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:

• Warrington College of Business –
  Chris Janiszewski, marketing
• College of Dentistry –
  Edward K.L. Chan, oral biology
• College of Design, Construction and Planning –
  Ilir Bejleri, urban and regional planning
• College of Education –
  Richard E. Ferdig, School of Teaching and Learning
• College of Engineering –
  David P. Norton, materials science and engineering
  Panos Pardalos, industrial and systems engineering
  Bhavani Sankar, mechanical and aerospace engineering
• College of Fine Arts –
  Melissa L. Hyde, School of Art & Art History
• Florida Museum of Natural History –
  Jacqueline Y. Miller, McGuire Center for Lepidoptera and Biodiversity
• College of Health & Human Performance –
  Christopher M. Janelle, applied physiology and kinesiology
• Institute of Food and Agricultural Sciences —
  Jeffrey K. Brecht, horticulture sciences
  Nicholas B. Comerford, soil and water science
  Jesse F. Gregory III, food science and human nutrition
  Jeffrey B. Jones, plant pathology
  Gary F. Peter, School of Forest Resources and Conservation
  James P. Syvertsen, plant pathology
• College of Journalism — ,
  Kim Walsh-Childers, journalism
• Levin College of Law –
  Mark Fenster
• College of Liberal Arts & Sciences –
  Darin E. Acosta, physics
  Benjamin M. Bolker, zoology
  George Christou, chemistry
  William Hager, mathematics
  Paul A. Mueller, geological sciences
  Carolyn M. Tucker, psychology
• Medicine —
  Laurence M. Morel, pathology, immunology and laboratory medicine
  David R. Nelson, medicine
  Dietmar W. Siemann, radiation oncology
  Sankar Swaminathan, internal medicine and molecular genetics and microbiology
  Charles S. Wingo, nephrology
• College of Nursing —
  Jennifer H. Elder, healthcare environment & systems
• College of Pharmacy —
  Jeffrey A. Hughes, pharmaceutics
• College of Public Health and Health Professions —
  R. Paul Duncan, health services research, management and policy
• College of Veterinary Medicine —
  Mary B. Brown, infectious diseases and pathology

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.”

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.

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

Scientists studying fruit fly cells discovered that slight changes in the protein scaffolds that support the genes “reaper” and “hid” — aptly named for their roles in triggering cell death — cause the cells to become naturally resistant to X-rays during early development.

“It turns out that a piece of DNA that is required for mediating this process of cell death is blocked,” said Lei Zhou, an associate professor of molecular genetics and microbiology in the UF College of Medicine. “When it is blocked, the cells just don’t die, even when subjected to heavy doses of radiation. This may be what is happening in some resistant cancer cells. The pro-apoptotic genes cannot be induced to cause cell death.”

The study may be the first to link apoptosis, the gene-driven process that leads to the necessary destruction of old, damaged, or infected cells, with epigenetics — the study of how gene function changes even when the genes themselves don’t change.

Scientists believe that defects in cell death regulation may be responsible for tumor formation and the spread of cancer because the cells escape the safeguards that normally clean up malignant cells.

In their experiments, UF researchers found the location of the DNA sequences known to trigger reaper, hid and other genes related to cell death in fruit flies. Similar genes exist in humans.

By monitoring gene activity levels and changes in chromatin — the protein spools that the genes wrap around — researchers were able to detect factors that made the cells resistant to radiation.

Scientists first noticed drastic changes in sensitivity to radiation in developing fruit fly cells in the mid-1970s. Similarly, a sensitive-to-resistant transformation takes place in people during the development of brain cells, which are extremely sensitive to radiation in their formative stages but more durable once they grow into adult neurons.

However, the underlying cellular and molecular causes of the transformations were undetected. The latest findings suggest that like the fruit fly cells, tumor cells may have a degree of epigenetic protection from radiotherapy or chemotherapy.

