Evaluation of the effect of stent strut profile on shear stress distribution using statistical moments

Background  

In-stent restenosis rates have been closely linked to the wall shear stress distribution within a stented arterial segment, which in turn is a function of stent design. Unfortunately, evaluation of hemodynamic performance can only be evaluated with long term clinical trials. In this work we introduce a set of metrics, based on statistical moments, that can be used to evaluate the hemodynamic performance of a stent in a standardized way. They are presented in the context of a 2D flow study, which analyzes the impact of different strut profiles on the wall shear stress distribution for stented coronary arteries.     

Cathodoluminescence Microscopy: A Useful Tool for Assessing Incremental Chemical Variation in Otoliths

Otoliths taken from fish from Eden Lake, Manitoba show yellow–green and red cathodoluminescence of varying intensity that corresponds to their annular structure. Proton-induced X-ray emission analysis shows manganese (Mn) concentrations of between 2 and 205ppm, zinc (Zn) concentrations between 2 and 290ppm and strontium (Sr) concentrations up to 1500ppm in the otoliths. The distribution of luminescence correlates with the distribution of Mn. The Mn, Zn and Sr are likely derived from the monzonitic rocks surrounding the lake. Variations in the distribution of cathodoluminescence may be a useful tool for evaluating changes in environmental chemistry and fish life histories.     

Mammalian mitochondrial methylenetetrahydrofolate dehydrogenase-cyclohydrolase derived from a trifunctional methylenetetrahydrofolate dehydrogenase-cyclohydrolase-synthetase

We have isolated the cDNA and the gene encoding the murine cytoplasmic methylenetetrahydrofolate dehydrogenase-methenyltetrahydrofolate cyclohydrolase-formyltetrahydrofolate synthetase (DCS). Comparison of these sequences with the 3'-untranslated region of the mitochondrial NAD(+)-dependent methylenetetrahydrofolate dehydrogenase-cyclohydrolase (mt-DC) revealed areas of significant homology. Both exon and intron sequences of the synthetase domain of DCS are homologous to sequences in the untranslated region of mt-DC. A similar comparison between the mt-DC and the DCS sequences of humans as well as Drosophila supports the conclusion that in higher eukaryotes the bifunctional mt-DC replaced a trifunctional precursor through inactivation of the synthetase domain. The mt-DC should be considered in models of one-carbon folate fluxes in mammals.     

Leaf Stripe and Stem Rot Caused by Burkholderia gladioli,a New Maize Disease in Mexico

A disease in maize plants, not previously observed, appeared in 2003–2004 in Cosoleacaque, Tlalixcoyan and Paso de Ovejas counties, in the state of Veracruz, Mexico. Initial symptoms on leaves were small white‐yellow watery spots, which coalesced into dry necrotic stripes 0.3 wide and up to 8 cm long. Reddening sometimes developed on these leaves. Stems developed a rot in the crown. The flag leaf became rot and necrotic at the base, rolled inwards and dried out. Necrosis developed at the base of the corn ears and their growth was inhibited. These symptoms were initially observed in Asgrow‐7573 commercial maize plantings. A bacterium characterized by white colonies, gram negative, aerobic, rod‐shape, opaque, round colonies with entire margins on casaaminoacid peptone and glucose media was consistently isolated from diseased maize plants. On King’s Medium B, the isolates produced yellow, non‐mucoid colonies, with the majority of the strains secreting a diffusible yellow pigment into the media. The bacterium identity was confirmed by PCR amplification and sequencing of 16S and 23S genes rDNA fragments. The bacterium was identified as Burkholderia gladioli. Its pathogenicity on maize plants in Mexico is a new record.     

Comparative analysis of the zeta-crystallin/quinone reductase gene in guinea pig and mouse

zeta-Crystallin is a novel nicotinamide adenine dinucleotide phosphate:quinone reductase, present at enzymatic levels in various tissues of different species, which is highly expressed in the lens of some hystricomorph rodents and camelids. We report here the complementary DNA (cDNA) cloning of zeta-crystallin from liver libraries in guinea pig (Cavia porcellus), where zeta-crystallin is highly expressed in the lens, and in the laboratory mouse (Mus musculus), where expression in the lens occurs only at enzymatic levels. A 5' untranslated sequence different from the one previously reported for the guinea pig lens cDNA was found in these clones. We also report the isolation of genomic clones including the complete guinea pig zeta-crystallin gene and the 5' region of this gene in mouse. These results show the presence of two promoters in the guinea pig zeta-crystallin gene, one responsible for expression at enzymatic levels and the other responsible for the high expression in the lens. The guinea pig lens promoter is not present in the mouse gene. This is the first example in which the recruitment of an enzyme as a lens crystallin can be explained by the acquisition of an alternative lens- specific promoter.      

GUCY2C opposes systemic genotoxic tumorigenesis by regulating AKT-dependent intestinal barrier integrity

The barrier separating mucosal and systemic compartments comprises epithelial cells, annealed by tight junctions, limiting permeability. GUCY2C recently emerged as an intestinal tumor suppressor coordinating AKT1-dependent crypt-villus homeostasis. Here, the contribution of GUCY2C to barrier integrity opposing colitis and systemic tumorigenesis is defined. Mice deficient in GUCY2C (Gucy2c(-/-)) exhibited barrier hyperpermeability associated with reduced junctional proteins. Conversely, activation of GUCY2C in mice reduced barrier permeability associated with increased junctional proteins. Further, silencing GUCY2C exacerbated, while activation reduced, chemical barrier disruption and colitis. Moreover, eliminating GUCY2C amplified, while activation reduced, systemic oxidative DNA damage. This genotoxicity was associated with increased spontaneous and carcinogen-induced systemic tumorigenesis in Gucy2c(-/-) mice. GUCY2C regulated barrier integrity by repressing AKT1, associated with increased junction proteins occludin and claudin 4 in mice and Caco2 cells in vitro. Thus, GUCY2C defends the intestinal barrier, opposing colitis and systemic genotoxicity and tumorigenesis. The therapeutic potential of this observation is underscored by the emerging clinical development of oral GUCY2C ligands, which can be used for chemoprophylaxis in inflammatory bowel disease and cancer.