96 results on '"Apfel, H"'
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2. Der Anteil des Endothels am elektrischen Widerstand arterieller Gefäßwandstreifen
- Author
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Apfel, H., Kaufmann, J., Assmann, G., editor, Betz, E., editor, Heinle, H., editor, and Schulte, H., editor
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- 1990
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3. Änderung der elektrischen Impedanz der Arteria carotis unter Streßbelastung
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Apfel, H., Assmann, G., editor, Betz, E., editor, Heinle, H., editor, and Schulte, H., editor
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- 1990
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4. Electrical Impedance of the Carotid Artery in Response to Various Types of Stress
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Apfel, H. and Liepsch, Dieter W., editor
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- 1990
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5. Recovery, Distribution, and Development of Acanthocheilonema viteae Third- and Early Fourth-Stage Larvae in Adult Jirds
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Eisenbeiss, Wilhelm F., Apfel, H., and Meyer, T. F.
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- 1991
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6. Thermal start-up behaviour and thermal management of SOFC's
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Apfel, H., Rzepka, M., Tu, H., and Stimming, U.
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- 2006
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7. Regulation of ion channels in rat hepatocytes
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Breit, S., Kolb, H.-A., Apfel, H., Haberland, C., Schmitt, M., Häussinger, D., Graf, J., and Lang, F.
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- 1997
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8. Pattern of pulmonary venous blood flow in the hypoplastic left heart syndrome in the fetus
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Better, D J, Apfel, H D, Zidere, V, and Allan, L D
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- 1999
9. Global, regional, national, and selected subnational levels of stillbirths, neonatal, infant, and under-5 mortality, 1980–2015: a systematic analysis for the Global Burden of Disease Study 2015
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Wang, H, Liddell, CA, Coates, MM, Mooney, MD, Levitz, CE, Schumacher, AE, Apfel, H, Iannarone, M, Phillips, B, Lofgren, KT, Sandar, L, Dorrington, RE, Rakovac, I, Jacobs, TA, Liang, X, Zhou, M, Zhu, J, Yang, G, Wang, Y, Liu, S, Li, Y, Ozgoren, AA, Abera, SF, Abubakar, I, Achoki, T, Adelekan, A, Ademi, Z, Alemu, ZA, Allen, PJ, AlMazroa, MA, Alvarez, E, Amankwaa, AA, Amare, AT, Ammar, W, Anwari, P, Cunningham, SA, Asad, MM, Assadi, R, Banerjee, A, Basu, S, Bedi, N, Bekele, T, Bell, ML, Bhutta, Z, Blore, JD, Basara, BB, Boufous, S, Breitborde, N, Bruce, NG, Bui, LN, Carapetis, JR, Cárdenas, R, Carpenter, DO, Caso, V, Castro, RE, Catalá-Lopéz, F, Cavlin, A, Che, X, Chiang, PP, Chowdhury, R, Christophi, CA, Chuang, TW, Cirillo, M, da Costa Leite, I, Courville, KJ, Dandona, L, Dandona, R, Davis, A, Dayama, A, Deribe, K, Dharmaratne, SD, Dherani, MK, Dilmen, U, Ding, EL, Edmond, KM, Ermakov, SP, Farzadfar, F, Fereshtehnejad, SM, Fijabi, DO, Foigt, N, Forouzanfar, MH, Garcia, AC, Geleijnse, JM, Gessner, BD, Goginashvili, K, Gona, P, Goto, A, Gouda, HN, Green, MA, Greenwell, KF, Gugnani, HC, Gupta, R, Hamadeh, RR, Hammami, M, Harb, HL, Hay, Simon, Hedayati, MT, Hosgood, HD, Hoy, DG, Idrisov, BT, Islami, F, Ismayilova, S, Jha, Vivekanand, Jiang, G, Jonas, JB, Juel, K, Kabagambe, EK, Kazi, DS, Kengne, AP, Kereselidze, M, Khader, YS, Khalifa, SE, Khang, YH, Kim, D, Kinfu, Y, Kinge, JM, Kokubo, Y, Kosen, S, Defo, BK, Kumar, GA, Kumar, K, Kumar, RB, Lai, T, Lan, Q, Larsson, A, Lee, JT, Leinsalu, M, Lim, SS, Lipshultz, SE, Logroscino, G, Lotufo, PA, Lunevicius, R, Lyons, RA, Ma, S, Mahdi, AA, Marzan, MB, Mashal, MT, Mazorodze, TT, McGrath, JJ, Memish, ZA, Mendoza, W, Mensah, GA, Meretoja, A, Miller, TR, Mills, EJ, Mohammad, KA, Mokdad, AH, Monasta, L, Montico, M, Moore, AR, Moschandreas, Joanna, Msemburi, WT, Mueller, UO, Muszynska, MM, Naghavi, M, Naidoo, KS, Narayan, KM, Nejjari, C, Ng, M, de Dieu Ngirabega, J, Nieuwenhuijsen, MJ, Nyakarahuka, L, Ohkubo, T, Omer, SB, Caicedo, AJ, Pillay-van Wyk, V, Pope, D, Pourmalek, F, Prabhakaran, D, Rahman, SU, Rana, SM, Reilly, RQ, Rojas-Rueda, D, Ronfani, L, Rushton, L, Saeedi, MY, Salomon, JA, Sampson, U, Santos, IS, Sawhney, M, Schmidt, JC, Shakh-Nazarova, M, She, J, Sheikhbahaei, S, Shibuya, K, Shin, HH, Shishani, K, Shiue, I, Sigfusdottir, ID, Singh, JA, Skirbekk, V, Sliwa, K, Soshnikov, SS, Sposato, LA, Stathopoulou, VK, Stroumpoulis, K, Tabb, KM, Talongwa, RT, Teixeira, CM, Terkawi, AS, Thomson, AJ, Thorne-Lyman, AL, Toyoshima, H, Dimbuene, ZT, Uwaliraye, P, Uzun, SB, Vasankari, TJ, Vasconcelos, AM, Vlassov, VV, Vollset, SE, Waller, S, Wan, X, Weichenthal, S, Weiderpass, E, Weintraub, RG, Westerman, R, Wilkinson, JD, Williams, HC, Yang, YC, Yentur, GK, Yip, P, Yonemoto, N, Younis, M, Yu, C, Jin, KY, El Sayed Zaki, M, Zhu, S, Vos, T, Lopez, AD, and Murray, CJ
- Abstract
Remarkable financial and political efforts have been focused on the reduction of child mortality during the past few decades. Timely measurements of levels and trends in under-5 mortality are important to assess progress towards the Millennium Development Goal 4 (MDG 4) target of reduction of child mortality by two thirds from 1990 to 2015, and to identify models of success.We generated updated estimates of child mortality in early neonatal (age 0-6 days), late neonatal (7-28 days), postneonatal (29-364 days), childhood (1-4 years), and under-5 (0-4 years) age groups for 188 countries from 1970 to 2013, with more than 29,000 survey, census, vital registration, and sample registration datapoints. We used Gaussian process regression with adjustments for bias and non-sampling error to synthesise the data for under-5 mortality for each country, and a separate model to estimate mortality for more detailed age groups. We used explanatory mixed effects regression models to assess the association between under-5 mortality and income per person, maternal education, HIV child death rates, secular shifts, and other factors. To quantify the contribution of these different factors and birth numbers to the change in numbers of deaths in under-5 age groups from 1990 to 2013, we used Shapley decomposition. We used estimated rates of change between 2000 and 2013 to construct under-5 mortality rate scenarios out to 2030.We estimated that 6·3 million (95% UI 6·0-6·6) children under-5 died in 2013, a 64% reduction from 17·6 million (17·1-18·1) in 1970. In 2013, child mortality rates ranged from 152·5 per 1000 livebirths (130·6-177·4) in Guinea-Bissau to 2·3 (1·8-2·9) per 1000 in Singapore. The annualised rates of change from 1990 to 2013 ranged from -6·8% to 0·1%. 99 of 188 countries, including 43 of 48 countries in sub-Saharan Africa, had faster decreases in child mortality during 2000-13 than during 1990-2000. In 2013, neonatal deaths accounted for 41·6% of under-5 deaths compared with 37·4% in 1990. Compared with 1990, in 2013, rising numbers of births, especially in sub-Saharan Africa, led to 1·4 million more child deaths, and rising income per person and maternal education led to 0·9 million and 2·2 million fewer deaths, respectively. Changes in secular trends led to 4·2 million fewer deaths. Unexplained factors accounted for only -1% of the change in child deaths. In 30 developing countries, decreases since 2000 have been faster than predicted attributable to income, education, and secular shift alone.Only 27 developing countries are expected to achieve MDG 4. Decreases since 2000 in under-5 mortality rates are accelerating in many developing countries, especially in sub-Saharan Africa. The Millennium Declaration and increased development assistance for health might have been a factor in faster decreases in some developing countries. Without further accelerated progress, many countries in west and central Africa will still have high levels of under-5 mortality in 2030.Bill & Melinda Gates Foundation, US Agency for International Development.
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- 2018
10. Outcome after prenatal diagnosis of the hypoplastic left heart syndrome
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Allan, L D, Apfel, H, and Printz, B
- Published
- 1998
11. Experimental arteriosclerosis: is the spatially irregular development of the plaque a consequence of locally differing electrical vector field?
