Newly discovered plant structure may lead to improved biofuel processing

Debra Mohnen, left, is a professor of biochemistry and molecular biology and a member of UGA’s Complex Carbohydrate Research Center. Li Tan is an assistant research scientist with the CCRC.

Athens, Ga. – When Li Tan approached his colleagues at the University of Georgia with some unusual data he had collected, they initially seemed convinced that his experiment had become contaminated; what he was seeing simply didn’t make any sense.

Tan was examining some of the sugars, proteins and polymers that make up plant cell walls, which provide the structural support and protection that allow plants to grow. Yet his samples contained a mixture of sugars that should not be present in the same structure.

However, Tan was convinced that his samples were pure so he and Debra Mohnen, who heads the lab, met again to pore over the data. They came to realize that there were hints in the data of a connection between two different types of cell wall glycans (sugars) and a specific cell wall protein known as arabinogalactan protein. This connection is not known to exist and does not conform to the commonly held scientific definitions of plant cell wall structure.

But Tan and Mohnen, who both work as part of the BioEnergy Science Center, one of three U.S. Department of Energy-funded research centers, were persistent, and they, along with an interdisciplinary team of chemists, molecular biologists and plant experts at UGA, began searching for answers. What they found could redefine our understanding of basic plant biology, and it may lead to significant improvements in the growth and processing of biofuel crops.

Exposure to pesticides in food, air and water increases risk of type 2 diabetes

From left to right, some of the researchers at the University of Granada laboratory: Juan Pedro Arrebola, Francisco Artacho and María Fernández

A study led by the University of Granada reveals that there is a direct relationship between the presence of Persistent Organic Pollutants in the body and the development of type 2 diabetes, regardless of the patient’s age, gender or body mass index.

A study conducted at the University of Granada has revealed that there is a direct relationship between exposure to pesticides (Persistent Organic Pollutants, CPOs) in food, air and water and prevalence of type 2 diabetes in adults, regardless of age, gender and body mass index. These substances tend to concentrate in body fat, and they might be one of the reasons why obese people are more likely to develop diabetes, since the more fat the higher the COP concentrations in the body.

In a paper recently published in the journal Environmental Research, researchers demonstrate that people with higher concentrations of DDE –the main metabolite in the pesticide DDT– are four times more likely to develop type 2 diabetes than other people. In addition, the risk of type 2 diabetes is also associated with exposure to β-HCH (beta-Hexachlorocyclohexane), which is present in the formula of the pesticide Lindano.

University of Pittsburgh Cancer Institute (UPCI) researchers reveal mechanism to halt cancer cell growth, discover potential therapy

Dr. Bennett Van Houten

University of Pittsburgh Cancer Institute (UPCI) researchers have uncovered a technique to halt the growth of cancer cells, a discovery that led them to a potential new anti-cancer therapy.

When deprived of a key protein, some cancer cells are unable to properly divide, a finding described in the cover story of the February issue of the Journal of Cell Science. This research is supported in part by a grant from the National Institutes of Health.

“This is the first time anyone has explained how altering this protein at a key stage in cell reproduction can stop cancer growth,” said Bennett Van Houten, Ph.D., the Richard M. Cyert Professor of Molecular Pharmacology at UPCI and senior author of the research paper. “Our hope is that this discovery will spur the development of a new type of cancer drug that targets this process and could work synergistically with existing drugs.”

All cells have a network of mitochondria, which are tiny structures inside cells that are essential for energy production and metabolism. Dynamin-related protein 1 (Drp1) helps mitochondria undergo fission, a process by which they split themselves into two new mitochondria.

In breast or lung cancer cells made to be deficient in Drp1, the researchers observed a huge network of highly fused mitochondria. These cancer cells appear to have stalled during a stage in cell division called G2/M. Unable to divide into new cells, the cancer growth stops. Those cells that do try to divide literally tear their chromosomes apart, causing more stress for the cell.

The cover of the Journal of Cell Science includes a colorful image of a breast cancer cell deficient in Drp1 that is stuck during the process of separating its chromosomes into two identical sets to be divided among two new cells. Lead author Wei Qian, Ph.D., a postdoctoral fellow in Dr. Van Houten’s laboratory, captured the image using a confocal microscope at Pitt’s Center for Biologic Imaging run by Simon Watkins, Ph.D., a co-author of this study.

