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3. Health sector spending and spending on HIV/AIDS, tuberculosis, and malaria, and development assistance for health: progress towards Sustainable Development Goal 3

Author

Micah, A, Su, Y, Bachmeier, S, Chapin, A, Cogswell, I, Crosby, S, Cunningham, B, Harle, A, Maddison, E, Moitra, M, Sahu, M, Schneider, M, Simpson, K, Stutzman, H, Tsakalos, G, Zende, R, Zlavog, B, Abbafati, C, Abebo, Z, Abolhassani, H, Abrigo, M, Ahmed, M, Akinyemi, R, Alam, K, Ali, S, Alinia, C, Alipour, V, Aljunid, S, Almasi, A, Alvis-Guzman, N, Ancuceanu, R, Andrei, T, Andrei, C, Anjomshoa, M, Antonio, C, Arabloo, J, Arab-Zozani, M, Aremu, O, Atnafu, D, Ausloos, M, Avila-Burgos, L, Ayanore, M, Azari, S, Babalola, T, Bagherzadeh, M, Baig, A, Bakhtiari, A, Banach, M, Banerjee, S, Barnighausen, T, Basu, S, Baune, B, Bayati, M, Berman, A, Bhageerathy, R, Bhardwaj, P, Bohluli, M, Busse, R, Cahuana-Hurtado, L, Camera, L, Castaneda-Orjuela, C, Catala-Lopez, F, Cevik, M, Chattu, V, Dandona, L, Dandona, R, Dianatinasab, M, Do, H, Doshmangir, L, El Tantawi, M, Eskandarieh, S, Esmaeilzadeh, F, Faraj, A, Farzadfar, F, Fischer, F, Foigt, N, Fullman, N, Gad, M, Ghafourifard, M, Ghashghaee, A, Gholamian, A, Goharinezhad, S, Grada, A, Haghparast Bidgoli, H, Hamidi, S, Harb, H, Hasanpoor, E, Hay, S, Hendrie, D, Henry, N, Herteliu, C, Hole, M, Hosseinzadeh, M, Hostiuc, S, Huda, T, Humayun, A, Hwang, B, Ilesanmi, O, Iqbal, U, Irvani, S, Islam, S, Islam, M, Jahani, M, Jakovljevic, M, James, S, Javaheri, Z, Jonas, J, Joukar, F, Jozwiak, J, Jurisson, M, Kalhor, R, Karami Matin, B, Karimi, S, Kayode, G, Kazemi Karyani, A, Kinfu, Y, Kisa, A, Kohler, S, Komaki, H, Kosen, S, Kotlo, A, Koyanagi, A, Kumar, G, Kusuma, D, Lansingh, V, Larsson, A, Lasrado, S, Lee, S, Lim, L, Lozano, R, Magdy Abd El Razek, H, Mahdavi, M, Maleki, S, Malekzadeh, R, Mansour-Ghanaei, F, Mansournia, M, Mantovani, L, Martinez, G, Masoumi, S, Massenburg, B, Menezes, R, Mengesha, E, Meretoja, T, Meretoja, A, Mestrovic, T, Milevska Kostova, N, Miller, T, Mirica, A, Mirrakhimov, E, Moghadaszadeh, M, Mohajer, B, Mohamadi, E, Mohammad Darwesh, A, Mohammadian-Hafshejani, A, Mohammadpourhodki, R, Mohammed, S, Mohebi, F, Mokdad, A, Morrison, S, Mosser, J, Mousavi, S, Muriithi, M, Muthupandian, S, Myint, C, Naderi, M, Nagarajan, A, Nguyen, C, Nguyen, H, Nonvignon, J, Noubiap, J, Oh, I, Olagunju, A, Olusanya, J, Olusanya, B, Omar Bali, A, Onwujekwe, O, Otstavnov, S, Otstavnov, N, Owolabi, M, Padubidri, J, Palladino, R, Panda-Jonas, S, Pandey, A, Postma, M, Prada, S, Pribadi, D, Rabiee, M, Rabiee, N, Rahim, F, Ranabhat, C, Rao, S, Rathi, P, Rawaf, S, Rawaf, D, Rawal, L, Rawassizadeh, R, Rezapour, A, Sabour, S, Sahraian, M, Salman, O, Salomon, J, Samy, A, Sanabria, J, Santos, J, Santric Milicevic, M, Sao Jose, B, Savic, M, Schwendicke, F, Senthilkumaran, S, Sepanlou, S, Servan-Mori, E, Setayesh, H, Shaikh, M, Sheikh, A, Shibuya, K, Shrime, M, Simonetti, B, Singh, J, Singh, P, Skryabin, V, Soheili, A, Soltani, S, Stefan, S, Tabares-Seisdedos, R, Topor-Madry, R, Tovani-Palone, M, Tran, B, Travillian, R, Undurraga, E, Valdez, P, van Boven, J, Vasankari, T, Violante, F, Vlassov, V, Vos, T, Wolfe, C, Wu, J, Yaya, S, Yazdi-Feyzabadi, V, Yip, P, Yonemoto, N, Younis, M, Yu, C, Zaidi, Z, Zaman, S, Zastrozhin, M, Zhang, Z, Zhao, Y, Murray, C, Dieleman, J, Micah A. E., Su Y., Bachmeier S. D., Chapin A., Cogswell I. E., Crosby S. W., Cunningham B., Harle A. C., Maddison E. R., Moitra M., Sahu M., Schneider M. T., Simpson K. E., Stutzman H. N., Tsakalos G., Zende R. R., Zlavog B. S., Abbafati C., Abebo Z. H., Abolhassani H., Abrigo M. R. M., Ahmed M. B., Akinyemi R. O., Alam K., Ali S., Alinia C., Alipour V., Aljunid S. M., Almasi A., Alvis-Guzman N., Ancuceanu R., Andrei T., Andrei C. L., Anjomshoa M., Antonio C. A. T., Arabloo J., Arab-Zozani M., Aremu O., Atnafu D. D., Ausloos M., Avila-Burgos L., Ayanore M. A., Azari S., Babalola T. K., Bagherzadeh M., Baig A. A., Bakhtiari A., Banach M., Banerjee S. K., Barnighausen T. W., Basu S., Baune B. T., Bayati M., Berman A. E., Bhageerathy R., Bhardwaj P., Bohluli M., Busse R., Cahuana-Hurtado L., Camera L. L. A., Castaneda-Orjuela C. A., Catala-Lopez F., Cevik M., Chattu V. K., Dandona L., Dandona R., Dianatinasab M., Do H. T., Doshmangir L., El Tantawi M., Eskandarieh S., Esmaeilzadeh F., Faraj A., Farzadfar F., Fischer F., Foigt N. A., Fullman N., Gad M. M., Ghafourifard M., Ghashghaee A., Gholamian A., Goharinezhad S., Grada A., Haghparast Bidgoli H., Hamidi S., Harb H. L., Hasanpoor E., Hay S. I., Hendrie D., Henry N. J., Herteliu C., Hole M. K., Hosseinzadeh M., Hostiuc S., Huda T. M., Humayun A., Hwang B. -F., Ilesanmi O. S., Iqbal U., Irvani S. S. N., Islam S. M. S., Islam M. M., Jahani M. A., Jakovljevic M., James S. L., Javaheri Z., Jonas J. B., Joukar F., Jozwiak J. J., Jurisson M., Kalhor R., Karami Matin B., Karimi S. E., Kayode G. A., Kazemi Karyani A., Kinfu Y., Kisa A., Kohler S., Komaki H., Kosen S., Kotlo A., Koyanagi A., Kumar G. A., Kusuma D., Lansingh V. C., Larsson A. O., Lasrado S., Lee S. W. H., Lim L. -L., Lozano R., Magdy Abd El Razek H., Mahdavi M. M., Maleki S., Malekzadeh R., Mansour-Ghanaei F., Mansournia M. A., Mantovani L. G., Martinez G., Masoumi S. Z., Massenburg B. B., Menezes R. G., Mengesha E. W., Meretoja T. J., Meretoja A., Mestrovic T., Milevska Kostova N., Miller T. R., Mirica A., Mirrakhimov E. M., Moghadaszadeh M., Mohajer B., Mohamadi E., Mohammad Darwesh A., Mohammadian-Hafshejani A., Mohammadpourhodki R., Mohammed S., Mohebi F., Mokdad A. H., Morrison S. D., Mosser J. F., Mousavi S. M., Muriithi M. K., Muthupandian S., Myint C. -Y., Naderi M., Nagarajan A. J., Nguyen C. T., Nguyen H. L. T., Nonvignon J., Noubiap J. J., Oh I. -H., Olagunju A. T., Olusanya J. O., Olusanya B. O., Omar Bali A., Onwujekwe O. E., Otstavnov S. S., Otstavnov N., Owolabi M. O., Padubidri J. R., Palladino R., Panda-Jonas S., Pandey A., Postma M. J., Prada S. I., Pribadi D. R. A., Rabiee M., Rabiee N., Rahim F., Ranabhat C. L., Rao S. J., Rathi P., Rawaf S., Rawaf D. L., Rawal L., Rawassizadeh R., Rezapour A., Sabour S., Sahraian M. A., Salman O. M., Salomon J. A., Samy A. M., Sanabria J., Santos J. V., Santric Milicevic M. M., Sao Jose B. P., Savic M., Schwendicke F., Senthilkumaran S., Sepanlou S. G., Servan-Mori E., Setayesh H., Shaikh M. A., Sheikh A., Shibuya K., Shrime M. G., Simonetti B., Singh J. A., Singh P., Skryabin V. Y., Soheili A., Soltani S., Stefan S. C., Tabares-Seisdedos R., Topor-Madry R., Tovani-Palone M. R., Tran B. X., Travillian R., Undurraga E. A., Valdez P. R., van Boven J. F. M., Vasankari T. J., Violante F. S., Vlassov V., Vos T., Wolfe C. D. A., Wu J., Yaya S., Yazdi-Feyzabadi V., Yip P., Yonemoto N., Younis M. Z., Yu C., Zaidi Z., Zaman S. B., Zastrozhin M. S., Zhang Z. -J., Zhao Y., Murray C. J. L., Dieleman J. L., Micah, A, Su, Y, Bachmeier, S, Chapin, A, Cogswell, I, Crosby, S, Cunningham, B, Harle, A, Maddison, E, Moitra, M, Sahu, M, Schneider, M, Simpson, K, Stutzman, H, Tsakalos, G, Zende, R, Zlavog, B, Abbafati, C, Abebo, Z, Abolhassani, H, Abrigo, M, Ahmed, M, Akinyemi, R, Alam, K, Ali, S, Alinia, C, Alipour, V, Aljunid, S, Almasi, A, Alvis-Guzman, N, Ancuceanu, R, Andrei, T, Andrei, C, Anjomshoa, M, Antonio, C, Arabloo, J, Arab-Zozani, M, Aremu, O, Atnafu, D, Ausloos, M, Avila-Burgos, L, Ayanore, M, Azari, S, Babalola, T, Bagherzadeh, M, Baig, A, Bakhtiari, A, Banach, M, Banerjee, S, Barnighausen, T, Basu, S, Baune, B, Bayati, M, Berman, A, Bhageerathy, R, Bhardwaj, P, Bohluli, M, Busse, R, Cahuana-Hurtado, L, Camera, L, Castaneda-Orjuela, C, Catala-Lopez, F, Cevik, M, Chattu, V, Dandona, L, Dandona, R, Dianatinasab, M, Do, H, Doshmangir, L, El Tantawi, M, Eskandarieh, S, Esmaeilzadeh, F, Faraj, A, Farzadfar, F, Fischer, F, Foigt, N, Fullman, N, Gad, M, Ghafourifard, M, Ghashghaee, A, Gholamian, A, Goharinezhad, S, Grada, A, Haghparast Bidgoli, H, Hamidi, S, Harb, H, Hasanpoor, E, Hay, S, Hendrie, D, Henry, N, Herteliu, C, Hole, M, Hosseinzadeh, M, Hostiuc, S, Huda, T, Humayun, A, Hwang, B, Ilesanmi, O, Iqbal, U, Irvani, S, Islam, S, Islam, M, Jahani, M, Jakovljevic, M, James, S, Javaheri, Z, Jonas, J, Joukar, F, Jozwiak, J, Jurisson, M, Kalhor, R, Karami Matin, B, Karimi, S, Kayode, G, Kazemi Karyani, A, Kinfu, Y, Kisa, A, Kohler, S, Komaki, H, Kosen, S, Kotlo, A, Koyanagi, A, Kumar, G, Kusuma, D, Lansingh, V, Larsson, A, Lasrado, S, Lee, S, Lim, L, Lozano, R, Magdy Abd El Razek, H, Mahdavi, M, Maleki, S, Malekzadeh, R, Mansour-Ghanaei, F, Mansournia, M, Mantovani, L, Martinez, G, Masoumi, S, Massenburg, B, Menezes, R, Mengesha, E, Meretoja, T, Meretoja, A, Mestrovic, T, Milevska Kostova, N, Miller, T, Mirica, A, Mirrakhimov, E, Moghadaszadeh, M, Mohajer, B, Mohamadi, E, Mohammad Darwesh, A, Mohammadian-Hafshejani, A, Mohammadpourhodki, R, Mohammed, S, Mohebi, F, Mokdad, A, Morrison, S, Mosser, J, Mousavi, S, Muriithi, M, Muthupandian, S, Myint, C, Naderi, M, Nagarajan, A, Nguyen, C, Nguyen, H, Nonvignon, J, Noubiap, J, Oh, I, Olagunju, A, Olusanya, J, Olusanya, B, Omar Bali, A, Onwujekwe, O, Otstavnov, S, Otstavnov, N, Owolabi, M, Padubidri, J, Palladino, R, Panda-Jonas, S, Pandey, A, Postma, M, Prada, S, Pribadi, D, Rabiee, M, Rabiee, N, Rahim, F, Ranabhat, C, Rao, S, Rathi, P, Rawaf, S, Rawaf, D, Rawal, L, Rawassizadeh, R, Rezapour, A, Sabour, S, Sahraian, M, Salman, O, Salomon, J, Samy, A, Sanabria, J, Santos, J, Santric Milicevic, M, Sao Jose, B, Savic, M, Schwendicke, F, Senthilkumaran, S, Sepanlou, S, Servan-Mori, E, Setayesh, H, Shaikh, M, Sheikh, A, Shibuya, K, Shrime, M, Simonetti, B, Singh, J, Singh, P, Skryabin, V, Soheili, A, Soltani, S, Stefan, S, Tabares-Seisdedos, R, Topor-Madry, R, Tovani-Palone, M, Tran, B, Travillian, R, Undurraga, E, Valdez, P, van Boven, J, Vasankari, T, Violante, F, Vlassov, V, Vos, T, Wolfe, C, Wu, J, Yaya, S, Yazdi-Feyzabadi, V, Yip, P, Yonemoto, N, Younis, M, Yu, C, Zaidi, Z, Zaman, S, Zastrozhin, M, Zhang, Z, Zhao, Y, Murray, C, Dieleman, J, Micah A. E., Su Y., Bachmeier S. D., Chapin A., Cogswell I. E., Crosby S. W., Cunningham B., Harle A. C., Maddison E. R., Moitra M., Sahu M., Schneider M. T., Simpson K. E., Stutzman H. N., Tsakalos G., Zende R. R., Zlavog B. S., Abbafati C., Abebo Z. H., Abolhassani H., Abrigo M. R. M., Ahmed M. B., Akinyemi R. O., Alam K., Ali S., Alinia C., Alipour V., Aljunid S. M., Almasi A., Alvis-Guzman N., Ancuceanu R., Andrei T., Andrei C. L., Anjomshoa M., Antonio C. A. T., Arabloo J., Arab-Zozani M., Aremu O., Atnafu D. D., Ausloos M., Avila-Burgos L., Ayanore M. A., Azari S., Babalola T. K., Bagherzadeh M., Baig A. A., Bakhtiari A., Banach M., Banerjee S. K., Barnighausen T. W., Basu S., Baune B. T., Bayati M., Berman A. E., Bhageerathy R., Bhardwaj P., Bohluli M., Busse R., Cahuana-Hurtado L., Camera L. L. A., Castaneda-Orjuela C. A., Catala-Lopez F., Cevik M., Chattu V. K., Dandona L., Dandona R., Dianatinasab M., Do H. T., Doshmangir L., El Tantawi M., Eskandarieh S., Esmaeilzadeh F., Faraj A., Farzadfar F., Fischer F., Foigt N. A., Fullman N., Gad M. M., Ghafourifard M., Ghashghaee A., Gholamian A., Goharinezhad S., Grada A., Haghparast Bidgoli H., Hamidi S., Harb H. L., Hasanpoor E., Hay S. I., Hendrie D., Henry N. J., Herteliu C., Hole M. K., Hosseinzadeh M., Hostiuc S., Huda T. M., Humayun A., Hwang B. -F., Ilesanmi O. S., Iqbal U., Irvani S. S. N., Islam S. M. S., Islam M. M., Jahani M. A., Jakovljevic M., James S. L., Javaheri Z., Jonas J. B., Joukar F., Jozwiak J. J., Jurisson M., Kalhor R., Karami Matin B., Karimi S. E., Kayode G. A., Kazemi Karyani A., Kinfu Y., Kisa A., Kohler S., Komaki H., Kosen S., Kotlo A., Koyanagi A., Kumar G. A., Kusuma D., Lansingh V. C., Larsson A. O., Lasrado S., Lee S. W. H., Lim L. -L., Lozano R., Magdy Abd El Razek H., Mahdavi M. M., Maleki S., Malekzadeh R., Mansour-Ghanaei F., Mansournia M. A., Mantovani L. G., Martinez G., Masoumi S. Z., Massenburg B. B., Menezes R. G., Mengesha E. W., Meretoja T. J., Meretoja A., Mestrovic T., Milevska Kostova N., Miller T. R., Mirica A., Mirrakhimov E. M., Moghadaszadeh M., Mohajer B., Mohamadi E., Mohammad Darwesh A., Mohammadian-Hafshejani A., Mohammadpourhodki R., Mohammed S., Mohebi F., Mokdad A. H., Morrison S. D., Mosser J. F., Mousavi S. M., Muriithi M. K., Muthupandian S., Myint C. -Y., Naderi M., Nagarajan A. J., Nguyen C. T., Nguyen H. L. T., Nonvignon J., Noubiap J. J., Oh I. -H., Olagunju A. T., Olusanya J. O., Olusanya B. O., Omar Bali A., Onwujekwe O. E., Otstavnov S. S., Otstavnov N., Owolabi M. O., Padubidri J. R., Palladino R., Panda-Jonas S., Pandey A., Postma M. J., Prada S. I., Pribadi D. R. A., Rabiee M., Rabiee N., Rahim F., Ranabhat C. L., Rao S. J., Rathi P., Rawaf S., Rawaf D. L., Rawal L., Rawassizadeh R., Rezapour A., Sabour S., Sahraian M. A., Salman O. M., Salomon J. A., Samy A. M., Sanabria J., Santos J. V., Santric Milicevic M. M., Sao Jose B. P., Savic M., Schwendicke F., Senthilkumaran S., Sepanlou S. G., Servan-Mori E., Setayesh H., Shaikh M. A., Sheikh A., Shibuya K., Shrime M. G., Simonetti B., Singh J. A., Singh P., Skryabin V. Y., Soheili A., Soltani S., Stefan S. C., Tabares-Seisdedos R., Topor-Madry R., Tovani-Palone M. R., Tran B. X., Travillian R., Undurraga E. A., Valdez P. R., van Boven J. F. M., Vasankari T. J., Violante F. S., Vlassov V., Vos T., Wolfe C. D. A., Wu J., Yaya S., Yazdi-Feyzabadi V., Yip P., Yonemoto N., Younis M. Z., Yu C., Zaidi Z., Zaman S. B., Zastrozhin M. S., Zhang Z. -J., Zhao Y., Murray C. J. L., and Dieleman J. L.

