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Samantha Bond on Her Disastrous Audition For London’s Scoundrels

first_img Was it difficult gaining confidence in yourself in a singer? It was. At first I didn’t want anybody to see my singing, and it took a very long time for me to overcome that. For a long time in rehearsals if anyone beside the musical director came in, I completely froze and turned my back on them again. It was quite a journey to go from singing in a cupboard to singing in front of 1,400 people [laughs]. It certainly feels like luxury casting to have you in this role. [Laughs.] I don’t know that [my colleagues] think that at the moment! But what’s been most extraordinary has been the love and support our ensemble has given me. There are moments where I have been literally shaking with terror and the young dancers have put their arms around me and held me and championed me and picked me up; I’ve literally been blown away by their support. Here you are in your first musical. Had you been angling to sing and dance on stage? No, it came completely the other way around! My agent rang and said, “They’re doing a new musical and I’ve suggested you for the part of Muriel,” and I said, “I don’t do musicals; Alex [Bond’s husband, Stephen Ward alum Alexander Hanson] does musicals,” and my agent said, “But I’m sure you can.” So I went away and thought about it and listened to [Muriel’s] big number and thought, well, if I was going to have this experience, it couldn’t be more phenomenal than to have it in this company. Tell us your thoughts on Muriel—she’s British in this version, which of course she was not on Broadway. Very British—she comes from Surrey! What was useful for me was that I never saw the show on Broadway or the film, so I was able to approach the whole thing totally fresh. I think of Muriel as someone incredibly wealthy who’s recently divorced and is looking for love, and her one drive in life is to be useful and helpful. She’s smitten very early on by Robert Lindsay, who beguiles her by pretending to be a prince. She’s an innocent, an absolute innocent. Samantha Bond was a Tony nominee for Amy’s View, played Moneypenny in the Bond (no relation) films, and appeared in Downton Abbey as Lady Rosamund—but only now is the 52-year-old actress tackling her first-ever musical. The new production of Dirty Rotten Scoundrels at the Savoy Theatre features Robert Lindsay and Rufus Hound as two con artists let loose on various unsuspecting Riviera culprits, with Bond as an Anglicized version of Muriel Eubanks, the glamorous divorcee originated on Broadway by Joanna Gleason. The protean actress spoke to Broadway.com about her fears of singing and dancing in public, and taking a vocal cue from her former Broadway and West End co-star, Judi Dench. With your two children, Tom and Molly, now entering the profession as actors, might we at some point see an all-Bond/Hanson project? [Laughs.] Only if someone writes a rather extraordinary play! Leaving the vocals aside, how does it feel to be part of a big West End musical, with all the expectations that entails? You become really aware with something like this of the scale of it and the fact that it’s a huge undertaking quite unlike being in a straight play. And I think when there’s so much riding on a project, then all the pressures are greater: musicals are such expensive machines. Did you take a leaf from your friend and former co-star Judi Dench (Amy’s View), who always says that she sings the way she speaks? I think that is the way to approach it. Even Alex, who sings properly, always says that the reason you break into song in a musical is because speech is no longer enough and, following that logic, that you should be singing as you speak, as it were. What Judi says about singing is all I can do. What’s been the most exhausting aspect of the job? The stairs at the Savoy! There are 55 stairs down to the stage and back up again to my dressing room and then there are 13 to the exit, and I’m forever going up and down. I added it up about a week ago and it was something like 976 steps that I have to climb every night. What was your audition like? There were ten people there, including [book writer] Jeffrey Lane, [composer] David Yazbek and [director/choreographer] Jerry Mitchell, and I sang the song with my back to the entire room—which is precisely what you’re taught not to do—and then read for them. Jerry put his arms up and twirled me around in a waltz and I left the room feeling the whole thing had been a total disaster, but thank heavens I wouldn’t have to do it again. Then before I knew it, I had the job. Good heavens! That’s a far cry from the demands of playing Lady Rosamund in Downton Abbey. How has that been? What’s been interesting is that my character only arrived in the last episode of the first series, so by the time I got there, I knew something extraordinary was happening. I think the older members of the cast in particular were aware that the show was being done so carefully and with such style—such attention to detail—that by the time I got there, it was as if a delicate perfume was hanging around the entire project. I’ve been filming again this week, mostly with Laura Carmichael [who plays Lady Edith], and I’ll be filming again over the summer. Had you really never sung in a show before? The last time I sang in public was in pantomime at the Bristol Old Vic some 30 years ago when I was a year or two out of drama school. I certainly didn’t think I’d ever be doing it again. View Commentslast_img read more

