Physical Growth, Biological Age, And Nutritional Transitions Of Adolescents Living At Moderate Altitudes In Peru

Background: Peru is experiencing a stage of nutritional transition where the principal characteristics are typical of countries undergoing development. Objectives: The objectives of this study were the following: (a) compare physical growth patterns with an international standard; (b) determine biological age; and (c) analyze the double nutritional burden of adolescents living at a moderate altitude in Peru. Design: Weight, standing height, and sitting height were measured in 551 adolescents of both sexes (12.0 to 17.9 years old) from an urban area of Arequipa, Peru (2328 m). Physical growth was compared with the international standard of the CDC-2000. Biological age was determined by using a non-invasive transversal technique based on years from age at peak height velocity (APHV). Nutritional state was determined by means of weight for age and height for age. Z scores were calculated using international standards from the CDC-2000. Results: Body weight for both sexes was similar to the CDC-2000 international standards. At all ages, the girls' height (p < 0.05) was below the standards. However, the boys' height (p < 0.05) was less at ages, 15, 16, and 17. Biological age showed up in girls at age 12.7 years and for boys at 15.2 years. Stunted growth (8.7% boys and 18.0% girls) and over weight (11.3% boys and 8.8% girls) occurred in both groups. A relationship existed in both sexes between the categories of weight for the age and stunted growth by sex. Conclusions: Adolescents living at a moderate altitude exhibited stunted linear growth and biological maturation. Furthermore, adolescents of both sexes showed the presence of the double nutritional burden (stunted growth and excessive weight).1210120821209

Defining the molecular basis of BubR1 kinetochore interactions and APC/C-CDC20 inhibition.

BubR1 is essential for the mitotic checkpoint that prevents aneuploidy in cellular progeny by triggering anaphase delay in response to kinetochores incorrectly/not attached to the mitotic spindle. Here, we define the molecular architecture of the functionally significant N-terminal region of human BubR1 and present the 1.8 A crystal structure of its tetratricopeptide repeat (TPR) domain. The structure reveals divergence from the classical TPR fold and is highly similar to the TPR domain of budding yeast Bub1. Shared distinctive features include a disordered loop insertion, a 3(10)-helix, a tight turn involving glycine positive Phi angles, and noncanonical packing of and between the TPR motifs. We also define the molecular determinants of the interaction between BubR1 and kinetochore protein Blinkin. We identify a shallow groove on the concave surface of the BubR1 TPR domain that forms multiple discrete and potentially cooperative interactions with Blinkin. Finally, we present evidence for a direct interaction between BubR1 and Bub1 mediated by regions C-terminal to their TPR domains. This interaction provides a mechanism for Bub1-dependent kinetochore recruitment of BubR1. We thus present novel molecular insights into the structure of BubR1 and its interactions at the kinetochore-microtubule interface. Our studies pave the way for future structure-directed engineering aimed at dissecting the roles of kinetochore-bound and other pools of BubR1 in vivo

Young tableau reconstruction via minors

The tableau reconstruction problem, posed by Monks (2009), asks the following. Starting with a standard Young tableau $T$, a 1-minor of $T$ is a tableau obtained by first deleting any cell of $T$, and then performing jeu de taquin slides to fill the resulting gap. This can be iterated to arrive at the set of $k$-minors of $T$. The problem is this: given $k$, what are the values of $n$ such that every tableau of size $n$ can be reconstructed from its set of $k$-minors? For $k=1$, the problem was recently solved by Cain and Lehtonen. In this paper, we solve the problem for $k=2$, proving the sharp lower bound $n \geq 8$. In the case of multisets of $k$-minors, we also give a lower bound for arbitrary $k$, as a first step toward a sharp bound in the general multiset case.Comment: 24 pages, 18 figure

Characterization of spindle checkpoint kinase Mps1 reveals domain with functional and structural similarities to tetratricopeptide repeat motifs of Bub1 and BubR1 checkpoint kinases.

Kinetochore targeting of the mitotic kinases Bub1, BubR1, and Mps1 has been implicated in efficient execution of their functions in the spindle checkpoint, the self-monitoring system of the eukaryotic cell cycle that ensures chromosome segregation occurs with high fidelity. In all three kinases, kinetochore docking is mediated by the N-terminal region of the protein. Deletions within this region result in checkpoint failure and chromosome segregation defects. Here, we use an interdisciplinary approach that includes biophysical, biochemical, cell biological, and bioinformatics methods to study the N-terminal region of human Mps1. We report the identification of a tandem repeat of the tetratricopeptide repeat (TPR) motif in the N-terminal kinetochore binding region of Mps1, with close homology to the tandem TPR motif of Bub1 and BubR1. Phylogenetic analysis indicates that TPR Mps1 was acquired after the split between deutorostomes and protostomes, as it is distinguishable in chordates and echinoderms. Overexpression of TPR Mps1 resulted in decreased efficiency of both chromosome alignment and mitotic arrest, likely through displacement of endogenous Mps1 from the kinetochore and decreased Mps1 catalytic activity. Taken together, our multidisciplinary strategy provides new insights into the evolution, structural organization, and function of Mps1 N-terminal region