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Harvard medical school Post stroke: Addressing thinking and memory problemsA stroke can disrupt your ability to think clearly and can cause problems with your memory, attention, and organizational abilities. Both speech and occupational therapists work with people to improve these areas and to develop strategies to compensate for problems — for example, using cue cards and detailed lists or simplifying daily routines.Coping with spatial neglect. One fairly common effect of stroke is called "neglect." This is a lack of awareness of one side of the body and the space around that side of the body. The left side is more commonly affected than the right. If you have neglect, you may bump into things on your left without noticing them, shave or apply makeup only on the right side of your face, or eat food on only the right side of your plate.Skin Care and RepairProtect your brain: That’s the strategy that Harvard doctors recommend in this report on preventing and treating stroke. Whether you’ve already had a mini-stroke or a major stroke, or have been warned that your high blood pressure might cause a future stroke, Stroke: Diagnosing, treating, and recovering from a "brain attack" provides help and advice.If you have this problem, occupational and speech therapists will cue you to look frequently toward your neglected side and then teach you to cue yourself. One example: A red line down the left margin of the page you are reading may help remind you to look all the way to the marker so you see all the words on that line. A variety of software programs and games can also help train people to pay attention to the things on the neglected side. Caregivers and family members can help by setting important objects (food, writing implements) on the person's neglected side to train him or her to focus more on that side. Prism glasses — which are shaped in a way that changes the focus point of your eyes — can be helpful to shift your view more toward the neglected side.To learn more about strokes and how they can affect you, read Stroke: Diagnosing, treating, and recovering from a "brain attack", a Special Health Report from Harvard Medical School.
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A tool that tracks and stops bacterial blight outbreaks in ricericetoday.irri.org/a-tool-that-tracks-and-stops-bacterial-blight-outbreaks-in-rice/A new, faster, and more accurate way of identifying infectious organisms—down to their genetic fingerprint—could finally put farmers a step ahead of bacterial blight. Severe bacterial blight infection in a susceptible rice variety from West Java, Indonesia. (Photo by R. Oliva)Severe bacterial blight infection in a susceptible rice variety from West Java, Indonesia. (Photo by R. Oliva)A revolutionary tool called the PathoTracer has been developed at the International Rice Research Institute (IRRI) and it can identify the exact strain of the bacterium that causes bacterial blight present in a field in a matter of days instead of several months of laboratory work.“It’s like a paternity test that uses DNA profiling, ” said Ricardo Oliva, a plant pathologist at IRRI. “It will not only tell you that you have bacterial blight in your plant. It will tell you the particular strain of the pathogen so that we can recommend varieties resistant to it.”For more than four years, Dr. Oliva and his team worked on deciphering the genetic code of Xanthomonas oryzae pv. oryzae, the pathogen that causes bacterial blight, to develop the test. Bacterial blight is one of the most serious diseases of rice. The earlier the disease occurs, the higher the yield loss—which could be as much as 70% in vulnerable varieties.“Bacterial blight is a persistent disease in rice fields, ” said Dr. Oliva. “The epidemic builds up every season when susceptible varieties are planted. The problem is that the bacterial strains vary from one place to another and farmers don’t know which are the resistant varieties for that region. We were always behind because the pathogens always moved and evolved faster.”Identifying the strains of bacterial blight present in the field requires a lot of labor and time. You need people to collect as many samples as they can over large areas to accurately monitor the pathogen population. In addition, isolating the pathogens in the lab is laborious and it typically takes several months or even a year to determine the prevalent strains in a region.The PathoTracer can identify the local bacteria in the field using small leaf discs as samples. The samples will be sent to a certified laboratory to perform the genetic test and the results will be analyzed by IRRI.The team that developed PathoTracer. Left row: Maritess Carillaga, Cipto Nugroho, Ian Lorenzo Quibod, and Genelou Grande. Right row: Veronica Roman-Reyna, Sapphire Thea Charlene Coronejo, and Dr. Oliva. Not in photo: Eula Gems Oreiro, EiEi Aung, and Marian Hanna Nguyen. (Photo by Isagani Serrano, IRRI)The team that developed PathoTracer. Left row (front to back): Maritess Carillaga, Cipto Nugroho, Ian Lorenzo Quibod, and Genelou Grande. Right row: Veronica Roman-Reyna, Sapphire Thea Charlene Coronejo, and Dr. Oliva. Not in photo: Eula Gems Oreiro, EiEi Aung, Epifania Garcia, Ismael Mamiit, and Marian Hanna Nguyen. (Photo by Isagani Serrano, IRRI)“It takes only a few days to analyze the samples, ” Dr. Oliva explained. “With the PathoTracer, we can bring a year’s work down to probably two weeks. Because the tool can rapidly and efficiently monitor the pathogen present in each season, the information can be available before the cropping season ends.”It’s like knowing the future, and predicting what would happen the next season can empower the farmers, according to Dr. Oliva.