New, ‘robust’ treatment for stroke uses genetic material from bone marrow

Aug. 26, 2013 — In the latest in a series of experiments testing the use of stem cells to treat neurological disease, researchers at Henry Ford Hospital have shown for the first time that microscopic material in the cells offers a “robust” treatment for crippling stroke.”In this study we pioneered a totally new treatment for stroke, and possibly for all neurological disease,” says Michael Chopp, Ph.D., scientific director of the Henry Ford Neuroscience Institute.The new study is published online in the current issue of Journal of Cerebral Blood Flow and Metabolism.It focused on exosomes, blister-like microscopic “bubbles” that once were thought to carry and get rid of “old” proteins that were no longer needed by the body. After they were recently found to also carry RNA, whole new fields of study were suggested — including the pioneering work at Henry Ford.The research team found that after inducing stroke in lab rats, injecting exosomes containing this genetic material into their blood prompted remodeling of the affected brain, including increased production of new brain cells, blood vessels and neural rewiring. Together, these effects significantly improved neurological function that had been impaired by stroke.Using bone marrow from the adult rats, the researchers extracted stem cells — specifically mesenchymal cells, or MSCs — that were then employed to generate exosomes.The researchers induced stroke by occluding an artery in the brain of each rat to block blood flow for two hours. Twenty-four hours later, they injected the exosomes into a vein in each rat’s tail.The rats’ physical agility and neurological responses were tested before stroke and after treatment with the exosomes, and the results were compared.”All rats showed severe functional loss one day after treatment, but gradual and eventually significant improvement during the four-week period that followed,” Dr. Chopp says. “This discovery provides a novel treatment for stroke, and possibly other neurological diseases.”Dr. Chopp and Henry Ford researchers earlier found that the beneficial effects of treatment of stroke with bone marrow cells are attributed to their production and release of exosomes. In addition, using a similar treatment with exosomes from bone marrow stem cells significantly reduced a particularly resistant form of malignant brain tumor in living lab rats.

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Scientists pinpoint 105 additional genetic errors that cause cystic fibrosis

Aug. 25, 2013 — Of the over 1,900 errors already reported in the gene responsible for cystic fibrosis (CF), it is unclear how many of them actually contribute to the inherited disease. Now a team of researchers reports significant headway in figuring out which mutations are benign and which are deleterious. In so doing, they have increased the number of known CF-causing mutations from 22 to 127, accounting for 95 percent of the variations found in patients with CF.In a summary of their research to be published online in Nature Genetics Aug. 25, the scientists say that characterizing those additional mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene will not only bring certainty to families about a CF diagnosis or carrier status, but will also accelerate the design process for new drugs tailored to a particular mutation. There already is one such individualized drug on the market.”Since not all mutations cause disease, sequencing the DNA in both copies of your CFTR gene and finding an abnormality in one wouldn’t tell us if you are a carrier for CF unless we knew if that abnormality causes CF,” says Garry Cutting, M.D., professor of pediatrics in the McKusick-Nathans Institute of Genetic Medicine at the Johns Hopkins University School of Medicine. “Until this new work, more than a quarter of couples in which both partners were found to carry a CFTR mutation were left wondering if their mutations were going to affect their offspring. Now it’s down to 9 percent,” he says.CF is the most common, lethal, recessive genetic disease affecting Caucasians, with approximately 70,000 to 80,000 cases worldwide. When two copies of a defective CFTR gene are inherited, one from each parent, a child’s body will not be able to create working CFTR proteins, resulting in the production of thickened mucus, which clogs the lungs and digestive system. Modern treatments to unclog the lungs and address other symptoms have allowed patients to survive into adulthood, but most will still die prematurely of lung disease.One in 30 Caucasians in the United States is a “carrier” of the disease, meaning their genomes include one abnormal copy of the CFTR gene but they experience no symptoms of the disease, and as many as a million Americans are tested each year for carrier status. …

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PHS gene prevents wheat from sprouting: Fewer crop losses anticipated

Aug. 20, 2013 — A new study about the common problem of preharvest sprouting, or PHS, in wheat is nipping the crop-killing issue in the bud.Researchers at Kansas State University and the U.S. Department of Agriculture-Agricultural Research Service, or USDA-ARS, found and cloned a gene in wheat named PHS that prevents the plant from preharvest sprouting. Preharvest sprouting happens when significant rain causes the wheat grain to germinate before harvest and results in significant crop losses.”This is great news because preharvest sprouting is a very difficult trait for wheat breeders to handle through breeding alone,” said Bikram Gill, university distinguished professor of plant pathology and director of the Wheat Genetics Resource Center. “With this study, they will have a gene marker to expedite the breeding of wheat that will not have this problem.”Gill conducted the study with Guihau Bai, a researcher with the Hard Winter Wheat Genetics Research Unit of the USDA-ARS, adjunct professor of agronomy at Kansas State University and the study’s lead author. Also involved were Harold Trick, professor of plant pathology; Shubing Liu, research associate in agronomy; Sunish Sehgal, senior scientist in plant pathology; Jiarui Li, research assistant professor; and Meng Lin, doctoral student in agronomy, all from Kansas State University; and Jianming Yu, Iowa State University.Their study, “Cloning and Characterization of a Critical Regulator for Pre-Harvest Sprouting in Wheat,” appears in a recent issue of the scientific journal Genetics.The finding will to be most beneficial to white wheat production, which loses $1 billion annually to preharvest sprouting, according to Gill.He said consumers prefer white wheat to the predominant red wheat because white wheat lacks the more bitter flavor associated with red wheat. Millers also prefer white wheat to red because it produces more flour when ground. The problem is that white wheat is very susceptible to preharvest sprouting.”There has been demand for white wheat in Kansas for more than 30 years,” Gill said. “The very first year white wheat was grown in the state, though, there was rain in June and then there was preharvest sprouting and a significant loss. The white wheat industry has not recovered since and has been hesitant to try again. …