“We are talking about a piece of DNA that is very sensitive when open, but modification of its supporting structure has caused it to condense,” said Zhou, who is affiliated with the UF Shands Cancer Center and the UF Genetics Institute. “If we reverse this and open the DNA supporting structure, we can conceivably make the cells sensitive to radiation once more. Controlling the blocking-unblocking mechanism to make the cells sensitive could potentially lead to better cancer therapy.”

Conceivably, certain drugs that open “enhancer” regions of cell-death genes in tumor cells could improve the effectiveness of cancer treatments.

“The scientists took a different approach to look at the regions of the genome important for DNA-damage induced cell death,” said Kristin White, an associate professor of dermatology at Harvard Medical School and Massachusetts General Hospital, who did not participate in the research. “One of the most interesting aspects of this work is the finding that changes in chromatin structure regulate the expression of genes that are important in this death, and that this regulation can extend over long distances in the genome.

“The research shows there is still a lot to learn about DNA damage-induced cell death,” she said. “We need to understand all aspects of this if we want to improve cancer therapy. This work suggests that we need to look harder at chromatin-modifying enzymes as new targets to alter the response of cancer cells to radiation.”

The research was supported by a National Institutes of Health grant.

“Within African-American and Latino families, children follow a cultural tradition that places a high value on respecting, obeying and learning from elders, and in our study they did indeed show more respect for parental authority,” said Julia Graber, a UF psychology professor.

However, when African-American and Latina girls do act up, their mothers consider the arguments more intense than those reported by white mothers who clash with their daughters, said Graber, whose study is published in the February issue of the Journal of Family Psychology.

Hispanic and black mothers, who value strong family connections, a deep sense of family loyalty and the importance of extended family and social support networks, seemed to be much more upset if daughters fell short of cultural, good girl expectations, Graber said. “It may be just the kind of issue that pushes their buttons more, thinking of their daughter as no longer being the good, respectful daughter,” she said.

For all girls, discipline was the only factor that influenced how much conflict they perceived in the relationship. The stricter and harsher mothers were, the less conflict their daughters reported, Graber said. However, as girls get older, stricter discipline may lead to greater conflict if girls try to disagree, she said.

The study differs from other research on mother-daughter conflict in that instead of looking at adolescence, it examines girls in middle to late childhood, at an average age of 8½, Graber said. The teenage years are naturally turbulent times for families, but understanding what happens immediately preceding them sets the stage for a smoother or rockier transition, she said.

Teen conflict is a risk for other behavior-related problems, Graber said. “It does seem that when there are higher levels of conflict, those daughters are more likely to have adjustment problems in terms of feeling more depression, sadness, anxiety and those problems,” she said.

The intensity of the conflicts aside, the study found that mothers’ and daughters’ reports of the frequency of conflict were similar, Graber said. The study, which Graber did with Sara Villanueva Dixon, a St. Edward’s University psychology professor, and Jeanne Brooks-Gunn, a Columbia University child development professor, involved 45 African-American, 23 Latina and 65 white girls recruited through fliers while in the third grade and their mothers. The girls and their families were from racially integrated, working and middle-class communities in a large metropolitan area.

The girls’ respect for authority was observed during a series of videotaped interactions with their mothers. Daughters were scored on their listening behaviors, which included attending to their mothers when their mothers were speaking, acknowledging their mothers’ comments and not interrupting their mothers. They also were evaluated for defiant behaviors, such as disobeying their mothers’ requests, being unwilling to cooperate with their mothers and ignoring their mothers during the interaction.

Not only do children need to be more aware of the expectations their parents have for them, but mothers may also want to reassess their feelings about particular issues, she said.

“The challenge for African-American and Latina mothers is they are in an environment where their children are potentially getting messages at school, on television and elsewhere about what normal childhood behavior is like that may conflict with their own expectations for these behaviors,” Graber said.

“In the higher conflict families where mothers and daughters are arguing much more often there seems to be less productive resolution going on and less learning of those skills,” she said. “Everybody feels mad afterwards rather than feeling the potential of moving forward.”

“This is a fascinating study that enhances our understanding of ethnic and racial differences in parent-child relationships,” said Judi Smetana, a University of Rochester psychologist. “One of its strengths is that it examines in a very careful and detailed way how different cultural values are expressed in mother-daughter interactions and how those values influence the quality of family relationships.”