“Recognizing the specific local bacteria present in the current season can help us plan for the next, ” he added. “We can come up with a list of recommended rice varieties that are resistant to the prevalent pathogen strains in the locality. By planting the recommended varieties, farmers can reduce the risk of an epidemic in the next season and increase their profits.”The PathoTracer was pilot tested in Mindanao in the southern part of the Philippines in April 2017. The rains came early in the region, just after the peak of the dry season, and that triggered an outbreak of bacterial blight.“We went there and took samples from different fields, ” Dr. Oliva said. “By the end of April, we had the results and we were able to come up with a list of resistant varieties that could stop the pathogen. We submitted our recommendation to give farmers a choice in reducing the risk. If the farmers planted the same rice varieties in the succeeding rainy seasons, I am 100% sure the results would be very bad.”The PathoTracer can run thousands of samples and can, therefore, easily cover large areas, making it an essential tool for extension workers of agriculture departments and private-sector rice producers, or it can be incorporated into monitoring platforms such as the Philippine Rice Information System (PRiSM) or Pest and Disease Risk Identification and Management (PRIME) to support national or regional crop health decision-making.“National breeding programs could also make more informed decisions, ” Dr. Oliva said. “If you know the pathogen population in the entire Philippines, for example, the country’s breeding program could target those strains.”IRRI is interested in expanding the genetic testing tool to include rice blast and, further down the road, all bacteria, viruses, and fungi that infect rice.The speed at which PathoTracer can identify the strains of bacterial blight present in the field can be used for recommending resistant rice varieties to farmers for planting in the next cropping season. (Photo: IRRI)The speed at which PathoTracer can identify the strains of bacterial blight present in the field can be used for recommending resistant rice varieties to farmers for planting in the next cropping season. (Photo: IRRI)The PathoTracer has been tested in other Asian countries and IRRI expects to roll it out early in 2018. When it becomes available, the expected potential impact of the PathoTracer on a devastating disease that affects rice fields worldwide would be huge.“Imagine if this tool prevented bacterial blight outbreaks every season across Asia, ” said Dr. Oliva. “It’s super cool!”For more information about bacterial blight, see Section II, Chapter 2 of IRRI’s Rice Diseases Online Resource
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In the future we won’t edit genomes—we’ll just print out new onesWhy redesigning the humble yeast could kick off the next industrial revolution.by Bryan Walsh February 16, 2018At least since thirsty Sumerians began brewing beer thousands of years ago, Homo sapiens has had a tight relationship with Saccharomyces cerevisiae, the unicellular fungus better known as brewer’s yeast. Through fermentation, humans were able to harness a microscopic species for our own ends. These days yeast cells produce ethanol and insulin and are the workhorse of science labs.That doesn’t mean S. cerevisiae can’t be further improved—at least not if Jef Boeke has his way. The director of the Institute for Systems Genetics at New York University’s Langone Health, Boeke is leading an international team of hundreds dedicated to synthesizing the 12.5 million genetic letters that make up a yeast’s cells genome.In practice, that means gradually replacing each yeast chromosome—there are 16 of them—with DNA fabricated on stove-size chemical synthesizers. As they go, Boeke and collaborators at nearly a dozen institutions are streamlining the yeast genome and putting in back doors to let researchers shuffle its genes at will. In the end, the synthetic yeast—called Sc2.0—will be fully customizable.“Over the next 10 years synthetic biology is going to be producing all kinds of compounds and materials with microorganisms, ” says Boeke. “We hope that our yeast is going to play a big role in that.”Think of the project as something like Henry Ford’s first automobile—hand built and, for now, one of a kind. One day, though, we may routinely design genomes on computer screens. Instead of engineering or even editing the DNA of an organism, it could become easier to just print out a fresh copy. Imagine designer algae that make fuel; disease-proof organs; even extinct species resurrected.Jef Boeke leads an effort to create yeast with a man-made genome.