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Causal mutations and their intra- and inter-locus interactions play a critical role in complex trait variation. It is often not easy to detect epistatic quantitative trait loci (QTL) due to complicated population structure requirements for detecting epistatic effects in linkage analysis studies and due to main effects often being hidden by interaction effects. Mapping their positions is even harder when they are closely linked. The data structure requirement may be overcome when information on linkage disequilibrium is used. We present an approach using a mixed linear model nested in an empirical Bayesian approach, which simultaneously takes into account additive, dominance and epistatic effects due to multiple QTL. The covariance structure used in the mixed linear model is based on combined linkage disequilibrium and linkage information. In a simulation study where there are complex epistatic interactions between QTL, it is possible to simultaneously map interacting QTL into a small region using the proposed approach. The estimated variance components are accurate and less biased with the proposed approach compared with traditional models.  相似文献   
204.
In a randomized crossover study 15 dysmenorrheic women were treated during two consecutive menstrual periods, once with the potent prostaglandin-synthesis inhibitor: ibuprofen and once with an identical looking placebo. Each patient was medicated for 12 hours during the first day of her menstrual flow and was subsequently fitted with a cervical cup for the collection of menstrual blood during three hours. In these samples the concentrations of prostaglandin (PG)F and PGE were measured by radioimmunoassay.The patients receiving placebo had high PGF levels 135 ± 27 ng/ml (Mean ± S.E.) which were significantly reduced by Ibuprofen to 24 ± 5 ng/ml (P<0.001). The PGE concentrations decreased from 5 ± 1 ng/ml to 2 ± 1 ng/ml (P<0.05). Ibuprofen also reduced the menstrual pain significantly (P<0.001). These results substantiate the earlier conclusion that a causal relationship exists between effective treatment with PG-synthesis inhibitors and decrease in menstrual blood PG levels, intrauterine pressure and dysmenorrheic pain.  相似文献   
205.
Identification of messenger RNA for human type II collagen   总被引:4,自引:0,他引:4  
The fluorescence polarization of acridine orange-stained, oriented lambda phages was measured. The parameters of DNA packing within the phage head cos2 theta and cos4 theta were calculated (theta, angle between the direction of a small segment of DNA and the phage axis). It is shown that simple models of lambda phage DNA tertiary structure are not consistent with calculated values. A new model is proposed.  相似文献   
206.
Stress caused by the 'mark-recapture' method to Coregonus albula (L)   总被引:1,自引:0,他引:1  
The aim of this study was to establish if capture and marking caused stress to C. albula , and if a 'mark-recapture' method was suitable for the estimation of a population of C. albula . The blood lactate and glucose levels and the liver and muscle glycogen content were determined during the initial handling and subsequent recovery of the fish in the autumn and spring.
The blood lactate content did not increase to the critical level. Usually the values were distinctly less than 100 mg %, but the blood glucose content increased throughout the whole experiment (24 h) until it reached 250 mg %. The glycogen content in liver and muscle decreased. The liver glycogen of female C. albula was below 0·3 % in autumn, while the values for males were 3–5 %. In spring, the corresponding values were about 0·5 % in both sexes. During handling, the critical period was when the glycogen reserves in the liver became negligible, and female C. albula in autumn had the greatest risk of dying because of their low liver glycogen content.
Spring seemed to be a better season for marking than the autumn. A steady increase in blood glucose indicated there was also stress in spring and the marking time in both seasons should be less than two hours.  相似文献   
207.
Family, twin and adoption studies have provided evidence for familial and genetic influences on individual differences in disease risk and in human behavior. Attempts to identify individual genes accounting for these differences have not been outstandingly successful to date, and at best, known genes account for only a fraction of the familiality of most traits or diseases. More detailed knowledge of the dynamics of gene action and of specific environmental conditions are needed. Twin and twin-family studies with multiple measurements of risk factors and morbidity over time can permit a much more detailed assessment of the developmental dynamics of disease risk and the unfolding of behavioral risk factors.  相似文献   
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