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An organized approach to 3-D tissue engineering: Getting closer to viable organ implants

Aug. 20, 2013 — Researchers at the Institute of Bioengineering and Nanotechnology (IBN) have developed a simple method of organizing cells and their microenvironments in hydrogel fibers. Their unique technology provides a feasible template for assembling complex structures, such as liver and fat tissues, as described in their recent publication in Nature Communications.According to IBN Executive Director Professor Jackie Y. Ying, “Our tissue engineering approach gives researchers great control and flexibility over the arrangement of individual cell types, making it possible to engineer prevascularized tissue constructs easily. This innovation brings us a step closer toward developing viable tissue or organ replacements.”IBN Team Leader and Principal Research Scientist, Dr Andrew Wan, elaborated, “Critical to the success of an implant is its ability to rapidly integrate with the patient’s circulatory system. This is essential for the survival of cells within the implant, as it would ensure timely access to oxygen and essential nutrients, as well as the removal of metabolic waste products. Integration would also facilitate signaling between the cells and blood vessels, which is important for tissue development.”Tissues designed with pre-formed vascular networks are known to promote rapid vascular integration with the host. Generally, prevascularization has been achieved by seeding or encapsulating endothelial cells, which line the interior surfaces of blood vessels, with other cell types. In many of these approaches, the eventual distribution of vessels within a thick structure is reliant on in vitro cellular infiltration and self-organization of the cell mixture. These are slow processes, often leading to a non-uniform network of vessels within the tissue. …

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Celery, artichokes contain flavonoids that kill human pancreatic cancer cells

Aug. 15, 2013 — Celery, artichokes, and herbs, especially Mexican oregano, all contain apigenin and luteolin, flavonoids that kill human pancreatic cancer cells in the lab by inhibiting an important enzyme, according to two new University of Illinois studies.”Apigenin alone induced cell death in two aggressive human pancreatic cancer cell lines. But we received the best results when we pre-treated cancer cells with apigenin for 24 hours, then applied the chemotherapeutic drug gemcitabine for 36 hours,” said Elvira de Mejia, a U of I professor of food chemistry and food toxicology.The trick seemed to be using the flavonoids as a pre-treatment instead of applying them and the chemotherapeutic drug simultaneously, said Jodee Johnson, a doctoral student in de Mejia’s lab who has since graduated.”Even though the topic is still controversial, our study indicated that taking antioxidant supplements on the same day as chemotherapeutic drugs may negate the effect of those drugs,” she said.”That happens because flavonoids can act as antioxidants. One of the ways that chemotherapeutic drugs kill cells is based on their pro-oxidant activity, meaning that flavonoids and chemotherapeutic drugs may compete with each other when they’re introduced at the same time,” she explained.Pancreatic cancer is a very aggressive cancer, and there are few early symptoms, meaning that the disease is often not found before it has spread. Ultimately the goal is to develop a cure, but prolonging the lives of patients would be a significant development, Johnson added.It is the fourth leading cause of cancer-related deaths, with a five-year survival rate of only 6 percent, she said.The scientists found that apigenin inhibited an enzyme called glycogen synthase kinase-3β (GSK-3β), which led to a decrease in the production of anti-apoptotic genes in the pancreatic cancer cells. Apoptosis means that the cancer cell self-destructs because its DNA has been damaged.In one of the cancer cell lines, the percentage of cells undergoing apoptosis went from 8.4 percent in cells that had not been treated with the flavonoid to 43.8 percent in cells that had been treated with a 50-micromolar dose. In this case, no chemotherapy drug had been added.Treatment with the flavonoid also modified gene expression. “Certain genes associated with pro-inflammatory cytokines were highly upregulated,” de Mejia said.According to Johnson, the scientists’ in vitro study in Molecular Nutrition and Food Research is the first to show that apigenin treatment can lead to an increase in interleukin 17s in pancreatic cells, showing its potential relevance in anti-pancreatic cancer activity.Pancreatic cancer patients would probably not be able to eat enough flavonoid-rich foods to raise blood plasma levels of the flavonoid to an effective level. But scientists could design drugs that would achieve those concentrations, de Mejia said.And prevention of this frightening disease is another story. “If you eat a lot of fruits and vegetables throughout your life, you’ll have chronic exposure to these bioactive flavonoids, which would certainly help to reduce the risk of cancer,” she noted.

