Toward a New Generation of Superplastics

Scientists are reporting an in-depth validation of the discovery of the world's first mass producible, low-cost, organoclays for plastics. The powdered material, made from natural clay, would be a safer, more environmentally friendly replacement for the compound widely used to make plastics nanocomposites.

would not exist.

However, quaternary amine organoclays are difficult to produce because of the health and environmental risks associated with quaternary amines, as well as the need to manufacture them in small batches. These and other disadvantages, including high cost, limit use of the materials.

The new organoclay uses resorcinol diphenyl phosphate (which is normally a flame retardant), to achieve mass producible organoclays which can be made in continuous processing. In addition these organoclays are cheaper, generate less dust, and are thermostable to much higher temperatures (beyond 600 degrees Fahrenheit). This clay has also been proven to be superior for flame retardance applications. In addition, unlike most quaternary amine based organoclays, it works well in styrene plastics, one of the most widely used kinds of plastic.

Journal Reference:

1. Seongchan Pack, Takashi Kashiwagi, Changhong Cao, Chad S. Korach, Menachem Lewin, Miriam H. Rafailovich. Role of Surface Interactions in the Synergizing Polymer/Clay Flame Retardant Properties. Macromolecules, 2010; 43 (12): 5338 DOI: 10.1021/ma100669g

Courtesy: ScienceDaily

Sea Lamprey Research Sheds Light on How Stress Hormones Evolved

Michigan State University researchers are the first to identify a stress hormone in the sea lamprey, using the 500 million-year-old species as a model to understand the evolution of the endocrine system.

Corticosteroid hormones control stress response in animals with backbones, including humans. While scientists have learned quite a bit about these so-called stress hormones in most modern animals, little was known about the hormones' earliest forms in prehistoric creatures such as lamprey.

"By identifying 11-deoxycortisol as a stress hormone in lamprey, it allows us to better understand how the endocrine system in vertebrates evolved into the complex systems we see in humans today," explained Weiming Li, professor of fisheries and wildlife who helped lead the project. Li also is a member of the Michigan Agricultural Experiment Station.

The hormone is the only one the researchers have found so far in the lamprey and Li said the researchers are hypothesizing that it may be the only corticosteroid hormone in the lamprey. Humans, in contrast, have more than 30 corticosteroid hormones.

The research is published in the July 19 edition of the Proceedings of the National Academy of Sciences.

Native to the Atlantic Ocean, sea lampreys are invasive species in the Great Lakes. They stay alive by attaching themselves to other fish, such as salmon and trout, and then suck out the fish's body fluids. One sea lamprey can kill 40 or more pounds of fish. The U.S. and Canadian governments spend about $10 million to $15 million per year on lamprey control.

Li led the groundbreaking research that identified the pheromone male lampreys use to attract females to their nests to mate. He has made a synthetic version of the pheromone and is testing its effectiveness as a control for the destructive parasites. While the identification of 11-deoxycortisol likely won't directly help his lamprey control work, Li said this new discovery will bolster understanding on how the fish has successfully adapted since the Paleozoic Era.

"Most jawless animals similar to the lamprey didn't survive into the modern era, so they're not available for us to use as we strive to learn more about how human systems developed," Li said. "The sea lamprey, a survivor, gives us a snapshot of what happened as vertebrates evolved into the animals we know today."

Li and his team plan to continue studying the lamprey, possibly investigating how the endocrine and other body systems became more integrated and successfully adapted to the changing environment.

Other paper authors are David Close, former doctoral student in Li's lab, now at the University of British Columbia; Sang-Seon Yun, former post-doctoral researcher now at Kunsan National University in Korea; Stephen McCormick, of U.S. Geological Survey Conte Anadromous Fish Research Center; and Andrews Wildbill, MSU undergraduate student.

The research is supported by the National Science Foundation, the Confederated Tribes of the Umatilla Indian Reservation, the Bonneville Power Administration, the Great Lakes Fishery Commission, the MSU College of Agriculture and Natural Resources, and the National Institute of Mental Health.

Li's research also is supported by the Michigan Agricultural Experiment Station.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Michigan State University.