Abstract

Background: Sustainable Development Goal (SDG) 3 aims to “ensure healthy lives and promote well-being for all at all ages”. While a substantial effort has been made to quantify progress towards SDG3, less research has focused on tracking spending towards this goal. We used spending estimates to measure progress in financing the priority areas of SDG3, examine the association between outcomes and financing, and identify where resource gains are most needed to achieve the SDG3 indicators for which data are available. Methods: We estimated domestic health spending, disaggregated by source (government, out-of-pocket, and prepaid private) from 1995 to 2017 for 195 countries and territories. For disease-specific health spending, we estimated spending for HIV/AIDS and tuberculosis for 135 low-income and middle-income countries, and malaria in 106 malaria-endemic countries, from 2000 to 2017. We also estimated development assistance for health (DAH) from 1990 to 2019, by source, disbursing development agency, recipient, and health focus area, including DAH for pandemic preparedness. Finally, we estimated future health spending for 195 countries and territories from 2018 until 2030. We report all spending estimates in inflation-adjusted 2019 US$, unless otherwise stated. Findings: Since the development and implementation of the SDGs in 2015, global health spending has increased, reaching $7·9 trillion (95% uncertainty interval 7·8–8·0) in 2017 and is expected to increase to $11·0 trillion (10·7–11·2) by 2030. In 2017, in low-income and middle-income countries spending on HIV/AIDS was $20·2 billion (17·0–25·0) and on tuberculosis it was $10·9 billion (10·3–11·8), and in malaria-endemic countries spending on malaria was $5·1 billion (4·9–5·4). Development assistance for health was $40·6 billion in 2019 and HIV/AIDS has been the health focus area to receive the highest contribution since 2004. In 2019, $374 million of DAH was provided for pandemic preparedness, less than 1% of

