Abstract: The present invention relates to alpha-amylase variants. The present invention also relates to polynucleotides encoding the variants; nucleic acid constructs, vectors, and host cells comprising the polynucleotides; and methods of using the variants.

Abstract: The present invention relates to alpha-amylase variants. The present invention also relates to polynucleotides encoding the variants; nucleic acid constructs, vectors, and host cells comprising the polynucleotides; and methods of using the variants.

Abstract: The present invention relates to alpha-amylase variants. The present invention also relates to polynucleotides encoding the variants; nucleic acid constructs, vectors, and host cells comprising the polynucleotides; and methods of using the variants.

Abstract: The present invention relates to alpha-amylase variants. The present invention also relates to polynucleotides encoding the variants; nucleic acid constructs, vectors, and host cells comprising the polynucleotides; and methods of using the variants.

Abstract: The present invention relates to alpha-amylase variants. The present invention also relates to polynucleotides encoding the variants; nucleic acid constructs, vectors, and host cells comprising the polynucleotides; and methods of using the variants.

Abstract: The present disclosure relates to a methodology that identifies the underlying mechanisms that lead to hepatotoxicity. This is done by using the alterations in cellular metabolite profiles obtained before and after therapy/drug treatment in combination with a model of liver metabolism. Subsequently, by using a covariance matrix adaptation followed by evolutionary selection, it compares the drug-induced metabolite profiles obtained experimentally with those generated using the in silico model, automatically shortlists potential parameters whose alterations could have produced the drug-treated metabolite profile. Values of these parameters are estimated by formulating an optimal control problem to minimize the differences between the model-generated metabolite values and experimentally observed data. The estimated parameters are given as an input to the homeostatic liver model and simulations are carried out, thereby the results providing a mechanistic explanation for the development of toxicity.

Abstract: One embodiment of the present invention provides systems and techniques to extract assume properties from a constrained random test-bench. During operation, the system can receive a constrained random test-bench for verifying the design-under-test (DUT), wherein the constrained random test-bench includes a statement which assigns a random value to a random variable according to a constraint. Next, the system can modify the constrained random test-bench by replacing the statement with another statement which assigns a free input variable's value to the random variable. The system can also add a statement to the constrained random test-bench that toggles a marker variable to localize the scope of the statement. The system can then generate an assume property which models the constraint on the free input variable. The assume property can then be used by a formal property verification tool to verify the DUT.

Abstract: The present invention comprises a new class of compounds useful for the prophylaxis and treatment of protein kinase mediated diseases, including inflammation and related conditions. The compounds have a general Formula I wherein B, R1, R2, R3, R4 and R5 are d.efined herein. The invention also comprises pharmaceutical compositions including one or more compounds of Formula I, uses of such compounds and compositions for treatment of kinase mediated diseases including rheumatoid arthritis, psoriasis and other inflammation disorders, as well as intermediates and processes useful for the preparation of compounds of Formula I.

Abstract: The present invention comprises a new class of compounds useful for the prophylaxis and treatment of protein kinase mediated diseases, including inflammation and related conditions. The compounds have a general Formula I wherein A, B, R1, R2, R3 and R4 are defined herein. The invention also comprises pharmaceutical compositions including one or more compounds of Formula I, uses of such compounds and compositions for treatment of P38 map kinase mediated diseases including rheumatoid arthritis, psoriasis and other inflammation disorders, as well as intermediates and processes useful for the preparation of compounds of Formula I.

Abstract: One embodiment of the present invention provides systems and techniques to extract assume properties from a constrained random test-bench. During operation, the system can receive a constrained random test-bench for verifying the design-under-test (DUT), wherein the constrained random test-bench includes a statement which assigns a random value to a random variable according to a constraint. Next, the system can modify the constrained random test-bench by replacing the statement with another statement which assigns a free input variable's value to the random variable. The system can also add a statement to the constrained random test-bench that toggles a marker variable to localize the scope of the statement. The system can then generate an assume property which models the constraint on the free input variable. The assume property can then be used by a formal property verification tool to verify the DUT.

Abstract: The present invention comprises a new class of compounds useful for the prophylaxis and treatment of protein kinase mediated diseases, including inflammation and related conditions. The compounds have a general Formula I wherein A, B, R1, R2, R3 and R4 are defined herein. The invention also comprises pharmaceutical compositions including one or more compounds of Formula I, uses of such compounds and compositions for treatment of P38 map kinase mediated diseases including rheumatoid arthritis, psoriasis and other inflammation disorders, as well as intermediates and processes useful for the preparation of compounds of Formula I.