ST. PETERSBURG, Florida (AP) ? Authorities said late Friday they had located country singer Mindy McCready's 5-year-old son in Arkansas and taken him into custody.
Florida Department of Children and Families spokeswoman Terri Durdaller said in an email Friday night that her agency was working with Arkansas officials to bring the boy back to his legal guardian in Florida, his maternal grandmother. Officials said he's safe and in good health.
Gayle Inge, Zander's grandmother and McCready's mother, was tearful when she talked about the news Friday night with The Associated Press.
"I'm real excited that he's safe," she said. "But I can't explain what this is like. We feel for Mindy and we feel for Zander."
Inge said Zander was taken into custody at McCready's boyfriend's home in Arkansas. Inge said her son ? McCready's half brother ? texted McCready, who responded with a text that said her mother would never see her again.
"I want to wrap my arms around her and tell her that I love her," Inge said.
Friday night's developments recap a dayslong saga between McCready and her family.
Authorities say McCready took the boy during a recent visit to her father's Florida home. A judge there signed an order Thursday telling authorities to take the boy into custody and return him.
It's not yet clear whether the singer could face criminal charges.
Inflammatory cues modulate goblet cell products important for intestinal barrier functionPublic release date: 2-Dec-2011 [ | E-mail | Share ]
Contact: Dr. H. Rex Gaskins hgaskins@illinois.edu 217-444-3165 Society for Experimental Biology and Medicine
In a paper published in the December 2011 issue of Experimental Biology and Medicine, a team of scientists at the University of Illinois, Urbana-Champaign led by Rex Gaskins, PhD have demonstrated that both microbial and host inflammatory factors modulate sulfomucin production in a human cell line, LS174T, that models intestinal goblet cells.
Sulfomucins, one of two primary types of acidomucins secreted by intestinal goblet cells, provide crucial protection to the intestinal mucosa. Therefore, it is not surprising that a loss of intestinal sulfomucins is associated with both inflammatory bowel disease (IBD) and colorectal cancer. However, the extent to which pathways involved in sulfomucin production are responsive to signals emanating directly from intestinal microbes or cues originating from host inflammatory cells is not known.
The research team at the University of Illinois compared the effects of bacterial flagellin to the mucogenic cytokine IL-13, and the proinflammatory cytokine TNF? on expression of genes encoding the Golgi sulfotransferases involved in addition of sulfate groups to mucin precursors and sulfomucin production. They observed high induction of carbohydrate (N-acetyl-glucosamine 6-O) sulfotransferase 5 (CHST5) as early as 12 h after treatment with IL-13. Flagellin, IL-13 and TNF all, on the other hand, induced expression of the other sulfotransferase galactose-3-O-sulfotransferase 2 (GAL3ST2). The observed induction of sulfotransferases was consistent with increased sulfomucin production by LS174T cells in response to IL-13 and flagellin, indicating that sulfotransferases and sulfomucin synthesis can be differentially modulated by particular inflammatory signals.
Galactose-3-O-sulfotransferase 2 is thought to be the sulfotransferase responsible for sulfate addition to the C-3 position of galactose in human colonic mucins. On the other hand, CHST5 is the most likely candidate for sulfation of the C-6 position of N-acetylglucosamine. GAL3ST2 expression was enhanced in LS174T cells following treatment with flagellin, IL-13 and TNF?, indicating that increased mucin sulfation at the C-3 position of galactose might be a common response to inflammatory stimuli.
Although cautious to point out that the present study derives from a well-differentiated, but transformed goblet cell line, Professor Gaskins said that "the data implicate biosynthesis of sulfomucins as a potential therapeutic target for the restoration of barrier function in chronic intestinal inflammatory disorders. Recent studies provide strong evidence that both ulcerative colitis (UC) and Crohn's disease (CD), the two primary types of IBD, result from multifactorial interactions among genetic, environmental and immunological factors that lead to a dysregulation of the innate immune response to the intestinal microbiota in genetically predisposed individuals."
