Publications

Found 55 results

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2011
Ngugi RW, Mohapatra S, Ratha D. "Remittances market in Kenya.". In: Remittance Markets in Africa. The World Bank; 2011.
Ngugi RW, Sennoga E, Mohapatra S, Ratha D. "Remittances market in Uganda.". In: Remittance Markets in Africa. The World Bank; 2011.
2010
Ngugi RW, Maana I, Amanja D, Adam CS, Collier P, Ndung’u N. "Capital market and economic growth in Kenya.". In: Kenya Policies for Prosperity. Oxford University Press; 2010.
O’Connell SA, Maturu BO, Mwega FM, Ndung’u N, Ngugi RW, Adam CS, Collier P. "Capital mobility, monetary policy and exchange rate management in Kenya.". In: Kenya Policies for Prosperity. Oxford University Press; 2010.
2009
Mbutu M, Ngugi RW, Njenga G. "Financial sector development and economic growth in Africa." Africa Finance Journal. 2009.
Ngugi RW, Agoti J. "Microstructure characteristics of the bonds market in Kenya." African Finance Journal. 2009.
2008
Ngugi RW, Sifunjo EK, Wainaina G, Pokhariyal G. "An analysis of the efficiency of foreign exchange market in Kenya." Economic Bulletin. 2008.
2007
Ngugi RW, Mwega FM, Ibi A. "Foreign Direct Investment in Kenya.". In: Foreign Direct Investment in Sub-Saharan Africa: Determinants, Origins, Targets, Impact and Potential. AERC; 2007.
2006
Ngugi RW, Nyang'oro O. "Insecurity And Investment Decisions.". 2006.Website
Ngugi RW, Nyang'oro O. "Investment Climate And Investment Growth.". 2006.Website
Ngugi RW, Were M, Makau P, Mensah J, Macmillan P. "Understanding the Reform Porcess in Kenya.". In: Understanding Economic Reforms in Kenya.; 2006.
2005
WANJIRU DRNGUGIROSE. "Growth of the NSE primary market: what can we learn? KIPPRA Discussion Paper # 47." The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2005.
Ngugi RW, Nyang'oro O. "Institutional Factors and FDI Flows: Implications For Kenya, KIPPRA Discussion Paper # 48." The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2005.
Were M, Ngugi RW, Makau P, Wambua J, Oyugi L. "Kenya’s reform experience: What have we learnt? KIPPRA Working Paper #12."; 2005.
Ngugi RW, Murinde V, Green C, Green CJ, Kirkpatrick C, Murinde V, Elgar E. "Stock market development, in Finance and Development: Surveys of Theory Evidence and Policy." The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2005.
Ngugi RW. "Zacchaeus Nicholas Vundi, Time Varying Risk Premium: An Empirical Investigation on the Nairobi Stock Exchange, University of Nairobi." The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2005.
2004
Ngugi RW. "Andati Samuel Obulemire, Duration dependence in stock prices: A duration analysis of bull and bear markets on NSE, University of Nairobi, 2004." The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2004.
WANJIRU DRNGUGIROSE. "Justus Nyameyio Agoti, The impact of dividend announcements on firm value: An event study of the case of the NSE, University of Nairobi, 2004." The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2004.
WANJIRU DRNGUGIROSE, Ngugi RW. "Luka Kandie Kiptui, Exchange rate pass-through to domestic prices in Kenya: 1972-2004, University of Nairobi, 2005." The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2004.
Ngugi RW, Kimenyi MS, Gakuru O, Nyang’oro O, Muriu P, Nderitu P, Kariuki E, Kimilu G, Bikuri K, Njuguna S. "Security Risk and Private sector growth in Kenya, KIPPRA Special Report #06."; 2004.
Ngugi RW;, Murinde V;, Green CJ. "Stock market development: What have we learned. .". 2004.Website
Ngugi RW. "Understanding the structure of interest rates in Kenya, KIPPRA Discussion Paper # 40." The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2004.