Published
2020

4. Future and potential spending on health 2015-40 : Development assistance for health, and government, prepaid private, and out-of-pocket health spending in 184 countries

Author

Dieleman, J. L., Campbell, M., Chapin, A., Eldrenkamp, E., Fan, V. Y., Haakenstad, A., Kates, J., Li, Z., Matyasz, T., Micah, A., Reynolds, A., Sadat, N., Schneider, M. T., Sorensen, R., Abbas, K. M., Abera, S. F., Ahmad Kiadaliri, A., Ahmed, M. B., Alam, K., Alizadeh-Navaei, R., Alkerwi, A., Amini, E., Ammar, W., Antonio, C. A. T., Atey, T. M., Avila-Burgos, L., Awasthi, A., Barac, A., Berheto, T. M., Beyene, A. S., Beyene, T. J., Birungi, C., Bizuayehu, H. M., Breitborde, N. J. K., Cahuana-Hurtado, L., Castro, R. E., Catalá-López, F., Dalal, Koustuv, Dandona, L., Dharmaratne, R. D. S. D., Dubey, M., Faro, A., Feigl, A. B., Fischer, F., Fitchett, J. R. A., Foigt, N., Giref, A. Z., Gupta, R., Hamidi, S., Harb, H. L., Hay, S. I., Hendrie, D., Horino, M., JÌrisson, M., Jakovljevic, M. B., Javanbakht, M., John, D., Jonas, J. B., Karimi, S. M., Khang, Y. -H, Khubchandani, J., Kim, Y. J., Kinge, J. M., Krohn, K. J., Kumar, G. A., Leung, R., Magdy Abd El Razek, H., Magdy Abd El Razek, M., Majeed, A., Malekzadeh, R., Malta, D. C., Meretoja, A., Miller, T. R., Mirrakhimov, E. M., Mohammed, S., Molla, G., Nangia, V., Olgiati, S., Owolabi, M. O., Patel, T., Paternina Caicedo, A. J., Pereira, D. M., Perelman, J., Polinder, S., Rafay, A., Rahimi-Movaghar, V., Rai, R. K., Ram, U., Ranabhat, C. L., Roba, H. S., Savic, M., Sepanlou, S. G., Te Ao, B. J., Tesema, A. G., Thomson, A. J., Tobe-Gai, R., Topor-Madry, R., Undurraga, E. A., Vargas, V., Vasankari, T., Violante, F. S., Wijeratne, T., Xu, G., Yonemoto, N., Younis, M. Z., Yu, C., Zaidi, Z., El Sayed Zaki, M., Murray, C. J. L., Network, Global Burden of Disease Health Financing Collaborator, Dieleman, J. L., Campbell, M., Chapin, A., Eldrenkamp, E., Fan, V. Y., Haakenstad, A., Kates, J., Li, Z., Matyasz, T., Micah, A., Reynolds, A., Sadat, N., Schneider, M. T., Sorensen, R., Abbas, K. M., Abera, S. F., Ahmad Kiadaliri, A., Ahmed, M. B., Alam, K., Alizadeh-Navaei, R., Alkerwi, A., Amini, E., Ammar, W., Antonio, C. A. T., Atey, T. M., Avila-Burgos, L., Awasthi, A., Barac, A., Berheto, T. M., Beyene, A. S., Beyene, T. J., Birungi, C., Bizuayehu, H. M., Breitborde, N. J. K., Cahuana-Hurtado, L., Castro, R. E., Catalá-López, F., Dalal, Koustuv, Dandona, L., Dharmaratne, R. D. S. D., Dubey, M., Faro, A., Feigl, A. B., Fischer, F., Fitchett, J. R. A., Foigt, N., Giref, A. Z., Gupta, R., Hamidi, S., Harb, H. L., Hay, S. I., Hendrie, D., Horino, M., JÌrisson, M., Jakovljevic, M. B., Javanbakht, M., John, D., Jonas, J. B., Karimi, S. M., Khang, Y. -H, Khubchandani, J., Kim, Y. J., Kinge, J. M., Krohn, K. J., Kumar, G. A., Leung, R., Magdy Abd El Razek, H., Magdy Abd El Razek, M., Majeed, A., Malekzadeh, R., Malta, D. C., Meretoja, A., Miller, T. R., Mirrakhimov, E. M., Mohammed, S., Molla, G., Nangia, V., Olgiati, S., Owolabi, M. O., Patel, T., Paternina Caicedo, A. J., Pereira, D. M., Perelman, J., Polinder, S., Rafay, A., Rahimi-Movaghar, V., Rai, R. K., Ram, U., Ranabhat, C. L., Roba, H. S., Savic, M., Sepanlou, S. G., Te Ao, B. J., Tesema, A. G., Thomson, A. J., Tobe-Gai, R., Topor-Madry, R., Undurraga, E. A., Vargas, V., Vasankari, T., Violante, F. S., Wijeratne, T., Xu, G., Yonemoto, N., Younis, M. Z., Yu, C., Zaidi, Z., El Sayed Zaki, M., Murray, C. J. L., and Network, Global Burden of Disease Health Financing Collaborator

Abstract

Background: The amount of resources, particularly prepaid resources, available for health can affect access to health care and health outcomes. Although health spending tends to increase with economic development, tremendous variation exists among health financing systems. Estimates of future spending can be beneficial for policy makers and planners, and can identify financing gaps. In this study, we estimate future gross domestic product (GDP), all-sector government spending, and health spending disaggregated by source, and we compare expected future spending to potential future spending. Methods: We extracted GDP, government spending in 184 countries from 1980-2015, and health spend data from 1995-2014. We used a series of ensemble models to estimate future GDP, all-sector government spending, development assistance for health, and government, out-of-pocket, and prepaid private health spending through 2040. We used frontier analyses to identify patterns exhibited by the countries that dedicate the most funding to health, and used these frontiers to estimate potential health spending for each low-income or middle-income country. All estimates are inflation and purchasing power adjusted. Findings: We estimated that global spending on health will increase from US$9.21 trillion in 2014 to $24.24 trillion (uncertainty interval [UI] 20.47-29.72) in 2040. We expect per capita health spending to increase fastest in upper-middle-income countries, at 5.3% (UI 4.1-6.8) per year. This growth is driven by continued growth in GDP, government spending, and government health spending. Lower-middle income countries are expected to grow at 4.2% (3.8-4.9). High-income countries are expected to grow at 2.1% (UI 1.8-2.4) and low-income countries are expected to grow at 1.8% (1.0-2.8). Despite this growth, health spending per capita in low-income countries is expected to remain low, at $154 (UI 133-181) per capita in 2030 and $195 (157-258) per capita in 2040. Increases in national hea

Published
2017
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5. Evolution and patterns of global health financing 1995-2014 : Development assistance for health, and government, prepaid private, and out-of-pocket health spending in 184 countries

