first_imgLiberty Global-owned cable operator UPC Czech Republic has launched a new bundled combining 240Mbps internet access with over 100 TV channels for CZK859 (€33.40) to those subscribers who sign up for a year.The cable operator has also boosted its HD offering with the addition of Film Europe HD, Deluxe Music HD and Auto Motor Sport HD to its line-up.last_img

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first_imgReviewed by Alina Shrourou, B.Sc. (Editor)Mar 22 2019UT Southwestern researchers have identified two proteins that act as gatekeepers to dampen a potentially life-threatening immune response to chronic infection.The proteins – the transcription factors SIX1 and SIX2 – activate cellular pathways required for fetal development and later switch to a new role in which they repress these pathways in adult immune system cells. The findings are published today in Nature.”This work provides insight into the molecular components required to limit tissue damage associated with uncontrolled inflammation, such as in septic shock, and reveals how cancer cells may suppress the innate immune system during tumor genesis,” said Dr. Neal Alto, Professor of Microbiology at UT Southwestern and corresponding author of the study.Transcription factors are proteins that bind to special regions of DNA to turn genes on (activate them) or off (repress them). “One of the surprising findings was that a transcription activator that is essential for the development of tissues and organs has been repurposed as a transcriptional repressor in the immune system. While transcription factors can be used differently in various stages of life, a switch from a transcriptional activator in the fetus to a suppressor in adult immune cells is infrequent,” said Dr. Alto, who holds the Lorraine Sulkin Schein Endowed Distinguished Professorship in Microbial Pathogenesis. Dr. Alto is also a UT Southwestern Presidential Scholar and a Rita C. and William P. Clements, Jr. Scholar in Medical Research.He added that the work provides a new pathway for controlling inflammation, which could be important for developing new drugs. It also might explain how cancer cells develop chemotherapy resistance.The researchers found that the two proteins showed inhibitory activities when bound to genes involved in inflammation. Specifically, SIX1 and SIX2 appeared to dampen the body’s immune response to prevent damage associated with a potentially life-threatening condition called a cytokine storm, which can occur in chronic inflammatory conditions. “A cytokine storm can occur when the body’s immune cells and activators (cytokines) show an overresponse to a health threat such as the flu,” he explained.Related StoriesComplement system shown to remove dead cells in retinitis pigmentosa, contradicting previous researchFibrinogen a key player in health and disease, says new studyChronic inflammation removes motivation by reducing dopamine in the brainAn experiment with transgenic mice found that expression of SIX1 in adulthood conferred near-complete recovery following exposure to a toxin released by gram-negative bacteria that can set off a cytokine storm. The two SIX proteins seem to dampen the response of the so-called noncanonical NF-κB pathway, a signaling cascade that is instrumental in the development of the lymph organs, the maturation of the immune system’s antibody-producing B cells, and the development of bone cells. The same pathway is involved in the body’s immune defense in adulthood.The studies, which initially focused on bacteria and viruses, also shed light on mechanisms of cancer cell resistance to drug treatment, Dr. Alto said.In one series of experiments, the team found that cancer cells derived from patients with treatment-resistant non-small cell lung cancer expressed high levels of the SIX1 and SIX2 proteins. The scientists used the CRISPR-Cas9 gene-editing technology to remove the genes that produce those two proteins, making the cancer cells dramatically more sensitive to a promising drug class called SMAC mimetics.”In summary, we have established that SIX family transcription factors function as immunological gatekeepers, regulating the activity of inflammatory genes in response to noncanonical NF-κB pathway activation,” he said. “These findings indicate that disruption of this pathway could have important consequences for the pathogenesis of human disease, including cancer.” Source:https://www.utsouthwestern.edu/newsroom/articles/year-2019/reducing-inflammation.htmllast_img read more