Scientists at the Monell Center have identified the location and certain genetic characteristics of taste stem cells on the tongue. Identification of progenitors may someday help treat clinical taste dysfunction

Scanning electron microscopy image illustrates the dorsal view of an E15.5 embryonic tongue and papilla types. Black arrowheads point to fungiform papillae on the anterior oral tongue; black arrow points to the single circumvallate papilla in the back. White arrowhead at the tip points to the median furrow. The straight line marks the orientation for sectioning in the sagittal plane. B: H and E stained sagittal section of an E15.5 tongue to illustrate the orientation for all images of tongue sections. Black arrowheads point to fungiform papillae. Scale bars: 250 μm.

Scientists at the Monell Center have identified the location and certain genetic characteristics of taste stem cells on the tongue. The findings will facilitate techniques to grow and manipulate new functional taste cells for both clinical and research purposes.

“Cancer patients who have taste loss following radiation to the head and neck and elderly individuals with diminished taste function are just two populations who could benefit from the ability to activate adult taste stem cells,” said Robert Margolskee, M.D., Ph.D., a molecular neurobiologist at Monell who is one of the study’s authors.

Taste cells are located in clusters called taste buds, which in turn are found in papillae, the raised bumps visible on the tongue’s surface.

Two types of taste cells contain chemical receptors that initiate perception of sweet, bitter, umami, salty, and sour taste qualities. A third type appears to serve as a supporting cell.

A remarkable characteristic of these sensory cells is that they regularly regenerate. All three taste cell types undergo frequent turnover, with an average lifespan of 10-16 days. As such, new taste cells must constantly be regenerated to replace cells that have died.

For decades, taste scientists have attempted to identify the stem or progenitor cells that spawn the different taste receptor cells. The elusive challenge also sought to establish whether one or several progenitors are involved and where they are located, whether in or near the taste bud.

UGA researchers invent new material for warm-white LEDs. Discovery brings hope to the widespread use of LEDs for indoor lighting

Light emitting diodes, more commonly called LEDs, are known for their energy efficiency and durability, but the bluish, cold light of current white LEDs has precluded their widespread use for indoor lighting.

Now, University of Georgia scientists have fabricated what is thought to be the world’s first LED that emits a warm white light using a single light emitting material, or phosphor, with a single emitting center for illumination. The material is described in detail in the current edition of the Nature Publishing Group journal “Light: Science and Applications.”

“Right now, white LEDs are mainly used in flashlights and in automotive lamps, but they give off a bluish, cool light that people tend to dislike, especially in indoor lighting,” said senior author Zhengwei Pan, an associate professor in the department of physics in the UGA Franklin College of Arts and Sciences and in the College of Engineering. “Our material achieves a warm color temperature while at the same time giving highly accurate color rendition, which is something no single-phosphor-converted LED has ever been shown to do.”

Severity of emphysema predicts mortality

HRCT scan imaging of a patient with IPF and emphysema. Upper zones of the lungs showing paraseptal emphysema and mild patchy peripheral reticular lesions (A). Lower zones of the lungs showing patchy peripheral reticular and honeycombing lesions (B).

Severity of emphysema, as measured by computed tomography (CT), is a strong independent predictor of all-cause, cardiovascular, and respiratory mortality in ever-smokers with or without chronic obstructive pulmonary disease (COPD), according to a study from researchers in Norway. In patients with severe emphysema, airway wall thickness is also associated with mortality from respiratory causes.

“Ours is the first study to examine the relationship between degree of emphysema and mortality in a community-based sample and between airway wall thickness and mortality,” said lead author Ane Johannessen, PhD, post-doctoral researcher at Haukeland University Hospital in Bergen, Norway. “Given the wide use of chest CT scans around the world, the predictive value of these measures on mortality risk is of substantial clinical importance.”

