32 resultados para brake even point
Resumo:
In a paper published in 1961, L. Cesari [1] introduces a method which extends certain earlier existence theorems of Cesari and Hale ([2] to [6]) for perturbation problems to strictly nonlinear problems. Various authors ([1], [7] to [15]) have now applied this method to nonlinear ordinary and partial differential equations. The basic idea of the method is to use the contraction principle to reduce an infinite-dimensional fixed point problem to a finite-dimensional problem which may be attacked using the methods of fixed point indexes.
The following is my formulation of the Cesari fixed point method:
Let B be a Banach space and let S be a finite-dimensional linear subspace of B. Let P be a projection of B onto S and suppose Г≤B such that pГ is compact and such that for every x in PГ, P-1x∩Г is closed. Let W be a continuous mapping from Г into B. The Cesari method gives sufficient conditions for the existence of a fixed point of W in Г.
Let I denote the identity mapping in B. Clearly y = Wy for some y in Г if and only if both of the following conditions hold:
(i) Py = PWy.
(ii) y = (P + (I - P)W)y.
Definition. The Cesari fixed paint method applies to (Г, W, P) if and only if the following three conditions are satisfied:
(1) For each x in PГ, P + (I - P)W is a contraction from P-1x∩Г into itself. Let y(x) be that element (uniqueness follows from the contraction principle) of P-1x∩Г which satisfies the equation y(x) = Py(x) + (I-P)Wy(x).
(2) The function y just defined is continuous from PГ into B.
(3) There are no fixed points of PWy on the boundary of PГ, so that the (finite- dimensional) fixed point index i(PWy, int PГ) is defined.
Definition. If the Cesari fixed point method applies to (Г, W, P) then define i(Г, W, P) to be the index i(PWy, int PГ).
The three theorems of this thesis can now be easily stated.
Theorem 1 (Cesari). If i(Г, W, P) is defined and i(Г, W, P) ≠0, then there is a fixed point of W in Г.
Theorem 2. Let the Cesari fixed point method apply to both (Г, W, P1) and (Г, W, P2). Assume that P2P1=P1P2=P1 and assume that either of the following two conditions holds:
(1) For every b in B and every z in the range of P2, we have that ‖b=P2b‖ ≤ ‖b-z‖
(2)P2Г is convex.
Then i(Г, W, P1) = i(Г, W, P2).
Theorem 3. If Ω is a bounded open set and W is a compact operator defined on Ω so that the (infinite-dimensional) Leray-Schauder index iLS(W, Ω) is defined, and if the Cesari fixed point method applies to (Ω, W, P), then i(Ω, W, P) = iLS(W, Ω).
Theorems 2 and 3 are proved using mainly a homotopy theorem and a reduction theorem for the finite-dimensional and the Leray-Schauder indexes. These and other properties of indexes will be listed before the theorem in which they are used.
Resumo:
Part I. The regions of sequence homology and non-homology between the DNA molecules of T2, T4, and T6 have been mapped by the electron microscopic heteroduplex method. The heteroduplex maps have been oriented with respect to the T4 genetic map. They show characteristic, reproducible patterns of substitution and deletion loops. All heteroduplex molecules show more than 85% homology. Some of the loop patterns in T2/T4 heteroduplexes are similar to those in T4/T6.
We find that the rII, the lysozyme and ac genes, the D region, and gene 52 are homologous in T2, T4, and T6. Genes 43 and 47 are probably homologous between T2 and T4. The region of greatest homology is that bearing the late genes. The host range region, which comprises a part of gene 37 and all of gene 38, is heterologous in T2, T4, and T6. The remainder of gene 37 is partially homologous in the T2/T4 heteroduplex (Beckendorf, Kim and Lielausis, 1972) but it is heterologous in T4/T6 and in T2/T6. Some of the tRNA genes are homologous and some are not. The internal protein genes in general seem to be non-homologous.
The molecular lengths of the T-even DNAs are the same within the limit of experimental error; their calculated molecular weights are correspondingly different due to unequal glucosylation. The size of the T2 genome is smaller than that of T4 or T6, but the terminally repetitious region in T2 is larger. There is a length distribution of the terminal repetition for any one phage DNA, indicating a variability in length of the DNA molecules packaged within the phage.
Part II. E. coli cells infected with phage strains carrying extensive deletions encompassing the gene for the phage ser-tRNA are missing the phage tRNAs normally present in wild type infected cells. By DNA-RNA hybridization we have demonstrated that the DNA complementary to the missing tRNAs is also absent in such deletion mutants. Thus the genes for these tRNAs must be clustered in the same region of the genome as the ser-tRNA gene. Physical mapping of several deletions of the ser-tRNA and lysozyme genes, by examination of heteroduplex DNA in the electron microscope, has enabled us to locate the cluster, to define its maximum size, and to order a few of the tRNA genes within it. That such deletions can be isolated indicates that the phage-specific tRNAs from this cluster are dispensable.
Part III. Genes 37 and 38 between closely related phages T2 and T4 have been compared by genetic, biochemical, and hetero-duplex studies. Homologous, partially homologous and non-homologous regions of the gene 37 have been mapped. The host range determinant which interacts with the gene 38 product is identified.
Part IV. A population of double-stranded ØX-RF DNA molecules carrying a deletion of about 9% of the wild-type DNA has been discovered in a sample cultivated under conditions where the phage lysozyme gene is nonessential. The structures of deleted monomers, dimers, and trimers have been studied by the electron microscope heteroduplex method. The dimers and trimers are shown to be head-to-tail repeats of the deleted monomers. Some interesting examples of the dynamical phenomenon of branch migration in vitro have been observed in heteroduplexes of deleted dimer and trimer strands with undeleted wild-type monomer viral strands.