Until now the revised March reading, along with January’s index, had been consumer confidence’s lowest level since December 1991, said Chris McCarty, director of UF’s Survey Research Center at the Bureau of Economic and Business Research.

“Consumer confidence in Florida is now at the same recessionary levels as it was during the 1990-91 recession,” McCarty said. “Unlike the relatively mild recession of 2001, the recession of 1990-91 resulted in a longer time to recover. This is a likely scenario for the current economy.”

Most economists believe the economy will pick up by late 2008 or early 2009, but the question remains whether it will get worse and follow the pattern of the 1973-75 recession, he said.

“The causes of lower consumer confidence are well-known to Floridians,” McCarty said. “Falling housing prices, stricter guidelines for all forms of credit, and rising gasoline and food prices are hitting consumers all at once. This has raised the possibility of ‘stagflation,’ a circumstance where gross domestic product retracts while inflation rises.”

Four of the five components that make up the index fell this month. The largest decrease was in perceptions of personal finances a year from now, which fell nine points to 79, a record low for that component. Perceptions of U.S. economic conditions over the next year fell six points to 52, perception of personal finances now compared with a year ago fell five points to 59, a record low for that component, and perceptions of U.S. economic conditions over the next five years fell four points to 72. Perceptions as to whether it is a good time to buy big-ticket consumer items rose three points to 67.

Nationally, consumer confidence as measured by the University of Michigan has fallen to a 26-year low, McCarty said. Hardest hit are low-income households that have a far more difficult time with higher energy and food prices, he said.

In Florida, consumer confidence hit a record low of 64 in December of 1991, McCarty said. Last month’s preliminary index was 68 but was revised up to 70 when the final results were in, he said.

“The question on everyone’s mind is how we are going to get out of this slow economy?” McCarty said. “The answer is probably time. Median house prices have been falling here in Florida since late 2006, and we expect prices to bottom out in much of Florida by July.”

Many homeowners have dealt with their adjustable rate mortgages being reset at higher rates by refinancing, making the required higher payments or leaving their home altogether, McCarty said. Most banks that made bad loans have reduced the book value of assets that are overvalued compared to their market value, and investors are adjusting to these write-downs, he said.

The economic stimulus package, though a welcome relief for many households, will probably not do much to change the course of events, he said.

The research center conducts the Florida Consumer Attitude Survey monthly. Respondents are 18 or older and live in households telephoned randomly. The preliminary index for April was conducted from 533 responses.

Consumer confidence is designed to help predict buying patterns by measuring the mood of consumers toward purchasing. Although other economic indicators also predict buying patterns, consumer confidence tends to be available sooner. The index is benchmarked to 1966, so a value of 100 represents the same level of confidence for that year. The value of the index is in comparing changes over time rather than looking at an isolated month.

In a study of 210 college students, UF researchers discovered a link between what psychologists call relational victimization in adolescence and depression and anxiety in early adulthood, according to findings published online this month in the journal Psychology in the Schools. Rather than threatening a child with physical violence, these bullies target a child’s social status and relationships by shunning them, excluding them from social activities or spreading rumors, said Allison Dempsey, a doctoral student in the UF College of Education and the study’s lead author.

“Even though people are outside of high school, the memories of these experiences continue to be associated with depression and social anxiety,” said Dempsey, who graduated from Columbine High School in Colorado one year before the 1999 school shooting there and now studies school prevention programs. “It was interesting to see these relationships still continue to exist even though they are in early adulthood now and in a completely different setting.

“I’m hoping this study will help shed light on the fact that this is a real problem and continues to be a real problem after students leave school.”

To uncover the relationships between social bullying and loneliness, depression and anxiety, researchers surveyed college undergraduates between the ages of 18 and 25 and asked them to recall their experiences from high school. They were also looking to see if having friends mitigated some of the effects of bullying and if there was any relationship between gender and the severity of psychological symptoms, said Eric Storch, an assistant professor of psychiatry in the UF College of Medicine and a co-author of the study.

