The Science Path project, in partnership with the school district, aims to tackle locally the national issue of students going to college underprepared for more rigorous science courses. The idea is that if the curriculum and instruction for these critical subjects are enhanced in K-12, students will be better prepared for the college coursework. PBSC also plans to partner with Florida Atlantic University on the initiative.

The Obama administration and Gov. Rick Scott are among those stressing the need for more workers with solid skills in science, technology, engineering and math (STEM) subjects. The U.S. Department of Commerce projects a 17 percent growth nationwide in STEM jobs by 2018.

“The current economic forecast for this industry outpaces even health care,” said Dr. Dennis Gallon, Palm Beach State president. “The College stands ready to partner and support the development of programs which support quality education for our students and prepare them to take their place in the workforce, advancing STEM industries.”

Just 1 in 3 ACT-tested high school graduates met the College Readiness Benchmark in Science in 2011 and at the state level only 20 percent of graduates were college ready in the subject, according to ACT Profile Reports.

On the local level, Palm Beach State College has experienced troubling withdrawal rates from its six introductory level biology and chemistry courses, raising serious questions about the preparation of the county’s high school graduates.

“We are excited to have the support of the Quantum Foundation in working together to significantly move the needle of students’ success in these two fields and ultimately help to grow a significant portion of our workforce,” said Pat Lord, major gifts director for the Palm Beach State College Foundation.

The College plans to launch a pilot program at the Palm Beach Gardens campus, the site of its existing Math and Science Summer Institute and the Employ Florida Banner Center for Life Sciences, working with area high schools. The program eventually will be expanded to other high schools in the county. While the Science Path project currently focuses on high school, to further enhance the science curriculum throughout the school district, the College is seeking other funding opportunities to align the curriculum of middle and elementary schools. In addition to curriculum alignment, the partnership will include shared professional development opportunities for college faculty and K-12 school teachers, the initial design of a virtual library of learning objects for faculty and teachers and the development of cooperative teams to identify students who demonstrate interest and potential in STEM.

The timing of the project comes just as the state has boosted its graduation requirements calling for all students beginning in 2013-2014 to pass biology, chemistry and one equally rigorous science course to receive a high school diploma.

It also falls in line with the more aggressive efforts of the Quantum Foundation to enhance science education in the county through the funding of programs that provide curriculum alignment, student pipelines into science and science teaching development.

Dr. Kwon joins MPFI from the Department of Neurobiology at Harvard Medical School, where he served as a post-doctoral fellow in the laboratory of Dr. Bernardo Sabatini, a Howard Hughes Medical Institute investigator. Dr. Taniguchi comes to the Institute from Cold Spring Harbor Laboratory, where he was a research investigator in the lab of Dr. Z. Josh Huang.

Dr. Taniguchi’s research probes the cellular and molecular mechanisms that are responsible for the development of neural circuits in the cerebral cortex, the largest and most complex area of the brain, whose proper function is critical for sensory perception, motor control, and cognition. He is highly regarded in the field for pioneering work that has made it possible to target molecular probes to specific classes of neurons in the cerebral cortex that utilize the inhibitory neurotransmitter GABA. This discovery has opened the door to a broad range of experiments that will make it possible to analyze the structure, function and development of GABAergic neurons, and to use this information to address a host of neurological and psychiatric disorders. Among other scientific goals, Dr. Taniguchi plans to work collaboratively with colleagues at Max Planck Florida Institute to expand his studies of GABA neurons and their roles in regulating the activity of circuits in cerebral cortex.

Their study, published in Neurosurgical Focus, suggests this tool, known as frontal near-infrared spectroscopy (NIRS), could offer hospital physicians a safe and cost-effective way to monitor patients who are being treated for a stroke, in real time.

“About one-third of stroke patients in the hospital suffer another stroke, and we have few options for constantly monitoring patients for such recurrences,” says the study’s senior investigator, neurocritical care specialist William Freeman, M.D., an associate professor of neurology at Mayo Clinic.

“This was a small pilot study initiated at Mayo Clinic’s campus in Florida, but we plan to study this device more extensively and hope that this bedside tool offers significant benefit to patients by helping physicians detect strokes earlier and manage recovery better,” he says.

“We have developed a procedure which can repair severed nerves within minutes so that the behavior they control can be partially restored within days and often largely restored within two to four weeks,” said Professor George Bittner from the University of Texas. “If further developed in clinical trials this approach would be a great advance on current procedures that usually imperfectly restore lost function within months at best.”

