UberX in LA: It's Illegal. It's Great. It Needs to Stop.

Despite the fact that it's currently banned in Los Angeles, UberX is defiantly still up and running. I used it for the first time this weekend. This so-called ride-sharing service from San Francisco-based Uber Technologies is supposedly the future of cabs. Much like similar services Lyft and Sidecar, UberX seeks to "disrupt" the taxi industry by using average people with a car (and without a taxi license) to shuttle others around. But it's pretty clear that they shouldn't be allowed to.

Using UberX was easy, affordable and pretty convenient. My driver was very nice, and I never felt in danger during my 11 minute, 53 second trip (the emailed receipt has stats) in what was essentially a random neighbor's Toyota Corolla. But that doesn't change the fact that Uber's ride-share service?which is currently operating in Los Angeles in defiance of the city's cease-and-desist order?should be shut down immediately.

I've lived without a car in Los Angeles for about two years now. Months ago, one of my brothers in Chicago emailed me a $10 credit for Uber. He and my other brother both swear by their black car service, and use it all the time. Neither of my two brothers in Chicago have cars and they both really can't say enough nice things about the service. But they've only ever used Uber's black car service, which (as far as we know) only uses city-licensed cars. Uber's ride-share service isn't available in Chicago.

So, when I found that I didn't have any singles for the bus, I decided to try out Uber with a little help from my brother's $10 credit. When my driver arrived (within 7 minutes of my hailing it through the app) my experience with Uber was almost immediately awkward. I approached the passenger side door of the Toyota Corolla and saw a plaid shirt on the front seat along with an orange on the floor. Was I supposed to sit in the back? That seems a bit... strange for a ride-share app, even if it was trying to emulate the full livery cab experience. My driver saw me opening the front passenger side door and kindly chucked the shirt in the backseat.

Aside from the initial awkwardness of the experience, everything else went more or less smoothly. Like I said, my driver was really nice. He looked like he was maybe in his mid-30s and told me that he drove for Uber part-time on the weekends to supplement his day-job at an auto body shop. Uber takes a 20% cut of every ride, he told me, and he drives about 10-15 people per day. I asked if he'd picked up any weirdos. Just drunk people, he said, but no one really creepy or anything. His friends who were cabbies weren't too happy about his part-time job. We shared a laugh about the obviousness of that statement.

And honestly, I'm not a huge fan of the taxi system in Los Angeles. It's virtually impossible to hail a cab on the street, unless you can find a hotel nearby. And unless my destination is the airport, cabbies in L.A. never know where anything is by memory; I'm almost always looking up directions (or at the very least an address) for them on my phone. But Uber doesn't really solve any of these problems with their disruption of the industry. The first thing my UberX driver asked me when I got in the cab was where I wanted to go. Wasn't this part of the process that should be automated with an app?

Those are just personal inconveniences, though. The real problem with UberX, and why it shouldn't be allowed to operate, is that its lack of oversight is cause for serious concern. When it comes to regulation, I tend to favor explicit consumer information as a bare-bones pre-requisite for putting a product or service into the world. Right now, Uber makes only sparse information available to the average consumer, even on their website.

Do you know what it does say there? "UberX: The convenience of Uber at a lower price with mid-range cars in a variety of colors. Seats up to 4 people." No mention of the fact that this is an unlicensed taxi in every sense of the concept. No mention that your driver will not be licensed by the city and will pull up in a car indistinguishable from any other on the road. These facts don't have to matter to you personally, but they probably should be considered when we're talking about issues of public safety.

I was never worried about my well-being during my UberX ride. I'm a large, white male, and I was traveling during daytime hours on relatively active streets. For me, using UberX was merely socially awkward. But we live in a world in which 1 in 5 American women have experienced sexual violence, where physical danger and robberies are all too common. Getting in an UberX car, for most people, becomes a complex mental equation about whether they trust the driver of this random Toyota Corolla?and by extension, whether they trust Uber.

Unfortunately, Uber gives us no reason to. I spent a large part of my morning going back and forth with the company trying to get the barest of details about what kind of training and screening UberX drivers in Los Angeles go through. Every response to my questions was boilerplate non-answer bullshit, wherein they tried to hang their hat on a temporary operating agreement with the California Public Utilities Commission (CPUC). Specific questions about their screening process went unanswered in the name of protecting trade secrets.