“I think this could be bigger than the space revolution or the computer revolution, ” says George Church, a genome scientist at Harvard Medical School.Researchers have previously synthesized the genetic instructions that operate viruses and bacteria. But yeast cells are eukaryotic—meaning they confine their genomes in a nucleus and bundle them in chromosomes, just as humans do. Their genomes are also much bigger.That’s a problem because synthesizing DNA is still nowhere near as cheap as reading it. A human genome can now be sequenced for $1, 000, with the cost still falling. By comparison, to replace every DNA letter in yeast, Boeke will have to buy $1.25 million worth of it. Add labor and computer power, and the total cost of the project, already under way for a decade, is considerably more.Along with Church, among others, Boeke is a leader of GP-write, an organization advocating for international research to reduce the cost of designing, engineering, and testing genomes by a factor of a thousand over the next decade. “We have all kinds of challenges facing ourselves as a species on this planet, and biology could have a huge impact on them, ” he says. “But only if we can drive down costs.”Bottom upA scientist named Ronald Davis at Stanford first suggested the possibility of synthesizing the yeast genome at a conference in 2004—though initially, Boeke didn’t see the point. “Why would anyone want to do this?” he recalls thinking.But Boeke came around to the idea that manufacturing a yeast genome might be the best way to comprehend the organism. By replacing each part, you might learn which genes are necessary and which the organism can live without. Some team members call the idea “build to understand.”“It’s a different take on trying to understand how living things work, ” says Leslie Mitchell, a postdoctoral fellow in the NYU lab and one of the main designers of the synthetic yeast. “We learn what gaps in our knowledge exist in a bottom-up genetic approach.”Joel Bader, a computer scientist at Johns Hopkins, signed on to develop software that let scientists see the yeast chromosomes on a screen and keep track of versions as they changed, like a Google Docs for biology. And in 2008, to make the DNA, Boeke launched an undergraduate course at Hopkins called “Build a Genome.” Students would learn basic molecular biology as each one assembled a continuous stretch of 10, 000 DNA letters that would go toward the synthetic-yeast project. Later, several institutions in China joined to share the workload, along with collaborators in Britain, Australia, and Japan.“We assign chromosomes to individual teams, like assigning a chapter of a book, and they have the freedom to decide how to do it, as long as it’s based 100 percent on what we design, ” says Patrick Cai, a synthetic biologist at the University of Manchester and the yeast project’s international coordinator.Next stepsIt took Boeke and his team eight years before they were able to publish their first fully artificial yeast chromosome. The project has since accelerated. Last March, the next five synthetic yeast chromosomes were described in a suite of papers in Science, and Boeke says that all 16 chromosomes are now at least 80 percent done. These efforts represent the largest amount of genetic material ever synthesized and then joined together.It helps that the yeast genome has proved remarkably resilient to the team’s visions and revisions. “Probably the biggest headline here is that you can torture the genome in a multitude of different ways, and the yeast just laughs, ” says Boeke.
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Sequencing Human Genome with Pocket-Sized “Nanopore” DeviceDr. Francis CollinsMinION sequencing deviceIt’s hard to believe, but it’s been almost 15 years since we successfully completed the Human Genome Project, ahead of schedule and under budget. I was proud to stand with my international colleagues in a celebration at the Library of Congress on April 14, 2003 (which happens to be my birthday), to announce that we had stitched together the very first reference sequence of the human genome at a total cost of about $400 million. As remarkable as that achievement was, it was just the beginning of our ongoing effort to understand the human genome, and to use that understanding to improve human health.That first reference human genome was sequenced using automated machines that were the size of small phone booths. Since then, breathtaking progress has been made in developing innovative technologies that have made DNA sequencing far easier, faster, and more affordable. Now, a report in Nature Biotechnology highlights the latest advance: the sequencing and assembly of a human genome using a pocket-sized device [1]. It was generated using several “nanopore” devices that can be purchased online with a “starter kit” for just $1, 000. In fact, this new genome sequence—completed in a matter of weeks—includes some notoriously hard-to-sequence stretches of DNA, filling several key gaps in our original reference