Courtesy: ScienceDaily

How Do Cells Die? Biophotonic Tools Reveal Real-Time Dynamics in Living Color

Apoptosis, programmed cell death, is essential to normal development, healthy immune system function, and cancer prevention. The process dramatically transforms cellular structures but the limitations of conventional microscopy methods have kept much about this structural reorganization a mystery.

Now, in research featured on the cover of the current issue of Proceedings of the National Academy of Sciences, University at Buffalo scientists have developed a biophotonic imaging approach capable of monitoring in real-time the transformations that cellular macromolecules undergo during programmed cell death.

The work could help realize the potential of customized molecular medicine, in which chemotherapy, for example, can be precisely targeted to cellular changes exhibited by individual patients. It can also be a valuable drug development tool for screening new compounds.

"This new ability provides us with a dynamic mapping of the transformations occurring in the cell at the molecular level," says study co-author Paras N. Prasad, PhD, executive director of the UB Institute for Lasers, Photonics and Biophotonics (ILPB) and SUNY Distinguished Professor in the departments of Chemistry, Physics, Electrical Engineering and Medicine. "It provides us with a very clear visual picture of the dynamics of proteins, DNA, RNA and lipids during the cell's disintegration."

Prasad notes that molecular medicine, in which treatments or preventive measures can be tailored to cellular properties exhibited by individual patients, depends on much better methods of visualizing what's happening during critical cellular processes.

"This research helps improve our understanding of cellular events at the molecular level," he says. "If we know that specific molecular changes constitute an early signature of a disease, or what changes may predispose a patient to that disease, then we can take steps to target treatment or even prevent the disease from developing in the first place."

To capture the cellular images, the interdisciplinary UB team of biologists, chemists and physicists, led by Prasad, utilized an advanced biophotonic approach that combines three techniques: a nonlinear, optical imaging system (CARS or Coherent anti-Stokes Raman scattering), TPEF (two-photon excited fluorescence), which images living tissue and cells at deep penetration and Fluorescence Recovery after Photobleaching to measure dynamics of proteins.

"For the first time, this approach allows us to monitor in a single scan, four different types of images, characterizing the distribution of proteins, DNA, RNA and lipids in the cell," says Aliaksandr V. Kachynski, PhD, research associate professor at the ILPB and co-author.

The resulting composite image integrates in one picture the information on all four types of biomolecules, with each type of molecule represented by a different color: proteins in red, RNA in green, DNA in blue and lipids in grey, as shown on the PNAS cover.

Multiplex imaging provided new information on the rate at which proteins diffuse through the cell nucleus, the UB scientists say.

Before apoptosis was induced, the distribution of proteins was relatively uniform, but once apoptosis develops, nuclear structures disintegrate, the proteins become irregularly distributed and their diffusion rate slows down, says Artem Pliss, PhD, research assistant professor at the ILPB and co-author on the paper.

"This research gives us the unique ability to study and improve our understanding of individual subcellular structures and the transformations they go through," says Pliss.

Such precise information will be especially useful for monitoring how specific cancer drugs affect individual cells.

"For example, say drug therapy is being administered to a cancer patient; this system will allow for the monitoring of cellular changes throughout the treatment process," notes Kachynski. "Clinicians will be able to determine the optimal conditions to kill a cancer cell for the particular type of disease. An improved understanding of the drug-biomolecule interactions will help discover the optimal treatment doses so as to minimize side effects."

Andrey Kuzmin, PhD, research assistant professor at the ILPB and co-author, adds that a new paper from the UB team, forthcoming in Biophysical Journal, further extends this work.

"The benefits of the UB multiplex imaging system and its molecular selectivity have been further extended into a new fundamental cellular study, structural reorganization throughout the mitotic cell cycle," he says.

The work was supported by a grant from the John R. Oishei Foundation of Buffalo, N.Y.

The researchers are active participants in the strategic strength in Integrated Nanostructured Systems identified in the UB 2020 strategic plan for academic, research and service excellence.

Journal Reference:

1. Artem Pliss, Andrey N. Kuzmin, Aliaksandr V. Kachynski, and Paras N. Prasad. Biophotonic probing of macromolecular transformations during apoptosis. Proceedings of the National Academy of Sciences, 2010; 107 (29): 12771-12776 DOI: 10.1073/pnas.1006374107

Courtesy: ScienceDaily

Database for Personalised Cancer Treatment: Largest Study of Genomes and Cancer Treatments Releases First Results

The largest study to correlate genetics with response to cancer drugs releases its first results. The researchers behind the study, based at Massachusetts General Hospital Cancer Center and the Wellcome Trust Sanger Institute, describe in this initial dataset the responses of 350 cancer samples to 18 anticancer therapeutics.