“About 20 years ago people thought of bullying as very physical,” Storch said. “As a result people thought guys did the bullying, and that it wasn’t really a big experience for girls. The problem is that isn’t actually true. There are different types of aggression.

“Boys do tend to be more physical, but both sexes engage in relational victimization. We wanted to see if gender affected strength of the relationship between depressive symptoms and victimization.”

But researchers found no gender difference in the link between this type of bullying and depression. They also discovered that having friends or other positive social relationships didn’t lessen rates of depression and anxiety in adulthood, a finding that surprised them, Dempsey said.

For some children, having friends and positive support can help make them more resilient to the slings and arrows from bullies, Storch said. But other children take the words and abuse more to heart and begin to believe what’s being said about them.

“Those types of negative thoughts are actually believed to be at the core of things like depression and anxiety,” Storch said. “Behaviorally what starts happening is you avoid interactions and situations that could be quite positive for you.”

Currently, there are few prevention or intervention programs that focus specifically on relational victimization, in part because it’s tougher to pinpoint and stop, Dempsey said.

“If a child tries to punch someone or kick someone, there’s evidence of that happening,” Dempsey said. “There’s a definite aggressor and a definite victim. When it comes to spreading rumors and gossiping, that’s a lot more difficult to prove who’s doing it. And it’s harder to provide consequences.”

Dempsey said she hopes this study and others will help other researchers and psychologists design programs that can help stop this form of bullying in schools.

“I think many people have the belief that victimization is a normal rite of passage in childhood,” Storch said. “While it certainly does happen to most kids, it’s not acceptable. And while I think it would be difficult to completely curtail it, by reducing it you’re going to help someone a tremendous amount to not have to go to school and be plagued by this environment of being tortured day in and day out.

“This isn’t a normative experience and we need to do something about it and recognize that not doing something could affect children who are really rising stars.”

Wendy Troop-Gordon, an assistant professor of psychology at North Dakota State University, said understanding how past relational bullying affects people in adulthood is an important step forward for research in this field.

“Turning 18 is not a magical age when you leave all of these experiences behind,” said Troop-Gordon, who is not affiliated with the study. “People do seem to carry these experiences with them.”

The students have designed a headset that shows promise of reducing the extremely loud, repetitive, industrial-like noises that accompany magnetic resonance image examinations. The noises, which range from beeping to whirring to grinding and can often be as loud as a jet engine, stem from the workings of the powerful magnets at the heart of the machines’ ability to produce sharply defined internal images of the body or body parts.

The headset would not only make the experience less off-putting, it might also reduce the number of needed exams, freeing up the machine for access by more patients, said Stephen Forguson, a senior majoring in electrical engineering.

“The sound often makes patients move or wriggle a bit,” he said. “Unfortunately, that can blur the image, which means the operators have to redo the exam.”

Forguson and Chad Dailey, Paul Norris and Christopher Ruesga, all also engineering seniors, designed the headset as part of the College of Engineering’s Integrated Product and Process Design Program. The program pairs student teams with corporate or government sponsors for yearlong design projects of products or processes intended to be useful to the sponsor. The sponsor of the headset project was Invivo Corporation, a Gainesville manufacturer of magnetic coils, monitors and other MRI accessories.

With battery-operated headphones that cancel internal airplane noise or other loud noises already commercially available, muffling the noise a patient hears when inserted into the cylinder-like MRI machines might seem a small challenge.

But the problem is that no electronics are permitted within the MRI chamber because the electronics can distort or disrupt the images scanned by the machines’ magnets. So the difficulty for the UF students was figuring out how to reduce noise without the use of any wires, switches or other electronics with the patient in the chamber.

“Passive” systems that use foam or other sound-deadening materials are insufficient to combat the noise. So the team attempted to solve the problem using existing “air phones,” or headphones attached to small tubes, connected via the tubes to specially crafted electronics and software located outside the MRI machine.