Giz: How many drivers have applied to drive in L.A. since you started in the city and how many have been rejected after not passing the background check and/or training?

Uber: Thousands have applied but we don't release specific numbers. We're committed to providing the safest most reliable service possible and our rejection process reflects that.

Giz: My driver yesterday said that his background check and training occurred at an office in Santa Monica. Is that the only such location in Southern California? Is that conducted by in-house Uber staff or do you bring in outside firms to conduct training? How long are these training sessions and could you explain what's involved?

Uber: We have several offices in Southern California and our training is carried out by Uber staff. The interviewing and training processes are intense and rigorous but we don't share the exact recipe for the secret Uber sauce.

Secret Uber sauce, indeed.

Uber wants to have it both ways. They distance themselves from the drivers, saying that "We don't employee [note: I think they mean employ] any of the drivers, or own the cars." But they also understand that they have to give consumers some amount of confidence in their product by using background checks (which is part of their temporary agreement with CPUC) and stressing in however vague terms that they do their own inspection of vehicles.

I spoke over the phone with Christopher Chow at the California Public Utilities Commission and he told me that they can expect a new decision at the state level on ride-sharing regulation either next week or later this month. Uber in Los Angeles is clearly biding their time in defiance of the city's cease and desist, deferring the move to comply with L.A. until this state decision is handed down.

Uber has met resistance at every turn, but not all of it exists simply to protect legacy business models. Objection to neoliberal fantasies around "disruption" and the free market isn't very trendy in Silicon Valley at the moment. But let's push these unlicensed cabs out of existence. It's better to put disruption in harm's way than ourselves.

Photo: Downtown Los Angeles by Matt Novak

Source: http://paleofuture.gizmodo.com/uberx-in-la-its-illegal-its-great-it-needs-to-stop-626060445

avengers soa

New understanding of tiny RNA molecules could have far-ranging medical applications

Public release date: 30-Jun-2013
[ | E-mail | Share ]

Contact: Mika Ono
mikaono@scripps.edu
858-784-2052
Scripps Research Institute

LA JOLLA, CA June 30, 2013 A team led by scientists at The Scripps Research Institute (TSRI) has identified a family of tiny RNA molecules that work as powerful regulators of the immune response in mammals. Mice who lack these RNA molecules lose their normal infection-fighting ability, whereas mice that overproduce them develop a fatal autoimmune syndrome.

"This finding gives us insights into immune regulation that could be very helpful in a range of medical applications, from viral vaccines to treatments for autoimmune diseases," said Changchun Xiao, assistant professor in TSRI's Department of Immunology and Microbial Science and senior investigator for the study, which appears in the June 30, 2013 issue of Nature Immunology.

Unraveling a Crucial Process

The finding concerns a key interaction between T cells and B cells, the allied lymphocyte armies that make up most of the adaptive immune system of mammals. B cells, which produce antibodies, usually lie in wait for pathogens in special zones called follicles within lymph nodes and the spleen. But to start proliferating normally and pumping out antibodies to fight an infection, these B cells have to be assisted, in effect, by T cells known as "follicular helper" T cells (TFH cells). "The TFH cells have to migrate into the B cell follicles and physically contact the B cells in order to provide help to them," said Xiao. "However, the molecular pathways that control TFH cell differentiation and migration have not been well understood."

In 2009, other researchers proposed that this crucial process requires the suppression of the miR-17~92 family of RNA molecules. These are among the thousands of short RNA molecules (often known as micro-RNAs, miRs, or miRNAs) that are made by mammalian cells and are meant to do their jobs while in RNA form. Typically an miRNA works inside the cell as a basic regulator or "dimmer switch" for the activity of tens to hundreds of genesit binds to transcripts of those genes and slows down their translation into proteins.

Xiao, who had been studying the miR-17~92 family since 2005, decided to examine their role in TFH differentiation. His team began by measuring the levels of these miRNAs in young, "nave" T cells and in the TFH cells to which these T cells gave birth after exposure to foreign antigens.

Surprising Finding

To the researchers' surprise, the miR-17~92s showed the opposite pattern of expression than expected: their levels jumped as the nave T cells began differentiating into TFH cells, but fell back by the time the process was finished. The finding suggested that, far from acting as a brake on TFH differentiation, miR-17~92s work as enablers of the process.