The team studied the mechanisms all animal cells use to repair damage to their membranes and focused on invertebrates, which have a superior ability to regenerate nerve axons compared to mammals. An axon is a long extension arising from a nerve cell body that communicates with other nerve cells or with muscles.

This research success arises from Bittner’s discovery that nerve axons of invertebrates which have been severed from their cell body do not degenerate within days, as happens with mammals, but can survive for months, or even years.

The severed proximal nerve axon in invertebrates can also reconnect with its surviving distal nerve axon to produce much quicker and much better restoration of behaviour than occurs in mammals.

“Severed invertebrate nerve axons can reconnect proximal and distal ends of severed nerve axons within seven days, allowing a rate of behavioural recovery that is far superior to mammals,” said Bittner. “In mammals the severed distal axonal stump degenerates within three days and it can take nerve growths from proximal axonal stumps months or years to regenerate and restore use of muscles or sensory areas, often with less accuracy and with much less function being restored.”

The team described their success in applying this process to rats in two research papers published today. The team were able to repair severed sciatic nerves in the upper thigh, with results showing the rats were able to use their limb within a week and had much function restored within 2 to 4 weeks, in some cases to almost full function.

“We used rats as an experimental model to demonstrate how severed nerve axons can be repaired. Without our procedure, the return of nearly full function rarely comes close to happening,” said Bittner. “The sciatic nerve controls all muscle movement of the leg of all mammals and this new approach to repairing nerve axons could almost-certainly be just as successful in humans.”

To explore the long term implications and medical uses of this procedure, MD’s and other scientist- collaborators at Harvard Medical School and Vanderbilt Medical School and Hospitals are conducting studies to obtain approval to begin clinical trials.

“We believe this procedure could produce a transformational change in the way nerve injuries are repaired,” concluded Bittner.

Traumatic brain injury, or TBI, is known as the signature injury of soldiers returning home from Afghanistan and Iraq. Blast forces sustained in combat often cause damage to parts of the brain critical to high-level functions influencing memory, attention, decision-making and motor skills. Many veterans developing symptoms after TBI also suffer from post-traumatic stress disorder (PTSD), according to the Department of Veterans Affairs (VA).

“Working with the VA, the Department of Defense and private research entities, we will develop novel studies – everything from drug discovery and preclinical work to clinical, social and behavioral trials,” said principal investigator Dr. Paul R. Sanberg, USF senior associate vice president for research and innovation and director of the USF Center of Excellence for Aging and Brain Repair. “Our multidisciplinary work will provide critical knowledge about TBI and its complications that could lead to more effective diagnosis and treatments for soldiers and veterans, as well as skills to improve their physical and psychological adjustment into civilian life.”

“This new federal award is a tremendous boost to USF’s efforts to build a research infrastructure to support our veterans reintegration strategy,” said Karen Holbrook, PhD, USF senior vice president for research, innovation and global affairs.

The two-year, DOD-funded grant joins faculty from across colleges and disciplines.

The grant involves four major projects:

• Researchers will assess in animal models how granulocyte colony stimulating factor (GCSF), a growth factor that mobilizes the body’s own stem cells, may help treat traumatic brain injury.
• A clinical trial will test whether GCSF reduces neurological damage and improves recovery of memory, decision-making and other cognitive functions in soldiers and veterans with TBI, even when administered a month or two after the initial injury. Patients will be recruited from the polytrauma rehabilitation and blast injury programs at James A. Haley Veterans’ Hospital.
• In an attempt to identify better diagnostic measures for mild TBI, a frequently underdiagnosed condition, a study will compare the balance, gait, hearing and vestibular functions of otherwise healthy USF student veterans with and without self-reported TBI to those of non-veteran students. Evaluations will be conducted at the USF School of Physical Therapy & Rehabilitation Sciences Human Functional Performance Laboratory.
• Using advanced technology researchers will monitor changes in patterns of everyday movement and the cognitive function of TBI patients undergoing smart house-based rehabilitation at the Tampa VA hospital’s Polytrauma Transitional Rehabilitation Program. The study will evaluate whether scientific analysis of movements, tracked by devices like radiofrequency identification and global positioning systems, can help assess therapeutic improvement. A second arm of the study will investigate whether variability in walking patterns is greater for USF student veterans reporting mild TBI than for those without this diagnosis.

