124 research outputs found
Linear Algebra Done Right
No full textNow available in Open Access, this best-selling textbook for a second course in linear algebra is aimed at undergraduate math majors and graduate students. The fourth edition gives an expanded treatment of the singular value decomposition and its consequences. It includes a new chapter on multilinear algebra, treating bilinear forms, quadratic forms, tensor products, and an approach to determinants via alternating multilinear forms. This new edition also increases the use of the minimal polynomial to provide cleaner proofs of multiple results. Also, over 250 new exercises have been added. The novel approach taken here banishes determinants to the end of the book. The text focuses on the central goal of linear algebra: understanding the structure of linear operators on finite-dimensional vector spaces. The author has taken unusual care to motivate concepts and simplify proofs. A variety of interesting exercises in each chapter helps students understand and manipulate the objects of linear algebra. Beautiful formatting creates pages with an unusually student-friendly appearance in both print and electronic versions. No prerequisites are assumed other than the usual demand for suitable mathematical maturity. The text starts by discussing vector spaces, linear independence, span, basis, and dimension. The book then deals with linear maps, eigenvalues, and eigenvectors. Inner-product spaces are introduced, leading to the finite-dimensional spectral theorem and its consequences. Generalized eigenvectors are then used to provide insight into the structure of a linear operator. From the reviews of previous editions: Altogether, the text is a didactic masterpiece. — zbMATH The determinant-free proofs are elegant and intuitive. — American Mathematical Monthly The most original linear algebra book to appear in years, it certainly belongs in every undergraduate library — CHOIC
Diastolic Function and Left Ventricular Filling Pressures should be measured with Advanced Echocardiography Doppler. Controversy. Olivier Axler : should be measured with Advanced Echocardiography Doppler.
No full textDiastolic Function and Left Ventricular Filling Pressures should be measured with Advanced Echocardiography Doppler. Controversy. Olivier Axler : should be measured with Advanced Echocardiography Doppler.
No full textDiastolic Function and Left Ventricular Filling Pressures should be measured with Advanced Echocardiography Doppler. Controversy. Olivier Axler : should be measured with Advanced Echocardiography Doppler.
No full textCharacterization of apoM in normal and genetically modified mice
No full textA novel human apolipoprotein [apolipoprotein M (apoM)l was recently described and demonstrated to be a lipocalin. We have now examined apoM in wild-type mice and mice with genetically altered lipoprotein metabolism. Liver and kidney showed high mRNA expression, whereas spleen, heart, brain, and testis demonstrated low expression. ApoM gene expression was initiated on embryonic day 10. Western blot analysis of plasma suggested that mouse apoM, like its human counterpart, is secreted with a retained signal peptide, but unlike human apoM it is not glycosylated. Gel filtration of plasma showed apoM to be associated with HDL-sized particles in wild-type and apoA-I-deficient mice and with HDL and LDL-sized particles in LDL receptor-deficient mice, whereas apoM was mainly found in VLDL-sized particles in high-fat, high-cholesterol-fed apoE-deficient mice. The plasma concentration of apoM was similar in wild-type, LDL receptor-deficient, and apoE-deficient mice but was reduced to 33% in apoA-I-deficient compared with wild-type mice (P = 0.007). These data suggest that apoM mainly associates with HDL in normal mice but also with the pathologically increased lipoprotein fraction in genetically modified mice. The substantially decreased apoM levels in apoA-I-deficient mice suggest a connection between apoM and apoA-I metabolism.-Faber, K., O. Axler, B. Dahlback, and L. B. Nielsen. Characterization of apoM in normal and genetically modified mice
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