genome.For most sequencing methods, DNA must be broken into smaller, more manageable fragments. That means all of the nucleotide “letters”— the As, Cs, Gs, and Ts—in the DNA code must be pieced back together in their correct order like a complex puzzle. While many methods are incredibly accurate at reassembling many parts of the puzzle, it’s much trickier to do this in highly repetitive stretches of DNA. When broken up, they produce puzzle pieces that are essentially identical.To get around that problem, some newer sequencing technologies are able to read out much longer stretches of DNA. In this latest report, an international team including Nicholas Loman at the University of Birmingham in the United Kingdom (U.K.), Matthew Loose at the University of Nottingham, U.K., and Adam Phillippy at NIH’s National Human Genome Research Institute, Bethesda, MD, relied on one such device: the hand-held MinION nanopore sequencer, produced by Oxford Nanopore Technologies.In fact, nanopore sequencing was named one of Science magazine’s “Breakthroughs of the Year” in 2016. The method involves threading single DNA strands through many tiny protein pores, i.e., nanopores, set in an electrically resistant polymer membrane. Inside the device, an ionic current is passed through the nanopore. When a single-stranded DNA molecule passes through the charged nanopore, it alters the current. In fact, the current is altered in different ways depending on which of DNA’s four unique nucletoides—adenine (A), cytosine (C), guanine (G), or thymine (T)—is passing through the pore. As a result, it’s possible to “read” off the DNA sequence, letter by letter!The nanopore sequencer was initially used primarily for sequencing smaller microbial genomes. In fact, Loman was part of a team that used the portable nanopore device to track Ebola and Zika viruses during the recent outbreaks in Africa and Brazil [2, 3]. The nanopore sequencer was also used on the International Space Station to do the very first DNA sequencing in zero gravity [4].The larger, more complex human genome represents a much stiffer challenge. But Loman and colleagues took on the challenge, betting that MinION was now up to the task based on recent improvements in its sequencing speed, computer software, and sample prep.The team, which included five labs in three countries, sequenced the complete genome of a well-studied human cell line in a matter of weeks. The researchers generated 91.2 gigabytes of DNA data, enough to cover the genome 30 times over, which helps to put the pieces together accurately. Most notably, they also generated ultra-long “reads” up to 882, 000 bases of contiguous DNA sequence. The researchers report that they have since read individual DNA molecules over a million bases long! Though the final cost ran about $23, 000 to sequence one human genome, further refinements should continue to drop the price.The real trick to getting such long reads is to prepare the DNA in such a way that the molecules don’t get cut or otherwise broken into small fragments, which the team has learned to do well. In fact, the team reports that in principle there may be no limit to the read-lengths that are possible using nanopore-based sequencing, including possibly entire chromosomes. The challenge will be getting the DNA molecules into the sequencing device without damaging them. Once a DNA molecule is threaded into a pore, there’s really no reason for it to stop until its passed all the way through.Despite those longer, easier-to-assemble reads, the researchers still required some big computers, including the high-performance computational resources in NIH’s Biowulf system, to make sense of the data, correct for errors, and piece together portions of the genome that had been impossible to assemble previously. For example, they resolved several highly repetitive genomic regions, including the sequences of some essential genes in immunity. They were also able to accurately estimate the lengths of highly repetitive telomeres, which act like “caps” at the tips of chromosomes. Telomere lengths are of great research interest for their implications in aging and cancer.Just as capabilities once only available through huge supercomputers can today be accessed though apps on smartphones, DNA sequencers continue to get better, smaller, and more portable. And as this study demonstrates, there’s no doubt that we’re pushing ever closer to a time when it may become both feasible and practical to sequence individual human genomes to bring greater precision to the delivery of health care for everyone.References:[1] Nanopore sequencing and assembly of a human genome with ultra-long reads. Jain M, Koren S, Miga KH, Quick J, Rand AC, Sasani TA, Tyson JR, Beggs AD, Dilthey AT, Fiddes IT, Malla S, Marriott H, Nieto T, O’Grady J, Olsen HE, Pedersen BS, Rhie A, Richardson H, Quinlan AR, Snutch TP, Tee L, Paten B, Phillippy AM, Simpson JT, Loman NJ, Loose M. Nature Biotech. 2018 Jan. 29. [Epub ahead of print][2] Real-time, portable genome sequencing for Ebola surveillance. Quick J, Loman NJ, Duraffour S, Simpson JT, Severi E, Cowley L, et al..Nature. 2016 Feb 11;530(7589):228-232.