The new DOD award adds momentum to USF’s plans to work with the VA and DOD to build a first-of-its kind Center for Rehabilitation, Science, Engineering and Medicine, an interdisciplinary research, education and treatment facility. Over the last three years, the university’s Veterans Reintegration Strategy program has joined researchers across colleges and disciplines to work on studies in areas including TBI, PTSD, robotics and prosthetics, gait and balance, and aging-related disorders.

“This award reflects USF’s collaborative efforts to leverage our research and academic expertise to enhance the quality of life of our men and women in uniform, and their families, who have so selflessly served this country,” said Lt. Gen. Martin Steele (USMC retired), executive director of USF Military Partnerships. “It builds, not only upon interdisciplinary research within the university, but also strengthens our longstanding ties with Tampa Bay’s military community through two major VA hospitals, MacDill Air Force Base, U.S. Central Command and U.S. Special Operations Command.”

The findings, published in PloS One, open new opportunities for understanding Alzheimer’s disease and other neurological diseases and for developing therapies to halt its progression, according to senior author Karen E. Duff, PhD, professor of pathology at CUMC and at the New York State Psychiatric Institute.

Alzheimer’s disease, the most common form of dementia, is characterized by the accumulation of plaques (composed of amyloid-beta protein) and fibrous tangles (composed of abnormal tau) in neurons. Postmortem studies of human brains and neuroimaging studies have suggested that the disease, especially the neurofibrillary tangle pathology, begins in the entorhinal cortex, which plays a key role in memory. Then as Alzheimer’s progresses, the disease appears in anatomically linked higher brain regions.

“Earlier research, including functional MRI studies in humans, have also supported this pattern of spread,” said study coauthor Scott A. Small, MD, professor of neurology in the Sergievsky Center and in the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain at CUMC.  “But these various findings do not definitively show that Alzheimer’s spreads directly from one brain region to another.”

To look further into this issue, the CUMC researchers developed a novel transgenic mouse in which the gene for abnormal human tau is expressed predominantly in the entorhinal cortex. The brains of the mice were analyzed at different time points over 22 months to map the spread of abnormal tau protein.

The researchers found that as the mice aged, the abnormal human tau spread along a linked anatomical pathway, from the entorhinal cortex to the hippocampus to the neocortex. “This pattern very much follows the staging that we see at the earliest stages of human Alzheimer’s disease,” said Dr. Duff.

The researchers also found evidence suggesting that the abnormal tau protein was moving from neuron to neuron across synapses, the junctions that these cells use to communicate with each other.

“If, as our data suggest, tau pathology starts in the entorhinal cortex and emanates from there, the most effective approach may be to treat Alzheimer’s the way we treat cancer—through early detection and treatment, before it has a chance to spread,” said Dr. Small. “The best way to cure Alzheimer’s may be to identify and treat it when it is just beginning, to halt progression. It is during this early stage that the disease will be most amenable to treatment. That is the exciting clinical promise down the road.”

Treatments could conceivably target tau during it extracellular phase, as it moves from cell to cell, added Dr. Duff. “If we can find the mechanism by which tau spreads from one cell to another, we could potentially stop it from jumping across the synapses — perhaps using some type of immunotherapy. This would prevent the disease from spreading to other regions of the brain, which is associated with more severe dementia.”

Florida Biologix provides either manual or automated filling services up to 4,000 vials per lot. They have significant experience with formulation and filling of complex biologic products such as proteins, protein complexes, adjuvanted vaccines, oligonucleotides, liquid small molecules and other parenterals. Associated services include drug product in-process and release testing, labeling, packaging, cGMP storage, stability studies, blind labeling, and distribution to clinical study sites.

In addition to this expanded capability, Florida Biologix has recently invested in GMP facility improvements and equipment, as well as outfitted additional classified support space and is adding new warehouse areas to better serve clients’ needs. The Associate Director of Florida Biologix, Dr. Joyce Francis, explains, “These improvements support our multi-year production contracts. As our business grows, we continue to make investments to improve our state-of-the-art facility and overall capabilities.”

A new University of Florida study (PLoS One) shows there may be a way to make insect-killing fungi a more potent weapon against fire ants and other pests. Scientists with UF’s Institute of Food and Agricultural Sciences modified the fungus so that it produces a peptide that helps regulate the fire ants’ nervous system.

The modified fungus was five to eight times as effective in killing fire ants, but had no increased effect on an unrelated insect, the greater wax moth. The researchers were surprised to learn that the modified fungus had another benefit — it disrupted the ants’ undertaker-like behavior.

