 Your new post is loading...
Your new post is loading...
It's a group effort - the curators:
get in touch if you want to help curate this topic
|
Scooped by
Cindy
|
Over the last two weeks, I have been reading Dan Graur’s book titled “Molecular and Genome Evolution”. This is a fantastic book that everyone should read before starting to work on any genome-related project. For the benefit of our readers, I will share some comments in this short post. If time permits, I will later follow up with a longer post on the book.
|
|
Scooped by
Cindy
|
In 2006, when Kevin and I started to examine Potti’s data on genetic signatures of cancer, both of us had tenure and resources to devote to the work. (We were funded to provide statistical support to faculty members and could easily argue that they would want to implement techniques Potti described.) Once we established (at least to our own satisfaction) that the results were simply wrong, it was harder to justify our work, but we couldn’t stop: patients were being enrolled in useless trials that would expose them to toxic agents.
AbstractSummary. We present a bioinformatics and systems biology visualization toolkit harmonizing real time interactive exploring and analyzing of big data, f
UCT Vaccinology Research Chair Professor Anna-Lise Williamson has been honoured with a gold medal from the SA Medical Research Council for her seminal scientific contributions.
Via Ed Rybicki
Meantime, stricter measures have been implemented in order to stop the spreading of the disease.
Via Ed Rybicki
|
|
Scooped by
Cindy
|
Since 2003, several researchers have noticed that scientists tend to study genes that are already well studied, and the genes that become popular aren’t necessarily the most biologically interesting ones. Even among genes, it seems, the rich get richer. This trend hasn’t changed in the past two decades, according to a new study from Thomas Stoeger from Northwestern University. Through a massive analysis of existing biomedical data, he found that he can predict how intensely a given gene is studied based on a small number of basic biochemical traits. Most of these, he says, reflect how easy a gene was to investigate in the 1980s and 1990s, rather than how important it is.
“People said that knowing all the genes was going to change everything,” says Luis Amaral, who led the new study. But the 16 percent of genes that were known in 1991 still accounted for half of all biomedical papers in 2015. By contrast, more recently discovered genes are more poorly known, and a quarter (27 percent) have never been the focus of a scientific paper. Based on current trends, Stoeger estimates that it would take at least five decades before every gene was characterized at the most basic level, let alone fully understood. “There’s a chance that we are missing out on a lot of interesting biology,” he says.
In what could address a critical bottleneck in biology research, Berkeley Lab researchers announced they have pioneered a new way to synthesize DNA sequences through a creative use of enzymes that promises to be faster, cheaper, and more accurate.
Inspired by the architectures of different organisms, MIT PhD student Zijay Tang is developing a living material that can sense and filter water contaminants.
Via Gerd Moe-Behrens
Extraviral components that can influence the accumulation and pathogenesis of their associated helper viruses are known as ‘satellites’. The maintenan…
|
|
Scooped by
Cindy
|
Here is your most reliable resource for tutorials in statistics, data science, and working with R prgramming Software created by Mike Marin and his partner in crime Ladan Hamadani . Initially made for Mike's Master's and PhD students at the University of British Columbia (UBC), these tutorials are now made available to everyone.
|
|
Scooped by
Cindy
|
The notion that the genetic inheritance of any species can be described as a single sequence has always been a convenient simplification. Most reference genomes are derived from only one or a small number of individuals, and diploid or polyploid species are typically represented as consensus haploid sequences or sequences with reduced heterozygosity produced by inbreeding. For the human genome, the current haploid reference assembly is based on DNA from only ∼50 people, with ∼70% of the sequence coming from just one of those genomes. Thus, it is missing most of the variation that defines the genetic identity of individuals, including variants with clinical relevance and regions of high diversity. In this issue, Garrison et al.1 take an important step toward addressing this deficiency with an approach that represents genetic variation and sequence assembly in a single graph structure. The variation graph (vg) approach promises to transform our ability to account for complex genetic variation across populations.
AbstractMotivation. The recent technological advances in genome sequencing techniques have resulted in an exponential increase in the number of sequenced human
|
|
|
Scooped by
Cindy
|
Sequencing human genomes is now routine at the Sanger Institute. Bacteria, yeast, worms, malaria, and other pathogens are also all regularly sequenced in their thousands. Our people are pretty well known for sequencing the human genome, but we’ve also contributed to the first sequencing of many others including the mouse, rat, zebrafish, pig and gorilla too.