How fat grizzly bears stay diabetesfree

first_img Email Click to view the privacy policy. Required fields are indicated by an asterisk (*) Every fall, grizzly bears pack on the pounds in preparation for their winter hibernation. In humans, such extreme weight gain would likely lead to diabetes or other metabolic diseases, but the bears manage to stay healthy year after year. Their ability to remain diabetes-free, researchers have now discovered, can be chalked up to the shutting down of a protein found in fat cells. The discovery could lead to new diabetes drugs that turn off the same pathway in humans.The findings are “provocative and interesting,” says biologist Sandy Martin of the University of Colorado, Denver, who was not involved in the new work. “They found a natural solution to a problem that we haven’t been able to solve.”As people gain weight, fat, liver, and muscle cells typically become less sensitive to the hormone insulin—which normally helps control blood sugar levels—and insulin levels rise. In turn, that increased insulin prevents the breakdown of fat cells, causing a vicious cycle that can lead to full-blown insulin resistance, or diabetes. 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 Zimbabwecenter_img Developing new diabetes drugs has been hampered by the fact that findings from many mouse models of diabetes have not translated to humans. So Kevin Corbit, a senior scientist at Thousand Oaks, California–based drug company Amgen, decided to start looking at obesity and metabolic disease in other animals. “When I was thinking about things that are quite fat, one of the first things I thought of was bears, and what they do to prepare to go into hibernation,” he says. “But of course you don’t see bears running around with diabetes and heart disease.”Corbit and scientists at the Washington State University Bear Center in Pullman measured blood sugar levels, insulin levels, body weight, and other markers of the metabolism in six captive grizzly bears before, during, and after hibernation—in October, January, and May. Surprisingly, even as each bear gained more than a hundred pounds in the fall, their cells remained sensitive to insulin, and their insulin and blood sugar levels stayed constant. In people, such an immense weight gain would likely cause insulin resistance. It wasn’t until well after they’d begun hibernating that bears experienced a temporary, seasonal episode of insulin resistance, but even that was completely reversed come springtime. “This type of physiology had never been described before and was completely opposite what’s seen in humans,” Corbit says.When he and his collaborators analyzed levels of more molecules in the bears’ blood, liver, and fat cells, they found out what was controlling the insulin sensitivity and resistance independently from weight gain or loss: a protein called PTEN. In the fall, the bears have switched-off versions of PTEN present in their fat cells, Corbit’s team reports today in Cell Metabolism. As a result, the cells continue responding to insulin—and the signals to store sugar—even as the bears gain weight. For bears, the shutdown protein helps maximize sugar storage in their bodies for the long winter ahead.The finding could also help humans, Corbit says. Because shutting off PTEN helps obese bears maintain insulin sensitivity, turning off the pathway in overweight people could prevent or treat diabetes, he suggests. Interestingly, he points out, a previous study found that people missing one gene for PTEN production are less likely to develop metabolic or cardiovascular disease even as they gain weight. Those people do develop other diseases, including cancer, but Corbit suspects that’s because the PTEN levels are diminished body-wide. If scientists could turn it off only in fat cells—like bears do—these side effects might be diminished.Metabolic disease specialist Abhimanyu Garg of the University of Texas Southwestern Medical Center in Dallas says that more evidence is needed to support any link between the bear finding and human diabetes. And you’d have to be careful with a drug that turns off PTEN, even if it’s only in fat cells, he says. Even if it could treat diabetes, it might also cause increased weight gain. After all, it helps bears store up their winter fat, Garg notes. “You might create a situation where patients are metabolically healthy but you’re trading that for joint problems and back problems and arthritis.” Sign up for our daily newsletter Get more great content like this delivered right to you! Countrylast_img read more