UA's information technology functions.
"Transforming Technology Support Services" is the most controversial of the 75 proposals submitted to Hay Oct. 13 as the first step in UA's reorganization process - at least on the Web site.
The IT proposal, written by UA Information Technology Services CIO Michele Norin, had 64 comments as of Friday, including one from the director of the BIO5 Institute. Most of the other proposals had zero to five comments, although a proposal calling for the merger of the colleges of science and engineering had 14.
"We all absolutely hate this proposal," said anthropology Professor David Killick, one of the many critics who commented on Norin's proposal. "We aren't a corporation. Each of (our) departments and research facilities have very different computing needs. This is just an effort to save money, but in the long run it will make things worse, not better."
Shelton announced in mid-September that "business as usual" was no longer an option at UA in the face of declining state support. He said a major reorganization was necessary and asked deans and department heads to consult their constituencies and develop "white papers" listing consolidations, eliminations or reorganizations that would strengthen UA's mission while cutting costs.
The proposals are being vetted by a subcommittee of UA's Strategic Planning and Budgetary Advisory Committee, whhich will turn them over to Hay on Monday with recommendations of which should be scrapped, which implemented immediately and which need further development or refinement.
Complaints about Norin's proposal centered on a lack of constituent input and fear that centralizing IT functions will harm research and cost money.
According to Norin's proposal, the goal is to "transition a majority of technology personnel, equipment and operational budgets currently managed and performed within colleges, departments, and support units to the responsibility of the CIO, whereby management is centralized yet personnel are distributed."
Vicki Chandler, director of UA's BIO5 Institute, wrote that Norin's proposal "by and large … will be extremely detrimental to the activities of BIO5."
"I am genuinely concerned that the design, motive and rationale listed in the proposal lacks understanding of how our research-intensive units function and the essential role for IT in our research missions," Chandler wrote in the comments section on the Transformation Plan Web site. "This is exactly the type of proposal that will do major harm to our university's ability to continue to pursue big science."
Chris Segrin, head of the Department of Communications, recalled past efforts at centralizing IT services that cost his department "several thousand dollars" and wrote that he was concerned centralizing IT functions again could result in departments being charged outrageous sums from Norin's office for computer technician services.
"If one does not like (University Information Technology Services) fee structure or cannot afford it, what recourse does she or he have?" Segrin wrote. "In my view, the most likely effect of this plan would be an increase in revenue flowing into central administration, absent any clear plan for how that would translate into cost savings at the college, department, and end user level."
A handful of comments supported at least part of Norin's proposal, including Dianne Horgan, associate dean of the Graduate College.
"I came to UA from another (not so prestigious) university where something very similar was tried. I, and everyone else, fought it," Horgan wrote. "But three years later, I had to admit I'd been wrong. It worked, saved the university lots of money, and we ended up with far superior service."
Unlike the other proposals, Norin's did not describe the consultation process she used to come up with her proposal, a lapse a number of comments noted.
The proposal rubrics from Hay state that proposals should include information about "the processes of consultation with deans, heads, faculty, staff, appointed personnel, and students and the extent to which this proposal has the support of those affected."
Norin, through her administrative assistant, declined to comment on her proposal Friday.
"Transforming Technology Support Services" is the most controversial of the 75 proposals submitted to Hay Oct. 13 as the first step in UA's reorganization process - at least on the Web site.
The IT proposal, written by UA Information Technology Services CIO Michele Norin, had 64 comments as of Friday, including one from the director of the BIO5 Institute. Most of the other proposals had zero to five comments, although a proposal calling for the merger of the colleges of science and engineering had 14.
"We all absolutely hate this proposal," said anthropology Professor David Killick, one of the many critics who commented on Norin's proposal. "We aren't a corporation. Each of (our) departments and research facilities have very different computing needs. This is just an effort to save money, but in the long run it will make things worse, not better."
Shelton announced in mid-September that "business as usual" was no longer an option at UA in the face of declining state support. He said a major reorganization was necessary and asked deans and department heads to consult their constituencies and develop "white papers" listing consolidations, eliminations or reorganizations that would strengthen UA's mission while cutting costs.
The proposals are being vetted by a subcommittee of UA's Strategic Planning and Budgetary Advisory Committee, whhich will turn them over to Hay on Monday with recommendations of which should be scrapped, which implemented immediately and which need further development or refinement.
Complaints about Norin's proposal centered on a lack of constituent input and fear that centralizing IT functions will harm research and cost money.
According to Norin's proposal, the goal is to "transition a majority of technology personnel, equipment and operational budgets currently managed and performed within colleges, departments, and support units to the responsibility of the CIO, whereby management is centralized yet personnel are distributed."
Vicki Chandler, director of UA's BIO5 Institute, wrote that Norin's proposal "by and large … will be extremely detrimental to the activities of BIO5."
"I am genuinely concerned that the design, motive and rationale listed in the proposal lacks understanding of how our research-intensive units function and the essential role for IT in our research missions," Chandler wrote in the comments section on the Transformation Plan Web site. "This is exactly the type of proposal that will do major harm to our university's ability to continue to pursue big science."
Chris Segrin, head of the Department of Communications, recalled past efforts at centralizing IT services that cost his department "several thousand dollars" and wrote that he was concerned centralizing IT functions again could result in departments being charged outrageous sums from Norin's office for computer technician services.
"If one does not like (University Information Technology Services) fee structure or cannot afford it, what recourse does she or he have?" Segrin wrote. "In my view, the most likely effect of this plan would be an increase in revenue flowing into central administration, absent any clear plan for how that would translate into cost savings at the college, department, and end user level."
A handful of comments supported at least part of Norin's proposal, including Dianne Horgan, associate dean of the Graduate College.
"I came to UA from another (not so prestigious) university where something very similar was tried. I, and everyone else, fought it," Horgan wrote. "But three years later, I had to admit I'd been wrong. It worked, saved the university lots of money, and we ended up with far superior service."
Unlike the other proposals, Norin's did not describe the consultation process she used to come up with her proposal, a lapse a number of comments noted.
The proposal rubrics from Hay state that proposals should include information about "the processes of consultation with deans, heads, faculty, staff, appointed personnel, and students and the extent to which this proposal has the support of those affected."
Norin, through her administrative assistant, declined to comment on her proposal Friday.
Friday, October 31, 2008
Corn Researchers Discover Novel Gene Shut-off Mechanisms
[Source: ScienceDaily] - University of Delaware scientists, in collaboration with researchers from the University of Arizona and South Dakota State University, have identified unusual differences in the natural mechanisms that turn off, or “silence,” genes in corn.
The discovery, which was made by comparing the impact of inactivating a gene that occurs in both corn and in the much-studied laboratory plant Arabidopsis, provides new insight into how one of the world's most important crops protects itself from mutation-causing mobile DNA elements and viruses.
The research was led by Blake Meyers, associate professor of plant and soil sciences, and Pamela Green, Crawford H. Greenewalt Chair and professor of plant and soil sciences and marine bioscience, and their laboratory groups at the Delaware Biotechnology Institute, a major center for biotechnology and life sciences research at the University of Delaware.
Collaborating with the University of Delaware team were Vicki Chandler, the Carl E. and Patricia Weiler Endowed Chair for Excellence in Agriculture and Life Sciences Regents' Professor at the University of Arizona, and Yang Yen, a professor at South Dakota State University.
The results were published in the Proceedings of the National Academy of Sciences of the United States of America.
Studies of Arabidopsis thaliana, a small flowering plant of the mustard family that is easy to grow in the lab, have provided a lot of what scientists know about gene silencing in plants.
An important key to the process is short sequences of ribonucleic acids known as “small RNAs” which act like biochemical switches that shut off genes, thus playing a fundamental role in plant development. Understanding how small RNAs work is a continuing quest for geneticists seeking to breed plants with improved crop yields, disease resistance and other characteristics.
Previously, the Meyers and Green labs had studied Arabidopsis plants with nonfunctional versions of a gene known as RNA-dependent RNA polymerase 2 (RDR2). Without an active copy of this gene, the plants were unable to produce a major class of small RNAs, which act to stabilize and protect genes on the chromosomes.
In that prior work, Meyers and Green took advantage of the nonfunctional gene to study microRNAs, an interesting type of small RNA that is usually “masked” by the major class of small RNAs produced by RDR2.
Independently of the UD groups, Chandler and her team at the University of Arizona had identified from corn an orthologous gene--a gene that has the same function in different organisms. In corn, this gene, which the Chandler lab found, is called the mediator of paramutation (MOP1). Its equivalent in Arabidopsis is the RDR2 gene.
Because the RDR2 and MOP1 genes should both produce the “protective” set of small RNAs, the research groups decided to collaborate to see if the small RNAs in corn behave the same way they do in Arabidopsis. The hypothesis was that the result would be the same in the two plant species, and the lab groups could use the MOP1 corn plants to focus their studies on the harder-to-examine microRNAs, as they had done previously in Arabidopsis.
“Yet we found something that had not been observed before in this plant--an odd class of small RNAs,” Meyers said. “I think it's pretty neat to work in a more complex system like corn and see things that Arabidopsis hadn't shown us,” he noted.