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Apfel, H., primary, Friedmann, B., additional, and Betz, E., additional
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- 1992
- Full Text
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12. Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013
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Vos, T, Barber, Rm, Bell, B, Bertozzi Villa, A, Biryukov, S, Bolliger, I, Charlson, F, Davis, A, Degenhardt, L, Dicker, D, Duan, L, Erskine, H, Feigin, Vl, Ferrari, Aj, Fitzmaurice, C, Fleming, T, Graetz, N, Guinovart, C, Haagsma, J, Hansen, Gm, Hanson, Sw, Heuton, Kr, Higashi, H, Kassebaum, N, Kyu, H, Laurie, E, Liang, X, Lofgren, K, Lozano, R, Macintyre, Mf, Moradi Lakeh, M, Naghavi, M, Nguyen, G, Odell, S, Ortblad, K, Roberts, Da, Roth, Ga, Sandar, L, Serina, Pt, Stanaway, Jd, Steiner, C, Thomas, B, Vollset, Se, Whiteford, H, Wolock, Tm, Ye, P, Zhou, M, Ãvila, Ma, Aasvang, Gm, Abbafati, C, Abbasoglu, Ozgoren, A, Abd Allah, F, Abdel, Aziz, Abera, Sf, Aboyans, V, Abraham, Jp, Abraham, B, Abubakar, I, Abu Raddad, Lj, Abu Rmeileh, Nm, Aburto, Tc, Achoki, T, Ackerman, In, Adelekan, A, Ademi, Z, Adou, Ak, Adsuar, Jc, Arnlov, J, Agardh, Ee, Khabouri, Al, Alam, Ss, Alasfoor, D, Albittar, Mi, Alegretti, Ma, Aleman, Av, Alemu, Za, Alfonso Cristancho, R, Alhabib, S, Ali, R, Alla, F, Allebeck, P, Allen, Pj, Almazroa, Ma, Alsharif, U, Alvarez, E, Alvis, Guzman, Ameli, N, O, Amini, H, Ammar, W, Anderson, Bo, Anderson, Hr, Antonio, Ca, Anwari, P, Apfel, H, Arsenijevic, Vs, Artaman, A, Asghar, Rj, Assadi, R, Atkins, Ls, Atkinson, C, Badawi, A, Bahit, Mc, Bakfalouni, T, Balakrishnan, K, Balalla, S, Banerjee, A, Barker Collo, Sl, Barquera, S, Barregard, L, Barrero, Lh, Basu, S, Basu, A, Baxter, A, Beardsley, J, Bedi, N, Beghi, E, Bekele, T, Bell, Ml, Benjet, C, Bennett, Da, Bensenor, Im, Benzian, H, Bernabe, E, Beyene, Tj, Bhala, N, Bhalla, A, Bhutta, Z, Bienhoff, K, Bikbov, B, Bin, Abdulhak, Blore, Jd, Blyth, Fm, Bohensky, Ma, Bora, Basara, B, Borges, G, Bornstein, Nm, Bose, D, Boufous, S, Bourne, Rr, Boyers, Ln, Brainin, M, Brauer, M, Brayne, Ce, Brazinova, A, Breitborde, Nj, Brenner, H, Briggs, Ad, Brooks, Pm, Brown, J, Brugha, Ts, Buchbinder, R, Buckle, Gc, Bukhman, G, Bulloch, Ag, Burch, M, Burnett, R, Cardenas, R, Cabral, Nl, Campos, Nonato, Campuzano, Ir, Carapetis, Jc, Carpenter, Do, Caso, V, Castaneda Orjuela, Ca, Catala Lopez, F, Chadha, Vk, Chang, Jc, Chen, H, Chen, W, Chiang, Pp, Chimed Ochir, O, Chowdhury, R, Christensen, H, Christophi, Ca, Chugh, Ss, Cirillo, Massimo, Coggeshall, M, Cohen, A, Colistro, V, Colquhoun, Sm, Contreras, Ag, Cooper, Lt, Cooper, C, Cooperrider, K, Coresh, J, Cortinovis, M, Criqui, Mh, Crump, Ja, Cuevas Nasu, L, Dandona, R, Dandona, L, Dansereau, E, Dantes, Hg, Dargan, Pi, Davey, G, Davitoiu, Dv, Dayama, A, La, De, Cruz, Gongora, De, V, Vega, La, De, Sf, Leo, D, Del, Pozo, Cruz, Dellavalle, Rp, Deribe, K, Derrett, S, Des, Jarlais, Dessalegn, M, Deveber, Ga, Dharmaratne, Sd, Diaz Torne, C, Ding, El, Dokova, K, Dorsey, Er, Driscoll, Tr, Duber, H, Durrani, Am, Edmond, Km, Ellenbogen, Rg, Endres, M, Ermakov, Sp, Eshrati, B, Esteghamati, A, Estep, K, Fahimi, S, Farzadfar, F, Fay, Df, Felson, Dt, Fereshtehnejad, Sm, Fernandes, Jg, Ferri, Cp, Flaxman, A, Foigt, N, Foreman, Kj, Fowkes, Fg, Franklin, Rc, Furst, T, Futran, Nd, Gabbe, Bj, Gankpe, Fg, Garcia, Guerra, Geleijnse, Fa, Gessner, Bd, Gibney, Kb, Gillum, Rf, Ginawi, Ia, Giroud, M, Giussani, G, Goenka, S, Goginashvili, K, Gona, P, Gonzalez, De, Cosio, T, Gosselin, Ra, Gotay, Cc, Goto, A, Gouda, Hn, Guerrant, Rl, Gugnani, Hc, Gunnell, D, Gupta, R, Gutierrez, Ra, Hafezi Nejad, N, Hagan, H, Halasa, Y, Hamadeh, Rr, Hamavid, H, Hammami, M, Hankey, Gj, Hao, Y, Harb, Hl, Haro, Jm, Havmoeller, R, Hay, Rj, Hay, S, Hedayati, Mt, Heredia, Pi, Heydarpour, P, Hijar, M, Hoek, Hw, Hoffman, Hj, Hornberger, Jc, Hosgood, Hd, Hossain, M, Hotez, Pj, Hoy, Dg, Hsairi, M, Hu, H, Hu, G, Huang, Jj, Huang, C, Huiart, L, Husseini, A, Iannarone, M, Iburg, Km, Innos, K, Inoue, M, Jacobsen, Kh, Jassal, Sk, Jeemon, P, Jensen, Pn, Jha, V, Jiang, G, Jiang, Y, Jonas, Jb, Joseph, J, Juel, K, Kan, H, Karch, A, Karimkhani, C, Karthikeyan, G, Katz, R, Kaul, A, Kawakami, N, Kazi, Ds, Kemp, Ah, Kengne, Ap, Khader, Ys, Khalifa, Se, Khan, Ea, Khan, G, Khang, Yh, Khonelidze, I, Kieling, C, Kim, D, Kim, S, Kimokoti, Rw, Kinfu, Y, Kinge, Jm, Kissela, Bm, Kivipelto, M, Knibbs, L, Knudsen, Ak, Kokubo, Y, Kosen, S, Kramer, A, Kravchenko, M, Krishnamurthi, Rv, Krishnaswami, S, Kuate, Defo, Kucuk, B, Bicer, B, Kuipers, Ej, Kulkarni, Vs, Kumar, K, Kumar, Ga, Kwan, Gf, Lai, T, Lalloo, R, Lam, H, Lan, Q, Lansingh, Vc, Larson, H, Larsson, A, Lawrynowicz, Ae, Leasher, Jl, Lee, Jt, Leigh, J, Leung, R, Levi, M, Li, B, Li, Y, Liang, J, Lim, S, Lin, Hh, Lind, M, Lindsay, Mp, Lipshultz, Se, Liu, S, Lloyd, Bk, Lockett, Ohno, S, Logroscino, G, Looker, Kj, Lopez, Ad, Lopez Olmedo, N, Lortet Tieulent, J, Lotufo, Pa, Low, N, Lucas, Rm, Lunevicius, R, Lyons, Ra, Ma, J, Ma, S, Mackay, Mt, Majdan, M, Malekzadeh, R, Mapoma, Cc, Marcenes, W, March, Lm, Margono, C, Marks, Gb, Marzan, Mb, Masci, Jr, Mason Jones, Aj, Matzopoulos, Rg, Mayosi, Bm, Mazorodze, Tt, Mcgill, Nw, Mcgrath, Jj, Mckee, M, Mclain, A, Mcmahon, Bj, Meaney, Pa, Mehndiratta, Mm, Mejia Rodriguez, F, Mekonnen, W, Melaku, Ya, Meltzer, M, Memish, Za, Mensah, G, Meretoja, A, Mhimbira, Fa, Micha, R, Miller, Tr, Mills, Ej, Mitchell, Pb, Mock, Cn, Moffitt, Te, Mohamed, Ibrahim, N, Mohammad, Ka, Mokdad, Ah, Mola, Gl, Monasta, L, Montico, M, Montine, Tj, Moore, Ar, Moran, Ae, Morawska, L, Mori, R, Moschandreas, J, Moturi, Wn, Moyer, M, Mozaffarian, D, Mueller, Uo, Mukaigawara, M, Murdoch, Me, Murray, J, Murthy, Ks, Naghavi, P, Nahas, Z, Naheed, A, Naidoo, Ks, Naldi, L, Nand, D, Nangia, V, Narayan, Km, Nash, D, Nejjari, C, Neupane, Sp, Newman, Lm, Newton, Cr, Ng, M, Ngalesoni, Fn, Nhung, Nt, Nisar, Mi, Nolte, S, Norheim, Of, Norman, Re, Norrving, B, Nyakarahuka, L, Ih, Oh, Ohkubo, T, Omer, Sb, Opio, Jn, Ortiz, A, Pandian, Jd, Panelo, Ci, Papachristou, C, Park, Ek, Parry, Cd, Caicedo, Aj, Patten, Sb, Paul, Vk, Pavlin, Bi, Pearce, N, Pedraza, Ls, Pellegrini, Ca, Pereira, Dm, Perez Ruiz, Fp, Perico, N, Pervaiz, A, Pesudovs, K, Peterson, Cb, Petzold, M, Phillips, Mr, Phillips, D, Phillips, B, Piel, Fb, Plass, D, Poenaru, D, Polanczyk, Gv, Polinder, S, Pope, Ca, Popova, S, Poulton, Rg, Pourmalek, F, Prabhakaran, D, Prasad, Nm, Qato, D, Quistberg, Da, Rafay, A, Rahimi, K, Rahimi Movaghar, V, Rahman, Su, Raju, M, Rakovac, I, Rana, Sm, Razavi, H, Refaat, A, Rehm, J, Remuzzi, G, Resnikoff, S, Ribeiro, Al, Riccio, Pm, Richardson, L, Richardus, Jh, Riederer, Am, Robinson, M, Roca, A, Rodriguez, A, Rojas Rueda, D, Ronfani, L, Rothenbacher, D, Roy, N, Ruhago, Gm, Sabin, N, Sacco, Rl, Ksoreide, K, Saha, S, Sahathevan, R, Sahraian, Ma, Sampson, U, Sanabria, Jr, Sanchez Riera, L, Santos, Is, Satpathy, M, Saunders, Je, Sawhney, M, Saylan, Mi, Scarborough, P, Schoettker, B, Schneider, Ij, Schwebel, Dc, Scott, Jg, Seedat, S, Sepanlou, Sg, Serdar, B, Servan Mori, Ee, Shackelford, K, Shaheen, A, Shahraz, S, Shamah, Levy, T, Shangguan, S, She, J, Sheikhbahaei, S, Shepard, Ds, Shi, P, Shibuya, K, Shinohara, Y, Shiri, R, Shishani, K, Shiue, I, Shrime, Mg, Sigfusdottir, Id, Silberberg, Dh, Simard, Ep, Sindi, S, Singh, Ja, Singh, L, Skirbekk, V, Sliwa, K, Soljak, M, Soneji, S, Soshnikov, Ss, Speyer, P, Sposato, La, Sreeramareddy, Ct, Stoeckl, H, Stathopoulou, Vk, Steckling, N, Stein, Mb, Stein, Dj, Steiner, Tj, Stewart, A, Stork, E, Stovner, Lj, Stroumpoulis, K, Sturua, L, Sunguya, Bf, Swaroop, M, Sykes, Bl, Tabb, Km, Takahashi, K, Tan, F, Tandon, N, Tanne, D, Tanner, M, Tavakkoli, M, Taylor, Hr, Ao, Te, Temesgen, Am, Ten, Have, M, Tenkorang, Ey, Terkawi, As, Theadom, Am, Thomas, E, Thorne Lyman, Al, Thrift, Ag, Tleyjeh, Im, Tonelli, M, Topouzis, F, Towbin, Ja, Toyoshima, H, Traebert, J, Tran, Bx, Trasande, L, Trillini, M, Truelsen, T, Trujillo, U, Tsilimbaris, M, Tuzcu, Em, Ukwaja, Kn, Undurraga, Ea, Uzun, Sb, Van, Brakel, Van, Wh, Vijver, De, Van, S, Dingenen, R, Van, Gool, Varakin, Yy, Vasankari, Tj, Vavilala, Ms, Veerman, Lj, Velasquez, Melendez, G, Venketasubramanian, N, Vijayakumar, L, Villalpando, S, Violante, Fs, Vlassov, Vv, Waller, S, Wallin, Mt, Wan, X, Wang, L, Wang, J, Wang, Y, Warouw, Ts, Weichenthal, S, Weiderpass, E, Weintraub, Rg, Werdecker, A, Wessells, Kr, Westerman, R, Wilkinson, Jd, Williams, Hc, Williams, Tn, Woldeyohannes, Sm, Wolfe, Cd, Wong, Jq, Wong, H, Woolf, Ad, Wright, Jl, Wurtz, B, Xu, G, Yang, G, Yano, Y, Yenesew, Ma, Yentur, Gk, Yip, P, Yonemoto, N, Yoon, Sj, Younis, M, Yu, C, Kim, Ky, Zaki, Mel, Zhang, Y, Zhao, Z, Zhao, Y, Zhu, J, Zonies, D, Zunt, Jr, Salomon, Ja, Murray, C. J., Vos, T, Barber, Rm, Bell, B, Bertozzi-Villa, A, Biryukov, S, Bolliger, I, Charlson, F, Davis, A, Degenhardt, L, Dicker, D, Duan, L, Erskine, H, Feigin, Vl, Ferrari, Aj, Fitzmaurice, C, Fleming, T, Graetz, N, Guinovart, C, Haagsma, J, Hansen, Gm, Hanson, Sw, Heuton, Kr, Higashi, H, Kassebaum, N, Kyu, H, Laurie ELiang, X, Lofgren, K, Lozano, R, Macintyre, Mf, Moradi-Lakeh, M, Naghavi, M, Nguyen, G, Odell, S, Ortblad, K, Roberts, Da, Roth, Ga, Sandar, L, Serina, Pt, Stanaway, Jd, Steiner, C, Thomas, B, Vollset, Se, Whiteford, H, Wolock, Tm, Ye, P, Zhou, M, Ãvila, Ma, Aasvang, Gm, Abbafati, C, Abbasoglu Ozgoren, A, Abd-Allah, F, Abdel Aziz MI, Abera, Sf, Aboyans, V, Abraham, Jp, Abraham, B, Abubakar, I, Abu-Raddad, Lj, Abu-Rmeileh, Nm, Aburto, Tc, Achoki TAckerman IN, Adelekan, A, Ademi, Z, Adou, Ak, Adsuar, Jc, Arnlov, J, Agardh, Ee, Al Khabouri MJ, Alam, S, Alasfoor, D, Albittar, Mi, Alegretti MAAleman AV, Alemu, Za, Alfonso-Cristancho, R, Alhabib, S, Ali, R, Alla, F, Allebeck, P, Allen, Pj, Almazroa, Ma, Alsharif, U, Alvarez, E, Alvis-Guzman NAmeli, O, Amini, H, Ammar, W, Anderson, Bo, Anderson, Hr, Antonio, Ca, Anwari, P, Apfel, H, Arsenijevic, V, Artaman, A, Asghar, Rj, Assadi, R, Atkins, L, Atkinson, C, Badawi, A, Bahit, Mc, Bakfalouni, T, Balakrishnan, K, Balalla, S, Banerjee, A, Barker-Collo, Sl, Barquera, S, Barregard, L, Barrero LHBasu, S, Basu, A, Baxter, A, Beardsley, J, Bedi, N, Beghi, E, Bekele, T, Bell, Ml, Benjet, C, Bennett, Da, Bensenor, Im, Benzian, H, Bernabe, E, Beyene TJBhala, N, Bhalla, A, Bhutta, Z, Bienhoff, K, Bikbov, B, Bin Abdulhak, A, Blore, Jd, Blyth, Fm, Bohensky, Ma, Bora Basara, B, Borges, G, Bornstein, Nm, Bose, D, Boufous, S, Bourne, Rr, Boyers, Ln, Brainin, M, Brauer, M, Brayne, Ce, Brazinova, A, Breitborde, Nj, Brenner, H, Briggs, Ad, Brooks, Pm, Brown JBrugha TS, Buchbinder, R, Buckle, Gc, Bukhman, G, Bulloch, Ag, Burch, M, Burnett, R, Cardenas, R, Cabral, Nl, Campos Nonato IR, Campuzano JCCarapetis JR, Carpenter, Do, Caso, V, Castaneda-Orjuela, Ca, Catala-Lopez, F, Chadha, Vk, Chang, Jc, Chen, H, Chen, W, Chiang, Pp, Chimed-Ochir, O, Chowdhury, R, Christensen, H, Christophi, Ca, Chugh, S, Cirillo, M, Coggeshall, M, Cohen, A, Colistro, V, Colquhoun, Sm, Contreras, Ag, Cooper LTCooper, C, Cooperrider, K, Coresh, J, Cortinovis, M, Criqui, Mh, Crump, Ja, Cuevas-Nasu, L, Dandona, R, Dandona, L, Dansereau, E, Dantes, Hg, Dargan, Pi, Davey, G, Davitoiu, Dv, Dayama, A, De la Cruz-Gongora, V, de la Vega SF, De Leo, D, del Pozo-Cruz, B, Dellavalle, Rp, Deribe, K, Derrett, S, Des Jarlais