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Research on the percentage of graduates in your school who actually landed jobs related to their majors. Research on the possibility of online schools taking over entirely from the standard educational institutions. It is evident that to find a popular topic, you need not look further than your nose or the newspaper that your dad reads every morning. Alternatively you could tune in to the topics that your friends talk about and perhaps get some ideas from them for the treatment you wish to pursue. Research paper format example is popular among students as they tend to learn to write effective research papers. If you are at lost with a specific task that needs to be completed, the best way of accomplishing such is to have someone extend a helping hand to you. Here, a thesis statement becomes very significant because it is the USP of your entire paper.
Other that the thesis you also need to give enough space to the arguments that your paper is going to present.
Our prices and services are specially designed so that our customers can benefit from them. On the second Tuesday of every month, about 20 researchers from a dozen or so cities around the world get on the horn to participate in a conference call that has been happening regularly for nearly a decade. Incidence of multiple sclerosis in the United Kingdom : findings from a population-based cohort. Pathway and network-based analysis of genome-wide association studies in multiple sclerosis. Baranzini SE, Galwey NW, Wang J, Khankhanian P, Lindberg R, Pelletier D, Wu W, Uitdehaag B M, Kappos L, Consortium GMSA, et al. Barcellos LF, Sawcer S, Ramsay PP, Baranzini SE, Thomson G, Briggs F, Cree BCA, Begovich AB, Villoslada P, Montalban X, et al. Gas6 increases myelination by oligodendrocytes and its deficiency delays recovery following cuprizone-induced demyelination. Broadley S, Sawcer S, D'Alfonso S, Hensiek A, Coraddu F, Gray J, Roxburgh R, Clayton D, Buttinelli C, Quattrone A, et al. These are just three examples of alternatives to classic white rice.  There are so many amazing and different grains that can really spice up a dish, and most of them are now just as readily available in average supermarkets and just as easy to make as (if not easier than!) white rice.  All it takes is a little creativity and a willingness to try something new, and you could wind up with a reinvented, healthier take on a family favorite in no time! Jessica Serdikoff is the chief blogger behind Floptimism, a blog where Jessica shares deliciously inspiring recipes and tales of life as a nutrition student.
The contents of this website represent the views and opinions of the writers only and not those of any third-party individuals or companies.
FDA Advisory Panel votes 8-2 in favor of an insulin dosing label update for Dexcom's G5 CGM!
A recent article in Nature Medicine titled “Microbes, metabolism, and medications” presents an exciting new tool that may soon find a place in the diabetes and obesity treatment arsenal. The microbes that live in our gut, also called the “gut microbiome” or “intestinal flora,” are a significant contributor to human health. Fascinating research on mice shows that transplanting the gut microbiome of an obese mouse can actually make a thin mouse become obese, suggesting that gut microbes influence obesity. This is an area of research that we expect to hear much more about in the coming years, for both type 1 and type 2 diabetes, as well as obesity. Our mission is to help individuals better understand their diabetes and to make our readers happier & healthier. Our mission is to help individuals better understand their diabetes and to make our readers happier and healthier.
Topic of your research paper talks about your creativity, thinking, life priorities, behavior. You don’t have to be an expert writer to take a good and clear look at how you feel about something deep inside. Students have to spend majority of their time searching for research matter and convey the matter in the proper format in writing. It has a long track record for helping its clients meet their literary requirements in any type of custom essay or paper, for the school or for business use. You can give your specifications as per your university’s normal requirements and leave the rest to us. Because of the multiple things that must be accomplished in writing a thesis, this academic activity can take over your life. That caused an opportunity and an obligation to turn that research into results, putting research and education together.
The sun is just peeking over the Australian skyline when participants dial in from Melbourne and Sydney. Learning more about the gut microbiome could lead to clues about how weight loss occurs and how complicated our metabolisms can be.
These organisms serve many important roles including helping with immune function and cell tissue growth. Recent animal studies have also found that metformin may actually play a role in shaping the gut microbiome.
When we realize that we have 10 trillion cells that are host to 100 trillion bacteria, it certainly puts the importance of the gut microbiome into perspective. Just as important as quality is for them, the client’s prerequisites are also prioritized in writing the paper.
If after receiving it, you or your research supervisor should see the need for some changes to made, such alterations are readily accommodated free of charge. Late nights at the library and endless editing in front of the computer screen are just few of the common scenarios one faces when one needs to come up with a thesis.