The air phones, which are similar to the headphones once distributed on commercial airplanes, pipe the sound via two tubes to tiny microphones connected to an amplifier and a signal processor several feet away.

That processor taps an algorithm, or set of computer instructions, to produce a sound signal that is the opposite of the signal just received. That opposite signal then gets piped back through a third tube to each of the patient’s ears.

Because the MRI sounds are repetitive and the piped-in sounds are timed to occur on top of the repetitions, the result is that the patient hears the same sound as he or she would have without any intervention — but at a lower volume.

Trials of the system using a loud beeping sound similar to some MRI noises showed it could reduce the noise by as much as 15 decibels. Ambient noise is about 60 decibels, with jet engines and other extremely loud noises reaching 120 decibels. The students were only able to reduce actual MRI sounds by a smaller level, but they said further tweaks of the system and algorithm are likely to improve that result.

The team’s results are “significant and make a difference,” said Gijs Bosman, a professor of electrical and computer engineering and the team’s faculty adviser. “Based on experiments and further testing of the prototype, the team has come up with several recommendations for further improvements.”

Sam Coons, a project manager with Invivo who worked with the UF team, said reducing the MRI noises is also challenging in part because as clinicians develop new scans, new noises emerge. But he said that improving the algorithm at the heart of the headset project should make it more effective against the variety of noises.

The noise-muffling technology is “a big piece” of Invivo’s entertainment system, he said. “We hopefully at some point will incorporate this into all of our systems because noise is such a problem,” he said. “If we can achieve our goals, we will ship this to everyone.”

“For HIV, it’s been shown that if you don’t take a very high percentage of your medication, you may as well not take medication at all,” said Dr. Richard Melker, a professor of anesthesiology at the UF College of Medicine and chief technology officer for Xhale.

Patients who take some but not all of their medication increase the likelihood the virus will mutate into a deadlier, drug-resistant form. Experts have tried literally hundreds, if not thousands, of ways to monitor drug adherence, ranging from daily log books to blister packs that record the time each pill is dispensed. Despite the money, time and effort devoted to these methods, Melker said only one works well: directly observed therapy, or DOT.

“If you have a disease that is deemed to be a public health risk, authorities can put you into a program where you have to come to the clinic every day and be observed putting the pill into your mouth and swallowing it,” Melker said.

But that process is inconvenient for patients, as well as for clinic personnel who have to track them down when they fail to show up. A breath-monitoring device developed by UF scientists and Xhale could change that, allowing patients to participate in a type of virtual DOT from home.

“The machine sits in your home and when it’s time for you to take your medication, it makes a beeping noise. If you don’t hit a button after about five minutes, it’s going to beep louder and louder until you come,” Melker said. “If you don’t come after a certain amount of time, the machine can call the clinical trial coordinator and indicate that subject or patient didn’t take the medication as prescribed.”

The device, which is slightly smaller than a shoebox, records the results of each breath test, allowing patients to bring a memory card or USB key to the clinic once a month and receive a printout of their results. Eventually, the researchers hope to reduce the size of their detection device to fit inside a cell phone. But for now, they’re satisfied that the technology works.

“The doctor can see how often you took it and exactly what time. If it made the patient really sick or dizzy and they didn’t take it, they can find out why,” Melker said. “It’s not just a question of did I or didn’t I take it, but when you took it or why you didn’t take it.”

The researchers developed the adherence monitor by incorporating minute amounts of an alcohol into a gel capsule. The additive, called 2-butanol, is one of many GRAS — Generally Recognized as Safe — compounds approved by the Food and Drug Administration for use in foods.

“We wanted (patients) to swallow a chemical and have it transform into something else that’s easy to monitor,” said Matthew Booth, an assistant professor of anesthesiology at the UF College of Medicine and an investigator in the study. “When it hits the stomach lining and liver, an enzyme converts the alcohol to a gas that can be measured in the breath.”

To determine how well the byproduct could be detected, six healthy volunteers swallowed empty pills in which the capsules contained trace amounts of 2-butanol. After five to 10 minutes, the scientists could measure the volatile byproduct in the volunteers’ breath using a small detector. The scientists say their device could also be used to monitor medication adherence in patients with other communicable diseases, such as tuberculosis.

