Forests crucial to green growth

The value of forests and tree-based ecosystems extends far beyond carbon sequestration; they are the foundation of sustainable societies.A new report, launched in Jakarta, Indonesia on 21 March — the International Day of Forests — promotes REDD+ and the Green Economy as together providing a new pathway to sustainable development that can benefit all nations. It claims this approach can conserve and even boost the economic and social benefits forests provide to human society.Building Natural Capital — How REDD+ Can Support a Green Economy was developed by the International Resources Panel. It outlines how REDD+ can be integrated into a Green Economy to support pro-poor development while maintaining or increasing forest cover.According to the report, REDD+ needs to be placed in a landscape-scale planning framework that goes beyond forests to consider all sectors of a modern economy and the needs of agriculture, energy, water resources, finance, transport, industry, trade and cities.In this way, REDD+ would add value to other initiatives, such as agroforestry projects that are being implemented within these sectors, and be a critical element in a green economy.The report provides recommendations on how to integrate REDD+ and Green Economy approaches, such as through better coordination, stronger private sector engagement, changes in fiscal incentive frameworks, greater focus on assisting policymakers to understand the role forests play in propping up economies, and equitable benefit sharing.While it is recognized that what lies ahead is a long process of societies adapting to new conditions, REDD+ could be integral to increasing agricultural and forestry outputs to meet future needs, while at the same time enhancing the conservation of forests and ecosystem services.Each year, the International Day of Forests highlights the unique role of forests in the environment and in sustaining livelihoods. The theme this year is Celebrating Forests for Sustainable Development.”It is important day to remind us to save our planet as it is the only one we know which has trees says Tony Simons the Director General of the World Agroforestry Centre (ICRAF). “Trees are what made Earth habitable for mammals, and destruction of forests will lead to the ultimate destruction of mammals — including humans. Trees are one of the few things which live longer than humans — a true intergenerational gift. He added.Forests and trees are key to sustainable development. Not only do they store carbon, they support biodiversity, regulate water flows and, reduce soil erosion. Nearly 1.6 billion people worldwide depend on forests as a source of food, medicines, timber and fuel.Story Source:The above story is based on materials provided by World Agroforestry Centre (ICRAF). Note: Materials may be edited for content and length.

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Distinct brain disorders biologically linked: Disruption to the gene TOP3B increases susceptibility to schizophrenia and a learning disorder

Aug. 4, 2013 — A team of researchers have shown that schizophrenia and a disorder associated with autism and learning difficulties share a common biological pathway. This is one of the first times that researchers have uncovered genetic evidence for the underlying causes of schizophrenia.The team found that a disruption of the gene TOP3B, an exceedingly rare occurrence in most parts of the world, is fairly common in a uniquely genetically distinct founder population from North-eastern Finland. In this population, which has grown in relative isolation for several centuries, the disruption of TOP3B is associated with an increased risk of schizophrenia as well as with impairment in intellectual function and learning.Furthermore, the biochemical investigation of the protein encoded by the TOP3B gene allowed the researchers to gain first insight into the cellular processes that might be disturbed in the affected individuals.Although the past two decades have revealed a wealth of information about the genetics of disease, we still know little about the biology behind schizophrenia. Many associations between schizophrenia and genetic risk factors have been reported, but only a very few can be considered schizophrenia susceptibility genes. This study uncovers an important biological pathway that appears to underlie schizophrenia and could contribute to the cognitive impairment that is an important component of this disorder.”This is a tremendous discovery for our team; not only have we uncovered vital information about the biology behind schizophrenia, but we have also linked this same biological process to a disorder associated with learning difficulties,” says Dr Aarno Palotie, lead author from the Wellcome Trust Sanger Institute, the Broad Institute of MIT and Harvard and the Institute for Molecular Medicine Finland. “Our findings offer great hope for future studies into the genetic basis of schizophrenia and other brain disorders, potentially finding new drug targets against them.”The North-eastern population of Finland has three times the frequency of schizophrenia compared to the national average in Finland, as well as a higher rate of intellectual impairment and learning difficulties. The team used data collected from this unique population to sift through genomic data for genetic deletions that may influence people’s susceptibility to schizophrenia.The team identified a rare genetic deletion affecting TOP3B in the North-eastern Finnish population that increases a person’s susceptibility to schizophrenia two-fold and that also is associated with an increased frequency of other disorders of brain development such as intellectual impairment. They speculate that this deletion directly disrupts the TOP3B gene to cause its effects on the brain.Having identified the link between TOP3B and schizophrenia, the researchers sought to understand why disrupting this gene might increase susceptibility to disease, and for this purpose they investigated the function of the protein that it encodes.”Such an approach is only possible when researchers from different disciplines — in our case geneticists and biochemists team up,” says Professor Utz Fischer, author from the University of Wurzburg. “Luckily, when we teamed up with the genetic team we had already worked on the TOP3B gene product for more than 10 years and hence had a good idea what this protein is doing.”TOP3B encodes a type of protein that typically helps the cell to unwind and wind DNA helices — essential to normal cell function. …