Author

Dieleman, J., Campbell, M., Chapin, A., Eldrenkamp, E., Fan, V. Y., Haakenstad, A., Kates, J., Liu, Y., Matyasz, T., Micah, A., Reynolds, A., Sadat, N., Schneider, M. T., Sorensen, R., Evans, T., Evans, D., Kurowski, C., Tandon, A., Abbas, K. M., Abera, S. F., Ahmad Kiadaliri, A., Ahmed, K. Y., Ahmed, M. B., Alam, K., Alizadeh-Navaei, R., Alkerwi, A., Amini, E., Ammar, W., Amrock, S. M., Antonio, C. A. T., Atey, T. M., Avila-Burgos, L., Awasthi, A., Barac, A., Bernal, O. A., Beyene, A. S., Beyene, T. J., Birungi, C., Bizuayehu, H. M., Breitborde, N. J. K., Cahuana-Hurtado, L., Castro, R. E., Catalá-López, F., Dalal, Koustuv, Dandona, L., Dandona, R., De Jager, P., Dharmaratne, S. D., Dubey, M., Farinha, C. S. E. S., Faro, A., Feigl, A. B., Fischer, F., Fitchett, J. R. A., Foigt, N., Giref, A. Z., Gupta, R., Hamidi, S., Harb, H. L., Hay, S. I., Hendrie, D., Horino, M., JÌrisson, M., Jakovljevic, M. B., Javanbakht, M., John, D., Jonas, J. B., Karimi, S. M., Khang, Y. -H, Khubchandani, J., Kim, Y. J., Kinge, J. M., Krohn, K. J., Kumar, G. A., Magdy Abd El Razek, H., Magdy Abd El Razek, M., Majeed, A., Malekzadeh, R., Masiye, F., Meier, T., Meretoja, A., Miller, T. R., Mirrakhimov, E. M., Mohammed, S., Nangia, V., Olgiati, S., Osman, A. S., Owolabi, M. O., Patel, T., Paternina Caicedo, A. J., Pereira, D. M., Perelman, J., Polinder, S., Rafay, A., Rahimi-Movaghar, V., Rai, R. K., Ram, U., Ranabhat, C. L., Roba, H. S., Salama, J., Savic, M., Sepanlou, S. G., Shrime, M. G., Talongwa, R. T., Te Ao, B. J., Tediosi, F., Tesema, A. G., Thomson, A. J., Tobe-Gai, R., Topor-Madry, R., Undurraga, E. A., Vasankari, T., Violante, F. S., Werdecker, A., Wijeratne, T., Xu, G., Yonemoto, N., Younis, M. Z., Yu, C., Zaidi, Z., El Sayed Zaki, M., Murray, C. J. L., Network, Global Burden of Disease Health Financing Collaborator, Dieleman, J., Campbell, M., Chapin, A., Eldrenkamp, E., Fan, V. Y., Haakenstad, A., Kates, J., Liu, Y., Matyasz, T., Micah, A., Reynolds, A., Sadat, N., Schneider, M. T., Sorensen, R., Evans, T., Evans, D., Kurowski, C., Tandon, A., Abbas, K. M., Abera, S. F., Ahmad Kiadaliri, A., Ahmed, K. Y., Ahmed, M. B., Alam, K., Alizadeh-Navaei, R., Alkerwi, A., Amini, E., Ammar, W., Amrock, S. M., Antonio, C. A. T., Atey, T. M., Avila-Burgos, L., Awasthi, A., Barac, A., Bernal, O. A., Beyene, A. S., Beyene, T. J., Birungi, C., Bizuayehu, H. M., Breitborde, N. J. K., Cahuana-Hurtado, L., Castro, R. E., Catalá-López, F., Dalal, Koustuv, Dandona, L., Dandona, R., De Jager, P., Dharmaratne, S. D., Dubey, M., Farinha, C. S. E. S., Faro, A., Feigl, A. B., Fischer, F., Fitchett, J. R. A., Foigt, N., Giref, A. Z., Gupta, R., Hamidi, S., Harb, H. L., Hay, S. I., Hendrie, D., Horino, M., JÌrisson, M., Jakovljevic, M. B., Javanbakht, M., John, D., Jonas, J. B., Karimi, S. M., Khang, Y. -H, Khubchandani, J., Kim, Y. J., Kinge, J. M., Krohn, K. J., Kumar, G. A., Magdy Abd El Razek, H., Magdy Abd El Razek, M., Majeed, A., Malekzadeh, R., Masiye, F., Meier, T., Meretoja, A., Miller, T. R., Mirrakhimov, E. M., Mohammed, S., Nangia, V., Olgiati, S., Osman, A. S., Owolabi, M. O., Patel, T., Paternina Caicedo, A. J., Pereira, D. M., Perelman, J., Polinder, S., Rafay, A., Rahimi-Movaghar, V., Rai, R. K., Ram, U., Ranabhat, C. L., Roba, H. S., Salama, J., Savic, M., Sepanlou, S. G., Shrime, M. G., Talongwa, R. T., Te Ao, B. J., Tediosi, F., Tesema, A. G., Thomson, A. J., Tobe-Gai, R., Topor-Madry, R., Undurraga, E. A., Vasankari, T., Violante, F. S., Werdecker, A., Wijeratne, T., Xu, G., Yonemoto, N., Younis, M. Z., Yu, C., Zaidi, Z., El Sayed Zaki, M., Murray, C. J. L., and Network, Global Burden of Disease Health Financing Collaborator

Abstract

Background: An adequate amount of prepaid resources for health is important to ensure access to health services and for the pursuit of universal health coverage. Previous studies on global health financing have described the relationship between economic development and health financing. In this study, we further explore global health financing trends and examine how the sources of funds used, types of services purchased, and development assistance for health disbursed change with economic development. We also identify countries that deviate from the trends. Methods: We estimated national health spending by type of care and by source, including development assistance for health, based on a diverse set of data including programme reports, budget data, national estimates, and 964 National Health Accounts. These data represent health spending for 184 countries from 1995 through 2014. We converted these data into a common inflation-adjusted and purchasing power-adjusted currency, and used non-linear regression methods to model the relationship between health financing, time, and economic development. Findings: Between 1995 and 2014, economic development was positively associated with total health spending and a shift away from a reliance on development assistance and out-of-pocket (OOP) towards government spending. The largest absolute increase in spending was in high-income countries, which increased to purchasing power-adjusted $5221 per capita based on an annual growth rate of 3.0%. The largest health spending growth rates were in upper-middle-income (5.9) and lower-middle-income groups (5.0), which both increased spending at more than 5% per year, and spent $914 and $267 per capita in 2014, respectively. Spending in low-income countries grew nearly as fast, at 4.6%, and health spending increased from $51 to $120 per capita. In 2014, 59.2% of all health spending was financed by the government, although in low-income and lower-middle-income countries, 29.1% and 58.0%

Published
2017
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6. Regulation of the Raf-1 kinase domain by phosphorylation and 14-3-3 association

Author

Yip-Schneider, M T, Miao, W, Lin, A, Barnard, D S, Tzivion, G, and Marshall, M S

Subjects
Tyrosine 3-Monooxygenase, hemic and immune systems, Binding, Competitive, Peptide Fragments, Oncogene Protein pp60(v-src), Protein Structure, Tertiary, Enzyme Activation, Proto-Oncogene Proteins c-raf, Phosphoserine, 14-3-3 Proteins, Catalytic Domain, COS Cells, Mutation, Animals, Tetradecanoylphorbol Acetate, Phosphorylation, Research Article, Protein Binding
Abstract

The Raf-1 kinase domain is kept in an inactive state by the N-terminal regulatory domain. Activation of the kinase domain occurs following release from the N-terminal repression and possible catalytic upregulation. To distinguish the regulatory mechanisms that directly influence the catalytic activity of the enzyme from those which act through the inhibitory domain, the catalytic domain of Raf-1 (CR3) was expressed in COS-7 cells. The role of phosphorylation in the direct regulation of this domain was determined by substituting non-phosphorylatable amino acids for known serine and tyrosine phosphorylation sites. The intrinsic activity of each mutant protein was determined as well as stimulation by v-Src and phorbol esters. Both v-Src and phorbol esters were potent activators of CR3, requiring the serine 338/339 (p21-activated protein kinase, Pak) and tyrosine 340/341 (Src) phosphorylation sites for full stimulation of CR3. In contrast, loss of the serine 497/499 protein kinase C phosphorylation sites had little effect on CR3 activation by either v-Src or phorbol esters. Loss of serine 621, a 14-3-3 adaptor-protein-binding site, prevented activation of CR3 by v-Src or phorbol esters and partially decreased the high basal activity of the kinase fragment. When co-expressed in COS-7 cells, 14-3-3 associated strongly with full-length Raf-1, weakly with wild-type CR3 and not at all with the A621 and D621 CR3 mutants. The role of 14-3-3 in maintaining the activity of the catalytic domain of Raf-1 was investigated further by performing peptide-competition studies with wild-type CR3, wild-type CR3 and v-Src or constitutively active CR3 (CR3[YY340/341DD]). In each case, incubation of the proteins with a phosphoserine-621 Raf-1 peptide, which we show displaced Raf-1 and CR3[YY340/341DD] from 14-3-3, was found to substantially reduce catalytic activity. Taken together, our results support a model of Raf regulation in which the activity of the Raf-1 catalytic domain is directly upregulated by phosphorylation, following relief of inhibition by the N-terminal regulatory domain upon Ras-GTP binding. Moreover, the presence of serine 621 in the free catalytic fragment is required for full CR3 activation by stimulatory factors, and the continuous presence of 14-3-3 at this site is necessary for retaining activity once the kinase is activated.

Published
2000

9. Health sector spending and spending on HIV/AIDS, tuberculosis, and malaria, and development assistance for health: progress towards Sustainable Development Goal 3

