WHAT: Demonstration of massive hurricane simulator and other unique equipment intended to mimic the effects of hurricanes as part of UF research aimed at toughening homes against the big storms. Researchers will use the 2,800-horsepower machine to blast a large mockup of a house with wind gusts and simulated wind-driven rain at speeds up to 120 mph. They will also conduct tests of flying debris using machines that launch shingles, roof tiles and other projectiles at high speeds. Other equipment to be demonstrated includes portable towers used for gathering data during land-falling hurricanes and a device that simulates hurricane conditions to test windows.
WHEN: May 19, 10 a.m. to 2 p.m.
WHERE: University of Florida Eastside Campus, 2160 N.E. Waldo Road, Gainesville. http://www.mapquest.com/maps/2160+NE+Waldo+Road+Gainesville+FL/
RSVP by May 14 to: Aaron Hoover, ahoover@ufl.edu, 352-392-0186. NOTE: Lunch will be available to all members of the news media who RSVP.
PHOTO OF EQUIPMENT AVAILABLE
BACKGROUND: A major goal of UF research is to determine how wind-driven rain finds its way past doors, windows, soffits and other openings in homes even when they remain intact . So-called “water intrusion” was a big problem after the 2004 and 2005 storms in Florida, when many homes built to the latest Florida building code remained standing yet sustained massive water damage to interiors. UF researchers are working closely with industry representatives to evaluate not only building components such as windows and doors, but also installation procedures, with the goal of ensuring that products perform properly in real homes. Another major goal of UF research is to learn more about the behavior of low-altitude hurricane winds — the kind that affect homes — in real storms. UF storm-chasing crews tow the hurricane towers to projected hurricane-landfall sites as part of the Florida Coastal Monitoring Program.
]]>The recognition goes to faculty members who have a distinguished current record of research and a strong research agenda likely to lead to continuing distinction in their fields.
The UFRF professors were recommended by their college deans based on nominations from department chairs, a personal statement and an evaluation of recent research accomplishments as evidenced by publications in scholarly journals, external funding, honors and awards, development of intellectual property and other measures..
“These nominating documents invariably use phrases like ‘cutting edge,’ ‘innovative,’ and ‘most productive’ to describe these researchers’ work,” said Win Phillips, UF’s vice president for research. “They — and hundreds of others like them — are the reason we have been able to move into the top tier of research universities nationally.”
The three-year award includes a $5,000 annual salary supplement and a one-time $3,000 grant.
The professorships are funded from the university’s share of royalty and licensing income on UF-generated products. Founded in 1986, the not-for-profit foundation provides a means by which research can be conducted flexibly and efficiently and by which discoveries, inventions, processes and work products of UF faculty, staff and students can be transferred from the laboratory to the public. Funds generated by licensing such discoveries are used to enhance research at the university.
The professors are:
It was announced today that Irma and Norman Braman, of Miami, Fla., have given $1 million toward establishing an endowed chair at the center. The gift, along with funds raised from other interested donors, will allow UF to hire a distinguished senior professor of Holocaust studies.
“This significant show of private support for a faculty position is exactly what the university needs to continue to excel, particularly in these times of state budget cuts,” said UF President Bernie Machen. “We are grateful to the Bramans for their generosity and foresight.”
“The senior-level position will galvanize our curriculum,” said Jack Kugelmass, Sam Melton Professor and director of the Center for Jewish Studies at UF.
“Recruiting a distinguished scholar in this field of study will amplify the quality of our course offerings in general and will encourage more graduate students to pursue masters and doctoral research in this particular area,” according to Kugelmass.
Today the field has become a core area of Jewish studies and helps to link Jewish studies with various European area studies programs, as well as to departments of comparative literature, film and philosophy. Indeed, the Holocaust as a subject of study has become integral to much of the humanities.
The Center for Jewish Studies at UF was established in 1973 by the College of Liberal Arts and Sciences. It offers both a major and minor, as well as study abroad programs. Overall, UF has at least five faculty members in different disciplines teaching in the area of Holocaust studies.
“We feel a very strong commitment to supporting Holocaust studies on the university level,” said Norman Braman. “The murder of 6,000,000 Jews for no crime other than being Jewish must be studied so that the world will never have to endure such inhumanity again. Our high opinion of the Center for Jewish Studies led us to direct our resources to UF.”
“We are also appreciative of the level of education our grandson (Alex Shack) received at UF,” continued Braman. “He came to UF four years ago as a boy and is graduating as a man.”
In recognition of their gift the faculty position will be named the Norman and Irma Braman Chair in Holocaust Studies.
