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Genetics probabilities

I told Jennifer that from her descriptions, both of her parents probably were depressed, even though neither had ever been formally diagnosed. Genetics probably accounts for 40 to 50 percent of mood disorders, including depression but because mental illness has been stigmatized for so long, many people who today would be considered depressed have never been diagnosed. [Pg.30]

Whatever the physiology of odor perception may be, the sense of smell is keener than that of taste (22). If flavors are classed into odors and tastes as is common practice in science, it can be calculated that there are probably more than 10 possible sensations of odor and only a few, perhaps five, sensations of taste (13,21,35—37). Just as a hereditary or genetic factor may cause taste variations between individuals toward phenylthiourea, a similar factor may be in operation with odor. The odor of the steroid androsterone, found in many foods and human sweat, may eflcit different responses from different individuals. Some are very sensitive to it and find it unpleasant. To others, who are less sensitive to it, it has a musk or sandalwood-like smell. Approximately 50% of the adults tested cannot detect any odor even at extremely high concentrations. It is befleved that this abiUty is genetically determined (38). [Pg.11]

Filter Press The filter press, one of the most frequently used filters in the early years or the chemical industry, is still widely employed. Often referred to genetically (in error) as the plate-and-frame filter, it has probably over 100 design variations. Two basic popular designs are the flush-plate, or plate-and-frame, design and the recessed-plate press. Both are available in a wide range of materials metals, coated metals, plastics, or wood. [Pg.1709]

S Greenland. Probability logic and probability induction. Epidemiology 9 322-332, 1998. GM Petersen, G Parmigiam, D Thomas. Missense mutations in disease genes A Bayesian approach to evaluate causality. Am J Hum Genet. 62 1516-1524, 1998. [Pg.345]

Appendix III contains failure rate estimates for various genetic types of mechanical and electrical equipment. Included ate listings of failure rates with range estimates for specified component failure modes, demand probabilities, and times to maintain repair. It also contains some discussion on such special topics as human errors, aircraft crash probabilities, loss of electric power, and pipe breaks. Appendix III contains a great deal of general information of use to analysts on the methodology of data assessment for PRA. [Pg.125]

Step 5 Loop through each bit of each chromosome in the population and perforin genetic mutation i.c. flip the bit-value (0 1 and 1 0) at each locus with some (typically small see below) probability, p,j. (In practice, this step is combined with step 4.)... [Pg.588]

There is a small probability of a genetic change occurring each time a cell divides. Therefore, selection of natural variants may result in increased yields but it is not possible to rely on such improvement, and techniques must be employed to increase the chances of improving the culture. [Pg.29]

Genetic transmission in nemaline myopathy is the subject of some uncertainty. A Japanese study of 50 pedigrees came to the conclusion that autosomal dominant with reduced penetrance was the most probable mode. However a Finnish study presented evidence for autosomal recessive transmission. There is no evidence that severe and mild forms are genetically distinct and several pedigrees contain members showing widely differing clinical severity. A candidate gene for autosomal dominant nemaline myopathy has been localized to chromosome Iq 21—23. [Pg.293]

The genetic trait for MH is not sex-linked and both men and women can inherit MH. Inheritance in humans appears to be autosomal dominant with variable penetrance. Studies of large families have documented an autosomal dominant pattern. McPherson and Taylor (1982) studied 93 families in whom MH occurred. Even though various patterns of inheritance did emerge in the study we should assume that 50% of children are at risk in MH susceptible families. Kalow and Britt (1992) suggested that, in some families, at least two different non-allelic genes are likely to be present, one of which is probably autosomal dominant but rare, and the other autosomal recessive but common. [Pg.401]


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See also in sourсe #XX -- [ Pg.131 , Pg.132 ]




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