[3] Establishment and cryptic transmission of Zika virus in Brazil and the Americas. Faria NR, Quick J, Claro IM, Thézé J, de Jesus JG, et al. Nature. 2017 Jun 15;546(7658):406-410.[4] Nanopore DNA Sequencing and Genome Assembly on the International Space Station. Castro-Wallace SL, Chiu CY, John KK, Stahl SE, Rubins KH, McIntyre ABR, Dworkin JP, Lupisella ML, Smith DJ, Botkin DJ, Stephenson TA, Juul S, Turner DJ, Izquierdo F, Federman S, Stryke D, Somasekar S, Alexander N, Yu G, Mason CE7, Burton AS. Sci Rep. 2017 Dec 21;7(1):18022.Links:DNA Sequencing (National Human Genome Research Institute/NIH)Loman Lab (University of Birmingham, United Kingdom)Matt Loose (University of Nottingham, U.K.)Adam Phillippy (National Human Genome Research Institute/NIH)MinION (Oxford Nanopore Technologies, U.K.)NIH Support: National Human Genome Research Institute; National Cancer Institute
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How To Evaluate Forensic DNA Quality With Quantifiler Trio DNA Quantification KitBy Angie Lackey04.05.2018Wouldn’t it be wonderful if there was a tool that forensic scientists could use to assess the quality of an unknown DNA sample before attempting to generate an STR profile? DNA samples collected from crime scenes range from DNA-rich fluids, like blood and saliva, to a few skin cells left behind from a casual touch. For example, there is generally much more DNA in a bloodstain than on, say, a knife handle. Getting an accurate estimate of DNA concentration is crucial to generating a robust DNA profile. But what if the process of DNA quantification could provide even more information? What if it could provide information about the quality of a DNA sample?Well, luckily there is the Quantifiler Trio Quantification Kit. The Quant Trio kit provides DNA concentration, in addition to quality assessments for degradation and inhibition of the sample. And it can help you make workflow decisions based on quantity of autosomal vs male DNA present.DNA can be degraded by environmental influences like sunlight, extreme heat, and humidity; degradation may manifest as a ski-slope pattern in the STR electropherogram. You see this pattern with degraded DNA because small fragments remain intact and amplify well, but the large fragments are damaged and don’t amplify well.To evaluate degradation in forensic samples, a Degradation Index, or DI, has been added to the Quantifiler Trio Kit. The DI is the ratio of the smaller to larger DNA fragments in a sample. It is automatically calculated in the software.The DI for intact DNA will be ≤1, as the concentration of the small and large fragments are approximately equal. Any DI over 1 could indicate degradation. To overcome degradation, you could target more DNA during STR amplification in an effort to increase the signal of the large DNA fragments.Impurities in a DNA extract can also suppress amplification of DNA – we call this inhibition of the reaction. Inhibition can occur at the quantification or amplification stages and can affect the interpretability of your DNA profile. Inhibition could appear similar to degradation, because large DNA fragments don’t amplify as well as small DNA fragments in the presence of the inhibitor.Although the STR profiles from degraded and inhibited samples may appear similar, don’t be fooled. Unlike with degraded DNA, increasing your target adds even more inhibitor to the reaction, making the inhibition even worse.The Internal PCR Control (IPC) is synthetic DNA that is amplified along with each sample. It just confirms that the assay worked as expected. Inhibitors can affect the IPC amplification; an increase in the threshold cycle value for the IPC indicates that it took the synthetic DNA longer than expected to reach a defined threshold; therefore something was impeding the reaction.There is one tricky thing about interpreting elevated IPC CTvalues. High concentrations of DNA in an extract (above 5ng/uL) can elevate the IPC Ct slightly because the entire reaction becomes saturated. Because of this, it is very important to evaluate the IPC CTvalue in conjunction with the DNA concentration. For example, if you were to question whether a sample that is at a concentration of 50ng/ul is inhibited, you would have to compare it to other samples or standards with a similarly high concentration. The same is true for a sample with a low concentration – you should only compare like to like.Because degradation and inhibition both affect large DNA targets more than small, it is necessary to assess the quality flags for degradation and inhibition together. For example, if the DI is elevated, and the IPC is as expected then the sample is degraded and not inhibited. However, if the IPC and DI are both elevated, you may not be able to determine if the sample is simply inhibited, or both degraded and inhibited. In a severely inhibited sample, the inhibition should be addressed by dilution or clean up and if necessary, the treated sample can be re-quantified to assess whether degradation is present.You can learn more from forensic scientists, who work with bone, and use real-time PCR analysis to make decisions that deliver improved recovery of alleles.