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New findings could help improve development of drugs for addiction

Aug. 2, 2013 — Scientists from the Florida campus of The Scripps Research Institute have described findings that could enable the development of more effective drugs for addiction with fewer side effects.The study, published in the August 2, 2013 issue of the Journal of Biological Chemistry, showed in a combination of cell and animal studies that one active compound maintains a strong bias towards a single biological pathway, providing insight into what future drugs could look like.The compound examined in the study, known as 6′- guanidinonaltrindole (6′-GNTI), targets the kappa opioid receptor (KOR). Located on nerve cells, KOR plays a role in the release of dopamine, a neurotransmitter that plays a key role in drug addiction. Drugs of abuse often cause the brain to release large amounts of dopamine, flooding the brain’s reward system and reinforcing the addictive cycle.”There are a number of drug discovery efforts ongoing for KOR,” said Laura Bohn, a TSRI associate professor, who led the study. “The ultimate question is how this receptor should be acted upon to achieve the best therapeutic effects. Our study identifies a marker that shows how things normally happen in live neurons — a critically important secondary test to evaluate potential compounds.”While KOR has become the focus for drug discovery efforts aimed at treating addiction and mood disorders, KOR can react to signals that originate independently from multiple biological pathways, so current drug candidates targeting KOR often produce unwanted side effects. Compounds that activate KOR can decrease the rewarding effects of abused drugs, but also induce sedation and depression.The new findings, from studies of nerve cells in the striatum (an area of the brain involved in motor activity and higher brain function), reveal a point on the KOR signaling pathway that may prove to be an important indicator of whether drug candidates can produce effects similar to the natural biological effects.”Standard screening assays can catch differences but those differences may not play out in live tissue,” Bohn noted. “Essentially, we have shown an important link between cell-based screening assays and what occurs naturally in animal models.”The first author of the study, ‘Functional Selectivity of 6′-guanidinonaltrindole (6’-GNTI) at Kappa Opioid Receptors in Striatal Neurons,” is Cullen L. Schmid of TSRI. Other authors include John M. …

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New designer compound treats heart failure by targeting cell nucleus

Aug. 1, 2013 — Researchers from Case Western Reserve University School of Medicine and the Dana-Farber Cancer Institute have made a fundamental discovery relevant to the understanding and treatment of heart failure — a leading cause of death worldwide. The team discovered a new molecular pathway responsible for causing heart failure and showed that a first-in-class prototype drug, JQ1, blocks this pathway to protect the heart from damage.In contrast to standard therapies for heart failure, JQ1 works directly within the cell’s command center, or nucleus, to prevent damaging stress responses. This groundbreaking research lays the foundation for an entirely new way of treating a diseased heart. The study is published in the August 1 issue of Cell.”As a practicing cardiologist, it is clear that current heart failure drugs fall alarmingly short for countless patients. Our discovery heralds a brand new class of drugs which work within the cell nucleus and offers promise to millions suffering from this common and lethal disease,” said Saptarsi Haldar, MD, senior author on the paper, assistant professor of medicine at Case Western Reserve and cardiologist at University Hospitals Case Medical Center.Heart failure occurs when the organ’s pumping capacity cannot meet the body’s needs. Existing drugs, most of which block hormones such as adrenaline at the cell’s outer surface, have improved patient survival. Unfortunately, several clinical studies have demonstrated that heart failure patients taking these hormone-blocking drugs still succumb to high rates of hospitalization and death. Leveraging a new approach, the research team turned their attention from the cell’s periphery to the nucleus — the very place that unleashes sweeping damage-control responses which, if left unchecked, ultimately destroy the heart.The team found that a new family of genes, called BET bromodomains, cause heart failure because they drive hyperactive stress responses in the nucleus. Prior research linking BET bromodomains to cancer prompted the laboratory of James Bradner, MD, the paper’s senior author and a researcher at the Dana-Farber, to develop a direct-acting BET inhibitor, called JQ1. …