2003
Ngugi RW. " Response of Emerging Stock Markets in Africa to the Reform Process, in Journal of African Business." The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2003.
WANJIRU DRNGUGIROSE. "Deregulation and management of interest rates, IPAR Discussion Paper # 38." The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2003.
Ngugi RW. "Determinants of Interest rate spread in Kenya." African Journal of Economic Policy. 2003.Website
Ngugi RW. "Kienjeku S. Mbuthia, Calendar anomalies in the NSE, University of Nairobi, 2003." The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2003.
Ngugi RW. "Muriu P. Wanjihia, Volatility of stock returns. University of Nairobi, 2003." The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2003.
WANJIRU DRNGUGIROSE. "Owen Nyango'ro, Tax and Capital structure: Case of listed firms in Kenya, University of Nairobi, 2003.". In: Paris 2011 World Cup in Paris, France. The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2003. Abstract
In contrast with mammalian cells, little is known about the control of Ca2+ entry into primitive protozoans. Here we report that Ca2+ influx in pathogenic Trypanosoma brucei can be regulated by phospholipase A2 (PLA2) and the subsequent release of arachidonic acid (AA). Several PLA2 inhibitors blocked Ca2+ entry; 3-(4-octadecyl)-benzoylacrylic acid (OBAA; IC50 0.4+/-0.1 microM) was the most potent. We identified in live trypanosomes PLA2 activity that was sensitive to OBAA and could be stimulated by Ca2+, suggesting the presence of positive feedback control. The cell-associated PLA2 activity was able to release [14C]AA from labelled phospholipid substrates. Exogenous AA (5-50 microM) also initiated Ca2+ entry in a manner that was inhibited by the Ca2+ antagonist La3+ (100 microM). Ca2+ entry did not depend on AA metabolism or protein kinase activation. The cell response was specific for AA, and fatty acids with greater saturation than tetraeicosanoic acid (AA) or with chain lengths less than C20 exhibited greatly diminished ability to initiate Ca2+ influx. Myristate and palmitate inhibited PLA2 activity and also inhibited Ca2+ influx. Overall, these results demonstrate that Ca2+ entry into T. brucei can result from phospholipid hydrolysis and the release of eicosanoic acids.
WANJIRU DRNGUGIROSE. "Rose W. Ngugi , Determinants of Interest rate spread in Kenya, African Journal of Economic Policy.". In: Paris 2011 World Cup in Paris, France. The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2003. Abstract
In contrast with mammalian cells, little is known about the control of Ca2+ entry into primitive protozoans. Here we report that Ca2+ influx in pathogenic Trypanosoma brucei can be regulated by phospholipase A2 (PLA2) and the subsequent release of arachidonic acid (AA). Several PLA2 inhibitors blocked Ca2+ entry; 3-(4-octadecyl)-benzoylacrylic acid (OBAA; IC50 0.4+/-0.1 microM) was the most potent. We identified in live trypanosomes PLA2 activity that was sensitive to OBAA and could be stimulated by Ca2+, suggesting the presence of positive feedback control. The cell-associated PLA2 activity was able to release [14C]AA from labelled phospholipid substrates. Exogenous AA (5-50 microM) also initiated Ca2+ entry in a manner that was inhibited by the Ca2+ antagonist La3+ (100 microM). Ca2+ entry did not depend on AA metabolism or protein kinase activation. The cell response was specific for AA, and fatty acids with greater saturation than tetraeicosanoic acid (AA) or with chain lengths less than C20 exhibited greatly diminished ability to initiate Ca2+ influx. Myristate and palmitate inhibited PLA2 activity and also inhibited Ca2+ influx. Overall, these results demonstrate that Ca2+ entry into T. brucei can result from phospholipid hydrolysis and the release of eicosanoic acids.
