Unai Emery praises Granit Xhaka’s performance and thanks fans for ‘helping’ Arsenal midfielder

first_img Metro Sport ReporterThursday 28 Nov 2019 11:37 pmShare this article via facebookShare this article via twitterShare this article via messengerShare this with Share this article via emailShare this article via flipboardCopy link169Shares Comment Unai Emery praises Granit Xhaka’s performance and thanks fans for ‘helping’ Arsenal midfielder Advertisement Unai Emery was pleased with Granit Xhaka’s display in Arsenal’s defeat to Eintracht Frankfurt (Picture: Getty)Unai Emery praised Granit Xhaka’s display in the aftermath of Arsenal’s woeful 2-1 defeat to Eintracht Frankfurt and thanked fans for supporting the midfielder.Xhaka was making his first appearance since his sweary outburst at fans last month but it was an evening to forget for the Swiss as Arsenal extended their winless run to seven games.The Gunners only needed a draw to secure a place in the Europa League knockout stages and Pierre-Emerick Aubameyang put them ahead right on half-time in front of a half-empty Emirates.However, a pair of lethal strikes from Daichi Kamada after the break secured a memorable win for the visitors to heap even more pressure on Emery.ADVERTISEMENT Emery appeared close to tears on the touchline during the second half (Picture: Getty)Boos rang out around the ground as Kamada struck home his second goal and Arsenal’s increasingly agitated support once again made their feelings known as Emery and his players made their way off the field.AdvertisementAdvertisementEmery is reportedly in a desperate battle to keep his job ahead of this weekend’s trip to Norwich, with Nuno Espirito Santo being lined up as a possible replacement. Kamada was Eintracht’s hero at the Emirates (Picture: Getty)Martin Keown suggested that Emery may consider stepping down as manager following the defeat.‘I think he may well have taken the team as far as he can,’ he said on BT Sport.‘We just witnessed an absolute shambles of a performance, the team motivation, the team selection, the performance, the subs, it was dreadful.‘The fans turned many years ago on Terry Neil, things got toxic, we’re getting close to that again. Is he able to motivate the team? He seems to have lost the players.More: FootballBruno Fernandes responds to Man Utd bust-up rumours with Ole Gunnar SolskjaerNew Manchester United signing Facundo Pellistri responds to Edinson Cavani praiseArsenal flop Denis Suarez delivers verdict on Thomas Partey and Lucas Torreira moves‘The desire has ebbed away. The subs he made – you’ve got Nicolas Pepe and Alexandre Lacazette sitting on the bench when you’re trying to get back into the game.‘He might even feel he needs to step aside now. Change was needed under Wenger but now it looks like the club need to go in another direction again. This is relegation form.‘Do the club really realise how tricky this is going to be? Decisions have to be made otherwise they are going to plunge even further down the table.‘It’s a sad day because we still love the club. It’s sad watching itMORE: Chelsea star Reece James told the area he must improve after Valencia draw Xhaka demanded to play on through the pain (Picture: Getty)Xhaka looked like he may have to be replaced towards the end of the first half after going down with a knock to his knee.However, the Switzerland international demanded to play on through the pain and remained on the pitch for the entire 90 minutes.‘It’s very good news with Granit. We played well and the supporters helped him and I think it’s good news,’ Emery said.More: FootballRio Ferdinand urges Ole Gunnar Solskjaer to drop Manchester United starChelsea defender Fikayo Tomori reveals why he made U-turn over transfer deadline day moveMikel Arteta rates Thomas Partey’s chances of making his Arsenal debut vs Man CityThe Spaniard added: ‘Xhaka wanted to continue playing.‘His match today was good and he helped the team.‘I am being positive but I’m also realistic and we lost against a good opponent.‘We have improved from our last match and we are still first and have the opportunity to qualify, but we missed the opportunity tonight.’ Advertisementlast_img read more