Funds received for the endowed position are eligible for matching funds from the state of Florida Trust Fund for Major Gifts, which would increase the value of the endowment for the chair significantly.
A national search for the position is expected to begin next fall.
The University of Florida is currently in a seven-year capital campaign themed Florida Tomorrow. As of March 31st, $646 million had been raised toward a goal of $1.5 billion. More information can be found at www.floridatomorrow.ufl.edu.
]]>In the first-ever study of the effects of the absence of microRNAs in the mammalian eye, an international team of researchers directed by the University of Florida and the Italian National Research Council describes a gradual structural decline in retinas that lack microRNAs — a sharp contrast to the immediate devastation that occurs in limbs, lungs and other tissues that develop without microRNAs.
The discovery, reported in today’s (May 7) issue of the Journal of Neuroscience, may lead to new understanding of some blinding diseases and further penetrates the cryptic nature of microRNAs — important gene regulators that a decade ago were considered to be little more than scraps floating around the cell’s working genetic machinery.
“MicroRNAs are behaving differently in the nervous system than they are in other bodily tissues,” said Brian Harfe, an assistant professor of molecular genetics and microbiology at the University of Florida College of Medicine. “Judging by our previous studies in limb development, I was expecting to see lots of immediate cell death in the retina. I was not expecting a normal-looking retina in terms of its form. It would be something like finding a perfectly formed arm at birth that just did not work.”
Production of microRNAs is dependent on Dicer, an enzyme widely used by living things to kick-start the process of silencing unwanted genetic messages. By breeding mice that lack one or both of the forms — or alleles — of the gene that produces Dicer in the retina, scientists were able to observe retinal development when Dicer levels were half of normal or completely eliminated.
Electrical activity in retinas devoid of Dicer was abnormally low at the time of eye opening and became progressively worse at 1-, 3- and 5-month stages. Structurally, the retinas initially appeared normal, but the cells progressively became disorganized, followed by widespread degeneration.
Retinas in animals equipped with a single form of the Dicer gene never underwent the inexorable structural decline that occurs in total absence of Dicer, but they also never functioned normally, according to electroretinograms.
“We have removed Dicer from about 30 different tissues,” said Harfe, a member of the UF Genetics Institute. “In all of those cases with half the amount of Dicer, you still had a normal animal. In the retina, there were functional abnormalities. This is the first indication that the dose of Dicer is important for normal retinal health.”
Inherited forms of retinal degeneration affect about 100,000 people in the United States, according to the National Eye Institute. The problems typically occur with the destruction of photoreceptor cells called rods and cones in the back of the eye. More than 140 genes have been linked to these diseases, which only account for a fraction of the cases.
“We have many types of retinal degeneration and not enough mutations to explain them,” said Enrica Strettoi, a senior researcher at the Institute of Neurosciences of the Italian National Research Council in Pisa, Italy. “Finding that ablation of Dicer causes retinal degeneration might be helpful in discovering candidate disease genes. What we’ve done is target virtually all microRNAs in the retina by ablating Dicer, the core enzyme regulating their synthesis. The next step is to try to address each one separately, and find the role of specific microRNAs. Removal of Dicer from other areas of the central nervous system has also produced functional and structural abnormalities, confirming the fundamental role of this enzyme in neurons.”
More than 400 microRNAs have been identified in both mice and humans, and each one has the potential to regulate hundreds of target genes. They have also been linked to human diseases such as diabetes, hepatitis C, leukemia, lymphoma, Kaposi’s sarcoma and breast cancer.
“This interesting study, together with recent findings reported from three other labs in the United States, provide strong evidence that the microRNA pathway is involved in the health and sickness of many parts of the mammalian nervous system,” said Fen-Biao Gao, an investigator at the Gladstone Institute of Neurological Disease at the University of California-San Francisco, who did not participate in the research. “Additional in-depth studies in the future will likely help develop new therapeutic approaches for many neurodegenerative diseases.”
Additional scientists who participated in the research include Devid Damiani of the Institute of Neurosciences in Pisa; John Alexander, Jason O’Rourke and William Hauswirth of the University of Florida; Michael McManus of the University of California-San Francisco; and Ashutosh Jadhav and Constance Cepko of Harvard Medical School.
]]>With all the arrogance of youth, Danny was busy explaining that his father was a “dull academic,” Homan said.
Danny jokingly accused Homan, who has published 10 books on Shakespeare and the modern playwrights, of simply feeding off the creativity of others and challenged him to write something original.
As for himself, Danny was at that point inexperienced and unpublished, yet convincingly unconcerned, Homan said. He would sit amid publishers’ rejection letters and confidently tell his father that someday, someone would want to read his work.