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Protein that helps plants tolerate drought, flooding, other stresses discovered

Aug. 12, 2013 — A team including Dartmouth researchers has uncovered a protein that plays a vital role in how plant roots use water and nutrients, a key step in improving the production and quality of crops and biofuels.Share This:The findings appear this week in the journal PNAS. The team included researchers from Dartmouth, the University of Aberdeen and the University of Lausanne.Plant roots use their endodermis, or inner skin, as a cellular gatekeeper to control the efficient use and movement of water and nutrients from the soil to the above-ground parts of the plant. A key part of that cellular barrier is the Casparian strip, which also helps plants to tolerate stresses such as salinity, drought and flooding. Until recently, little was known about the genes that drive the formation of the Casparian strip, which is composed of a fine band of lignin, the polymer that gives wood its strength.In their study, the researchers identified a protein, ESB1, involved in the deposition of lignin patches early in the development of the Casparian strip and the fusion of these patches into a continuous band of lignin as the Casparian strip matures.Plants use lignin deposition in many different cell types and in response to various environmental stresses. A better understanding of lignin deposition may eventually help scientists to manipulate lignin content in plants and boost crop and biofuels production, including in locations where growth conditions are not ideal.Share this story on Facebook, Twitter, and Google:Other social bookmarking and sharing tools:|Story Source: The above story is based on materials provided by Dartmouth College, via EurekAlert!, a service of AAAS. Note: Materials may be edited for content and length. For further information, please contact the source cited above. Journal Reference:Prashant S. Hosmani, Takehiro Kamiya, John Danku, Sadaf Naseer, Niko Geldner, Mary Lou Guerinot, and David E. …

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Eavesdropping plants prepare to be attacked

Aug. 7, 2013 — In a world full of hungry predators, prey animals must be constantly vigilant to avoid getting eaten. But plants face a particular challenge when it comes to defending themselves.”One of the things that makes plants so ecologically interesting is that they can’t run away,” says John Orrock, a zoology professor at the University of Wisconsin-Madison. “You can’t run, you can’t necessarily hide, so what can you do? Some plants make themselves less tasty.”Some do this either by boosting their production of toxic or unpleasant-tasting chemicals (think cyanide, sulfurous compounds, or acids) or through building physical defenses such as thorns or tougher leaves.But, he adds, “Defense is thought to come at a cost. If you’re investing in chemical defenses, that’s energy that you could be putting into growth or reproduction instead.”To balance those costs with survival, it may behoove a plant to be able to assess when danger is nigh and defenses are truly necessary. Previous research has shown that plants can induce defenses against herbivores in response to airborne signals from wounded neighbors.But cues from damaged neighbors may not always be useful, especially for the first plant to be attacked, Orrock says. Instead he asked whether plants — here, black mustard, a common roadside weed — can use other types of cues to anticipate a threat.In a presentation Aug. 6 at the 2013 Ecological Society of America Annual Meeting in Minneapolis, he and co-author Simon Gilroy, a UW-Madison botany professor, reported that the plants can eavesdrop on herbivore cues to mount a defensive response even before any plant is attacked.Slugs and snails are generalist herbivores that love to munch on mustard plants and can’t help but leave evidence of their presence — a trail of slime, or mucus. Where there’s slime, there’s a snail. …

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Why don’t we all get Alzheimer’s disease?

Aug. 7, 2013 — Though one might think the brains of people who develop Alzheimer’s disease (AD) possess building blocks of the disease absent in healthy brains, for most sufferers, this is not true. Every human brain contains the ingredients necessary to spark AD, but while an estimated 5 million Americans have AD — a number projected to triple by 2050 — the vast majority of people do not and will not develop the devastating neurological condition.For researchers like Subhojit Roy, MD, PhD, associate professor in the Departments of Pathology and Neurosciences at the University of California, San Diego School of Medicine, these facts produce a singular question: Why don’t we all get Alzheimer’s disease?In a paper published in the August 7 issue of the journal Neuron, Roy and colleagues offer an explanation — a trick of nature that, in most people, maintains critical separation between a protein and an enzyme that, when combined, trigger the progressive cell degeneration and death characteristic of AD.”It’s like physically separating gunpowder and match so that the inevitable explosion is avoided,” said principal investigator Roy, a cell biologist and neuropathologist in the Shiley-Marcos Alzheimer’s Disease Research Center at UC San Diego. “Knowing how the gunpowder and match are separated may give us new insights into possibly stopping the disease.”The severity of AD is measured in the loss of functioning neurons. In pathological terms, there are two tell-tale signs of AD: clumps of a protein called beta-amyloid “plaques” that accumulate outside neurons and threads or “tangles” of another protein, called tau, found inside neurons. Most neuroscientists believe AD is caused by the accumulating assemblies of beta-amyloid protein triggering a sequence of events that leads to impaired cell function and death. This so-called “amyloid cascade hypothesis” puts beta-amyloid protein at the center of AD pathology.Creating beta-amyloid requires the convergence of a protein called amyloid precursor protein (APP) and an enzyme that cleaves APP into smaller toxic fragments called beta-secretase or BACE.”Both of these proteins are highly expressed in the brain,” said Roy, “and if they were allowed to combine continuously, we would all have AD.”But that doesn’t happen. Using cultured hippocampal neurons and tissue from human and mouse brains, Roy — along with first author Utpal Das, a postdoctoral fellow in Roy’s lab, and colleagues — discovered that healthy brain cells largely segregate APP and BACE-1 into distinct compartments as soon as they are manufactured, ensuring the two proteins do not have much contact with each other.”Nature seems to have come up with an interesting trick to separate co-conspirators,” said Roy.The scientists also found that the conditions promoting greater production of beta-amyloid protein boost the convergence of APP and BACE. Specifically, an increase in neuronal electrical activity — known to increase the production of beta-amyloid — also led to an increase in APP-BACE convergence. Post-mortem examinations of AD patients revealed increased physical proximity of the proteins as well, adding support to the pathophysiological significance of this phenomenon in human disease.Das said the findings are fundamentally important because they elucidate some of the earliest molecular events triggering AD and show how a healthy brain naturally avoids them. …