To confirm their suspicion, team members developed mutant mouse lines in which some or all of the miR-17~92 miRNAs were knocked out of T cells. These miR-17~92-deficient T cells turned out to be much less able to differentiate into TFH cells. As a result, the follicle-dwelling B cells that depend on TFH assistance also lost much of their ability to respond to an immune challenge. "These mutant mice showed a deficient antibody response to a standard immune-provoking protein," said Seung Goo Kang, a postdoctoral research associate in the Xiao laboratory who was the leading author of the study.

Collaborating TSRI scientists led by John Teijaro, a senior research associate in the laboratory of Michael B. A. Oldstone, professor in the Department of Immunology and Microbial Science, showed further that these transgenic miceunlike ordinary lab micecould not clear a chronic virus infection that is used as a standard challenge in immunological experiments.

By contrast, when the team raised transgenic mice whose T cells produced four to six times the normal amount of miR-17~92s, these T cells differentiated into TFH cells spontaneouslythat is, without an immune-stimulating inoculation.

These mice developed antibody responses to their own tissues, and died young, with swollen spleen and lymph nodes. "The accumulation of autoantibodies is also seen in lupus and other autoimmune diseases in humans," said Wen-Hsien Liu, another postdoctoral research associate in the Xiao laboratory and a co-first author of the paper.

Important Targets

Liu and Kang were able to track down a key target gene of miR-17~92s, which the miRNAs suppress to enable TFH cell differentiation. The targeted gene codes for Phlpp2, a recently discovered signaling inhibitor. "Lowering Phlpp2 protein levels in our miR-17~92-knockout T cells restored much of their ability to become TFH cells," Kang said.

"Phlpp2 is one important target, but we believe there are others too, and we are now looking for those," Xiao said. He and his colleagues also plan to investigate methods for manipulating miR-17~92s and their TFH cell-related pathways, in order to boost antibody responses to vaccines for exampleor alternatively to lower autoantibody productions in people with autoimmune diseases.

###

The study, "miR-17~92 family microRNAs are critical regulators of T follicular helper cell differentiation," was a collaboration that also involved the laboratory of Hai Qi at Tsinghua University in Beijing and the laboratory of Eric Verdin at the Gladstone Institute of Virology and Immunology at the University of California, San Francisco. A co-first author of the study was Peiwen Lu of the Qi laboratory; other co-authors were Hyung W. Lim of the Verdin laboratory, Daniel Fremgen of the Oldstone laboratory and Hyun Yong Jin and Jovan Shepherd of the Xiao laboratory.

The study was funded by the PEW Charitable Trusts, the Cancer Research Institute, the Lupus Research Institute, the American Heart Association (grant 11POST7430106 ), the National Institutes of Health (R01AI019484 and R01AI087634) and the National Natural Science Foundation of China (81161120405).

---

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?

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

Public release date: 30-Jun-2013
[ | E-mail | Share ]

Contact: Mika Ono
mikaono@scripps.edu
858-784-2052
Scripps Research Institute

LA JOLLA, CA June 30, 2013 A team led by scientists at The Scripps Research Institute (TSRI) has identified a family of tiny RNA molecules that work as powerful regulators of the immune response in mammals. Mice who lack these RNA molecules lose their normal infection-fighting ability, whereas mice that overproduce them develop a fatal autoimmune syndrome.

"This finding gives us insights into immune regulation that could be very helpful in a range of medical applications, from viral vaccines to treatments for autoimmune diseases," said Changchun Xiao, assistant professor in TSRI's Department of Immunology and Microbial Science and senior investigator for the study, which appears in the June 30, 2013 issue of Nature Immunology.

Unraveling a Crucial Process

The finding concerns a key interaction between T cells and B cells, the allied lymphocyte armies that make up most of the adaptive immune system of mammals. B cells, which produce antibodies, usually lie in wait for pathogens in special zones called follicles within lymph nodes and the spleen. But to start proliferating normally and pumping out antibodies to fight an infection, these B cells have to be assisted, in effect, by T cells known as "follicular helper" T cells (TFH cells). "The TFH cells have to migrate into the B cell follicles and physically contact the B cells in order to provide help to them," said Xiao. "However, the molecular pathways that control TFH cell differentiation and migration have not been well understood."