Using a technique known as sequencing by synthesis (SBS), provided by Illumina in Hayward, Calif., coupled with state-of-the-art bioinformatics in Meyers' lab, the research team found that the MOP1 and RDR2 genes are not fully equivalent based on an assessment of small RNA complexity.
The researchers found that there are lots more RNAs of an unusual class known as “small interfering RNAs” in corn than there are in Arabidopsis.
“This class of RNAs mainly functions to repress repetitive sequences, including mobile DNA elements called transposons,” Meyers said. “Thus, small interfering RNAs act to protect the genome,” he noted.
“Corn contains an extra layer of protective small RNAs that had not been observed in Arabidopsis, so there must be additional genes other than MOP1 that produce this,” Meyers said.
The scientific community is sequencing the corn genome now, Meyers said. Once the genome is available, the work of matching up small RNAs to specific traits in corn will be much easier, he noted.
“This research is helping us to better understand the biology of corn--one of the most important plants in the world--and gives us new avenues for exploring a novel class of small RNAs,” Meyers said.
The discovery, which was made by comparing the impact of inactivating a gene that occurs in both corn and in the much-studied laboratory plant Arabidopsis, provides new insight into how one of the world's most important crops protects itself from mutation-causing mobile DNA elements and viruses.
The research was led by Blake Meyers, associate professor of plant and soil sciences, and Pamela Green, Crawford H. Greenewalt Chair and professor of plant and soil sciences and marine bioscience, and their laboratory groups at the Delaware Biotechnology Institute, a major center for biotechnology and life sciences research at the University of Delaware.
Collaborating with the University of Delaware team were Vicki Chandler, the Carl E. and Patricia Weiler Endowed Chair for Excellence in Agriculture and Life Sciences Regents' Professor at the University of Arizona, and Yang Yen, a professor at South Dakota State University.
The results were published in the Proceedings of the National Academy of Sciences of the United States of America.
Studies of Arabidopsis thaliana, a small flowering plant of the mustard family that is easy to grow in the lab, have provided a lot of what scientists know about gene silencing in plants.
An important key to the process is short sequences of ribonucleic acids known as “small RNAs” which act like biochemical switches that shut off genes, thus playing a fundamental role in plant development. Understanding how small RNAs work is a continuing quest for geneticists seeking to breed plants with improved crop yields, disease resistance and other characteristics.
Previously, the Meyers and Green labs had studied Arabidopsis plants with nonfunctional versions of a gene known as RNA-dependent RNA polymerase 2 (RDR2). Without an active copy of this gene, the plants were unable to produce a major class of small RNAs, which act to stabilize and protect genes on the chromosomes.
In that prior work, Meyers and Green took advantage of the nonfunctional gene to study microRNAs, an interesting type of small RNA that is usually “masked” by the major class of small RNAs produced by RDR2.
Independently of the UD groups, Chandler and her team at the University of Arizona had identified from corn an orthologous gene--a gene that has the same function in different organisms. In corn, this gene, which the Chandler lab found, is called the mediator of paramutation (MOP1). Its equivalent in Arabidopsis is the RDR2 gene.
Because the RDR2 and MOP1 genes should both produce the “protective” set of small RNAs, the research groups decided to collaborate to see if the small RNAs in corn behave the same way they do in Arabidopsis. The hypothesis was that the result would be the same in the two plant species, and the lab groups could use the MOP1 corn plants to focus their studies on the harder-to-examine microRNAs, as they had done previously in Arabidopsis.
“Yet we found something that had not been observed before in this plant--an odd class of small RNAs,” Meyers said. “I think it's pretty neat to work in a more complex system like corn and see things that Arabidopsis hadn't shown us,” he noted.
Using a technique known as sequencing by synthesis (SBS), provided by Illumina in Hayward, Calif., coupled with state-of-the-art bioinformatics in Meyers' lab, the research team found that the MOP1 and RDR2 genes are not fully equivalent based on an assessment of small RNA complexity.
The researchers found that there are lots more RNAs of an unusual class known as “small interfering RNAs” in corn than there are in Arabidopsis.
“This class of RNAs mainly functions to repress repetitive sequences, including mobile DNA elements called transposons,” Meyers said. “Thus, small interfering RNAs act to protect the genome,” he noted.
“Corn contains an extra layer of protective small RNAs that had not been observed in Arabidopsis, so there must be additional genes other than MOP1 that produce this,” Meyers said.
The scientific community is sequencing the corn genome now, Meyers said. Once the genome is available, the work of matching up small RNAs to specific traits in corn will be much easier, he noted.
“This research is helping us to better understand the biology of corn--one of the most important plants in the world--and gives us new avenues for exploring a novel class of small RNAs,” Meyers said.
Monday, October 27, 2008
Diatom Genome Helps Explain Their Great Diversity and Success in Trapping Excess Carbon in Oceans
[Source: Deborah Daun, BIO5] - Diatoms, mighty microscopic algae, have profound influence on climate, producing 20 percent of the oxygen we breathe by capturing atmospheric carbon and in so doing, countering the greenhouse effect. Since their evolutionary origins these photosynthetic wonders have come to acquire advantageous genes from bacterial, animal and plant ancestors enabling them to thrive in today’s oceans. These findings, based on the analysis of the latest sequenced diatom genome, Phaeodactylum tricornutum, are published in the October 15, 2008 edition of the journal Nature by an international team of researchers led by the U.S. Department of Energy Joint Genome Institute (DOE JGI) and the Ecole Normale Supérieure of Paris. The research team includes Carolyn Napoli, PhD, a research professor with the BIO5 Institute; and Rich Jorgensen, PhD, professor of plant sciences at The University of Arizona.
The researchers compared Phaeodactylum with the diatom Thalassiosira pseudonana, previously sequenced by DOE JGI, revealing a wealth of information about diatom biology, particularly the rapid diversification among the hundreds of thousands of diatom species that exist today. Phaeodactylum was targeted for sequencing due to its value as a diatom model, given the ease with which it can be grown in the lab and the availability of tools to genetically transform it, and the comparisons with the previously sequenced diatom genome of Thalassiosira pseudonana.
“These organisms represent a veritable melting pot of traits—a hybrid of genetic mechanisms contributed by ancestral lineages of plants, animals, and bacteria, and optimized over the relatively short evolutionary timeframe of 180 million years since they first appeared,” says first author Chris Bowler of the Ecole Normale Supérieure. “Our findings show that gene transfer between diatoms and other organisms has been extremely common, making diatoms ‘transgenic by nature’,” he adds.
The wholesale acquisition of genetic material has provided food for thought to researchers bent on characterizing the diatom’s staying power and ability to cope with environmental change.
“We believe this is the first time bacterial horizontal gene transfer has been observed in eukaryotes at such scale,” says senior author Igor Grigoriev of DOE JGI. “This study gets us closer to explaining the dramatic diversity across the genera of diatoms, morphologically, behaviorally, but we still haven’t yet explained all the differences conferred by the genes contributed by the other taxa.”
From plants, the diatom inherited photosynthesis, and from animals the production of urea. Bowler speculates that the diatom uses urea to store nitrogen, not to eliminate it like animals do, because nitrogen is a precious nutrient in the ocean. What’s more, the tiny alga draws the best of both worlds—it can convert fat into sugar, as well as sugar into fat—extremely useful in times of nutrient shortage.
The team documented more than 300 genes sourced from bacteria and found in both types of diatoms, pointing to their ancient origin and suggesting novel mechanisms of managing nutrients—for example utilization of organic carbon and nitrogen—and detecting cues from their environment.
Diatoms, encapsulated by elaborate lacework-like shells made of glass, are only about one-third of a strand of hair in diameter. “The diatom genomes will help us to understand how they can make these structures at ambient temperatures and pressures, something that humans are not able to do. If we can learn how they do it, we could open up all kinds of new nanotechnologies, like for building miniature silicon chips or for biomedical applications,” says Bowler.
Diatoms reside in fresh or salt water and can be divided into two camps, centrics and pennates. The centric Thalassiosira resemble a round “Camembert” cheese box (only much smaller) and pennates like Phaeodactylum look more like a cross between a boomerang and a narrow three-cornered hat—hence the species name, tricornutum. Not only is their shape and habitat diverse, so too is their behavior; for instance, the former get around by floating, the latter by gliding through the water or on surfaces.
The lifestyle of diatoms can be characterized as “bloom or bust.” When light and nutrient conditions in the upper reaches of the ocean are favorable, particularly at the onset of spring, diatoms gain an edge and tend to dominate their phytoplankton brethren. When food is scarce, they die and sink, carrying their complement of carbon dioxide to the deeper recesses.
Bowler and his colleagues are also trying to understand the role that iron plays in the Phaeodactylum’s development. Iron is even more precious than nitrogen in the ocean and its absence in the southern hemisphere is likely a major cause of oceanic deserts of photosynthesis there. Bowler’s team has demonstrated that when iron deficiency occurs processes such as photosynthesis and nitrogen assimilation are suppressed. Other studies, which hail diatoms as champions in capturing carbon dioxide, suggest a bold strategy of using iron as a fertilizer to provoke massive diatom blooms. “Once they have feasted, the weight of their silicon shells, which resemble glass, causes the diatoms to sink to the bottom of the ocean when they die, and the carbon that they assimilated is trapped there for millennia,” says Bowler. “By sequestering carbon in this way we could reverse the damage from the burning of fossil fuels.”
