This work describes how reactions of oxidative addition of N-C and C-H bonds are in competition in the PNP-ligated Rh and Ir complexes. Iridium appears to have a higher preference than Rh for the C-H activation over the N-C activation, and the Ir C-H activated complexes are more kinetically stable than their Rh analogues. A new generation of a diarylamido-based PNP pincer is presented, a "tied" PNP ligand 1c based on the iminodibenzyl substructure. This ligand is more definitively prearranged for binding to a metal center in a meridional, anionic PNP fashion. As a result, its N-C cleavage reactions (that lead to complexes of anionic PNP) are faster than for the "untied" ligands 1a,b. Structural evidence indicates that the "tied" anionic PNP pincer ligand is bulkier than the "untied" ligands when bearing the same substituents on the donor atoms because of the influence of the conformation of the pincer backbone. The "tied" pincer ligand also allows for the observation of the products of activation of the C-H bonds of the central N-CH 3 group, which are not detected with the "untied" ligands. The N-C oxidative addition reaction with "untied" ligands proceeds in the solid state as well as in solution. A remarkable result is reported where the solid-state N-C oxidative addition reaction displays superior selectivity to the solution reaction. The mechanistic studies are augmented by the investigations of the isotopically labeled ( 2 H and 13 C) ligands.

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"Obesity cardiomyopathy" effects have been widely described; however, the specific contribution of metabolic changes and altered adipokine secretion are still uncharacterized. Moreover, a diagnosis based on body mass index might not be the most accurate to identify increased adiposity and its outcomes. In this study, we aimed to determine the impact of a Western-type diet [hypercaloric diet (HCD)] ingestion on biventricular structure and function, as well as the metabolic and endocrine changes that occur before the establishment of overt obesity. Wistar rats were fed for 6 wk with a regular diet or HCD. At the end of the protocol, metabolic tests, cardiac structure, and functional evaluation were performed, and blood and tissue samples collected to perform histological, molecular biology, and functional studies. The animals that ingested the HCD presented increased adiposity and larger adipocyte cross-sectional area, but similar body weight compared with the regular diet group. At the cardiac level, HCD induced biventricular cardiomyocyte hypertrophy, fibrosis, increased stiffness, and impaired relaxation. Galectin-3 plasma expression was likewise elevated in the same animals. The nutritional modulation also altered the secretory pattern of the adipose tissue, originating a proinflammatory systemic environment. In this study, we observed that before "clinical" overweight or frank obesity is established, the ingestion of a HCD-induced cardiac remodeling manifests by increased biventricular stiffness and diastolic dysfunction. The mechanism triggering the cardiac alterations appears to be the proinflammatory environment promoted by the adipose tissue dysfunction. Furthermore, galectin-3, a profibrotic molecule, might be a potential biomarker for the myocardial alterations promoted by the HCD before overweight or obesity.

Rapid maxillary expansion resulted in a reduction in hearing loss, yearly rate of ENT infections and parentally assessed symptoms of upper airway obstruction, compared with no treatment. These findings are probably related to expanded oronasal space, due to rapid maxillary expansion.