Definition: In this task, you are given a text of many news articles seperated by special token "|||||". Your task is to summarize them.
Input: A generic blood pressure drug could prevent hyperactive brain cell firing associated with early stages of autism spectrum disorder, according to a new study. 
  
 Injecting pregnant mice with Bumetanide, a diuretic, appears to correct a developmental switch flipped during childbirth that reverses the firing characteristics of neurons in newborns, according to a study published online Thursday in the journal Science. 
  
 Bumetanide mimics the effects of oxytocin, a hormone released during labor that helps protect newborns from the stresses and complications of birth, the study found. That surge of oxytocin changes the way a neurotransmitter regulates neurons -- it no longer encourages the firing of neurons and becomes a kind of electrochemical brake in the adult brains. 
  
 Overly excited brain circuits are strongly linked with autism spectrum disorder, a disease that strikes an estimated 1 of every 88 children, causing them to have restricted interests, and impaired communication and social skills. 
  
 The drug was tested for only two types of autism that constitute a minority of cases of the perplexing disorder: a genetic mutation that causes Fragile X Syndrome, and autism sparked by prenatal exposure to the anticonvulsive valproic acid. 
  
 Researchers warned that further testing will be needed to determine both the efficacy of the drug in children and its potential for causing side effects. And because there is no way to diagnose autism risks to fetuses, it remains unlikely that such a therapy would be administered prenatally, as a prevention of autism. 
  
 “I’m not convinced that the hope is one day to be able to treat during pregnancy,” said neurologist Yehezkel Ben-Ari, of the French Institute of Health and Medical Research, the lead author of the study. “The hope is after birth, provided we have a good diagnosis.” 
  
 Early clinical trials in Europe have shown that the drug diminished autism symptoms among 60 children age 3-11. Further trials are underway, Ben-Ari said. 
  
 Researchers have long suspected the role of gamma aminobutyric acid, or GABA, but have not understood the intricacies of the “GABA switch” that is apparently thrown at birth, nor how it might be altered. 
  
 They focused on a kind of biochemical trade balance of chloride ions in neurons of the hippocampus. A surplus inside fetal neurons gradually decreases as a chloride exporter comes to dominate the equation, and oxytocin appears to mediate this change, according to the study. 
  
 “During delivery, you have important reactions that, if they fail, you have a higher likelihood of autism,” Ben-Ari said. “The delivery has a major priming effect on what is going to happen subsequently.” 
  
 But that priming doesn’t happen in mice with the Fragile X mutation or those exposed to valproic acid in utero, the researchers found. Chloride export was reduced in both. And GABA continued to excite the neurons of the newborns of both type rats, rather than inhibit them. This led to more active circuits, according to the study. 
  
 Bumetanide administered to pregnant mice changed the aberrant chloride profile in the the neurons of mice offspring, which also exhibited fewer autism-like characteristics in their vocalizations, according to the study. 
  
 Andrew Zimmerman, a pediatric neurologist at the Center for Autism and Neurodevelopmental Disorders at the University of Massachusetts Medical School in Worcester, said the findings were encouraging. 
  
 “They’ve further defined this GABA switch that we’ve suspected is present in normal brain development but is probably abnormal in autism brain development,” Zimmerman said. “This is direct confirmation, as close as you can get in animals.” 
  
 Zimmerman noted that 80% of autism cases arise from unknown causes unrelated to Fragile X syndrome or exposure to valproic acid. Still, he added, the fact that two widely different causes of autism showed a chloride imbalance suggests that this may be a common denominator in other cases. ||||| A drug aimed at eliminating symptoms in people with certain forms of autism is in the early stages of work, and animal studies show promise, researchers report. 
  
 In experiments in mice and rats, the drug reversed the effects of a faulty mechanism during birth that might lead the offspring to develop autism, and alleviated the symptoms of autism that certain offspring would normally demonstrate, according to studies published today (Feb. 6) in the journal Science. 
  
 The drug, called bumetanide, is a diuretic already approved to treat people with liver and heart disease. It is being tested for safety in children with autism, and researchers will be looking to see if it can achieve similar results in children as seen in the early experiments. 
  
 "If you administer a diuretic to the mother 24 hours before delivery, the offspring is, so to speak, cured," study author Yehezkel Ben-Ari, a neurobiologist at the French Institute of Health and Medical Research in Paris, told reporters. 
  
 Normally, nerve signaling in a fetus is excited during early development, and then, leading up to and during birth, the hormone oxytocin causes a switch in that excitement. But in certain cases, there appears to be a buildup of chloride, which prevents that switch from happening. This starts a pathway that could lead to autism, the researchers said. [10 Things You Didn't Know About the Brain] 
  
 But the drug given in the study appears to stop that problem, Ben-Ari said. 
  
 The drug is used to flush water and salt from the body. Because it is generic, Ben-Ari said, there has been difficulty generating funding for research on it. At present, he said, his colleagues are at work on a compound that can be patented to remove that obstacle. 
  
 While bumetanide is being tested in children to see if it can eliminate autism symptoms, it's far from clear whether the positive early results in mice and rats will carry over to people. 
  
 "I think 90 percent of this paper is really earth-shattering, but there's always the caution of, 'is this going to work in humans, a more advanced mammal?'" said G. Ian Gallicano, a molecular and cell biologist at Georgetown University in Washington DC, who was not involved in the new research. 
  
 Mice and rats develop differently from humans in utero, and the first few months of life in humans are comparable, in terms of development, to the last week or so of pregnancy in mice and rats. So it remains to be seen whether giving the drug to infants early in life will match the effects of administering the drug to a pregnant mouse or rat. 
  
 Autism cannot be diagnosed prenatally, but certain conditions that often lead to autism, such as fragile X syndrome, can be diagnosed in that early stage. Some of the animals in the study were models of fragile X. 
  