Researchers find that simple blood test can help identify trauma patients at greatest risk of death. Study of more than 9,500 patients discovered that some trauma patients are up to 58 times more likely to die than others, regardless of the severity of their original injuries

A simple, inexpensive blood test performed on trauma patients upon admission can help doctors easily identify patients at greatest risk of death, according to a new study by researchers at Intermountain Medical Center in Salt Lake City.

The Intermountain Medical Center research study of more than 9,500 patients discovered that some trauma patients are up to 58 times more likely to die than others, regardless of the severity of their original injuries.

Researchers say the study findings provide important insight into the long-term prognosis of trauma patients, something not previously well understood.

“The results were very surprising,” said Sarah Majercik, MD, an Intermountain Medical Center surgeon and trauma researcher, whose team discovered that a tool developed at Intermountain Medical Center, called the Intermountain Risk Score, can predict mortality among trauma patients.

Dr. Majercik will present the findings from the study Friday at the 27th annual Scientific Session of the Eastern Association for the Surgery of Trauma in Phoenix.

A quantum leap in gene therapy of Duchenne muscular dystrophy

Dongsheng Duan, University of Missouri, and his research team have been able to reduce muscle disease and improve muscle strength in a dystrophic dog.
Credit: Christian Basi/University of Missouri

Usually, results from a new study help scientists inch their way toward an answer whether they are battling a health problem or are on the verge of a technological breakthrough. Once in a while, those results give them a giant leap forward. In a preliminary study in a canine model of Duchenne muscular dystrophy (DMD), University of Missouri scientists showed exactly such a leap using gene therapy to treat muscular dystrophy. The results of the study will be published in the journal Molecular Therapy on Jan. 15, 2013.

Muscular dystrophy occurs when damaged muscle tissue is replaced with fibrous, bony or fatty tissue and loses function. Duchenne muscular dystrophy is the most common type of muscular dystrophy predominantly affecting boys. Patients with DMD have a gene mutation that disrupts the production of dystrophin, a protein essential for muscle cell survival and function. Absence of dystrophin starts a chain reaction that eventually leads to muscle cell degeneration and death. For years, scientists have been working to find the key to restoring dystrophin, but they have faced many challenges.

Kaiser Permanente study: Change in PSA levels over time can help predict aggressive prostate cancer

Measurements taken over time of prostate specific antigen, the most commonly used screening test for prostate cancer in men, improve the accuracy of aggressive prostate cancer detection when compared to a single measurement of PSA, according to a Kaiser Permanente study published today in the British Journal of Urology International.

The retrospective study examined the electronic health records of nearly 220,000 men ages 45 and older over a 10-year period who had at least one PSA measurement and no previous diagnosis of prostate cancer. The study found that annual percent changes in PSA more accurately predicted the presence of aggressive prostate cancer when compared to single measurements of PSA alone, but only marginally improved the prediction of prostate cancer overall.

“The use of a single, elevated PSA level to screen for prostate cancer is considered controversial given the questionable benefits of PSA screening on prostate cancer mortality. The screening may also result in unnecessary prostate biopsies and subsequent treatments for localized prostate cancer, as it does not distinguish well between slow-growing and aggressive disease,” said Lauren P. Wallner, PhD, MPH, study lead author and post-doctoral research fellow at Kaiser Permanente Southern California’s Department of Research & Evaluation. “Our study demonstrates that repeated measurements of PSA over time could provide a more accurate – and much needed – detection strategy for aggressive forms of prostate cancer.”

Borderline personality disorder: The “perfect storm” of emotion dysregulation

Borderline Personality Disorder (BPD) Abnormal Brain Structures

Originally, the label “borderline personality disorder” was applied to patients who were thought to represent a middle ground between patients with neurotic and psychotic disorders. Increasingly, though, this area of research has focused on the heightened emotional reactivity observed in patients carrying this diagnosis, as well as the high rates with which they also meet diagnostic criteria for posttraumatic stress disorder and mood disorders.

New research now published in Biological Psychiatry from Dr. Anthony Ruocco at the University of Toronto and his colleagues paints perhaps the sharpest picture we have so far of the patterns of brain activity which may underlie the intense and unstable emotional experiences associated with this diagnosis.

