1,212 research outputs found

    Modeling of anionic polymerization in flow with coupled variations of concentration, viscosity and diffusivity

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    Abstract This paper explains the reasons behind the very low polydispersity index (PDI) obtained in living anionic polymerizations in microstructured reactors. From the results, it can be explained that a narrow molecular weight distribution can be obtained due to the presence of a highly segregated flow behavior, even in microflow conditions, provided that the mean residence time is high enough. This paper investigates the feasibility of a living anionic polymerization reaction under micro-fluidic conditions. This is accomplished using a multiphysics model that accounts for the changes in viscosity and diffusivity. These properties descend with the increase in weight of the polymer, and could not be un-coupled from hydrodynamics and mass transfer. The results of the model are used to understand the reasons behind the very low PDI that can be experimentally obtained in microflow conditions. This leads to the conclusion that the increased viscosity almost "suppresses" the diffusion of the monomer, even at the very short characteristic lengths of a micro-device. These conditions generate a fully segregated flow that yields an almost monodisperse polymer regardless of the effective residence time distribution encountered in the reactor

    Diagnosis Of Alpha-1-antitrypsin Deficiency By Dna Analysis Of Children With Liver Disease.

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    Alpha-1-antitrypsin deficiency is a genetic disorder which is transmitted in a co-dominant, autosomal form. Alpha-1-antitrypsin deficiency affects mainly the lungs and the liver leading, in the latter case, to neonatal cholestasis, chronic hepatitis or cirrhosis. A precise diagnosis of Alpha-1-antitrypsin deficiency may be obtained by biochemical or molecular analysis. The purpose of this study was to use DNA analysis to examine the presence of an alpha-1-antitrypsin deficiency in 12 children suspected of having this deficiency and who showed laboratory and clinical characteristics of the disease. Twelve patients, aged 3 months to 19 years, who had serum alpha-1-antitrypsin levels lower than normal and/or had hepatic disease of undefined etiology were studied. The mutant alleles S and Z of the alpha-1-antitrypsin gene were investigated in the 12 children. Alpha-1-antitrypsin gene organization was analyzed by amplification of genome through the polymerase chain reaction and digestion with the restriction enzymes Xmnl (S allele) and Taq-1 (Z allele). Seven of the 12 patients had chronic liver disease of undefined etiology and the other five patients had low serum levels of alpha-1-antitrypsin as well as a diagnosis of neonatal cholestasis and/or chronic liver disease of undefined etiology. Five of the 12 patients were homozygous for the Z allele (ZZ) and two had the S allele with another allele (*S) different from Z. These results show that alpha-1-antitrypsin deficiency is relatively frequent in children with chronic hepatic disease of undefined etiology and/or low alpha-1-antitrypsin levels (41.6%). A correct diagnosis is important for effective clinical follow-up and for genetic counseling.3863-

    Diagnosis Of Alpha-1-antitrypsin Deficiency By Dna Analysis Of Children With Liver Disease