The 25 genomes project is an entirely different beast. It’s posing some new, and frankly very odd, challenges. The diversity of the new species means we’ve had a steep learning curve. Here’s a peek at some of the weird and wonderful things we’ve discovered so far:
|
|
Scooped by
Cindy
|
Box 1. Hurdles to writing that all scientists can face
Types of Writing Resistance
Evaluation: “This draft stinks.”
Inspiration: “I don’t have a good idea yet.”
Motivation: “I just don’t feel like it.”
Optimization: “I need to make this sentence perfect.”
Procrastination: “I will start working on it tomorrow.”
Separation: “I need a lot of time in a quiet place to write.”
Temptation: “My lab bench is really disorganized; it needs to be cleaned now.”
|
|
Scooped by
Cindy
|
Today I’m excited to announce the first part of our new system, a new set of massive online open courses called Chromebook Data Science. These MOOCs are for anyone from high schoolers on up to get into data science. If you can read and follow instructions you can learn data science from these courses!
The reason they are called Chromebook Data Science is because philosophically our goal was that anyone with a Chromebook could do the courses. All you need is a web browser and an internet connection. The courses all take advantage of RStudio Cloud so that all course work can be completed entirely in a web browser. No need to install software or have the latest MacBook Computer.
|
|
Scooped by
Cindy
|
Introduction to de novo genome assembly (2016 edition)
When it emerged that two people infected with monkeypox had travelled by plane through one of the world's busiest airports, a media storm arose, with irresponsible headlines and exaggerations of risks for others in the UK and across the globe. The two patients—currently recovering in specialist units in London and Liverpool, UK—probably contracted the infection, which produces symptoms such as fever, headache, malaise, and the typical smallpox-like vesicular rash, from animals in Nigeria, where there is an ongoing outbreak of the virus. The Nigeria Centre for Disease Control has recorded 262 suspected cases of monkeypox since the outbreak began in September, 2017, including 113 confirmed cases and seven deaths. The Nigerian outbreak is likely to be the result of a local zoonotic spillover event from the virus' natural hosts—rodents. The disease, caused by a virus of the Orthopox genus, is usually self-limiting—although it has a mortality rate of 1–10%.
Via Ed Rybicki
Nidhi Shah, Michael G Nute, Tandy Warnow, Mihai Pop; Misunderstood parameter of NCBI BLAST impacts the correctness of bioinformatics workflows, Bioinformatics,
|
Scooped by
Ed Rybicki
|
In 2009, the co-circulation of H5N1 and H1N1pdm09 raised concerns that a reassortment event may lead to highly pathogenic influenza strains. H1N1pdm09 and H5N1 are able to infect the same target cells of the lower respiratory tract.
A 64-year-old otherwise healthy virology professor comes to your office complaining of flu symptoms. She has had fever, cough, and sore throat for the last day or so that she attributes to one of her students. She has been furiously sanitizing her hands and comes to the office wearing a face mask. Being the savvy patient, she brings reverse transcriptase–polymerase chain reaction (RT-PCR) results that confirm she has influenza A virus (as does the student). She is febrile but hemodynamically stable with no signs of lower respiratory tract infection. She asks about available treatment options, explaining that she will be presenting at a conference tomorrow. How would you proceed? In this week’s NEJM, Hayden and colleagues report the results of two double-blind, randomized-controlled trials comparing single-dose baloxavir versus placebo or oseltamivir in patients with uncomplicated influenza in Japan and the United States during the 2015–2017 flu seasons. Baloxavir marboxil (Xofluza) is an important new addition to the armamentarium against flu because it represents a new class of antiviral drugs that target a different process than the other two classes available (amadantanes and neuraminidase inhibitors), and has antiviral activity against strains resistant to those agents. Baloxavir also has the advantage of requiring a single dose, as compared to 5 days of twice daily oseltamivir (Tamiflu). Baloxavir is a cap-dependent endonuclease inhibitor that blocks viral replication by blocking the initiation of mRNA synthesis (read more here). In the phase 3 trial (CAPSTONE-1), the investigators randomized 1436 patients (age range, 12–64 years) with uncomplicated flu to receive a single dose of baloxavir (40 mg), oseltamivir (75 mg twice daily for 5 days), or matching placebos (with those aged 12-19 assigned only to baloxavir or placebo). Uncomplicated flu was defined as fever ≥38.0°C, at least one systemic symptom and one respiratory symptom, and presentation with 48 hours of symptom onset. Pregnant women and those requiring hospitalization were excluded. The primary endpoint was the time