This book is an edited collection of papers by leading experts on the population genetics and evolutionary biology of malaria, a disease which results in three million deaths

Inhoudsopgave:

Preface		ix
Contributors		xi
1. Introduction
Krishna R. Dronamraju
1. The Haldane Hypothesis		2	(3)
2. Glucose-6-Phosphate Dehydrogenase Deficiency and Malarial Resistance		5	(1)
3. Phagocytosis of Ring Forms		6	(1)
4. Evolutionary Considerations: Malaria`s Eve Hypothesis		6	(2)
5. Malaria Vaccines		8	(2)
References		10	(6)
2. J.B.S. Haldane (1892-1964)
Krishna R. Dronamraju
1. Population Genetics		16	(1)
2. Beanbag Genetics		17	(1)
3. Terminology		17	(1)
4. Human Genetics		18	(1)
5. Genetic Load Theory		19	(1)
6. Immunogenetics		19	(2)
7. Sociobiology		21	(1)
8. Daedalus and Eugenics		21	(1)
References		22	(3)
3. Removal of Early Parasite Forms from Circulation as a Mechanism of Resistance Against Malaria in Widespread Red Blood Cell Mutations
Paolo Arese, Kodjo Ayi, Aleksei Skorokhod and Franco Turrini
1. Introduction		25	(2)
2. Malaria is Responsible for High Frequency and Regional Distribution of Major Protective RBC Mutations: Geographical Evidence		27	(2)
3. Epidemiological Evidence: Degree of Protection Afforded by RBC Mutations		29	(3)
3.1. Hemoglobin AS (Sickle-Cell Trait)		29	(1)
3.2. Thalassemias		29	(1)
3.3. Hemoglobin C		30	(1)
3.4. Hemoglobin E		30	(1)
3.5. Glucose-6-Phosphate Dehydrogenase		31	(1)
3.6. Southeast Asian Ovalocytosis		32	(1)
4. A Critical Assessment of the Current Mechanism of Protection by Widespread RBC Mutations		32	(7)
4.1. Sickle-Cell Anemia		36	(1)
4.2. Beta-Thalassemia		36	(1)
4.3. Alpha-Thalassemia		37	(1)
4.4. Glucose-6-Phosphate Dehydrogenase Deficiency		38	(1)
5. Modifications in the RBC Membrane Elicited by the Developing
Parasite Induce Phagocytosis		39	(1)
5.1. Similarity of Ring Phagocytosis to Phagocytosis
of Normal Senescent or Oxidatively Stressed RBCs		39	(2)
6. Enhanced Phagocytosis of Ring Forms as a Model of Protection for Widespread RBC Mutations		41	(7)
6.1. Membrane Binding of Hemichromes, Autologous IgG, Complement C3c Fragment; Aggregated Band 3 and Phagocytosis in Nonparasitized and Ring-Parasitized Normal and Mutant RBCs		41	(2)
6.2. Why are Rings Developing in Beta-Thalassemia, Sickle-Cell Trait, HbH, and G6PD-deficient RBCs Phagocytosed More Intensely than Rings Developing in Normal RBCs?		43	(2)
6.3. What is the Evidence that Ring-Parasitized Mutant RBCs are Also Preferentially Removed In Vivo?		45	(1)
6.4. Why is Preferential Removal of Ring-Forms Advantageous to the Host?		46	(1)
6.5. Why are Rings Developing in Alpha-Thalassemia Very Similar to Controls?		46	(2)
7. Conclusions		48	(2)
References		50	(6)
4. Clinical, Epidemiological, and Genetic Investigations on Thalassemia and Malaria in Italy
Stefano Canali and Gilberto Corbellini
1. The Evolution of the Knowledge of Thalassemia Genetics: The Italian Contribution		56	(2)
2. Early Observations on the Association between Malaria and Thalassemia		58	(5)
3. Collaboration of Silvestroni and Bianco with Montalenti: At Work on Haldane`s Hypothesis		63	(5)
4. Research of Carcassi et al.		68	(1)
5. Studies on Microcythemia Genetics in Italy Funded by the Rockefeller Foundation		69	(5)
6. The Results of Siniscalco`s Genetic Studies on the Distribution of Thalassemia, G-6-PD Deficit, and of Malaria		74	(1)
7. The Malaria Hypothesis and the Consequences of Eradicating the Plasmodia and of Thalassemia Prevention		75	(1)
8. Conclusions		76	(1)
Acknowledgements		77	(1)
References		77	(4)
5. Resistance to Antimalarial Drugs: Parasite and Host Genetic Factors
Rajeev K. Mehlotra and Peter A. Zimmerman
1. Introduction		81	(1)
2. Malaria		82	(1)
3. Antimalarial Chemotherapy and Chemoprophylaxis		83	(3)
3.1. Drugs Available for Treatment of Malaria		83	(3)
4. Antimalarial Drug Resistance		86	(10)
4.1. Current Status of Drug-Resistant Malaria		86	(3)
4.2. Parasite Genetic Polymorphism As a Basis for Antimalarial Resistance		89	(1)
4.3. Genes Associated with Chloroquine Resistance in P. falciparum		90	(3)
4.4. Mechanism of Resistance to Antifolate Combination Drugs in P. falciparum		93	(1)
4.5. Mechanism of Atovaquone Resistance in P. falciparum		94	(1)
4.6. Mechanisms of Drug Resistance in P. vivax		95	(1)
5. Human Drug Metabolism		96	(13)
5.1. Cytochrome P450 Enzyme Superfamily		96	(2)
5.2. Uridine Diphosphate Glucuronosyltransferase Enzyme Superfamily		98	(2)
5.3. Antimalarial Drug Metabolism		100	(4)
5.4. Antimalarial Drug Levels and Treatment Outcome		104	(5)
6. Conclusions		109	(1)
Acknowledgments		110	(1)
References		110	(15)
6. Evolutionary Origins of Human Malaria Parasites
Stephen M. Rich and Francisco J. Ayala
1. The Phylum Apicomplexa		125	(2)
2. The Genus Plasmodium		127	(5)
3. Transfers Between Human and Monkey Hosts		132	(3)
4. Population Structure of Plasmodium falciparum		135	(2)
5. Malaria`s Eve Hypothesis		137	(3)
6. Malaria`s Eve Counterarguments		140	(2)
Appendix		142	(1)
References		143	(4)
7. Vector Genetics in Malaria Control
V.P. Sharma
Abstract		147	(1)
1. Introduction		147	(2)
2. The Anopheles culicifacies Complex		149	(7)
2.1. Paradox Resolved		154	(2)
3. Application in Malaria Control		156	(8)
3.1. Stratification		157	(1)
3.2. Insecticide Resistance		158	(4)
3.3. Bioenvironmental Malaria Control		162	(2)
Acknowledgments		164	(1)
References		165	(4)
8. The Rate of Mutation of Human Genes		169	(6)
J.B.S. Haldane
9. Disease and Evolution		175	(14)
J.B.S. Haldane
Index		189

Extra informatie: Gebonden: harde kaft, 190 pagina's Verschenen: februari 2006 Gewicht: 476 gram Formaat: 235 x 159 x 19 mm Springer Verlag

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