Maurine R. Hobbs

TL;DR: The findings suggest that HRPT2 is a tumor-suppressor gene, the inactivation of which is directly involved in predisposition to HPT–JT and in development of some sporadic parathyroid tumors.

TL;DR: GNA11 mutations predicted disrupted protein structures, and assessment on the basis of in vitro expression showed that familial hypocalciuric hypercalcemia type 2-associated mutations decreased the sensitivity of cells expressing calcium-sensing receptors to changes in extracellular calcium concentrations, whereas autosomal dominant hypocalcemia types 1 and 2- associated mutations increased cell sensitivity.

TL;DR: Increased NO production in individuals with the NOS2 promoter -1173 C-->T single nucleotide polymorphism lends support to a protective role for NO against these syndromes.

TL;DR: Nitric oxide (NO) production and mononuclear cell NO synthase 2 (NOS2) expression are high in healthy Tanzanian children but low in those with cerebral malaria, and analysis by logistic regression showed that hypoargininaemia was significantly associatedWith cerebral malaria case-fatality.

TL;DR: The results of this analysis expand the spectrum of HPT‐JT‐associated tumours to include uterine tumours, and these may account for the decreased reproductive fitness in females from HPT-JT families.