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Starring role discovered for supporting cells in inner ear

July 25, 2013 — Researchers have found in mice that supporting cells in the inner ear, once thought to serve only a structural role, can actively help repair damaged sensory hair cells, the functional cells that turn vibrations into the electrical signals that the brain recognizes as sound.The study in the July 25, 2013 online edition of the Journal of Clinical Investigation reveals the rescuing act that supporting cells and a chemical they produce called heat shock protein 70 (HSP70) appear to play in protecting damaged hair cells from death. Finding a way to jumpstart this process in supporting cells offers a potential pathway to prevent hearing loss caused by certain drugs, and possibly by exposure to excess noise. The study was led by scientists at the National Institutes of Health.Over half a million Americans experience hearing loss every year from ototoxic drugs — drugs that can damage hair cells in the inner ear. These include some antibiotics and the chemotherapy drug cisplatin. In addition, about 15 percent of Americans between the ages of 20 and 69 have noise-induced hearing loss, which also results from damage to the sensory hair cells.Once destroyed or damaged by noise or drugs, sensory hair cells in the inner ears of humans don’t grow back or self-repair, unlike the sensory hair cells of other animals such as birds and amphibians. This has made exploring potential pathways to protect or regrow hair cells in humans a major focus of hearing research.”If you’re looking to protect hair cells, you should be looking at supporting cells,” said senior author Lisa Cunningham, Ph.D., whose laboratory of sensory cell biology at the National Institute on Deafness and other Communication Disorders (NIDCD), a component of NIH, led the study. “Our study indicates that when the inner ear is under stress, the cell that responds by generating protective proteins is not a hair cell, but a supporting cell.”Earlier work by Dr. Cunningham’s group and other labs had shown that HSP70 — a protein produced in the inner ear after exposure to stressors such as environmental toxins, oxidative stress, chemical toxins, and noise — can protect hair cells. However, the mechanism wasn’t fully understood.In this study, researchers exposed mouse utriclesto heat and then rapidly preserved them. The scientists found robust expression of HSP70; however, microscopy techniques showed that the protein was located only in the supporting cells, not the hair cells.Further experiments showed that the supporting cells don’t keep the HSP70 to themselves — they secrete HSP70, which can then protect neighboring hair cells. …

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Chemical reaction could streamline manufacture of pharmaceuticals and other compounds

July 22, 2013 — Researchers at The University of Texas at Austin have discovered a new chemical reaction that has the potential to lower the cost and streamline the manufacture of compounds ranging from agricultural chemicals to pharmaceutical drugs.The reaction resolves a long-standing challenge in organic chemistry in creating phenolic compounds from aromatic hydrocarbons quickly and cheaply.Phenolic compounds, or phenols, are broadly used as disinfectants, fungicides and drugs to treat many ailments such as Parkinson’s disease. Creating a phenol seems deceptively simple. All it requires is replacing a hydrogen molecule on an aromatic hydrocarbon with an oxygen molecule.”This is a chemical transformation that is underdeveloped and at the same time pivotal in the production of many chemicals important to life as we know it,” said Dionicio Siegel, an assistant professor of chemistry in the College of Natural Sciences at The University of Texas at Austin.The secret that Siegel and his colleagues discovered is a substance called phthaloyl peroxide. This chemical was studied in the late 1950s and early 1960s, but it has been largely ignored during the intervening years.The scientists were conducting basic studies on phthaloyl peroxide, building on previous research, and decided to use it to tackle the age-old problem of transforming aromatic hydrocarbons into phenols.The advantage to using phthaloyl peroxide is that the reaction does not require the use of acids or catalysts to work, and it can add oxygen to a wide variety of starting materials.”There are no special conditions,” said Siegel. “You just combine the reagents, mix them and go. It’s very simple and straight forward.”The paper describing this discovery was published last week in Nature.The new process can be applied to other problems in organic chemistry. One particular area of interest is creating metabolites to drugs. Metabolites are the products left after the body finishes breaking down, or metabolizing, a substance. When testing drugs, scientists need to take into account not just how the drug itself reacts in the body, but also how the metabolites react.”We’ve had a long-standing interest in accessing metabolites of drugs or compounds that are used in biological systems,” said Siegel. “Just as it’s important that the drug doesn’t have deleterious side effects, it’s equally important that the metabolite doesn’t have an effect. …