In 2009, other researchers proposed that this crucial process requires the suppression of the miR-17~92 family of RNA molecules. These are among the thousands of short RNA molecules (often known as micro-RNAs, miRs, or miRNAs) that are made by mammalian cells and are meant to do their jobs while in RNA form. Typically an miRNA works inside the cell as a basic regulator or "dimmer switch" for the activity of tens to hundreds of genesit binds to transcripts of those genes and slows down their translation into proteins.

Xiao, who had been studying the miR-17~92 family since 2005, decided to examine their role in TFH differentiation. His team began by measuring the levels of these miRNAs in young, "nave" T cells and in the TFH cells to which these T cells gave birth after exposure to foreign antigens.

Surprising Finding

To the researchers' surprise, the miR-17~92s showed the opposite pattern of expression than expected: their levels jumped as the nave T cells began differentiating into TFH cells, but fell back by the time the process was finished. The finding suggested that, far from acting as a brake on TFH differentiation, miR-17~92s work as enablers of the process.

To confirm their suspicion, team members developed mutant mouse lines in which some or all of the miR-17~92 miRNAs were knocked out of T cells. These miR-17~92-deficient T cells turned out to be much less able to differentiate into TFH cells. As a result, the follicle-dwelling B cells that depend on TFH assistance also lost much of their ability to respond to an immune challenge. "These mutant mice showed a deficient antibody response to a standard immune-provoking protein," said Seung Goo Kang, a postdoctoral research associate in the Xiao laboratory who was the leading author of the study.

Collaborating TSRI scientists led by John Teijaro, a senior research associate in the laboratory of Michael B. A. Oldstone, professor in the Department of Immunology and Microbial Science, showed further that these transgenic miceunlike ordinary lab micecould not clear a chronic virus infection that is used as a standard challenge in immunological experiments.

By contrast, when the team raised transgenic mice whose T cells produced four to six times the normal amount of miR-17~92s, these T cells differentiated into TFH cells spontaneouslythat is, without an immune-stimulating inoculation.

These mice developed antibody responses to their own tissues, and died young, with swollen spleen and lymph nodes. "The accumulation of autoantibodies is also seen in lupus and other autoimmune diseases in humans," said Wen-Hsien Liu, another postdoctoral research associate in the Xiao laboratory and a co-first author of the paper.

Important Targets

Liu and Kang were able to track down a key target gene of miR-17~92s, which the miRNAs suppress to enable TFH cell differentiation. The targeted gene codes for Phlpp2, a recently discovered signaling inhibitor. "Lowering Phlpp2 protein levels in our miR-17~92-knockout T cells restored much of their ability to become TFH cells," Kang said.

"Phlpp2 is one important target, but we believe there are others too, and we are now looking for those," Xiao said. He and his colleagues also plan to investigate methods for manipulating miR-17~92s and their TFH cell-related pathways, in order to boost antibody responses to vaccines for exampleor alternatively to lower autoantibody productions in people with autoimmune diseases.

###

The study, "miR-17~92 family microRNAs are critical regulators of T follicular helper cell differentiation," was a collaboration that also involved the laboratory of Hai Qi at Tsinghua University in Beijing and the laboratory of Eric Verdin at the Gladstone Institute of Virology and Immunology at the University of California, San Francisco. A co-first author of the study was Peiwen Lu of the Qi laboratory; other co-authors were Hyung W. Lim of the Verdin laboratory, Daniel Fremgen of the Oldstone laboratory and Hyun Yong Jin and Jovan Shepherd of the Xiao laboratory.

The study was funded by the PEW Charitable Trusts, the Cancer Research Institute, the Lupus Research Institute, the American Heart Association (grant 11POST7430106 ), the National Institutes of Health (R01AI019484 and R01AI087634) and the National Natural Science Foundation of China (81161120405).

---

[ | E-mail | Share ]

?

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

Source: http://www.eurekalert.org/pub_releases/2013-06/sri-nuo062613.php

Diwali elmo

Justice Kennedy denies motion to halt gay marriage

WASHINGTON (AP) ? Supreme Court Justice Anthony Kennedy has denied a request from Proposition 8 supporters in California to halt the issuance of same-sex marriage licenses in the nation's most populous state.

Kennedy turned away the request on Sunday with no additional comment.

Same-sex marriage opponents asked him to step in on Saturday, a day after the federal appeals court in San Francisco allowed same-sex marriages to go forward. Numerous weddings were performed at San Francisco City Hall following the court decisions.

The opponents said the appeals court had acted about three weeks too soon. Proposition 8 supporters could continue their efforts to halt gay marriage by filing their request with another Supreme Court justice.