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Gene Editing for GoodHow CRISPR Could Transform Global DevelopmentBy Bill GatesToday, more people are living healthy, productive lives than ever before. This good news may come as a surprise, but there is plenty of evidence for it. Since the early 1990s, global child mortality has been cut in half. There have been massive reductions in cases of tuberculosis, malaria, and HIV/AIDS. The incidence of polio has decreased by 99 percent, bringing the world to the verge of eradicating a major infectious disease, a feat humanity has accomplished only once before, with smallpox. The proportion of the world’s population in extreme poverty, defined by the World Bank as living on less than $1.90 per day, has fallen from 35 percent to about 11 percent.Continued progress is not inevitable, however, and a great deal of unnecessary suffering and inequity remains. By the end of this year, five million children under the age of five will have died—mostly in poor countries and mostly from preventable causes. Hundreds of millions of other children will continue to suffer needlessly from diseases and malnutrition that can cause lifelong cognitive and physical disabilities. And more than 750 million people—mostly rural farm families in sub-Saharan Africa and South Asia—still live in extreme poverty, according to World Bank estimates. The women and girls among them, in particular, are denied economic opportunity.Some of the remaining suffering can be eased by continuing to fund the development assistance programs and multilateral partnerships that are known to work. These efforts can help sustain progress, especially as the world gets better at using data to help guide the allocation of resources. But ultimately, eliminating the most persistent diseases and causes of poverty will require scientific discovery and technological innovations.That includes CRISPR and other technologies for targeted gene editing. Over the next decade, gene editing could help humanity overcome some of the biggest and most persistent challenges in global health and development. The technology is making it much easier for scientists to discover better diagnostics, treatments, and other tools to fight diseases that still kill and disable millions of people every year, primarily the poor. It is also accelerating research that could help end extreme poverty by enabling millions of farmers in the developing world to grow crops and raise livestock that are more productive, more nutritious, and hardier. New technologies are often met with skepticism. But if the world is to continue the remarkable progress of the past few decades, it is vital that scientists, subject to safety and ethics guidelines, be encouraged to continue taking advantage of such promising tools as CRISPR.FEEDING THE WORLDEarlier this year, I traveled to Scotland, where I met with some extraordinary scientists associated with the Centre for Tropical Livestock Genetics and Health at the University of Edinburgh. I learned about advanced genomic research to help farmers in Africa breed more productive chickens and cows. As the scientists explained, the breeds of dairy cows that can survive in hot, tropical environments tend to produce far less milk than do Holsteins—which fare poorly in hot places but are extremely productive in more moderate climates, thanks in part to naturally occurring mutations that breeders have selected for generations. The scientists in Scotland are collaborating with counterparts in Ethiopia, Kenya, Nigeria, Tanzania, and the United States. They are studying ways to edit the genes of tropical breeds of cattle to give them the same favorable genetic traits that make Holsteins so productive, potentially boosting the tropical breeds’ milk and protein production by as much as 50 percent. Conversely, scientists are also considering editing the genes of Holsteins to produce a sub-breed with a short, sleek coat of hair, which would allow the cattle to tolerate heat.This sort of research is vital, because a cow or a few chickens, goats, or sheep can make a big difference in the lives of the world’s poorest people, three-quarters of whom get their food and income by farming small plots of land. Farmers with livestock can sell eggs or milk to pay for day-to-day expenses. Chickens, in particular, tend to be raised by women, who are more likely than men to use the proceeds to buy household necessities. Livestock help farmers’ families get the nutrition they need, setting children up for healthy growth and success in school.Similarly, improving the productivity of crops is fundamental to ending extreme poverty. Sixty percent of people in sub-Saharan Africa earn their living by working the land. But given the region’s generally low agricultural productivity—yields of basic cereals are five times higher in North America—Africa remains a net importer of food. This gap between supply and demand will only grow as the number of mouths to feed increases. Africa’s population is expected to more than double by 2050, reaching 2.5 billion, and its food production will need to match that growth to feed everyone on the continent. The challenge will become even more difficult as climate change threatens the livelihoods of smallholder farmers in Africa and South Asia.Gene editing to make crops more abundant and resilient could be a lifesaver on a massive scale. The technology is already beginning to show results, attracting public and private investment, and for good reason. Scientists are developing crops with traits that enhance their growth, reduce the need for fertilizers and pesticides, boost their nutritional value, and make the plants hardier during droughts and hot spells. Already, many crops that have been improved by gene editing are being developed and tested in the field, including mushrooms with longer shelf lives, potatoes low in acrylamide (a potential carcinogen), and soybeans that produce healthier oil.Improving the productivity of crops is fundamental to ending extreme poverty.For a decade, the Bill & Melinda Gates Foundation has been backing research into the use of gene editing in agriculture. In one of the first projects we funded, scientists from the University of Oxford are developing improved varieties of rice, including one called C4 rice. Using gene editing and other tools, the Oxford scientists were able to rearrange the cellular structures in rice plant leaves, making C4 rice a remarkable 20 percent more efficient at photosynthesis, the process by which plants convert sunlight into food. The result is a crop that not only produces higher yields but also needs less water. That’s good for food security, farmers’ livelihoods, and the environment, and it will also help smallholder farmers adapt to climate change.Such alterations of the genomes of plants and even animals are not new. Humans have been doing this for thousands of years through selective breeding. Scientists began recombining DNA molecules in the early 1970s, and today, genetic engineering is widely used in agriculture and in medicine, the latter to mass-produce human insulin, hormones, vaccines, and many drugs. Gene editing is different in that it does not produce transgenic plants or