“It is encouraging that the biological and chemical elements of the adherence system work as predicted. We were able to conclusively show who swallowed the capsules containing the 2-butanol. With further optimization, we are optimistic the device will perform very well,” said Dr. Donn Dennis, the Joachim S. Gravenstein professor of anesthesiology at the UF College of Medicine and an investigator in the study.

The researchers say the device may prove equally helpful for monitoring adherence in clinical trials.

“If you enroll HIV/AIDS patients in a clinical trial and they don’t take the medication, then you may not get adequate proof that the drug is effective,” Melker said. “It might be effective, but some of the patients aren’t taking it.”

Phase 2 trials are often conducted in the community, rather than at research institutions, making it difficult for researchers to monitor adherence. As a result, many trials enroll a larger group of subjects than needed, in hopes they’ll obtain enough data to determine the safety and efficacy of the medication.

“If we had a good way of doing DOT that’s realistic, instead of having someone come to your house or you going to clinic every day of your life, then we would know whether these people stopped taking their medication and why. Right now, nobody knows any of that.” Melker said. “The implications of being able to understand what normal human behavior is in a clinical trial and, of course, in the real world, are huge.”

For the past decade Hygrophila polysperma — a southern Asian plant known as “hygrophila” for short — has been taking over the ecological niche left when hydrilla was eradicated from waterways, said Jim Cuda, a UF associate professor of entomology. It’s now a significant problem in South and Central Florida.

Like hydrilla, hygrophila (“high-GRAW-fill-uh”) was sold as an aquarium plant, got into Florida waters decades ago and survived. But the similarities end there.

Hydrilla is strictly a water weed, and can be controlled with herbicides, hungry grass carp or mechanical harvesting. Hygrophila can grow fully submerged or up on river banks. Herbicides aren’t very effective, grass carp don’t like it, and mechanical harvesting breaks its stems into tiny pieces capable of spawning new plants.

Given that scenario, Cuda and colleagues with UF’s Institute of Food and Agricultural Sciences are looking for natural enemies that attack the plant on its home turf in India.

‘There aren’t any good, cost-effective management options for hygrophila,” Cuda said. “That’s why there’s interest in biological control.”

Last fall, Cuda and entomology graduate student Abhishek Mukherjee made a collecting trip to several Indian states, described in an article published in the spring issue of Aquatics, journal of the Florida Aquatic Plant Management Society.

The researchers found evidence of at least one insect Mukherjee hopes to capture on a return trip this summer. They also collected samples of wild hygrophila that are being genetically analyzed to determine if they’re identical to plants found in Florida.

If so, that would mean insects and diseases found in the same parts of India would be likely to attack the Florida hygrophila. If not, the researchers may keep trying to pinpoint the original home of Florida hygrophila and seek enemies there.

The UF team — which includes Cuda, Mukherjee and Bill Overholt, also a UF associate professor of entomology — recently discovered that the larvae of a native moth species will feed on hygrophila.

The moth has no value as a biological control agent because it isn’t host-specific — the larvae attack more than 60 plants — and is unlikely to put a dent in hygrophila populations. But it can be a great research tool, enabling researchers to find out if hygrophila can survive defoliation, Cuda said.

Hygrophila closely resembles native alligatorweed, he said. Residents who think they’ve found a patch should not try to destroy it, but instead contact their county extension office, which can be found at www.solutionsforyourlife.com.

In the United States, hygrophila is currently growing wild only in Florida and Texas. It’s been officially confirmed in 10 Florida counties, though Cuda suspects it’s present in at least 20. Previous research indicates the weed can survive cold climates, and could potentially spread as far as hydrilla did — from Delaware to Florida, all along the Gulf Coast, and north to Washington state.

In Texas, hygrophila has already become established in two lakes and a river system, said Marcos De Jesus, a state fisheries biologist with the Texas Parks and Wildlife Department. But right now, the population is small and other invasive aquatic weeds take priority.