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It’s not just the heat, it’s the ozone: Hidden heat wave dangers exposed

July 19, 2013 — During heat waves — when ozone production rises — plants’ ozone absorption is curtailed, leaving more pollution in the air.This resulted in the loss of an estimated 460 lives in the UK in the hot summer of 2006.Vegetation plays a crucial role in reducing air pollution, but new research by the Stockholm Environment Institute (SEI) at the University of York shows that they may not protect us when we need it most: during extreme heat, when ozone formation from traffic fumes, industrial processes and other sources is at its worst.The reason, explained lead author Dr Lisa Emberson, is that during heat waves — when the ground is especially dry — plants become stressed and shut their stomata (small pores on their leaves) to conserve water. This natural protective mechanism makes them more resilient to extreme heat and high ozone levels, but it also stops them from absorbing ozone and other pollutants.”Vegetation can absorb as much as 20 per cent of the global atmospheric ozone production, so the potential impact on air quality is substantial,” says Dr Emberson, a senior lecturer in the Environment Department at the University of York and director of SEI’s York Centre. “What we set out to do in this study was to quantify that impact in terms of increased ozone levels and the toll on human life.”The research team, which also included scientists at King’s College, London, focused on the summer of 2006, when a heat wave and drought occurred across the UK and much of Europe. They combined two models used for human health and ecosystem risk assessment to compare two scenarios, one with perfect ozone uptake by plants, and one with minimal ozone absorption.The difference between perfect and minimal uptake was equivalent to 16 days of ozone levels above the threshold for human safety across the entire UK — and as many as 20 days in the East Midlands and eastern UK. Using these same scenarios, the team also estimated that 970 premature deaths due to ozone would have occurred under minimal plant ozone uptake conditions over the June to July period; of these 460 could have been avoided if plants had been absorbing ozone at full capacity. All estimated premature deaths are in addition to human health and mortality impacts from the heat itself.”The most vulnerable people to ozone pollution are those with existing respiratory and cardiovascular diseases,” explains Dr Emberson. “For example, ground-level ozone can lead to lung inflammation, decreased lung function, and an increase in asthma attacks. That is why, during high ozone episodes, especially in urban areas, people are generally advised not to do physical activity.”The study findings were published this week in the peer-reviewed journal Atmospheric Chemistry and Physics. The research was financed by the UK Department for Environment, Food and Rural Affairs (Defra).The timing of the publication coincides with yet another major heat wave in the UK, and Dr Emberson says it is likely that ozone uptake by vegetation is once again curtailed. The extent of the problem, however, will depend on how dry the soil is, since it is the combination of heat and drought that stresses plants the most.Dr Emberson says the study highlights the importance of understanding the frequency with which such heat waves and droughts will occur in the future as well as how ozone uptake by vegetation is affected by droughts, extreme heat, and interaction with other pollutants.”The more we know, the better we will be able to judge how successful our emission reduction efforts have been so far, and whether we need additional efforts — in the UK, across Europe and beyond, since we know that pollutants such as ozone and its precursors can carried around the globe,” she says.The research can also inform public-health responses, Dr Emberson says. …

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Cells in the early embryo battle each other to death for becoming part of the organism

July 11, 2013 — Spanish researchers at the Centro Nacional de Investigaciones Cardiovasculares (CNIC) have found that during the early stages of mammalian development, embryonic cells embark on a battle for survival. Through this battle, the less active of these cells are eliminated by their stronger sisters.The work is published today in the journal Nature.This phenomenon, termed cell competition, occurs in a defined time window, between days 3 and 7 of mouse development. During this period all embryonic cells compete with each other, as explained by Dr. Cristina Claveria, first author of the study, and Dr. Miguel Torres, director of this work and Head of the Department of Cardiovascular Development and Repair at CNIC.”Thanks to cell competition the developing organism optimizes itself by selecting the cells theoretically more capable of supporting vital functions throughout the life of the new individual,” says Dr. Claveria. According to the authors, this would be particularly important in long-lived organisms, like humans, where the functionality of their tissues must be maintained throughout a long life.Dr. Miguel Torres also explains that when cell competition is prevented, cells that normally would have lost the battle now become able to contribute to the new organism: “We think, however, that this organism will probably be less capable than the one which would have been formed under normal circumstances. In what sense will it be less adequate is a matter of great interest that we will address in the coming years.”Indeed, the researchers are able to determine in advance which cells will win this battle: those with higher levels of the Myc protein, an important controller of cell metabolic capacity. Moreover, using a new technique that they have developed for the production of genetic mosaics, they are able to manipulate the levels of Myc protein in cells, thus changing the outcome of the fight.According to Claveria and Torres, the study shows that the early embryo is a mosaic of cells with very different levels of Myc ,in which cells with higher levels of Myc eliminate those with lower levels. …

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Mapping the benefits of our ecosystems