WANJIRU DRNGUGIROSE. "Rose W. Ngugi , Development of the NSE: A historical perspective, KIPPRA Discussion Paper # 27.". In: Paris 2011 World Cup in Paris, France. The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2003. Abstract
In contrast with mammalian cells, little is known about the control of Ca2+ entry into primitive protozoans. Here we report that Ca2+ influx in pathogenic Trypanosoma brucei can be regulated by phospholipase A2 (PLA2) and the subsequent release of arachidonic acid (AA). Several PLA2 inhibitors blocked Ca2+ entry; 3-(4-octadecyl)-benzoylacrylic acid (OBAA; IC50 0.4+/-0.1 microM) was the most potent. We identified in live trypanosomes PLA2 activity that was sensitive to OBAA and could be stimulated by Ca2+, suggesting the presence of positive feedback control. The cell-associated PLA2 activity was able to release [14C]AA from labelled phospholipid substrates. Exogenous AA (5-50 microM) also initiated Ca2+ entry in a manner that was inhibited by the Ca2+ antagonist La3+ (100 microM). Ca2+ entry did not depend on AA metabolism or protein kinase activation. The cell response was specific for AA, and fatty acids with greater saturation than tetraeicosanoic acid (AA) or with chain lengths less than C20 exhibited greatly diminished ability to initiate Ca2+ influx. Myristate and palmitate inhibited PLA2 activity and also inhibited Ca2+ influx. Overall, these results demonstrate that Ca2+ entry into T. brucei can result from phospholipid hydrolysis and the release of eicosanoic acids.
WANJIRU DRNGUGIROSE. "Rose W. Ngugi, What defines the liquidity of stock market? The case for Nairobi Stock Exchange, KIPPRA Discussion Paper # 29.". In: Paris 2011 World Cup in Paris, France. The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2003. Abstract
In contrast with mammalian cells, little is known about the control of Ca2+ entry into primitive protozoans. Here we report that Ca2+ influx in pathogenic Trypanosoma brucei can be regulated by phospholipase A2 (PLA2) and the subsequent release of arachidonic acid (AA). Several PLA2 inhibitors blocked Ca2+ entry; 3-(4-octadecyl)-benzoylacrylic acid (OBAA; IC50 0.4+/-0.1 microM) was the most potent. We identified in live trypanosomes PLA2 activity that was sensitive to OBAA and could be stimulated by Ca2+, suggesting the presence of positive feedback control. The cell-associated PLA2 activity was able to release [14C]AA from labelled phospholipid substrates. Exogenous AA (5-50 microM) also initiated Ca2+ entry in a manner that was inhibited by the Ca2+ antagonist La3+ (100 microM). Ca2+ entry did not depend on AA metabolism or protein kinase activation. The cell response was specific for AA, and fatty acids with greater saturation than tetraeicosanoic acid (AA) or with chain lengths less than C20 exhibited greatly diminished ability to initiate Ca2+ influx. Myristate and palmitate inhibited PLA2 activity and also inhibited Ca2+ influx. Overall, these results demonstrate that Ca2+ entry into T. brucei can result from phospholipid hydrolysis and the release of eicosanoic acids.
2002
Ngugi RW, Murinde V, Green C. " How emerging market respond to the revitalization process: Evidence on the Nairobi Stock Exchange, in Africa Finance Journal." The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2002.
2001
Ngugi RW. ""Techniques, Methods and Procedures of Privatization" The context of Privatization in Kenya, edited by Professor Anyang Nyong'o.". The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2001.