 Other animals modeled what happens when a fetus is exposed to a compound in certain drugs a mother might take, including epilepsy medication, which might mean that another drug can be given in combination with it to reduce negative outcomes in children. 
  
 "I think you're going to have ample parents wanting to try this, if they know that their child has a genetic disorder that is going to lead to autism," Gallicano told Live Science. 
  
 Ben-Ari said the key to successful treatment, as with other therapies, is going to be early intervention. An early change from normal development as shown in this case can result in further problems if left untreated. However, he said, the research may not reach the point where the drug would be given to a pregnant woman rather than the child, after birth. 
  
 "What we must do is work in the development and biology earlier so we see, this is insufficient and how we can treat it earlier," he said. 
  
 Follow Joe Brownstein @joebrownstein. Follow Live Science @livescience, Facebook & Google+. Original article on Live Science. ||||| Autism may result from a faulty chemical switch that doesn't get flipped in time to help the brain develop normally, a new research study suggests. 
  
 Researchers are finding genetic differences that help explain why autism is more frequent in boys than girls. (Photo: Doug Kapustin for USA TODAY) Story Highlights Drug is being tested on dozens of European children with autism 
  
 Autism affects at least 1 in 88 U.S. schoolchildren 
  
 Previous attempts to develop an effective drug for autism have either failed or are still experimental 
  
 Building on what they hope will be an important insight into the cause of autism, French researchers are testing a high blood pressure medication on dozens of European children with autism. 
  
 The team, which has a financial stake in the drug, has tried it on 30 children with autism; now they are testing it in more, hoping to improve core characteristics of autism for the first time. 
  
 There are drugs to treat some of autism's symptoms, but none that address the underlying social and communication difficulties and repetitive behaviors, which define the condition. Previous attempts to develop an effective drug against the condition, which affects at least one in 88 U.S. schoolchildren, have either failed or are also still experimental. 
  
 In a study out today in the journal Science, the researchers offer an explanation for the promise of their drug, bumetanide, a generic diuretic long used to treat the fluid retention of high blood pressure. 
  
 The researchers found that the drug, given during pregnancy, could reverse autism symptoms in newborn mice bred with a genetic condition that often causes autism in people, and in rats exposed to the epilepsy drug valproic acid, which is known to trigger autism. 
  
 They suspect that bumetanide is flipping a chemical switch in the brain — changing the chemical GABA from stimulating electrical activity in the brain to tamping it down. This switch needs to be flipped during or near birth for the brain to develop normally, says lead researcher Yehezkel Ben-Ari of the French Institut National de la Santé et de la Recherche Médicale, in Marseilles, France. 
  
 Because this switch fails to flip in rodents with two very different triggers of autism, the researchers say they may have found an underlying cause of the condition. 
  
 That is a "pretty incredible finding and really great," says Andrew Zimmerman, a pediatric neurologist and autism expert at the University of Massachusetts Medical School in Worcester, Mass. 
  
 He and other researchers note that it's too early for people to try the drug outside of carefully watched clinical trials. There are just so many unknowns, from what the drug will do to the developing brain to how much of the drug to give and when. 
  
 "So many things cure cancer in mice and rats, and so many things cure all kinds of things and then when we give them to humans they have adverse affects and don't fix the problems we thought they could fix," says Gary Goldstein, president and CEO of the Kennedy Krieger Institute, a Baltimore-based clinic and research center. "I wouldn't give it to my child, I can tell you that." 
  
 Ben-Ari and his colleagues have patented a version of bumetanide and formed a company, Neurochlore, in Marseilles, to test the drug in children. He says bumetanide should not be given to pregnant women — despite his success with rodents — because it is impossible to determine which children will go on to develop autism and unethical to test on healthy ones. 
  
 It should be used as early in childhood as possible, Ben-Ari says, and his team is testing the drug in children as young as 2. Autism is typically diagnosed around age 4, but experts are working to push that diagnosis earlier. It is widely believed that the sooner treatment begins, the more effective it is likely to be. 
  
 Ben-Ari says he is hopeful that the drug will show benefits across a broad spectrum of children with autism, but behavioral therapy and possibly other pharmaceutical treatments will likely still be needed, too, he says. 
  
 "It's important for people to understand there is no drug to cure a medical disease as complicated as autism," he says. 
  
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Output:
French researchers have been testing a diuretic on kids with autism, and in a study released yesterday in Science, they explain why they think the drug, a version of bumetanide they have patented, has so much promise: because of their experiments with mice. As USA Today explains, a chemical switch needs to be flipped in the brain at or near birth in order for the brain to develop normally; the "flip" changes "the chemical GABA from stimulating electrical activity in the brain to tamping it down." As LiveScience explains, the hormone oxytocin would normally cause a switch, but it seems that in some cases, a buildup of chloride prevents the flip. Bumetanide removes salt from the body, and when the researchers administered the drug to pregnant mice and rats "modeled for autism" just before delivery, the flip, which seemingly wouldn't have occurred, seemingly did. The LAT notes a pretty important facet of the study: The drug was tested on just two types of autism that amount to a minority of overall autism instances. Still, an autism expert calls it a "pretty incredible finding." The researchers caution against administering bumetanide to all pregnant mothers, as that could be dangerous, and it's not possible to prenatally know which children will eventually develop autism. But early diagnosis is key, and they're testing their drug in kids as young as 2 (diagnosis typically comes two years later, notes USA Today). At Forbes, Emily Willingham pokes holes at the study, noting that, for one, "This 'brain-protective' action of oxytocin has been established in rodents. It has not been established in humans. If it were relevant, one would expect a strong autism signal among children born via planned cesarean section, as that generally doesn't involve oxytocin influence."