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By Gary D. Berkovitz MD (auth.), Dr. Stuart Handwerger MD (eds.)

In Molecular and mobile Pediatric Endocrinology, Stuart Handwerger, MD and a unusual panel of clinicians and specialists evaluate the main major contemporary advancements in molecular and mobile biology, robust advances that experience produced new diagnostic tools and more advantageous remedies for lots of pediatric endocrine ailments. subject matters diversity from the expansion hormone/prolactin/placental lactogen gene relations and their rules of progress, to steroid hormones, sexual improvement, and mineral corticoid motion. extra chapters study the pathophysiology of insulin-dependent diabetes mellitus, the molecular genetics of thyroid melanoma, the molecular foundation of hypophosphatemic rickets, and inherited diabetes insipidus.
Molecular and mobile Pediatric Endocrinology bargains present day clinicians and researchers not just the newest findings on endocrine problems of their pediatric manifestations, but in addition hugely sensible insights into brand new state-of-the-art diagnostics, rising remedy recommendations, and robust new therapeutics.

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Extra resources for Molecular and Cellular Pediatric Endocrinology

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Since tumors frequently secrete, in abnormal amounts andin an unregulated fashion, substances that have a role in normal physiology, it is plausible that the phosphate wasting observed in patients who have tumor induced osteomalacia is caused by overproduction of a factor( s) that normally controls renal phosphate reabsorption. Wehave referred to this factor as "phosphatonin" (24). Unfortunately, this factor has only been partially purified (25,26) and its role in the phosphate wasting seen in HYP has yet to be determined.

The hallmark of this disease is isolated renal phosphate wasting with inappropriately normal calcitriol concentrations. An osteablast defect has also been proposed to contribute to impaired From: Molecu/ar and Cellular Pediatric Endocrinology Edited by: S. , Totowa, NJ 39 40 Econs and Strom mineralization in the disorder (see below). Classically, patients present with lower extremity deformities, rickets, growth retardation, hone pain, tooth abscesses, enthesopathy, and osteomalacia (2). However, the severity ofthe disease is variable and affected members of the same family, who have the same genetic defect, may have markedly different phenotypes.

IGF-1 acts tbrougb its own receptor to enbance tbe proliferation and maturation of many tissues including bone, cartilage, and skeletal muscle. In addition to promoting growth of different tissues through these various effects, GH bas also been sbown to exert a variety of other biological effects including lactogenic, diabetogenic, lipolytic, protein-anabolic, and sodium/water-retention (1). From: Molecu/ar and Ce/lu/ar Pediatric Endocrinology Edited by: S. , Totowa, NJ 23 Cogan and Phillips 24 Fig.

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