The results with TNF are of particular interest because of its association with IBD and the alterations in mucin sulfation seen with active IBD. As IBD is characterized by dysregulated immune responsiveness, it may be that individuals with IBD fail to respond appropriately to TNF? and, hence, fail to increase the production of sulfomucins. However, much additional work will be needed to better understand the mechanisms by which flagellin, IL-13, and TNF enhance expression of specific sulfotransferases and sulfomucin production.
Dr. Steve Goodman, Editor-in-Chief of Experimental Biology and Medicine said "Crohn's disease and ulcerative colitis (UC), the two primary types of inflammatory bowel disease (IBD), afflict 0.1-0.5% of individuals in Western countries with approximately 1 million Americans suffering from the disease at a cost of over $2 billion. This impressive study by Gaskins and colleagues identifies sulfomucins as potential targets for future therapies for chronic intestinal inflammatory disorders".
###
Experimental Biology and Medicine is the journal of the Society of Experimental Biology and Medicine. To learn about the benefits of society membership visit http://www.sebm.org. If you are interested in publishing in the journal please visit http://ebm.rsmjournals.com.
[ | 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.
Inflammatory cues modulate goblet cell products important for intestinal barrier functionPublic release date: 2-Dec-2011 [ | E-mail | Share ]
Contact: Dr. H. Rex Gaskins hgaskins@illinois.edu 217-444-3165 Society for Experimental Biology and Medicine
In a paper published in the December 2011 issue of Experimental Biology and Medicine, a team of scientists at the University of Illinois, Urbana-Champaign led by Rex Gaskins, PhD have demonstrated that both microbial and host inflammatory factors modulate sulfomucin production in a human cell line, LS174T, that models intestinal goblet cells.
Sulfomucins, one of two primary types of acidomucins secreted by intestinal goblet cells, provide crucial protection to the intestinal mucosa. Therefore, it is not surprising that a loss of intestinal sulfomucins is associated with both inflammatory bowel disease (IBD) and colorectal cancer. However, the extent to which pathways involved in sulfomucin production are responsive to signals emanating directly from intestinal microbes or cues originating from host inflammatory cells is not known.
The research team at the University of Illinois compared the effects of bacterial flagellin to the mucogenic cytokine IL-13, and the proinflammatory cytokine TNF? on expression of genes encoding the Golgi sulfotransferases involved in addition of sulfate groups to mucin precursors and sulfomucin production. They observed high induction of carbohydrate (N-acetyl-glucosamine 6-O) sulfotransferase 5 (CHST5) as early as 12 h after treatment with IL-13. Flagellin, IL-13 and TNF all, on the other hand, induced expression of the other sulfotransferase galactose-3-O-sulfotransferase 2 (GAL3ST2). The observed induction of sulfotransferases was consistent with increased sulfomucin production by LS174T cells in response to IL-13 and flagellin, indicating that sulfotransferases and sulfomucin synthesis can be differentially modulated by particular inflammatory signals.
Galactose-3-O-sulfotransferase 2 is thought to be the sulfotransferase responsible for sulfate addition to the C-3 position of galactose in human colonic mucins. On the other hand, CHST5 is the most likely candidate for sulfation of the C-6 position of N-acetylglucosamine. GAL3ST2 expression was enhanced in LS174T cells following treatment with flagellin, IL-13 and TNF?, indicating that increased mucin sulfation at the C-3 position of galactose might be a common response to inflammatory stimuli.
Although cautious to point out that the present study derives from a well-differentiated, but transformed goblet cell line, Professor Gaskins said that "the data implicate biosynthesis of sulfomucins as a potential therapeutic target for the restoration of barrier function in chronic intestinal inflammatory disorders. Recent studies provide strong evidence that both ulcerative colitis (UC) and Crohn's disease (CD), the two primary types of IBD, result from multifactorial interactions among genetic, environmental and immunological factors that lead to a dysregulation of the innate immune response to the intestinal microbiota in genetically predisposed individuals."