until flu symptoms became absent or mild for at least 21.5 hours. The intention-to-treat infected population included only RT-PCR-positive patients. Roughly 85% of patients in the three treatment groups were infected with influenza A (H3N2) and most (77%) were recruited in Japan. The time to alleviation of symptoms was significantly shorter (by 26.5 hours) in the baloxavir group, when compared with the placebo group (median, 53.7 vs. 80.2 hours), and similar to the oseltamivir group (53.5 vs. 53.8 hours). Baloxavir was associated with significantly more rapid decline in potentially infectious viral load as compared to both oseltamivir and placebo. The rate of adverse events was similar in the three groups. Emergence of mutations conferring reduced baloxavir susceptibility occurred in fewer than 10% of baloxavir recipients, which prolonged time to resolution of symptoms by about 13 hours. Per CDC recommendations, only individuals with acute influenza who are at high risk of related complications (e.g., in a chronic care facility, pregnant, age ≥65 years) should receive antiviral treatment. Hence, the results of this trial are not likely to affect current practice or treatment of the professor described above. The importance of this study lies in the demonstration of the safety and efficacy of baloxavir for treatment of uncomplicated acute influenza in otherwise healthy patients. These encouraging results will form the basis for future study of baloxavir in higher risk populations, where its utility and future clinical indications may lie. Browse more From Pages to Practice » Tenzing T. Lama, MD, MScRes, is a resident physician in the Department of Anesthesiology and Pain Medicine at the University of Washington and a Fellow at the Ethics and Transformative Values Center at the Massachusetts Institute of Technology. He graduated from Harvard Medical School and Oxford.
Via Ed Rybicki
|
|
Scooped by
Cindy
|
In 2009, the co-circulation of H5N1 and H1N1pdm09 raised concerns that a reassortment event may lead to highly pathogenic influenza strains. H1N1pdm09 and H5N1 are able to infect the same target cells of the lower respiratory tract. To investigate the capacity of the emergence of reassortant viruses, we characterized viruses obtained from the co-infection of cells with H5N1 (A/Turkey/13/2006) and H1N1pdm09 (A/Lyon/969/2009 H1N1). In our analysis, all the screened reassortants possessed the PB2, HA, and NP segments from H5N1 and acquired one or two of the H1N1pdm09 segments. Moreover, the in vivo infections showed that the acquisition of the NS segment from H1N1pdm09 increased the virulence of H5N1 in mice. We conclude, therefore, that reassortment can occur between these two viruses, even if this process has never been detected in nature.
The molecular processes that determine the outcome of influ- enza virus infection in humans are multifactorial and involve a complex interplay between host, viral and bacterial fac- tors 1 . However, it is generally accepted that a strong innate immune dysregulation known as ‘cytokine storm’ contributes to the pathology of infections with the 1918 H1N1 pandemic or the highly pathogenic avian influenza viruses of the H5N1 subtype 2–4 . The RNA sensor retinoic acid-inducible gene I (RIG-I) plays an important role in sensing viral infection and initiating a signalling cascade that leads to interferon expres- sion 5 . Here, we show that short aberrant RNAs (mini viral RNAs (mvRNAs)), produced by the viral RNA polymerase during the replication of the viral RNA genome, bind to and activate RIG-I and lead to the expression of interferon-β . We find that erroneous polymerase activity, dysregulation of viral RNA replication or the presence of avian-specific amino acids underlie mvRNA generation and cytokine expression in mam- malian cells. By deep sequencing RNA samples from the lungs of ferrets infected with influenza viruses, we show that mvR- NAs are generated during infection in vivo. We propose that mvRNAs act as the main agonists of RIG-I during influenza virus infection.
|
|
Scooped by
Cindy
|
CRISPR-Cas systems function by uptake and integration of foreign genetic element sequences into the CRISPR array, which constitutes a genomic archive of iterative vaccination events. Consequently, CRISPR spacers can be investigated to reconstruct interplay between viruses and bacteria, and metagenomic sequencing data can be exploited to provide insights into host-phage interactions within a niche. Here, we show how the CRISPR spacer content of commensal and pathogenic bacteria can be used to determine the evidence of their phage exposure. This framework opens new opportunities for investigating host-virus dynamics in metagenomic data, and highlights the need to dedicate more efforts for virome sampling and sequencing.
AbstractSummary. Phylogenetic profiles form the basis for tracing proteins and their functions across species and through time. Novel genome sequences nowadays
Cases of monkeypox confirmed in England.
|
Scoop.it!