There are a few factors that are compulsory for thesis presentation like table of contents, abstract, tables, graphics, acknowledgements etc. As illustrated by John Gardner in this quote, research is an inevitable part of education and education could not exist without research.
You simply place an order with the writing instructions you have been given, and before you know it, your essay or term paper, completely finished and unique, will be completed and sent back to you. Their colleagues in Boston and other cities across the United States reach for their office phones during more reasonable work hours, while those in Norway, Finland, and Sweden might already be wearing pajamas.
This growing new field of study linking the gut to type 2 diabetes and obesity is in its infancy, and many hope future therapies could be developed from this research. An emerging area of research concerns the role of the intestinal flora in “host metabolism” – in other words, the organisms in our gut actually influence how we digest our food. Metformin is a first-line drug for treating type 2 diabetes, but it is also sometimes prescribed for overweight and obese individuals seeking to lose weight. And remember that the next time you eat, to think about your own health along with the health of your gut microbiome! The symbiotic relationship between this two goes to show that each is dependent upon the other. For the members of the International Multiple Sclerosis Genetics Consortium (IMSGC), the years of calls have held the group together, not just by keeping the far-flung collaborators informed of projects under way, but also by providing the means for would-be competitors to develop enough trust to share their hunches, their plans, and their data.  When the IMSGC formed, in 2002, the idea of competing labs pooling their resources—and of principal investigators forgoing primary authorship on research papers—was still novel.
What’s more, the intestinal flora is directly shaped by our genetics, medications, our exposure to different bacteria, diet, and more. Although metformin has been used for decades, new research suggests it could hold the key to new treatments that target the intestinal flora.
And just because such topics are of common interest, the burden on the writer discussing a popular research paper topic will be how to treat it with sufficient originality to retain the interest of the readers who may have read previous articles on the same essay topic.
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For students who have too much things in their hand can get the assistance they need when thesis writing is concerned. For example, some research suggests that consuming a high-fat diet can negatively impact the gut microbiome. Preliminary studies reveal the positive effects of metformin – changes in the metabolic pathways of bacteria and growth of helpful bacteria, to name a few.
Also the topic should fit to the concept of the discipline, problem posed by your professor.
In practical application, this quote represents the inescapable task of every student to comply with multiple research paper writing task once he steps in an academe.
The malady clearly clustered in families; 15% to 20% of patients have a relative with the disease, and having a twin with MS confers a 30% risk of developing the illness. While the exact details remain unknown, it’s fascinating to find that the medications we take can actually affect the microbes we host. In this section you will find information about popular topics for research papers, outline template, examples. The MHC family of genes, called the human leukocyte antigen (HLA) system in humans, encodes proteins on the cell surface that present antigens—typically, small chunks of foreign or a person’s own proteins—to T cells. Among other things, this process helps the immune system distinguish invaders from its own components. Researchers first correlated certain HLAs with MS in the early 1970s and, as genotyping technology evolved, traced the bulk of the disease-risk effect to specific alleles, or variants, of the genes, most significantly HLA DRB1*1501 (Barcellos et al., 1996).
This locus accounted for a sizable chunk of the genetic, as opposed to the environmental, component of risk for the disease.
Unlike disorders such as cystic fibrosis or Huntington disease, which stem from glitches in a single gene, MS arises from a combination of genetic and environmental factors. Each of the multiple genes involved exerts a small influence on whether someone develops the disease, as do a variety of environmental factors.
Tracking this legion of modest effects required many more study subjects than scientists initially realized.
A study published in August 2011, by far the biggest of its kind for MS, brought to 57 the number of spots on the human genome where variations were associated with increased risk of the disease. Since then, three more have been identified, and further follow-up work is poised to push the total number over 100 within the next year.
Geneticists are still developing basic techniques for analyzing such studies; figuring out which gene corresponds to a variant is far from straightforward, and identifying the function of any novel gene can consume an entire career. By the 1990s, researchers were beginning to realize the limitations of going solo, and small-scale cooperative efforts were beginning to emerge, for example among researchers in Nordic countries or across Australia and New Zealand.
Most gene-mining projects had deployed a technique called linkage analysis, in which researchers use well-defined sequences of DNA as markers to track how risk for MS is inherited within individual families.