These first results, made freely available on the Genomics of Drug Sensitivity website (http://www.sanger.ac.uk/genetics/CGP/translation/), will help cancer researchers around the world to seek better understanding of cancer genetics and could help to improve treatment regimens.

"Today is our first glimpse of this complex interface, where genomes meet cancer medicine," says Dr Andy Futreal, co-leader of the Cancer Genome Project at the Wellcome Trust Sanger Institute. "We will, over the course of this work, add to this picture, identifying genetic changes that can inform clinical decisions, with the hope of improving treatment.

"By producing a carefully curated set of data to serve the cancer research community, we hope to produce a database for improving patient response during cancer treatment."

How a patient responds to anticancer treatment is known to be determined in large part by the combination of mutations in her or his cancer cells. The better this relationship is understood, the better treatment can be targeted to the particular tumour.

The aim of the five-year, international drug-sensitivity study is to find the best combinations of treatments for a wide range of cancer types: roughly 1000 cancer cell lines will be exposed to 400 anticancer treatments, alone or in combination, to determine the most effective drug or combination of drugs in the lab.

The therapies include known anticancer drugs as well as others in pre-clinical development.

To make the study as comprehensive as possible, the researchers have selected 1000 genetically characterised cell lines that include common cancers such as breast, colorectal and lung. Each cell line has been genetically fingerprinted and this data will also be publicly available on the website. Importantly, the researchers will take promising leads from the cancer samples in the lab to be verified in clinical specimens: the findings will be used to design clinical studies in which treatment will be selected based on a patient's cancer mutation spectrum.

The newly released data draw on large-scale analyses of cancer genomes to identify genomic markers of sensitivity to anticancer drugs.

The first data release confirms several genes that predict therapeutic response in different cancer types. These include sensitivity of melanoma, a deadly form of skin cancer, with activating mutations in the gene BRAF to molecular therapeutics targeting this protein, a therapeutic strategy that is currently being exploited in the clinical setting. These first results provide a striking example of the power of this approach to identify genetic factors that determine drug response.

"It is very encouraging that we are able to clearly identify drug-gene interactions that are known to have clinical impact at an early stage in the study," says Dr Ultan McDermott, Faculty Investigator at the Wellcome Trust Sanger Institute. "It suggests that we will discover many novel interactions even before we have the full complement of cancer cell lines and drugs screened.

"We have already studied more gene mutation-drug interactions than any previous work but, more importantly, we are putting in place a mechanism to ensure rapid dissemination of our results to enable worldwide collaborative research. By ensuring that all the drug sensitivity data and correlative analysis is freely available in an easy-to-use website, we hope to enable and support the important work of the wider community of cancer researchers."

Further results from this study should, over its five-year term, identify interactions between mutations and drug sensitivities most likely to translate into benefit for patients: at the moment we do not have sufficient understanding of the complexity of cancer drug response to optimise treatment based on a person's genome.

"We need better information linking tumour genotypes to drug sensitivities across the broad spectrum of cancer heterogeneity, and then we need to be in position to apply that research foundation to improve patient care," says Professor Daniel Haber, Director of the Cancer Centre at Massachusetts General Hospital and Harvard Medical School. "The effectiveness of novel targeted cancer agents could be substantially improved by directing treatment towards those patients that genetic study suggests are most likely to benefit, thus 'personalising' cancer treatment."

The comprehensive results include correlating drug sensitivity with measurements of mutations in key cancer genes, structural changes in the cancer cells (copy number information) and differences in gene activity, making this the largest project of its type and a unique resource for cancer researchers around the world.

"This is one of the Sanger Institute's first large-scale explorations into the therapeutics of human disease," says Professor Mike Stratton, co-leader of the Cancer Genome Project and Director of the Wellcome Trust Sanger Institute. "I am delighted to see the early results from our partnership with the team at Massachusetts General Hospital. Collaboration is essential in cancer research: this important project is part of wider efforts to bring international expertise to bear on cancer."

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Wellcome Trust Sanger Institute.