Other DOE JGI authors on the Nature study include Alan Kuo, Robert Otillar, Asaf Salamov, Chris Detter, Erika Lindquist, Susan Lucas, Harris Shapiro, Daniel Rokhsar, and Igor Grigoriev as well as Jane Grimwood and Jeremy Schmutz of JGI at the HudsonAlpha Institute.
The U.S. Department of Energy Joint Genome Institute, supported by the DOE Office of Science, unites the expertise of five national laboratories -- Lawrence Berkeley, Lawrence Livermore, Los Alamos, Oak Ridge, and Pacific Northwest -- along with the HudsonAlpha Institute for Biotechnology -- to advance genomics in support of the DOE missions related to clean energy generation and environmental characterization and cleanup. DOE JGI’s Walnut Creek, CA, Production Genomics Facility provides integrated high-throughput sequencing and computational analysis that enable systems-based scientific approaches to these challenges.
The researchers compared Phaeodactylum with the diatom Thalassiosira pseudonana, previously sequenced by DOE JGI, revealing a wealth of information about diatom biology, particularly the rapid diversification among the hundreds of thousands of diatom species that exist today. Phaeodactylum was targeted for sequencing due to its value as a diatom model, given the ease with which it can be grown in the lab and the availability of tools to genetically transform it, and the comparisons with the previously sequenced diatom genome of Thalassiosira pseudonana.
“These organisms represent a veritable melting pot of traits—a hybrid of genetic mechanisms contributed by ancestral lineages of plants, animals, and bacteria, and optimized over the relatively short evolutionary timeframe of 180 million years since they first appeared,” says first author Chris Bowler of the Ecole Normale Supérieure. “Our findings show that gene transfer between diatoms and other organisms has been extremely common, making diatoms ‘transgenic by nature’,” he adds.
The wholesale acquisition of genetic material has provided food for thought to researchers bent on characterizing the diatom’s staying power and ability to cope with environmental change.
“We believe this is the first time bacterial horizontal gene transfer has been observed in eukaryotes at such scale,” says senior author Igor Grigoriev of DOE JGI. “This study gets us closer to explaining the dramatic diversity across the genera of diatoms, morphologically, behaviorally, but we still haven’t yet explained all the differences conferred by the genes contributed by the other taxa.”
From plants, the diatom inherited photosynthesis, and from animals the production of urea. Bowler speculates that the diatom uses urea to store nitrogen, not to eliminate it like animals do, because nitrogen is a precious nutrient in the ocean. What’s more, the tiny alga draws the best of both worlds—it can convert fat into sugar, as well as sugar into fat—extremely useful in times of nutrient shortage.
The team documented more than 300 genes sourced from bacteria and found in both types of diatoms, pointing to their ancient origin and suggesting novel mechanisms of managing nutrients—for example utilization of organic carbon and nitrogen—and detecting cues from their environment.
Diatoms, encapsulated by elaborate lacework-like shells made of glass, are only about one-third of a strand of hair in diameter. “The diatom genomes will help us to understand how they can make these structures at ambient temperatures and pressures, something that humans are not able to do. If we can learn how they do it, we could open up all kinds of new nanotechnologies, like for building miniature silicon chips or for biomedical applications,” says Bowler.
Diatoms reside in fresh or salt water and can be divided into two camps, centrics and pennates. The centric Thalassiosira resemble a round “Camembert” cheese box (only much smaller) and pennates like Phaeodactylum look more like a cross between a boomerang and a narrow three-cornered hat—hence the species name, tricornutum. Not only is their shape and habitat diverse, so too is their behavior; for instance, the former get around by floating, the latter by gliding through the water or on surfaces.
The lifestyle of diatoms can be characterized as “bloom or bust.” When light and nutrient conditions in the upper reaches of the ocean are favorable, particularly at the onset of spring, diatoms gain an edge and tend to dominate their phytoplankton brethren. When food is scarce, they die and sink, carrying their complement of carbon dioxide to the deeper recesses.
Bowler and his colleagues are also trying to understand the role that iron plays in the Phaeodactylum’s development. Iron is even more precious than nitrogen in the ocean and its absence in the southern hemisphere is likely a major cause of oceanic deserts of photosynthesis there. Bowler’s team has demonstrated that when iron deficiency occurs processes such as photosynthesis and nitrogen assimilation are suppressed. Other studies, which hail diatoms as champions in capturing carbon dioxide, suggest a bold strategy of using iron as a fertilizer to provoke massive diatom blooms. “Once they have feasted, the weight of their silicon shells, which resemble glass, causes the diatoms to sink to the bottom of the ocean when they die, and the carbon that they assimilated is trapped there for millennia,” says Bowler. “By sequestering carbon in this way we could reverse the damage from the burning of fossil fuels.”
Other DOE JGI authors on the Nature study include Alan Kuo, Robert Otillar, Asaf Salamov, Chris Detter, Erika Lindquist, Susan Lucas, Harris Shapiro, Daniel Rokhsar, and Igor Grigoriev as well as Jane Grimwood and Jeremy Schmutz of JGI at the HudsonAlpha Institute.
The U.S. Department of Energy Joint Genome Institute, supported by the DOE Office of Science, unites the expertise of five national laboratories -- Lawrence Berkeley, Lawrence Livermore, Los Alamos, Oak Ridge, and Pacific Northwest -- along with the HudsonAlpha Institute for Biotechnology -- to advance genomics in support of the DOE missions related to clean energy generation and environmental characterization and cleanup. DOE JGI’s Walnut Creek, CA, Production Genomics Facility provides integrated high-throughput sequencing and computational analysis that enable systems-based scientific approaches to these challenges.
UA researchers are finding a new way to reduce food-borne illness in humans
[Source: Susan McGinley, UA College of Agriculture and Life Sciences] - Most people are familiar with Salmonella and its potential to make people ill. But fewer know about Campylobacter jejuni – even though it makes more people sick. Raw chicken is one of the most common carriers of the bacteria, often encountered when cooked meat is placed on unwashed cutting boards previously used for trimming raw chicken, or when chicken is not cooked to 165 degrees Fahrenheit.
"Campylobacter is now the No. 1 food-borne pathogen in the United States and the world, surpassing Salmonella," said Lynn Joens, a professor in The University of Arizona department of veterinary science and microbiology and a BIO5 member. "In the United States alone, 2.4 million cases are reported annually, with costs exceeding $1 billion."
A new poultry vaccine in development at the UA offers a unique approach in controlling Campylobacter jejuni infection in chickens before it reaches the dinner table. In research trials the vaccine has significantly reduced the pathogen's ability to colonize young chickens' intestines, where the infection begins. The goal is to halt the contamination before it spreads and survives on raw chicken sold in stores.
"Yet chickens don't actually cause the disease (nor does it make them ill). It's the organism they carry that makes people sick," Joens said. "Right now you can go to any grocery store, get a raw chicken, test it in a laboratory and find Campylobacter jejuni. Twenty to 80 percent of all broiler houses become contaminated with Campylobacter."
The most common symptoms of human Campylobacter poisoning, which mimic those of Salmonella and other gastrointestinal pathogens, include fever, cramps, watery diarrhea and sometimes dysentery. More severe infections can lead to peritonitis, autoimmune disease or death.
Funded by the U.S. Department of Agriculture, Joens and UA graduate students started analyzing Campylobacter's infection process about four years ago, looking for a way to interrupt it. The laboratory team, which included graduate research associate James Theoret and assistant research professor Bibiana Law, eventually discovered that the pathogen first attached itself to the surface of the chick's intestines and then began to multiply. Attacking the "sticking" mechanism seemed to be the key.
When the UA researchers sequenced the intestinal surface protein they identified the gene responsible for producing Campylobacter’s adherence protein. Then they built a trial vaccine around it using Salmonella bacteria as a vector, with the assistance of Roy Curtiss, professor and director of the Center for Infectious Diseases and Vaccinology at Arizona State University. Curtiss’ group inserted the adherence gene into Salmonella bacteria, which is nonpathogenic for poultry. The resulting live vaccine – containing Salmonella programmed to make the Campylobacter adhering protein – was fed to young chickens to protect them.
“Once the Salmonella in the vaccine produced the Campylobacter protein, the chicks made antibodies against it in their intestines,” Joens says. "In our first study of 15 birds we got a very significant reduction – 98 percent – in Campylobacter infection, compared with a control group. We're now repeating the trial on a larger scale."
The vaccination process is simple, easy to produce and protective to the chick, according to Joens. The Salmonella lives four to five days, enough time to stimulate antibody production, and dies. Chickens need to be vaccinated early because they become infected at just two to three weeks of age.
Joens' preliminary figures show that 270 million Campylobacter organisms were present in non-vaccinated birds, compared with 67,000 organisms in the vaccinated birds.
"You need at least 500 organisms to produce disease in humans," he explained. "The chlorine in the packinghouse chillers usually reduces numbers of bacteria by 1,000 to 100,000 organisms, so the chickens should be free of Campylobacter after processing."
