Bradley set for tough introduction to EPL

first_imgMANCHESTER, England (AP): Ask people to describe Swansea’s style of play and most would detail the free-flowing, possession-based approach that has been the hallmark of teams under managers such as Roberto Martinez, Brendan Rodgers and Michael Laudrup over the last decade. Some have even dubbed them “Swanselona” over the years, a reference to Swansea’s passable imitation of Barcelona’s preferred style. Bob Bradley has to decide if it’s time for a change. The American coach was hired by Swansea last week, taking charge of a team that has lost five of its last six games in the English Premier League (EPL) under the fired Francesco Guidolin and languishes in 17th place. Bradley arrives with a reputation for preferring a more pragmatic, direct style of football, which would be at odds with what Swansea typically produces. A shift in approach might just be what the team needs to stay up this season. The 58-year-old Bradley said in his presentation press conference that he likes “good, passing football” and that Swansea has been a team that is “fun to watch,” but it’s not helping at the moment. Taking the game to Manchester City and Liverpool in the last two rounds, the Swans were brave but ultimately lost both matches. They haven’t kept a clean sheet since the opening round. Next up is a trip to third-place Arsenal tomorrow, something of a daunting introduction to the Premier League for Bradley. Tightening up and being harder to beat might be the name of the game for the new coach. “Whenever there’s a change at any club, it’s a fresh start for everybody,” Bradley said yesterday. “You can see that on certain faces, that’s clear. Even at a time in a season when it’s been difficult, when there’s been managerial change, you see enthusiasm and a certain amount of excitement. “That doesn’t automatically mean because you’ve changed some things, everything’s going to come together right away. But, it’s a start.” Arsenal have won their last five games in all competitions and can be a devastating force when the team’s sprightly attacking unit containing the likes of Mesut Ozil, Santi Cazorla, Theo Walcott and Alexis Sanchez is given space to perform. Sanchez, in particular, is thriving as a so-called ‘false nine’ up front in the absence of injured striker Olivier Giroud. But Arsene Wenger’s team can struggle and get frustrated when teams sit back and defend in numbers. Bradley, an experienced, savvy coach who has watched the Premier League from afar for years, values teamwork highly and that will be needed at Emirates Stadium. “I believe he is equipped to deal with what is requested of him,” Wenger said yesterday, when asked if Bradley would be a success at Swansea. Bradley will look to continue Swansea’s good recent record against Arsenal, with three wins in their last five meetings most recently a 2-1 win at the Emirates in March. “It is a tough first game (under Bradley), but we don’t mind playing that,” Swansea defender Neil Taylor said. “We would be probably written off even if we were in form.” DEVASTATING FORCE MANCHESTER CITY VS EVERTON UNBEATEN SPURS Wayne Rooney would love nothing more than to score against Liverpool tomorrow. He may not get the chance. Rooney has started on the bench for Man United’s last two league games and was also dropped by England this week, demoted to a substitute’s role against Slovenia on Tuesday. The former Everton forward has previously said he “hates” Liverpool, comments which are regularly brought up to add an inflammatory edge to what already is traditionally the biggest game in English football. Northwest rivals United (20) and Liverpool (18) have more league titles than any other teams in the country. Liverpool are in fourth place, three points ahead of sixth-place United. LIVERPOOL VS MANCHESTER UNITED It’s a first managerial meeting tomorrow between two disciples of Johan Cruyff: Pep Guardiola and Ronald Koeman. Koeman acted as a mentor for a young Guardiola when they played together under Cruyff at Barcelona in the early 1990s, with both players central to the style desired by the late Dutch great. Now they are two of the most respected coaches around. Guardiola, in his first season in English football, has guided City to first place in the league with six wins from seven games, while Everton are in fifth place in Koeman’s first season at Goodison Park. Boosted by a 2-0 win over Manchester City last time out, second-place Tottenham protects the league’s only unbeaten record when they visit West Bromwich Albion tomorrow, when it’s also Chelsea vs Leicester, Bournemouth vs Hull, Stoke vs Sunderland and Crystal Palace vs West Ham. On Sunday, Middlesbrough host Watford and Southampton are at home to Burnley.last_img read more