IN PICTURES: MIRACLE ESCAPE AS RUNAWAY BUS WRECKS CARS IN MOVILLE

first_imgTHIS was the scene in the centre of Moville today after a runaway bus ploughed into cars on the main street.Incredibly no-one was injured in the incident which happened at around 8.30am.“It could have been so much worse,” said one eye-witness. Gardai have sealed off the area and were diverting traffic while an investigation takes place.“No-one has been hurt in the incident and Gardai are now at the scene,” said a Garda spokesman.Six cars and the bus have been damaged in the incident.Bus company owner Joe McGonagle said the bus – which was due to drive to Derry – was evacuated after the handbrake caused problems. After the driver got the passengers off, he thought he had secured it and went to see of he could get some help.But while he was gone the bus took off, smashing into the cars.IN PICTURES: MIRACLE ESCAPE AS RUNAWAY BUS WRECKS CARS IN MOVILLE was last modified: October 20th, 2012 by BrendaShare this:Click to share on Facebook (Opens in new window)Click to share on Twitter (Opens in new window)Click to share on LinkedIn (Opens in new window)Click to share on Reddit (Opens in new window)Click to share on Pocket (Opens in new window)Click to share on Telegram (Opens in new window)Click to share on WhatsApp (Opens in new window)Click to share on Skype (Opens in new window)Click to print (Opens in new window) Tags:IN PICTURES: MIRACLE ESCAPE AS RUNAWAY WRECKS CARS IN MOVILLElast_img read more

Biologists identify the backup systems that ensure genes build limbs

first_img Click to view the privacy policy. Required fields are indicated by an asterisk (*) Sign up for our daily newsletter Get more great content like this delivered right to you! Country 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 COLD SPRING HARBOR, NEW YORK—Some aspects of our genomes would make a NASA engineer proud. Whereas spacecraft have many redundant systems that can kick in, such as when a thruster fails, cells have their own backup systems for regulating gene activity. But they are extraordinarily hard to understand, as was made clear last week when molecular biologists for the first time described the regulatory backups for two genes involved in mammalian limb formation. Understanding these redundancies, and how to bypass them, could be important for biomedical researchers wishing to manipulate gene activity to treat human diseases.Genes may carry information for building proteins, but a host of other factors, including the DNA between genes that doesn’t encode proteins, tells them when to make their proteins. And this so-called noncoding DNA plays a role in some diseases, studies have shown. Noncoding DNA includes stretches called enhancers, short sequences that help control a target gene.  Geneticists have identified hundreds of thousands of potential enhancers in our genome, but verifying their role in DNA regulation and disease is a daunting proposition. “We still don’t have a good understanding of what [many do],” says Yang Li, a computational biologist at Stanford University in Palo Alto, California.For the new study, presented last week at the Biology of Genomes meeting here, molecular biologist Marco Osterwalder of Lawrence Berkeley National Laboratory in Berkeley, California, and colleagues harnessed a powerful new gene-editing technique called CRISPR to figure out exactly how some of these candidate enhancers work. The method speeds up the development of “knockout” mice that lack a particular enhancer, helping reveal its function.center_img The lab already had preliminary evidence for more than 1200 enhancers. And in the new tests, Osterwalder used CRISPR to knock out 10 of the enhancers in different mouse embryos. These enhancers were located close to genes involved in limb development, so he and his colleagues expected the embryo’s limbs to be defective in some way. But to their dismay, there were no such abnormalities, he reported last week. Wondering whether other enhancers pick up the slack—providing a backup system to keep limb development on track—Osterwalder and his colleagues bred mice lacking a pair of enhancers specifically implicated in digit formation.  Those mouse embryos developed extra digits, just as an embryo would have if the enhancers’ target gene, Gli3, itself had been defective, he reported at the meeting.To further explore this redundancy, the team then knocked out one or both of those enhancers in mice in which they had also knocked out one of the pair of Gli3 genes that control digit number. Typically, with one copy of that gene out of commission, embryos make only half the normal amount of Gli3 protein—and an extra thumb forms. When scientists also knocked out just one of the enhancers in the same mice, the embryos again grew an extra thumb. But when scientists knocked out both enhancers in the mice with one missing Gli3, the mice grew several extra digits. Those results are the same if the enhancers are intact but both copies of the gene itself are defective, indicating that the amount of protein determines the number of digits. The enhancers “are redundant on an organismal level, but additive at a molecular level,” Osterwalder concluded. “It is really a wonderful experiment” says William Greenleaf, a biophysicist at Stanford who was not involved with the work. “It represents the logical next step in the mapping of regulatory elements.”Three years ago, another team studying enhancers in the development of the mouse face and skull uncovered similar complexity. And studies in Drosophila suggest, too, that interactions of multiple enhancers are commonplace. Already, researchers have linked noncoding DNA to Crohn disease, heart disease, multiple sclerosis, and other disorders, suggesting that enhancers could be targets for medical manipulation. And “we are finding more associations all the time,” says Joseph Pickrell, an evolutionary geneticist at the New York Genome Center in New York City. But given the complexity revealed by the CRISPR experiments, understanding how enhancers interact with diseases “is going to be a marathon,” he predicts. Emaillast_img read more