Growth, structural, and optical characterization of ZnO-coated cellulosic fibers

Rod-shaped ZnO particles were grown over wood cellulose fibers using a two-step process. In the first step, the formation of ZnO seeds at cellulose fibers surfaces was induced by the alkaline hydrolysis of aqueous Zn(II); in the second step, the growth of the ZnO seeds into larger nanoparticles was promoted by the controlled hydrolysis of Zn(II)−amine complexes. In particular, we will report the use of hexamethylenetetramine (C6H12N4) and triethanolamine (C6H15NO3) to grow, respectively, ZnO nanorods and microrods at the cellulose fibers surfaces. Photoluminescence measurements performed on the nanocomposite materials showed the typical excitonic ZnO recombination peaked between 3.38 and 3.34 eV, at low temperature. The full width at half-maximum of the excitonic line is dependent on the ZnO particles morphology and can be as narrow as 30 meV for some of the materials investigated.EU-SUSTAINPACK IP-500311-2FCT-POCI/CTM/55945/200

ClinGen--the Clinical Genome Resource

On autopsy, a patient is found to have hypertrophic cardiomyopathy. The patient’s family pursues genetic testing that shows a “likely pathogenic” variant for the condition on the basis of a study in an original research publication. Given the dominant inheritance of the condition and the risk of sudden cardiac death, other family members are tested for the genetic variant to determine their risk. Several family members test negative and are told that they are not at risk for hypertrophic cardiomyopathy and sudden cardiac death, and those who test positive are told that they need to be regularly monitored for cardiomyopathy on echocardiography. Five years later, during a routine clinic visit of one of the genotype-positive family members, the cardiologist queries a database for current knowledge on the genetic variant and discovers that the variant is now interpreted as “likely benign” by another laboratory that uses more recently derived population-frequency data. A newly available testing panel for additional genes that are implicated in hypertrophic cardiomyopathy is initiated on an affected family member, and a different variant is found that is determined to be pathogenic. Family members are retested, and one member who previously tested negative is now found to be positive for this new variant. An immediate clinical workup detects evidence of cardiomyopathy, and an intracardiac defibrillator is implanted to reduce the risk of sudden cardiac deat