Cause of rare immune disease identified

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Country Email Country * Afghanistan Aland Islands Albania Algeria Andorra Angola Anguilla Antarctica Antigua and Barbuda Argentina Armenia Aruba Australia Austria Azerbaijan Bahamas Bahrain Bangladesh Barbados Belarus Belgium Belize Benin Bermuda Bhutan Bolivia, Plurinational State of Bonaire, Sint Eustatius and Saba Bosnia and Herzegovina Botswana Bouvet Island Brazil British Indian Ocean Territory Brunei Darussalam Bulgaria Burkina Faso Burundi Cambodia Cameroon Canada Cape Verde Cayman Islands Central African Republic Chad Chile China Christmas Island Cocos (Keeling) Islands Colombia Comoros Congo Congo, the Democratic Republic of the Cook Islands Costa Rica Cote d’Ivoire Croatia Cuba Curaçao Cyprus Czech Republic Denmark Djibouti Dominica Dominican Republic Ecuador Egypt El Salvador Equatorial Guinea Eritrea Estonia Ethiopia Falkland Islands (Malvinas) Faroe Islands Fiji Finland France French Guiana French Polynesia French Southern Territories Gabon Gambia Georgia Germany Ghana Gibraltar Greece Greenland Grenada Guadeloupe Guatemala Guernsey Guinea Guinea-Bissau Guyana Haiti Heard Island and McDonald Islands Holy See (Vatican City State) Honduras Hungary Iceland India Indonesia Iran, Islamic Republic of Iraq Ireland Isle of Man Israel Italy Jamaica Japan Jersey Jordan Kazakhstan Kenya Kiribati Korea, Democratic People’s Republic of Korea, Republic of Kuwait Kyrgyzstan Lao People’s Democratic Republic Latvia Lebanon Lesotho Liberia Libyan Arab Jamahiriya Liechtenstein Lithuania Luxembourg Macao Macedonia, the former Yugoslav Republic of Madagascar Malawi Malaysia Maldives Mali Malta Martinique Mauritania Mauritius Mayotte Mexico Moldova, Republic of Monaco Mongolia Montenegro Montserrat Morocco Mozambique Myanmar Namibia Nauru Nepal Netherlands New Caledonia New Zealand Nicaragua Niger Nigeria Niue Norfolk Island Norway Oman Pakistan Palestine Panama Papua New Guinea Paraguay Peru Philippines Pitcairn Poland Portugal Qatar Reunion Romania Russian Federation Rwanda Saint Barthélemy Saint Helena, Ascension and Tristan da Cunha Saint Kitts and Nevis Saint Lucia Saint Martin (French part) Saint Pierre and Miquelon Saint Vincent and the Grenadines Samoa San Marino Sao Tome and Principe Saudi Arabia Senegal Serbia Seychelles Sierra Leone Singapore Sint Maarten (Dutch part) Slovakia Slovenia Solomon Islands Somalia South Africa South Georgia and the South Sandwich Islands South Sudan Spain Sri Lanka Sudan Suriname Svalbard and Jan Mayen Swaziland Sweden Switzerland Syrian Arab Republic Taiwan Tajikistan Tanzania, United Republic of Thailand Timor-Leste Togo Tokelau Tonga Trinidad and Tobago Tunisia Turkey Turkmenistan Turks and Caicos Islands Tuvalu Uganda Ukraine United Arab Emirates United Kingdom United States Uruguay Uzbekistan Vanuatu Venezuela, Bolivarian Republic of Vietnam Virgin Islands, British Wallis and Futuna Western Sahara Yemen Zambia Zimbabwe Scientists have already identified several rare but painful diseases in which the immune system triggers inappropriate inflammation in various parts of the body. These conditions differ from autoimmune diseases like rheumatoid arthritis and type I diabetes because a different branch of the immune system, which includes the body’s first responders to foreign invaders, malfunctions. Some of the Belgian family’s symptoms resembled the symptoms of one of these so-called autoinflammatory diseases, familial Mediterranean fever (FMF), but they were much worse. In FMF, for instance, fever lasts for a few days, not months.FMF results from mutations in the gene for pyrin, a protein inside many immune cells that detects infections by certain microbes. One attempt to track down the genetic flaw in the Belgian sufferers suggested that they could carry a defect in the same gene, but researchers dismissed the possibility because their symptoms were so different from those in people with FMF, says immunologist Seth Masters of the Walter and Eliza Hall Institute of Medical Research in Parkville, Australia, a co-author on the new paper. “It really didn’t look like the same disease.”Yet when