DC, Dessalegn, M, Deveber, Ga, Dharmaratne, Sd, Diaz-Torne, C, Ding, El, Dokova, K, Dorsey, Er, Driscoll, Tr, Duber, H, Durrani, Am, Edmond, Km, Ellenbogen, Rg, Endres, M, Ermakov, Sp, Eshrati, B, Esteghamati, A, Estep, K, Fahimi, S, Farzadfar, F, Fay, Df, Felson, Dt, Fereshtehnejad SMFernandes JG, Ferri, Cp, Flaxman, A, Foigt, N, Foreman, Kj, Fowkes, Fg, Franklin, Rc, Furst, T, Futran, Nd, Gabbe, Bj, Gankpe, Fg, Garcia-Guerra 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Kissela, Bm, Kivipelto MKnibbs, L, Knudsen, Ak, Kokubo, Y, Kosen, S, Kramer, A, Kravchenko, M, Krishnamurthi, Rv, Krishnaswami, S, Kuate Defo, B, Kucuk Bicer, B, Kuipers EJKulkarni VS, Kumar, K, Kumar, Ga, Kwan, Gf, Lai, T, Lalloo, R, Lam, H, Lan, Q, Lansingh, Vc, Larson, H, Larsson, A, Lawrynowicz, Ae, Leasher, Jl, Lee, Jt, Leigh, J, Leung, R, Levi, M, Li, B, Li, Y, Liang, J, Lim, S, Lin, Hh, Lind, M, Lindsay, Mp, Lipshultz, Se, Liu, S, Lloyd, Bk, Lockett Ohno, S, Logroscino, G, Looker, Kj, Lopez, Ad, Lopez-Olmedo, N, Lortet-Tieulent, J, Lotufo, Pa, Low, N, Lucas, Rm, Lunevicius, R, Lyons, Ra, Ma, J, Ma, S, Mackay MTMajdan, M, Malekzadeh, R, Mapoma, Cc, Marcenes, W, March, Lm, Margono, C, Marks, Gb, Marzan, Mb, Masci, Jr, Mason-Jones, Aj, Matzopoulos RGMayosi BM, Mazorodze, Tt, Mcgill, Nw, Mcgrath, Jj, Mckee, M, Mclain, A, Mcmahon, Bj, Meaney, Pa, Mehndiratta, Mm, Mejia-Rodriguez, F, Mekonnen, W, Melaku, Ya, Meltzer, M, Memish, Za, Mensah, G, Meretoja, A, Mhimbira, Fa, Micha, R, 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Ryan, Westerman, Ronny, Wilkinson, James D., Williams, Hywel C., Williams, Thomas N., Woldeyohannes, Solomon M., Wolfe, Charles D.A., Wong, John Q., Wong, Haidong, Woolf, Anthony D., Wright, Jonathan L., Wurtz, Brittany, Xu, Gelin, Yang, Gonghuan, Yano, Yuichiro, Yenesew, Muluken A., Yentur, Gokalp K., Yip, Paul, Yonemoto, Naohiro, Yoon, Seok-Jun, Younis, Mustafa, Yu, Chuanhua, Kim, Kim Yun, Zaki, Maysaa El Sayed, Zhang, Yong, Zhao, Zheng, Zhao, Yong, Zhu, Jun, Zonies, David, Zunt, Joseph R., Salomon, Joshua A., Murray, Christopher J.L., Cell biology, Gastroenterology & Hepatology, Epidemiology, Health Technology Assessment (HTA), and Public Health
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Male ,Gerontology ,Nutrition and Disease ,Epidemiology ,years lived with disability, Global burden of disease, acute and chronic diseases, countries ,Prevalence ,Disease ,Global Health ,Medical and Health Sciences ,Conduct disorder ,Otitis-media ,Cost of Illness ,Residence Characteristics ,Voeding en Ziekte ,80 and over ,Global health ,2.2 Factors relating to the physical environment ,2.1 Biological and endogenous factors ,countries ,Aetiology ,Child ,Aged, 80 and over ,Medicine(all) ,education.field_of_study ,ATTENTION-DEFICIT/HYPERACTIVITY DISORDER ,Incidence ,Mortality rate ,Incidence (epidemiology) ,Pain Research ,Neglected Diseases ,Alcohol dependence ,General Medicine ,Middle Aged ,Global burden of disease ,Global Burden of Disease Study 2013 Collaborators ,Mental Health ,Infectious Diseases ,Attention deficit/Hyperactivity disorder ,Burden of Illness ,Child, Preschool ,Acute Disease ,Female ,Life Sciences & Biomedicine ,Adult ,medicine.medical_specialty ,Adolescent ,GBD 2013 ,Population ,acute and chronic diseases ,Young Adult ,Mental-disorders ,Age Distribution ,Medicine, General & Internal ,Weights ,General & Internal Medicine ,medicine ,Humans ,Life Science ,Disabled Persons ,Sex Distribution ,Preschool ,education ,Developing Countries ,VLAG ,Aged ,Science & Technology ,business.industry ,Developed Countries ,Cutaneous Leishmaniasis ,Infant, Newborn ,Infant ,Health outcomes ,Newborn ,medicine.disease ,Comorbidity ,Brain Disorders ,years lived with disability ,Good Health and Well Being ,Disease, injury, incidence, prevalence, YLDs, GBD 2010 ,Chronic Disease ,Wounds and Injuries ,business ,2.4 Surveillance and distribution ,Iron-deficiency ,Demography - Abstract
Summary Background Up-to-date evidence about levels and trends in disease and injury incidence, prevalence, and years lived with disability (YLDs) is an essential input into global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013), we estimated these quantities for acute and chronic diseases and injuries for 188 countries between 1990 and 2013. Methods Estimates were calculated for disease and injury incidence, prevalence, and YLDs using GBD 2010 methods with some important refinements. Results for incidence of acute disorders and prevalence of chronic disorders are new additions to the analysis. Key improvements include expansion to the cause and sequelae list, updated systematic reviews, use of detailed injury codes, improvements to the Bayesian meta-regression method (DisMod-MR), and use of severity splits for various causes. An index of data representativeness, showing data availability, was calculated for each cause and impairment during three periods globally and at the country level for 2013. In total, 35 620 distinct sources of data were used and documented to calculated estimates for 301 diseases and injuries and 2337 sequelae. The comorbidity simulation provides estimates for the number of sequelae, concurrently, by individuals by country, year, age, and sex. Disability weights were updated with the addition of new population-based survey data from four countries. Findings Disease and injury were highly prevalent; only a small fraction of individuals had no sequelae. Comorbidity rose substantially with age and in absolute terms from 1990 to 2013. Incidence of acute sequelae were predominantly infectious diseases and short-term injuries, with over 2 billion cases of upper respiratory infections and diarrhoeal disease episodes in 2013, with the notable exception of tooth pain due to permanent caries with more than 200 million incident cases in 2013. Conversely, leading chronic sequelae were largely attributable to non-communicable diseases, with prevalence estimates for asymptomatic permanent caries and tension-type headache of 2·4 billion and 1·6 billion, respectively. The distribution of the number of sequelae in populations varied widely across regions, with an expected relation between age and disease prevalence. YLDs for both sexes increased from 537·6 million in 1990 to 764·8 million in 2013 due to population growth and ageing, whereas the age-standardised rate decreased little from 114·87 per 1000 people to 110·31 per 1000 people between 1990 and 2013. Leading causes of YLDs included low back pain and major depressive disorder among the top ten causes of YLDs in every country. YLD rates per person, by major cause groups, indicated the main drivers of increases were due to musculoskeletal, mental, and substance use disorders, neurological disorders, and chronic respiratory diseases; however HIV/AIDS was a notable driver of increasing YLDs in sub-Saharan Africa. Also, the proportion of disability-adjusted life years due to YLDs increased globally from 21·1% in 1990 to 31·2% in 2013. Interpretation Ageing of the world's population is leading to a substantial increase in the numbers of individuals with sequelae of diseases and injuries. Rates of YLDs are declining much more slowly than mortality rates. The non-fatal dimensions of disease and injury will require more and more attention from health systems. The transition to non-fatal outcomes as the dominant source of burden of disease is occurring rapidly outside of sub-Saharan Africa. Our results can guide future health initiatives through examination of epidemiological trends and a better understanding of variation across countries. Funding Bill & Melinda Gates Foundation. Background Up-to-date evidence about levels and trends in disease and injury incidence, prevalence, and years lived with disability (YLDs) is an essential input into global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013), we estimated these quantities for acute and chronic diseases and injuries for 188 countries between 1990 and 2013. Methods Estimates were calculated for disease and injury incidence, prevalence, and YLDs using GBD 2010 methods with some important refinements. Results for incidence of acute disorders and prevalence of chronic disorders are new additions to the analysis. Key improvements include expansion to the cause and sequelae list, updated systematic reviews, use of detailed injury codes, improvements to the Bayesian meta-regression method (DisMod-MR), and use of severity splits for various causes. An index of data representativeness, showing data availability, was calculated for each cause and impairment during three periods globally and at the country level for 2013. In total, 35 620 distinct sources of data were used and documented to calculated estimates for 301 diseases and injuries and 2337 sequelae. The comorbidity simulation provides estimates for the number of sequelae, concurrently, by individuals by country, year, age, and sex. Disability weights were updated with the addition of new population-based survey data from four countries. Findings Disease and injury were highly prevalent; only a small fraction of individuals had no sequelae. Comorbidity rose substantially with age and in absolute terms from 1990 to 2013. Incidence of acute sequelae were predominantly infectious diseases and short-term injuries, with over 2 billion cases of upper respiratory infections and diarrhoeal disease episodes in 2013, with the notable exception of tooth pain due to permanent caries with more than 200 million incident cases in 2013. Conversely, leading chronic sequelae were largely attributable to non-communicable diseases, with prevalence estimates for asymptomatic permanent caries and tension-type headache of 2·4 billion and 1·6 billion, respectively. The distribution of the number of sequelae in populations varied widely across regions, with an expected relation between age and disease prevalence. YLDs for both sexes increased from 537·6 million in 1990 to 764·8 million in 2013 due to population growth and ageing, whereas the age-standardised rate decreased little from 114·87 per 1000 people to 110·31 per 1000 people between 1990 and 2013. Leading causes of YLDs included low back pain and major depressive disorder among the top ten causes of YLDs in every country. YLD rates per person, by major cause groups, indicated the main drivers of increases were due to musculoskeletal, mental, and substance use disorders, neurological disorders, and chronic respiratory diseases; however HIV/AIDS was a notable driver of increasing YLDs in sub-Saharan Africa. Also, the proportion of disability-adjusted life years due to YLDs increased globally from 21·1% in 1990 to 31·2% in 2013. Interpretation Ageing of the world's population is leading to a substantial increase in the numbers of individuals with sequelae of diseases and injuries. Rates of YLDs are declining much more slowly than mortality rates. The non-fatal dimensions of disease and injury will require more and more attention from health systems. The transition to non-fatal outcomes as the dominant source of burden of disease is occurring rapidly outside of sub-Saharan Africa. Our results can guide future health initiatives through examination of epidemiological trends and a better understanding of variation across countries. Funding Bill & Melinda Gates Foundation.