WANJIRU DRNGUGIROSE. "Rose W. Ngugi, An Empirical Analysis of Interest Rate Spread in Kenya. AERC Research Paper # 106.". In: Paris 2011 World Cup in Paris, France. The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2001. Abstract
In contrast with mammalian cells, little is known about the control of Ca2+ entry into primitive protozoans. Here we report that Ca2+ influx in pathogenic Trypanosoma brucei can be regulated by phospholipase A2 (PLA2) and the subsequent release of arachidonic acid (AA). Several PLA2 inhibitors blocked Ca2+ entry; 3-(4-octadecyl)-benzoylacrylic acid (OBAA; IC50 0.4+/-0.1 microM) was the most potent. We identified in live trypanosomes PLA2 activity that was sensitive to OBAA and could be stimulated by Ca2+, suggesting the presence of positive feedback control. The cell-associated PLA2 activity was able to release [14C]AA from labelled phospholipid substrates. Exogenous AA (5-50 microM) also initiated Ca2+ entry in a manner that was inhibited by the Ca2+ antagonist La3+ (100 microM). Ca2+ entry did not depend on AA metabolism or protein kinase activation. The cell response was specific for AA, and fatty acids with greater saturation than tetraeicosanoic acid (AA) or with chain lengths less than C20 exhibited greatly diminished ability to initiate Ca2+ influx. Myristate and palmitate inhibited PLA2 activity and also inhibited Ca2+ influx. Overall, these results demonstrate that Ca2+ entry into T. brucei can result from phospholipid hydrolysis and the release of eicosanoic acids.
2000
WANJIRU DRNGUGIROSE. "Njuguna Ndung'u and Rose W. Ngugi. Banking Sector Interest Rate Spread in Kenya. KIPPRA Discussion Paper # 5.". In: Paris 2011 World Cup in Paris, France. The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2000. Abstract
In contrast with mammalian cells, little is known about the control of Ca2+ entry into primitive protozoans. Here we report that Ca2+ influx in pathogenic Trypanosoma brucei can be regulated by phospholipase A2 (PLA2) and the subsequent release of arachidonic acid (AA). Several PLA2 inhibitors blocked Ca2+ entry; 3-(4-octadecyl)-benzoylacrylic acid (OBAA; IC50 0.4+/-0.1 microM) was the most potent. We identified in live trypanosomes PLA2 activity that was sensitive to OBAA and could be stimulated by Ca2+, suggesting the presence of positive feedback control. The cell-associated PLA2 activity was able to release [14C]AA from labelled phospholipid substrates. Exogenous AA (5-50 microM) also initiated Ca2+ entry in a manner that was inhibited by the Ca2+ antagonist La3+ (100 microM). Ca2+ entry did not depend on AA metabolism or protein kinase activation. The cell response was specific for AA, and fatty acids with greater saturation than tetraeicosanoic acid (AA) or with chain lengths less than C20 exhibited greatly diminished ability to initiate Ca2+ influx. Myristate and palmitate inhibited PLA2 activity and also inhibited Ca2+ influx. Overall, these results demonstrate that Ca2+ entry into T. brucei can result from phospholipid hydrolysis and the release of eicosanoic acids.
WANJIRU DRNGUGIROSE. "Rose W. Ngugi, Victor Murinde, and Christopher Green, , Key microstructure and policy issues for emerging stock markets. What have we learned? Finance and Development Research Programme Working Paper # 16 May, ISBN 1902518780, Being revised for the SUERF .". In: Paris 2011 World Cup in Paris, France. The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2000. Abstract
In contrast with mammalian cells, little is known about the control of Ca2+ entry into primitive protozoans. Here we report that Ca2+ influx in pathogenic Trypanosoma brucei can be regulated by phospholipase A2 (PLA2) and the subsequent release of arachidonic acid (AA). Several PLA2 inhibitors blocked Ca2+ entry; 3-(4-octadecyl)-benzoylacrylic acid (OBAA; IC50 0.4+/-0.1 microM) was the most potent. We identified in live trypanosomes PLA2 activity that was sensitive to OBAA and could be stimulated by Ca2+, suggesting the presence of positive feedback control. The cell-associated PLA2 activity was able to release [14C]AA from labelled phospholipid substrates. Exogenous AA (5-50 microM) also initiated Ca2+ entry in a manner that was inhibited by the Ca2+ antagonist La3+ (100 microM). Ca2+ entry did not depend on AA metabolism or protein kinase activation. The cell response was specific for AA, and fatty acids with greater saturation than tetraeicosanoic acid (AA) or with chain lengths less than C20 exhibited greatly diminished ability to initiate Ca2+ influx. Myristate and palmitate inhibited PLA2 activity and also inhibited Ca2+ influx. Overall, these results demonstrate that Ca2+ entry into T. brucei can result from phospholipid hydrolysis and the release of eicosanoic acids.