Markers close to the genes or sequences that stir up the biological trouble would be passed down with the miscreant DNA, pointing researchers to short stretches of the genome in which the culprits lie. Linkage studies work well to identify mutations that play a large role in a disease. But in cases of complex inheritance, when many alleles contribute to disease risk, related family members are likely to have different assortments, making the relevance of each one harder to demonstrate statistically and rendering linkage studies ineffective. A different approach was needed: association studies, which fish out disease-associated variants by comparing markers among large numbers of affected and unaffected individuals instead of comparing inheritance patterns within families. So-called genome-wide association studies (GWAS) scan hundreds of thousands of points along the genome and identify alleles that are more common in those who have the disease compared to those who do not. In the late 1990s, Compston, at Cambridge, decided to get groups across Europe to pool their samples and expertise and to take the first serious stab at conducting an association study for MS. The collaborators called the effort GAMES (Genetic Analysis of Multiple Sclerosis in Europeans Consortium). A theoretical paper had suggested that a map of 6000 markers in 200 MS patients and 200 controls would provide sufficient statistical power (Barcellos et al., 1997). As knowledge about immunology exploded, showering the terrain with newly discovered molecules, he realized that he and his colleagues needed a scaffold for MS on which to hang these immune components. He reached out to genomicist Eric Lander, then also at Harvard, to learn about complex genetics and genome sequencing. By 2002, those founders of the IMSGC who had already been involved with genetics consortia dedicated to MS began to discuss how they could again work together; Hafler also began to chat with Stephen Hauser of the University of California, San Francisco, about the idea of a new international consortium for MS.
At around this time, while at a conference in Copenhagen, Hafler and Compston continued those conversations with several colleagues including Haines and Margaret Pericak-Vance, now at the University of Miami in Florida. They envisioned an ambitious goal: discovering all of the common genetic risk variants in MS. A Boston venture capitalist named Martha Crowninshield, who has a long-standing interest in MS and has remained closely involved with the IMSGC’s work, helped them refine the proposal and contributed the first $1 million. She also hosted an event at which a handful of potential donors were invited to hear about the consortium’s plans from Hafler, Lander, and Joseph Martin, then the dean of Harvard Medical School. We started working on this problem in the early 1980s, and now it’s 30 years later.’” The initial crew members knew they would have to replace guarded competition with trust, so one of their first steps was to create a charter—appropriated and amended from the International Inflammatory Bowel Disease Genetics Consortium—that addressed issues such as authorship, seniority, sample and data sharing, bringing in new members, and settling disputes. This policy was meant to ensure that the boundaries between IMSGC projects and individual labs’ work were known to everyone in advance. The founding members also agreed that the collaboration would stay small until time had proven that it could work. First on the group’s agenda, then, was a linkage study to end all linkage studies—that is, a linkage study powerful enough to definitively determine whether the technique could identify genetic risk factors outside the MHC.
The answer to the question, based on a study of 700 families, turned out to be a resounding “no” (Sawcer et al., 2005). The analysis once again pointed to the HLA DRB1*1501 allele in the MHC, and it identified no other signals anywhere near as strong, despite being many orders of magnitude more sensitive than previous MS linkage studies.  Meanwhile, the technology that powers genetic research was on the verge of a revolution.
In the 2000s, researchers were turning to single-nucleotide polymorphisms (SNPs)—single-base variations in the genome—which could serve as much denser, more accurate markers than those previously used. Initiatives sparked by the Human Genome Project, such as the SNP Consortium and the International HapMap Project, were identifying tens of thousands of SNPs common enough to be found in 1% to 5% of the population. This development meant that researchers could use a microchip that contained upward of 100,000 such SNPs to scan a person’s entire genome and assess which variants were more common in people with a specific disease.  With linkage a failure, the group was divided about how to proceed.
Some members were eager to try GWAS in MS; however, the technique was costly and unproven, and others thought it more prudent to wait for the technology to mature. Researchers linked its overactivity to the disease in a 2001 report of 15 patients with relapsing-remitting MS (Ramanathan et al., 2001), but subsequent studies of the gene were inconclusive. When IMSGC participants and others further investigated the gene, they found that the risk variant changes how it is spliced, which likely causes it to generate reduced amounts of the protein’s alpha chain in the membrane and increased amounts in the cytoplasm (Gregory et al., 2007). Because this portion of the protein must lie in the membrane for the receptor to work properly, the location change curbs its ability to do its job.