Author

Priya Rathi, Ritesh G. Menezes, Edris Hasanpoor, Sanni Yaya, Mohsen Bayati, Maciej Banach, Raffaele Palladino, Mikhail Sergeevich Zastrozhin, Siamak Sabour, Theo Vos, Tuomo J. Meretoja, Dimas Ria Angga Pribadi, Shahin Soltani, Simona Cătălina Ștefan, Behzad Karami Matin, Cyrus Alinia, Tudorel Andrei, Mehdi Bohluli, Nikita Otstavnov, Yanfang Su, Mohammad Ali Mansournia, Simon I. Hay, Mansour Ghafourifard, Songhomitra Panda-Jonas, Pushpendra Singh, Salman Rawaf, Morteza Arab-Zozani, Robert Ancuceanu, Samer Hamidi, Maarten J. Postma, Vijay Kumar Chattu, Ted R. Miller, Stanislav S. Otstavnov, Gbenga A. Kayode, Chhabi Lal Ranabhat, João Vasco Santos, Savita Lasrado, Jonathan F. Mosser, Chaw Yin Myint, Mihajlo Jakovljevic, Masoud Moghadaszadeh, Tanvir M. Huda, Fakher Rahim, Seyedeh Zahra Masoumi, Yingxi Zhao, Aziz Sheikh, Subramanian Senthilkumaran, Sheikh Mohammed Shariful Islam, Fariborz Mansour-Ghanaei, Andrew T Olagunju, Atif Amin Baig, Ali H. Mokdad, Anders Larsson, Atte Meretoja, Bach Xuan Tran, Lal B. Rawal, Brandon Cunningham, Vahid Alipour, Sowmya J. Rao, Anamika Pandey, Vahid Yazdi-Feyzabadi, Salime Goharinezhad, Angela E Micah, Leticia Avila-Burgos, Hayley N Stutzman, Farshad Farzadfar, M. Mofizul Islam, Sharareh Eskandarieh, Saqib Ali, Srikanta Banerjee, Zhi-Jiang Zhang, Anirudh Kotlo, Ravensara S. Travillian, Aziz Rezapour, Huong Lan Thi Nguyen, Sergio I. Prada, Biagio Simonetti, Maitreyi Sahu, Sadaf G. Sepanlou, Carlos A Castañeda-Orjuela, Hoa Thi Do, Farahnaz Joukar, Aso Mohammad Darwesh, Syed Mohamed Aljunid, Modhurima Moitra, In-Hwan Oh, Ayman Grada, Kenji Shibuya, Sojib Bin Zaman, Steven D Bachmeier, Hilda L Harb, Edson Serván-Mori, Bahram Mohajer, Van C. Lansingh, Ali Almasi, German Martinez, Till Bärnighausen, Reza Malekzadeh, Adam E. Berman, Matthew T. Schneider, Michael K. Hole, Reza Rawassizadeh, Bing-Fang Hwang, Bianca S. Zlavog, Mohammad Rabiee, Moses K. Muriithi, Anton C Harle, Mokhtar Mahdavi, Yohannes Kinfu, Olatunde Aremu, Cristiana Abbafati, Nelson Alvis-Guzman, Joseph L Dieleman, Lucero Cahuana-Hurtado, Abdollah Mohammadian-Hafshejani, Soewarta Kosen, Zeleke Hailemariam Abebo, Muge Cevik, Hassan Abolhassani, Farnam Mohebi, Job F M van Boven, Nataliya Foigt, Neda Milevska Kostova, Abdallah M. Samy, Roman Topor-Madry, Golsum Tsakalos, Benjamin B. Massenburg, Spencer L. James, Erkin M. Mirrakhimov, Miloje Savic, Mehdi Hosseinzadeh, Sawyer W Crosby, Ayesha Humayun, Hamidreza Setayesh, G Anil Kumar, Juan Sanabria, Jalal Arabloo, Milena M Santric Milicevic, Ai Koyanagi, Shokofeh Maleki, Junjie Wu, Nathaniel J Henry, Efat Mohamadi, Francesco Saverio Violante, Samad Azari, Delia Hendrie, Ahad Bakhtiari, Olayinka Stephen Ilesanmi, Pankaj Bhardwaj, Ahamarshan Jayaraman Nagarajan, Adnan Kisa, Masood Ali Shaikh, Shafiu Mohammed, Justice Nonvignon, Firooz Esmaeilzadeh, Eduardo A. Undurraga, Khurshid Alam, Muktar Beshir Ahmed, Mohamed M. Gad, Mikk Jürisson, Usman Iqbal, Chuanhua Yu, Luis Camera, Mohammad Ali Jahani, Abigail Chapin, Pascual R. Valdez, Reinhard Busse, Tomislav Mestrovic, Paul S. F. Yip, Christopher J L Murray, Jacob Olusegun Olusanya, Salah Eddin Karimi, Mustafa Z. Younis, Michael R.M. Abrigo, Rahul R. Zende, Mina Anjomshoa, Shane D. Morrison, Marcel Ausloos, Bruno Piassi Sao Jose, Zohre Javaheri, Saravanan Muthupandian, Valentin Yurievich Skryabin, Endalkachew Worku Mengesha, Lalit Dandona, Jacek Jerzy Jozwiak, Omar Mukhtar Salman, Rakhi Dandona, Mojtaba Bagherzadeh, Mostafa Dianatinasab, Reza Mohammadpourhodki, Seyed Sina Naghibi Irvani, Nancy Fullman, Claudiu Herteliu, Andreea Mirica, Jasvinder A. Singh, Amin Soheili, Lee Ling Lim, Charles D.A. Wolfe, Catalina Liliana Andrei, Ali Kazemi Karyani, Bolajoko O. Olusanya, Carl Abelardo T. Antonio, Tommi Vasankari, Jean Jacques Noubiap, Mehdi Naderi, Jagadish Rao Padubidri, Bernhard T. Baune, Navid Rabiee, Mark G. Shrime, Mayowa O. Owolabi, Lorenzo G. Mantovani, Desta Debalkie Atnafu, Vasily Vlassov, Kyle E. Simpson, Sorin Hostiuc, Shaun Wen Huey Lee, Cuong Tat Nguyen, Ian E Cogswell, Tesleem Kayode Babalola, Sanjay Basu, Hassan Haghparast Bidgoli, Leila Doshmangir, Marcos Roberto Tovani-Palone, Maha El Tantawi, Obinna Onwujekwe, Mohammad Ali Sahraian, Ahmed Omar Bali, Joshua A. Salomon, Hamidreza Komaki, David Laith Rawaf, Zoubida Zaidi, Hassan Magdy Abd El Razek, Reshmi Bhageerathy, Emilie R Maddison, Naohiro Yonemoto, Ahmad Ghashghaee, Asadollah Gholamian, Ferrán Catalá-López, Stefan Kohler, Rafael Tabarés-Seisdedos, Anwar Faraj, Rafael Lozano, Rufus Akinyemi, Florian Fischer, Jost B. Jonas, Dian Kusuma, Martin Amogre Ayanore, Rohollah Kalhor, Falk Schwendicke, Seyyed Meysam Mousavi, Micah, A. E., Su, Y., Bachmeier, S. D., Chapin, A., Cogswell, I. E., Crosby, S. W., Cunningham, B., Harle, A. C., Maddison, E. R., Moitra, M., Sahu, M., Schneider, M. T., Simpson, K. E., Stutzman, H. N., Tsakalos, G., Zende, R. R., Zlavog, B. S., Abbafati, C., Abebo, Z. H., Abolhassani, H., Abrigo, M. R. M., Ahmed, M. B., Akinyemi, R. O., Alam, K., Ali, S., Alinia, C., Alipour, V., Aljunid, S. M., Almasi, A., Alvis-Guzman, N., Ancuceanu, R., Andrei, T., Andrei, C. L., Anjomshoa, M., Antonio, C. A. T., Arabloo, J., Arab-Zozani, M., Aremu, O., Atnafu, D. D., Ausloos, M., Avila-Burgos, L., Ayanore, M. A., Azari, S., Babalola, T. K., Bagherzadeh, M., Baig, A. A., Bakhtiari, A., Banach, M., Banerjee, S. K., Barnighausen, T. W., Basu, S., Baune, B. T., Bayati, M., Berman, A. E., Bhageerathy, R., Bhardwaj, P., Bohluli, M., Busse, R., Cahuana-Hurtado, L., Camera, L. L. A., Castaneda-Orjuela, C. A., Catala-Lopez, F., Cevik, M., Chattu, V. K., Dandona, L., Dandona, R., Dianatinasab, M., Do, H. T., Doshmangir, L., El Tantawi, M., Eskandarieh, S., Esmaeilzadeh, F., Faraj, A., Farzadfar, F., Fischer, F., Foigt, N. A., Fullman, N., Gad, M. M., Ghafourifard, M., Ghashghaee, A., Gholamian, A., Goharinezhad, S., Grada, A., Haghparast Bidgoli, H., Hamidi, S., Harb, H. L., Hasanpoor, E., Hay, S. I., Hendrie, D., Henry, N. J., Herteliu, C., Hole, M. K., Hosseinzadeh, M., Hostiuc, S., Huda, T. M., Humayun, A., Hwang, B. -F., Ilesanmi, O. S., Iqbal, U., Irvani, S. S. N., Islam, S. M. S., Islam, M. M., Jahani, M. A., Jakovljevic, M., James, S. L., Javaheri, Z., Jonas, J. B., Joukar, F., Jozwiak, J. J., Jurisson, M., Kalhor, R., Karami Matin, B., Karimi, S. E., Kayode, G. A., Kazemi Karyani, A., Kinfu, Y., Kisa, A., Kohler, S., Komaki, H., Kosen, S., Kotlo, A., Koyanagi, A., Kumar, G. A., Kusuma, D., Lansingh, V. C., Larsson, A. O., Lasrado, S., Lee, S. W. H., Lim, L. -L., Lozano, R., Magdy Abd El Razek, H., Mahdavi, M. M., Maleki, S., Malekzadeh, R., Mansour-Ghanaei, F., Mansournia, M. A., Mantovani, L. G., Martinez, G., Masoumi, S. Z., Massenburg, B. B., Menezes, R. G., Mengesha, E. W., Meretoja, T. J., Meretoja, A., Mestrovic, T., Milevska Kostova, N., Miller, T. R., Mirica, A., Mirrakhimov, E. M., Moghadaszadeh, M., Mohajer, B., Mohamadi, E., Mohammad Darwesh, A., Mohammadian-Hafshejani, A., Mohammadpourhodki, R., Mohammed, S., Mohebi, F., Mokdad, A. H., Morrison, S. D., Mosser, J. F., Mousavi, S. M., Muriithi, M. K., Muthupandian, S., Myint, C. -Y., Naderi, M., Nagarajan, A. J., Nguyen, C. T., Nguyen, H. L. T., Nonvignon, J., Noubiap, J. J., Oh, I. -H., Olagunju, A. T., Olusanya, J. O., Olusanya, B. O., Omar Bali, A., Onwujekwe, O. E., Otstavnov, S. S., Otstavnov, N., Owolabi, M. O., Padubidri, J. R., Palladino, R., Panda-Jonas, S., Pandey, A., Postma, M. J., Prada, S. I., Pribadi, D. R. A., Rabiee, M., Rabiee, N., Rahim, F., Ranabhat, C. L., Rao, S. J., Rathi, P., Rawaf, S., Rawaf, D. L., Rawal, L., Rawassizadeh, R., Rezapour, A., Sabour, S., Sahraian, M. A., Salman, O. M., Salomon, J. A., Samy, A. M., Sanabria, J., Santos, J. V., Santric Milicevic, M. M., Sao Jose, B. P., Savic, M., Schwendicke, F., Senthilkumaran, S., Sepanlou, S. G., Servan-Mori, E., Setayesh, H., Shaikh, M. A., Sheikh, A., Shibuya, K., Shrime, M. G., Simonetti, B., Singh, J. A., Singh, P., Skryabin, V. Y., Soheili, A., Soltani, S., Stefan, S. C., Tabares-Seisdedos, R., Topor-Madry, R., Tovani-Palone, M. R., Tran, B. X., Travillian, R., Undurraga, E. A., Valdez, P. R., van Boven, J. F. M., Vasankari, T. J., Violante, F. S., Vlassov, V., Vos, T., Wolfe, C. D. A., Wu, J., Yaya, S., Yazdi-Feyzabadi, V., Yip, P., Yonemoto, N., Younis, M. Z., Yu, C., Zaidi, Z., Zaman, S. B., Zastrozhin, M. S., Zhang, Z. -J., Zhao, Y., Murray, C. J. L., Dieleman, J. L., Global Burden of Disease Health Financing Collaborator Network, Violante FS, Micah, A, Su, Y, Bachmeier, S, Chapin, A, Cogswell, I, Crosby, S, Cunningham, B, Harle, A, Maddison, E, Moitra, M, Sahu, M, Schneider, M, Simpson, K, Stutzman, H, Tsakalos, G, Zende, R, Zlavog, B, Abbafati, C, Abebo, Z, Abolhassani, H, Abrigo, M, Ahmed, M, Akinyemi, R, Alam, K, Ali, S, Alinia, C, Alipour, V, Aljunid, S, Almasi, A, Alvis-Guzman, N, Ancuceanu, R, Andrei, T, Andrei, C, Anjomshoa, M, Antonio, C, Arabloo, J, Arab-Zozani, M, Aremu, O, Atnafu, D, Ausloos, M, Avila-Burgos, L, Ayanore, M, Azari, S, Babalola, T, Bagherzadeh, M, Baig, A, Bakhtiari, A, Banach, M, Banerjee, S, Barnighausen, T, Basu, S, Baune, B, Bayati, M, Berman, A, Bhageerathy, R, Bhardwaj, P, Bohluli, M, Busse, R, Cahuana-Hurtado, L, Camera, L, Castaneda-Orjuela, C, Catala-Lopez, F, Cevik, M, Chattu, V, Dandona, L, Dandona, R, Dianatinasab, M, Do, H, Doshmangir, L, El Tantawi, M, Eskandarieh, S, Esmaeilzadeh, F, Faraj, A, Farzadfar, F, Fischer, F, Foigt, N, Fullman, N, Gad, M, Ghafourifard, M, Ghashghaee, A, Gholamian, A, Goharinezhad, S, Grada, A, Haghparast Bidgoli, H, Hamidi, S, Harb, H, Hasanpoor, E, Hay, S, Hendrie, D, Henry, N, Herteliu, C, Hole, M, Hosseinzadeh, M, Hostiuc, S, Huda, T, Humayun, A, Hwang, B, Ilesanmi, O, Iqbal, U, Irvani, S, Islam, S, Islam, M, Jahani, M, Jakovljevic, M, James, S, Javaheri, Z, Jonas, J, Joukar, F, Jozwiak, J, Jurisson, M, Kalhor, R, Karami Matin, B, Karimi, S, Kayode, G, Kazemi Karyani, A, Kinfu, Y, Kisa, A, Kohler, S, Komaki, H, Kosen, S, Kotlo, A, Koyanagi, A, Kumar, G, Kusuma, D, Lansingh, V, Larsson, A, Lasrado, S, Lee, S, Lim, L, Lozano, R, Magdy Abd El Razek, H, Mahdavi, M, Maleki, S, Malekzadeh, R, Mansour-Ghanaei, F, Mansournia, M, Mantovani, L, Martinez, G, Masoumi, S, Massenburg, B, Menezes, R, Mengesha, E, Meretoja, T, Meretoja, A, Mestrovic, T, Milevska Kostova, N, Miller, T, Mirica, A, Mirrakhimov, E, Moghadaszadeh, M, Mohajer, B, Mohamadi, E, Mohammad Darwesh, A, Mohammadian-Hafshejani, A, Mohammadpourhodki, R, Mohammed, S, Mohebi, F, Mokdad, A, Morrison, S, Mosser, J, Mousavi, S, Muriithi, M, Muthupandian, S, Myint, C, Naderi, M, Nagarajan, A, Nguyen, C, Nguyen, H, Nonvignon, J, Noubiap, J, Oh, I, Olagunju, A, Olusanya, J, Olusanya, B, Omar Bali, A, Onwujekwe, O, Otstavnov, S, Otstavnov, N, Owolabi, M, Padubidri, J, Palladino, R, Panda-Jonas, S, Pandey, A, Postma, M, Prada, S, Pribadi, D, Rabiee, M, Rabiee, N, Rahim, F, Ranabhat, C, Rao, S, Rathi, P, Rawaf, S, Rawaf, D, Rawal, L, Rawassizadeh, R, Rezapour, A, Sabour, S, Sahraian, M, Salman, O, Salomon, J, Samy, A, Sanabria, J, Santos, J, Santric Milicevic, M, Sao Jose, B, Savic, M, Schwendicke, F, Senthilkumaran, S, Sepanlou, S, Servan-Mori, E, Setayesh, H, Shaikh, M, Sheikh, A, Shibuya, K, Shrime, M, Simonetti, B, Singh, J, Singh, P, Skryabin, V, Soheili, A, Soltani, S, Stefan, S, Tabares-Seisdedos, R, Topor-Madry, R, Tovani-Palone, M, Tran, B, Travillian, R, Undurraga, E, Valdez, P, van Boven, J, Vasankari, T, Violante, F, Vlassov, V, Vos, T, Wolfe, C, Wu, J, Yaya, S, Yazdi-Feyzabadi, V, Yip, P, Yonemoto, N, Younis, M, Yu, C, Zaidi, Z, Zaman, S, Zastrozhin, M, Zhang, Z, Zhao, Y, Murray, C, Dieleman, J, University of Helsinki, Clinicum, HUS Comprehensive Cancer Center, HUS Neurocenter, Helsinki University Hospital Area, University of St Andrews. School of Medicine, University of St Andrews. Infection and Global Health Division, Groningen Research Institute for Asthma and COPD (GRIAC), Value, Affordability and Sustainability (VALUE), and Real World Studies in PharmacoEpidemiology, -Genetics, -Economics and -Therapy (PEGET)