In their report, the investigators describe two critical brain underpinnings of emotion dysregulation in borderline personality disorder: heightened activity in brain circuits involved in the experience of negative emotions and reduced activation of brain circuits that normally suppress negative emotion once it is generated.

To accomplish this, they undertook a meta-analysis of previously published neuroimaging studies to examine dysfunctions underlying negative emotion processing in borderline personality disorder. A thorough literature search identified 11 relevant studies from which they pooled the results to further analyze, providing data on 154 patients with borderline personality disorder and 150 healthy control subjects.

Ruocco commented, “We found compelling evidence pointing to two interconnected neural systems which may subserve symptoms of emotion dysregulation in this disorder: the first, centered on specific limbic structures, which may reflect a heightened subjective perception of the intensity of negative emotions, and the second, comprised primarily of frontal brain regions, which may be inadequately recruited to appropriately regulate emotions.”

Researchers identify genetic mutation for rare cancer. Gene sequencing program gives researchers new leads to improve cancer treatment

Dan Robinson, research fellow with the Michigan Center for Translational Pathology
Read: going to a new website Identification of recurrent NAB2-STAT6 gene fusions in solitary fibrous tumor by integrative sequencing

By looking at the entire DNA from this one patient’s tumor, researchers have found a genetic anomaly that provides an important clue to improving how this cancer is diagnosed and treated.

Researchers at the University of Michigan Comprehensive Cancer Center sequenced the tumor’s genome through a new program called MI-ONCOSEQ, which is designed to identify genetic mutations in tumors that might be targeted with new therapies being tested in clinical trials.

The sequencing also allows researchers to find new mutations. In this case, an unusual occurrence of two genes – NAB2 and STAT6 – fusing together. This is the first time this gene fusion has been identified.

“In most cases, mutations are identified because we see them happening again and again. Here, we had only one case of this. We knew NAB2-STAT6 was important because integrated sequencing ruled out all the known cancer genes. That allowed us to focus on what had been changed,” says lead study author Dan R. Robinson, research fellow with the Michigan Center for Translational Pathology.

Once they found the aberration, the researchers looked at 51 other tumor samples from benign and cancerous solitary fibrous tumors, looking for the NAB2-STAT6 gene fusion. It showed up in every one of the samples. Results are published online in Nature Genetics.

“Genetic sequencing is extremely important with rare tumors,” says study co-author Scott Schuetze, M.D., associate professor of internal medicine at the U-M Medical School. “Models of rare cancers to study in the laboratory are either not available or very limited. The sequencing helps us to learn more about the disease that we can use to develop better treatments or to help diagnose the cancer in others.”

The NAB2-STAT6 fusion may prove to be a difficult target for therapies, but researchers believe they may be able to attack the growth signaling cycle that leads to this gene fusion.

“Understanding the changes induced in the cell by the NAB2-STAT6 gene fusion will help us to select novel drugs to study in patients with advanced solitary fibrous tumors. Currently this is a disease for which there are no good drug therapies available and patients are in great need of better treatments,” Schuetze says.

Schizophrenia linked to social inequality. Urban neighbourhoods with high deprivation, population density and inequality found to have higher rates of schizophrenia

Genetic Causes
Schizophrenia has a strong hereditary component. Individuals with a first-degree relative (parent or siblng) who has schizophrenia have 10 percent chance of developing the disorder, as opposed to the 1 percent chance of general population. But schizophrenia is only influenced by genetics, not determined by it. While schizophrenia runs in families, about 60% of schizophrenics have no family members with the disorder. Furthermore, individuals who are genetically predisposed to schizophrenia don’t always develop the disease, which shows that biology is not destiny.
Environmental Causes
Twin and adoption studies suggest that inherited genes make a person vulnerable to schizophrenia and then environmental factors act this vulnerability to trigger the disorder. As for the environmental factors involved, more and more research is pointing to stress, either during pregnancy or at a later stage of development. High levels of stress are believed to trigger schizophrenia by increasing the body ‘s production of the hormone cortisol. Research points to several stress-inducing environmental factors that may be involved in schizophrenia, including:
* Prenatal exposure to a viral infection
* Low oxygen levels during birth (from prolonged labor or premature birth)
* Exposure to a virus during infancy
* Early parental loss or separation
* Physical or sexual abuse in childhood
Abnormal Brain Structures
In addition to abnormal brain chemistry, abnormalities in brain structure may also play a role in schizophrenia. Enlarged brain ventricles are seen in some schizophrenics, indicating a deficit in the volume of brain tissue. There is also evidence of abnormally low activity in the frontal lobe, the area of the brain responsible for planning, reasoning, and decision-making.
Some studies also suggest that abnormalities in the temporal lobes, hippocampus, and amygdala are connected to schizophrenia’s positive symptoms. But despite the evidence of brain abnormalities, it is highly unlikely that schizophrenia is the result of any one problem in any one region of the brain.