The results with TNF are of particular interest because of its association with IBD and the alterations in mucin sulfation seen with active IBD. As IBD is characterized by dysregulated immune responsiveness, it may be that individuals with IBD fail to respond appropriately to TNF? and, hence, fail to increase the production of sulfomucins. However, much additional work will be needed to better understand the mechanisms by which flagellin, IL-13, and TNF enhance expression of specific sulfotransferases and sulfomucin production.
Dr. Steve Goodman, Editor-in-Chief of Experimental Biology and Medicine said "Crohn's disease and ulcerative colitis (UC), the two primary types of inflammatory bowel disease (IBD), afflict 0.1-0.5% of individuals in Western countries with approximately 1 million Americans suffering from the disease at a cost of over $2 billion. This impressive study by Gaskins and colleagues identifies sulfomucins as potential targets for future therapies for chronic intestinal inflammatory disorders".
###
Experimental Biology and Medicine is the journal of the Society of Experimental Biology and Medicine. To learn about the benefits of society membership visit http://www.sebm.org. If you are interested in publishing in the journal please visit http://ebm.rsmjournals.com.
[ | 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.
MEXICO CITY ? The president of Mexico's former ruling party resigned Friday amid a financial scandal that had begun to weigh on the party's hopes to regain the presidency in 2012.
Humberto Moreira, who headed the Institutional Revolutionary Party, or PRI, said he is leaving the post because he doesn't want to hurt the party.
"I've resigned because I'm not going to allow a media war that is trying to harm our party to continue," Moreira said told party members. "I also do it because I believe in a man who is the hope for Mexico, Enrique Pena Nieto."
Pena Nieto, the PRI's presidential candidate, has recently begun publicly distancing himself from the party leader.
Moreira fought to remain in office despite a growing scandal over the revelation he left a 34 billion peso ($2.8 billion) debt in the state of Coahuila when he resigned as governor to take over the PRI.
A close former aide to Moreira also is under investigation for amassing unexplained wealth, buying property in the U.S. and becoming CEO of two firms and a shareholder in Mexican radio stations on a modest state salary.
Moreira, 45, has called the claims a smear campaign against the PRI as it is poised to regain the presidency it lost in 2000 after 71 years of rule.
But Pena Nieto and other party leaders have tried to show the party is now more democratic and transparent, most notably in its open process of choosing candidates, who in the past were simply appointed before by their predecessors.
Cristina Sanchez, who was the PRI's general secretary, replaced Moreira.
That's the question Britain's electronic listening agency, GCHQ, is asking in an online campaign to find the next generation of cyber specialists.
GCHQ quietly launched a cryptic website last month featuring a box of code made up of numbers and letters. There is no branding on the site, only the phrase "Can you crack it?"
The agency has now revealed it is behind the campaign, and said Friday it's trying to reach individuals with "a keen interest in code breaking and ethical hacking" for careers at GCHQ.
"It's to arouse interest in people who perhaps might not be caught by our normal recruitment campaigns," a GCHQ spokesman said, speaking on customary condition of anonymity.
Cracking the code reveals a keyword, which when entered into a space on the website prompts the GCHQ job-recruitment website to appear.
The agency is currently recruiting for cyber security specialists ? at a pay grade of around 25,000 pounds ($39,000) ? and hopes to recruit around 35 people over the next few months, the spokesman said.
More than 50 people have successfully cracked the code so far ? of which 80 percent have submitted an application, the spokesman said.
GCHQ said the fast-moving pace of the digital arena and cybersecurity means it must find new ways to engage with prospective candidates, who typically have entered the agency as graduates.
"With the threats to information and computer technology constantly evolving, it is essential that GCHQ allows candidates who may be self taught, but have a keen interest in code breaking and ethical hacking, to enter the recruitment route too," it said in a statement.
But career hackers beware: "Anyone applying who has hacked illegally will not be eligible to continue in the recruitment process," GCHQ warned.