“Potentially, it’s important because if you can disrupt this behavior, you may be able to increase the efficacy of the fungus in the nest, because they won’t take the dead out and you can spread the infection throughout the nest better. In theory, you could use the same amount of fungus and it would be more effective,” said Nemat Keyhani, a UF associate professor of microbiology and cell science and the study’s lead author.

Keyhani also led a research team in a similar study of mosquitoes, publishing the findings in this month’s issue of Nature Biotechnology: Exploiting host molecules to augment mycoinsecticide virulence

In that study, the scientists tested Beauveria bassiana against mosquitoes, modifying the fungus so that it produced another peptide, called TMOF (trypsin-modulating oostatic factor). This hormone, discovered by a UF/IFAS entomologist, stops the mosquitoes from producing a crucial digestive enzyme called trypsin. Though TMOF is important for the normal digestive process, too much of it causes mosquitoes to starve, unable to take nutrients from food.

Keyhani said the goal of both studies was to show that a host molecule, such as a peptide or hormone that an insect uses for a normal physiological process, can be used against it, disrupting that process and making it more susceptible to microbial infections.

In the mosquito study, combining the fungus with TMOF reduced the survival time of the mosquitoes by 25 percent, reduced females’ trypsin activity by 50 percent, and resulted in female mosquitoes laying 40 percent fewer eggs.

“So we’ve now proven the concept in two different ways — one against mosquitoes and one against fire ants,” Keyhani said.

Acoustic waves from music, particularly rap, were found to effectively recharge the pressure sensor. Such a device might ultimately help to treat people stricken with aneurisms or incontinence due to paralysis.

The heart of the sensor is a vibrating cantilever, a thin beam attached at one end like a miniature diving board. Music within a certain range of frequencies, from 200-500 hertz, causes the cantilever to vibrate, generating electricity and storing a charge in a capacitor, said Babak Ziaie, a Purdue University professor of electrical and computer engineering and biomedical engineering.

“The music reaches the correct frequency only at certain times, for example, when there is a strong bass component,” he said. “The acoustic energy from the music can pass through body tissue, causing the cantilever to vibrate.”

When the frequency falls outside of the proper range, the cantilever stops vibrating, automatically sending the electrical charge to the sensor, which takes a pressure reading and transmits data as radio signals. Because the frequency is continually changing according to the rhythm of a musical composition, the sensor can be induced to repeatedly alternate intervals of storing charge and transmitting data.

“You would only need to do this for a couple of minutes every hour or so to monitor either blood pressure or pressure of urine in the bladder,” Ziaie said. “It doesn’t take long to do the measurement.”

“Creating highly purified and functional human Alzheimer’s neurons in a dish – this has never been done before,” said senior study author Lawrence Goldstein, PhD, professor in the Department of Cellular and Molecular Medicine, Howard Hughes Medical Institute Investigator and director of the UC San Diego Stem Cell Program. “It’s a first step. These aren’t perfect models. They’re proof of concept. But now we know how to make them. It requires extraordinary care and diligence, really rigorous quality controls to induce consistent behavior, but we can do it.”

The feat, published in the journal Nature, represents a new and much-needed method for studying the causes of AD, a progressive dementia that afflicts approximately 5.4 million Americans. More importantly, the living cells provide an unprecedented tool for developing and testing drugs to treat the disorder.

“We’re dealing with the human brain. You can’t just do a biopsy on living patients,” said Goldstein. “Instead, researchers have had to work around, mimicking some aspects of the disease in non-neuronal human cells or using limited animal models. Neither approach is really satisfactory.”

Goldstein and colleagues extracted primary fibroblasts from skin tissues taken from two patients with familial AD (a rare, early-onset form of the disease associated with a genetic predisposition), two patients with sporadic AD (the common form whose cause is not known) and two persons with no known neurological problems. They reprogrammed the fibroblasts into induced pluripotent stem cells (iPSCs) that then differentiated into working neurons.

The iPSC-derived neurons from the Alzheimer’s patients exhibited normal electrophysiological activity, formed functional synaptic contacts and, critically, displayed tell-tale indicators of AD. Specifically, they possessed higher-than-normal levels of proteins associated with the disorder.

With the in vitro Alzheimer’s neurons, scientists can more deeply investigate how AD begins and chart the biochemical processes that eventually destroy brain cells associated with elemental cognitive functions like memory. Currently, AD research depends heavily upon studies of post-mortem tissues, long after the damage has been done.