Craniofacial shape from pre- to post-adolescence.

AIM: Craniofacial growth demonstrates significant variation and is difficult to predict. The aim of the present investigation was twofold: (1) to assess the association (covariation) between craniofacial shape at pre- and post-adolescence and (2) to evaluate if pre-adolescent craniofacial shape is related (covaries) with growth magnitude and direction. SUBJECTS AND METHODS: One hundred fifty subjects (86 males and 64 females) untreated orthodontically were selected from AAOF Craniofacial Growth Legacy Collection. Each subject had cephalograms taken before 9 (pre-adolescent stage) and after 15 years of age (post-adolescent). Fourteen curves comprising 123 points (10 fixed and 113 sliding semilandmarks) comprehensively covering the craniofacial skeleton were digitally traced on each cephalogram. Procrustes alignment, principal component analysis, 2-block partial least squares (2B-PLS) analysis, and regression analysis were done after sliding the semilandmarks to minimize bending energy. RESULTS: The first 16 principal components (PCs) were non-trivial and explained 85.2% of total shape variability in the sample. PC1 depicted mainly variability in the vertical direction, PC2 represented mostly variability in the saddle angle and in the antero-posterior position of the mandible, and PC3 depicted primarily variability of the mandibular shape (steep versus flat mandibular plane). The covariation between pre- and post-adolescent facial shape was statistically significant, both in the pooled sample (RV coefficient = 0.604) and in boys (RV = 0.639) and girls (RV = 0.629). The pre-adolescent shape was weakly associated with the magnitude of facial change-2-block PLS analysis demonstrated that blocks 1 and 2 were independent (P = 0.118, RV = 0.035). CONCLUSIONS: The pre-adolescent shape of the craniofacial complex explained approximately 60% of the post-adolescent shape of the craniofacial complex; however, the relationship between pre-adolescent shape of the craniofacial complex and magnitude of its change was weak.

Chiral Cryptates Derived from a Hexaazamacrocycle.

The reactions of hexaazamacrocycle 1 with 2,6-bis(bromomethyl)pyridine or 2,6-bis[(tosyloxy)methyl)]pyridine in the presence of appropriate carbonates result in the formation of derivatives of cryptand 6: enantiopure azacryptates of sodium and potassium. Crystal structures of these compounds indicate interaction of a metal ion with four pyridine nitrogen atoms and four tertiary amine atoms. The competition reactions monitored by NMR spectroscopy indicate preferential binding of Na+ over K+ as well as higher affinity of 6 for Na+ in comparison with the [2.2.1] cryptand.

Endothelial dysfunction in young healthy men is associated with aspirin resistance.

The aim of this study was to investigate the relation between endothelial dysfunction and aspirin response in a young healthy population (102 men aged 18-40). Initial concentrations of the NO pathway metabolites (ADMA, l-arginine, SDMA), cardiovascular risk markers, oxidative stress markers (MDA, thiol index), sICAM1, sVCAM1, PAI-1, sE-selectin, sP-selectin, VEGF, thromboxane B2, 6-keto-PGF1α and arachidonate-induced platelet aggregation (to separate aspirin resistant from sensitive group) were measured. Flow-mediated-vasodilation (FMD) was measured before and after intravenous infusion of 16.0 g of l-arginine. Measurements were repeated following aspirin administration (75 mg/24 h) for 4 days. Both groups were homogenous regarding demographic and biochemical characteristics reflecting cardiovascular risk. Aspirin resistant subjects were characterized by lower baseline FMD and higher FMD following aspirin and l-arginine treatment, as compared to aspirin sensitive control. MDA and nitrotyrosine were greater, whereas thiol index was lower in aspirin resistant men. The sICAM1, sVCAM1, PAI-1, sE-selectin, sP-selectin and VEGF levels were similar in the analyzed groups. Thromboxane in aspirin resistant subjects was greater both at baseline and following aspirin therapy. However, a significant decrease following aspirin treatment was present in both groups. Aspirin resistance in young men is associated with endothelial dysfunction, which could be due to oxidative stress resulting from lipid peroxidation.