The UA group was the first to discover the adherence protein, which is only produced when Campylobacter jejuni colonizes certain surfaces, like chicken intestine and skin. They have a patent pending in both the United States and the European Union for the gene that produces it.
"If everything goes right we could have a commercial vaccine in three to five years," Joens said. The vaccine's effect could be significant: About 8.9 billion broilers go to market annually in the U.S., with a value of $21.5 billion. Europe has similar broiler production figures. Americans consumed 86 pounds of chicken per person in 2006, the most recent numbers available.
"The vaccine would be a great intervention method for Campylobacter when the USDA and FDA (Food and Drug Administration) mandate reduced numbers of food-borne pathogens in chicken – probably in two to three years," Joens said. "Once it becomes available, the vaccine should cost about a penny per chick. More importantly, it should greatly reduce the number of cases of human Campylobacter gastroenteritis."
"Campylobacter is now the No. 1 food-borne pathogen in the United States and the world, surpassing Salmonella," said Lynn Joens, a professor in The University of Arizona department of veterinary science and microbiology and a BIO5 member. "In the United States alone, 2.4 million cases are reported annually, with costs exceeding $1 billion."
A new poultry vaccine in development at the UA offers a unique approach in controlling Campylobacter jejuni infection in chickens before it reaches the dinner table. In research trials the vaccine has significantly reduced the pathogen's ability to colonize young chickens' intestines, where the infection begins. The goal is to halt the contamination before it spreads and survives on raw chicken sold in stores.
"Yet chickens don't actually cause the disease (nor does it make them ill). It's the organism they carry that makes people sick," Joens said. "Right now you can go to any grocery store, get a raw chicken, test it in a laboratory and find Campylobacter jejuni. Twenty to 80 percent of all broiler houses become contaminated with Campylobacter."
The most common symptoms of human Campylobacter poisoning, which mimic those of Salmonella and other gastrointestinal pathogens, include fever, cramps, watery diarrhea and sometimes dysentery. More severe infections can lead to peritonitis, autoimmune disease or death.
Funded by the U.S. Department of Agriculture, Joens and UA graduate students started analyzing Campylobacter's infection process about four years ago, looking for a way to interrupt it. The laboratory team, which included graduate research associate James Theoret and assistant research professor Bibiana Law, eventually discovered that the pathogen first attached itself to the surface of the chick's intestines and then began to multiply. Attacking the "sticking" mechanism seemed to be the key.
When the UA researchers sequenced the intestinal surface protein they identified the gene responsible for producing Campylobacter’s adherence protein. Then they built a trial vaccine around it using Salmonella bacteria as a vector, with the assistance of Roy Curtiss, professor and director of the Center for Infectious Diseases and Vaccinology at Arizona State University. Curtiss’ group inserted the adherence gene into Salmonella bacteria, which is nonpathogenic for poultry. The resulting live vaccine – containing Salmonella programmed to make the Campylobacter adhering protein – was fed to young chickens to protect them.
“Once the Salmonella in the vaccine produced the Campylobacter protein, the chicks made antibodies against it in their intestines,” Joens says. "In our first study of 15 birds we got a very significant reduction – 98 percent – in Campylobacter infection, compared with a control group. We're now repeating the trial on a larger scale."
The vaccination process is simple, easy to produce and protective to the chick, according to Joens. The Salmonella lives four to five days, enough time to stimulate antibody production, and dies. Chickens need to be vaccinated early because they become infected at just two to three weeks of age.
Joens' preliminary figures show that 270 million Campylobacter organisms were present in non-vaccinated birds, compared with 67,000 organisms in the vaccinated birds.
"You need at least 500 organisms to produce disease in humans," he explained. "The chlorine in the packinghouse chillers usually reduces numbers of bacteria by 1,000 to 100,000 organisms, so the chickens should be free of Campylobacter after processing."
The UA group was the first to discover the adherence protein, which is only produced when Campylobacter jejuni colonizes certain surfaces, like chicken intestine and skin. They have a patent pending in both the United States and the European Union for the gene that produces it.
"If everything goes right we could have a commercial vaccine in three to five years," Joens said. The vaccine's effect could be significant: About 8.9 billion broilers go to market annually in the U.S., with a value of $21.5 billion. Europe has similar broiler production figures. Americans consumed 86 pounds of chicken per person in 2006, the most recent numbers available.
"The vaccine would be a great intervention method for Campylobacter when the USDA and FDA (Food and Drug Administration) mandate reduced numbers of food-borne pathogens in chicken – probably in two to three years," Joens said. "Once it becomes available, the vaccine should cost about a penny per chick. More importantly, it should greatly reduce the number of cases of human Campylobacter gastroenteritis."
UA Departments of Chemistry and Biochemistry and Molecular Biophysics to Merge
[Source: Johnny Cruz, University Communications] - Faculty in The University of Arizona's departments of chemistry and biochemistry and molecular biophysics have overwhelmingly agreed to develop a plan to merge their respective departments, instantly creating one of the nation's most highly ranked chemistry departments.
The new department of chemistry and biochemistry will rank among the top 12 such departments in the country – as measured by federal research expenditures. There are approximately 160 doctoral degree-granting chemistry and biochemistry departments in the country, and most of them share a similar model to the new UA department.
The combined departments will form a teaching and research powerhouse, along with becoming the UA's third largest teaching program – behind only mathematics and English.
"The University Transformation gives us an opportunity to better position the disciplines represented by many departments around campus by aligning the strengths of the disparate units," said Joaquin Ruiz, dean of the UA College of Science. "There is perhaps no better example of this than the merger of the departments of chemistry and biochemistry and molecular biophysics. This merger will elevate the national ranking of the new unit, but more importantly will allow for exciting new opportunities in research and teaching."
The new department will house more than 650 undergraduate majors and 210 Ph.D. students – with combined teaching in excess of 40,000 student credit hours per year.
"Both of the faculty and staff groups merging are incredibly strong in research and teaching, as well as service," said Mark Smith, head of the UA department of chemistry. "Many of the ways we compete for resources depend on being able to project a formidable strength, and this merger will accomplish just that."
Smith also believes that the merger will enhance the UA's ability to compete with the nation's most prestigious institutions for the very best students, faculty and staff. "For perhaps the first time, chemistry and biochemistry at the UA will be recognized as the research and teaching leaders they are," Smith said.
"I have been a member of the two departments (chemistry and biochemistry and molecular biophysics) for the past 8 years and have experienced firsthand the great strengths that each department brings to the proposed merger," said Vicki Wysocki, head of the UA department of biochemistry and molecular biophysics. "This is an excellent example of bringing together two different cultures to form a new department that will be stronger than the sum of the parts."
When combined, the new department will attract approximately $16 million annually in federal research support to department research groups, which interact with faculty from nine other UA colleges. Chemistry and biochemistry faculty have collaborative research programs with UA researchers in optical sciences, astronomy, planetary science, the BIO5 Institute, molecular and cellular biology, medicine and other departments.
"This merger is about excellence, and it exemplifies the spirit of what the UA is striving for through the Transformation Plan," said Meredith Hay, UA executive vice president and provost. "These two strong departments joining forces will result in an exceptional unification of talent, greater quality through more collaborative research and more opportunities for our students through the combined resources of chemistry and biochemistry."
The teaching program will include undergraduate and graduate degrees in the traditional fields of chemistry and biochemistry as well as an accelerated master's degree, a graduate degree and distance learning programs for science teachers. The department also will continue educating medical school students and will join forces to become the UA's largest Ph.D. program.
The nationally ranked faculty in chemistry and biochemistry and molecular biophysics will continue performing research over a broad range of molecular science, which includes areas such as solar energy, chemistry of the planets and interstellar space and intervention in disease.
According to Smith, the merger will promote the best training of future scientists and technologists that will help Arizona to solidify its economic base. "It is strength in science that will help the state of Arizona weather the economic storm," Smith said.
Chemistry and biochemistry and molecular biophysics have been separate departments at the UA since 1977.
The new department of chemistry and biochemistry will rank among the top 12 such departments in the country – as measured by federal research expenditures. There are approximately 160 doctoral degree-granting chemistry and biochemistry departments in the country, and most of them share a similar model to the new UA department.
The combined departments will form a teaching and research powerhouse, along with becoming the UA's third largest teaching program – behind only mathematics and English.
"The University Transformation gives us an opportunity to better position the disciplines represented by many departments around campus by aligning the strengths of the disparate units," said Joaquin Ruiz, dean of the UA College of Science. "There is perhaps no better example of this than the merger of the departments of chemistry and biochemistry and molecular biophysics. This merger will elevate the national ranking of the new unit, but more importantly will allow for exciting new opportunities in research and teaching."
The new department will house more than 650 undergraduate majors and 210 Ph.D. students – with combined teaching in excess of 40,000 student credit hours per year.
"Both of the faculty and staff groups merging are incredibly strong in research and teaching, as well as service," said Mark Smith, head of the UA department of chemistry. "Many of the ways we compete for resources depend on being able to project a formidable strength, and this merger will accomplish just that."
Smith also believes that the merger will enhance the UA's ability to compete with the nation's most prestigious institutions for the very best students, faculty and staff. "For perhaps the first time, chemistry and biochemistry at the UA will be recognized as the research and teaching leaders they are," Smith said.