July 1, 2013 — We rely on our physical environment for many things — clean water, land for crops or pastures, storm water absorption, and recreation, among others. Yet it has been challenging to figure out how to sustain the many benefits people obtain from nature — so-called “ecosystem services” — in any given landscape because an improvement in one may come at the cost of another.Two ecologists at the University of Wisconsin-Madison report this week (July 1) in the Proceedings of the National Academy of Sciences a novel approach to analyzing the production and location of 10 different ecosystem services across a landscape, opening the door to being able to identify factors governing their synergies and tradeoffs.Monica Turner, the Eugene P. Odum Professor of Zoology, and graduate student Jiangxiao Qiu mapped the production, distribution, and interactions of the services in three main categories: provisioning (providing resources like food, fiber, or fresh water), cultural (such as aesthetics and hunting), and regulating (including improving ground and surface water quality, handling floodwater, preventing erosion, and storing carbon). They focused on the Yahara River watershed, which covers much of central portion of Dane County and parts of Columbia and Rock Counties in southern Wisconsin and includes the chain of Madison lakes.”We found that the main ecosystem services are not independent of each other. They interact spatially in very complex ways,” says Qiu, lead author of the new study.Some of those interactions were not surprising — for example, higher levels of crop production were generally associated with poorer surface and ground water quality. However, two other sets of services showed positive associations: flood regulation, pasture and freshwater supply all went together, as did forest recreation, soil retention, carbon storage and surface water quality.”If you manage for one of these services, you can probably enhance others, as well,” says Turner. “It also means that you can’t take a narrow view of the landscape. You have to consider all of the things that it produces for us and recognize that we have to manage it very holistically.”Even in the expected tradeoff between crop production and water quality, the researchers found something unexpected.”There is a strong tradeoff between crop production and surface and groundwater quality,” Qiu says. “But despite this, there are still some locations that can be high for all three services — exceptions that can produce high crop yield and good water quality in general.”Preliminary analysis of these “win-win” areas suggests that factors like flat topography, a deep water table, less field runoff, soil with high water-holding capacity, more adjoining wetlands and proximity to streams with riparian vegetation may contribute to maintaining both crop production and good water quality.The results also show that nearly all of the land in the watershed provides a high level of at least one of the measured services but that they are not uniformly distributed. Most areas offer a high level of just one or two services. …

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Protein is involved with colon cancer cell’s ability to invade other cells

June 27, 2013 — Understanding how the protein km23-1 enables in the spread of colon cancer may lead to new treatments for the disease, according to researchers at Penn State College of Medicine.Previous research shows that km23-1 is involved in the movement of cancer cells and in the control of specific proteins at the leading edge of moving cells. Kathleen Mulder, professor of biochemistry and molecular biology, who discovered the protein, now says km23-1 is used in the cancer cell’s ability to move out of a tumor in the early stages ofinvasion.”km23-1 may be able to help in this process due to its role in the assembly of large groups of proteins favorable to cancer invasion,” Mulder said.Colorectal cancer is the third most common cancer in the United States. Tumors spreading to other parts of the body are the greatest threat to a patient’s survival.The researchers limited the amount of km23-1 available in the cells they studied, which allowed them to see how it affects cell behavior. A reduction in km23-1 caused a decrease in the production of transforming growth factor beta (TGF-beta). In healthy cells, TGF-beta helps prevent cancer growth. However, in cancer cells, the protein actually aids in the spread of tumors. Limiting km23-1 also blocks the activity of proteins previously shown to lead to TGF-beta production. Researchers reported their results in PLOS One.The researchers also find that cells with less km23-1 have reduced amounts of a protein that forms a framework structure associated with the spread of cancer. This scaffolding holds together key factors that help the cancer cells move and invade to form secondary tumors.Mulder and colleagues say that by decreasing km23-1, colon cancer cells do not spread as much. This also affects several proteins known to make a cancer cell invasive, demonstrating that km23-1 is an important potential target for cancer therapies.The researchers also looked at another protein that influences cell survival, migration and invasion, called ERK, which has higher activity in cancer cells. …

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Molecule that reduces fats in blood identified

June 24, 2013 — Hyperlipidemia, a condition with high levels of fats circulating in the bloodstream, is a known risk factor for various cardiovascular and metabolic disorders. While the Western diet often contributes to high levels of lipids such as cholesterol and triglycerides, over-production of the body’s own lipoproteins can lead to hyperlipidemia, independent of food intake.In a discovery that may pave the way towards new treatments for high cholesterol, researchers led by M. Mahmood Hussain, PhD, Professor of Cell Biology at SUNY Downstate Medical Center, found that a regulatory RNA molecule interferes with the production of lipoproteins and, in a mouse model, reduces hyperlipidemia and atherosclerosis. Their study was published recently in the online edition of Nature Medicine.Dr. Hussain, whose laboratory focuses on molecular mechanisms of intestinal lipoprotein assembly, says, “High plasma lipid and lipoprotein levels are a risk factor for atherosclerosis, and lowering plasma lipid levels is a national goal. While current medications and changes in diet can be effective, cardiovascular disease remains the number one cause of death in the United States, and additional approaches to decrease lipid levels are needed.”In their Nature Medicine article, Dr. Hussain and colleagues note that “overproduction of lipoproteins, a process that is dependent on microsomal triglyceride transfer protein (MTP), can contribute to hyperlipidemia.” They demonstrate that microRNA-30c (miR-30c), a genetic regulator, interacts with MTP and induces its degradation, leading to reductions in MTP activity, the production of lipoproteins, plasma lipids, and atherosclerosis. This molecule also reduces lipid synthesis independently of MTP thereby avoiding complications associated with drug therapies aimed at lowering lipoprotein production.The authors conclude that a medication mimicking miR-30c could potentially be effective in reducing hyperlipidemia in humans.This work was supported in part by U.S. National Institutes of Health grants R01DK046900, from the National Institute of Diabetes and Digestive and Kidney Diseases, and R01HL095924, from the National Heart, Lung and Blood Institute.