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- 2015
13. Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: A systematic analysis for the Global Burden of Disease Study 2013
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Naghavi, M, Wang, H, Lozano, R, Davis, A, Liang, X, Zhou, M, Vollset, SE, Abbasoglu Ozgoren, A, Abdalla, S, Abd-Allah, F, Abdel Aziz, MI, Abera, SF, Aboyans, V, Abraham, B, Abraham, JP, Abuabara, KE, Abubakar, I, Abu-Raddad, LJ, Abu-Rmeileh, NME, Achoki, T, Adelekan, A, Ademi, Z, Adofo, K, Adou, AK, Adsuar, JC, Ärnlov, J, Agardh, EE, Akena, D, Al Khabouri, MJ, Alasfoor, D, Albittar, M, Alegretti, MA, Aleman, AV, Alemu, ZA, Alfonso-Cristancho, R, Alhabib, S, Ali, MK, Ali, R, Alla, F, Al Lami, F, Allebeck, P, AlMazroa, MA, Al-Shahi Salman, R, Alsharif, U, Alvarez, E, Alviz-Guzman, N, Amankwaa, AA, Amare, AT, Ameli, O, Amini, H, Ammar, W, Anderson, HR, Anderson, BO, Antonio, CAT, Anwari, P, Apfel, H, Argeseanu Cunningham, S, Arsic Arsenijevic, VS, Artaman, A, Asad, MM, Asghar, RJ, Assadi, R, Atkins, LS, Atkinson, C, Badawi, A, Bahit, MC, Bakfalouni, T, Balakrishnan, K, Balalla, S, Banerjee, A, Barber, RM, Barker-Collo, SL, Barquera, S, Barregard, L, Barrero, LH, Barrientos-Gutierrez, T, Basu, A, Basu, S, Basulaiman, MO, Beardsley, J, Bedi, N, Beghi, E, Bekele, T, Bell, ML, Benjet, C, Bennett, DA, Bensenor, IM, Benzian, H, Bertozzi-Villa, A, Beyene, TJ, Bhala, N, Bhalla, A, Bhutta, ZA, Bikbov, B, Bin Abdulhak, A, Biryukov, S, Blore, JD, Blyth, FM, Bohensky, MA, Borges, G, Naghavi, M, Wang, H, Lozano, R, Davis, A, Liang, X, Zhou, M, Vollset, SE, Abbasoglu Ozgoren, A, Abdalla, S, Abd-Allah, F, Abdel Aziz, MI, Abera, SF, Aboyans, V, Abraham, B, Abraham, JP, Abuabara, KE, Abubakar, I, Abu-Raddad, LJ, Abu-Rmeileh, NME, Achoki, T, Adelekan, A, Ademi, Z, Adofo, K, Adou, AK, Adsuar, JC, Ärnlov, J, Agardh, EE, Akena, D, Al Khabouri, MJ, Alasfoor, D, Albittar, M, Alegretti, MA, Aleman, AV, Alemu, ZA, Alfonso-Cristancho, R, Alhabib, S, Ali, MK, Ali, R, Alla, F, Al Lami, F, Allebeck, P, AlMazroa, MA, Al-Shahi Salman, R, Alsharif, U, Alvarez, E, Alviz-Guzman, N, Amankwaa, AA, Amare, AT, Ameli, O, Amini, H, Ammar, W, Anderson, HR, Anderson, BO, Antonio, CAT, Anwari, P, Apfel, H, Argeseanu Cunningham, S, Arsic Arsenijevic, VS, Artaman, A, Asad, MM, Asghar, RJ, Assadi, R, Atkins, LS, Atkinson, C, Badawi, A, Bahit, MC, Bakfalouni, T, Balakrishnan, K, Balalla, S, Banerjee, A, Barber, RM, Barker-Collo, SL, Barquera, S, Barregard, L, Barrero, LH, Barrientos-Gutierrez, T, Basu, A, Basu, S, Basulaiman, MO, Beardsley, J, Bedi, N, Beghi, E, Bekele, T, Bell, ML, Benjet, C, Bennett, DA, Bensenor, IM, Benzian, H, Bertozzi-Villa, A, Beyene, TJ, Bhala, N, Bhalla, A, Bhutta, ZA, Bikbov, B, Bin Abdulhak, A, Biryukov, S, Blore, JD, Blyth, FM, Bohensky, MA, and Borges, G
- Abstract
Background Up-to-date evidence on levels and trends for age-sex-specific all-cause and cause-specific mortality is essential for the formation of global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013) we estimated yearly deaths for 188 countries between 1990, and 2013. We used the results to assess whether there is epidemiological convergence across countries. Methods We estimated age-sex-specific all-cause mortality using the GBD 2010 methods with some refinements to improve accuracy applied to an updated database of vital registration, survey, and census data. We generally estimated cause of death as in the GBD 2010. Key improvements included the addition of more recent vital registration data for 72 countries, an updated verbal autopsy literature review, two new and detailed data systems for China, and more detail for Mexico, UK, Turkey, and Russia. We improved statistical models for garbage code redistribution. We used six different modelling strategies across the 240 causes; cause of death ensemble modelling (CODEm) was the dominant strategy for causes with sufficient information. Trends for Alzheimer's disease and other dementias were informed by meta-regression of prevalence studies. For pathogen-specific causes of diarrhoea and lower respiratory infections we used a counterfactual approach. We computed two measures of convergence (inequality) across countries: the average relative difference across all pairs of countries (Gini coefficient) and the average absolute difference across countries. To summarise broad findings, we used multiple decrement life-tables to decompose probabilities of death from birth to exact age 15 years, from exact age 15 years to exact age 50 years, and from exact age 50 years to exact age 75 years, and life expectancy at birth into major causes. For all quantities reported, we computed 95% uncertainty intervals (UIs). We constrained cause-specific fractions within each age-sex-country-y
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- 2015
14. Quantitative measurement of local blood flow with heat clearance
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Müller-Schauenburg, W., Apfel, H., Benzing, H., and Betz, E.
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- 1975
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15. Ein zwei-Elektroden-Meßverfahren zur in vivo-Bestimmung der elektrischen Impedanz arterieller Blutgefäße im Frequenzbereich von 1 kHz bis 100 kHz
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Apfel, H., primary
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- 2009
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16. Performance of Alternative Oxide Anodes for the Electrochemical Oxidation of Hydrogen and Methane in Solid Oxide Fuel Cells
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Tu, H., primary, Apfel, H., additional, and Stimming, U., additional
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- 2006
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17. Quantitative three dimensional echocardiography in patients with pulmonary hypertension and compressed left ventricles: comparison with cross sectional echocardiography and magnetic resonance imaging.
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Apfel, H. D., primary, Shen, Z., additional, Gopal, A. S., additional, Vangi, V., additional, Solowiejczyk, D., additional, Altmann, K., additional, Barst, R. J., additional, Boxt, L. M., additional, Allan, L. D., additional, and King, D. L., additional
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- 1996
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18. Electrophysiological effects of progesterone on hepatocytes
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Waldegger, S., primary, Beisse, F., additional, Apfel, H., additional, Breit, S., additional, Kolb, H.-A., additional, Häussinger, D., additional, and Lang, F., additional
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- 1995
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19. Inhibition of Rat Hepatocyte K+Conductance by Serotonin
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Apfel, H., primary, Wagner, C.A., additional, Schmitt, M., additional, Waldegger, S., additional, Häussinger, D., additional, and Lang, F., additional
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- 1995
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20. Protective immunity linked with a distinct developmental stage of a filarial parasite.
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Eisenbeiss, W F, primary, Apfel, H, additional, and Meyer, T F, additional
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- 1994
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21. Inhibition of Rat Hepatocyte K+ Conductance by Serotonin.
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Apfel, H., Wagner, C.A., Schmitt, M., Waldegger, S., Häussinger, D., and Lang, F.
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- 1995
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22. Molecular cloning and demonstration of an aminopeptidase activity in a filarial nematode glycoprotein
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Harnett, W., Houston, K.M., Tate, R., Garate, T., Apfel, H., Adam, R., Haslam, S.M., Panico, M., Paxton, T., and Dell, A.
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- 1999
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23. Molecular cloning and characterization of an Echinococcus multilocularis and Echinococcus granulosus stress protein homologous to the mammalian 78 kDa glucose regulated protein
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Muehlschlegel, F., Frosch, P., Castro, A., Apfel, H., Mueller, A., and Frosch, M.
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- 1995
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24. Research Note PCR-based amplification of total cDNA with high fidelity and high yield from minute amounts of parasite RNA
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Lattemann, C. T. and Apfel, H.
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- 1997
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25. Acetylcholine induces overdrive excitation in sheep Purkinje fibres
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APFEL, H., primary and VASSALLE, M., additional
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- 1988
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26. Durch Elektrostimulation erzeugte arteriosklerotische Veränderungen von Arterienwänden und deren elektrische Leitfähigkeit
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Apfel, H., primary and Bete, E., additional
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- 1986
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27. Ein zwei-Elektroden-Meßverfahren zur in vivo-Bestimmung der elektrischen Impedanz arterieller Blutgefäße im Frequenzbereich von 1 kHz bis 100 kHz.
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Apfel, H.
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- 1988
28. Durch Elektrostimulation erzeugte arteriosklerotische Veränderungen von Arterien wänden und deren elektrische Leitfähigkeit.
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Apfel, H.(Tübingen) and Bete, E.
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- 1986
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29. Two-dimensional echocardiographic assessment of right ventricular function as a predictor of outcome in hypoplastic left heart syndrome.
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Altmann, Karen, Printz, Beth F., Altmann, K, Printz, B F, Solowiejczky, D E, Gersony, W M, Quaegebeur, J, and Apfel, H D
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ECHOCARDIOGRAPHY , *RIGHT heart ventricle , *PHYSIOLOGY - Abstract
This study was undertaken to assess the importance of right ventricular function at the time of initial presentation on early and intermediate outcome in patients with hypoplastic left heart syndrome (HLHS). Several studies have attempted to define physiologic risk factors for poor early outcome following the Norwood palliation for HLHS. No clinical or hemodynamic factors including right ventricular function have been found to reliably predict Norwood I operative survival. The relation between initial ventricular function and later survival has not been investigated. To assess the importance of right ventricular (RV) function at the time of initial presentation on outcome in patients with HLHS, systolic function was determined by qualitative and quantitative methods in 60 consecutive patients before surgical intervention. The effects on stage I operative survival, survival to stage II, and overall survival were analyzed. Initial RV function did not impact on stage I survival. However, analysis of later outcome of the stage I survivors showed that those with prestage I RV dysfunction had significantly greater mortality before stage II. Actuarial survival 18 months after Norwood surgery was 93% for patients with initially normal RV function compared with 47% for those with abnormal function (p = <0.005). The relative risk for later mortality was approximately 11 times greater for patients with initial RV dysfunction. Thus, RV dysfunction identifiable soon after initial presentation does not impact on early survival after Norwood I operation for HLHS. Intermediate and overall survival, however, is significantly decreased in patients with initially diminished RV function. [ABSTRACT FROM AUTHOR]
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- 2000
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30. Serial echocardiographic measurements of the pulmonary autograft in the aortic valve position after the Ross operation in a pediatric population using normal pulmonary artery dimensions as the reference standard.
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Solowiejczyk, David E., Bourlon, Francois, Solowiejczyk, D E, Bourlon, F, Apfel, H D, Hordof, A J, Hsu, D T, Crabtree, G, Galantowicz, M, Gersony, W M, and Quaegebeur, J M
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AUTOTRANSPLANTATION , *PULMONARY artery , *ECHOCARDIOGRAPHY - Abstract
Serial echocardiographic measurements of the annulus and sinus were obtained in children before the Ross operation, and early and late postoperatively. Values were compared with normal standards for the aorta and pulmonary artery (PA). There was no significant difference between PA annulus measurements before surgery and the corresponding autograft immediately afterward (1.73 +/- 0.60 cm preoperatively; 1. 63 +/- 0.58 cm postoperatively, p = NS). Late after surgery the mean annulus diameter was enlarged compared with the normal aorta (DeltaZ 1.9 +/- 2.4), but remained relatively unchanged compared with the normal PA (DeltaZ 0.7 +/- 1.1, p <0.01). In contrast, the autograft sinus was dilated early after surgery (1.83 +/- 0.58 cm preoperatively; 2.18 +/- 0.73 cm postoperatively, p <0.01). Mean sinus Z score further increased compared with both the aorta (DeltaZ 1.3 +/- 1.7) and PA (DeltaZ 1.3 +/- 1.6). Use of standard PA measurements may be important in the assessment of autograft enlargement. Minimal change in autograft Z scores over time suggests that annulus enlargement is mainly due to somatic growth. In contrast, the autograft sinus showed an immediate and continued disproportionate increase in size over time, suggesting that sinus enlargement is largely due to passive dilation. [ABSTRACT FROM AUTHOR]
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- 2000
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31. Usefulness of preoperative echocardiography in predicting left ventricular outflow obstruction after primary repair of interrupted aortic arch with ventricular septal defect.