Scientists Identify Molecular Predictor of Prognosis for Pancreatic Cancer Patients

Pancreatic cancer is one of the most challenging tumors to treat. Identifying patients who have more aggressive disease could better inform treatment decisions and predict survival prognosis. A new finding from scientists at UNC Lineberger Comprehensive Cancer Center may help.

The team analyzed gene profiles of pancreatic tumors from patients with both localized and metastasized disease. They identified a six-gene "signature" associated with metastatic disease. Their study is the first to demonstrate that molecular differences in metastatic pancreatic cancer can be identified at earlier stages and that these differences are predictive of future disease behavior. This finding, if verified in further clinical studies, could help patients and physicians make more informed decisions about treatment and could offer new research opportunities into potential therapeutic targets to treat the disease.

Their findings were reported in the July 2010 issue of PLoS Medicine, published by the Public Library of Science.

"In our study we showed our six-gene signature to be superior to current methods used to stage disease and estimate prognosis," says study senior author, Jen Jen Yeh, MD, assistant professor of surgery and pharmacology at the UNC School of Medicine. "If we can better stage patients' disease, we can better determine those who may benefit most from chemotherapy before surgery or from surgery alone. As more therapies become available, this signature may be used to tailor treatment options."

Pancreatic cancer is often not diagnosed until it is advanced because the most common tumor type -- called pancreatic ductal adenocarcimona, that comprises over 90 percent of all pancreatic cancer -- rarely causes early noticeable symptoms. Survival rates for cancer that has spread are poor, on average only five to eight months. At present, treatment decisions and clinical prognosis are based on tumor size and lymph node status.

Study scientists compared and evaluated 30 tumor samples from patients with early and late-stage disease and identified the six-gene signature associated with late-stage disease. They then tested the prognostic value of this signature on a group of 67 patients with localized pancreatic cancer and confirmed the validity of the signature to identify patients with high-risk, aggressive disease.

At present, the only possibility of cure for pancreatic cancer is surgery which involves removal of the tumor, usually the head of the pancreas, part of the small intestine, a portion of the stomach, and other nearby tissues, a method called a Whipple procedure.

Says Yeh, "If patients have high risk, aggressive disease, this signature may be helpful for consideration of chemotherapy before surgery or, if patients are at increased risk for complications from the surgery, this information may help them decide whether or not to have the surgery."

Other UNC scientists are: Channing Der, PhD, and Jeran Stratford, PhD, from the department of pharmacology; Leigh Thorne, MD, from the department of pathology and laboratory medicine; Benjamin Calvo, MD; Hong Jin Kim, MD; and Jonathan Samuel, MD, from the department of surgery; Chuck Perou, PhD, from the department of genetics; J.S. Marron, PhD, department of biostatistics; Keith Volmar, MD, clinical pathologist at Rex Hospital, and Laura Caskey, research specialist, and Cheng Fan, research associate.

Other research team scientists are from UNC, Northwestern University, Chicago, IL; Eppley Cancer Institute, Omaha, NE; Northshore University HealthSystem, Baltimore MD; and Johns Hopkins Medical Institutions, Baltimore, MD.

Journal Reference:

1. Jeran K Stratford, David J Bentrem, Judy M Anderson, Cheng Fan, Keith A Volmar, J S Marron, Elizabeth D Routh, Laura S Caskey, Jonathan C Samuel, Channing J Der, Leigh B Thorne, Benjamin F Calvo, Hong Jin Kim, Mark S Talamonti, Christine A Iacobuzio-Donahue, Michael A Hollingsworth, Charles M Perou, Jen Jen Yeh. A Six-Gene Signature Predicts Survival of Patients with Localized Pancreatic Ductal Adenocarcinoma. PLoS Medicine, 2010; DOI: 10.1371/journal.pmed.1000307

Courtesy: ScienceDaily

Scientists Identify Molecular Predictor of Prognosis for Pancreatic Cancer Patients

Pancreatic cancer is one of the most challenging tumors to treat. Identifying patients who have more aggressive disease could better inform treatment decisions and predict survival prognosis. A new finding from scientists at UNC Lineberger Comprehensive Cancer Center may help.

