Plans Underway for World's First Bicycle Superhighway
Bike paths? Protected bike lanes? You're thinking way too small! The city of London is thinking much bigger, as befits a city with a population of more than 8 million where cycling is rapidly becoming a favored means of commuting.
The city's transportation agency, Transport for London, last week approved the world's first bicycle superhighway. It would run along the bank of the Thames River, which flows east-west through southern England, including the entire width of London. The plan is part of the city's Road Modernization Plan, proposed by Transport for London (TfL), the city's transportation coordinating agency. It received final approval yesterday. A subsection of the plan touts Mayor Boris Johnson's "Vision for Cycling."
Describing the superhighway, Johnson said, "My flagship route will run for at least 15 miles, very substantially segregated, from the western suburbs, through the heart of the Capital, to the City, Canary Wharf and Barking in the east. It will, we believe, be the longest substantially segregated continuous cycle route of any city in Europe. It will use a new segregated cycle track along, among other places, the Victoria Embankment and the Westway flyover. The Westway, the ultimate symbol of how the urban motorway tore up our cities, will become the ultimate symbol of how we are claiming central London for the bike."
With the number of cyclists on London's main roads tripling in the last decade, a study of cycling was undertaken in the spring of 2013, leading to the development of the plan. It projects to double the number of people cycling by 2020 through what it calls a "Tube network for bikes," a series of high capacity, joined-up tracks, many running parallel to bus, rail and Underground routes; more segregated, mandatory bike lanes and junctions; and a network of direct, back-street "Quietway" routes to encourage those concerned about safety on London's busier main streets. In addition to the east-west "superhighway," there will be several shorter mini superhighways including a north-south route.
To get there, the plan doubles the amount of money spent on cycling. London's first-ever cycling commissioner Andrew Gilligan, appointed two years ago, will oversee the execution of the plan. Work could start within weeks and the new routes could be open by the spring of 2016.
According to The Guardian of London, "The forces in favour seem overwhelming: Johnson, with all his political capital and democratic mandate, is a key proponent, and a nine-week consultation involving 21,500 people or organisations found 84 percent in favour."
But it also notes the plan has faced opposition from some business groups and the Licensed Tax Drivers Association (LTDA), which wants a judicial review of the process. LTDA general secretary Steve McNamara claims cyclists have been attacking him.
“You can’t believe the amount of emails and tweets I’ve been getting," he told The Guardian. "Some of it is quite outrageous. I’ve been threatened with violence. But I’m 6ft 2in, I weigh 15 stone, and I grew up in Hackney. They don’t scare me."
While the TfL study showed that most London cyclists are young and male, Johnson, who is a cyclist himself, wants to mix it up more.
"I want cycling to be normal, a part of everyday life," he said. "I want it to be something you feel comfortable doing in your ordinary clothes, something you hardly think about. I want more women cycling, more older people cycling, more black and minority ethnic Londoners cycling, more cyclists of all social backgrounds–without which truly mass participation can never come. As well as the admirable Lycra-wearers, and the enviable east Londoners on their fixed-gear bikes, I want more of the kind of cyclists you see in Holland, going at a leisurely pace on often clunky steeds."
Johnson says that the cycling plan will benefit all of the city's citizens, including those crabby cabbies.
"At the very heart of this strategy is my belief that helping cycling will not just help cyclists," he said. "It will create better places for everyone. It means less traffic, more trees, more places to sit and eat a sandwich. It means new life, new vitality and lower crime on underused streets. It means more seats on the Tube, less competition for a parking place and fewer cars in front of yours at the lights."
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From the mythical minotaur to the mule, creatures created from merging two or more distinct organisms – hybrids – have played defining roles in human history and culture. However, not all hybrids are as fantastic as the minotaur or as dependable as the mule; in fact, some of them cause human diseases.