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Apfel, Howard D., Levenbraun, Joseph, Quaegebeur, Jan M., Allen, Lindsey D., Apfel, H D, Levenbraun, J, Quaegebeur, J M, and Allan, L D
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ECHOCARDIOGRAPHY - Abstract
Residual left ventricular outflow tract (LVOT) obstruction is a significant problem after repair of interrupted aortic arch (IAA) and ventricular septal defect. Resection of subaortic tissue at the time of primary repair, however, is associated with increased morbidity and mortality. We reviewed the preoperative echocardiograms and the postoperative clinical course and echocardiograms of 23 consecutive patients who underwent primary repair of IAA without widening of the subaortic region. Nine patients (39%) developed significant LVOT obstruction (pressure gradient >40 mm Hg). LVOT obstruction was noted postoperatively in 7 of 9 patients by 1 month, 8 of 9 by 2 months, and 9 of 9 by 1 year. On retrospective analysis of the preoperative echocardiograms, the indexed cross-sectional area of the LVOT, the subaortic diameter index, and the subaortic diameter Z score were all significantly smaller in those requiring reintervention (p <0.04, p <0.05, p <0.05, respectively). Of these, indexed cross-sectional area had the least reproducibility and subaortic diameter index the most (coefficient of variation of 26.3% vs 11.2%). In conclusion, most patients who develop significant LVOT obstruction after repair of IAA do so within 1 month of operation. Although subaortic indexed cross-sectional area is the most sensitive predictor of LVOT obstruction after primary repair of IAA, other more simple standardized measurements of the subaortic diameter were comparably predictive and had better reproducibility. [ABSTRACT FROM AUTHOR]
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- 1998
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32. Global, regional, and national levels of neonatal, infant, and under-5 mortality during 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013
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Karen Sliwa, Xiaofeng Liang, Vivekanand Jha, Dorairaj Prabhakaran, Rakhi Dandona, Gonghuan Yang, Xuan Che, Soewarta Kosen, Sergei Petrovich Ermakov, Ted R. Miller, Samath D Dharmaratne, Philimon Gona, Sergey Soshnikov, Atsushi Goto, Costas A. Christophi, Zacharie Tsala Dimbuene, Elena Alvarez, Yanping Wang, Peggy Pei-Chia Chiang, Mohammad H. Forouzanfar, Giancarlo Logroscino, Massimo Cirillo, Knud Juel, Johanna M. Geleijnse, Stefan Ma, Samaya Ismayilova, Karen Fern Greenwell, Michelle L. Bell, Saad B. Omer, Ademola Lukman Adelekan, Joshua A. Salomon, Dhruv S. Kazi, Jed D. Blore, Walid Ammar, Carly E Levitz, Kovin Naidoo, Solveig A. Cunningham, Stephen G. Waller, Anand Dayama, James D. Wilkinson, Vasiliki Stathopoulou, Meghan D. Mooney, Mall Leinsalu, Jonathan R. Carapetis, Paul S. F. Yip, Anders Larsson, Abbas Ali Mahdi, Hideaki Toyoshima, Guohong Jiang, Xia Wan, Chuanhua Yu, Soufiane Boufous, Ivy Shiue, Bulat Idrisov, Qing Lan, Chelsea A. Liddell, Austin E Schumacher, Valeria Caso, Nigel Bruce, Paulo A. Lotufo, Ibrahim Abubakar, Roberto Tchio Talongwa, Luke Nyakarahuka, Edward J Mills, Iuri da Costa Leite, Semaw Ferede Abera, Ana C. Garcia, Ayse Abbasoglu Ozgoren, Matthew M Coates, Konstantinos Stroumpoulis, Bradford D. Gessner, Kebede Deribe, Tommi Vasankari, Logan Sandar, Kenji Shibuya, Karen M. Tabb, Troy Jacobs, Christopher J L Murray, Chakib Nejjari, Katherine T. Lofgren, Melvin Barrientos Marzan, Haidong Wang, Joanna Moschandreas, Raimundas Lunevicius, Nataliya Foigt, Rashmi Gupta, Ziad A. Memish, Victoria Pillay-van Wyk, Randah R. Hamadeh, Azmeraw T. Amare, Lalit Dandona, Uchechukwu K.A. Sampson, Monika Sawhney, Vasiliy Victorovich Vlassov, Farhad Islami, Palwasha Anwari, Mustafa Z. Younis, Amitava Banerjee, Ruben Castro, David O. Carpenter, Karzan Abdulmuhsin Mohammad, Taavi Lai, Yousef Khader, Sara Sheikhbahaei, Atte Meretoja, Zanfina Ademi, Ivo Rakovac, Yang Yang, Hilda L Harb, Daniel Pope, Jun She, Yichong Li, Andrew L. Thorne-Lyman, Adrian Davis, Stein Emil Vollset, Andre Pascal Kengne, Henry Apfel, Mark J. Nieuwenhuijsen, John J. McGrath, Yoshihiro Kokubo, Jonas Minet Kinge, Elisabete Weiderpass, Rajiv Chowdhury, Damian G Hoy, Jürgen C Schmidt, Seyed-Mohammad Fereshtehnejad, Harish Chander Gugnani, Hywel C Williams, Karen Edmond, Peter J. Allen, Marina Shakh-Nazarova, Tom Achoki, Edmond K. Kabagambe, Naohiro Yonemoto, Jun Zhu, Simon I. Hay, Karen J. Courville, Ketevan Goginashvili, Theo Vos, Kim Yun Jin, Kawkab Shishani, Lorenzo Monasta, H. Dean Hosgood, Uʇur Dilmen, Marcella Montico, Shankuan Zhu, Ami R. Moore, Marie Ng, Maigeng Zhou, Hebe N. Gouda, Linh N Bui, Sanjay Basu, Mouhanad Hammami, Mohammad T Mashal, Bryan K. Phillips, Marissa Iannarone, Ronan A Lyons, Young-Ho Khang, Robert G. Weintraub, Luca Ronfani, Daniel Kim, Alanur Çavlin, Ferrán Catalá-López, Ronny Westerman, Maia Kereselidze, Itamar S. Santos, Reza Assadi, Hwashin Hyun Shin, Carolina Maria Teixeira, Berrak Bora Basara, David Rojas-Rueda, Abdullah Sulieman Terkawi, Adansi A. Amankwaa, Nicholas J K Breitborde, Gokalp Kadri Yentur, Kaushalendra Kumar, Daniel Obadare Fijabi, Neeraj Bedi, Robert Quentin Reilly, Ana Maria Nogales Vasconcelos, Scott Weichenthal, Mark A. Green, Selen Begüm Uzun, Mukesh Dherani, Shams Eldin Ali Hassan Khalifa, Majed Asad, Jasvinder A. Singh, Angel J Paternina Caicedo, Eric L. Ding, Jost B. Jonas, Tolesa Bekele, Alan J Thomson, Steven E. Lipshultz, Rosario Cárdenas, Sajjad Ur Rahman, George A. Mensah, Jongmin Lee, Inga Dora Sigfusdottir, Mohammad Yahya Saeedi, Magdalena M. Muszyńska, Ulrich O Mueller, Stephen S Lim, Barthelemy Kuate Defo, Alan D. Lopez, Luciano A. Sposato, G Anil Kumar, Farshad Pourmalek, Zulfiqar A Bhutta, Maysaa El Sayed Zaki, Shiwei Liu, K.M. Venkat Narayan, William Msemburi, Ting Wu Chuang, Zewdie Aderaw Alemu, Saleem M Rana, Mohammad Taghi Hedayati, Mohsen Naghavi, Vegard Skirbekk, Walter Mendoza, Ali H. Mokdad, Yohannes Kinfu, Jean de Dieu Ngirabega, Takayoshi Ohkubo, Parfait Uwaliraye, Tasara T. Mazorodze, Farshad Farzadfar, Rob E. Dorrington, Mohammad A. AlMazroa, R. Kumar, Lesley Rushton, Wang, H, Liddell, Ca, Coates, Mm, Mooney, Md, Levitz, Ce, Schumacher, Ae, Apfel, H, Iannarone, M, Phillips, B, Lofgren, Kt, Sandar, L, Dorrington, Re, Rakovac, I, Jacobs, Ta, Liang, X, Zhou, M, Zhu, J, Yang, G, Wang, Y, Liu, S, Li, Y, Ozgoren, Aa, Abera, Sf, Abubakar, I, Achoki, T, Adelekan, A, Ademi, Z, Alemu, Za, Allen, Pj, Almazroa, Ma, Alvarez, E, Amankwaa, Aa, Amare, At, Ammar, W, Anwari, P, Cunningham, Sa, Asad, Mm, Assadi, R, Banerjee, A, Basu, S, Bedi, N, Bekele, T, Bell, Ml, Bhutta, Z, Blore, J, Basara, Bb, Boufous, S, Breitborde, N, Bruce, Ng, Bui, Ln, Carapetis, Jr, Cárdenas, R, Carpenter, Do, Caso, V, Castro, Re, Catalá Lopéz, F, Cavlin, A, Che, X, Chiang, Pp, Chowdhury, R, Christophi, Ca, Chuang, Tw, Cirillo, Massimo, da Costa Leite, I, Courville, Kj, Dandona, L, Dandona, R, Davis, A, Dayama, A, Deribe, K, Dharmaratne, Sd, Dherani, Mk, Dilmen, U, Ding, El, Edmond, Km, Ermakov, Sp, Farzadfar, F, Fereshtehnejad, Sm, Fijabi, Do, Foigt, N, Forouzanfar, Mh, Garcia, Ac, Geleijnse, Jm, Gessner, Bd, Goginashvili, K, Gona, P, Goto, A, Gouda, Hn, Green, Ma, Greenwell, Kf, Gugnani, Hc, Gupta, R, Hamadeh, Rr, Hammami, M, Harb, Hl, Hay, S, Hedayati, Mt, Hosgood, Hd, Hoy, Dg, Idrisov, Bt, Islami, F, Ismayilova, S, Jha, V, Jiang, G, Jonas, Jb, Juel, K, Kabagambe, Ek, Kazi, D, Kengne, Ap, Kereselidze, M, Khader, Y, Khalifa, Se, Khang, Yh, Kim, D, Kinfu, Y, Kinge, Jm, Kokubo, Y, Kosen, S, Defo, Bk, Kumar, Ga, Kumar, K, Kumar, Rb, Lai, T, Lan, Q, Larsson, A, Lee, Jt, Leinsalu, M, Lim, S, Lipshultz, Se, Logroscino, G, Lotufo, Pa, Lunevicius, R, Lyons, Ra, Ma, S, Mahdi, Aa, Marzan, Mb, Mashal, Mt, Mazorodze, Tt, Mcgrath, Jj, Memish, Za, Mendoza, W, Mensah, Ga, Meretoja, A, Miller, Tr, Mills, Ej, Mohammad, Ka, Mokdad, Ah, Monasta, L, Montico, M, Moore, Ar, Moschandreas, J, Msemburi, Wt, Mueller, Uo, Muszynska, Mm, Naghavi, M, Naidoo, K, Narayan, Kv, Nejjari, C, Ng, M, de Dieu Ngirabega, J, Nieuwenhuijsen, Mj, Nyakarahuka, L, Ohkubo, T, Omer, Sb, Caicedo, Aj, Wyk, Vp, Pope, D, Prabhakaran, D, Rahman, Su, Rana, Sm, Reilly, Rq, Rojas Rueda, D, Ronfani, L, Rushton, L, Saeedi, My, Salomon, J, Sampson, U, Santos, I, Sawhney, M, Schmidt, Jc, Shakh Nazarova, M, She, J, Sheikhbahaei, S, Shibuya, K, Shin, Hh, Shishani, K, Shiue, I, Sigfusdottir, Id, Singh, Ja, Skirbekk, V, Sliwa, K, Soshnikov, S, Sposato, La, Stathopoulou, Vk, Stroumpoulis, K, Tabb, Km, Talongwa, Rt, Teixeira, Cm, Terkawi, A, Thomson, Aj, Thorne Lyman, Al, Toyoshima, H, Dimbuene, Zt, Uwaliraye, P, Uzun, Sb, Vasankari, Tj, Vasconcelos, Am, Vlassov, Vv, Vollset, Se, Vos, T, Waller, S, Wan, X, Weichenthal, S, Weiderpass, E, Weintraub, Rg, Westerman, R, Wilkinson, Jd, Williams, Hc, Yang, Yc, Yentur, Gk, Yip, P, Yonemoto, N, Younis, M, Yu, C, Jin, Ky, El Sayed Zaki, M, Zhu, S, Lopez, Ad, and Murray, C. J.