The team analyzed gene profiles of pancreatic tumors from patients with both localized and metastasized disease. They identified a six-gene "signature" associated with metastatic disease. Their study is the first to demonstrate that molecular differences in metastatic pancreatic cancer can be identified at earlier stages and that these differences are predictive of future disease behavior. This finding, if verified in further clinical studies, could help patients and physicians make more informed decisions about treatment and could offer new research opportunities into potential therapeutic targets to treat the disease.

Their findings were reported in the July 2010 issue of PLoS Medicine, published by the Public Library of Science.

"In our study we showed our six-gene signature to be superior to current methods used to stage disease and estimate prognosis," says study senior author, Jen Jen Yeh, MD, assistant professor of surgery and pharmacology at the UNC School of Medicine. "If we can better stage patients' disease, we can better determine those who may benefit most from chemotherapy before surgery or from surgery alone. As more therapies become available, this signature may be used to tailor treatment options."

Pancreatic cancer is often not diagnosed until it is advanced because the most common tumor type -- called pancreatic ductal adenocarcimona, that comprises over 90 percent of all pancreatic cancer -- rarely causes early noticeable symptoms. Survival rates for cancer that has spread are poor, on average only five to eight months. At present, treatment decisions and clinical prognosis are based on tumor size and lymph node status.

Study scientists compared and evaluated 30 tumor samples from patients with early and late-stage disease and identified the six-gene signature associated with late-stage disease. They then tested the prognostic value of this signature on a group of 67 patients with localized pancreatic cancer and confirmed the validity of the signature to identify patients with high-risk, aggressive disease.

At present, the only possibility of cure for pancreatic cancer is surgery which involves removal of the tumor, usually the head of the pancreas, part of the small intestine, a portion of the stomach, and other nearby tissues, a method called a Whipple procedure.

Says Yeh, "If patients have high risk, aggressive disease, this signature may be helpful for consideration of chemotherapy before surgery or, if patients are at increased risk for complications from the surgery, this information may help them decide whether or not to have the surgery."

Other UNC scientists are: Channing Der, PhD, and Jeran Stratford, PhD, from the department of pharmacology; Leigh Thorne, MD, from the department of pathology and laboratory medicine; Benjamin Calvo, MD; Hong Jin Kim, MD; and Jonathan Samuel, MD, from the department of surgery; Chuck Perou, PhD, from the department of genetics; J.S. Marron, PhD, department of biostatistics; Keith Volmar, MD, clinical pathologist at Rex Hospital, and Laura Caskey, research specialist, and Cheng Fan, research associate.

Other research team scientists are from UNC, Northwestern University, Chicago, IL; Eppley Cancer Institute, Omaha, NE; Northshore University HealthSystem, Baltimore MD; and Johns Hopkins Medical Institutions, Baltimore, MD.

Journal Reference:

1. Jeran K Stratford, David J Bentrem, Judy M Anderson, Cheng Fan, Keith A Volmar, J S Marron, Elizabeth D Routh, Laura S Caskey, Jonathan C Samuel, Channing J Der, Leigh B Thorne, Benjamin F Calvo, Hong Jin Kim, Mark S Talamonti, Christine A Iacobuzio-Donahue, Michael A Hollingsworth, Charles M Perou, Jen Jen Yeh. A Six-Gene Signature Predicts Survival of Patients with Localized Pancreatic Ductal Adenocarcinoma. PLoS Medicine, 2010; DOI: 10.1371/journal.pmed.1000307

Courtesy: ScienceDaily

Early Alzheimer's Identification Method Discovered

Abnormal brain images combined with examination of the composition of the fluid that surrounds the spine may offer the earliest signs identifying healthy older adults at risk of developing Alzheimer's disease, well before cognitive problems emerge, a study by researchers at UC Davis has found.

"Our findings indicate that a distinctive pattern of imaging and biomarker deviations from typical adults may be an early warning sign of neurobiological pathology and an early sign of Alzheimer's disease," said Laurel Beckett, a professor of public health sciences at UC Davis and the lead study author. "By the time people get diagnosed with Alzheimer's using cognitive tests, there's already a lot of brain damage. We hope that in the future methods that combine brain imaging and biomarker assessments can push the diagnosis back, while learning more about the mechanisms causing Alzheimer's disease, so we can develop better treatments."

Published in the journal Neurobiology of Aging in June, the study analysis picked out a subgroup of healthy adults who later would experience a decline in memory performance typical of early Alzheimer's disease long before other study participants.