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Biochemical mapping helps explain who will respond to antidepressants

July 18, 2013 — Duke Medicine researchers have identified biochemical changes in people taking antidepressants — but only in those whose depression improves. These changes occur in a neurotransmitter pathway that is connected to the pineal gland, the part of the endocrine system that controls the sleep cycle, suggesting an added link between sleep, depression and treatment outcomes.The study, published on July 17, 2013, in the journal PLOS ONE, uses an emerging science called pharmacometabolomics to measure and map hundreds of chemicals in the blood in order to define the mechanisms underlying disease and to develop new treatment strategies based on a patient’s metabolic profile.”Metabolomics is teaching us about the differences in metabolic profiles of patients who respond to medication, and those who do not,” said Rima Kaddurah-Daouk, PhD, associate professor of psychiatry and behavioral sciences at Duke Medicine and leader of the Pharmacometabolomics Research Network.”This could help us to better target the right therapies for patients suffering from depression who can benefit from treatment with certain antidepressants, and identify, early on, patients who are resistant to treatment and should be placed on different therapies.”Major depressive disorder — a form of depression characterized by a severely depressed mood that persists two weeks or more — is one of the most prevalent mental disorders in the United States, affecting 6.7% of the adult population in a given year.Selective serotonin reuptake inhibitors (SSRIs) are the most commonly prescribed antidepressants for major depressive disorder, but only some patients benefit from SSRI treatment. Others may respond to placebo, while some may not find relief from either. This variability in response creates dilemmas for treating physicians where the only choice they have is to test one drug at a time and wait for several weeks to determine if a patient is going to respond to the specific SSRI.Recent studies by the Duke team have used metabolomics tools to map biochemical pathways implicated in depression and have begun to distinguish which patients respond to treatment with an SSRI or placebo based on their metabolic profiles. These studies have pointed to several metabolites on the tryptophan metabolic pathway as potential contributing factors to whether patients respond to antidepressants.Tryptophan is metabolized in different ways. One pathway leads to serotonin and subsequently to melatonin and an array of melatonin-like chemicals called methoxyindoles produced in the pineal gland. In the current study, the researchers analyzed levels of metabolites within branches of the tryptophan pathway and correlated changes with treatment outcomes.Seventy-five patients with major depressive disorder were randomized to take sertraline (Zoloft) or placebo in the double-blind trial. After one week and four weeks of taking the SSRI or placebo, the researchers measured improvement in symptoms of depression to determine response to treatment, and blood samples were taken and analyzed using a metabolomics platform build to measure neurotransmitters.The researchers observed that 60 percent of patients taking the SSRI responded to the treatment, and 50 percent of those taking placebo also responded. Several metabolic changes in the tryptophan pathway leading to melatonin and methoxyindoles were seen in patients taking the SSRI who responded to the treatment; these changes were not found in those who did not respond to the antidepressant.The results suggest that serotonin metabolism in the pineal gland may play a role in the underlying cause of depression and its treatment outcomes, based on the biochemical changes that were seen to be associated with improvements in depression.”This study revealed that the pineal gland is involved in mechanisms of recovery from a depressed state,” said Kaddurah-Daouk. “We have started to map serotonin which is believed to be implicated in depression, but now realize that it may not be serotonin itself that is important in depression recovery. …

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Nanog protein promotes growth of head and neck cancer