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    Background - Alpha-1-antitrypsin deficiency is a genetic disorder which is transmitted in a co-dominant, autosomal form. Alpha-1-antitrypsin deficiency affects mainly the lungs and the liver leading, in the latter case, to neonatal cholestasis, chronic hepatitis or cirrhosis. A precise diagnosis of Alpha-1-antitrypsin deficiency may be obtained by biochemical or molecular analysis. Objective - The purpose of this study was to use DNA analysis to examine the presence of an alpha-1-antitrypsin deficiency in 12 children suspected of having this deficiency and who showed laboratory and clinical characteristics of the disease. Patients and Methods - Twelve patients, aged 3 months to 19 years, who had serum alpha-1-antitrypsin levels lower than normal and/or had hepatic disease of undefined etiology were studied. The mutant alleles S and Z of the alpha-1-antitrypsin gene were investigated in the 12 children. Alpha-1-antitrypsin gene organization was analyzed by amplification of genoma through the polymerase chain reaction and digestion with the restriction enzymes Xmnl (S allele) and Taq 1 (Z allele). Results - Seven of the 12 patients had chronic liver disease of undefined etiology and the other five patients had low serum levels of alpha-1-antitrypsin as well as a diagnosis of neonatal cholestasis and/or chronic liver disease of undefined etiology. Five of the 12 patients were homozygous for the Z allele (ZZ) and two had the S allele with another allele (*S) different from Z. Conclusion - These results show that alpha-1-antitrypsin deficiency is relatively frequent in children with chronic hepatic disease of undefined etiology and/or low alpha-1-antitrypsin levels (41.6%). A correct diagnosis is important for effective clinical follow-up and for genetic counseling.3816368Alagille, D., Cholestasis in the first three months of life (1979) Prog Liver Dis, 6, pp. 471-485Andresen, B.S., Knudsen, I., Jensen, P.K.A., Gregersen, N., Two novel nonradioactive polymerase chain reaction-based assays of dried blood spots, genomic DNA, or whole cells for fast, reliable detection of Z and S mutations in the alpha-1-antitrypsin gene (1992) Clin Chem, 38, pp. 2100-2107Balistreri, W.F., Schubert, W.K., Liver disease in infancy and childhood (1993) Diseases of the Liver. 7.ed., pp. 1099-1203. , Schiff L, Schiff ER, editors. Philadelphia: LippincottBillingsley, G.D., Cox, D.W., Functional assessment of genetic variants of alpha 1-antitrypsin (1982) Hum Genet, 61, pp. 118-122Brantly, M., Nukiwa, T., Crystal, R.G., Molecular basis of alpha-1-antitrypsin deficiency (1988) Am J Med, 84, pp. 13-31Carlson, J.A., Rogers, R.B., Sifers, R., Acumulation of PiZ alpha 1-antitrypsin causes liver damage in transgenic mice (1989) J Clin Invest, 83, pp. 1183-1190Carrel, R.W., Alpha 1-antitrypsin: Molecular pathology, leukocytes and tissue damage (1986) J Clin Invest, 78, pp. 1427-1431Cox, D.W., Woo, S.L., Mansfield, T., DNA restriction fragments associated with alpha 1-antitrypsin indicate a single origin for deficiency allele PI Z (1985) Nature, 316, pp. 79-81Crystal, R.G., Brantly, M.L., Hubbard, R.C., Curiel, D.T., States, D.J., Holmes, M.D., The alpha 1-antitrypsin gene and its mutations. Clinical consequences and strategies for therapy (1989) Chest, 95, pp. 196-208Crystal, R.G., Ferrans, V.J., Basset, F., Biologic basis of pulmonary fibrosis (1991) The Lung: Scientific Foundations, pp. 2031-2046. , Crystal RG, West JB, Barnes PJ, Cherniack S, editors. New YorkRaven PressCuriel, D., Brantly, M., Curiel, E., Crystal, R.G., Alpha-1-antitrypsin deficiency caused by the alpha-1-antitrypsin Nullmattawa gene. An insertion mutation rendering the alpha-1-antitrypsin gene incapable of producing alpha-1-antitrypsin (1989) J Clin Invest, 83, pp. 1144-1152Dermer, S.J., Johnson, E.M., Rapid DNA analysis of alpha 1-antitrypsin deficiency: Application of an improved method for amplifying mutated gene sequence (1988) Lab Invest, 59, pp. 403-408Deutsch, J., Becker, H., Auböck, L., Histopathological features of liver disease in alpha 1-antitrypsin deficiency (1994) Acta Paediatr, 393 (SUPPL.), pp. 8-12Dubel, J.R., Finwick, R., Hejtmancik, J.F., Denaturing gradient gel electrophoresis of the alpha 