“The money goes into chemical control or mechanical removal of these other species and hygrophila hasn’t spread enough to warrant a lot of attention,” he said.

The barrier deflects damage from radiation or chemotherapy, making some cancer cells difficult to destroy, but researchers from UF and the University of North Carolina at Chapel Hill may have discovered why. Their study revealed that mutations in the tumor-suppressing p53 protein lead to overabundance of a second protein called focal adhesion kinase, or FAK, which makes the cells less vulnerable to attack.

“These findings are significant to future cancer research and the development of new therapies,” said Vita Golubovskaya, an assistant professor in the UF department of surgery, who presented the findings. “The high correlation between these two markers is critical for predicting patient prognosis.”

The next step will involve developing cancer therapies that target this interaction, Golubovskaya added.

Both p53 and FAK are found in low levels in normal, healthy cells. The p53 protein ensures that cells strike a wholesome balance between growth and death. In its normal state, p53 suppresses the FAK protein and weakens the molecular force field around cancer cells. But mutations in the p53 protein can interfere with this regulatory function.

Mutations in the p53 gene are commonly found in patients with cancer, and those with more aggressive forms of the disease boast particularly high levels of p53 and FAK. Most cancer therapies are largely ineffective against the resulting FAK force field, which has been identified in melanoma and most solid tumors of the breast, lung, brain, thyroid and colon.

Scientists are still unsure what causes mutations in p53 and why FAK binds to the damaged protein. But the study revealed that the interaction interferes with the signaling process that normally induces cell death, allowing cancer cells to grow unchecked.

The population-based study centered on 600 patients with breast cancer. UNC researchers, led by Kathleen Conway-Dorsey, an assistant professor of cancer epidemiology, analyzed p53 mutations in tumor tissue samples from the patients. UF researchers then identified the FAK protein in the breast cancer samples and performed a statistical analysis, finding that the p53 mutation is associated with overabundance of FAK.

“Basically, tumors of breast cancer patients with p53 had a higher probability of high expression of FAK,” said Golubovskaya. “We have shown before that FAK overexpression will highly correlate with more aggressive breast cancers.”

The findings provide important information from human tumor samples about how the tumor suppressor p53 acts to negatively regulate FAK expression, said David D. Schlaepfer, a professor of reproductive medicine at the Moores Cancer Center at the University of California, San Diego.

“The results connecting p53 mutations and increased FAK expression further our understanding of the factors that modulate FAK expression during tumor progression,” he said.

Results from the current study could help predict patient prognoses, researchers say. Many patients with mutant p53 and an overabundance of FAK don’t fare well, but new therapies could change that by targeting the protein interaction. The next step will involve identifying the types of p53 mutations that contribute to an overabundance in FAK.

Surgery remains the treatment of choice for patients with cancer, Golubovskaya said. Scientists and surgeons often focus their efforts on determining why cancer developed. Overabundance of the FAK protein can be detected during very early stages of breast cancer, even in pre-malignant tissues. UF cancer researchers are currently developing FAK inhibitors that will pave the way for future therapies.

“We now need to answer questions about why the interaction happens and what regulates it,” Golubovskaya said. “If FAK is overexpressed, how can we stop it early to slow cancer growth and metastasis? Answering these questions together with surgeons and scientists can help to fight this deadly disease.”

The research was supported by Golubovskaya’s grant from Komen for the Cure and a National Institutes of Health grant held by surgical oncologist Dr. William Cance, chairman of the UF College of Medicine’s department of surgery.

Cance and colleagues were the first to pull FAK out of human tumors to show that cancers make the molecule in large quantities. In 1996, the team was the first to show that if a tumor is prevented from producing the enzyme it dies. In 2004, the team found the regulatory region of this protein and in 2005, found the interaction of FAK and p53 proteins. The significance of this finding was reviewed by Golubovskaya and Cance in the journal International Review of Cytology last year.

“These findings put together another piece of the complex cancer puzzle and open the way for highly specific molecular cancer therapy that can target the p53-FAK interaction,” said Cance, who also is an associate director at the UF Shands Cancer Center.