And gaming the website isn't a guarantee for joining GCHQ's ranks. The spokesman said that while anyone who cracks the code likely has an aptitude for GCHQ's type of work, it won't catapult code-crackers ahead of other job applicants automatically.
The agency said it has been using social media to get the word out and that the site has attracted about 8,000 hits.
___
Online:
http://www.canyoucrackit.co.uk/
_________
Cassandra Vinograd can be reached at http://twitter.com/CassVinograd
LOS ANGELES (TheWrap.com) ? Real Housewives of Beverly Hills" star Taylor Armstrong, whose estranged husband Russell killed himself in August, is penning a memoir about her life experiences, TheWrap has confirmed.
The book, to be published by Simon & Schuster imprint Gallery Books, will be published in February 2012. It bears the tentative title "Hiding From Reality: My Story of Love, Loss, and Finding the Courage Within" and will weigh in at 272 pages.
Armstrong's husband Russell was found dead in the Los Angeles home where he was staying in August, in what the coroner's office would ultimately determine to be a suicide. Taylor had filed for divorce from Russell, a venture capitalist, the month before. He was 47.
In September, during an interview with "Entertainment Tonight"'s Nancy O'Dell, Armstrong revealed a long history of physical abuse in her marriage to Russell, noting that her estranged husband told her he was worried he might kill her at some point.
"He had mentioned he was afraid he might kill me, and I think he meant it in almost an accidental way, that he would get so angry at me at some time that he would hit me, and I would hit something, or he would grab me by the neck and something would go wrong," Armstrong said.
ST. PETERSBURG, Fla. (AP) ? Country singer Mindy McCready is pushing her luck with the legal system by not following a judge's order to return her 5-year-old son to the care of her mother in Florida, her ex-boyfriend and father of the boy said Friday.
McCready said Thursday she would not bring her son back from Tennessee, despite violating a custody arrangement.
McCready took the boy during a recent visit at her father's Florida home, and a judge signed an order Thursday ordering authorities to take the boy into custody and return him. It's not yet clear whether the singer could face criminal charges.
"I'm doing all this to protect Zander, not stay out of trouble," McCready wrote in an email to The Associated Press on Thursday. "I don't think I should be in trouble for protecting my son in the first place."
McCready says she is in Tennessee and cannot travel because she's nearly seven months pregnant with twins.
The judge's order means law enforcement anywhere can pick up the boy and bring him back to Florida.
The boy's father, Billy McKnight, told the NBC "Today" show Friday he spoke on the phone with McCready and their boy after the judge's deadline expired.
"He did sound healthy and ok. He wasn't crying or scared," McKnight said about their son.
"I think she believes she has a case and doesn't realize she's pushing her luck on this one," he said.
McCready and her mother have had a long custody battle over the boy. The boy was living with McCready's mother, who was awarded guardianship in 2007. McCready says her son has suffered abuse at her mother's house; her mother, Gayle Inge, denies the abuse allegations.
"Once the child is located, we will pick him up and bring him back to Florida," said Terri Durdaller, a spokeswoman for the Florida Department of Children and Families. "Although these circumstances are unfortunate for a young child, his safety and well-being are our number one priority."
McCready provided a series of emails to the AP with Lee County Judge James Seals' ruling to return the boy.
"Mom has violated the court's custody order and we are simply restoring the child back into our custody," the judge wrote. "Nothing more. Nothing less. The court makes no judgment about whether Mom will or will not competently care for the child while in her custody. It only wants the child back where the court placed him."
McCready found fame in the mid-1990s and has lived a complicated life in recent years.
In August, she filed a libel suit against her mother and the National Enquirer's parent company, American Media Inc., over a story published in the tabloid newspaper that quoted Inge.
And in 2008, McCready was admitted to a hospital after police said she cut her wrists and took several pills in a suicide attempt.
During the TV show "Celebrity Rehab 3" in 2010, McCready came off as a sympathetic figure, and host Dr. Drew Pinsky called her an angel in the season finale.
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Public release date: 2-Dec-2011
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