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trends ,Pediatrics ,medicine.medical_specialty ,Nutrition and Disease ,democracy ,Developing country ,coverage ,VDP::Medisinske fag: 700::Helsefag: 800::Epidemiologi medisinsk og odontologisk statistikk: 803 ,millennium development goals ,Global Health ,survival ,03 medical and health sciences ,0302 clinical medicine ,Risk Factors ,030225 pediatrics ,Voeding en Ziekte ,Infant Mortality ,Global health ,Humans ,Organizational Objectives ,Medicine ,030212 general & internal medicine ,10. No inequality ,VLAG ,business.industry ,Mortality rate ,Infant, Newborn ,1. No poverty ,Infant ,health ,General Medicine ,Millennium Development Goals ,Infant mortality ,maternal education ,3. Good health ,Secular variation ,Child mortality ,Socioeconomic Factors ,income countries ,Child, Preschool ,Child Mortality ,developing-countries ,VDP::Midical sciences: 700::Health sciences: 800::Epidemiology, medical and dental statistics: 803 ,International development ,business ,Demography ,child-mortality - Abstract
Summary Background Remarkable financial and political efforts have been focused on the reduction of child mortality during the past few decades. Timely measurements of levels and trends in under-5 mortality are important to assess progress towards the Millennium Development Goal 4 (MDG 4) target of reduction of child mortality by two thirds from 1990 to 2015, and to identify models of success. Methods We generated updated estimates of child mortality in early neonatal (age 0–6 days), late neonatal (7–28 days), postneonatal (29–364 days), childhood (1–4 years), and under-5 (0–4 years) age groups for 188 countries from 1970 to 2013, with more than 29 000 survey, census, vital registration, and sample registration datapoints. We used Gaussian process regression with adjustments for bias and non-sampling error to synthesise the data for under-5 mortality for each country, and a separate model to estimate mortality for more detailed age groups. We used explanatory mixed effects regression models to assess the association between under-5 mortality and income per person, maternal education, HIV child death rates, secular shifts, and other factors. To quantify the contribution of these different factors and birth numbers to the change in numbers of deaths in under-5 age groups from 1990 to 2013, we used Shapley decomposition. We used estimated rates of change between 2000 and 2013 to construct under-5 mortality rate scenarios out to 2030. Findings We estimated that 6·3 million (95% UI 6·0–6·6) children under-5 died in 2013, a 64% reduction from 17·6 million (17·1–18·1) in 1970. In 2013, child mortality rates ranged from 152·5 per 1000 livebirths (130·6–177·4) in Guinea-Bissau to 2·3 (1·8–2·9) per 1000 in Singapore. The annualised rates of change from 1990 to 2013 ranged from −6·8% to 0·1%. 99 of 188 countries, including 43 of 48 countries in sub-Saharan Africa, had faster decreases in child mortality during 2000–13 than during 1990–2000. In 2013, neonatal deaths accounted for 41·6% of under-5 deaths compared with 37·4% in 1990. Compared with 1990, in 2013, rising numbers of births, especially in sub-Saharan Africa, led to 1·4 million more child deaths, and rising income per person and maternal education led to 0·9 million and 2·2 million fewer deaths, respectively. Changes in secular trends led to 4·2 million fewer deaths. Unexplained factors accounted for only −1% of the change in child deaths. In 30 developing countries, decreases since 2000 have been faster than predicted attributable to income, education, and secular shift alone. Interpretation Only 27 developing countries are expected to achieve MDG 4. Decreases since 2000 in under-5 mortality rates are accelerating in many developing countries, especially in sub-Saharan Africa. The Millennium Declaration and increased development assistance for health might have been a factor in faster decreases in some developing countries. Without further accelerated progress, many countries in west and central Africa will still have high levels of under-5 mortality in 2030. Funding Bill & Melinda Gates Foundation, US Agency for International Development.
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- 2014
33. Global, regional, and national levels of neonatal, infant, and under-5 mortality during 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013.
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Wang H, Liddell CA, Coates MM, Mooney MD, Levitz CE, Schumacher AE, Apfel H, Iannarone M, Phillips B, Lofgren KT, Sandar L, Dorrington RE, Rakovac I, Jacobs TA, Liang X, Zhou M, Zhu J, Yang G, Wang Y, Liu S, Li Y, Ozgoren AA, Abera SF, Abubakar I, Achoki T, Adelekan A, Ademi Z, Alemu ZA, Allen PJ, AlMazroa MA, Alvarez E, Amankwaa AA, Amare AT, Ammar W, Anwari P, Cunningham SA, Asad MM, Assadi R, Banerjee A, Basu S, Bedi N, Bekele T, Bell ML, Bhutta Z, Blore JD, Basara BB, Boufous S, Breitborde N, Bruce NG, Bui LN, Carapetis JR, Cárdenas R, Carpenter DO, Caso V, Castro RE, Catalá-Lopéz F, Cavlin A, Che X, Chiang PP, Chowdhury R, Christophi CA, Chuang TW, Cirillo M, da Costa Leite I, Courville KJ, Dandona L, Dandona R, Davis A, Dayama A, Deribe K, Dharmaratne SD, Dherani MK, Dilmen U, Ding EL, Edmond KM, Ermakov SP, Farzadfar F, Fereshtehnejad SM, Fijabi DO, Foigt N, Forouzanfar MH, Garcia AC, Geleijnse JM, Gessner BD, Goginashvili K, Gona P, Goto A, Gouda HN, Green MA, Greenwell KF, Gugnani HC, Gupta R, Hamadeh RR, Hammami M, Harb HL, Hay S, Hedayati MT, Hosgood HD, Hoy DG, Idrisov BT, Islami F, Ismayilova S, Jha V, Jiang G, Jonas JB, Juel K, Kabagambe EK, Kazi DS, Kengne AP, Kereselidze M, Khader YS, Khalifa SE, Khang YH, Kim D, Kinfu Y, Kinge JM, Kokubo Y, Kosen S, Defo BK, Kumar GA, Kumar K, Kumar RB, Lai T, Lan Q, Larsson A, Lee JT, Leinsalu M, Lim SS, Lipshultz SE, Logroscino G, Lotufo PA, Lunevicius R, Lyons RA, Ma S, Mahdi AA, Marzan MB, Mashal MT, Mazorodze TT, McGrath JJ, Memish ZA, Mendoza W, Mensah GA, Meretoja A, Miller TR, Mills EJ, Mohammad KA, Mokdad AH, Monasta L, Montico M, Moore AR, Moschandreas J, Msemburi WT, Mueller UO, Muszynska MM, Naghavi M, Naidoo KS, Narayan KM, Nejjari C, Ng M, de Dieu Ngirabega J, Nieuwenhuijsen MJ, Nyakarahuka L, Ohkubo T, Omer SB, Caicedo AJ, Pillay-van Wyk V, Pope D, Pourmalek F, Prabhakaran D, Rahman SU, Rana SM, Reilly RQ, Rojas-Rueda D, Ronfani L, Rushton L, Saeedi MY, Salomon JA, Sampson U, Santos IS, Sawhney M, Schmidt JC, Shakh-Nazarova M, She J, Sheikhbahaei S, Shibuya K, Shin HH, Shishani K, Shiue I, Sigfusdottir ID, Singh JA, Skirbekk V, Sliwa K, Soshnikov SS, Sposato LA, Stathopoulou VK, Stroumpoulis K, Tabb KM, Talongwa RT, Teixeira CM, Terkawi AS, Thomson AJ, Thorne-Lyman AL, Toyoshima H, Dimbuene ZT, Uwaliraye P, Uzun SB, Vasankari TJ, Vasconcelos AM, Vlassov VV, Vollset SE, Waller S, Wan X, Weichenthal S, Weiderpass E, Weintraub RG, Westerman R, Wilkinson JD, Williams HC, Yang YC, Yentur GK, Yip P, Yonemoto N, Younis M, Yu C, Jin KY, El Sayed Zaki M, Zhu S, Vos T, Lopez AD, and Murray CJ
- Subjects
- Child, Preschool, Global Health statistics & numerical data, Humans, Infant, Infant, Newborn, Organizational Objectives, Risk Factors, Socioeconomic Factors, Child Mortality trends, Global Health trends, Infant Mortality trends
- Abstract
Background: Remarkable financial and political efforts have been focused on the reduction of child mortality during the past few decades. Timely measurements of levels and trends in under-5 mortality are important to assess progress towards the Millennium Development Goal 4 (MDG 4) target of reduction of child mortality by two thirds from 1990 to 2015, and to identify models of success., Methods: We generated updated estimates of child mortality in early neonatal (age 0-6 days), late neonatal (7-28 days), postneonatal (29-364 days), childhood (1-4 years), and under-5 (0-4 years) age groups for 188 countries from 1970 to 2013, with more than 29,000 survey, census, vital registration, and sample registration datapoints. We used Gaussian process regression with adjustments for bias and non-sampling error to synthesise the data for under-5 mortality for each country, and a separate model to estimate mortality for more detailed age groups. We used explanatory mixed effects regression models to assess the association between under-5 mortality and income per person, maternal education, HIV child death rates, secular shifts, and other factors. To quantify the contribution of these different factors and birth numbers to the change in numbers of deaths in under-5 age groups from 1990 to 2013, we used Shapley decomposition. We used estimated rates of change between 2000 and 2013 to construct under-5 mortality rate scenarios out to 2030., Findings: We estimated that 6·3 million (95% UI 6·0-6·6) children under-5 died in 2013, a 64% reduction from 17·6 million (17·1-18·1) in 1970. In 2013, child mortality rates ranged from 152·5 per 1000 livebirths (130·6-177·4) in Guinea-Bissau to 2·3 (1·8-2·9) per 1000 in Singapore. The annualised rates of change from 1990 to 2013 ranged from -6·8% to 0·1%. 99 of 188 countries, including 43 of 48 countries in sub-Saharan Africa, had faster decreases in child mortality during 2000-13 than during 1990-2000. In 2013, neonatal deaths accounted for 41·6% of under-5 deaths compared with 37·4% in 1990. Compared with 1990, in 2013, rising numbers of births, especially in sub-Saharan Africa, led to 1·4 million more child deaths, and rising income per person and maternal education led to 0·9 million and 2·2 million fewer deaths, respectively. Changes in secular trends led to 4·2 million fewer deaths. Unexplained factors accounted for only -1% of the change in child deaths. In 30 developing countries, decreases since 2000 have been faster than predicted attributable to income, education, and secular shift alone., Interpretation: Only 27 developing countries are expected to achieve MDG 4. Decreases since 2000 in under-5 mortality rates are accelerating in many developing countries, especially in sub-Saharan Africa. The Millennium Declaration and increased development assistance for health might have been a factor in faster decreases in some developing countries. Without further accelerated progress, many countries in west and central Africa will still have high levels of under-5 mortality in 2030., Funding: Bill & Melinda Gates Foundation, US Agency for International Development., (Copyright © 2014 Elsevier Ltd. All rights reserved.)
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- 2014
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34. Noncardiac chest pain and psychopathology in children and adolescents.
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Lipsitz JD, Masia C, Apfel H, Marans Z, Gur M, Dent H, and Fyer AJ
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- Adolescent, Anxiety Disorders epidemiology, Chest Pain epidemiology, Child, Diagnostic and Statistical Manual of Mental Disorders, Electrocardiography, Female, Health Status, Humans, Male, Panic Disorder epidemiology, Prevalence, Psychophysiologic Disorders epidemiology, Anxiety Disorders diagnosis, Chest Pain diagnosis, Heart physiology, Panic Disorder diagnosis, Psychophysiologic Disorders diagnosis
- Abstract
Objective: We sought to examine the prevalence of DSM-IV psychiatric disorders in children and adolescents with complaints of noncardiac chest pain (NCCP)., Method: We assessed 27 youngsters (ages 8-17 years) referred to a pediatric cardiology practice with complaints of NCCP. Each child and a parent were interviewed using the Anxiety Disorders Interview Schedule for Children., Results: Sixteen youngsters (59%) were diagnosed with a current DSM-IV disorder. Fifteen (56%) had a current anxiety disorder, nine of whom were diagnosed with panic disorder. One participant was diagnosed with a depressive disorder., Conclusion: Results of this preliminary study suggest that DSM-IV anxiety disorders may be common in youngsters with NCCP. No evidence was found for high prevalence of depression in this sample. Larger controlled studies are needed to determine the prevalence and impact of psychopathology in youngsters with NCCP.
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- 2005
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35. Anxiety and depressive symptoms and anxiety sensitivity in youngsters with noncardiac chest pain and benign heart murmurs.
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Lipsitz JD, Masia-Warner C, Apfel H, Marans Z, Hellstern B, Forand N, Levenbraun Y, and Fyer AJ
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- Adolescent, Anxiety diagnosis, Chest Pain diagnosis, Child, Depression diagnosis, Female, Humans, Male, Sensitivity and Specificity, Surveys and Questionnaires, Anxiety epidemiology, Anxiety etiology, Chest Pain psychology, Depression epidemiology, Depression etiology
- Abstract
Objective: Chest pain in children and adolescents is rarely associated with cardiac disease. We sought to examine psychological symptoms in youngsters with medically unexplained chest pain. We hypothesized that children and adolescents with medically unexplained chest pain would have high rates of anxiety and depressive symptoms., Methods: We assessed 65 youngsters with noncardiac chest pain (NCCP) and 45 comparison youngsters with benign heart murmurs using self-report measures of anxiety and depressive symptoms and anxiety sensitivity., Results: Compared with the asymptomatic benign-murmur group, youngsters with NCCP had higher levels of some anxiety symptoms and anxiety sensitivity. Differences on depressive symptoms were not significant., Conclusions: Though preliminary, results suggest that youngsters with chest pain may experience increased levels of some psychological symptoms. Future studies of noncardiac chest pain in youngsters should include larger samples and comprehensive diagnostic assessments as well as long-term follow-up evaluations.
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- 2004
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36. Autodisplay: development of an efficacious system for surface display of antigenic determinants in Salmonella vaccine strains.