Associated Press

Source: http://hosted2.ap.org/APDEFAULT/386c25518f464186bf7a2ac026580ce7/Article_2013-06-30-Gay%20Marriage-California-Motion/id-7ad3b9958a474ea38d8ad812af94dd49

usher James Holmes

Combo Crew (for Android)

Combo Crew, the latest Android title from developer The Game Bakers, aims to eliminate one of the problems inherent to mobile action games: poor touch screen controls. Instead of requiring gamers to continuously jam their digits onto a glass screen, Combo Crew maps punches, kicks, and super moves to swipes?a far superior way to interact with a touchscreen interface. While it's easy to unleash moves in this arena-style 2D brawler, design elements intended to streamline the controls remove the challenge and the need for move set mastery.

Welcome to the Jungle
Combo Crew opens with a generic backstory that plays out as a pseudo-parody of games of this type: Mr. Boss invites Gina (a Hair-Fu practitioner), Dolph (an action movie star), and Parker (a video game junkie) to his Boss Tower for dinner?but it's a trap! The baddie simply wants to challenge and defeat the best fighters in order to stroke his ego.

Although Combo Crew introduces you to three cutesy protagonists, only Gina and Parker are available for fisticuffs duty right away; you unlock Dolph after you've fought a few matches and earned 20 in-game credits (that's right, in-game currency?no cash needed). A fourth character, Sammo, is also a 20-credit buy.

Each brawler starts with four attacks?a mix of regular blows, guard breakers, and crow ground attacks. New moves are unlocked as you complete chapters, while other moves are unlocked after successfully completing missions in Combo Crew mode (a series of fight-based challenges). Once new moves are acquired, you can use them to replace the old ones if you'd like, but you can only carry four attacks at a time. Spending credits in the Shop lets you purchase Boosts (temporary power-ups such as a health-replenishing burger) or Perks (permanent character improvements such as a greater damage output).

Fight Club
Swipe-based inputs are how you unleash your fury onto Mr. Boss' foot soldiers. Swiping up, down, left, or right executes basic attacks, but there are advanced methods, too. Tapping the screen, holding, and then swiping toward an enemy delivers a guard breaker that crumbles a block defense. Swiping with two fingers uncorks impressive auto-combos that string multiple hits together without any further input. When your super-meter is full, tapping the super-attack icon lets you bust out a flurry of hard-hitting moves. There's a surprisingly amount of depth to the combat system: you can even do air juggles and knockdown attacks. Your combos are tallied as you land blows, and the music gets remixed on the fly as the total grows.

The simplified combat works well and the hits are quite satisfying, but there are some associated tradeoffs. You don't actually move your opponent; swiping causes your character to dash toward a foe and attack. You can't rely on positioning to set up attacks/dodges as you can with classic beat 'em ups like Double Dragon or River City Ransom. If you want to avoid an attack, you must swipe attack when an exclamation point appears over an enemy's head to perform a counter. The streamlined controls also result in button-mashing as a viable combat scheme, which removes the challenge.

Combo Crew is a solo experience, but there is an unusual (and creative) asynchronous co-op element. Suppose a bad guy gives you the business and whittles your health down to zero. Instead enduring a game over, you can ask a Combo Crew-playing friend to remotely take over your game. Your buddy has the opportunity to finish up your mess, and if s/he beats the round, your friend's score is converted into health for your character. When your fighter's health gauge is filled, any remaining points are added to your score.

Knuckle Up
Combo Crew is an entertaining diversion that should scratch genre fans' beat 'em up itch. It's cute, colorful, and had a surprisingly deep combat system. Still, you don't necessarily need to learn it; button-mashing can get the job done, too. What makes Combo Crew work, the simple control scheme, also works against it. Still, those who want to punch a few grunts in the face will find a lot to like.

Source: http://feedproxy.google.com/~r/ziffdavis/pcmag/~3/ctQKZOPkw8o/0,2817,2421192,00.asp

vincent jackson vicki gunvalson

Google, Microsoft slate spying bill

Internet, technology giants oppose proposed obligations in eavesdropping legislation.

Internet and software giants Google and Microsoft have slammed legislation that could see the Government try to force them to make their systems available for interception by the Government Communications Security Bureau (GCSB).