"I have been a member of the two departments (chemistry and biochemistry and molecular biophysics) for the past 8 years and have experienced firsthand the great strengths that each department brings to the proposed merger," said Vicki Wysocki, head of the UA department of biochemistry and molecular biophysics. "This is an excellent example of bringing together two different cultures to form a new department that will be stronger than the sum of the parts."
When combined, the new department will attract approximately $16 million annually in federal research support to department research groups, which interact with faculty from nine other UA colleges. Chemistry and biochemistry faculty have collaborative research programs with UA researchers in optical sciences, astronomy, planetary science, the BIO5 Institute, molecular and cellular biology, medicine and other departments.
"This merger is about excellence, and it exemplifies the spirit of what the UA is striving for through the Transformation Plan," said Meredith Hay, UA executive vice president and provost. "These two strong departments joining forces will result in an exceptional unification of talent, greater quality through more collaborative research and more opportunities for our students through the combined resources of chemistry and biochemistry."
The teaching program will include undergraduate and graduate degrees in the traditional fields of chemistry and biochemistry as well as an accelerated master's degree, a graduate degree and distance learning programs for science teachers. The department also will continue educating medical school students and will join forces to become the UA's largest Ph.D. program.
The nationally ranked faculty in chemistry and biochemistry and molecular biophysics will continue performing research over a broad range of molecular science, which includes areas such as solar energy, chemistry of the planets and interstellar space and intervention in disease.
According to Smith, the merger will promote the best training of future scientists and technologists that will help Arizona to solidify its economic base. "It is strength in science that will help the state of Arizona weather the economic storm," Smith said.
Chemistry and biochemistry and molecular biophysics have been separate departments at the UA since 1977.
Thursday, October 16, 2008
Economic crisis could slow UA research into drugs, therapies
[Source: ALAN FISCHER, Tucson Citizen] - The continuing economic crisis could see the development of lifesaving drugs and therapies delayed.
Biotech researchers, already stung by funding cutbacks, fear the $700 billion bailout will further crimp their efforts to bring new drugs to market.
While it is too early to gauge exactly what the most recent financial upheavals will mean, researchers say they are already hurting.
"The bulk of research dollars at the University of Arizona come from the federal government," said Vicki Chandler, director of UA's BIO5 Institute. "I think we're in for a slowing of research."
Federal budget problems, fueled by the bailout, hurricane relief and the war in Iraq, mean less money for bioscience efforts, Chandler said.
The timing is poor.
"We've collected massive amounts of data were poised to really take advantage of," she said. "To do that, it takes money, people and facilities."
Local researchers are struggling, she said.
Three to four years ago, 20 percent to 25 percent of biotech grant requests made to the National Institutes of Health were funded. That has dropped to a funding success rate between 8 and 10 percent, Chandler said.
The National Science Foundation, another leading federal provider of science research funding, has seen a similar decline, she said.
"That's already hit UA in a big way," said Elaine Jacobson, UA professor of pharmacology and co-founder of Niadyne Inc., which develops and markets niacin-based products and therapeutics.
Some researchers have not received funding approval and have reduced their staffs and scientific efforts, she said.
The $700 billion bailout, which some analysts believe will cost closer to $2 trillion, will make things worse for researchers working to bring drugs to market.
"You just can't create grant money out of thin air, and there is a cash shortage," Jacobson said. "That's really going to hurt."
Niadyne next week will begin seeking private funding to move new therapeutics toward federal approval for use by humans.
A year ago, it would have been much easier to secure funding, Jacobson said. But with the Dow Jones industrial average dropping from the 12,000s to the 9,000s since then, all bets are off.
Venture funds will do fewer investments and reserve more cash per investment for capital-intensive biotech projects, said Shaun A. Kirkpatrick, president and CEO of Research Corporation Technologies, a Tucson-based venture capital operation.
He sees a decrease in funding available for life sciences projects, and believes small funds may leave the biotech arena because of the large amount of money needed.
On the bright side, investors hammered by the stock market may see biotech firms as good opportunities and invest, Chandler said.
And foreign investors may be drawn to biotech because of the weakness of the dollar, she said.
Drug development takes many years, and a pipeline of near-ready new products exists for the short term, she said.
But if the economic problems continue for a long time, that pipeline could be reduced to a trickle.
Biotech researchers, already stung by funding cutbacks, fear the $700 billion bailout will further crimp their efforts to bring new drugs to market.
While it is too early to gauge exactly what the most recent financial upheavals will mean, researchers say they are already hurting.
"The bulk of research dollars at the University of Arizona come from the federal government," said Vicki Chandler, director of UA's BIO5 Institute. "I think we're in for a slowing of research."
Federal budget problems, fueled by the bailout, hurricane relief and the war in Iraq, mean less money for bioscience efforts, Chandler said.
The timing is poor.
"We've collected massive amounts of data were poised to really take advantage of," she said. "To do that, it takes money, people and facilities."
Local researchers are struggling, she said.
Three to four years ago, 20 percent to 25 percent of biotech grant requests made to the National Institutes of Health were funded. That has dropped to a funding success rate between 8 and 10 percent, Chandler said.
The National Science Foundation, another leading federal provider of science research funding, has seen a similar decline, she said.
"That's already hit UA in a big way," said Elaine Jacobson, UA professor of pharmacology and co-founder of Niadyne Inc., which develops and markets niacin-based products and therapeutics.
Some researchers have not received funding approval and have reduced their staffs and scientific efforts, she said.
The $700 billion bailout, which some analysts believe will cost closer to $2 trillion, will make things worse for researchers working to bring drugs to market.
"You just can't create grant money out of thin air, and there is a cash shortage," Jacobson said. "That's really going to hurt."
Niadyne next week will begin seeking private funding to move new therapeutics toward federal approval for use by humans.
A year ago, it would have been much easier to secure funding, Jacobson said. But with the Dow Jones industrial average dropping from the 12,000s to the 9,000s since then, all bets are off.
Venture funds will do fewer investments and reserve more cash per investment for capital-intensive biotech projects, said Shaun A. Kirkpatrick, president and CEO of Research Corporation Technologies, a Tucson-based venture capital operation.
He sees a decrease in funding available for life sciences projects, and believes small funds may leave the biotech arena because of the large amount of money needed.
On the bright side, investors hammered by the stock market may see biotech firms as good opportunities and invest, Chandler said.
And foreign investors may be drawn to biotech because of the weakness of the dollar, she said.
Drug development takes many years, and a pipeline of near-ready new products exists for the short term, she said.
But if the economic problems continue for a long time, that pipeline could be reduced to a trickle.
From Jellyfish to Plants to Everything Alive: How a Magic Marker Altered Bioscience
[Source; Deb Daun, BIO5] - In a fortunate stroke of collaboration, a University of Arizona scientist has helped transform the Nobel-prize winning idea of marking cells with the bright green glow of a jellyfish into a basic tool of modern bioscience.
Plant Sciences Professor and BIO5 member David Galbraith, PhD, said today that he felt a personal attachment to the Nobel Prize given on Wednesday to Martin Chalfie and two others. The prize honored Chalfie’s paper in 1994 that showed how to use the jellyfish’s glow—caused by a Green Fluorescent Protein, or GFP, gene in its DNA—to mark a worm’s nerve cells.
With days of the publication of that paper, Galbraith, working in Arizona, was struck by an idea. That marker could become a much larger breakthrough for researchers trying to study cells in organs where individual cells were difficult, often impossible, to separate out and analyze.
”I read the jellyfish paper, and right away I thought, we should put that to use in plant cells,” Galbraith said.
Galbraith asked Chalfie to help him put the GFP gene to immediate use. Chalfie sent him samples of the DNA that encodes the green fluorescence, and some encouragement, and 14 years later the Nobel Prize has recognized both the initial breakthrough and the expanding applications that Galbraith was among the first to envision.
The discovery altered the way bioscience is conducted, Galbraith said, because GFP has proven effective in marking cells that had been all but impossible to study in the live tissues of organisms from bacteria to mice to other plants and animals used as models.
That crucial step—a simple way to label living cells with a fluorescent marker—now lets researchers in medicine, agriculture and basic cell biology examine the function of cells in any living organism. Since 1980, Galbraith says, he had been looking for a technique to label plant cells according to their function, where marking was more difficult than in animal cells.
”We engineered the Green Fluorescent Protein into plants so that it was produced only in specific cells,” Galbraith says. ”We have been working with that technique ever since that time, to make it possible to do cell sorting to isolate these different cells. Using our methods, we now can describe all of the genes that are active within any cell type within virtually any organism. Without the discovery of GFP, none of this would have been possible.”
Along with Chalfie, a biological sciences professor at Columbia University, the other co-winners of the 2008 Nobel Prize were Osamu Shimomura, of the Marine Biological Laboratory in Woods Hole, Mass., and Boston University Medical School, and Roger Y. Tsien, 56, a professor of pharmacology at the University of California, San Diego.
Plant Sciences Professor and BIO5 member David Galbraith, PhD, said today that he felt a personal attachment to the Nobel Prize given on Wednesday to Martin Chalfie and two others. The prize honored Chalfie’s paper in 1994 that showed how to use the jellyfish’s glow—caused by a Green Fluorescent Protein, or GFP, gene in its DNA—to mark a worm’s nerve cells.