animals—meaning it does not involve combining DNA from different organisms. With CRISPR, enzymes are used to target and delete a section of DNA or alter it in other ways that result in favorable or useful traits. Most important, it makes the discovery and development of innovations much faster and more precise.ENDING MALARIA In global health, one of the most promising near-term uses of gene editing involves research on malaria. Although insecticide-treated bed nets and more effective drugs have cut malaria deaths dramatically in recent decades, the parasitic disease still takes a terrible toll. Every year, about 200 million cases of malaria are recorded, and some 450, 000 people die from it, about 70 percent of them children under five. Children who survive often suffer lasting mental and physical impairments. In adults, the high fever, chills, and anemia caused by malaria can keep people from working and trap families in a cycle of illness and poverty. Beyond the human suffering, the economic costs are staggering. In sub-Saharan Africa, which is home to 90 percent of all malaria cases, the direct and indirect costs associated with the disease add up to an estimated 1.3 percent of GDP—a significant drag on countries working to lift themselves out of poverty.With sufficient funding and smart interventions using existing approaches, malaria is largely preventable and treatable—but not completely. Current tools for prevention, such as spraying for insects and their larvae, have only a temporary effect. The standard treatment for malaria today—medicine derived from artemisinin, a compound isolated from an herb used in traditional Chinese medicine—may relieve symptoms, but it may also leave behind in the human body a form of the malaria parasite that can still be spread by mosquitoes. To make matters worse, the malaria parasite has begun to develop resistance to drugs, and mosquitoes are developing resistance to insecticides.Efforts against malaria must continue to make use of existing tools, but moving toward eradication will require scientific and technological advances in multiple areas. For instance, sophisticated geospatial surveillance systems, combined with computational modeling and simulation, will make it possible to tailor antimalarial efforts to unique local conditions. Gene editing can play a big role, too. There are more than 3, 500 known mosquito species worldwide, but just a handful of them are any good at transmitting malaria parasites between people. Only female mosquitoes can spread malaria, and so researchers have used CRISPR to successfully create gene drives—making inheritable edits to their genes—that cause females to become sterile or skew them toward producing mostly male offspring. Scientists are also exploring other ways to use CRISPR to inhibit mosquitoes’ ability to transmit malaria—for example, by introducing genes that could eliminate the parasites as they pass through a mosquito’s gut on their way to its salivary glands, the main path through which infections are transmitted to humans. In comparable ways, the tool also holds promise for fighting other diseases carried by mosquitoes, such as dengue fever and the Zika virus.It will be several years, however, before any genetically edited mosquitoes are released into the wild for field trials. Although many questions about safety and efficacy will have to be answered first, there is reason to be optimistic that creating gene drives in malaria-spreading mosquitoes will not do much, if any, harm to the environment. That’s because the edits would target only the few species that tend to transmit the disease. And although natural selection will eventually produce mosquitoes that are resistant to any gene drives released into the wild, part of the value of CRISPR is that it expedites the development of new approaches—meaning that scientists can stay one step ahead.THE PATH FORWARDLike other new and potentially powerful technologies, gene editing raises legitimate questions and understandable concerns about possible risks and misuse. How, then, should the technology be regulated? Rules developed decades ago for other forms of genetic engineering do not necessarily fit. Noting that gene-edited organisms are not transgenic, the U.S. Department of Agriculture has reasonably concluded that genetically edited plants are like plants with naturally occurring mutations and thus are not subject to special regulations and raise no special safety concerns.The benefits of emerging technologies should not be reserved only for people in developed countries.Gene editing in animals or even humans raises more complicated questions of safety and ethics. In 2014, the World Health Organization issued guidelines for testing genetically modified mosquitoes, including standards for efficacy, biosafety, bioethics, and public participation. In 2016, the National Academy of Sciences built on the WHO’s guidelines with recommendations for responsible conduct in gene-drive research on animals. (The Gates Foundation co-funded this work with the National Institutes of Health, the Foundation for the National Institutes of Health, and the Defense Advanced Research Projects Agency.) These recommendations emphasized the need for thorough research in the lab, including interim evaluations at set points, before scientists move to field trials. They also urged scientists to assess any ecological risks and to actively involve the public, especially in the communities and countries directly affected by the research. Wherever gene-editing research takes place, it should involve all the key stakeholders—scientists, civil society, government leaders, and local communities—from wherever it is likely to be deployed.Part of the challenge in regulating gene editing is that the rules and practices in different countries may differ widely. A more harmonized policy environment would prove more efficient, and it would probably also raise overall standards. International organizations, especially of scientists, could help establish global norms. Meanwhile, funders of gene-editing research must ensure that it is conducted in compliance with standards such as those advanced by the WHO and the National Academy of Sciences, no matter where the research takes place.When it comes to gene-editing research on malaria, the Gates Foundation has joined with others to help universities and other institutions in the regions affected by the disease to conduct risk assessments and advise regional bodies on experiments and future field tests. The goal is to empower affected countries and communities to take the lead in the research, evaluate its costs and benefits, and make informed decisions about whether and when to apply the resulting technology.Finally, it’s important to recognize the costs and risks of failing to explore the use of new tools such as CRISPR for global health and development. The benefits of emerging technologies should not be reserved only for people in developed countries. Nor should decisions about whether to take advantage of them. Used responsibly, gene editing holds the potential to save millions of lives and empower millions of people to lift themselves out of poverty. It would be a tragedy to pass up the opportunity.