“Searching for the presence of this gene may be one way to better identify patients who are at an increased risk for the phenomenon,” said Dr. David S. Sheps, a professor and associate chairman of cardiovascular medicine at UF’s College of Medicine and the Malcom Randall Veterans Affairs Medical Center.

Those with the gene variation are three times more likely to experience dangerous decreases in blood flow to the heart — a condition doctors call ischemia — than heart disease patients without it. Ischemia increases the chance these patients will suffer a heart attack, heart rhythm abnormalities or sudden death, UF researchers report in the April 14 issue of Archives of Internal Medicine.

“There’s no question that in certain populations it is associated with worse prognosis than in patients who do not have mental stress-induced ischemia in terms of overall adverse events and also mortality,” Sheps said. “And it has become apparent that it is far more prevalent than we initially thought. Most of the studies that have been published to date have involved populations of patients who had coronary disease and positive exercise stress tests. But recently we and other investigators have shown that a much broader category of patients also are prone to mental stress ischemia.”

Past studies have shown that as many as two-thirds of patients with coronary artery disease who experience exercise-related reductions in blood flow to the heart respond similarly to mental stress. These bouts often produce no symptoms of chest pain and are rarely detectable on a standard electrocardiogram. Yet previous UF research has shown that these patients have a threefold greater risk of dying — as large a risk factor as cigarette smoking or high cholesterol. Other studies have linked stress experienced after mass disasters or natural catastrophes with a rise in heart attacks and sudden death.

Psychological stress can leave the heart more prone to developing arrhythmias or electrical instability and the blood more prone to clotting. Stress appears to raise heart rate and rapidly hike blood pressure, increasing the heart’s need for oxygen-rich blood, Sheps said. Yet less oxygen is supplied, in part because coronary arteries constrict, impeding blood flow. Doctors are concerned that this reaction to stress in the laboratory is simply a snapshot of how patients respond to the stress of life on a daily basis.

An estimated 10 percent of all patients with coronary disease experience detectable mental stress-induced reductions in blood flow to the heart. In some subsets of patients the phenomenon may be even more prevalent, involving up to 40 percent of these patients.

UF researchers studied 148 patients with coronary artery disease who were on average about 65 years old. Participants were asked to perform a public speaking test designed to induce stress. Images were taken of blood flow to the heart at rest and during the speech task. Blood samples also were collected and analyzed for five common gene variations.

About a fourth of the patients experienced mental stress-induced reduced blood flow to the heart, and about two-thirds of them harbored a particular variation of the adrenergic beta-1 receptor genotype that was associated with a three-fold increased risk of this phenomenon, said Dr. Mustafa Hassan, the study’s lead author and a research fellow in UF’s division of cardiovascular medicine. This receptor typically helps the body respond to stress by regulating blood pressure and heart rate, but a common variability in its gene may make certain patients more vulnerable to the effects of psychological stress.

The study was funded by the National Heart, Lung and Blood Institute and also was supported by the Malcom Randall Veterans Affairs Medical Center and the UF colleges of Pharmacy and Dentistry.

Why does mental stress restrict blood flow in some patients even when exercise fails to have the same effect? The effects of mental stress could predominantly affect the heart’s smaller vessels, causing them to spasm and temporarily limiting blood flow, Sheps speculated. In contrast, exercise tends to affect the heart’s blood supply through different mechanisms.

“We should focus our research on two areas,” he said. “One is better identification of patients who are prone to have this problem and two is looking for effective treatments once we know they have it. We need to know whether we can reverse this phenomenon. We are embarking on other treatment studies fairly soon.”

UF researchers are hunting for other genetic subtypes that could identify other patients at increased risk, he added.

“One of the advantages of detecting these sorts of things is that we may be able to in the future be more specific about what kind of treatment might work better in certain patients depending on their genetic makeup,” Sheps said. “That is one of the important things happening in many fields of medicine. There are many diseases that already have been shown to respond differently to different types of treatment based on genetic differences.”