Higher rates of schizophrenia in urban areas can be attributed to increased deprivation, increased population density and an increase in inequality within a neighbourhood, new research reveals. The research, led by the University of Cambridge in collaboration with Queen Mary University of London, was published today in the journal Schizophrenia Bulletin.

Dr James Kirkbride, lead author of the study from the University of Cambridge, said: “Although we already know that schizophrenia tends to be elevated in more urban communities, it was unclear why. Our research suggests that more densely populated, more deprived and less equal communities experience higher rates of schizophrenia and other similar disorders. This is important because other research has shown that many health and social outcomes also tend to be optimal when societies are more equal.”

The scientists used data from a large population-based incidence study (the East London first-episode psychosis study directed by Professor Jeremy Coid at the East London NHS Foundation Trust and Queen Mary, University of London) conducted in three neighbouring inner city, ethnically diverse boroughs in East London: City & Hackney, Newham, and Tower Hamlets.

427 people aged 18-64 years old were included in the study, all of whom experienced a first episode of psychotic disorder in East London between 1996 and 2000. The researchers assessed their social environment through measures of the neighbourhood in which they lived at the time they first presented to mental health services because of a psychotic disorder. Using the 2001 census, they estimated the population aged 18-64 years old in each neighbourhood, and then compared the incidence rate between neighbourhoods.

The incidence of schizophrenia (and other similar disorders where hallucinations and delusions are the dominant feature) still showed variation between neighbourhoods after taking into account age, sex, ethnicity and social class. Three environmental factors predicted risk of schizophrenia – increased deprivation (which includes employment, income, education and crime) increased population density, and an increase in inequality (the gap between the rich and poor).

Fertile soil doesn’t fall from the sky. The contribution of bacterial remnants to soil fertility has been underestimated until now

The Damma Glacier, on which a broad range of studies is being conducted, has become an important outdoor laboratory not only for climate researchers, but for ecologists as well. The soil investigated with the samples was between 0 and 120 years old and thus allowed insight into early processes of soil development.
Photo: Christian Schurig/ UFZ
CC BY 3.0 (http://creativecommons.org/licenses/by/3.0/de/)

Leipzig. Remains of dead bacteria have far greater meaning for soils than previously assumed. Around 40 per cent of the microbial biomass is converted to organic soil components, write researchers from the Helmholtz Centre for Environmental Research (UFZ), the Technische Universität Dresden (Technical University of Dresden) , the University of Stockholm, the Max-Planck-Institut für Entwicklungsbiologie (Max Planck Institute for Developmental Biology) and the Leibniz-Universität Hannover (Leibniz University Hannover) in the professional journal Biogeochemistry. Until now It was assumed that the organic components of the soil were comprised mostly of decomposed plant material which is directly converted to humic substances. In a laboratory experiment and in field testing the researchers have now refuted this thesis. Evidently the easily biologically degradable plant material is initially converted to microbial biomass which then provides the source material to soil organic matter.
Soil organic matter represent the largest fraction of terrestrially bound carbon in the biosphere. The compounds therefore play an important role not only for soil fertility and agricultural yields. They are also one of the key factors controlling the concentration of carbon dioxide in the atmosphere. Climatic change can therefore be slowed down or accelerated, according to the management of the soil resource.

