Resistance mechanism, genetic

While the mechanism of resistance to various synthetic pyrethroids in flies has been elucidated in terms of physiology, biochemistry, and genetics, it seems that the resistance mechanism is mostly common to mosquitoes. 

Bacteria can obtain the various types of resistance mechanisms described previously by undergoing modifications in their genetic constitution. Many bacteria simply inherit their resistance genes from their forerunners. In addition, genetic mutations can occur that can confer a new trait. For example, it has been estimated that bacteria undergo spontaneous mutation at a frequency of approximately 1 in 10 cells. These mutations can confer resistant traits to the subsequent progeny. Mutations are believed... 

Multidrug resistance (Mdr) is a serious problem in enteric and other Gramnegative bacteria [41, 71, 273-283] (Table 4.17). As distinct from plasmid-mediated resistance, described above, Mdr is a term employed to describe a resistance mechanism by genes that comprise part of the normal cell genome. These genes are activated by induction or mutation caused by some types of stress, considered below. Because the genes are ubiquitously distributed, there is no need for genetic transfer. 

Immunization of plants via priming for expression of latent genetic information encoding disease resistance mechanisms may be... 

The use of herbicide rotation to avoid resistance will not be successful in cases where resistance is conferred by non-specific detoxification mechanisms that act on herbicides with different modes of action. In this case, selection for weeds resistant to members of two or more mode-of-action groups can and does occur [9]. Therefore, alternating or rotating amongst herbicides from different mode-of-action groups does necessarily delay resistance development. Clearly, there is no simple herbicide rotation solution to resistance avoidance. The tremendous genetic diversity in some seed populations allows the evolution of resistance, with the resistance mechanism simply reflecting the nature of the selection pressure that was applied. 

Many different bioassays and biochemical or genetic tests have been developed to identify resistant weeds. However, these are normally conducted after the suspected development of resistance, not in a proactive or preventive manner. The potential for evolution of resistance to a new herbicide can be examined in several ways wild-type populations can be screened for resistant individuals, model plant populations can be muta-genized and screened for resistance, resistant cells can be selected in culture, with or without prior exposure to the herbicide, or biochemical or genetic assays can be used to identify known resistance mechanisms. However, more complex or obscure resistance mechanisms may exist, and certain mechanisms may only be expressed in whole plants, not in cell cultures. More recent techniques focused on rapid genetic evolution can also provide a clue to the relative ease with which resistance can be generated, but still require a large investment. However, as in many predictive studies, it is often difficult to relate the results of such experiments to resistance evolution in the field. 

Current evidence suggests that accumulation of fat in NAFLD is a consequence of insulin resistance. A variety of mechanisms may lead to insulin resistance, including genetic predisposition, increased concentrations of free fatty acids, and presence of cytokines such as tumor necrosis factor alpha (TNF-a). Since TNF-a is produced by fat cells, correlates with body fat, and is critical to development of insulin resistance in obesity,it may be a key factor in development of NAFLD. The pathogenesis is likely to be more complicated, however, as a variety of other factors lead to increased fat accumulation in the liver, including increased carbohydrate intake, certain drugs, and mutations in lipid synthesis, but have not been associated with development of NASH. 

Genetic analysis of different resistant mechanisms against the herbicidal antibiotic... 

Definition of existing and potential resistance mechanisms and their genetic basis. 

Resistance to pesticides arises primarily through changes in the sensitivity of the site of action or in the metabolism of the pesticide (25,27.28). Many pesticides are activated metabolically. While it is theoretically possible to generate resistance through reduced activation, it seems much more common to observe increased detoxification in resistant strains. In some cases decreased uptake or enhanced excretion also contribute. It is an obvious prerequisite for any type of scientifically-based attempt to combat resistance that the resistance mechanism and its genetic basis must be defined. 

HI. Hackbarth, C. J., and Chambers, H. F., Methicillin-resistant staphylococci Genetics and mechanisms of resistance. Antimicrob. Agents Chemother. 33, 991-994 (1989). 

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