WANJIRU DRNGUGIROSE. "Rose W. Ngugi. Financial Reform Process in Kenya 1989-1996, African Development Review.". In: Paris 2011 World Cup in Paris, France. The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 2000. Abstract
In contrast with mammalian cells, little is known about the control of Ca2+ entry into primitive protozoans. Here we report that Ca2+ influx in pathogenic Trypanosoma brucei can be regulated by phospholipase A2 (PLA2) and the subsequent release of arachidonic acid (AA). Several PLA2 inhibitors blocked Ca2+ entry; 3-(4-octadecyl)-benzoylacrylic acid (OBAA; IC50 0.4+/-0.1 microM) was the most potent. We identified in live trypanosomes PLA2 activity that was sensitive to OBAA and could be stimulated by Ca2+, suggesting the presence of positive feedback control. The cell-associated PLA2 activity was able to release [14C]AA from labelled phospholipid substrates. Exogenous AA (5-50 microM) also initiated Ca2+ entry in a manner that was inhibited by the Ca2+ antagonist La3+ (100 microM). Ca2+ entry did not depend on AA metabolism or protein kinase activation. The cell response was specific for AA, and fatty acids with greater saturation than tetraeicosanoic acid (AA) or with chain lengths less than C20 exhibited greatly diminished ability to initiate Ca2+ influx. Myristate and palmitate inhibited PLA2 activity and also inhibited Ca2+ influx. Overall, these results demonstrate that Ca2+ entry into T. brucei can result from phospholipid hydrolysis and the release of eicosanoic acids.
1999
Ngugi RW, Mbui W. "Macroeconomic Structure and Outlook" Kenya's Strategic Policies for the 21st Century, Edited by Kimuyu, Wagacha and Abagi." The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 1999.
Ndung'u N, Ngugi RW. "Njuguna Ndung'u and Rose W. Ngugi. Adjustment and liberalization in Kenya: The Financial and Foreign Exchange Market, Journal of International Development." The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 1999.
WANJIRU DRNGUGIROSE. "Kiragu M.R.; Market concentration and firm's profitability in the food processing sub-sector, 1999, University of Nairobi.". In: Paris 2011 World Cup in Paris, France. The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 1999. Abstract
In contrast with mammalian cells, little is known about the control of Ca2+ entry into primitive protozoans. Here we report that Ca2+ influx in pathogenic Trypanosoma brucei can be regulated by phospholipase A2 (PLA2) and the subsequent release of arachidonic acid (AA). Several PLA2 inhibitors blocked Ca2+ entry; 3-(4-octadecyl)-benzoylacrylic acid (OBAA; IC50 0.4+/-0.1 microM) was the most potent. We identified in live trypanosomes PLA2 activity that was sensitive to OBAA and could be stimulated by Ca2+, suggesting the presence of positive feedback control. The cell-associated PLA2 activity was able to release [14C]AA from labelled phospholipid substrates. Exogenous AA (5-50 microM) also initiated Ca2+ entry in a manner that was inhibited by the Ca2+ antagonist La3+ (100 microM). Ca2+ entry did not depend on AA metabolism or protein kinase activation. The cell response was specific for AA, and fatty acids with greater saturation than tetraeicosanoic acid (AA) or with chain lengths less than C20 exhibited greatly diminished ability to initiate Ca2+ influx. Myristate and palmitate inhibited PLA2 activity and also inhibited Ca2+ influx. Overall, these results demonstrate that Ca2+ entry into T. brucei can result from phospholipid hydrolysis and the release of eicosanoic acids.