For the study, Beckett and her team used data from the Alzheimer's Disease Neuroimaging Initiative, which provides researchers with access to brain scans, clinical data and other laboratory results from spinal fluid and blood tests from more than 800 older adults. Some study participants began with a clean slate of cognitive health, some with mild cognitive impairment -- a condition that often presages Alzheimer's -- and others with mild or moderate Alzheimer's disease.

The researchers analyzed data from 220 normal older adults who had undergone structural magnetic resonance imaging (MRI) and clinical examinations. About half also provided spinal fluid samples. Among the 96 participants, cluster analysis identified three distinct subgroups of individuals based solely on their baseline imaging and laboratory measures. During the next three years, few of these healthy people showed any cognitive change. But cognitive tests for people in one of the subgroups -- about 10 percent of the sample -- declined at nearly five times the rate as healthy older adults. The researchers believe this group, which had the most extreme MRI and spinal fluid measurements, may represent the earliest stages of subclinical cognitive decline and Alzheimer's disease.

Beckett said that the finding is an important step toward discovering the constellation of imaging and fluid biomarkers that foreshadow cognitive decline, as well as a means of determining whether new treatments are effective.

"The problem with current clinical trials is that we don't know who is on the edge of experiencing dementia. And even if we did, how would we know if a treatment was working, since they haven't shown any clinical problems?" Beckett said. "This method could improve clinical trials for prevention and reduce the numbers of study participants necessary to speed drug discovery -- and eventually change how the pharmaceutical industry and National Institutes of Health conduct Alzheimer's disease clinical trials."

Other study authors include Jasmine Nettiksimmons, Danielle Harvey, Owen Carmichael and Charles DeCarli of UC Davis; James Brewer of UC San Diego; Clifford R. Jack Jr. and Ronald Petersen of the Mayo Clinic College of Medicine; and Leslie Shaw, John Trojanowski and Michael Weiner of UC San Francisco.

The study was funded by the Alzheimer's Disease Neuroimaging Initiative, the National Institutes of Health and the Dana Foundation.

Journal Reference:

1. J. Nettiksimmons, D. Harvey, J. Brewer, O. Carmichael, C. DeCarli, C.R. Jack Jr, R. Petersen, L.M. Shaw, J.Q. Trojanowski, M.W. Weiner. Subtypes based on cerebrospinal fluid and magnetic resonance imaging markers in normal elderly predict cognitive decline. Neurobiology of Aging, 2010; 31 (8): 1419 DOI: 10.1016/j.neurobiolaging.2010.04.025

Courtesy: ScienceDaily

Scientists Use Computer Algorithms to Develop Seasonal Flu Vaccines

Defeating the flu is challenging because the virus responsible for the disease undergoes frequent changes of its genetic code, making it difficult for scientists to manufacture effective vaccines for the seasonal flu in a timely manner.

Now, a University of Miami (UM) computer scientist, Dimitris Papamichail, and a team of researchers from Stony Brook University have developed a rapid and effective approach to produce vaccines for new strains of influenza viruses. The researchers hope to develop the new technology and provide an efficient method to confront the threat of seasonal epidemics.

The novel approach uses computer algorithms created by Papamichail and scientists from Stony Brook University to design viruses that serve as live vaccines, which are then synthesized to specification. The new method is called Synthetic Attenuated Virus Engineering (SAVE). The findings are available in a study titled "Live attenuated influenza virus vaccines by computer-aided rational design," now available as an advance online publication by Nature Biotechnology.

"We have been able to produce an entirely novel method to systematically design vaccines using computer algorithms," says Papamichail, assistant professor of Computer Science in the College of Arts and Sciences at UM and co-author of the study. "Our approach is not only useful for influenza; it is also applicable to a wide range of viruses."

One way to make an anti-viral vaccine is to weaken a virus to the point where it cannot cause sickness, and then use the weakened virus as a live vaccine. Although such weakened viruses often make very effective vaccines, they suffer from the possibility that the virus can sometimes mutate to regain virulence.

In this study, the researchers used a novel approach to weaken the influenza virus: they made a synthetic genome of the virus containing hundreds of changes to its genetic code. The computer algorithms indicate the best places in the genome to make the changes, such that the new synthetic genome encodes exactly the same proteins as the wild-type genome, but in lesser quantities.