1-antitrypsin gene: Application to prenatal diagnosis (1991) Am J Med Genet, 41, pp. 39-43Evans, H.E., Levi, M., Mandl, I., Serum enzyme inhibitor concentrations in the respiratory distress syndrome (1970) Am Rev Resp Dis, 101, pp. 359-363Fagerhol, M.K., Cox, D.W., The PI polimorphism: Genetic, biochemical and clinical aspects of human alpha-1-antitrypsin (1981) Human Genetic, pp. 1-62. , Harris H, Hirchorn, K, editors. New York: PlenumGartner, J.C., Zitelli, B.J., Malatak, J.J., Shaw, B.W., Iwatsuki, S., Starzl, T.E., Orthotopic liver transplantation in children: Two-year experience with 47 patients (1984) Pediatrics, 74, pp. 140-145Ishak, K.G., Hepatic morphology in inherited metabolic diseases (1986) Sem Liver Dis, 6, pp. 246-258Jeppsson, J.O., Laurell, C.B., Fagerhol, M.K., Properties of isolated alpha-1-antitrypsin of Pi types M, S and Z (1978) Eur J Biochem, 83, pp. 143-153Lai, E.C., Kao, F.T., Law, M.L., Woo, S.L., Assignment of the alpha 1-antitrypsin gene and a sequence-related gene to human chromossome 14 by molecular hybridization (1983) Am J Hum Genet, 35, pp. 385-392Laurell, C.B., Eriksson, S., The electrophoretic alpha-1-globulin pattern of serum in alpha-1-antitrypsin deficiency (1963) Scand J Clin Lab Invest, 15, pp. 132-140Laurell, C.B., Kullander, S., Thorell, J., Effect of administration of a combined strogen-progestin contraceptive on the level of individual plasma proteins (1968) Scand J Clin Lab Invest, 21, pp. 337-343Massi, G., Chiarelli, C., Alpha 1-antitrypsin: Molecular and the Pi system (1994) Acta Paediatr, 393 (SUPPL.), pp. 1-4Mowat, A.P., Avaliação laboratorial das afecçÔes hepatobiliares (1991) Doenças Hepåticas Em Pediatria. 2.ed., pp. 410-430. , Mowat AP. Rio de Janeiro: RevinterNukiwa, T., Brantly, M., Ogushi, F., Crystal, R.G., Characterization of the M1(ala 213) type of alpha-1-antitrypsin, a newly recognized common "normal" alpha-1-antitrypsin haplotype (1987) Biochemistry, 26, pp. 5259-5267Okayama, H., Curiel, D.T., Brantly, M.L., Holmes, M.D., Crystal, R.G., Rapid nonradioactive detection of mutations in the human genome by allele-specific amplification (1989) J Lab Clin Med, 114, pp. 105-113Perlmutter, D.H., The cellular basis for liver injury in alpha-1-antitrypsin deficiency (1991) Hepatology, 13, pp. 172-185Perlmutter, D.H., Clinical manifestations of alpha 1-antitrypsin deficiency (1995) Gastroenterol Clin North Am, 24, pp. 27-43Schroeder, W.T., Miller, M.F., Woo, S.L., Saunders, G.F., Chromosomal localization of the human alpha 1-antitrypsin gene (PI) to 14q31-32 (1985) Am J Hum Genet, 37, pp. 868-872Serra, H.G., (1998) Identificação Molecular Dos Alelos S e Z Do Gene Da Alfa-1-antitripsina Em Um Grupo de Pacientes Portadores de Doença Pulmonar CrÎnica [tese de Doutorado], , Campinas, SP: Instituto de Biologia da Universidade Estadual de CampinasSilverman, E.K., Miletich, J.P., Pierce, J.A., Sherman, L.A., Endicott, S.K., Broze, G.J., Campbell, E.J., Alpha-1-antitrypsin deficiency. High prevalence in the St. Louis area determined by direct population screening (1989) Am Rev Respir Dis, 140, pp. 961-966Sveger, T., Liver disease in alpha 1-antitrypsin deficiency detected by screening of 200,000 infants (1976) N Engl J Med, 294, pp. 1316-1321Sveger, T., The natural history of liver disease in alpha 1-antitrypsin deficient children (1988) Acta Paediatr Scand, 77, pp. 847-851Sveger, T., Ericksson, S., The liver in adolescents with alpha 1-antitrypsin deficiency (1995) Hepatology, 22, pp. 514-517Talbot, I.C., Mowat, A.P., Liver disease in infancy. Histological features and relationship to alpha 1-antitrypsin phenotype (1975) J Clin Pathol, 28, pp. 559-563Travis, J., Salvesen, G.S., Human plasma proteinase inhibitors (1983) Annu Rev Biochem, 52, pp. 655-709Van Steenbergen, W., Alpha 1-antitrypsin deficiency: An overview (1993) Acta Clin Belg, 48 (3), pp. 171-189Wewers, M.D., Casolaro, M.A., Sellers, S.E., Swayze, S.C., McPhaul, K.M., Wittes, J.T., Crystal, R.G., Replacement therapy deficiency associated with emphysema (1987) N Engl J Med, 316, pp. 1055-1062Woodhead, J.L., Fallon, R., Figuered, H., Longdale, J., Malcom, A.D.B., Alternative methodology of gene diagnosis (1986) Human Genetic Diseases - a Pratical Approach, pp. 51-64. , Davies KE, editor. Oxford: IRL Pres