With days of the publication of that paper, Galbraith, working in Arizona, was struck by an idea. That marker could become a much larger breakthrough for researchers trying to study cells in organs where individual cells were difficult, often impossible, to separate out and analyze.
”I read the jellyfish paper, and right away I thought, we should put that to use in plant cells,” Galbraith said.
Galbraith asked Chalfie to help him put the GFP gene to immediate use. Chalfie sent him samples of the DNA that encodes the green fluorescence, and some encouragement, and 14 years later the Nobel Prize has recognized both the initial breakthrough and the expanding applications that Galbraith was among the first to envision.
The discovery altered the way bioscience is conducted, Galbraith said, because GFP has proven effective in marking cells that had been all but impossible to study in the live tissues of organisms from bacteria to mice to other plants and animals used as models.
That crucial step—a simple way to label living cells with a fluorescent marker—now lets researchers in medicine, agriculture and basic cell biology examine the function of cells in any living organism. Since 1980, Galbraith says, he had been looking for a technique to label plant cells according to their function, where marking was more difficult than in animal cells.
”We engineered the Green Fluorescent Protein into plants so that it was produced only in specific cells,” Galbraith says. ”We have been working with that technique ever since that time, to make it possible to do cell sorting to isolate these different cells. Using our methods, we now can describe all of the genes that are active within any cell type within virtually any organism. Without the discovery of GFP, none of this would have been possible.”
Along with Chalfie, a biological sciences professor at Columbia University, the other co-winners of the 2008 Nobel Prize were Osamu Shimomura, of the Marine Biological Laboratory in Woods Hole, Mass., and Boston University Medical School, and Roger Y. Tsien, 56, a professor of pharmacology at the University of California, San Diego.
Researchers working on cancer detection blood test
[Source: ALAN FISCHER, Tucson Citizen] - Researchers are working on a simple blood test to detect cancer a year before symptoms develop.
"Stopping cancer early is the best solution," Dr. Samir M. Hanash told about 270 people attending the Biosciences Leadership Symposium: Translational Medicine at the University of Arizona Monday. The event continues Tuesday.
"We're on a fast-track development of a blood-based cancer biomarker using proteomics," said Hanash, molecular diagnostics program head at the Fred Hutchinson Cancer Research Center in Seattle. "We are searching through thousands of proteins to see which one is a good marker for this or that type of cancer."
By using proteomics, the study of the structures and functions of proteins, cancers such as breast, lung, pancreatic and others can be detected a year before symptoms develop, Hanash said.
He is using specimens collected at early stages of tumor development - before the onset of symptoms - from a variety of institutions, clinical trials and studies to have a broad base of samples, he said.
"This could have a great impact on treating cancer, before it metastasizes," said Laurence Hurley, associate director of the UA BIO5 Institute. "The earlier you can treat the cancer the better."
Bioscience is also leading to new technologies in rapid pathogen detection and identification, said Linda S. Powers, the Thomas R. Brown Professor of Bioengineering at UA.
She uses intrinsic fluorescence optical signatures to find microbial contaminants in water, air, food, mail and other places. The microbes give off light when excited by light having higher energy.
The detection technology is real time and uses no sample contact or added chemical reagents, she said.
"We look for the toxin itself," she said. "We're capable of pulling it out of very large volumes."
A BioBadge, which can be worn around the neck like an identification card, "breathes" air into a chip that can be tested for bacteria, toxins and viruses, she said.
Mobile sensor technology provides quick and inexpensive tests for water supplies that can keep drinking water safe from contamination, she said.
One application was testing water wells to see if they were safe following Hurricane Katrina, she said
"Stopping cancer early is the best solution," Dr. Samir M. Hanash told about 270 people attending the Biosciences Leadership Symposium: Translational Medicine at the University of Arizona Monday. The event continues Tuesday.
"We're on a fast-track development of a blood-based cancer biomarker using proteomics," said Hanash, molecular diagnostics program head at the Fred Hutchinson Cancer Research Center in Seattle. "We are searching through thousands of proteins to see which one is a good marker for this or that type of cancer."
By using proteomics, the study of the structures and functions of proteins, cancers such as breast, lung, pancreatic and others can be detected a year before symptoms develop, Hanash said.
He is using specimens collected at early stages of tumor development - before the onset of symptoms - from a variety of institutions, clinical trials and studies to have a broad base of samples, he said.
"This could have a great impact on treating cancer, before it metastasizes," said Laurence Hurley, associate director of the UA BIO5 Institute. "The earlier you can treat the cancer the better."
Bioscience is also leading to new technologies in rapid pathogen detection and identification, said Linda S. Powers, the Thomas R. Brown Professor of Bioengineering at UA.
She uses intrinsic fluorescence optical signatures to find microbial contaminants in water, air, food, mail and other places. The microbes give off light when excited by light having higher energy.
The detection technology is real time and uses no sample contact or added chemical reagents, she said.
"We look for the toxin itself," she said. "We're capable of pulling it out of very large volumes."
A BioBadge, which can be worn around the neck like an identification card, "breathes" air into a chip that can be tested for bacteria, toxins and viruses, she said.
Mobile sensor technology provides quick and inexpensive tests for water supplies that can keep drinking water safe from contamination, she said.
One application was testing water wells to see if they were safe following Hurricane Katrina, she said
Monday, September 29, 2008
Cepheid Receives FDA Clearance for First Rapid On-Demand Molecular Diagnostic Test for MRSA and S. aureus
[Source: PRNewswire-FirstCall via COMTEX] - Cepheid today announced it has received clearance from the U.S. Food & Drug Administration (FDA) to market its Xpert(TM) MRSA/SA Skin and Soft Tissue Infection (SSTI) test, which runs on the GeneXpert(R) System, for the rapid detection of Methicillin-resistant Staphylococcus aureus (MRSA) and Staphylococcus aureus (SA, typically Methicillin-sensitive) in skin and soft tissue infections.
In less than one hour, Cepheid's Xpert MRSA/SA SSTI test processes specimens from suspected skin and soft tissue infection swabs to determine if a patient is infected with MRSA or SA, giving physicians and surgeons a powerful new tool to aid in selecting the most effective antibiotic therapy to improve patient management.
"The ability to detect MRSA or SA in less than one hour, versus two to three days with current culture methods, will enable clinicians to make real- time decisions as to the best course of treatment or management. The ability to accurately identify MRSA and SA on a more timely basis is important in managing both hospital-acquired and community-acquired infections. According to data from the Centers for Disease Control (CDC), there are approximately 12 million patient visits in the U.S. each year for skin infections," said John Bishop, Cepheid's Chief Executive Officer. "We are very pleased to announce the first molecular SSTI diagnostic test for MRSA and SA, building on our established position as the leader in the HAI (Healthcare Acquired Infections) testing market. With our expanding test menu, we expect Cepheid's GeneXpert System to continue to be the molecular platform of choice for the management of HAIs."
MRSA is a bacterium that has become resistant to multiple antibiotics including penicillin and cephalosporins. Current culture-based lab testing methods require 48-72 hours to determine if a skin or soft tissue infection is caused by MRSA or SA. As a result, physicians and surgeons often prescribe broad-spectrum antimicrobial therapies while awaiting culture results.
"Millions of patients visit emergency departments and urgent care clinics each year for treatment of 'staph' infections in skin and underlying tissue, many caused by MRSA. Because culture-based antibiotic test results are not available to physicians for several days, physicians have been forced to make decisions about wound drainage and antibiotic therapy without having the benefit of supportive laboratory data," said Dr. Donna Wolk, Division Chief of Clinical Microbiology, College of Medicine; and Research Associate, BIO5 Institute at The University of Arizona. "Our clinical trial data show that this new laboratory test makes it possible to accurately detect a staph infection before a patient is released, and it provides information to support treatment choices. In addition, the GeneXpert System supports informed antibiotic choices whereby prescribing antibiotics of last resort can be reserved for those patients truly infected with MRSA, therefore, reducing the chances of microbes further developing antibiotic resistance."
Community Acquired Infections in the ER & Healthcare Acquired Surgical Site Infections
MRSA and SA infections are national medical concerns that place millions of lives at risk and add millions of dollars to healthcare costs each year - both in outpatient, or community-acquired infections, and in-patient, or surgical site infections acquired within the healthcare environment.
The Centers for Disease Control recently reported that an estimated 12 million people in the United States seek outpatient medical attention each year for skin and soft tissue infections, of which MRSA plays a major role. Significant incremental healthcare costs associated with these infections are a result of additional follow-up visits, changes in antimicrobial therapy, and transmission of infections to family members and the community.
The Institute of Healthcare Improvement reports that about 800,000 surgeries are complicated by infections annually. Cost to the health care system to treat these infections is estimated at $9.5 billion, largely due to extended hospital stays following surgery. According to a study published in Clinical Infectious Diseases, increased length of stay is 18 days following a MRSA infection and 9 days for a SA infection.