Subjects
Economic growth, Financing, Government, Psychological intervention, HIV Infections, burden of disease, 030204 cardiovascular system & hematology, DISEASE, ALLOCATION, 0302 clinical medicine, RA0421, RA0421 Public health. Hygiene. Preventive Medicine, Sustainable development, Global health, health economics, Healthcare Financing, HIV Infection, 030212 general & internal medicine, 10. No inequality, 11 Medical and Health Sciences, DALY, Healthy lives, 1. No poverty, Public Health, Global Health, Social Medicine and Epidemiology, 3rd-DAS, General Medicine, Sustainable Development, 3. Good health, tuberculosis, IMPOVERISHMENT, TERRITORIES, Financing, Human, Financing, Personal, Resource (biology), Tuberculosi, 195 COUNTRIES, Developing Countrie, 03 medical and health sciences, SDG 3 - Good Health and Well-being, Acquired immunodeficiency syndrome (AIDS), General & Internal Medicine, SYSTEMATIC ANALYSIS, medicine, Humans, Burden, HIV/AIDS, tubercolosis, malaria, Human resources, Developing Countries, Government, Acquired Immunodeficiency Syndrome, Health economics, business.industry, DISABILITY, CATASTROPHE, Global Burden of Disease Health Financing Collaborator Network, GLOBAL BURDEN, medicine.disease, Malaria, SDG, health sector spending, development assistant for health, Health Expenditure, Folkhälsovetenskap, global hälsa, socialmedicin och epidemiologi, 3121 General medicine, internal medicine and other clinical medicine, NA, Health Expenditures, business, EXPENDITURE
Abstract

BACKGROUND: Sustainable Development Goal (SDG) 3 aims to "ensure healthy lives and promote well-being for all at all ages". While a substantial effort has been made to quantify progress towards SDG3, less research has focused on tracking spending towards this goal. We used spending estimates to measure progress in financing the priority areas of SDG3, examine the association between outcomes and financing, and identify where resource gains are most needed to achieve the SDG3 indicators for which data are available. METHODS: We estimated domestic health spending, disaggregated by source (government, out-of-pocket, and prepaid private) from 1995 to 2017 for 195 countries and territories. For disease-specific health spending, we estimated spending for HIV/AIDS and tuberculosis for 135 low-income and middle-income countries, and malaria in 106 malaria-endemic countries, from 2000 to 2017. We also estimated development assistance for health (DAH) from 1990 to 2019, by source, disbursing development agency, recipient, and health focus area, including DAH for pandemic preparedness. Finally, we estimated future health spending for 195 countries and territories from 2018 until 2030. We report all spending estimates in inflation-adjusted 2019 US$, unless otherwise stated. FINDINGS: Since the development and implementation of the SDGs in 2015, global health spending has increased, reaching $7·9 trillion (95% uncertainty interval 7·8-8·0) in 2017 and is expected to increase to $11·0 trillion (10·7-11·2) by 2030. In 2017, in low-income and middle-income countries spending on HIV/AIDS was $20·2 billion (17·0-25·0) and on tuberculosis it was $10·9 billion (10·3-11·8), and in malaria-endemic countries spending on malaria was $5·1 billion (4·9-5·4). Development assistance for health was $40·6 billion in 2019 and HIV/AIDS has been the health focus area to receive the highest contribution since 2004. In 2019, $374 million of DAH was provided for pandemic preparedness, less than 1% of DAH. Although spending has increased across HIV/AIDS, tuberculosis, and malaria since 2015, spending has not increased in all countries, and outcomes in terms of prevalence, incidence, and per-capita spending have been mixed. The proportion of health spending from pooled sources is expected to increase from 81·6% (81·6-81·7) in 2015 to 83·1% (82·8-83·3) in 2030. INTERPRETATION: Health spending on SDG3 priority areas has increased, but not in all countries, and progress towards meeting the SDG3 targets has been mixed and has varied by country and by target. The evidence on the scale-up of spending and improvements in health outcomes suggest a nuanced relationship, such that increases in spending do not always results in improvements in outcomes. Although countries will probably need more resources to achieve SDG3, other constraints in the broader health system such as inefficient allocation of resources across interventions and populations, weak governance systems, human resource shortages, and drug shortages, will also need to be addressed. For complete list of authors see http://dx.doi.org/10.1016/S0140-6736(20)30608-5

Published
2020
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10. Comparison of skin closure techniques in patients undergoing open pancreaticoduodenectomy: A single center experience.

