NYs Governor and Some Big City Mayors Ban Official Travel to North

first_imgShare2Tweet2ShareEmail4 SharesGov. Cuomo & Chairman Prendergast Ride E Train / Metropolitan Transportation Authority of the State of New YorkMarch 28, 2016; ABC News (Associated Press)The governor of New York has joined Mayor Ed Murray of Seattle and San Francisco’s Mayor Ed Lee in banning nonessential publically funded travel to North Carolina in response to N.C.’s House Bill 2, which blocks anti-discrimination protections for gay, lesbian, and transgender people. The law overrides local ordinances in the state that provide such protections, prevents cities and counties from passing anti-discrimination rules, and imposes a statewide standard that leaves out protections based on sexual orientation and gender identity.N.Y. Governor Andrew Cuomo issued the travel ban with this statement:In New York, we believe that all people—regardless of their gender identity or sexual orientation—deserve the same rights and protections under the law. From Stonewall to marriage equality, our state has been a beacon of hope and equality for the LGBT community, and we will not stand idly by as misguided legislation replicates the discrimination of the past. As long as there is a law in North Carolina that creates the grounds for discrimination against LGBT people, I am barring non-essential state travel to that state.Last week, North Carolina lawmakers approved and Republican Gov. Pat McCrory signed legislation voiding a Charlotte ordinance that would have provided wide protections against discrimination in public accommodations. Technology giants Apple, Google, and Facebook are among a dozen big companies, or their top executives, who have objected to the law. Governor Cuomo and the mayors are joining for-profit companies, public corporations, and associations and clubs who oppose the law by working an angle that works well for influencing decisions in a capitalist country: hitting the state’s pocketbook.Some of the roughly 20,000 retail and interior design companies that attend the twice-a-year High Point furniture market say they won’t travel to the North Carolina city next month because of HB2. The taxpayer-supported High Point Market Authority said Monday that dozens of buyers have said their employees wouldn’t attend to shop the new offerings of manufacturers and wholesalers. Opponents of the law also are on social media calling for a boycott of the market, which has an annual statewide economic impact of $5 billion. High Point Market Authority CEO Tom Conley says the impact of a threatened boycott won’t be known for weeks or months.Others are going the legal route. Lambda Legal, the American Civil Liberties Union, the ACLU of North Carolina, and Equality NC joined together in filing a federal lawsuit against House Bill 2. As reported in the Associated Press, at a press conference in Raleigh, North Carolina Attorney General Roy Cooper announced that his office would not defend HB2, which was pushed through during an unprecedented special legislative session of the N.C. General Assembly. (Cooper, a Democrat, is running against McCrory for governor in November.)Cooper has stated that the law is unconstitutional, and that he would join with the North Carolina Treasurer’s office to defend their non-discrimination policy, requiring equal treatment for LGBT people.—Marian ConwayShare2Tweet2ShareEmail4 Shareslast_img read more

Sweet fatty foods could remodel the brain to drive overeating

first_img We know fatty, sugary foods can transform our waistlines. Much less is known about how they might transform the brain. Now, researchers have found that switching a mouse from standard chow to more fattening fare changes the activity of certain neurons that regulate eating, wearing out the cellular “brakes” that limit intake. If the same is true for people, the finding could help explain our tendency to overeat.Changing an animal’s diet “is a subtle manipulation,” says Randy Seeley, a behavioral neuroscientist at the University of Michigan Nutrition Obesity Research Center in Ann Arbor who was not involved in the work. “The fact that you can go in and see different properties of these cells is an amazing finding.”Neurobiologist Garret Stuber and a team at the University of North Carolina at Chapel Hill wanted to understand the brain changes that accompany obesity. They were particularly interested in an area at the bottom of the brain known to regulate feeding, called the lateral hypothalamus. With collaborators in the United Kingdom, Stuber—now at the University of Washington in Seattle—sequenced RNA from cells in this area of the mouse brain and grouped them according to what genes they expressed. By comparing gene expression between obese mice on a high-fat diet and control animals on a standard one, the researchers identified a subset of neurons that changed most dramatically with the obesity-inducing diet. Sign up for our daily newsletter Get more great content like this delivered right to you! Country When lean mice become obese, neurons linked to feeding change their gene expression and activity levels. 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Required fields are indicated by an asterisk (*) That set expressed the gene for an excitatory signaling molecule, glutamate. The researchers used a two-photon microscope to observe these so-called glutamatergic cells in the brains of living mice. They endowed the cells with a gene that made them fluoresce when they took up calcium—an indicator of neural firing. Then they watched the cells while mice lapped calorie-rich sugar water from a spout. If a lean mouse had just eaten, the neurons were more active in response to the sugar than if it had just been fasting. The cells seemed to act as a brake, signaling, “That’s enough!”But as lean mice became obese from a diet high in fat and sugar, these cells became less lively. By 12 weeks after the diet switch, the glutamatergic cells were roughly 80% less active in response to the sugar drink, the team reports today in Science.The study is one of the first to use calcium imaging to observe brain activity in animals long-term, says Lora Heisler, a neuroscientist at the University of Aberdeen in the United Kingdom. It’s “a clever approach” to investigating how obesity develops, she says. One interpretation of the study: Regularly eating sweet, fatty foods “change[s] the way that our brain’s appetite centers function,” she says. “And by making the brain less responsive to the sweet stuff, it means that we will eat more than we need to.”But the study doesn’t distinguish which changed the neural activity: a feature of the diet or the weight gain itself. It also doesn’t prove the change in brain activity itself caused the animals to overeat and gain weight, Seeley notes. The taste of the new diet might have prompted mice to up their calories—worn-out brake or no. “You probably haven’t tasted rodent chow,” he says. “I have. It’s terrible. It is dry, salty, bland grossness.” High-fat mouse diets, on the other hand, usually “taste like sugar cookie dough.” Still, he says, the reduced activity of the glutamatergic neurons might have perpetuated obesity in the mice by failing to tamp down their appetites even as their weight climbed.“There are a lot of interesting areas for appetite in the brain. This paper makes the case that these neurons deserve additional attention,” says Scott Sternson, a neuroscientist at the Howard Hughes Medical Institute’s Janelia Research Campus in Ashburn, Virginia. If future studies reveal a receptor present on this subset of neurons—but absent from most other cells—researchers could try to target it with drugs to selectively bump up activity. But that won’t be easy. Strongly stimulating these neurons is apparently unpleasant; mice in the study avoided electrical zaps to the area. So the approach would require a delicate tap on the appetite brake, Sternson says, “not slamming on it full-force.”last_img read more