WANJIRU DRNGUGIROSE. "Rose W. Ngugi, Health Seeking Behavior in Reform Process for Rural Households The Case of Mwea-Kirinyaga District. AERC Research paper # 95.". In: Paris 2011 World Cup in Paris, France. The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 1999. Abstract
In contrast with mammalian cells, little is known about the control of Ca2+ entry into primitive protozoans. Here we report that Ca2+ influx in pathogenic Trypanosoma brucei can be regulated by phospholipase A2 (PLA2) and the subsequent release of arachidonic acid (AA). Several PLA2 inhibitors blocked Ca2+ entry; 3-(4-octadecyl)-benzoylacrylic acid (OBAA; IC50 0.4+/-0.1 microM) was the most potent. We identified in live trypanosomes PLA2 activity that was sensitive to OBAA and could be stimulated by Ca2+, suggesting the presence of positive feedback control. The cell-associated PLA2 activity was able to release [14C]AA from labelled phospholipid substrates. Exogenous AA (5-50 microM) also initiated Ca2+ entry in a manner that was inhibited by the Ca2+ antagonist La3+ (100 microM). Ca2+ entry did not depend on AA metabolism or protein kinase activation. The cell response was specific for AA, and fatty acids with greater saturation than tetraeicosanoic acid (AA) or with chain lengths less than C20 exhibited greatly diminished ability to initiate Ca2+ influx. Myristate and palmitate inhibited PLA2 activity and also inhibited Ca2+ influx. Overall, these results demonstrate that Ca2+ entry into T. brucei can result from phospholipid hydrolysis and the release of eicosanoic acids.
1998
Ngugi RW, Kabubo J. "Financial Sector Reforms and Interest Rate Determination: The Kenya case. AERC Research Paper # 72.". The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 1998.
WANJIRU DRNGUGIROSE. "Chacha, R. Njeri; Factors determining the development of NSE, 1998, University of Nairobi.". In: Paris 2011 World Cup in Paris, France. The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 1998. Abstract
In contrast with mammalian cells, little is known about the control of Ca2+ entry into primitive protozoans. Here we report that Ca2+ influx in pathogenic Trypanosoma brucei can be regulated by phospholipase A2 (PLA2) and the subsequent release of arachidonic acid (AA). Several PLA2 inhibitors blocked Ca2+ entry; 3-(4-octadecyl)-benzoylacrylic acid (OBAA; IC50 0.4+/-0.1 microM) was the most potent. We identified in live trypanosomes PLA2 activity that was sensitive to OBAA and could be stimulated by Ca2+, suggesting the presence of positive feedback control. The cell-associated PLA2 activity was able to release [14C]AA from labelled phospholipid substrates. Exogenous AA (5-50 microM) also initiated Ca2+ entry in a manner that was inhibited by the Ca2+ antagonist La3+ (100 microM). Ca2+ entry did not depend on AA metabolism or protein kinase activation. The cell response was specific for AA, and fatty acids with greater saturation than tetraeicosanoic acid (AA) or with chain lengths less than C20 exhibited greatly diminished ability to initiate Ca2+ influx. Myristate and palmitate inhibited PLA2 activity and also inhibited Ca2+ influx. Overall, these results demonstrate that Ca2+ entry into T. brucei can result from phospholipid hydrolysis and the release of eicosanoic acids.