Fast forward about two years. A son’s good-natured challenge has materialized into his father’s first book outside the scholarly realm, and Danny’s self-assured perseverance has paid off in the form of a soon-to-be-published fantasy novel debut.
“A Fish in the Moonlight,” a collection of stories from Homan’s childhood as told to pediatric cancer patients during his participation in the Shands Arts in Medicine program, is due for release from the Purdue University Press in June.
Danny’s “The Queen of Hearts,” a fantasy novel rife with allegorical undertones of current events ranging from the war in Iraq to the Pinochet regime in Chile, will be released by Prime Books in November.
Ever since that day in Central Park, the father-son pair has profited from a symbiotic creative rivalry.
“I never would have tried ‘A Fish in the Moonlight’ if it weren’t for the kid saying I was a dull academic,” Homan said. “When you’re challenged by your kid, you respond.”
But it wasn’t all competition. Homan and his son have provided valuable perspective for each other as co-editors.
“You need someone else to be a critic of your own writing,” Homan said. “We agreed from the beginning that we would be honest with each other.”
The two spent many hours reading each other’s work aloud, taking turns reading each new paragraph to stay focused.
“A Fish in the Moonlight” isn’t fiction per se — the events Homan talks about did actually happen. For example, his beer-bellied, black-sheep Uncle Eddie really did show up drunk to Uncle Arthur’s funeral and jump into the coffin with his dead brother while the family looked on in horror. But Homan isn’t about to pledge that every detail and quotation is exactly accurate. There may be some embellishment. These are stories, after all.
Homan said writing a book like this required him to fundamentally change the way he thinks and writes compared to his scholarly approach to books on the theater.
“It demands a different kind of language, a different kind of vocabulary,” he said. “When you are writing for yourself, the options are tremendous.”
Homan’s effort, however, has paid a handsome wage.
“’A Fish in the Moonlight’ gives me more pleasure than anything I’ve ever done,” he said. “As thrilling as it is to work in the theater, it’s so pleasurable now to just sit in front of my computer and create my own worlds.”
Where to go from here? Homan isn’t sure, but he has a sequel in the works and no plans to retire.
“You go in one direction your whole life, and then you change,” he said. “I have no idea where this book is going to take me.”
]]>WHAT: Machen is announcing UF’s budget cuts today and will hold a news conference to answer questions about those cuts.
WHEN: 4 p.m. today.
WHERE: President’s Conference Room, Tigert Hall, Room 226.
BACKGROUND: Machen has asked deans to create plans for reducing their budgets by 6 percent for the fiscal year that begins July 1. UF is reducing spending by $47 million in the next fiscal year because of reduced funding from the state Legislature. UF has already trimmed $22 million from the current budget.
FOR OUT-OF-TOWN MEDIA: To attend the news conference by phone, call 888-537-7715 and enter pass code 42677223#.
CONTACT: Steve Orlando, director, UF News Bureau, 352-392-0186.
]]>The findings, which appear in today’s (May 1) edition of the American Heart Association journal Hypertension, could lead to a new class of antihypertensive drugs designed to address two major problems associated with cardiovascular disease: high blood pressure and the tissue damage associated with it, known as fibrosis.
“When people have heart attacks (or suffer from hypertension) the blood vessels get more rigid,” said study author David Ostrov, an assistant professor in the UF College of Medicine’s department of pathology, immunology and laboratory medicine. “We discovered a compound that reverses the fibrosis that makes the blood vessels more rigid.”
The American Heart Association estimates that 72 million people in the United States have high blood pressure, a major risk factor for stroke, heart attack and death.
Angiotensin-converting enzyme plays a key role in the development of high blood pressure. It produces angiotensin II, a potent hormone that triggers the condition and contributes to the development of cardiovascular disease by constricting blood vessels, causing blood pressure to rise. That’s why millions of Americans with hypertension and cardiovascular disease take ACE inhibitors. But these drugs have limited capacity to repair heart function and to reverse tissue damage.
In contrast, the enzyme ACE2 not only lowers levels of angiotensin II but also converts it to a hormone that helps protect the cardiovascular system.
“Only recently has it come to be appreciated that ACE and ACE2 play a very important role in balancing the activity of the other one to maintain normal blood pressure,” Ostrov said. “They work in harmony.”
Hypothesizing that activating ACE2 could be beneficial, UF scientists set out to discover a compound that enhances the enzyme’s activity.