Only network operators such as Telecom, Vodafone and 2degrees are obliged to make their networks available for eavesdropping by the GCSB, SIS and police.

The new Telecommunications (Interception Capability and Security) bill being considered by Parliament's law and order committee would allow the Government to place the same obligations on internet service companies such as Google, Facebook and Microsoft-owned Skype.

Google submitted that the bill would harm innovation to the detriment of New Zealand customers and would raise privacy issues.

While Google recognised interception tools were necessary, it was concerned the new obligations were broader than necessary.

The additional costs, time and challenges imposed "may discourage both local and international entities from making new service offerings in New Zealand. It could also lead to existing providers exiting the New Zealand market or reducing their offerings", Google submitted.

Google also warned that the bill would require global internet companies based outside New Zealand to undertake interception, "even if doing so would conflict with those companies' legal obligations in their home jurisdiction".

It said ministers should only be able to impose interception obligations on internet service companies "following the transparency of a parliamentary process" rather than a simple ministerial direction which the bill allows for. That ministerial direction and other processes under the bill lacked transparency and "would likely raise public fears of unjustified intrusion into their privacy", Google said.

Microsoft also said the bill could result in obligations being placed on overseas-based internet companies that may "conflict with pre-existing obligations that they have under overseas laws".

The committee's consideration of submissions continues this week while the security and intelligence committee is to hear submissions on the GCSB bill from tomorrow.

Bugging bill

Only network operators such as Telecom, Vodafone and 2degrees are obliged to make their networks available for eavesdropping by the GCSB, SIS and police.

The new bill being considered would allow the Government to place the same obligations on internet service companies.

By Adam Bennett Email Adam

Source: http://www.nzherald.co.nz/nz/news/article.cfm?c_id=1&objectid=10893987&ref=rss

andy williams Lady Gaga

Rare giant catfish faces new threat in Southeast Asia's Mekong

Laos' controversial Xayaburi dam could bring the Giant Catfish to extinction, as well as devastate the Mekong River's other fisheries. The challenge: How to build a dam that allows a 600-pound fish to swim up stream?

By Elizabeth Barber,?Contributor / June 22, 2013

Two Thai fishermen show a 293-kilogram (646-pound) giant catfish they caught from the Mekong River in Chiang Khong district of Chiang Rai province, northern Thailand in 2005.

Suthep Kritsanavarin/AP

Enlarge

The Giant Catfish is an enormous fish with thin, down-turned lips that give it a lonely look. And such a "mournful" visage is not unwarranted.

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Already one of the most endangered fish in the world, a new study has found that a dam underway in Laos could push it to extinction.?

So rare that it is nearly a legend of the Mekong River?s depths, the Giant Catfish belongs to the?shark catfish family and reach upwards of 600 pounds and some 10 feet in length. The brobdingnagian?fish has dwindled in number an estimated 90 percent over the past 20 years ???possibly to just a few hundred animals, though tracking the elusive fish is difficult. It is now found only in the lower Mekong, which runs like a mud-colored vein carrying the economic lifeblood of Southeast Asia through Laos, Myanmar, Thailand, Cambodia, and Vietnam. In recent years, though, progress had been made in rescuing Giant Catfish fish from extinction, as those five countries introduced new protections that banned fishing it.

Now, Laos's controversial Xayaburi dam threatens to undo that.

?The Giant Catfish is endangered, but there?s still a chance for it, and all the countries involved have gotten on board to restrict fishing ? but just when we solved one problem we?re now facing this new one,? says Zeb Hogan, the?study?s author and associate research professor at the University of Nevada,?in a telephone interview.

The Xayabari, the first dam in the lower Mekong, will if finished block the Giant Catfish from making its lifecycle migration from the floodplain rearing areas to upstream spawning sites in northern Laos and Thailand, the study said. The dam could also alter Mekong flows, disrupting the natural cues the fish needs to spawn.

This is not the first warning that the Xayabari project could mean the end for the Giant Catfish. Two years ago, the Mekong River Commission???an advisory body established in 1995 as part of an agreement between five Southeast Asian countries on the development of the Mekong ??convened a panel of experts who concluded that the dam would obstruct the migrations of some 23 to 100 species of fish, including the Great Catfish. The panel recommended a 10-year hold on the Xayaburi project, pending more information on how the dam would affect the river?s ecology.