Author

Flick KF, Simpson RE, Soufi M, Fennerty ML, Yip-Schneider MT, Colgate CL, Ceppa EP, House MG, Zyromski NJ, Nakeeb A, and Schmidt CM

Subjects
Aged, Female, Follow-Up Studies, Humans, Incidence, Male, Middle Aged, Prognosis, Retrospective Studies, United States epidemiology, Pancreaticoduodenectomy methods, Postoperative Complications epidemiology, Wound Closure Techniques
Abstract

Background: This study evaluated closure techniques and incisional surgical site complications (SSCs) and incisional surgical site infections (SSIs) after pancreaticoduodenectomy (PD)., Methods: Retrospective review of open PDs from 2015 to 2018 was performed. Outcomes were compared among closure techniques (subcuticular + topical skin adhesive (TSA); staples; subcuticular only). SSCs were defined as abscess, cellulitis, seroma, or fat necrosis. SSIs were defined according to the National Surgical Quality Improvement Program (NSQIP)., Results: Patients with subcuticular + TSA (n = 205) were less likely to develop an incisional SSC (9.8%) compared to staples (n = 139) (20.1%) and subcuticular (n = 74) (16.2%) on univariable analysis (P = 0.024). Multivariable analysis revealed no statistically significant difference in incisional SSC between subcuticular + TSA and subcuticular (P = 0.528); a significant difference remained between subcuticular + TSA and staples (P = 0.014). Unadjusted median length of stay (LOS) (days) was significantly longer for staples (9) vs. subcuticular (8) vs. subcuticular + TSA (7); P < 0.001. Incisional SSIs were evaluated separately according to the NSQIP definition. When comparing rates, the subcuticular + TSA group experienced lower incisional SSIs compared to the other two techniques (4.9% vs. 10.1%, 10.8%). However, this difference was not statistically significant by either univariable or multivariable analysis., Conclusions: Subcuticular suture + TSA reduces the risk of incisional SSCs when compared to staples alone after pancreaticoduodenectomy., Competing Interests: Declaration of competing interest None declared., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Published
2020
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12. Early morphologic changes in trapeziometacarpal joint bones with osteoarthritis.

Author

Schneider MTY, Zhang J, Walker CG, Crisco JJ, Weiss AC, Ladd AL, Nielsen PMF, and Besier T

Subjects
Carpometacarpal Joints physiopathology, Disease Progression, Female, Follow-Up Studies, Humans, Male, Middle Aged, Osteoarthritis physiopathology, Thumb diagnostic imaging, Time Factors, Carpometacarpal Joints diagnostic imaging, Osteoarthritis diagnosis, Range of Motion, Articular physiology, Thumb physiopathology, Tomography, X-Ray Computed methods
Abstract

Objective: Characterising the morphological differences between healthy and early osteoarthritic (EOA) trapeziometacarpal (TMC) joints is important for understanding osteoarthritis onset, and early detection is important for treatment and disease management. This study has two aims: first, to characterise morphological differences between healthy and EOA TMC bones. The second aim was to determine the efficacy of using a statistical shape model (SSM) to detect early signs of osteoarthritis (OA)., Methods: CT image data of TMC bones from 22 asymptomatic volunteers and 47 patients with EOA were obtained from an ongoing study and used to generate a SSM. A linear discriminant analysis (LDA) classifier was trained on the principal component (PC) weights to characterise features of each group. Multivariable statistical analysis was performed on the PC to investigate morphologic differences. Leave-one-out classification was performed to evaluate the classifiers performance., Results: We found that TMC bones of EOA subjects exhibited a lower aspect ratio (P = 0.042) compared with healthy subjects. The LDA classifier predicted that protrusions (up to 1.5 mm) at the volar beak of the first metacarpal were characteristic of EOA subjects. This was accompanied with widening of the articular surface, deepening of the articular surface, and protruding bone growths along the concave margin. These characteristics resulted in a leave-one-out classification accuracy of 73.9% (95% CI [61.9%, 83.8%]), sensitivity of 89.4%, specificity of 40.9%, and precision of 75.9%., Conclusion: Our findings indicate that morphological degeneration is well underway in the EOA TMC joint, and shows promise for a clinical tool that can detect these features automatically., (Copyright © 2018 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.)

Published
2018
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13. Men and women have similarly shaped carpometacarpal joint bones.

Author

Schneider MT, Zhang J, Crisco JJ, Weiss AP, Ladd AL, Nielsen P, and Besier T

Subjects
Adult, Carpometacarpal Joints anatomy & histology, Carpometacarpal Joints diagnostic imaging, Female, Humans, Male, Middle Aged, Radiography, Sex Characteristics, Thumb anatomy & histology, Thumb diagnostic imaging, Trapezium Bone diagnostic imaging, Young Adult, Trapezium Bone anatomy & histology
Abstract

Characterizing the morphology of the carpometacarpal (CMC) joint bones and how they vary across the population is important for understanding the functional anatomy and pathology of the thumb. The purpose of this paper was to develop a statistical shape model of the trapezium and first metacarpal bones to characterize the size and shape of the whole bones across a cohort of 50. We used this shape model to investigate the effects of sex and age on the size and shape of the CMC joint bones and the articulating surface area of the CMC joint. We hypothesized that women have similar shape trapezium and first metacarpal bones compared to men, following scaling for overall size. We also hypothesized that age would be a significant predictor variable for CMC joint bone changes. CT image data and segmented point clouds of 50 CMC bones from healthy adult men and women were obtained from an ongoing study and used to generate two statistical shape models. Statistical analysis of the principal component weights of both models was performed to investigate morphological sex and age differences. We observed sex differences, but were unable to detect any age differences. Between men and women the only difference in morphology of the trapezia and first metacarpal bones was size. These findings confirm our first hypothesis, and suggest that the women have similarly shaped trapezium and first metacarpal bones compared to men. Furthermore, our results reject our second hypothesis, indicating that age is a poor predictor of CMC joint morphology., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Published
2015
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14. Cell cycle effects of nonsteroidal anti-inflammatory drugs and enhanced growth inhibition in combination with gemcitabine in pancreatic carcinoma cells.

Author

Yip-Schneider MT, Sweeney CJ, Jung SH, Crowell PL, and Marshall MS

Subjects
Apoptosis drug effects, Blotting, Western, Cell Cycle Proteins biosynthesis, Cell Division drug effects, Cyclooxygenase 2, Cyclooxygenase 2 Inhibitors, Cyclooxygenase Inhibitors pharmacology, Deoxycytidine analogs & derivatives, Humans, Isoenzymes biosynthesis, Isoenzymes drug effects, Male, Membrane Proteins, Pancreatic Neoplasms metabolism, Prostaglandin-Endoperoxide Synthases biosynthesis, Prostaglandin-Endoperoxide Synthases drug effects, Sulindac pharmacology, Tumor Cells, Cultured, Gemcitabine, Anti-Inflammatory Agents, Non-Steroidal pharmacology, Cell Cycle drug effects, Deoxycytidine pharmacology, Enzyme Inhibitors pharmacology, Pancreatic Neoplasms pathology
Abstract

Increased cyclooxygenase-2 (COX-2) expression in human pancreatic adenocarcinomas, as well as the growth-inhibitory effect of nonsteroidal anti-inflammatory drugs (NSAIDs) in vitro, suggests that NSAIDs may be an effective treatment for pancreatic cancer. Gemcitabine is currently the most effective chemotherapeutic drug available for patients with pancreatic cancer, but is only minimally effective against this aggressive disease. Clearly, other treatment options must be identified. To design successful therapeutic strategies involving compounds either alone or in combination with others, it is necessary to understand their mechanism of action. In the present study, we evaluated the effects of three NSAIDs (sulindac, indomethacin, and NS-398) or gemcitabine in two human pancreatic carcinoma cell lines, BxPC-3 (COX-2-positive) and PaCa-2 (COX-2-negative), previously shown to be growth-inhibited by these NSAIDs. Effects on cell cycle and apoptosis were investigated by flow cytometry or Western blotting. Treatment with NSAIDs or gemcitabine altered the cell cycle phase distribution as well as the expression of multiple cell cycle regulatory proteins in both cell lines, but did not induce substantial levels of apoptosis. Furthermore, we demonstrated that the combination of the NSAID sulindac or NS-398 with gemcitabine inhibited cell growth to a greater degree than either compound alone. These results indicate that the antiproliferative effects of NSAIDs and gemcitabine in pancreatic tumor cells are primarily due to inhibition of cell cycle progression rather than direct induction of apoptotic cell death, regardless of COX-2 expression. In addition, NSAIDs in combination with gemcitabine may hold promise in the clinic for the treatment of pancreatic cancer.

Published
2001

15. Pancreatic tumor cells with mutant K-ras suppress ERK activity by MEK-dependent induction of MAP kinase phosphatase-2.

Author

Yip-Schneider MT, Lin A, and Marshall MS

Subjects
Animals, Blotting, Western, Carcinoma enzymology, Cell Line, Down-Regulation, Dual-Specificity Phosphatases, Enzyme Inhibitors pharmacology, Humans, Kinetics, Mitogen-Activated Protein Kinase Phosphatases, Pancreatic Neoplasms enzymology, Phosphorylation drug effects, Protein Phosphatase 2, Rats, Signal Transduction, Time Factors, Tumor Cells, Cultured, Up-Regulation, Vanadates pharmacology, Carcinoma genetics, Gene Expression Regulation, Enzymologic, Genes, ras genetics, Mitogen-Activated Protein Kinase Kinases metabolism, Mitogen-Activated Protein Kinases metabolism, Mutation, Pancreatic Neoplasms genetics, Protein Tyrosine Phosphatases metabolism
Abstract

Activating mutations within the K-ras gene occur in a high percentage of human pancreatic carcinomas. We reported previously that the presence of oncogenic, activated K-ras in human pancreatic carcinoma cell lines did not result in constitutive activation of the extracellular signal-regulated kinases (ERK1 and ERK2). In the present study, we further characterized the ERK signaling pathway in pancreatic tumor cell lines in order to determine whether the ERK pathway is subject to a compensatory downregulation. We found that the attenuation of serum-induced ERK activation was not due to a delay in the kinetics of ERK phosphorylation. Treatment with the tyrosine phosphatase inhibitor orthovanadate increased the level of ERK phosphorylation, implicating a vanadate-sensitive tyrosine phosphatase in the negative regulation of ERK. Furthermore, expression of a dual specificity phosphatase capable of inactivating ERK known as mitogen-activated protein (MAP) kinase phosphatase-2 (MKP-2) was elevated in most of the pancreatic tumor cell lines and correlated with the presence of active MAP kinase kinase (MEK). Taken together, these results suggest that pancreatic tumor cells expressing oncogenic K-ras compensate, in part, by upregulating the expression of MKP-2 to repress the ERK signaling pathway., (Copyright 2001 Academic Press.)

Published
2001
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16. Regulation of the Raf-1 kinase domain by phosphorylation and 14-3-3 association.