Xpert MRSA/SA SSTI delivers actionable test results to assist physicians and surgeons in selecting accurate treatment plans for improved patient outcomes, better antimicrobial stewardship, and a reduction in both community- acquired and healthcare-acquired infections.
In less than one hour, Cepheid's Xpert MRSA/SA SSTI test processes specimens from suspected skin and soft tissue infection swabs to determine if a patient is infected with MRSA or SA, giving physicians and surgeons a powerful new tool to aid in selecting the most effective antibiotic therapy to improve patient management.
"The ability to detect MRSA or SA in less than one hour, versus two to three days with current culture methods, will enable clinicians to make real- time decisions as to the best course of treatment or management. The ability to accurately identify MRSA and SA on a more timely basis is important in managing both hospital-acquired and community-acquired infections. According to data from the Centers for Disease Control (CDC), there are approximately 12 million patient visits in the U.S. each year for skin infections," said John Bishop, Cepheid's Chief Executive Officer. "We are very pleased to announce the first molecular SSTI diagnostic test for MRSA and SA, building on our established position as the leader in the HAI (Healthcare Acquired Infections) testing market. With our expanding test menu, we expect Cepheid's GeneXpert System to continue to be the molecular platform of choice for the management of HAIs."
MRSA is a bacterium that has become resistant to multiple antibiotics including penicillin and cephalosporins. Current culture-based lab testing methods require 48-72 hours to determine if a skin or soft tissue infection is caused by MRSA or SA. As a result, physicians and surgeons often prescribe broad-spectrum antimicrobial therapies while awaiting culture results.
"Millions of patients visit emergency departments and urgent care clinics each year for treatment of 'staph' infections in skin and underlying tissue, many caused by MRSA. Because culture-based antibiotic test results are not available to physicians for several days, physicians have been forced to make decisions about wound drainage and antibiotic therapy without having the benefit of supportive laboratory data," said Dr. Donna Wolk, Division Chief of Clinical Microbiology, College of Medicine; and Research Associate, BIO5 Institute at The University of Arizona. "Our clinical trial data show that this new laboratory test makes it possible to accurately detect a staph infection before a patient is released, and it provides information to support treatment choices. In addition, the GeneXpert System supports informed antibiotic choices whereby prescribing antibiotics of last resort can be reserved for those patients truly infected with MRSA, therefore, reducing the chances of microbes further developing antibiotic resistance."
Community Acquired Infections in the ER & Healthcare Acquired Surgical Site Infections
MRSA and SA infections are national medical concerns that place millions of lives at risk and add millions of dollars to healthcare costs each year - both in outpatient, or community-acquired infections, and in-patient, or surgical site infections acquired within the healthcare environment.
The Centers for Disease Control recently reported that an estimated 12 million people in the United States seek outpatient medical attention each year for skin and soft tissue infections, of which MRSA plays a major role. Significant incremental healthcare costs associated with these infections are a result of additional follow-up visits, changes in antimicrobial therapy, and transmission of infections to family members and the community.
The Institute of Healthcare Improvement reports that about 800,000 surgeries are complicated by infections annually. Cost to the health care system to treat these infections is estimated at $9.5 billion, largely due to extended hospital stays following surgery. According to a study published in Clinical Infectious Diseases, increased length of stay is 18 days following a MRSA infection and 9 days for a SA infection.
Xpert MRSA/SA SSTI delivers actionable test results to assist physicians and surgeons in selecting accurate treatment plans for improved patient outcomes, better antimicrobial stewardship, and a reduction in both community- acquired and healthcare-acquired infections.
BIO5 to Host 7th Arizona Biosciences Leadership Symposium
[Source University of Arizona Communications] - Scott Patterson, executive director for medical services at Amgen, is the keynote speaker at the 7th Arizona Biosciences Leadership Symposium, taking place at The University of Arizona's Student Union Memorial Center.
The event is hosted by the UA's BIO5 Institute on behalf of the Flinn Foundation and the Arizona Biomedical Research Commission. The program begins at Oct. 6 at 9 a.m. and concludes on Oct. 7 at 1 p.m.
This year's event features a new format with speakers from around the country. Session topics and leaders are:
Case Histories in Translational Medicine: Ronald Marler, Mayo Clinic Phoenix
Personalized Medicine: Dr. Daniel D. Von Hoff, Translational Genomics Research Institute
Arizona Funding Sources for Translational Research: Laurence H. Hurley, BIO5 Institute and UA College of Pharmacy
New Technologies: Jennifer Barton, UA's Arizona Research Laboratories
A poster session highlighting Arizona Roadmap-themed research is planned.
To register and to submit posters, go to visit www.bio5.org.
The event is hosted by the UA's BIO5 Institute on behalf of the Flinn Foundation and the Arizona Biomedical Research Commission. The program begins at Oct. 6 at 9 a.m. and concludes on Oct. 7 at 1 p.m.
This year's event features a new format with speakers from around the country. Session topics and leaders are:
Case Histories in Translational Medicine: Ronald Marler, Mayo Clinic Phoenix
Personalized Medicine: Dr. Daniel D. Von Hoff, Translational Genomics Research Institute
Arizona Funding Sources for Translational Research: Laurence H. Hurley, BIO5 Institute and UA College of Pharmacy
New Technologies: Jennifer Barton, UA's Arizona Research Laboratories
A poster session highlighting Arizona Roadmap-themed research is planned.
To register and to submit posters, go to visit www.bio5.org.
Thursday, September 25, 2008
Understanding Underground Stems Focus of $4 million NSF Grant
[Source: Deborah Daun, BIO5] - Anyone who's tried to remove Bermuda grass from their yard knows about plant rhizomes. These stubborn underground stems give weeds—and other plants—many advantages, not the least of which is that even after you remove the above-ground plant, only a small portion of the underground stem needs to remain for the plant to survive and try to take over your yard once more.
Understanding the genetics and development of rhizomes is the focus of a four-year, $4 million National Science Foundation (NSF) grant awarded to a UA-led team of scientists. "We want to find the genes responsible for producing rhizomes," says BIO5 member David Gang, PhD, associate professor of Plant Sciences, College of Agriculture and Life Sciences. "The genetic triggers, the signals, the regulators, and also the genes that actually build the plant."
Gang is principal investigator for the grant; his co-PIs are BIO5 member Carol Soderlund, UA research associate professor of Plant Sciences, and Jay Thelen, assistant professor of Biochemistry at the University of Missouri. The plant biologists plan to study the rhizomes of a wide range of medicinal and weedy plants, from primitive ferns and rushes to complex flowering plants.
The fact that both simple and complex plants have rhizomes is part of what makes them so interesting. The original plant stem, the one used by all early land plants, was the rhizome. Early on in the evolution of plants, rhizomes remained common, but then—perhaps because there were evolutionary advantages to growing upwards instead of along the ground—plants abandoned the underground stems for a time. Yet rhizomes re-emerged in later plants, perhaps because of the benefits rhizomes confer—things like being able to resist fire or search far afield for water—became valuable once more.
Bermuda grass isn't the only rhizome-bearing weed to frustrate farmers and homeowners. "Most of the world's 10 worst weeds use rhizomes," Gang says. "They've adapted them as a mechanism to invade new territory and crowd out other plants." Gang says better understanding rhizomes may one day help us better control weedy grasses, which cause huge economic losses worldwide every year, as well as waterway weeds like giant salvinia, which is contaminating or destroying freshwater sources worldwide. "If we can understand the genetics of what makes a weedy rhizome so invasive, then we might be able to come up with strategies to control them better--strategies that affect just the rhizomes, so that we don't have to rely so heavily on broad-spectrum herbicides."
The practical applications of understanding rhizomes extend well beyond weed control, however. "If we can understand how a rhizome grows and how it is different from an upright stem, then we can better understand how upright stems grow and develop as well," Gang says. That understanding could ultimately help improve the yields of everything from trees that supply paper pulp to biofuel sources and food crops. "So maybe you can use less land to produce more food," Gang says. "In the next 50 years especially, doing so is going to be an important issue around the world. There's a huge potential impact here."
Tuesday, September 23, 2008
Tucson-created cancer drug advances: South Korea in licensing accord for still-in-trials Amplimexon
[Source: Arizona Daily Star] - A local drug-development company with links to the University of Arizona got a boost from a drug-licensing deal with a South Korean company -- even before the cancer drug is approved by U.S. regulators.
Tucson-based AmpliMed Corp. said Wednesday that it has entered into a license agreement with a leading South Korean-based pharmaceutical company for exclusive rights to its developmental cancer drug Amplimexon in the Asian nation.
Under terms of the agreement with Seoul-based Handok Pharmaceuticals, Handok will receive marketing and distribution rights for all cancer uses for Amplimexon in South Korea.
The company will pay AmpliMed an upfront fee, plus additional payments based on certain development and regulatory milestones. Additional financial terms of the deal were not disclosed.
AmpliMed CEO Robert Dorr said deals like these don't usually happened until results from randomized trials are returned, but Handok came looking to make an investment in the drug.
"Handok was willing to make a substantial investment before the trials were over," Dorr said. "It's a real vote of confidence in the technology."
A local biotech industry official said the deal is a big step for AmpliMed's technology.
"The drug's going to move forward through this relationship," said Nina Ossanna, director of business development for the UA's Bio5 Institute. Bio5 is the UA's cross-campus genetics institute.
