Barry S Marx

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Congenital malformations now represent the largest single cause of mortality in the infant of the diabetic mother. The mechanism by which diabetes exerts its teratogenic effects is not known. This study evaluated whether arachidonic acid might be involved, a possibility raised by the role of arachidonic acid in palatal elevation and fusion, processes(More)
The contribution of nociceptive Adelta-fibres and C-fibres of the central pad of the foot to nociceptive spinal flexor reflex pathways (FRA-type) and to nociceptive excitatory reflex pathways to foot extensors (non-FRA type) was investigated in high spinal cats by blocking A-fibres completely by TTX; effects persisting after TTX were attributed to(More)
We attempted to confirm the results of a previous study in which patients with hypogonadotropic hypogonadism (HH) could be readily distinguished from normal adolescents with constitutional delay of growth and development (CDGD) by their lower serum PRL responses to TRH. We compared the PRL responses to TRH of 13 teenaged males with HH to those of 14(More)
Our work on teratogen-induced cleft palate in rodents indicates that a functional deficiency of arachidonic acid mediates the defect. Because of analogous embryologic processes, we have hypothesized that the failure of neural tube fusion seen in diabetic embryopathy may involve a similar mechanism. This hypothesis was tested in two animal models of diabetic(More)
FSH, LH and prolactin (pro) responses to GNRH/TRH testing do not distinguish patients with idiopathic sexual precocity from those with hypothalamic hamartoma. Post-operative GNRH testing however, may be useful in the follow-up of cases due to organic lesions.A 2 9/12 year old white female with breast development, rapid weight gain and linear growth since(More)
Inborn errors of steroidogenesis present either with the classic clinical findings of congenital adrenal hyperplasia (CAH) or, as more recently described, in women with the clinical findings associated with the polycystic ovarian syndrome (PCOS). The present study evaluated serum 17 hydroxyprogesterone (17 OH-Prog) and 17 hydroxypregnenolone (17 OH-Preg)(More)
The lack of virilization in newborn males with 3β -HSD deficiency has been attributed to their inability to synthesize Δ 4 steroids, particularly T. However, no steroidal studies using radioimmunoassay technology have been performed in the newborn with this disorder. A newborn male with pseudovaginal perineoscrotal hypospadias was found to have a serum 17(More)