Away from the membrane, it is no longer available to respond to a cytokine called IL-7, which normally helps certain lymphocytes survive and promotes development of B and T cells. Perhaps dampening T- and B-cell maturation could knock immune cell function off kilter and contribute to MS, researchers conjectured. Researchers took a long time to understand how many subjects were needed to render GWAS useful, Sawcer says, in large part because the number required depends on the relative number of SNPs and risk genes—and on how strongly the genes involved boost the likelihood of getting the disease. Taking these issues into consideration, investigators have now calculated that a minimum of 2000 cases and as many controls are needed to achieve statistical significance, Sawcer says—about twice as many individuals as were included in the 2007 study. Additional subjects would increase the study’s power even more. As other susceptibility loci—most of them with unknown roles in the body—began to trickle in through subsequent studies, the group began planning a GWAS with 10 times as many patients. Several consortium members estimate that the IMSGC now comprises about 9 out of every 10 researchers working on MS genetics worldwide.
Candidates must bring something new to the group—almost always patient samples, although in some cases, expertise. Going through written approvals and waiting for materials to be aliquotted, checked, and shipped from a home laboratory could easily add 6 months to an experiment.
In contrast, the consortium repositories are geared to prep large numbers of samples for action as quickly as possible.  That setup helped the consortium to get moving on its latest GWAS, a $5 million to $6 million effort that included 9772 patients and 17,376 controls.

It was conducted as part of the Wellcome Trust Case Control Consortium, a massive study of genetic variation in common diseases. The resulting report, published in August 2011, scanned about 600,000 SNPs—covering approximately 80% of the genome—and brought the total number of confirmed risk variants for MS to 57 (IMSGC et al., 2011). Because these features are present from before birth, he says, “the genetics are telling us about the earliest events in MS—events we were never really able to capture before.” An initial analysis, in which researchers looked for associations between the risk genes and other aspects of the disease, such as its type and severity, suggested that these genes might play a role in whether a person gets the disease, but not in the disease’s course. If that’s the case, the genes might not prove to be good targets for new therapies, says Jan Hillert, a neurologist at the Karolinska Institute in Stockholm, Sweden, who started the Nordic MS genetics consortium in 1994 and joined the IMSGC about 4 years ago.
The vast majority of genes identified in the study have immune functions, De Jager says, strongly supporting the latter explanation. Sergio Baranzini, an MS geneticist at the University of California, San Francisco, points out that tremendous overlap exists between genes that operate in different physiological processes, and that the so-called immune genes could also function in the nervous system. Many of the genes with the strongest association to MS, including HLA DRB1*1501, appear to be regulated by vitamin D, says MS geneticist George Ebers of Oxford University in the U.K.
Because vitamin D levels strongly depend on sunlight, the observation fits with epidemiological studies showing that lack of sun exposure is an important risk factor for the disease. A study published in December 2011, which identified three more variants in addition to the 57 found in the latest GWAS, also compared risk genes for MS with those for ulcerative colitis, diabetes, psoriasis, and other autoimmune diseases. It found that a sizable minority of risk genes shared with celiac disease and other conditions have an opposite effect—protective rather than injurious—to that in MS (Patsopoulos et al., 2011).
But researchers are slowly starting to tie the known MS risk genes to biological processes that could affect disease onset (see "Altered Immunity, Crippled Neurons"). Kilpatrick’s group is studying a family of proteins known as the TAM receptors, one of which—MERTK—is associated with MS. At least one plasma-borne TAM receptor ligand shows initial promise as a biomarker of disease, Kilpatrick said during a presentation at the November 2011 Society for Neuroscience meeting in Washington, D.C. Such studies are beginning to show how some genes might be involved in MS, but they so far provide only the barest hints of mechanism. Understanding the functions of genes uncovered by GWAS starts with mapping the precise location of the SNPs that identify a risk variant. Some SNPs lie in the protein-coding section of the gene, making it likely, researchers say, that the genetic spelling variations correspond to codon differences. But the vast majority of SNPs reside in difficult-to-interpret areas, either in introns—stretches within a gene that can influence which versions of it are transcribed—or in even murkier regions between genes. Furthermore, a variant on one part of the genome can control a gene on a completely different chromosome. Often, the matchup between SNP and gene is a best guess, made by choosing the closest known gene. Sometimes the gene can be identified by a process called fine-mapping, in which researchers use an increasing number of markers to home in on sequences in nearby regions, “but a lot of these areas just won’t break down with fine-mapping,” Kilpatrick says.
His group identified one risk locus on chromosome 12 that could have been tied to any one of 17 genes. Researchers ascribed it to a gene called CYP27B1, which is involved in converting vitamin D to its active form, simply because that made the most sense, he says, but that is a so-called biased approach. Progress might not be linear, however; some argue that it will come only when a critical mass of risk variants is identified. But with 50 or 100 SNPs associated with the disease, “we can start mapping to hopefully coherent pathways.” Uncovering missing heritabilityEach gene identified by the IMSGC represents a minuscule portion of the disease’s heritability, at least in the simplest analysis. Researchers use a measure called an odds ratio to describe the size of an effect; the greater than 1 it is, the greater the likelihood that the SNP or gene in question is associated with the disease.
