Titlebook: Mathematics and Computing; ICMC 2022, Vellore, B. Rushi Kumar,S. Ponnusamy,Barbara Carminati Conference proceedings 2022 The Editor(s) (if

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somnambulism

On Some Properties of ,-type Block Matrices in the Context of Complementarity Problemck triangular .-matrices. We show that the solution of linear complementarity problem with .-type block matrices can be obtained by solving a linear programming problem. We show that block triangular .-matrices satisfy the least element property. We prove that hidden block triangular .-matrices are

预感

Families of Mordell Curves with Non-trivial Torsion and Rank of at Least Three at least three. We do this by using parametrizations due to Euler to obtain two rational points on these curves and obtain the third point from an elliptic curve of rank equal to two. We then show that the three points are of infinite order and are generally linearly independent.

Lucubrate

On the Genus of the Annihilator-Ideal Graph of Commutative Ring graph with the vertex set ., and two distinct vertices . and . are adjacent if and only if .. In this paper, we characterize all isomorphism classes of Artinian commutative rings whose . has genus one and crosscap one.

ANA

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抚育

uss different diseases associated with protein misfolding anAmyloid-forming proteins are implicated in over 30 human diseases. The proteins involved in each disease have unrelated sequences and dissimilar native structures, but they all undergo conformational alterations to form fibrillar polymers.

conformity

Pillory

Anjali Dhiman,S. Balakrishnane structures, but they all undergo conformational alterations to form fibrillar polymers. The fibrillar assemblies accumulate progressively into disease-specific lesions in vivo. Substantial evidence suggests these lesions are the end state of aberrant protein folding whereas the actual disease-caus

怪物

A. V. S. Kameshwari,S. Balakrishnane structures, but they all undergo conformational alterations to form fibrillar polymers. The fibrillar assemblies accumulate progressively into disease-specific lesions in vivo. Substantial evidence suggests these lesions are the end state of aberrant protein folding whereas the actual disease-caus