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Kramer U, Rizos K, Apfel H, Autenrieth IB, and Lattemann CT
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- Adhesins, Escherichia coli genetics, Adhesins, Escherichia coli metabolism, Animals, Antigens, Bacterial genetics, Antigens, Bacterial metabolism, Antigens, Surface genetics, Antigens, Surface metabolism, Chaperonin 60 genetics, Chaperonin 60 metabolism, Female, Gram-Negative Bacteria genetics, Gram-Negative Bacteria immunology, Immunization, Interferon-gamma metabolism, Mice, Mice, Inbred C57BL, Recombinant Fusion Proteins immunology, Salmonella Vaccines genetics, Salmonella Vaccines metabolism, T-Lymphocytes immunology, Adhesins, Escherichia coli immunology, Antigens, Bacterial immunology, Antigens, Surface immunology, Chaperonin 60 immunology, Genetic Vectors, Salmonella Vaccines immunology
- Abstract
To optimize antigen delivery by Salmonella vaccine strains, a system for surface display of antigenic determinants was established by using the autotransporter secretion pathway of gram-negative bacteria. A modular system for surface display allowed effective targeting of heterologous antigens or fragments thereof to the bacterial surface by the autotransporter domain of AIDA-I, the Escherichia coli adhesin involved in diffuse adherence. A major histocompatibility complex class II-restricted epitope, comprising amino acids 74 to 86 of the Yersinia enterocolitica heat shock protein Hsp60 (Hsp60(74-86)), was fused to the AIDA-I autotransporter domain, and the resulting fusion protein was expressed at high levels on the cell surface of E. coli and Salmonella enterica serovar Typhimurium. Colonization studies in mice vaccinated with Salmonella strains expressing AIDA-I fusion proteins demonstrated high genetic stability of the generated vaccine strain in vivo. Furthermore, a pronounced T-cell response against Yersinia Hsp60(74-86) was induced in mice vaccinated with a Salmonella vaccine strain expressing the Hsp60(74-86)-AIDA-I fusion protein. This was shown by monitoring Yersinia Hsp60-stimulated IFN-gamma secretion and proliferation of splenic T cells isolated from vaccinated mice. These results demonstrate that the surface display of antigenic determinants by the autotransporter pathway deserves special attention regarding the application in live attenuated Salmonella vaccine strains.
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- 2003
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37. Septation of the single ventricle: revisited.
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Margossian RE, Solowiejczyk D, Bourlon F, Apfel H, Gersony WM, Hordof AJ, and Quaegebeur J
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- Child, Child Welfare, Child, Preschool, Follow-Up Studies, Heart Septal Defects, Ventricular complications, Heart Septal Defects, Ventricular mortality, Heart Ventricles abnormalities, Humans, Infant, Infant Welfare, Length of Stay, Monaco, New York, Perioperative Care, Postoperative Complications etiology, Postoperative Complications mortality, Survival Analysis, Treatment Outcome, Ventricular Function, Left physiology, Fontan Procedure, Heart Septal Defects, Ventricular surgery, Heart Ventricles surgery
- Abstract
Background: Septation of a single ventricle into 2 functioning ventricles can provide an alternative to the Fontan operation. However, early experiences with septation reported unacceptable morbidity and mortality. The present study selected only those patients with large volume-overloaded hearts, 2 well-functioning atrioventricular valves, and an absence of severe outlet obstruction. Early and intermediate outcomes are evaluated., Methods and Results: Between June 1990 and March 1999, 11 patients underwent septation in 1 or 2 stages. Diagnoses of the patients included double-inlet left ventricle in 9, double-inlet right ventricle in 1 patient, and indeterminate ventricle in 1 patient. Five had l-transposition and 3 had d-transposition of the great arteries. Six had septation as 1 stage, 5 as planned 2-stage operations (2/5 completed). The median age for septation in 1 stage was 2.1 years (range 4 months to 5.8 years); for 2 stages, the median age was 7.2 months (range 3 to 14 months). Median follow-up time was 2.3 years. Eight of 11 patients survived (73%), with 2 early deaths and 1 late death. Seven of the 8 survivors have undergone complete septation (5 as single stage, 2 as 2 stages). Complications included surgically induced complete atrioventricular block in 1 patient and significant residual ventricular septal defects in another. Qualitatively, left ventricular function by echocardiography is normal in all patients, whereas right ventricular function is mildly decreased in 1 patient. All patients are clinically well., Conclusion: The septation procedure for single ventricle hearts may be a reasonable alternative to the Fontan operation in selected patients.
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- 2002
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38. Noninvasive prediction of pulmonary artery pressure in patients with isolated ventricular septal defect.
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Liberman L, Kaufman S, Alfayyadh M, Hordof AJ, and Apfel HD
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- Blood Pressure, Cardiac Catheterization, Child, Preschool, Humans, Infant, Predictive Value of Tests, Heart Septal Defects, Ventricular physiopathology, Pulmonary Artery physiopathology
- Abstract
Management of patients with isolated ventricular septal defect (VSD) requires information regarding pulmonary artery pressure (PAP). The purpose of this study was to evaluate the individual predictive value of noninvasive methods for assessment of PAP and to determine if any combination of techniques significantly improved their predictive power. We reviewed the clinical history, electrocardiogram, and echocardiogram of 31 patients (age 1.9 +/- 1. 73 years) who underwent catheterization for isolated VSD. Noninvasive data were compared for patients with mean PAP <20 mmHg (group 1) and those with mean PAP > or =20 (group 2) at catheterization. Fourteen (45%) patients were in group 1 and 17 (55%) in group 2. Doppler estimation of VSD gradient, right ventricular hypertrophy by echocardiogram, interventricular septal orientation, and VSD size had predictive value for elevated mean PAP (p < 0.01). All patients (n = 6) with normal findings in all four variables had normal PAP. All patients (n = 12) with at least three of four abnormal findings had elevated PAP. Six patients in group 1 had at least one variable that incorrectly predicted high PAP, whereas 3 patients with normal findings on three of the four variables nevertheless had elevated PAP. No single noninvasive variable accurately predicted PAP in all cases. However, normal findings for all four significant variables did predict normal PAP and suggest that cardiac catheterization is unnecessary in that setting. However, any other combination of normal and abnormal findings for the four significant variables did not reliably predict PAP and such patients may require catheterization to directly measure PAP.
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- 2000
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39. Up-regulation of extracellular copper/zinc superoxide dismutase mRNA after transmission of the filarial parasite Acanthocheilonema viteae in the vertebrate host Meriones unguiculatus.
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Lattemann CT, Matzen A, and Apfel H
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- Amino Acid Sequence, Animals, Dipetalonema Infections enzymology, Dipetalonema Infections transmission, Molecular Sequence Data, RNA, Helminth analysis, RNA, Messenger analysis, Reactive Oxygen Species metabolism, Sequence Homology, Amino Acid, Up-Regulation, Dipetalonema Infections veterinary, Gene Expression Regulation, Enzymologic, Gerbillinae parasitology, Rodent Diseases enzymology, Superoxide Dismutase genetics
- Abstract
The gene encoding the cytoplasmic copper/zinc superoxide dismutase (AVSOD1) from the filarial parasite Acanthocheilonema viteae was isolated from a genomic DNA library using a degenerate oligonucleotide probe. Additionally, cDNAs of the AVSOD1 and the secreted extracellular SOD (AVSOD2) were both cloned by RT-PCR, and the AVSOD2 was expressed at high levels in E. coli. The amino acid sequence of the AVSOD1 is 89.5 and 87.5% identical to that of the corresponding enzymes of Brugia pahangi and Onchocerca volvulus, respectively. In contrast, the AVSOD2 shows a lower degree of identity to the other filarial SODs and is extensively glycosylated. RT-PCR studies demonstrate the expression of both SOD subtypes in all developmental stages of A. viteae and indicate up-regulation of the AVSOD2 expression after transmission from the vector to the definitive host. This suggests an enhanced requirement for SOD activity in post-infective larval stages and adults of A. viteae. ELISAs performed with purified recombinant AVSOD2 show that the AVSOD2 is not a major target for the immune system in naturally infected jirds.
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- 1999
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40. Immunogenicity of the extracellular copper/zinc superoxide dismutase of the filarial parasite Acanthocheilonema viteae delivered by a two-phase vaccine strain of Salmonella typhimurium.
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Lattemann CT, Yan ZX, Matzen A, Meyer TF, and Apfel H
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- Administration, Oral, Animals, Antibodies, Helminth blood, Bacterial Vaccines immunology, Dipetalonema enzymology, Drug Carriers, Gerbillinae, Recombinant Proteins immunology, Salmonella typhimurium immunology, Superoxide Dismutase genetics, Antigens, Helminth immunology, Dipetalonema immunology, Superoxide Dismutase immunology
- Abstract
The recombinant extracellular copper/zinc superoxide dismutase of the filarial parasite Acanthocheilonema viteae (AVSOD2) was cloned in an expression vector under control of the bacteriophage T7 promoter and the resulting plasmid pLAT7 was introduced in tha aroA attenuated Salmonella typhimurium vaccine strain SL3261:pYZ84. This vaccine strain carries a chromosomally integrated two phase expression system containing inducible T7 RNA polymerase. The recombinant AVSOD2 was efficiently expressed, constituting up to 5% of the total bacterial protein. Furthermore, the plasmid vector containing the AVSOD2 cDNA was shown to be stable over a long period of time in the vaccine strain without antibiotic selection in vitro and in vivo. Jirds which were immunised orally with the recombinant vaccine strain expressing the A. viteae EC-SOD produced a strong humoral immune response.
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- 1999
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41. Regulation of ion channels in rat hepatocytes.
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Breit S, Kolb H, Apfel H, Haberland C, Schmitt M, Häussinger D, Graf J, and Lang F
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- Animals, Bucladesine pharmacology, Calcium pharmacology, Chloride Channels drug effects, Chloride Channels physiology, Colforsin pharmacology, Electric Conductivity, Humans, Ion Channel Gating, Ionomycin pharmacology, Membrane Potentials, Patch-Clamp Techniques, Potassium Channels drug effects, Potassium Channels physiology, Potassium Chloride pharmacology, Rats, Ion Channels physiology, Liver physiology
- Abstract
Patch-clamp studies have been performed to elucidate single ion channels in rat hepatocytes. In rat hepatocytes two types of ion channel have been identified: an inwardly rectifying K+ channel with a mean inward conductance of 55 +/- 6.5 pS (n = 20) and a mean outward conductance of 25 +/- 3.2 pS (n = 20) in the inside-out configuration with 145 mmol/l KCl on either side of the patch as well as an outwardly rectifying Cl- channel with a mean outward conductance of 30 +/- 4.5 pS (n = 8) and a mean inward conductance of 10 +/- 2.3 pS (n = 6) in the inside-out configuration with symmetrical 145 mmol/l KCl. The open probability of these channels is virtually insensitive to Ca2+ activity on the intracellular side. Accordingly, the Ca2+ ionophore ionomycin had no effect on cell membrane potential. Dibutyryl-cAMP (db-cAMP) hyperpolarizes the cell membrane and increases the activity of the 55-pS inwardly rectifying K+ channel by reducing the duration of closure between bursts. Forskolin similarly hyperpolarizes the cell membrane. The inwardly rectifying K+ channel is inhibited by progesterone, while the outwardly rectifying Cl- channel is insensitive to progesterone.
- Published
- 1998
- Full Text
- View/download PDF
42. Late left ventricular function after surgery for children with chronic symptomatic mitral regurgitation.
- Author
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Krishnan US, Gersony WM, Berman-Rosenzweig E, and Apfel HD
- Subjects
- Adolescent, Adult, Child, Child, Preschool, Chronic Disease, Echocardiography, Humans, Infant, Mitral Valve Insufficiency diagnostic imaging, Myocardial Contraction physiology, Postoperative Period, Risk Factors, Stroke Volume, Time Factors, Mitral Valve Insufficiency physiopathology, Mitral Valve Insufficiency surgery, Ventricular Function, Left physiology
- Abstract
Background: The use of quantitative echocardiography has been emphasized in optimizing timing of surgery in adult patients with mitral regurgitation to avoid irreversible left ventricular dysfunction. In contrast, surgery for infants and children is often delayed until the appearance of severe symptoms because of the patient's size and anticoagulation requirements and the possible need for early reoperation. The purpose of this study was to determine long-term ventricular function after mitral valve surgery in symptomatic children and to analyze risk factors for adverse outcome., Methods and Results: Thirty-three patients (0.5 to 19 years old) operated on for mitral regurgitation as a single hemodynamically significant lesion were studied. All but 3 had medically refractory symptoms. One patient died during surgery, and 32 were followed for 0.3 to 17.1 years (mean, 4.5 years). The mean preoperative left ventricular shortening fraction was 0.38+/-0.09. Successful mitral valvuloplasty or replacement was documented by long-term normalization of end-diastolic dimensions. Early postoperative shortening fraction was significantly reduced (0.28+/-0.1, P<.01), but it improved to 0.40+/-0.07 (P<.01) on late follow-up, at which time only 1 patient had ventricular dysfunction. Preoperative shortening fractions did not correlate well with early or late postoperative values (r=.18 and r=.31, respectively). Seven of 32 surviving patients had preoperative shortening fractions <0.33 (mean, 0.26+/-0.05) and 25 >0.33 (mean, 0.39+/-0.08). Analysis of these subgroups showed no significant differences between the groups in early or late postoperative function. Duration of mitral insufficiency appeared to be associated with the development of atrial arrhythmias., Conclusions: Late left ventricular function normalizes in children after surgical correction of mitral insufficiency. In contrast to adults, delay of surgery in children with significant mitral regurgitation until the onset of severe symptoms does not increase the risk for long-term ventricular dysfunction, although late atrial arrhythmias are more likely to be encountered.