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Simple tips to fight inflammation The awareness of the intersection between inflammation and chronic disease has spawned a plethora of diet plans, nutritional supplements, and lifestyle programs, many implying they offer new ways to improve your health by quelling inflammation. It's true that scientists are uncovering new complexities and expanding their knowledge of factors that may contribute to inflammation or help counter it. But much of the heavily hyped guidance for an anti-inflammation lifestyle boils down to the same no-nonsense health advice your grandmother might have given you.Understanding Inflammation Chronic inflammation plays a central role in some of the most challenging diseases of our time, including rheumatoid arthritis, cancer, heart disease, diabetes, asthma, and even Alzheimer’s. This report will examine the role that chronic inflammation plays in these conditions, and will also provide information on the breadth of drugs currently available to alleviate symptoms. Drug choices range from simple aspirin, a nonsteroidal anti-inflammatory drug that’s been available for more than a century, to disease-modifying drugs and so-called biologics that promise more targeted treatments.Make healthy food choicesOur diets play an important role in chronic inflammation because our digestive bacteria release chemicals that may spur or suppress inflammation. The types of bacteria that populate our gut and their chemical byproducts vary according to the foods we eat. Some foods encourage the growth of populations of bacteria that stimulate inflammation, while others promote the growth of bacteria that suppress it.Fortunately, you are probably already enjoying many of the foods and beverages that have been linked to reductions in inflammation and chronic disease. They include the following:Fruits and vegetables. Most fruits and brightly colored vegetables naturally contain high levels of antioxidants and polyphenols — potentially protective compounds found in plants.Nuts and seeds. Studies have found that consuming nuts and seeds is associated with reduced markers of inflammation and a lower risk of cardiovascular disease and diabetes.Beverages. The polyphenols in coffee and the flavonols in cocoa are thought to have anti-inflammatory properties. Green tea is also rich in both polyphenols and antioxidants.Inflammation is a key component of arthritis and other chronic joint diseases. Gout, a painful and potentially debilitating form of inflammatory arthritis, develops when tiny, needle-shaped crystals of uric acid (a biological waste product) accumulate in the joints. The presence of these uric acid crystals triggers the release of cytokines, and these inflammatory messengers attract neutrophils and other white blood cells to the scene. Gout usually affects one joint at a time, most often the big toe, but sometimes it occurs in a knee, ankle, wrist, foot, or finger.Early on, gout flare-ups tend to be intermittent. If gout persists for a long time, the joint pain can be ongoing and mimic other types of arthritis. After several years, uric acid crystals may collect in the joints or tendons. They can also collect under the skin, forming whitish deposits. They are called tophi, lumps of tissue that form under the skin of fingers, knuckles, and elsewhere.Most people with gout make too much uric acid. Often they have a family history of the disease, are overweight and have high blood pressure, high cholesterol, or diabetes. High protein diets, especially those rich in organ foods such as liver, kidney, and sweetbreads can raise uric acid levels and increase the chance of gouty attacks. Some people develop gout because their kidneys excrete too little uric acid.In addition, obesity, sudden weight gain, or alcohol use can elevate uric acid levels. Some medications, particularly diuretics, also can boost levels of uric acid.To learn more about how inflammation affects your body, read Understanding Inflammation, the Harvard Medical School Online Guide.
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