Researchers used one of the world’s most powerful supercomputers to process 140,000 prospective drug compounds in a matter of weeks. The computer predicted which molecules would be most likely to enhance the activity of ACE2, rotating them in thousands of different orientations to see how they would bind to certain pockets on the enzyme’s surface.
“This project had a very small likelihood of succeeding because it’s much easier to inhibit activity rather than to enhance it. By analogy, it’s easier to break something than to build it,” Ostrov said. “If you consider the structure of an enzyme’s active site it’s easy to see that if you plug up the active site it’s not going to work. But how can one make the enzyme actually work better? This seemed to be a very significant challenge we were probably not likely to overcome. We tried anyway.”
And it worked.
“That in itself is a significant accomplishment because no one has ever specifically identified a compound that enhances the activity of an enzyme using a rational structure-based approach,” he said. “In other words, no one has ever done this before on purpose. People have discovered molecules that enhance the activity of enzymes by trial and error, but no group has ever done it in a specifically pointed way like this.”
Ostrov said the enzyme exists in two forms: like a Pac-Man with a mouth that has chomped closed, and like a Pac-Man with a mouth that remains wide open. The molecule that worked best fit in a structural pocket in the enzyme’s open conformation.
“So in other words, stabilizing the open conformation may be the reason why we enhance the activity of the enzyme,” he said
After hitting on the “lead” compound, UF researchers then tested it in hypertensive rats that had developed fibrosis of the heart and kidney. The animals received the drug for two weeks. Tissue samples from treated animals revealed a significant decrease in fibrosis of the heart, kidney and blood vessels, said Ostrov, who described the findings as “striking and reproducible.”
The study was funded by grants from the National Institutes of Health and the American Heart Association and was a collaborative effort of the UF colleges of Medicine, Pharmacy and Liberal Arts and Sciences. Researchers also included Mohan Raizada, a distinguished professor of physiology and functional genomics, Michael J. Katovich, a professor of pharmacodynamics, and Ronald K. Castellano, an assistant professor of chemistry, among others.
Early results also show the compound inhibits inflammation, which has significant implications for a number of human diseases, including autoimmune diseases such as type 1 diabetes and rheumatoid arthritis as well as other diseases involving fibrosis, such as Alzheimer’s, Ostrov said.
Additional research will continue to explore the compound’s effectiveness in animals and humans.
]]>Testing a new class of blood pressure drugs, University of Florida researchers have been working to enhance a key enzyme called Ace-2. The enhanced Ace-2 enzyme helps relax blood vessels. But researcher David Ostrov and his team found that the enzyme has another more surprising effect.
Ostrov: “Not only did these compounds work in terms of reducing blood pressure and lowering heart rate, but they had a dramatic result that was not entirely anticipated and that result is that we are actually capable of reversing fibrosis, which means we are actually capable of reversing scarring in the heart and the kidney.”
When the study began, researchers had thought the enzyme might stop or inhibit that scarring, but it proved even more successful than that.
Ostrov: “If you think about it, we’re reversing scarring. There are currently no drugs capable of reversing scarring in any context that I’m aware of. But apparently this drug we’ve discovered has that property.”
Human trials may not start for several years, but researchers say their results suggest they may have found a key to combatting various forms of scarring.
]]>Testing a new class of blood pressure drugs, University of Florida researchers have been working to enhance a key enzyme called Ace-2. The enhanced Ace-2 enzyme helps relax blood vessels. But researcher David Ostrov and his team found that the enzyme has another more surprising effect.
Ostrov: “Not only did these compounds work in terms of reducing blood pressure and lowering heart rate, but they had a dramatic result that was not entirely anticipated and that result is that we are actually capable of reversing fibrosis, which means we are actually capable of reversing scarring in the heart and the kidney.”
When the study began, researchers had thought the enzyme might stop or inhibit that scarring, but it proved even more successful than that.
Ostrov: “If you think about it, we’re reversing scarring. There are currently no drugs capable of reversing scarring in any context that I’m aware of. But apparently this drug we’ve discovered has that property.”
Human trials may not start for several years, but researchers say their results suggest they may have found a key to combatting various forms of scarring.
]]>No matter what their inclination, as of June 1 many anglers will have to add three tools to their tackle boxes. New state and federal regulations will require fishermen angling for reef species in the Gulf of Mexico to carry circle hooks when fishing with natural bait, a dehooking device and a venting tool.
With the rule change fast approaching, Florida Sea Grant, in affiliation with the University of Florida’s Institute of Food and Agricultural Sciences, aims to quickly help bring fishermen up to speed.
Along with developing Web sites and brochures, Sea Grant will host workshops across the state along with the Florida Fish and Wildlife Conservation Commission.
