Why has Trump caught Clinton in the polls?PGA Tour commissioner Timothy Finchem said Mr Trump’s current profile had made it “difficult” to attract sponsors.”It’s fundamentally a sponsorship issue,” said Mr Finchem.Luxury car maker Cadillac has reportedly not renewed its sponsorship deal.”Donald Trump is a brand, a big brand, and when you’re asking a company to invest millions of dollars in branding a tournament and they’re going to share that brand with the host, it’s a difficult decision,” he said.However, Mr Finchem insisted the decision to move the event to Mexico City from Florida, where it has been held for the past 55 years, was not political.”From a golf standpoint we have no issues with Donald Trump. From a political standpoint we are neutral. PGA Tour has never been involved or cares to be involved in presidential politics,” he added.The PGA Tour has signed new seven-year sponsorship deal with Grupo Salinas, and the first WGC-Mexico Championship will held in March next year.Mr Trump said the decision marked a “sad day for Miami, the US and the game of golf”.”This decision only further embodies the very reason I am running for president of the United States,” he said.The venue for the event has not been officially confirmed, but media reports say it will take place at the Club de Golf Chapultapec outside Mexico City.”I hope they have kidnapping insurance,” Mr Trump told Fox News.Mr Finchem said that a member of his staff had already confirmed that this was in place.”I haven’t inquired about the detail,” he said. “But I made the point that maybe that’s something we don’t want to advertise.” Mr Trump said the PGA had “put profit ahead of thousands of American jobs”.On the campaign trail, Mr Trump has portrayed Mexico as undermining the US economy.
At Freelancers Union, we know that independent workers shouldn’t have to look out for their interests alone. We are stronger when we join together, which is why we’ve decided to make candidate endorsements. Find out why we support Rafael Espinal for Public Advocate in New York City’s special election on February 26 here.Why now?Freelancers Union represents 425,000 members, including 150,000 in New York City. Freelancers are the backbone of the economy, yet policy has not kept apace with the shift reflected in the workforce. We want to change that.And we can! When we organize our members around important policy issues, like Freelance Isn’t Free, we have been able to drive meaningful change. We believe that supporting candidates who back freelance issues is an important step to building our collective political voice.We’re kicking off our efforts with the New York City Public Advocate race, an office with a history of supporting worker rights. In making our endorsement, we reached out to candidates in the field and asked them to complete a questionnaire. We wanted to better understand their track records supporting issues like the Freelance Isn’t Free law, as well as their future plans to improve the lives of independent workers.In the coming months, we plan to expand candidate endorsements to key city and statewide races. To be successful, we need members who are interested in helping us shape our next policy agenda and engaging directly with candidate on the issues that matter most. Together, we can become a more influential political voice and drive meaningful change to improve the lives of freelancers.To get involved, and receive regular updates sign up for our advocacy mailing list:SIGN UP FOR ADVOCACY LIST To help us organize in support of Rafael Espinal, join our Text Banking Party on February 20:RSVP FOR TEXT BANKING I look forward to continuing the conversation with you as we build together.
Jun 21 2018Oxidative stress can help tumors thrive, but one way novel cancer treatments work is by pushing levels to the point where it instead helps them die, scientists report.Adoptive T cell therapy appears to reprogram the metabolism of tumor cells, increasing their level of reactive oxygen species, or ROS, and their destruction, says Dr. Gang Zhou, immunologist at the Georgia Cancer Center and Department of Medicine at the Medical College of Georgia at Augusta University.Scientists treated mice that had large, localized colorectal tumors with adoptive T cell therapy after preconditioning them with a chemotherapy drug known to help with the expansion and persistence of these infused T cells. The T cells are a patient’s own cells, but engineered to better fight cancer.The therapy appeared to deliver a deadly double-whammy to the cancer cells, says Zhou, corresponding author of the study in the journal Cell Metabolism.The scientists found the treatment interfered with production of glutathione, a natural antioxidant found in all cells, as it heightened production and accumulation of ROS inside tumor cells.Results included increased production by T cells of proinflammatory cytokines – including tumor necrosis factor alpha – which regulate many functions cancer needs to control like cell proliferation, differentiation and death.”We started by asking questions about how immunotherapy can change the metabolism of tumor cells. Our studies show tumor necrosis factor alpha can act directly on tumor cells and induce ROS inside them,” Zhou says.The bottom line of the metabolic changes include, for example, complete tumor regression in nearly all the tested mice.The scientists found similar effects – higher ROS levels correlated with high tumor cell death – when the therapy was used in models of breast cancer and lymphoma.Tumor necrosis factor alpha appears key to these desired results following adoptive T cell therapy, because when the scientists eliminated it from the equation, tumor cell death decreased dramatically.Scavenging ROS had a similar effect. When they gave the antioxidant N-acetylcysteine – a precursor to glutathione – it also hampered the curative effect of adoptive T cell therapy, they report.They also found that tumor necrosis factor alpha synergizes with chemotherapy to increase oxidative stress and cancer cell death. And, that giving pro-oxidants – drugs known to raise ROS levels – can somewhat replicate the tumor-killing benefit of adoptive T cell therapy. It’s known that these drugs may increase oxidative stress in cancer cells and push them toward death, or apoptosis, Zhou says.Related StoriesResearchers identify potential drug target for multiple cancer typesLiving with advanced breast cancerHow cell-free DNA can be targeted to prevent spread of tumors”Their baseline is already high and if you further disrupt their ability to deal with these free radicals, they will go toward apoptosis,” Zhou says.In fact, in an apparent failed attempt to fight off the higher ROS, the scientists found increased expression of several antioxidant genes in treated tumor cells.The significant, cancer-lethal ROS increases they found were limited to the tumor cells, not other nearby cell types.The scientists note that the direct killing of tumors by ROS they saw does not negate the possibility that tumor necrosis factor alpha also is working through its previously known method of killing off blood supplies to tumors.Antioxidant therapy in patients with active cancer has drawn mixed results, but most studies indicate that it worsens cancer, particularly in smokers, according to the National Cancer Institute. Preclinical studies in mice indicate the therapy promotes tumor growth and metastasis. Studies exploring the benefit of antioxidant therapy in preventing cancer have largely shown no benefit or harm, the NCI says.Tumors are known to impact T cells. In fact scientists have shown that the two can compete for nutrition and energy in the tumor microenvironment, remote sites tumors establish to successfully spread, the scientists write. It’s T cells that usually get short shrift in the struggle.Comparatively little focus has been on what T cells do to tumors, Zhou and his colleagues report. But better understanding of that impact should help improve immunotherapies, like adoptive T cell therapy, that seek to enable T cells to better target tumors.Adoptive T cell therapy is still under development for treatment of colorectal cancer. This therapeutic approach was already known to essentially poke holes in cancer cells to kill them.ROS are chemicals like peroxide and superoxide that are byproducts of necessary body functions like the use of oxygen and energy production by cell powerhouses called mitochondria. One reason cancer cells have naturally higher ROS levels is they have a high energy demand, Zhou says, constantly working to grow and spread.Some level of ROS also benefits our healthy cells, including cell proliferation and differentiation. But, too much is also deadly to normal cells, even damaging to DNA.Source: https://www.augusta.edu/mcg/