This process allows a wide margin of safety, explains Papamichail. "The probability of all the changes reverting themselves to produce a virulent strain is extremely unlikely," he says.

Although the new sequence and the original sequence both direct the synthesis of exactly the same proteins, the new sequence gives a weakened version of the virus; for that reason the live vaccine is capable of eliciting an immune reaction against the wild-type virus, but is not strong enough to cause disease symptoms. This method used to weaken the influenza virus is a general one, and may allow the creation of safe, effective vaccines against many different types of viruses.

In the future, the researchers would like to explore the applicability of their techniques, with the ultimate goal of methodically and computationally design from scratch synthetic organisms with predetermined functions and controlled properties, with broad applications in medicine.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Miami.

Courtesy: ScienceDaily

Gene Knockout Makes Female Mice Masculine

The mammalian fucose mutarotase enzyme is known to be involved in incorporating the sugar fucose into protein. Female mice that lack the fucose mutarotase (FucM) gene refuse to let males mount them, and will attempt copulation with other female mice. Researchers writing in BioMed Central's open access journal BMC Genetics created the FucM mouse mutants in order to investigate the role of this enzyme in vivo.

Chankyu Park worked with a team of researchers from the Korea Advanced Institute of Science and Technology and intriguingly gained some insight into the neurological basis of sexual preference. He said, "The FucM knockout mice displayed drastically reduced sexual receptivity, although pregnancy after forced mating attempts by normal sexually experienced males showed that the animals were fertile. The FucM knock-out mice have reduced levels of alpha-fetoprotein, a protein thought to be involved in development of parts of the brain responsible for reproductive behavior."

The mutant female mice were healthy, and behaved normally towards young mice. When approached by male mice, however, they would not adopt the sexually receptive 'lordosis' position. Furthermore, they lost interest in investigating male urine, unlike normal females, and would attempt to mount other females.

Speaking about the results, Park said, "We speculate that these behavioural changes are likely to be related to a neurodevelopmental change in pre-optic area of the female mutant brain , becoming similar to that of a normal male."

Journal Reference:

1. Dongkyu Park, Dongwook Choi, Junghoon Lee, Dae-sik Lim, Chankyu Park. Male-like sexual behavior of female mouse lacking fucose mutarotase. BMC Genetics, 2010; 11 (1): 62 DOI: 10.1186/1471-2156-11-62

Courtesy: ScienceDaily

Origins of Multicellularity: All in the Family

One of the most pivotal steps in evolution-the transition from unicellular to multicellular organisms-may not have required as much retooling as commonly believed, found a globe-spanning collaboration of scientists led by researchers at the Salk Institute for Biological Studies and the US Department of Energy's Joint Genome Institute.

A comparison of the genomes of the multicellular algae Volvox carteri and its closest unicellular relative Chlamydomonas reinhardtii revealed that multicellular organisms may have been able to build their more complex molecular machinery largely from the same list of parts that was already available to their unicellular ancestors.

"If you think of proteins in terms of lego bricks Chlamydomonas already had a great lego set," says James Umen, Ph.D., assistant professor in the Plant Molecular and Cellular Biology Laboratory at the Salk Institute. "Volvox didn't have to buy a new one, and instead could experiment with what it had inherited from its ancestor."

Altogether the findings, published in the journal Science, suggest that very limited protein-coding innovation occurred in the Volvox lineage. "We expected that there would be some major differences in genome size, number of genes, or gene families sizes between Volvox and Chlamydomonas," says Umen. "Mostly that turned out not to be the case."

The evolution of multicellularity occurred repeatedly and independently in diverse lineages including animals, plants, fungi, as well as green and red algae. "This transition is one of the great evolutionary events that shaped life on earth," says co-first author Simon E. Prochnik, Ph.D., a Computationial Scientist at the DOE Joint Genome Institute. "It has generated much thought and speculation about what makes multicellular organisms different or more complex than their unicellular ancestors."

In most cases the switch from a solitary existence to a communal one happened so long ago-over 500 million years-that the genetic changes enabling it are very difficult to trace. An interesting exception to the rule are volvocine green algae. For them, the transition to multicellularity happened in a series of small, potentially adaptive changes, and the progressive increase in morphological and developmental complexity can still be seen in contemporary members of the group (see slide show).