“Florida is the number one fishing destination in America,” said Chuck Adams, IFAS marine economics specialist for Sea Grant. “But history has shown us that we have to work to keep it that way.”
Saltwater angling is an $8 billion industry for the Sunshine State, but the millions who cast lines can contribute to overfishing. As a result, the types, sizes and numbers of fish that can be caught have become tightly regulated, leading to a rise in popularity of catch-and-release practices.
“It’s worked — to a degree,” Adams said. “It’s not a stopping point, though. There are more anglers every year, and the fish don’t get any better at not biting.”
The three new tools are designed to improve a fish’s chance of surviving once released. The most tried and true are circle hooks, used with live or cut bait.
Shaped like a capital “G” instead of the conventional j shape, the rounded hook with its inwardly angled point is designed to slip out of a fish’s throat or stomach, but easily catch on the fish’s lip.
The benefits to the fish are obvious, but the circle hooks have their own pluses for anglers.
J-hooks must be “set” by a perfectly timed jerk of the line that imbeds the hook just as the fish takes the bait. A proper set can be frustratingly elusive. In contrast, circle hooks rely on a smooth motion that allows the hook to set on its own.
Once the fish is reeled in, the next tool comes into play.
A dehooker is a straight piece of wire with a curve or loop at the end. It’s used to dislodge the hook from the fish’s mouth without removing the fish from the water.
“The less you handle the fish out of the water, the better its chances are going to be,” says Bryan Fluech, Collier County Sea Grant marine agent. Keeping the fish out of water deprives it of oxygen, and handling its skin or scales removes a protective layer of mucous.
But taking the fish out of water can sometimes be the best way to save it. Often, when fish are caught in deep water, the pressure change while being rapidly drawn to the surface can cause an interior organ called a swim bladder to expand or rupture.
When that happens, the escaped gas gets trapped in the fish’s body cavity and exerts pressure on its internal organs. Releasing a fish in this condition renders it unable to return to its home depth and exposes it to predators.
However, a properly trained angler can help the fish survive using a venting tool.
A preferred variety of the tool, developed by IFAS and the Mote Marine Laboratory, is much like a hypodermic syringe with the plunger pulled out. The angler lays the fish on its side, sticks the needle in behind the pectoral fin at a 45-degree angle, and waits for the deflating-balloon sound to stop.
After venting, the fish can hide from predators and make a speedy recovery.
“Individually, fish are a lot more resilient than we give them credit for,” Adams said. “This is a good thing — because, collectively, people can be a lot more damaging than we like to think.”
State wildlife officials say they will give anglers time to adjust to the new rules before aggressively enforcing them.
For more information about catch and release techniques and changes to Gulf reef fishing regulations, please visit:
http://myfwc.com/marine/gearrules
This headset can reduce the loud and repetitive noises magnetic resonance imaging machines make. The sounds created by powerful magnets range from whirring to grinding noises as loud as a jet engine. Patients already stressed out from the experience often wiggle around because of the noise. Engineer Stephen Forguson says that causes a problem.
Forguson: “Any motion inside while they’re taking those pictures can cause image distortion and they’ll have to restart, so just for the patient’s side, having a quieter environment is more beneficial.”
Fewer repeat exams can also free up the machine for other patients. The MRI presented special challenges in designing the headset, since any metal in the chamber can distort the images.
Forguson: “All these were hard technical difficulties to overcome, but mostly it’s that we couldn’t put any electronics in there. And we had to come up with a new way to cancel noise that really had never been done as far as we could tell.”
The system pipes in sounds on top of the repetitive noises the MRI makes. So far engineers have reduced noise similar to an MRI by fifteen decibels.
]]>This headset can reduce the loud and repetitive noises magnetic resonance imaging machines make. The sounds created by powerful magnets range from whirring to grinding noises as loud as a jet engine. Patients already stressed out from the experience often wiggle around because of the noise. Engineer Stephen Forguson says that causes a problem.
Forguson: “Any motion inside while they’re taking those pictures can cause image distortion and they’ll have to restart, so just for the patient’s side, having a quieter environment is more beneficial.”
Fewer repeat exams can also free up the machine for other patients. The MRI presented special challenges in designing the headset, since any metal in the chamber can distort the images.
Forguson: “All these were hard technical difficulties to overcome, but mostly it’s that we couldn’t put any electronics in there. And we had to come up with a new way to cancel noise that really had never been done as far as we could tell.”
The system pipes in sounds on top of the repetitive noises the MRI makes. So far engineers have reduced noise similar to an MRI by fifteen decibels.
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