- Published
- 1997
- Full Text
- View/download PDF
43. Comparison of three-dimensional echocardiographic assessment of volume, mass, and function in children with functionally single left ventricles with two-dimensional echocardiography and magnetic resonance imaging.
- Author
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Altmann K, Shen Z, Boxt LM, King DL, Gersony WM, Allan LD, and Apfel HD
- Subjects
- Adolescent, Adult, Child, Child, Preschool, Female, Heart Ventricles pathology, Heart Ventricles physiopathology, Humans, Infant, Male, Observer Variation, Reproducibility of Results, Stroke Volume, Echocardiography, Echocardiography, Three-Dimensional, Heart Ventricles abnormalities, Magnetic Resonance Imaging
- Abstract
Diminished systolic function or inappropriate hypertrophy are considered risk factors for outcome following the Fontan procedure. These parameters are difficult to assess in univentricular hearts that do not conform to the uniform shapes prescribed by conventional 2-dimensional imaging volume algorithms. Three-dimensional echocardiography requires no geometric assumptions and has been validated in both normal and distorted left ventricles. To assess the feasibility and accuracy of this technique in patients with univentricular hearts, we compared 2- and 3-dimensional echocardiographic estimates of ventricular volume, ejection fraction, and mass in patients with functionally single left ventricles with results obtained by magnetic resonance imaging (MRI). Twelve patients with functionally single left ventricles (6 months to 22 years) underwent examination by all 3 modalities. Correlation and agreement with MRI were calculated for volumes, ejection fraction, and mass. Three-dimensional echocardiographic comparison with MRI yielded a bias of 3.4 +/- 5.5 ml and 14.2 +/- 8.3 ml for systolic and diastolic volumes, respectively. Agreement analysis for mass showed a bias of 5.8 +/- 8.4 grams. Two-dimensional echocardiography showed less agreement for both volumes and mass (bias of -2.9 +/- 8.1, 2.9 +/- 10.4 ml and -8.3 +/- 12.0 g for volume and mass, respectively, p >0.05). Ejection fraction by 3-dimensional echocardiography showed significantly closer agreement with MRI (bias of 4.4 +/- 5.3%) than 2-dimensional echocardiography (bias of 8.5 +/- 10.3%, p = 0.04). Thus, 3-dimensional echocardiography provides estimates of ventricular volumes, ejection fraction, and mass that are comparable to MRI in this select group of patients with single ventricles of left ventricular morphology.
- Published
- 1997
- Full Text
- View/download PDF
44. PCR-based amplification of total cDNA with high fidelity and high yield from minute amounts of parasite RNA.
- Author
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Lattemann CT and Apfel H
- Subjects
- Animals, DNA Primers, Dipetalonema growth & development, Dipetalonema Infections parasitology, Female, Gerbillinae, Microfilariae genetics, RNA Precursors genetics, DNA, Complementary genetics, Dipetalonema genetics, Parasitology methods, Polymerase Chain Reaction methods, RNA, Helminth genetics
- Abstract
cDNA, synthesised from total RNA from Acanthocheilonema viteae, was amplified by PCR with a primer derived from the spliced leader 1 sequence of nematodes and oligo-dT. Due to the great number of side products observed in the reaction, a biotinylated oligo-dT primer was used for cDNA-synthesis and the first cycles of PCR. After binding of the PCR products to streptavidin/paramagnetic particles, the (+)strands of the cDNAs were recovered and reamplified. Analysis of the PCR products obtained revealed the presence of full-length cDNAs of at least 1.7 kbp in size in amplified total cDNA from microfilariae, postinfective L3, and adult worms. The total cDNA, from only 20 ex vivo recovered postinfective L3, was efficiently amplified.
- Published
- 1997
- Full Text
- View/download PDF
45. Radiological case of the month. Homozygous familial hypercholesterolemia.
- Author
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Apfel HD, Boxt LM, Wasserman HS, Jacobson MS, Reagen K, Starc TJ, and Wood BP
- Subjects
- Adolescent, Arterial Occlusive Diseases diagnosis, Coronary Angiography, Coronary Disease diagnosis, Exercise Test, Female, Humans, Magnetic Resonance Imaging, Homozygote, Hyperlipoproteinemia Type II genetics
- Published
- 1997
- Full Text
- View/download PDF
46. Feasibility of a two-dimensional echocardiographic method for the clinical assessment of right ventricular volume and function in children.
- Author
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Apfel HD, Solowiejczyk DE, Printz BF, Challenger M, Blood DK, Boxt LM, Barst RJ, and Gersony WM
- Subjects
- Adolescent, Adult, Child, Child, Preschool, Feasibility Studies, Female, Humans, Infant, Magnetic Resonance Imaging, Male, Radionuclide Angiography, Stroke Volume, Cardiac Volume, Echocardiography, Ventricular Function, Right
- Abstract
The relative ease of acquisition and safety of two-dimensional echocardiography has established it as the mainstay for routine cardiac imaging. Translation of imaging data into useful quantitative information, however, requires fitting the ventricle to a specific geometric model. Because of its complex shape and anterior position, many attempts at right ventricular quantitation by two-dimensional echocardiography have been criticized as impractical and not reproducible. A simple method incorporating subcostal and apical imaging was introduced in 1984. This approach appeared to combine accuracy and practicability but was never validated in a clinical setting because of the difficulties of subcostal imaging in adults. This study assessed the feasibility and accuracy of this technique in the pediatric population. Results of volume comparison to values derived by magnetic resonance imaging were r = 0.96, standard error of the estimate (SEE) = 19.3 ml, and mean difference = 15 +/- 19.4 ml and r = 0.97, SEE = 12.3 ml, and bias = 5 +/- 11.8 ml for diastolic and systolic volumes, respectively. Comparison of estimates of ejection fraction with magnetic resonance imaging demonstrated r = 0.90, SEE = 5.9%, and bias = 3% +/- 5.7%. Interobserver and intraobserver variability was 9.9% and 8.2%, respectively, for systolic volumes and 11.5% and 8.9%, respectively, for diastolic volumes. Evaluation of right ventricular size and function by this approach is comparable to determinations by magnetic resonance imaging and may be clinically useful in the management of pediatric patients.
- Published
- 1996
- Full Text
- View/download PDF
47. Tyrosine phosphorylation-dependent suppression of a voltage-gated K+ channel in T lymphocytes upon Fas stimulation.
- Author
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Szabò I, Gulbins E, Apfel H, Zhang X, Barth P, Busch AE, Schlottmann K, Pongs O, and Lang F
- Subjects
- Apoptosis, Benzoquinones, Electric Conductivity, Enzyme Inhibitors pharmacology, Humans, Ion Channel Gating, Lactams, Macrocyclic, Lymphocyte Specific Protein Tyrosine Kinase p56(lck), Membrane Potentials, Phosphorylation, Quinones pharmacology, Rifabutin analogs & derivatives, Signal Transduction, Tumor Cells, Cultured, src-Family Kinases antagonists & inhibitors, Phosphotyrosine metabolism, Potassium Channels metabolism, T-Lymphocytes metabolism, fas Receptor physiology
- Abstract
Selective cell death plays a critical role in the development of the immune system and in the elimination of target cells expressing foreign antigens. Most of programmed cell death occurs by apoptosis. Apoptotic cell death of lymphocytes can be triggered by ligation of APO-1/Fas (CD95) antigen (Suda, T., and Nagata, S. (1994) J. Exp. Med. 179, 873-879; Nagata, S., and Golstein, P. (1995) Science 267, 1449-1456). We find that activation of Fas leads to the inhibition of the voltage-dependent n-type K+ channels (Kv1.3) studied by patch clamp technique in Jurkat T lymphocytes. Tyrosine kinases have been shown to be crucial in Fas-induced cell death (Eischen, C. M., Dick, C. J., and Leibson, P. J. (1994) J. Immunol. 153, 1947-1954). The inhibition of the current is correlated with the tyrosine phosphorylation of immunoprecipitated and blotted K+ channel protein. We show, that the Src-like protein-tyrosine kinase inhibitor herbimycin A and the deficiency of the p56(lck) tyrosine kinase in mutant Jurkat cells abolished the channel inhibition and phosphorylation by anti-Fas antibody, while reconstitution of the p56(lck) kinase partly restored these effects of Fas receptor triggering. These results suggest a regulation of n-type K+ channels by tyrosine kinases upon Fas receptor triggering, which might be important for apoptosis.
- Published
- 1996
- Full Text
- View/download PDF
48. Ca2+ entry and vasoconstriction during osmotic swelling of vascular smooth muscle cells.
- Author
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Lang F, Busch GL, Zempel G, Ditlevsen J, Hoch M, Emerich U, Axel D, Fingerle J, Meierkord S, and Apfel H
- Subjects
- Animals, Aorta, Thoracic cytology, Aorta, Thoracic drug effects, Aorta, Thoracic metabolism, Cell Size physiology, Cells, Cultured, Electrophysiology, Fura-2, Guinea Pigs, Humans, Hydrogen-Ion Concentration, Hypotonic Solutions, In Vitro Techniques, Membrane Potentials drug effects, Membrane Potentials physiology, Muscle Tonus physiology, Muscle, Smooth, Vascular cytology, Muscle, Smooth, Vascular drug effects, Osmolar Concentration, Patch-Clamp Techniques, Vasoconstriction drug effects, Calcium Channels metabolism, Muscle, Smooth, Vascular metabolism, Vasoconstriction physiology
- Abstract
Exposure of aortic strips from guinea-pigs to hypotonic extracellular fluid is followed by marked vasoconstriction, which is inhibited by D-600 (3 microM), a blocker of voltage-sensitive Ca2+ channels. Conventional electrophysiology, patch-clamp studies, pH determination with 2',7' bis(2-carboxyethyl)-5,6-carboxyfluorescein (BCECF) and Ca2+ measurements with Fura-2 have been performed on smooth muscle cells cultured either from rat or human aorta to further elucidate the underlying mechanisms. Exposure of the cells to a 25% hypotonic extracellular fluid leads to a rapid and fully reversible depolarization, paralleled by an increase of the selectivity and conductance of the cell membrane to Cl-, an acidification of the cytoplasm and an increase of intracellular Ca2+ concentration ([Ca2+]i). The latter is inhibited by the Ca2+ channel blocker D-600 (1-3 microM). It is concluded that osmotic cell swelling leads to the activation of an anion channel. The subsequent depolarization of the cell membrane activates voltage-sensitive Ca2+ channels which increases [Ca2+]i, thus stimulating the contraction of vascular smooth muscle cells.
- Published
- 1995
- Full Text
- View/download PDF
49. Molecular cloning and characterization of an Echinococcus multilocularis and Echinococcus granulosus stress protein homologous to the mammalian 78 kDa glucose regulated protein.
- Author
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Mühlschlegel F, Frosch P, Castro A, Apfel H, Müller A, and Frosch M
- Subjects
- Amino Acid Sequence, Animals, Base Sequence, Cloning, Molecular, DNA Primers genetics, DNA, Helminth genetics, Endoplasmic Reticulum Chaperone BiP, Mammals, Molecular Sequence Data, Sequence Homology, Amino Acid, Carrier Proteins genetics, Echinococcus genetics, HSP70 Heat-Shock Proteins genetics, Heat-Shock Proteins, Helminth Proteins genetics, Molecular Chaperones genetics
- Published
- 1995
- Full Text
- View/download PDF
50. Changes in the surface composition after transmission of Acanthocheilonema viteae third stage larvae into the jird.
- Author
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Apfel H, Eisenbeiss WF, and Meyer TF
- Subjects
- Animals, Autoradiography, Carbohydrate Metabolism, Chromatography, Thin Layer, Dipetalonema growth & development, Female, Gerbillinae, Iodine Radioisotopes, Male, Membrane Lipids metabolism, Membrane Proteins metabolism, Cell Membrane metabolism, Dipetalonema metabolism, Dipetalonema Infections parasitology
- Abstract
This study describes the dynamics and the biochemical nature of changes in the surface of the filarial nematode Acanthocheilonema viteae after its transmission into the vertebrate host. Vector-derived third-stage larvae (mL3) were inoculated into naive Meriones unguiculatus and recovered from the tissues at different times post-infection until their moult to fourth-stage larvae (L4). Surface-specific labelling with fluoresceinated lectins revealed that the larvae are covered by a carbohydrate envelope. Although the mL3 envelope was strongly reduced one day after transmission, new surface carbohydrates appeared until the onset of moulting, some of which could also be identified on the surface of L4. In general, surface carbohydrates were partially shed by moving larvae, suggesting a loose association of these components in the epicuticle. The fate of cuticular lipids and proteins of L3 and L4 was monitored by external 125I-labelling and differential extraction of the components. Thin-layer chromatography of surface-labelled lipids revealed only minor changes 1 day after parasite transmission. Afterwards the number of lipids accessible to label decreased further until moulting was complete. Two-dimensional sodium dodecyl sulphate-polyacrylamide gel electrophoresis of surface-labelled proteins showed a consistent surface exposure of mL3 specific proteins until 1 day post-infection. Thereafter, the composition of surface-labelled proteins changed rapidly, resembling that of the L4 as early as several days before moulting. During this period individual differences in the composition of surface proteins were evident.
- Published
- 1992
- Full Text
- View/download PDF
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