    Gastropods Colour Patterns in Cassiopids and Naticids from Romualdo Formation, Araripe Basin, Northeast Brazil

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    The phylum Mollusca includes one of the most beautiful examples of colour patterns in present-day shells. However, they are rare in the fossil record because they demand excellent fossilization. In Brazil, colour patterns in fossil mollusk shells are recorded in gastropods Natica aff. bulbulus White, 1887 from the Riachuelo Formation (Aptian-Albian), Sergipe-Alagoas Basin. This paper presents the first gastropod shells from the Romualdo Formation with colour patterns, visible under natural and UV light, belonging to the families Naticidae and Cassiopidae, collected at Santo AntĂŽnio outcrop municipality of Exu, Pernambuco and, Pinheiro and Serra do MĂŁozinha sites, municipality of MissĂŁo Velha and Romualdo site, municipality of Crato, CearĂĄ. Among the cassiopids more than 100 specimens were tested, with 1/3 of them showing a residual colour pattern under UV light exposure, after chemical preparation. They correspond to the species Paraglauconia (Diglauconia) araripensis (Beurlen, 1964), Paraglauconia (Diglauconia) lyrica Maury, 1934, Gymnentome (Gymnentome) carregozica (Maury, 1934) and Gymnentome (Gymnentome) romualdoi Beurlen, 1964. The colour pattern is virtually similar in both genera, with fluorescent stripes on a dark background, showing the taxonomic similarity between them. As for the naticids, about 20 specimens were collected and 15 show good preservation, observing the visible colour pattern under natural light in Natica sp. and Euspira sp.; both new taxa for the Araripe Basin. The residual colour pattern in naticids ranges from spiral stripes to sigmoidal lines and blotches of brown and yellowish tones on a paler background, as observed in fossil species of the same family in the Cenozoic. The new occurrences increase the fossiliferous diversity of mollusks of the Romualdo Formation and extend the understanding of the diversity of colouration patterns of Lower Cretaceous gastropods

    Co-axial capillaries microfluidic device for synthesizing size- and morphology-controlled polymer core-polymer shell particles

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    An easy assembling-disassembling co-axial capillaries microfluidic device was built up for the production of double droplets. Uniform polymer core-polymer shell particles were synthesized by polymerizing the two immiscible monomer phases composing the double droplet. Thus poly(acrylamide) core-poly(tripropylenglycol-diacrylate) shell particles with controlled core diameter and shell thickness were simply obtained by adjusting operating parameters. An empirical law was extracted from experiments to predict core and shell sizes. Additionally uniform and predictable non-spherical polymer objects were also prepared without adding shape-formation procedures in the experimental device. An empirical equation for describing the lengths of rod-like polymer particles is also presented

    Online monitoring of vinyl chloride polymerization in a microreactor using raman spectroscopy

