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Biomedical subjects

M B Foster

Publications and source records attributed to M B Foster.

4 recordsLinked to original sources

Aberrant puberty.

With the emergence of an understanding of the processes at the cellular level that control the differentiated functions of tissues and eventually manifest as the developmental sequence in the whole animal, it is possible to describe pubertal aberrations in terms that are at once grounded in fundamental concepts of cellular biology and of practical value to the clinician. Delayed puberty and its treatment represent a relatively straightforward problem, submitting to division into two groups of patients: those whose gonadotropin levels are elevated (hypergonadotropic hypogonadism), implying primary gonadal failure; and those whose gonadotropin levels are low (hypogonadotropic hypogonadism), implying either a failure of the central control axis or an adaptive response to a disruptive stress. Precocious puberty is also usefully separable into two distinct groups of patients: those in whom the normal central control axis is activated and those in whom it is not. The workup beyond the basic general stage and the approach to therapy are both determined by into the group into which the patient can be assigned. Advances in imaging technology have enhanced the diagnostic process, and chemical remodeling of the hypothalamic peptide, which mediates control of the pituitary's contribution, has revolutionized the treatment of CMPP, making it imperative that the clinician be able to distinguish those conditions that merit treatment from those that may be observed safely.

Adolescent

HLA type and the genetic risk for type 1 diabetes mellitus.

One hundred twenty-nine type 1 diabetic children and 176 non-diabetic siblings from the Louisville referral area were HLA typed by microlymphocytotoxicity technique. DR antigen frequencies were compared to frequencies for the Southeast USA population. Frequencies of DR3 and DR4 were significantly increased in both the diabetics and their unaffected siblings relative to the general population and DR2 was decreased. Forty-six percent of diabetic children possessed both DR3 and DR4 antigens while only 7% had neither. The findings are consistent with those in other geographical areas and give strong support to the role of DR3 and DR4 antigens as markers for diabetes susceptibility genes.

Child