"The gaps in knowledge on the number of migratory fish species, their biomass and their ability to successfully pass a dam and reservoir leads to considerable uncertainty about the scale of impact on fisheries and associated livelihoods, both locally and in a transboundary context," the report said.

But in November 2012, Laos officially began what is expected to be seven years of construction of the Xayabari dam, the first in several controversial dams planned for the lower Mekong.?

Source: http://rss.csmonitor.com/~r/feeds/science/~3/CCrYxnsRm6U/Rare-giant-catfish-faces-new-threat-in-Southeast-Asia-s-Mekong

dan marino godaddy

Reading DNA, backward and forward: Biologists reveal how cells control the direction in which the genome is read

June 24, 2013 ? MIT biologists have discovered a mechanism that allows cells to read their own DNA in the correct direction and prevents them from copying most of the so-called "junk DNA" that makes up long stretches of our genome.

Only about 15 percent of the human genome consists of protein-coding genes, but in recent years scientists have found that a surprising amount of the junk, or intergenic DNA, does get copied into RNA -- the molecule that carries DNA's messages to the rest of the cell.

Scientists have been trying to figure out just what this RNA might be doing, if anything. In 2008, MIT researchers led by Institute Professor Phillip Sharp discovered that much of this RNA is generated through a process called divergent expression, through which cells read their DNA in both directions moving away from a given starting point.

In a new paper appearing in Nature on June 23, Sharp and colleagues describe how cells initiate but then halt the copying of RNA in the upstream, or non-protein-coding direction, while allowing it to continue in the direction in which genes are correctly read. The finding helps to explain the existence of many recently discovered types of short strands of RNA whose function is unknown.

"This is part of an RNA revolution where we're seeing different RNAs and new RNAs that we hadn't suspected were present in cells, and trying to understand what role they have in the health of the cell or the viability of the cell," says Sharp, who is a member of MIT's Koch Institute for Integrative Cancer Research. "It gives us a whole new appreciation of the balance of the fundamental processes that allow cells to function."

Graduate students Albert Almada and Xuebing Wu are the lead authors of the paper. Christopher Burge, a professor of biology and biological engineering, and undergraduate Andrea Kriz are also authors.

Choosing direction

DNA, which is housed within the nucleus of cells, controls cellular activity by coding for the production of RNAs and proteins. To exert this control, the genetic information encoded by DNA must first be copied, or transcribed, into messenger RNA (mRNA).

When the DNA double helix unwinds to reveal its genetic messages, RNA transcription can proceed in either direction. To initiate this copying, an enzyme called RNA polymerase latches on to the DNA at a spot known as the promoter. The RNA polymerase then moves along the strand, building the mRNA chain as it goes.

When the RNA polymerase reaches a stop signal at the end of a gene, it halts transcription and adds to the mRNA a sequence of bases known as a poly-A tail, which consists of a long string of the genetic base adenine. This process, known as polyadenylation, helps to prepare the mRNA molecule to be exported from the cell's nucleus.

By sequencing the mRNA transcripts of mouse embryonic stem cells, the researchers discovered that polyadenylation also plays a major role in halting the transcription of upstream, noncoding DNA sequences. They found that these regions have a high density of signal sequences for polyadenylation, which prompts enzymes to chop up the RNA before it gets very long. Stretches of DNA that code for genes have a low density of these signal sequences.

The researchers also found another factor that influences whether transcription is allowed to continue. It has been recently shown that when a cellular factor known as U1 snRNP binds to RNA, polyadenylation is suppressed. The new MIT study found that genes have a higher concentration of binding sites for U1 snRNP than noncoding sequences, allowing gene transcription to continue uninterrupted.

A widespread phenomenon

The function of all of this upstream noncoding RNA is still a subject of much investigation. "That transcriptional process could produce an RNA that has some function, or it could be a product of the nature of the biochemical reaction. This will be debated for a long time," Sharp says.

His lab is now exploring the relationship between this transcription process and the observation of large numbers of so-called long noncoding RNAs (lncRNAs). He plans to investigate the mechanisms that control the synthesis of such RNAs and try to determine their functions.

"Once you see some data like this, it raises many more questions to be investigated, which I'm hoping will lead us to deeper insights into how our cells carry out their normal functions and how they change in malignancy," Sharp says.

The research was funded by the National Institutes of Health, the National Cancer Institute and the National Institute of General Medical Sciences.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/top_health/~3/vK48xKSPdxQ/130624141412.htm

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