Previously unknown mechanism identified in oncogene-induced senescence. Reported in The American Journal of Pathology

Prototypic oncogene-induced senescence (OIS) by Ras/Raf/Mek. Activated Ras/Raf/Mek oncogenes damage DNA, thereby triggering cellular DNA damage response (DDR) signaling involving ATM/ATR kinases and various components of the double strand break (DSB) repair machinery. Signals from unresolved DSB are relayed to the tumor suppressor p53, PML and pRB, which eventually promote a dynamic process of local, senescence-associated heterochromatin foci (SAHF) formation with the help of histone methyltransferases (such as Suv39h1) in the vicinity of E2F-responsive target genes, thereby transcriptionally silencing E2F-dependent S-phase genes. Moreover, persistent DSB may also trigger a second senescence-associated response, the massive production of largely pro-inflammatory cytokines and other secretable factors (termed “senescence-associated secretory phenotype [SASP]”), considered to reinforce the senescent arrest. Notably, the Myc oncogene is also known to evoke reactive oxygen species (ROS) and DNA replication stress like Ras/Raf-type oncogenes, and, a small fraction of Myc-activated cells directly enter senescence in a cell-autonomous fashion.

Cell aging, or cellular senescence, has an important role in the natural physiological response to tumor development. Activated oncogenes are able to induce senescence, and recent findings have suggested that oncogene-induced senescence (OIS) could play a key role in future cancer therapy. Researchers have now identified a previously unknown mechanism in the regulation of OIS. This study is published online in advance of the January issue of The American Journal of Pathology.

In many types of normal cells, OIS depends on induction of DNA damage response. Oxidative stress and hyper-replication of genomic DNA have already been proposed as major causes of DNA damage in OIS cells. A group of investigators from New York, Oregon, and Michigan reports that down-regulation of deoxyribonucleoside pools is another endogenous source of DNA damage. In normal human cells, “OIS represents an important fail-safe mechanism that suppresses proliferation of pre-malignant cells,” explains lead investigator Dr Mikhail Nikiforov, PhD, Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, New York. “Compelling evidence suggests that one of the intrinsic processes required for the induction of OIS is the cellular response to DNA damage.”

Discovery in Ghent could improve screening for sudden cardiac death

Screening cardiac

Unfortunately, newspaper articles about young athletes dying suddenly on the field are not unheard of. Such reports fuel discussions about compulsory screening, for example of young footballers, for heart failure. Research by scientists from Ghent (VIB/UGent) and Italy will benefit these screening methods. They have discovered a link between mutations in a certain gene and the heart condition Arrhythmogenic Right Ventricular Cardiomyopathy.

Arrhythmogenic Right Ventricular Cardiomyopathy or ARVC
ARVC is a hereditary heart condition in which the heart muscle (particularly the right ventricle) is partly replaced by fatty tissue and connective tissue. Cardiac arrhythmias can occur as a result of the changes in the heart muscle. Severe arrhythmias can cause dizziness or even lead to fainting or an acute cardiac arrest (= sudden death). ARVC is a progressive disease that usually presents during the teenage years.

‘Smart stethoscope’, developed by scientists from the University of Southampton, used in monitoring treatment of kidney stones

Prototype of ‘Smart Stethoscope.’
Credit: University of Southampton

A new listening device, developed by scientists from the University of Southampton, is being used to monitor the effectiveness of the treatment of kidney stones – saving patients unnecessary repeat therapy and x-ray monitoring.

If kidney stones cannot be dissolved by drugs, the favoured procedure is lithotripsy. Lithotripsy works by focusing thousands of shock waves onto the kidney stones in an effort to break them into pieces small enough to urinate out of the body or be dissolved by drugs.

However, it is difficult to discover exactly when the treatment has succeeded in breaking the stone and patients frequently have to experience more shocks than necessary, or be sent home when an insufficient number of shocks have been delivered to break the stone.

The new ‘Smart stethoscope’ has been developed by a team from the University’s Faculty of Engineering and the Environment in collaboration with Guy’s and St Thomas’ Foundation Trust (GSTT) and Precision Acoustics Ltd. The programme was led by Professor Tim Leighton from the University’s Institute of Sound and Vibration Research (ISVR).