Masters and colleagues sequenced the DNA of the Belgian family, they found a mutation in the gene for pyrin. It’s in a different location than in most people with FMF, the team reports today in Science Translational Medicine. After searching disease databases and hearing from other doctors who had patients with the similar symptoms, the researchers identified three other families in Lebanon, France, and the United Kingdom that had the same mutation. They’ve named the resulting disease pyrin-associated autoinflammation with neutrophilic dermatosis (PAAND).Although the same gene is mutated in people with FMF, the type and severity of the symptoms confirm that PAAND is a unique disease, Kastner says. “It’s not FMF. Period.” It’s rare for different mutations in the same gene to cause distinct diseases, but PAAND and FMF are not the only examples, says medical geneticist Wayne Grody of the University of California, Los Angeles (UCLA), who wasn’t connected to the study. He notes, for instance, that mutations in the CFTR gene can trigger the potentially lethal disease cystic fibrosis or a milder illness that results in male infertility.Masters and colleagues further determined how the mutation in PAAND patients causes pyrin to go awry. When pyrin senses toxins released by some kinds of bacteria, it spurs formation of a structure called the inflammasome that in turn triggers inflammation. To prevent pyrin from switching on prematurely, cells typically shield it with another protein until they are in trouble. But the scientists found that this shield falls off the version of pyrin that the Belgian family produced, resulting in an overactive molecule. “In effect you take away the brake,” says co-author Adrian Liston, an immunologist at the University of Leuven in Belgium.What makes the paper stand out, says Grody, is the team’s thorough investigation. “They really have a mechanism—we don’t have anything like that to explain FMF,” he says. The work also points to a potential treatment, a drug that blocks an inflammation-promoting molecule that was abundant in the patients. When the researchers treated one member of the Belgian family with the drug, “all the signs of disease disappeared within a couple of weeks,” Liston says. “It was really quite remarkable.” The scientists now plan to launch a clinical trial of the drug in more PAAND patients. Masters and Liston say that the results could also help researchers better understand the role of inflammation in non–auto-inflammatory illnesses, including Alzheimer’s disease and inflammatory bowel disease.The study might provide more immediate benefits for some people as well. FMF is relatively common for an autoinflammatory disease, but even in the Mediterranean region only about one in 200 to one in 1000 people suffer from it. Although PAAND isn’t likely to be prevalent, researchers think that more patients are waiting for a diagnosis. Large numbers of people with the disease could live in populous countries such as India and China, Masters says. Grody and his colleagues at the FMF clinic at UCLA will be on the lookout for new cases. “I’m certain there are other families out there,” he says.center_img Click to view the privacy policy. Required fields are indicated by an asterisk (*) The Belgian family had puzzled doctors for more than a decade. Beginning when they were children, some members were prone to bouts of fever that could last for months. Their muscles and joints ached, their blood vessels were inflamed, and their skin erupted with sores that ranged from severe acne to abscesses and ulcers. One patient’s heart was so badly damaged that he needed a transplant at the age of 20.Now, researchers have figured out why the family members became ill, revealing that they suffer from a previously undiscovered genetic disease that unleashes a protein that normally helps protect us from microbes. Armed with the findings, doctors might be able to recognize other people with similar symptoms who have gone undiagnosed and offer treatment. In addition, the researchers say, the results might provide insight into more common diseases such as inflammatory bowel disease, where inflammation is out of control.“The paper beautifully works out the biochemistry” of how the mutation that causes the new disease alters a key immune protein, says geneticist Daniel Kastner of the National Human Genome Research Institute in Bethesda, Maryland, who wasn’t connected to the research.last_img read more