Paternity index

The results should include aU the information requested by the client and necessary for the interpretation of the test results and all information required by the method used. If the weight of evidence is calculated, it must be based on likelihood ratio principles, such as the paternity index. 

The probability of paternity (W) and the paternity index (PI) are two closely related values that express the likelihood that the tested man is truly the father rather than another man who by chance shares alleles at a tested locus. Calcula-... 

Baur MP, Elston RC, Gurtler H, Henningsen K, Hummel K, Matsumoto H, et al. No fallacies in the formulation of the paternity index. Am J Human Genetics 1986 39 528-36. 

A 38-year-old man with a family history of cardiovascular and cerebrovascular disease makes an appointment for a routine physical examination with a physician he has not seen before. He explains that his father died young of a heart attack and that two paternal uncles have suffered strokes in their late 40s. Physical examination reveals yellowish lumps on his eyelids (xanthelasmas, which are often associated with a lipid disorder) and a resting blood pressure of 186/95 mm Hg. There is some excess visceral fat, and his body mass index calculates to 26.5. Total serum cholesterol (476 mg/dL) and triglycerides (288 mg/dL) are elevated and subsequent angiography reveals atherosclerotic restrictions of at least two coronary arteries. 

Forensic laboratories in the United States have agreed on 13 core STR loci that are most accurate for identification of an individual. Based on these 13 loci, a Combined DNA Index System (CODIS) has been established to serve as a registry of convicted offenders. If the profile of sequences from a known individual and the profile from DNA obtained at a crime scene match, the probability is approximately 82 billion to 1 that the DNA is from the same individual. In paternity cases, where the DNA of father and offspring are related but not fully identical, the identity of the father can be established with a probability of 100,000 to 1. 

Patient Population. The proband of the B family, T.B., was referred to the Lipid Research Clinic at The Johns Hopkins Hospital at the age of five years because of hypercholesterolemia of 900 mg/100 ml. She had multiple planar xanthomas that had first appeared at three years of age. The patient was free of symptoms of ischemic heart disease. The index lipoprotein pattern was type lib (57), with marked hypercholesterolemia, hyperbeta-lipoproteinemia, a mild hyperprebetalipoproteinemia and hypertriglyceridemia. None of the relatives of T.B. had xanthomas or corneal arcus one (J.S.) developed signs of premature coronary atherosclerosis at the age of 43 years. Increased total plasma and LDL cholesterol levels were transmitted over three generations on both maternal and paternal sides of the family (Fig. I). The parents of the proband, S.B. and K.B., had endogenous hypertriglyceridemia as well. Two normolipidemic members of this family (S.B., Jr. and E.B.), were also studied. 

In a rabbit study, hydroquinone at 150 mg kg day produced minimal developmental alterations in the presence of maternal toxicity. The no-observed-effect level for developmental toxicity was 75mgkg day In rat studies, maternal toxic effects from exposure to hydroquinone included changes in the ovaries, fallopian tubes, and menstrual cycle. Postimplantation mortality was also observed in rat studies. Observed paternal toxic effects from exposure to hydroquinone included changes in the testes, epididymis, sperm duct, prostate, seminal vesicle, Cowper s gland, accessory glands, and male fertility index. Further, exposure to hydroquinone produced skeletal malformations in chickens and ocular and skeletal malformations in rabbits. Hydroquinone can induce renal tubule adenomas, bladder carcinomas, hepatocellular neoplasms, and mononuclear cell leukemia in experimental animals. 

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