WANJIRU DRNGUGIROSE. "Makoma, L. Wanza; the demand for municipal solid waste disposal services; An econometric analysis of willingness to pay; 1998, University of Nairobi.". In: Paris 2011 World Cup in Paris, France. The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 1998. Abstract
In contrast with mammalian cells, little is known about the control of Ca2+ entry into primitive protozoans. Here we report that Ca2+ influx in pathogenic Trypanosoma brucei can be regulated by phospholipase A2 (PLA2) and the subsequent release of arachidonic acid (AA). Several PLA2 inhibitors blocked Ca2+ entry; 3-(4-octadecyl)-benzoylacrylic acid (OBAA; IC50 0.4+/-0.1 microM) was the most potent. We identified in live trypanosomes PLA2 activity that was sensitive to OBAA and could be stimulated by Ca2+, suggesting the presence of positive feedback control. The cell-associated PLA2 activity was able to release [14C]AA from labelled phospholipid substrates. Exogenous AA (5-50 microM) also initiated Ca2+ entry in a manner that was inhibited by the Ca2+ antagonist La3+ (100 microM). Ca2+ entry did not depend on AA metabolism or protein kinase activation. The cell response was specific for AA, and fatty acids with greater saturation than tetraeicosanoic acid (AA) or with chain lengths less than C20 exhibited greatly diminished ability to initiate Ca2+ influx. Myristate and palmitate inhibited PLA2 activity and also inhibited Ca2+ influx. Overall, these results demonstrate that Ca2+ entry into T. brucei can result from phospholipid hydrolysis and the release of eicosanoic acids.
WANJIRU DRNGUGIROSE. "Njuguna Isaac Kiambo; an empirical study of the efficient market hypothesis on the NSE, 1998, University of Nairobi.". In: Paris 2011 World Cup in Paris, France. The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 1998. Abstract
In contrast with mammalian cells, little is known about the control of Ca2+ entry into primitive protozoans. Here we report that Ca2+ influx in pathogenic Trypanosoma brucei can be regulated by phospholipase A2 (PLA2) and the subsequent release of arachidonic acid (AA). Several PLA2 inhibitors blocked Ca2+ entry; 3-(4-octadecyl)-benzoylacrylic acid (OBAA; IC50 0.4+/-0.1 microM) was the most potent. We identified in live trypanosomes PLA2 activity that was sensitive to OBAA and could be stimulated by Ca2+, suggesting the presence of positive feedback control. The cell-associated PLA2 activity was able to release [14C]AA from labelled phospholipid substrates. Exogenous AA (5-50 microM) also initiated Ca2+ entry in a manner that was inhibited by the Ca2+ antagonist La3+ (100 microM). Ca2+ entry did not depend on AA metabolism or protein kinase activation. The cell response was specific for AA, and fatty acids with greater saturation than tetraeicosanoic acid (AA) or with chain lengths less than C20 exhibited greatly diminished ability to initiate Ca2+ influx. Myristate and palmitate inhibited PLA2 activity and also inhibited Ca2+ influx. Overall, these results demonstrate that Ca2+ entry into T. brucei can result from phospholipid hydrolysis and the release of eicosanoic acids.
WANJIRU DRNGUGIROSE. "Onyancha C.; Are foreign exchange and stock markets related? An empirical analysis of the Kenyan case, 1998, University of Nairobi.". In: Paris 2011 World Cup in Paris, France. The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 1998. Abstract
In contrast with mammalian cells, little is known about the control of Ca2+ entry into primitive protozoans. Here we report that Ca2+ influx in pathogenic Trypanosoma brucei can be regulated by phospholipase A2 (PLA2) and the subsequent release of arachidonic acid (AA). Several PLA2 inhibitors blocked Ca2+ entry; 3-(4-octadecyl)-benzoylacrylic acid (OBAA; IC50 0.4+/-0.1 microM) was the most potent. We identified in live trypanosomes PLA2 activity that was sensitive to OBAA and could be stimulated by Ca2+, suggesting the presence of positive feedback control. The cell-associated PLA2 activity was able to release [14C]AA from labelled phospholipid substrates. Exogenous AA (5-50 microM) also initiated Ca2+ entry in a manner that was inhibited by the Ca2+ antagonist La3+ (100 microM). Ca2+ entry did not depend on AA metabolism or protein kinase activation. The cell response was specific for AA, and fatty acids with greater saturation than tetraeicosanoic acid (AA) or with chain lengths less than C20 exhibited greatly diminished ability to initiate Ca2+ influx. Myristate and palmitate inhibited PLA2 activity and also inhibited Ca2+ influx. Overall, these results demonstrate that Ca2+ entry into T. brucei can result from phospholipid hydrolysis and the release of eicosanoic acids.
