Bio

DR. NGUGI ROSE WANJIRU CV

Publications


2011

Ngugi, RW, Sennoga E, Mohapatra S, Ratha D.  2011.  Remittances market in Uganda. Remittance Markets in Africa. : The World Bank
Ngugi, RW, Mohapatra S, Ratha D.  2011.  Remittances market in Kenya. Remittance Markets in Africa. : The World Bank

2010

Ngugi, RW, Maana I, Amanja D, Adam CS, Collier P, Ndung’u N.  2010.  Capital market and economic growth in Kenya. Kenya Policies for Prosperity. : Oxford University Press
O’Connell, SA, Maturu BO, Mwega FM, Ndung’u N, Ngugi RW, Adam CS, Collier P.  2010.  Capital mobility, monetary policy and exchange rate management in Kenya. Kenya Policies for Prosperity. : Oxford University Press

2009

Ngugi, RW, Agoti J.  2009.  Microstructure characteristics of the bonds market in Kenya. African Finance Journal.
Mbutu, M, Ngugi RW, Njenga G.  2009.  Financial sector development and economic growth in Africa. Africa Finance Journal.

2008

Ngugi, RW, Sifunjo EK, Wainaina G, Pokhariyal G.  2008.  An analysis of the efficiency of foreign exchange market in Kenya. Economic Bulletin.

2007

Ngugi, RW, Mbewa M, Kithinji A.  2007.  The development of bonds market in Kenya, KIPPRA Discussion Paper.
Ngugi, RW, Mwega FM, Ibi A.  2007.  Foreign Direct Investment in Kenya. Foreign Direct Investment in Sub-Saharan Africa: Determinants, Origins, Targets, Impact and Potential. : AERC

2006

Ngugi, RW, Nyang'oro O.  2006.  Investment Climate And Investment Growth. Website
Ngugi, RW, Nyang'oro O.  2006.  Insecurity And Investment Decisions. Website
Ngugi, RW, Were M, Makau P, Mensah J, Macmillan P.  2006.  Understanding the Reform Porcess in Kenya. Understanding Economic Reforms in Kenya.

2005

Were, M, Ngugi RW, Makau P, Wambua J, Oyugi L.  2005.  Kenya’s reform experience: What have we learnt? KIPPRA Working Paper #12
WANJIRU, DRNGUGIROSE.  2005.  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
Ngugi, RW, Murinde V, Green C, Green CJ, Kirkpatrick C, Murinde V, Elgar E.  2005.  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
Ngugi, RW, Nyang'oro O.  2005.  Institutional Factors and FDI Flows: Implications For Kenya, KIPPRA Discussion Paper # 48. : The Icfai University Journal of Architecture, Vol. II No.1, February 2010
Ngugi, RW.  2005.  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

2004

Ngugi, RW;, Murinde V;, Green CJ.  2004.  Stock market development: What have we learned. . Website
Ngugi, RW, Kimenyi MS, Gakuru O, Nyang’oro O, Muriu P, Nderitu P, Kariuki E, Kimilu G, Bikuri K, Njuguna S.  2004.  Security Risk and Private sector growth in Kenya, KIPPRA Special Report #06.
Ngugi, RW.  2004.  Understanding the structure of interest rates in Kenya, KIPPRA Discussion Paper # 40. : The Icfai University Journal of Architecture, Vol. II No.1, February 2010
Ngugi, RW.  2004.  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
WANJIRU, DRNGUGIROSE, Ngugi RW.  2004.  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
WANJIRU, DRNGUGIROSE.  2004.  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

2003

WANJIRU, DRNGUGIROSE.  2003.  Deregulation and management of interest rates, IPAR Discussion Paper # 38. : The Icfai University Journal of Architecture, Vol. II No.1, February 2010
WANJIRU, DRNGUGIROSE.  2003.  Rose W. Ngugi, What defines the liquidity of stock market? The case for Nairobi Stock Exchange, KIPPRA Discussion Paper # 29 Paris 2011 World Cup in Paris, France. : The Icfai University Journal of Architecture, Vol. II No.1, February 2010 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.  2003.  Rose W. Ngugi , Development of the NSE: A historical perspective, KIPPRA Discussion Paper # 27. Paris 2011 World Cup in Paris, France. : The Icfai University Journal of Architecture, Vol. II No.1, February 2010 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.
Ngugi, RW.  2003.   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
Ngugi, RW.  2003.  Kienjeku S. Mbuthia, Calendar anomalies in the NSE, University of Nairobi, 2003. : The Icfai University Journal of Architecture, Vol. II No.1, February 2010
WANJIRU, DRNGUGIROSE.  2003.  Rose W. Ngugi , Determinants of Interest rate spread in Kenya, African Journal of Economic Policy. Paris 2011 World Cup in Paris, France. : The Icfai University Journal of Architecture, Vol. II No.1, February 2010 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.
Ngugi, RW.  2003.  Muriu P. Wanjihia, Volatility of stock returns. University of Nairobi, 2003. : The Icfai University Journal of Architecture, Vol. II No.1, February 2010
WANJIRU, DRNGUGIROSE.  2003.  Owen Nyango'ro, Tax and Capital structure: Case of listed firms in Kenya, University of Nairobi, 2003. Paris 2011 World Cup in Paris, France. : The Icfai University Journal of Architecture, Vol. II No.1, February 2010 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.
Ngugi, RW.  2003.  Determinants of Interest rate spread in Kenya. African Journal of Economic Policy. : The Icfai University Journal of Architecture, Vol. II No.1, February 2010Website

2002

Ngugi, RW, Murinde V, Green C.  2002.   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

2001

WANJIRU, DRNGUGIROSE.  2001.  Rose W. Ngugi, An Empirical Analysis of Interest Rate Spread in Kenya. AERC Research Paper # 106. Paris 2011 World Cup in Paris, France. : The Icfai University Journal of Architecture, Vol. II No.1, February 2010 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.
Ngugi, RW.  2001.  "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

2000

WANJIRU, DRNGUGIROSE.  2000.  Njuguna Ndung'u and Rose W. Ngugi. Banking Sector Interest Rate Spread in Kenya. KIPPRA Discussion Paper # 5. Paris 2011 World Cup in Paris, France. : The Icfai University Journal of Architecture, Vol. II No.1, February 2010 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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