Author

Yip-Schneider MT, Miao W, Lin A, Barnard DS, Tzivion G, and Marshall MS

Subjects
14-3-3 Proteins, Animals, Binding, Competitive, COS Cells, Catalytic Domain, Enzyme Activation drug effects, Mutation genetics, Oncogene Protein pp60(v-src) genetics, Oncogene Protein pp60(v-src) metabolism, Peptide Fragments chemistry, Peptide Fragments metabolism, Phosphorylation, Phosphoserine metabolism, Protein Binding, Protein Structure, Tertiary, Proto-Oncogene Proteins c-raf genetics, Tetradecanoylphorbol Acetate pharmacology, Tyrosine 3-Monooxygenase genetics, Proto-Oncogene Proteins c-raf chemistry, Proto-Oncogene Proteins c-raf metabolism, Tyrosine 3-Monooxygenase metabolism
Abstract

The Raf-1 kinase domain is kept in an inactive state by the N-terminal regulatory domain. Activation of the kinase domain occurs following release from the N-terminal repression and possible catalytic upregulation. To distinguish the regulatory mechanisms that directly influence the catalytic activity of the enzyme from those which act through the inhibitory domain, the catalytic domain of Raf-1 (CR3) was expressed in COS-7 cells. The role of phosphorylation in the direct regulation of this domain was determined by substituting non-phosphorylatable amino acids for known serine and tyrosine phosphorylation sites. The intrinsic activity of each mutant protein was determined as well as stimulation by v-Src and phorbol esters. Both v-Src and phorbol esters were potent activators of CR3, requiring the serine 338/339 (p21-activated protein kinase, Pak) and tyrosine 340/341 (Src) phosphorylation sites for full stimulation of CR3. In contrast, loss of the serine 497/499 protein kinase C phosphorylation sites had little effect on CR3 activation by either v-Src or phorbol esters. Loss of serine 621, a 14-3-3 adaptor-protein-binding site, prevented activation of CR3 by v-Src or phorbol esters and partially decreased the high basal activity of the kinase fragment. When co-expressed in COS-7 cells, 14-3-3 associated strongly with full-length Raf-1, weakly with wild-type CR3 and not at all with the A621 and D621 CR3 mutants. The role of 14-3-3 in maintaining the activity of the catalytic domain of Raf-1 was investigated further by performing peptide-competition studies with wild-type CR3, wild-type CR3 and v-Src or constitutively active CR3 (CR3[YY340/341DD]). In each case, incubation of the proteins with a phosphoserine-621 Raf-1 peptide, which we show displaced Raf-1 and CR3[YY340/341DD] from 14-3-3, was found to substantially reduce catalytic activity. Taken together, our results support a model of Raf regulation in which the activity of the Raf-1 catalytic domain is directly upregulated by phosphorylation, following relief of inhibition by the N-terminal regulatory domain upon Ras-GTP binding. Moreover, the presence of serine 621 in the free catalytic fragment is required for full CR3 activation by stimulatory factors, and the continuous presence of 14-3-3 at this site is necessary for retaining activity once the kinase is activated.

Published
2000
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17. Transcriptional induction of pim-1 protein kinase gene expression by interferon gamma and posttranscriptional effects on costimulation with steel factor.

Author

Yip-Schneider MT, Horie M, and Broxmeyer HE

Subjects
Base Sequence, Binding Sites genetics, Drug Synergism, Gene Expression drug effects, Humans, Leukemia metabolism, Molecular Sequence Data, Promoter Regions, Genetic genetics, Protein Serine-Threonine Kinases biosynthesis, Protein Serine-Threonine Kinases genetics, Proto-Oncogene Proteins genetics, Proto-Oncogene Proteins c-pim-1, RNA, Messenger biosynthesis, Recombinant Proteins, Stem Cell Factor, Transcription, Genetic drug effects, Tumor Cells, Cultured, Hematopoietic Cell Growth Factors pharmacology, Interferon-gamma pharmacology, Proto-Oncogene Proteins biosynthesis
Abstract

Steel factor (SLF) synergizes with interferon gamma (IFN gamma) to stimulate proliferation of the human factor-dependent cell line MO7e. We examined the effects of IFN gamma and SLF treatment, alone or in combination, on the expression of a 33-kD cytoplasmic protein serine/threonine kinase designated pim-1 whose expression has been closely associated with proliferation induced by related myeloid cytokines. IFN gamma alone, but not SLF, stimulated expression of pim-1 RNA and protein in MO7e cells; compared with IFN gamma alone, costimulation with IFN gamma and SLF resulted in a twofold to threefold increase in pim-1 message and protein expression, correlating with synergistic effects on cell proliferation. Both IFN gamma and IFN gamma/SLF induced pim-1 mRNA in the absence of de novo protein synthesis. Nuclear run-on assays showed that, although IFN gamma alone increased the rate of pim-1 gene transcription, costimulation with IFN gamma and SLF did not further potentiate this effect; however, the stability of pim-1 message was significantly enhanced in the presence of both cytokines. An IFN gamma-responsive element within the 5' flanking region of the pim-1 gene that could confer IFN gamma responsiveness on a heterologous promoter was identified. This sequence, designated PMGAS, formed a specific complex with Stat (signal transducers and activators of transcription) 1 alpha (the p91 subunit of the transcription factor ISGF3 [interferon-stimulated gene factor 3]) in IFN gamma-treated cell extracts, suggesting that the transcriptional effects of IFN gamma on pim-1 expression may be mediated by Stat 1 alpha.

Published
1995

18. Characterization of interleukin-7-induced changes in tyrosine phosphorylation and c-myc gene expression in normal human T cells.

Author

Yip-Schneider MT, Horie M, and Broxmeyer HE

Subjects
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine, Blotting, Northern, Cell Division, Humans, Immunoblotting, Isoquinolines pharmacology, Molecular Weight, Phosphorylation, Phosphotyrosine, Piperazines pharmacology, Protein Kinase Inhibitors, Protein Kinases metabolism, Signal Transduction, T-Lymphocytes cytology, Tetradecanoylphorbol Acetate pharmacology, Transcription, Genetic, Tyrosine metabolism, Gene Expression drug effects, Genes, myc, Interleukin-7 pharmacology, Phosphoproteins metabolism, T-Lymphocytes metabolism, Tyrosine analogs & derivatives
Abstract

Interleukin-7 (IL-7) is a growth factor involved in regulating lymphopoiesis. We have chosen to study the signal transduction pathway of IL-7 in normal human peripheral blood T lymphocytes. Two early events that occur as a consequence of specific ligand-receptor interaction were examined: activation of protein tyrosine kinases and induction of primary response gene expression. Following treatment of human peripheral blood T cells with IL-7, four cellular proteins with relative molecular weights of 95- (doublet), 105-, and 130-kd were rapidly tyrosine phosphorylated as detected by immunoblotting with an antiphosphotyrosine monoclonal antibody (MAB). The 105-kd tyrosine-phosphorylated protein was membrane-associated after IL-7 stimulation. Treatment of human peripheral blood T cells with IL-7 enhanced expression of the primary response gene c-myc approximately three-fold, as detected by Northern blotting, in the presence or absence of protein synthesis. The rate of c-myc gene transcription increased in the presence of IL-7 and could account for the observed elevation of c-myc RNA levels. In addition, IL-7 treatment induced a slight increase in c-myc message stability. Experiments performed with the protein tyrosine kinase inhibitor genistein and the serine-threonine kinase inhibitor 1-(5-isoquinolinylsulfonyl)-2-methyl-piperazine (H-7) demonstrated that these kinases were required for IL-7 enhancement of c-myc expression. Treatment with tetradecanoyl phorbol acetate (TPA), a potent activator of protein kinase C (PKC), in combination with IL-7 induced a level of c-myc expression greater than that elicited by either factor alone, suggesting that TPA and IL-7 utilize cooperative signaling pathways to increase c-myc gene expression.

Published
1993

20. Fine structural characteristics and synaptic connections of trigeminocerebellar projection neurons in rat trigeminal nucleus oralis.

Author

Falls WM, Moore BJ, and Schneider MT

Subjects
Animals, Male, Microscopy, Electron, Rats, Rats, Inbred Strains, Cerebellum ultrastructure, Neurons, Afferent ultrastructure, Trigeminal Nerve ultrastructure
Abstract

In order to classify the presynaptic terminals contacting trigeminocerebellar projection neurons (TCPNs) in rat trigeminal nucleus oralis (Vo), electron-microscopic examination of sequential thin sections made from TCPNs located in the border zone (BZ) of Vo, labeled by the retrograde transport of horseradish peroxidase, was undertaken. The use of BZ TCPNs, labeled in Golgi-like fashion so that many of their dendrites and axons were visible, allowed for the determination of the distribution of each bouton type along the soma and dendrites, as well as for the characterization of the morphology and synaptic relations of the labeled axon and its terminals. Three types of axon terminals contacting labeled BZ TCPNs have been recognized, depending upon whether they contain primarily spherical-shaped, agranular synaptic vesicles (S endings); predominantly flattened, agranular synaptic vesicles (F endings); or a population of pleomorphic-shaped, agranular synaptic vesicles (P endings). The S endings represent the majority of axon terminals contacting labeled BZ TCPNs and establish asymmetrical axosomatic and axodendritic synaptic contacts. Many S endings are situated in one of two types of synaptic glomeruli. One type of glomerulus has a large S ending at its core, whereas the other contains a small S ending. Large-S-ending glomeruli include only labeled distal dendrites of BZ TCPNs; small-S-ending glomeruli contain either a labeled soma, proximal dendrite, or distal dendritic shaft. The remaining S endings are extraglomerular, synapsing on distal dendrites. P endings are less frequently encountered and establish intermediate axosomatic and axodendritic synapses. These endings exhibit a generalized distribution along the entire somatodendritic tree. F endings make symmetrical axodendritic synapses with distal dendrites, are only found in glomeruli containing small S endings, and are the least frequently observed ending contacting labeled BZ TCPNs. The majority of axonal endings synapsing on labeled BZ TCPNs are located along distal dendrites, with only a relatively few synapsing terminals situated on proximal dendrites and somata. The axons of labeled BZ TCPNs arise from the cell body and generally give rise to a single short collateral near their points of origin. This collateral remains unbranched and generates several boutons within BZ, while the parent axon acquires a myelin sheath and, without branching further, travels dorsolaterally toward the inferior cerebellar peduncle. The collateral boutons resemble extraglomerular S endings. They contain agranular, spherical-shaped synaptic vesicles and make asymmetrical axodendritic synapses with small-diameter unlabeled dendritic shafts in the BZ neuropil.

Published
1990
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