Ossanna, who also chairs the Bioindustry Organization of Southern Arizona, said such early licensing deals provide "third-party validation" of a drug's potential.
Dorr said AmpliMed -- founded in 1989 by UA cancer researchers -- will retain the drug's rights in the United States but may look to sell similar rights to its drug in the European Union and Japan.
So far, the company said it has raised $29.3 million since 2004 to help fund its research.
The drug has undergone rigorous trials and is making progress toward approval by the U.S. Food and Drug Administration, said Dorr, who is a UA professor of pharmacology and toxicology and director of pharmacology for the Arizona Cancer Center.
Amplimexon, a spinoff from UA research, has shown results in fighting melanoma, breast, lung, prostate and pancreatic cancer, the company said.
Representatives from Handok noted the drug's potential in the fight against cancer.
"Amplimexon is poised to be a leading product in Handok's cancer pipeline, and we anticipate this promising agent will improve the quality of life for cancer patients," Handok CEO Young-jin Kim said in a press release.
Currently, Amplimexon is in Phase II clinical trials combined with gemcitabine to test for use against pancreatic cancer.
Dorr said that Phase II trials should be completed by the second quarter of 2010, with Phase III trials to wrap up by 2013.
Phase III trials are typically the last step before a drug is submitted for final approval.
The company also plans to start a Phase II trial of Amplimexon in combination with the chemotherapy drug taxotere in patients with non-small-cell lung cancer later this year.
More tests for other cancers, as well as potential further deals with Handok are in the works.
AmpliMed plans to hold trials of Amplimexon in South Korea to combat gastric cancer, Dorr said.
"I foresee further interaction with Handok in the future," he said.
Tucson-based AmpliMed Corp. said Wednesday that it has entered into a license agreement with a leading South Korean-based pharmaceutical company for exclusive rights to its developmental cancer drug Amplimexon in the Asian nation.
Under terms of the agreement with Seoul-based Handok Pharmaceuticals, Handok will receive marketing and distribution rights for all cancer uses for Amplimexon in South Korea.
The company will pay AmpliMed an upfront fee, plus additional payments based on certain development and regulatory milestones. Additional financial terms of the deal were not disclosed.
AmpliMed CEO Robert Dorr said deals like these don't usually happened until results from randomized trials are returned, but Handok came looking to make an investment in the drug.
"Handok was willing to make a substantial investment before the trials were over," Dorr said. "It's a real vote of confidence in the technology."
A local biotech industry official said the deal is a big step for AmpliMed's technology.
"The drug's going to move forward through this relationship," said Nina Ossanna, director of business development for the UA's Bio5 Institute. Bio5 is the UA's cross-campus genetics institute.
Ossanna, who also chairs the Bioindustry Organization of Southern Arizona, said such early licensing deals provide "third-party validation" of a drug's potential.
Dorr said AmpliMed -- founded in 1989 by UA cancer researchers -- will retain the drug's rights in the United States but may look to sell similar rights to its drug in the European Union and Japan.
So far, the company said it has raised $29.3 million since 2004 to help fund its research.
The drug has undergone rigorous trials and is making progress toward approval by the U.S. Food and Drug Administration, said Dorr, who is a UA professor of pharmacology and toxicology and director of pharmacology for the Arizona Cancer Center.
Amplimexon, a spinoff from UA research, has shown results in fighting melanoma, breast, lung, prostate and pancreatic cancer, the company said.
Representatives from Handok noted the drug's potential in the fight against cancer.
"Amplimexon is poised to be a leading product in Handok's cancer pipeline, and we anticipate this promising agent will improve the quality of life for cancer patients," Handok CEO Young-jin Kim said in a press release.
Currently, Amplimexon is in Phase II clinical trials combined with gemcitabine to test for use against pancreatic cancer.
Dorr said that Phase II trials should be completed by the second quarter of 2010, with Phase III trials to wrap up by 2013.
Phase III trials are typically the last step before a drug is submitted for final approval.
The company also plans to start a Phase II trial of Amplimexon in combination with the chemotherapy drug taxotere in patients with non-small-cell lung cancer later this year.
More tests for other cancers, as well as potential further deals with Handok are in the works.
AmpliMed plans to hold trials of Amplimexon in South Korea to combat gastric cancer, Dorr said.
"I foresee further interaction with Handok in the future," he said.
Thursday, September 18, 2008
Small RNA Molecules Provide Big Tools for Understanding Plant Development
[Source: Deborah Daun, BIO5 Insitute, UA] - University of Arizona researchers are among those who have discovered a source of previously scarce small RNA molecules. Their finding, which was recently published in the Proceedings of the National Academy of Sciences, provides a valuable new tool for better understanding how plants grow and develop.
All living things contain small RNA molecules, explains Vicki Chandler, PhD, UA Regents' Professor and director of the BIO5 Institute. Some small RNA molecules help the genes in cells to carry out their instructions; others silence genes and prevent them from acting. In plants, two types of small RNA molecules have been studied, one of them 21 nucleotides long, the other 24 nucleotides long. (Nucleotides are the atomic "building blocks" of all genetic material.)
Working with a mutant strain of maize, Chandler and her colleagues have honed in on a distinct class of small RNA molecule, one that's 22 nucleotides long. The 21- and 22-nucleotide RNAs are scarce in most plants—including wild maize—but in the mutant strain, the researchers discovered that they were common because the 24-nucleotide RNAs are dramatically reduced.
Having a reliable source of the 21- and 22-nucleotide RNA means plant biologists can now study these molecules in depth, and work out the pathways they follow to regulate plant genes. "We don't yet know exactly what it [the 22-nucleotide RNA] is doing in the cells, so there'll be a whole new line of experiments as we try to figure it out," Chandler says. She adds that there may well be other understudied small RNA molecules waiting to be looked at as well. "I think we've only seen the tip of the iceberg with these small regulatory RNAs. There's still a lot to learn, and that's exciting."
The information that results from studying "new" small RNAs will become doubly valuable as other plant biologists (including BIO5 member Rod Wing) finish refining the genetic sequence of maize. "The two together [the small RNA molecules and the sequenced maize genome] will provide a lot of new tools for better understanding plant growth and function," Chandler says.
That work could ultimately have implications for everything from environmental and ecological issues to agriculture and medicine. "Gene regulation is fundamental to so many issues," Chandler says. "This [the 22-nucleotide RNA molecule] is one example of a pathway that—once it's worked out—could be targeted to address them."
Tuesday, September 9, 2008
Laurence Hurley has been awarded one of 38 NIH grants for research projects that could have an extraordinary impact on many areas of science.
[Source: University of Arizona Communications] - Laurence Hurley, professor of pharmacy at The University of Arizona and associate director of the BIO5 Institute, has been awarded one of 38 National Institutes of Health grants for exceptionally innovative research projects that could have an extraordinary impact on many areas of science.
The grants totaling $42.2 million are the first made in a new program called EUREKA (Exceptional, Unconventional Research Enabling Knowledge Acceleration), which helps investigators test novel and often unconventional hypotheses or tackle major technical challenges.
Hurley is designing a molecular system that permits the design of simple drugs that turn off cancer genes.
Each EUREKA researcher will receive approximately $200,000 per year for up to four years, subject to the availability of appropriations.
"EUREKA projects promise remarkable outcomes that could revolutionize science," said NIH Director Dr. Elias A. Zerhouni. "The program reflects NIH's commitment to supporting potentially transformative research, even if it carries a greater than usual degree of scientific risk."
"EUREKA is an experiment in how to attract, identify and support particularly creative approaches that, if successful, could move science forward dramatically," said Jeremy M. Berg, director of the National Institute of General Medical Sciences, or NIGMS, which led the development of the EUREKA program. "One way EUREKA does this is through a specialized application and review process focusing on the significance and innovation of the proposal."
In addition to NIGMS, the other NIH divisions funding EUREKA projects are the National Institute of Neurological Disorders and Stroke, the National Institute of Mental Health and the National Institute on Drug Abuse.
The grants totaling $42.2 million are the first made in a new program called EUREKA (Exceptional, Unconventional Research Enabling Knowledge Acceleration), which helps investigators test novel and often unconventional hypotheses or tackle major technical challenges.
Hurley is designing a molecular system that permits the design of simple drugs that turn off cancer genes.
Each EUREKA researcher will receive approximately $200,000 per year for up to four years, subject to the availability of appropriations.
"EUREKA projects promise remarkable outcomes that could revolutionize science," said NIH Director Dr. Elias A. Zerhouni. "The program reflects NIH's commitment to supporting potentially transformative research, even if it carries a greater than usual degree of scientific risk."
"EUREKA is an experiment in how to attract, identify and support particularly creative approaches that, if successful, could move science forward dramatically," said Jeremy M. Berg, director of the National Institute of General Medical Sciences, or NIGMS, which led the development of the EUREKA program. "One way EUREKA does this is through a specialized application and review process focusing on the significance and innovation of the proposal."
In addition to NIGMS, the other NIH divisions funding EUREKA projects are the National Institute of Neurological Disorders and Stroke, the National Institute of Mental Health and the National Institute on Drug Abuse.
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