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first_imgRisk reduction for Alzheimer’s disease is now more critical than ever due to the continued lack of a cure or effective disease-slowing treatment,”Dr. Joshua S. Talboom, a Postdoctoral Fellow in TGen’s Neurogenomics Division, and a member of Dr. Huentelman’s lab Reviewed by James Ives, M.Psych. (Editor)Jun 21 2019Results from a study of nearly 60,000 individuals suggest those at higher risk of developing Alzheimer’s disease due to family history may demonstrate changes in memory performance as early as their 20s.Researchers from the Translational Genomics Research Institute (TGen), an affiliate of City of Hope, and the University of Arizona gathered the data through an online word-pair memory test called MindCrowd, one of the world’s largest scientific assessments of how healthy brains function.Published today in the scientific journal eLife, study data suggests that those with a family history of Alzheimer’s disease, and who are younger than 65, on average do not perform as well as their peers who do not have a family history of Alzheimer’s, the most common form of dementia.The study results suggest that the family history effect is particularly pronounced among men, as well as those with lower educational attainment, diabetes, and carriers of a common genetic change in APOE, a gene long associated with Alzheimer’s disease risk.While family history has previously been associated with the risk of Alzheimer’s, this is the first study of its kind, and in these numbers, that indicates this risk can be detected up to four decades before the typical age of onset. The study looked at 59,571 MindCrowd participants aged 18-85, and the effect of family history was shown across every age group, up until age 65.”In this study we show that family history is associated with reduced paired-associate learning performance as many as four decades before the typical onset of Alzheimer’s disease,” said Dr. Matt Huentelman, TGen Professor of Neurogenomics, and the study’s senior authorBecause there is no cure or proven way of slowing progressive memory-loss among those with Alzheimer’s, early indicators of the disease can help those at risk to focus on ways to help stave off dementia. Related StoriesGenetic contribution to distractibility helps explain procrastinationResearchers identify gene mutations linked to leukemia in children with Down’s syndromeStudy reveals link between inflammatory diet and colorectal cancer risk”This study supports recommendations underscoring the importance of living a healthy lifestyle and properly treating disease states such as diabetes,” said Dr. Talboom, the study’s lead author. “Our findings specifically highlight the positive effects of such interventions for those with a family history risk of Alzheimer’s, opening the door to the development of more targeted risk-reduction approaches to combat the disease.”In addition, this study underscores the utility of web-based participant recruitment to research studies like MindCrowd, facilitating large sample sizes in a cost- and time-effective fashion, said Dr. Lee Ryan, a University of Arizona Alzheimer’s researcher, who along with the UA’s Dr. Betty Glisky, helped Dr. Huentelman develop MindCrowd. Drs. Ryan and Glisky were contributing authors to the study.”It should be acknowledged that that web-based studies are not without concerns. However, we propose that the advantage of considerably larger sample sizes and enriched participant diversity in online research mostly diminishes the potential disadvantages,” Dr. Ryan said.The MindCrowd study began in 2013. By August 2018, it had nearly 60,000 qualified participants, whose performance is reflected in the study. Today, more than 115,000 people, aged 18-95 — from all 50 states and 150 nations around the world — have completed the MindCrowd assessment.MindCrowd cannot tell you if you have Alzheimer’s. What it does give researchers is a set of data baselines about how people not suffering from the disease perform at different ages; among men and women, among those with quick and slow physical responses, among those who smoke and those who don’t, and among many other demographic, lifestyle and health factors.Establishing these baselines will help researchers to more properly evaluate Alzheimer’s patients and usher in a new era of what the MindCrowd developers describe as Precision Aging.Alzheimer’s is a progressive neurological disorder that typically presents clinically as deficits in memory and thinking. It is estimated that more than 5 million Americans are living with Alzheimer’s, and that by 2050 that number will nearly triple to almost 14 million. Source:The Translational Genomics Research InstituteJournal reference:Talboom, J. et al. (2019) Family history of Alzheimer’s disease alters cognition and is modified by medical and genetic factors. eLife. doi.org/10.7554/eLife.46179last_img read more

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first_imgNEW DELHI (Reuters) – U.S. President Donald Trump faced criticism for saying Pakistan’s arrest of the alleged mastermind of the 2008 attacks on Mumbai had come after a 10-year search, as the suspected militant had been living in plain view. U.S. President Donald Trump speaks during a campaign rally in Greenville, North Carolina July 17, 2019. REUTERS/Kevin LamarquePakistani authorities on Wednesday arrested Hafiz Saeed, the founder of the Lashkar-e-Taiba militant group that is accused by India and the United States of carrying out the Mumbai attacks, on terrorism financing charges. More than 160 people were killed in the four-day militant attacks. Saeed is designated a terrorist by the United States and the United Nations. Trump, who is due to host Pakistan Prime Minister Imran Khan for talks at the White House next week, welcomed Saeed’s arrest and said it was the result of pressure from his administration on Pakistan to get tougher on militants. “After a ten year search, the so-called “mastermind” of the Mumbai Terror attacks has been arrested in Pakistan. Great pressure has been exerted over the last two years to find him!,” Trump tweeted. But Saeed has been in and out of Pakistan prisons for the last decade and even addressed public rallies. The U.S. House Foreign Affairs Committee countered Trump’s comments with a tweet of its listing the eight times Saeed had been arrested and freed by Pakistan authorities since 2001. “FYI Pakistan wasn’t searching for him for 10 years. He’s been living freely..” it said and suggested Trump hold the applause till Saeed is convicted by Pakistani authorities. Former Pakistan ambassador to the United States Husain Haqqani said Trump had been ill-advised about Saeed’s case. “Finding him was never an issue. He operated freely and was highly visible. He has been arrested and released many times over. @POTUS shd immediately fire whoever gave him the wrong information,” he said in a tweet, referring to Trump. Pakistan said Saeed was arrested while he was going to a court to seek pre-arrest bail. Saeed has denied any involvement and Pakistani authorities say they have not found any evidence against him either. India says Pakistan’s failure to act against the suspected militant is one of the reasons it won’t resume peace talks with the arch rival. Christian Fair, a South Asia specialist at Georgetown University, said Trump was also wrong to describe Saeed as the “so-called mastermind” of the Mumbai attacks. “@POTUS shows AGAIN that he’s a complete dumbass,” said Fair. Reporting by Sanjeev Miglani; Editing by Michael PerryOur Standards:The Thomson Reuters Trust Principles.last_img read more

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