1997
1996
WANJIRU DRNGUGIROSE. "Rose, W. Ngugi, Ikiara, M. M. and Makhoha J., 1996. Solid waste management in the city of Nairobi, perceptions, practices, and possibilities, SYLFF Working Paper # 2 November (JREX International Award Winning Research Paper, a condition for the publicatio.". In: Paris 2011 World Cup in Paris, France. The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 1996. Abstract
In contrast with mammalian cells, little is known about the control of Ca2+ entry into primitive protozoans. Here we report that Ca2+ influx in pathogenic Trypanosoma brucei can be regulated by phospholipase A2 (PLA2) and the subsequent release of arachidonic acid (AA). Several PLA2 inhibitors blocked Ca2+ entry; 3-(4-octadecyl)-benzoylacrylic acid (OBAA; IC50 0.4+/-0.1 microM) was the most potent. We identified in live trypanosomes PLA2 activity that was sensitive to OBAA and could be stimulated by Ca2+, suggesting the presence of positive feedback control. The cell-associated PLA2 activity was able to release [14C]AA from labelled phospholipid substrates. Exogenous AA (5-50 microM) also initiated Ca2+ entry in a manner that was inhibited by the Ca2+ antagonist La3+ (100 microM). Ca2+ entry did not depend on AA metabolism or protein kinase activation. The cell response was specific for AA, and fatty acids with greater saturation than tetraeicosanoic acid (AA) or with chain lengths less than C20 exhibited greatly diminished ability to initiate Ca2+ influx. Myristate and palmitate inhibited PLA2 activity and also inhibited Ca2+ influx. Overall, these results demonstrate that Ca2+ entry into T. brucei can result from phospholipid hydrolysis and the release of eicosanoic acids.
1993
WANJIRU DRNGUGIROSE. "Yong Yoon; World economic booms and crisis, adjustment policies and the current account: A decomposition analysis for Kenya 1972-1993, University of Nairobi.". In: Paris 2011 World Cup in Paris, France. The Icfai University Journal of Architecture, Vol. II No.1, February 2010; 1993. Abstract
In contrast with mammalian cells, little is known about the control of Ca2+ entry into primitive protozoans. Here we report that Ca2+ influx in pathogenic Trypanosoma brucei can be regulated by phospholipase A2 (PLA2) and the subsequent release of arachidonic acid (AA). Several PLA2 inhibitors blocked Ca2+ entry; 3-(4-octadecyl)-benzoylacrylic acid (OBAA; IC50 0.4+/-0.1 microM) was the most potent. We identified in live trypanosomes PLA2 activity that was sensitive to OBAA and could be stimulated by Ca2+, suggesting the presence of positive feedback control. The cell-associated PLA2 activity was able to release [14C]AA from labelled phospholipid substrates. Exogenous AA (5-50 microM) also initiated Ca2+ entry in a manner that was inhibited by the Ca2+ antagonist La3+ (100 microM). Ca2+ entry did not depend on AA metabolism or protein kinase activation. The cell response was specific for AA, and fatty acids with greater saturation than tetraeicosanoic acid (AA) or with chain lengths less than C20 exhibited greatly diminished ability to initiate Ca2+ influx. Myristate and palmitate inhibited PLA2 activity and also inhibited Ca2+ influx. Overall, these results demonstrate that Ca2+ entry into T. brucei can result from phospholipid hydrolysis and the release of eicosanoic acids.

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