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    A novel capillary-based microfluidic device has been designed to follow the vinyl chloride polymerization reaction. The use of a co-flow generation system enabled obtaining monodisperse vinyl chloride droplets within 200 ”m in diameter, each one being considered as a polymerization reactor. During polymerization VCM droplets were visualized with a high speed camera. At the end of the reaction PVC grains were observed with a Scanning Electron Microscopy technique. Real-time non-invasive Raman measurement has been performed on stationary vinyl chloride monomer droplets and has provided values of effective reaction orders n and effective rate constants k. This microdevice allowed the investigation in difficult conditions (pressure, temperature) with a minimal amount of reagents and consequently under safe conditions

    Accelerating biphasic biocatalysis through new process windows

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    Process intensification through continuous flow reactions has increased the production rates of fine chemicals and pharmaceuticals. Catalytic reactions are accelerated through an unconventional and unprecedented use of a high‐performance liquid/liquid counter current chromatography system. Product generation is significantly faster than in traditional batch reactors or in segmented flow systems, which is exemplified through stereoselective phase‐transfer catalyzed reactions. This methodology also enables the intensification of biocatalysis as demonstrated in high yield esterifications and in the sesquiterpene cyclase‐catalyzed synthesis of sesquiterpenes from farnesyl diphosphate as high‐value natural products with applications in medicine, agriculture and the fragrance industry. Product release in sesquiterpene synthases is rate limiting due to the hydrophobic nature of sesquiterpenes, but a biphasic system exposed to centrifugal forces allows for highly efficient reactions

    Stationary, continuous, and sequential surface-enhanced raman scattering sensing based on the nanoscale and microscale polymer-metal composite sensor particles through microfluidics: a review

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    Surface-enhanced Raman scattering (SERS) is a label-free and accurate analytical technique for the detection of a broad range of various analytes such as, biomolecules, pesticides, petrochemicals, as well as, cellular and other biological systems. A key component for the SERS analysis is the substrate which is required to be equipped with plasmonic features of metal nanostructures that directly interact with light and targeted analytes. Either metal nanoparticles can be deposited on the solid support (glass or silicon) which is suitable for stationary SERS analysis or dispersed in the solution (freely moving nanoparticles). Besides these routinely utilizing SERS substrates, polymer-metal composite particles are promising for sustained SERS analysis where metal nanoparticles act as plasmon-active (hence SERS-active) components and polymer particles act as support to the metal nanoparticles. Composite sensor particles provide 3D interaction possibilities for analytes, suitable for stationary, continuous, and sequential analysis, and they are reusable/regenerated. Therefore, this review is focused on the experimental procedures for the development of multiscale, uniform, and reproducible composite sensor particles together with their application for SERS analysis. The microfluidic reaction technique is highly versatile in the production of uniform and size-tunable composite particles, as well as, for conducting SERS analysis

    Early detection of hearing loss

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    The universal newborn hearing screening (UNHS) is currently spreading in Germany, as well, even though there can be no talk of a comprehensive establishment. The introduction of UNHS in several federal states such as Hamburg, Hessen, and Schleswig-Holstein can be ascribed to the personal commitment of individual pediatric audiologists. Apart from the procurement of the screening equipment and the training of the staff responsible for the examination of the newborns, the tracking, i.e. the follow-up on children with conspicuous test results, is of utmost importance. This involves significant administration effort and work and is subject to data protection laws that can differ substantially between the various federal states. Among audiologists, there is consensus that within the first three months of a child’s life, a hearing loss must be diagnosed and that between the age of 3 and 6 months, the supply of a hearing aid must have been initiated. For this purpose, screening steps 1 (usually a TEOAE measurement) and 2 (AABR testing) need to be conducted in the maternity hospital. The follow-up of step 1 then comprises the repetition of the TEOAE- and AABR measurement for conspicuous children by a specialized physician. The follow-up of step 2 comprises the confirmatory diagnostics in a pediatric audiological center. This always implies BERA diagnostics during spontaneous sleep or under sedation. The subsequent early supply of a hearing aid should generally be conducted by a (pediatric) acoustician specialized on children
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