By Kenneth M. Smith and Max A. Lauffer (Eds.)
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Utilizing as a subject the stumble upon among protozoan parasites and macrophages, this quantity brings jointly phone biologists, immunologists and protozoologists to check present advancements during this wide and dynamic learn zone. mentioned are methods protozoans determine their intracellular area of interest, how they turn on macrophage effector services, what those features are, and capacity in which numerous protozoans subvert macrophage task.
It really is now 17 years because the junior author's publication Parasitic protozoa was once first released, and thirteen years because it obtained restricted revision. The research of symbiotic protozoa has in the meantime stepped forward, and masses of the content material of the sooner booklet has been outdated if no longer displaced by means of contemporary wisdom. We think that there's nonetheless a spot for an introductory textbook, conventionally prepared on a taxonomic body paintings, in this such a lot attention-grabbing workforce of organisms.
The previous 12 months has been one in every of viral panic—panic approximately viruses, that's. via headlines, public overall healthiness warnings, and a minimum of one home made hazmat swimsuit, we have been reminded of the robust strength of viruses. they're the smallest dwelling issues recognized to technology, but they could carry the total planet of their sway.
- Biomarker Discovery in the Developing World: Dissecting the Pipeline for Meeting the Challenges
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- Transgenic Models of Human Viral and Immunological Disease
- Virus as populations : composition, complexity, dynamics, and biological implications
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The assumption that a single event results in a mutation is expressed by the equation m = 1- e-rkt in which rri is the fraction of mutants in the total population and r is the fraction of events which arc mutating events. When T is small in relation to Ict, m becomes approximately equal to rkt. The fraction of the total population which can be detected as mutants is that fraction, M , which has been mutated but not killed. Thus, A4 = ms = rkte& and from which it can be seen that M will have a maximum value when k t is equal to 1, and Mundry and Gierer found that they did observe a maximum value for A4 when k t was 1 (the fraction of survivors is 37% when kt is equal to l), and also that reasonably good agreement was found between experimental values for M / M,,,, at different kt‘s and the theoretical values derived from the above equation.
25 26 26 27 28 29 31 31 33 42 43 44 45 46 47 55 58 I. INTRODUCTION One of the outstanding problems of biology is the nature of the relationship between gene and gene product. Viruses offer a useful material for attacking this problem because virus particles consist of a small number of genes and one to several gene products. The smalI ribonucleic acid-containing viruses are particularly useful for this purpose because many of them contain only enough nucleic acid to comprise a small number of genes and only a single species of protein as a gene product.
Chemical Mutagenesis In contrast to the absence of conclusive evidence for mutagenicity of in vivo treatments of the virus-host system or of irradiation of virus preparations in uitro, little doubt exists concerning the mutation-inducing power of at least one chemical reagent, nitrous acid. The chief reason for the Iack of uncertainty lies in an exceptionally high frequency mutation induction with this reagent. a. Nitrous Acid. i. The killing and mutagenic effect of nitrous acid. The efficacy of nitrous acid as a mutagen for TMV was first demonstrated by Mundry and Gierer (1958) (see also Gierer and Mundry, 1958).