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.

“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.

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.”

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.

Postdoctoral student Parag Katira and his adviser, Roger T. Bonnecaze, department chair in the Cockrell School of Engineering and T. Brockett Hudson Professor, worked with Muhammad Zaman of Boston University to devise a 3-D cancer model that shows the softening of cells and changes in cell binding cause cancerous behavior in cells. These mechanical property changes cause cells to divide uncontrollably, making them less likely to die and resulting in malignant tumor growth. The findings present a unique physics-based perspective on understanding cancer progression and were published recently in the American Physical Society’s journal Physical Review Letters: “How Changes in Cell Mechanical Properties Induce Cancerous Behavior.

“To date, cancer research has focused on biochemical factors,” said Katira. “Instead of looking to solve numerous interdependent biochemical carcinogenic factors, we can now focus on a small number of mechanical factors. It’s a new approach.”

Cancers are caused by various genetic and carcinogenic factors, such as synthetic chemicals, radiation, the environment and physical stress. However, there is an uncanny similarity in mechanical property changes, such as degree of stiffness and ability to bind to other cells, that differentiate healthy and cancerous cells, as previously observed for several types of cancers.

Cancer cells are softer than healthy cells, and when surrounded by stiffer, healthy cells, cancerous cells stay compact and do not spread. When the number of neighboring cancerous cells increases, however, the resisting force from stiffer cells is lowered and softer cancerous cells relax and expand to cover a larger surface area. Stretching of cells increases their multiplication rate and lowers cells’ probability of death.

The team’s computational model replicates the life cycle of cells within a tissue and is used to observe how mechanical property changes affect a cell’s behavior and fate within that tissue. The team started with a completely healthy tissue where all the cells had the same stiffness and binding ability, and then softened a small cluster of cells at the center of the tissue. As long as the number of softened cells was less than a critical value, the tissue remained stable and healthy.

Past this threshold, there was an increase in the multiplication rate of softer cells compared with healthy, stiffer cells. Beyond this point, tumors grew by replacing surrounding healthy tissue and displayed clinically observed characteristics of malignant tumors. The researchers also analyzed how a cell’s ability to bind, or stick, to other cells affected metastasis, or progression. They observed that changes in the inter-cellular binding ability of softened cells controlled the rate and form of growing tumors.

The researchers believe this model identifies a common physical mechanism by which various biochemical carcinogenic or genetic factors can drive cancer progression.

The con occurs when a virus injects its DNA into a bacterium living in a phosphorus-starved region of the ocean. Such bacteria, stressed by the lack of phosphorus — which they use as a nutrient — have their phosphorus-gathering machinery in high gear. The virus senses the host’s stress and offers what seems like a helping hand: bacterial genes nearly identical to the host’s own that enable the host to gather more phosphorus. The host uses those genes — but the additional phosphorus goes primarily toward supporting the virus’s replication of its own DNA.

Once that process is complete, about 10 hours after infection, the virus explodes its host, releasing progeny viruses back into the ocean where they can invade other bacteria and repeat this process. The additional phosphorus-gathering genes provided by the virus keep its reproduction cycle on schedule.

In essence, the virus, or phage, is co-opting a very sophisticated component of the host’s regulatory machinery to enhance its own reproduction — something never before documented in a virus-bacteria relationship.

“This is the first demonstration of a virus of any kind — even those heavily studied in biomedical research — exploiting this kind of regulatory machinery in a host cell, and it has evolved in response to the extreme selection pressures of phosphorus limitation in many parts of the global oceans,” says Sallie “Penny” W. Chisholm, a professor of civil and environmental engineering (CEE) and biology at MIT, who is principal investigator of the research and co-author of a paper published in the Jan. 24 issue of Current Biology. “The phages have evolved the capability to sense the degree of phosphorus stress in the host they’re infecting and have captured, over evolutionary time, some components of the bacteria’s machinery to overcome the limitation.”

“Increasing investment in federally funded research, as the President called for in his address, is important. It takes public and private companies to translate that research into cures and useful technologies. We look forward to working with the Administration and the Congress to pursue public policies that will unleash the promise of biotechnology.

“Curing diseases, first and foremost, means saving lives. But it also means reducing health care costs. With science-based regulatory systems, appropriate tax policy and incentives to encourage continued innovation, America’s biotechnology sector can help drive substantial job growth in the United States and advance our nation’s competitiveness over the long term. The proposals detailed in our ‘Unleashing the Promise of Biotechnology’ plan are designed to transform the innovative ideas of today into the realities of tomorrow.

“The President has been a supporter of building a strong biobased economy. The U.S. biobased economy is growing in large part from the innovation and commercial development of the industrial biotechnology sector. Biorefineries that deploy biotechnology to convert renewable agricultural feedstocks and other organic raw material to chemicals and biofuels or more cleanly manufacture consumer products can help revitalize U.S. manufacturing and generate high-quality jobs. Growth of the bioeconomy can strengthen our nation’s economic security and energy security by reducing dependence on foreign oil. And it could improve the health of our nation’s citizens and its environmental health through more efficient manufacturing.

“America is the world leader in biotechnology. Our nation’s biotechnology industry is comprised of scientists, entrepreneurs, and large and small companies in all 50 states engaged in translating the latest scientific discoveries into innovative new medical therapies and environmental products, increased agricultural production and farm incomes, and greener bio-based products and biofuels. Nationwide, our industry directly employs more than 1.4 million people and indirectly generates jobs for an additional 6.6 million people. These are high-quality jobs, paying substantially more than the average U.S. wage.

“Realizing the promise of biotechnology requires a comprehensive national strategy that fine-tunes some policies and overhauls others. The biotechnology sector continues to stand ready to work with President Obama, his Administration and the Congress to help create jobs and drive economic growth.”

Ren calls his technique “individual-particle electron tomography,” or IPET. The work is described in PLoS One: “IPET and FETR: Experimental Approach for Studying Molecular Structure Dynamics by Cryo-Electron Tomography of a Single-Molecule Structure.”

The 3-D images reported in the paper include those of a single IgG antibody and apolipoprotein A-1 (ApoA-1), a protein involved in human metabolism. Ren’s goal is to produce individual 3-D images of medically significant proteins, such as HDL— the heart-protective “good cholesterol” whose structure has eluded the efforts of legions of scientists armed with far more powerful protein modeling tools. “We are well on our way,” says Ren.

Ren has the credentials of one who knows what he can do. He was recruited to work at Berkeley Lab in August 2010 from the University of California at San Francisco, where he had used a cryo-electron microscope and more conventional averaging techniques to discern the 3-D structure of LDL – the “bad cholesterol” thought to be a major risk factor for heart disease.

His images of single proteins are a bit fuzzy, even after they are cleaned up by complex computer filtering, but very informative to the trained observer. These individual particles are extraordinarily tiny, requiring Ren to zero in on a spot of less than 20 nanometers. He has reported protein images as small as 70 kDa. That’s kilodaltons, a Lilliputian scale (expressed in units of mass) set aside for taking the measure of atoms, molecules, and snippets of DNA. It’s a more useful way to size soft objects like proteins that can be clumped, stringy, or floppy.

Unlike the sculptural images of protein models, a suite of these photographs can convey a sense of these particles in all their nanoscale floppiness. Within the complex structure of these proteins lies the secrets of their function, and perhaps keys to drugs that block bad ones and promote good ones. With some additional computer filtering, a high-contrast model of protein can be generated from the images and animated to show its moving parts in 3-D.