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Finasteride, medication for male pattern hair loss, may also decrease drinking

June 13, 2013 — Finasteride is a synthetic drug for the treatment of male pattern hair loss (MPHL) and an enlarged prostate. The side effects of finasteride for treatment of these two conditions can include increased rates of sexual dysfunction, such as low libido and erectile dysfunction; in fact, some men who have discontinued the medication continue to experience persistent sexual side effects. Building on the discovery that finasteride has also been shown to reduce alcohol intake and suppress alcohol preference in mice, a new study has found that a majority of men with finasteride-related sexual side effects noticed a decrease in their alcohol consumption.Results will be published in the November 2013 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.”Finasteride is a synthetic medication used to treat enlarged prostates in older men,” explained Michael S. Irwig, assistant professor of medicine at The George Washington University and sole author of the study. “It is also used by younger men for male pattern baldness. In younger men with male pattern baldness, [less than] five percent have developed sexual side effects. Finasteride has not been used for alcohol reduction in humans; our study is among the first to look at its effects on drinking in humans.””Finasteride is a 5α-reductase inhibitor that blocks the production of a variety of cholesterol-derived hormones and modulators, including certain androgens and other steroids that are active in both the body and brain,” explained Chuck Zorumski, the Samuel B. Guze Professor and head of psychiatry at Washington University School of Medicine. “Neuroactive steroids like allopregnanolone help to regulate brain networks involved in emotion, motivation, and cognition. There is considerable interest in whether these neurosteroids contribute to psychiatric illnesses. …

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Tumors disable immune cells by using up sugar

June 6, 2013 — Cancer cells’ appetite for sugar may have serious consequences for immune cell function, researchers at Washington University School of Medicine in St. Louis have learned.The scientists found that when they kept sugar away from critical immune cells called T cells, the cells no longer produced interferon gamma, an inflammatory compound important for fighting tumors and some kinds of infection.”T cells can get into tumors, but unfortunately they are often ineffective at killing the cancer cells,” said Erika Pearce, PhD, assistant professor of pathology and immunology. “Lack of the ability to make interferon gamma could be one reason why they fail to kill tumors. By understanding more about how sugar metabolism affects interferon production, we may be able to develop treatments that fight tumors by enhancing T cell function. “According to Pearce, inhibiting interferon gamma production also may help scientists treat autoimmune disorders in which T cells cause too much inflammation.The results appear June 6 in Cell.Pearce’s insights arose from her research into the metabolism of T cells.Like most cells, T cells can make energy either by using an efficient process called oxidative phosphorylation or a less efficient pathway called aerobic glycolysis.Cells normally make most of their energy via oxidative phosphorylation, but they need oxygen to do so. If oxygen runs short, most cells switch to aerobic glycolysis. Low sugar levels can also force cells to use oxidative phosphorylation for their energy.Scientists aren’t sure why, but many cells, including T cells, switch to aerobic glycolysis when they need to reproduce rapidly. T cells proliferate quickly as they begin to respond to invaders or tumors, and scientists have assumed their switch to aerobic glycolysis was essential for this replicative process.For the new study, Chih-Hao Chang, PhD, a postdoctoral researcher in the Pearce lab and first author of the study, set up a system that allowed him to control the resources available to T cells in test tubes. Switching the sugars available to the cells let him force the cells to use either oxidative phosphorylation or aerobic glycolysis.”The conventional view was that proliferating T cells needed to use glycolysis, ” Chang said. “We found that wasn’t true: they could also use oxidative phosphorylation to support proliferation.”After proliferation starts, the T cells can sustain themselves with either energy-making process. …

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The intensity of land use doubled in the 20th century