Volvox, the most sophisticated member of the lineage, is believed to have evolved from a Chlamydomonas-like ancestor within the last 200 million years, making the two living organisms an appealing model to study the evolutionary changes that brought about multicellularity and cellular differentiation.

To gather data for the comparative genomic analysis, the researchers sequenced the 138 million base pair Volvox genome using a whole genome shotgun strategy. The genome itself is 17% larger than the previously sequenced genome of Chlamydomonas and the sequence divergence between the two is comparable to that between human and chicken.

Despite the modest increase in genome size, the number of predicted proteins turned out to be very similar for the two organisms (14,566 in Volvox vs. 14,516 in Chlamydomonas) and no significant differences could be identified in the repertoires of protein domains or domain combinations. Protein domains are parts of proteins that can evolve, function, and exist independently of the rest of the protein chain.

"This was somewhat unexpected," explains Umen, "since innovation at the domain level was previously thought to play a role in the evolution of multicellularity in the plant and animal lineages."

In contrast to the overall lack of innovation, protein families specific to volvocine algae, such as extracellular matrix proteins, were enriched in Volvox compared to Chlamydomonas. Each mature Volvox colony is composed of numerous flagellated cells similar to Chlamydomonas, which are embedded in the surface of a spheroid of elaborately patterned extracellular matrix (ECM) that is clearly related to the Chlamydomonas cell wall. Maybe not surprisingly, the difference in size and complexity between the Volvox extracellular matrix and Chlamydomonas cell wall is mirrored by a dramatic increase in the number and variety of Volvox genes for two major ECM protein families, pherophorins and VMPs.

Additionally, Umen and his collaborators identified an increase in the number of cyclin D proteins in Volvox, which govern cell division and may be necessary to ensure the complex regulation of cell division during Volvox development. Last but not least, Volvox adapted a few of its existing genes to acquire novel functions. Members of the pherophorin family, for one, not only help build the extracellular matrix; some subtypes evolved into a diffusible hormonal trigger for sexual differentiation.

Researchers who also contributed to this work include Alan Kuo, Uffe Hellsten, Jarrod Chapman, Astrid Terry, Jasmyn Pangilinan, Asaf Salamov, Harris Shapiro, Erika Lindquist, Susan Lucas, Igor V Grigoriev, Harris Shapiro and Daniel S. Rokhsar at U.S. Department of Energy Joint Genome Institute in Walnut Creek, Patrick Ferris at the Salk Institute for Biological Studies, Aurora Nedelcu at the University of New Brunswick in Fredericton, Canada, Arman Hallmann at the University of Bielefeld, Germany, Stephen M. Miller at the University of Maryland, Baltimore, Ichiro Nishii at the Nara Women's University in Nara-shi, Japan, Lillian K. Fritz-Laylin at the Center for Integrative Genomics, Berkeley, Oleg Simakov at the EMBL in Heidelberg, Germany, Stefan A. Rensing at the University of Freiburg, Germany, Vladimir Kapitonov and Jerzy Jurka at the Genetic Information Research Institute in Mountain View, Jeremy Schmutz at the HudsonAlpha Institute in Huntsville, Rüdiger Schmitt at the University of Regensburg, Germany and David Kirk at Washington University in St. Louis.

Journal Reference:

1. Simon E. Prochnik, James Umen, Aurora M. Nedelcu, Armin Hallmann, Stephen M. Miller, Ichiro Nishii, Patrick Ferris, Alan Kuo, Therese Mitros, Lillian K. Fritz-Laylin, Uffe Hellsten, Jarrod Chapman, Oleg Simakov, Stefan A. Rensing, Astrid Terry, Jasmyn Pangilinan, Vladimir Kapitonov, Jerzy Jurka, Asaf Salamov, Harris Shapiro, Jeremy Schmutz, Jane Grimwood, Erika Lindquist, Susan Lucas, Igor V. Grigoriev, Rüdiger Schmitt, David Kirk, and Daniel S. Rokhsar. Genomic Analysis of Organismal Complexity in the Multicellular Green Alga Volvox carteri. Science, 2010; 329 (5988): 223-226 DOI: 10.1126/science.1188800

Courtesy: ScienceDaily

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