June 18, 2013 — A new study led by researchers at The Ohio State University Comprehensive Cancer Center — Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC-James) has identified a biochemical pathway in cancer stem cells that is essential for promoting head and neck cancer.The study shows that a protein called Nanog, which is normally active in embryonic stem cells, promotes the growth of cancer stem cells in head and neck cancer. The findings provide information essential for designing novel targeted drugs that might improve the treatment of head and neck cancer.Normally, Nanog helps healthy embryonic stem cells maintain their undifferentiated, uncommitted (i.e., pluripotent) state. But recent evidence suggests that Nanog promotes tumor growth by stimulating the proliferation of cancer stem cells.”This study defines a signaling axis that is essential for head and neck cancer progression, and our findings show that this axis may be disrupted at three key steps,” says principal investigator Quintin Pan, PhD, associate professor of otolaryngology at the OSUCCC — James. “Targeted drugs that are designed to inhibit any or all of these three steps might greatly improve the treatment of head and neck cancer.”The findings were published in a recent issue of the journal Oncogene.Specifically, the study shows that an enzyme called “protein kinase C-epsilon” (PKCepsilon) adds energy-packing phosphate groups to the Nanog molecule. This phosphorylation of Nanog stabilizes and activates the molecule.It also triggers a series of events: Two Nanog molecules bind together, and these are joined by a third “co-activating” molecule called p300. This molecular complex then binds to the promoter region of a gene called Bmi1, an event that increases the expression of the gene. This, in turn, stimulates proliferation of cancer stem cells.”Our work shows that the PKCepsilon/Nanog/Bmi1 signaling axis is essential to promote head and neck cancer,” Pan says. “And it provides initial evidence that the development of inhibitors that block critical points in this axis might yield a potent collection of targeted anti-cancer therapeutics that could be valuable for the treatment of head and neck cancer.”Funding from the NIH/National Cancer Institute (grant CA135096), the American Cancer Society; The Michelle Theado Memorial Grant from The Joan Bisesi Fund for Head and Neck Oncology Research, and The Sloman Foundation supported this research.Other researchers involved in this study were X. …

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Metabolic molecule drives growth of aggressive brain cancer

June 14, 2013 — A study led by researchers at The Ohio State University Comprehensive Cancer Center — Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC — James) has identified an abnormal metabolic pathway that drives cancer-cell growth in a particular glioblastoma subtype. The finding might lead to new therapies for a subset of patients with glioblastoma, the most common and lethal form of brain cancer.The physician scientists sought to identify glioblastoma subtype-specific cancer stem cells. Genetic analyses have shown that high-grade gliomas can be divided into four subtypes: proneural, neural, classic and mesenchymal.This study shows that the mesenchymal subtype is the most aggressive subtype, that it has the poorest prognosis among affected patients, and that cancer stem cells isolated from the mesenchymal subtype have significantly higher levels of the enzyme ALDH1A3 compared with the proneural subtype.The findings, published recently in the Proceedings of the National Academy of Sciences, show that high levels of the enzyme drive tumor growth.”Our study suggests that ALDH1A3 is a potentially functional biomarker for mesenchymal glioma stem cells, and that inhibiting that enzyme might offer a promising therapeutic approach for high-grade gliomas that have a mesenchymal signature,” says principal investigator Ichiro Nakano, MD, PhD, associate professor of neurosurgery at the OSUCCC — James. “This indicates that therapies for high-grade gliomas should be personalized, that is, based on the tumor subtype instead of applying one treatment to all patients,” he says.The National Cancer Institute estimates that 23,130 Americans will be diagnosed with brain and other nervous system tumors in 2013, and that 14,000 people will die of these malignancies. Glioblastoma accounts for about 15 percent of all brain tumors, is resistant to current therapies and has a survival as short as 15 months after diagnosis.Little is known, however, about the metabolic pathways that drive the growth of individual glioblastoma subtypes — knowledge that is crucial for developing novel and effective targeted therapies that might improve treatment for these lethal tumors.For this study, Nakano and his collaborators used cancer cells from 40 patients with high-grade gliomas, focusing on tumor cells with a stem-cell signature. The researchers then used microarray analysis and pre-clinical animal assays to identify two predominant glioblastoma subtypes, proneural and mesenchymal.Key technical findings include:Genes involved in glycolysis and gluconeogenesis, particularly ALDH1A3, were significantly up-regulated in mesenchymal glioma stem cells compared to proneural stem cells; Mesenchymal glioma stem cells show significantly higher radiation resistance and high expression of DNA-repair genes; Radiation induces transformation of proneural glioma stem cells into mesenchymal-like glioma stem cells that are highly resistant to radiation treatment; inhibiting the ALDH1 pathway reverses this resistance. Inhibiting ALDH1A3-mediated pathways slows the growth of mesenchymal glioma stem cells and might provide a promising therapeutic approach for glioblastomas with a mesenchymal signature. “Overall, our data suggest that a novel signaling mechanism underlies the transformation of proneural glioma stem cells to mesenchymal-like cells and their maintenance as stem-like cells,” Nakano says. …

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