Researchers say that the 60 genes outside the MHC together explain only a small percentage of MS’s heritability, significantly less than that explained by the MHC. IMSGC scientists posit that even with small effect sizes, genes could reveal pathways that play a central role in the disease. But, he adds, “if I was spending this amount of time and money on this and I came up with genes that explain [so little] of the risk, I’d be disappointed.” Part of the problem might lie in the assumptions underlying the interpretation of GWAS data.
Risk alleles are generally treated additively in statistical analyses, simply because this is the easiest way to model the enormous amounts of data that GWAS produce.
The method, however, does not incorporate the possibility that genes’ activities could combine in more complicated ways. In May 2011, Michael Demetriou, an immunologist at the University of California, Irvine, identified a connection between MS and disruption of a process called N-glycosylation, which attaches complex sugars to proteins and can modify their function (Mkhikian et al., 2011).
The IL2RA, IL7RA, and MGAT1 risk alleles—but not those associated with other genes—disrupt N-glycosylation and cause symptoms characteristic of MS in mice.
When the three are present together, however, MGAT1 negates the deleterious effects of the other two.
Vitamin D delivers the same mitigating effect, revealing a complex interplay of genetic and environmental factors. A paper published in January by Lander’s group at the Broad Institute in Cambridge, Massachusetts, suggests that this idea might be generally true for illnesses associated with relatively common gene variants, but identifying such interactions might require enormous studies of hundreds of thousands of patients (Zuk et al., 2012).
So far, however, no clear method exists for systematically detecting how risk variants enhance or slash one another’s effects, he adds.
Results to date suggest that common variants do appear to behave additively, De Jager says, “but the problem is that the studies are underpowered to detect” synergistic interactions that might be present. Gene interactions might be particularly relevant in specific subsets of patients, he says, but currently no meaningful approach parses out such groups. Hillert’s lab is working on a database that will tie information about individuals’ disease course and relevant environmental factors—whether they smoked or were infected with Epstein-Barr virus (EBV), for example—to their genotype in order to begin systematically searching for such interactions (see "Viral Villain"). Researchers within and outside the IMSGC propose several other possibilities for where the missing heritability might lie. First, with GWAS to date covering only about 80% of the genome, additional common risk variants might lie in areas with poor SNP coverage. Additionally, Baranzini notes, risk alleles might be distributed along key pathways that are misregulated in the disease. For example, a particular SNP associated with the disease might be found in, say, 20% of the population.
But another SNP, present in another 20% of the population, might participate in the same physiological process as the first one. Uniting all of these small effects under the umbrella of a single pathway might flush out more of the missing heritability. Another avenue of exploration is rare variants that occur sporadically in certain families but are uncommon in MS patients in general.
Such variants can’t easily be found with GWAS; rather, their identification requires whole-genome sequencing or at least sequencing of the coding region of the genome and comparing the results among affected and unaffected family members. Techniques to carry out such experiments are becoming available, and Baranzini and his colleagues have sequenced DNA from 12 individuals in one family: siblings, cousins, and an aunt, of whom six have the disease and six do not.
A handful of reports have suggested that the risk of developing MS differs depending on whether individuals inherit a particular allele from their father or their mother. Such a pattern would arise if the chromosomal regions harboring these genes are “imprinted,” carrying epigenetic marks that turn genes on and off.            Meanwhile, IMSGC researchers are focusing on the identified risk alleles to determine whether they can somehow be used to predict the chances that an individual will get MS—not in the general population, but in people who have a close relative with it or who have experienced an isolated neurological episode or have MS-like lesions. De Jager’s group is developing an algorithm that uses genetic and environmental information to stratify such people based on their risk.
The researchers are now conducting a study to determine which, if any, of these factors correlate with asymptomatic disease, as captured by MRI. With the identification of the common risk variants for the disease close to its logical conclusion, researchers are now well positioned to transform current knowledge into a springboard for the next stage of research. Despite the complexity and the caveats, IMSGC researchers say, the investment so far has been well worth it. How much do they uncover novel disease mechanisms?What can genes that are associated with other autoimmune disorders contribute to researchers’ understanding of MS?Are any genetic markers associated with subpopulations of patients (according to disease type or lifestyle factors, for instance) or disease factors such as viral status or response to specific therapies?

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