When Looking Through a Microscope Isn’t Close Enough.<p>For the last few years, <a href="http://www.rokaslab.org/" target="_blank">our team at Vanderbilt University</a>, <a href="https://www.researchgate.net/lab/Gustavo-Goldman-Lab" target="_blank">Gustavo Goldman's team at São Paulo University in Brazil</a> and many other collaborators around the world have been collecting samples of fungi from patients infected with different species of <em>Aspergillus</em> molds. One of the species we are particularly interested in is <a href="https://doi.org/10.1006/rwgn.2001.0082" target="_blank"><em>Aspergillus nidulans</em>, a relatively common and generally harmless fungus</a>. Clinical laboratories typically identify the species of <em>Aspergillus</em> causing the infection by examining cultures of the fungi under the microscope. The problem with this approach is that very closely related species of <em>Aspergillus</em> tend to look very similar in their broad morphology or physical appearance when viewing them through a microscope.</p><p>Interested in examining the varying abilities of different <em>A. nidulans</em> strains to cause disease, we decided to analyze their total genetic content, or genomes. What we saw came as a total surprise. We had not collected <em>A. nidulans</em> but <em>Aspergillus latus</em>, a close relative of <em>A. nidulans</em> and, as we were to soon find out, <a href="https://doi.org/10.1016/j.cub.2020.04.071" target="_blank">a hybrid species that evolved through the fusion of the genomes</a> of two other <em>Aspergillus</em> species: <em>Aspergillus spinulosporus</em> and an unknown close relative of <em>Aspergillus quadrilineatus</em>. Thus, we realized not only that these patients harbored infections from an entirely different species than we thought they were, but also that this species was the first ever <em>Aspergillus</em> hybrid known to cause human infections.</p>
Several Different Fungal Hybrids Cause Human Disease.<p>Hybrid fungi that can cause infections in humans are well known to occur in several different lineages of single-celled fungi known as yeasts. Notable examples include multiple different species of <a href="https://doi.org/10.1002/yea.3242" target="_blank">yeast hybrids</a> that cause the human diseases <a href="https://rarediseases.info.nih.gov/diseases/6218/cryptococcosis" target="_blank">cryptococcosis</a> and <a href="https://www.cdc.gov/fungal/diseases/candidiasis/index.html" target="_blank">candidiasis</a>. Although pathogenic yeast hybrids are well known, our discovery that the <em>A. latus</em> pathogen is a hybrid is a first for molds that cause disease in humans.</p>
(Left) Candida yeasts live on parts of the human body. Imbalance of microbes on the body can allow these yeasts, some of which are hybrids, to grow and cause infection. (Right) Cryptococcus yeasts, including ones that are hybrids, can cause life-threatening infections in primarily immunocompromised people. Centers for Disease Control and Prevention<p><a href="https://doi.org/10.1371/journal.ppat.1008315" target="_blank">Why certain <em>Aspergillus</em> species are so deadly</a> while others are harmless remains unknown. This may in part be because <a href="https://doi.org/10.1016/j.fbr.2007.02.007" target="_blank">combinations of traits, rather than individual traits</a>, underlie organisms' ability to cause disease. So why then are hybrids frequently associated with human disease? Hybrids inherit genetic material from both parents, which may result in new combinations of traits. This may make them more similar to one parent in some of their characteristics, reflect both parents in others or may differ from both in the rest. It is precisely this mix and match of traits that hybrids have inherited from their parental species that <a href="https://www.nytimes.com/2010/09/14/science/14creatures.html" target="_blank">facilitates their evolutionary success</a>, including their ability to cause disease.</p>
The Evolutionary Origin of an Aspergillus Hybrid.<p>Multiple evolutionary paths can lead to the emergence of hybrids. One path is through mating, just as the horse and donkey mate to create a mule. Another path is through the merging or fusion of genetic material from cells of different species.</p><p>It is this second path that appears to have been taken by our fungus. <em>A. latus</em> appears to have two of almost everything compared to its parental species: twice the genome size, twice the total number of genes and so on. But unlike other hybrids, which are often sterile like the mule, we found that <em>A. latus</em> is capable of reproducing both asexually and sexually.</p><p>But how distinct were the parents of <em>A. latus</em>? By comparing the parts contributed by each parent in the <em>A. latus</em> genome, we estimate that its parents are approximately 93% genetically similar, which is about as related as we humans are with lemurs. In other words, <em>A. latus</em>, an agent of infectious disease, is the fungal equivalent of a human-lemur hybrid.</p>
How A. Latus Differs From its Parents.<p>Elucidating the identity of closely related fungal pathogens and how they differ from each other in infection-relevant characteristics is a key step toward reducing the burden of fungal disease. For example, we found that <em>A. latus</em> was three times more resistant than <em>A. nidulans</em>, the species it was originally identified as using microscopy-based methods, to one of the most common antifungal drugs, <a href="https://www.drugbank.ca/drugs/DB00520" target="_blank">caspofungin</a>. This result provides a clear example of the potential importance of accurate identification of the <em>Aspergillus</em> pathogen causing an infection.</p><p>We also examined how <em>A. latus</em> and <em>A. nidulans</em> interact with cells from our immune system. We found that immune cells were less efficient at combating <em>A. latus</em> compared to <em>A. nidulans</em>, suggesting the hybrid fungus may be trickier for our immune systems to identify and destroy.</p><p>In the midst of the COVID-19 pandemic, our quest to understand <em>Aspergillus</em> pathogens is becoming more urgent. Growing evidence suggests that <a href="https://doi.org/10.1111/myc.13096" target="_blank">a fraction of COVID-19 patients are also infected with <em>Aspergillus</em>.</a> More worrying is that these <a href="https://doi.org/10.3201/eid2607.201603" target="_blank">secondary <em>Aspergillus</em> infections</a> can worsen the clinical outcomes for those infected with the novel coronavirus. That being said, we stress that little is known about <em>Aspergillus</em> infections in COVID-19 patients due to a lack of systematic testing, and none of the infections identified so far appear to have been caused by hybrids.</p><p>So, when it comes to hybrids, some are fantastic (the minotaur), some are helpful (the mule) and some are dangerous (<em>Aspergillus latus</em>). Understanding more about the biology of <em>Aspergillus latus</em> may help in our understanding of how microbial pathogens arise and how to best prevent and combat their infections.</p>
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