June 4, 2013 — The growth of green plants — which can be measured in terms of “net primary production,” or NPP for short — provides the energetic foundation for all life on earth. The share of NPP appropriated by humans (HANPP) through agriculture and forestry, bioenergy production, and vegetation fires doubled over the course of the past century. Researchers at the Institute of Social Ecology at the AAU have shown that while land is used more efficiently, simultaneously, the intensity of land use has increased continuously.In a study published in PNAS (Proceedings of the National Academy of Sciences), researchers warn that an increased expansion of bioenergy use would drastically raise HANPP to over 40%.The growing global population and its increasing hunger for resources gives cause for concern for various reasons, in particular with regard to the sustainability of the current and future use of natural resources. The so-called HANPP indicator is a measurement for the intensity with which humans use land and biomass. HANPP stands for “Human Appropriation of Net Primary Production” and provides information about the impact of human activity upon the biosphere. HANPP reveals the percentage of the annual plant-based biomass production that is co-opted by humans through land use activities such as agriculture and forestry, bioenergy production, construction of buildings and infrastructures, soil degradation, or human induced vegetation fires — and thus not available to other ecosystem processes.A study recently published in PNAS quantifies for the first time long term trends in HANPP during global industrialization covering the period from 1910 to 2005. The authors, including Fridolin Krausmann, Karl-Heinz Erb, Simone Gingrich, Helmut Haberl, Veronika Gaube, Christian Lauk and Christoph Plutzar from the Institute of Social Ecology, and Tim Searchinger from Princeton University arrived at a surprising result: While global population increased fourfold over the past century, and economic output increased 17-fold, HANPP “only” doubled. “This shows us that land use became more and more efficient across the globe: The production of food and other products has increased at a much faster rate than HANPP. Nevertheless, HANPP has climbed from 13 to 25 per cent during the past century,” Fridolin Krausmann, lead author of the article, explains.While global consumption has increased dramatically, the amount of biomass harvested and used per capita has dropped significantly. Krausmann elaborates: “One of the reasons for this is that — seen from a global perspective — bioenergy has increasingly been replaced by fossil energy. …

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Chickens with bigger gizzards are more efficient

Apr. 11, 2013 — According to animal scientists, farmers could further protect the environment by breeding chickens with larger digestive organs. This research, published in the February issue of the Journal of Animal Science, could solve a major problem in poultry production.

In some areas, large poultry operations release nitrogen and phosphorus into the environment. These pollutants come from chicken waste, and they can cause ecological problems like algal blooms in rivers and lakes.

“These result in a loss of plant and animal species and have negative impacts on the use of water for human consumption,” said study co-author Dr. Agnes Narcy in an interview.

Narcy, along with and fellow researchers from the French National Institute For Agricultural Research (INRA) and France’s Center of Agricultural Research for Development (CIRAD), bred chickens to test whether selecting for larger digestive organ size could reduce the amount of waste that the chicken excreted.

The key organs were the proventriculus and the gizzard. The proventriculus is a stomach-like organ that softens food using acids and digestive enzymes. The gizzard is a compartment with thick, muscular walls that grinds food. Together, these organs prepare foods for digestion in the small intestine.

Narcy and fellow researchers hypothesized that chickens with larger, better functioning digestive organs would absorb more nutrients from their feed and therefore produce less waste. To test this hypothesis, the researchers selected chickens and raised three lines with differing abilities to digest feed.

After rearing nine generations of each line, the researchers found that chickens with larger digestive organs ate less feed and produced less waste. The researchers concluded that selecting for this trait could make poultry production more environmentally and economically sustainable. They say that a farmer raising 20,000 chickens could save 9.76 tons of feed per hatch.

“Furthermore, such selection would not affect body composition and meat and bone quality traits at slaughter age,” said Narcy.

Narcy said the next step is for animal scientists to identify the genes that control digestive efficiency in chickens. By pinpointing the right genes, researchers could help farmers select the most efficient chickens for breeding.

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Cell-based alternative to animal testing? Genomic biomarker signature can predict skin sensitizers, study finds

Aug. 8, 2011 — European legislation restricts animal testing within the pharmaceutical and cosmetic industries and companies are increasingly looking at alternative systems to ensure that their products are safe to use. Research published in BioMed Central’s open access journal BMC Genomics demonstrates that the response of laboratory grown human cells can now be used to classify chemicals as sensitizing, or non-sensitizing, and can even predict the strength of allergic response, so providing an alternative to animal testing.


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Allergic contact dermatitis can result in itching and eczema and is often due to repeated exposure to chemicals at work or in everyday life such as machine oil, detergents, soaps, and cosmetics. Unless the source of the sensitizing chemical is found the resulting rashes can be an ongoing source of misery for the sufferer. The 2009, 7th Amendment to the Cosmetic Directive bans testing of cosmetic products and ingredients on animals meaning that there is currently no way of ensuring new products are hypoallergenic.

Researchers from Lund University in Sweden used genome-wide profiling to measure the response of a human myeloid leukemia cell line to known chemicals. From this they defined a ‘biomarker signature’ of 200 genes, which could accurately discriminate between sensitizing and non-sensitizing chemicals. By comparing this signature with the known action of these chemicals they were also able to use this system to predict sensitizing potency.

Prof Borrebaeck said, “REACH (Registration, Evaluation, and Authorization of Chemicals) regulation requires that all new and existing chemicals within the European Union are tested for safety. The number of chemicals this includes is over 30,000 and is increasing all the time. Our lab-based alternative to animal testing, although in an early stage of production, is faster, out-performs present alternatives, and, because the cells are human in origin, is more relevant. It provides a way of ensuring the continued safety of consumers and users and, by identifying chemicals and products with low immunogenicity, reducing the suffering due to eczema.”

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The above story is reprinted from materials provided by BioMed Central, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Henrik Johansson, Malin Lindstedt, Ann-Sofie Albrekt and Carl AK Borrebaeck. A genomic biomarker signature can predict skin sensitizers using a cell-based in vitro alternative to animal tests. BMC Genomics, August 2011 [link]

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