159 resultados para Payroll deductions
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Mode of access: Internet.
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Most existing requirements engineering approaches focus on the modelling and specification of the IT artefacts ignoring the environment where the application is deployed. Although some requirements engineering approaches consider the stakeholder’s goals, they still focus on the IT artefacts’ specification. However, IT artefacts are embedded in a dynamic organisational environment and their design and specification cannot be separated from the environment’s constant evolution. Therefore, during the initial stages of a requirements engineering process it is advantageous to consider the integration of IT design with organisational design. We proposed the ADMITO (Analysis, Design and Management of IT and Organisations) approach to represent the dynamic relations between social and material entities, where the latter are divided into technological and organisational entities. In this paper we show how by using ADMITO in a concrete case, the Queensland Health Payroll (QHP) case, it is possible to have an integrated representation of IT and organisational design supporting organisational change and IT requirements specification.
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The objective of this paper is to identify and analyze the main problems in the taxation—regarding both taxes themselves and compliance costs of taxation—of civil society organizations in Brazil. This study is qualitative descriptive research. A multiple case study with 26 organizations was performed. The results show that the problems mainly affect organizations with lower revenue and that do not work in the areas of education, health or social care. The main problems involve the taxation of the payroll and the difficulties related to obtaining and maintaining certifications. The study concludes with suggestions for the improvement of the regulatory framework.
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Inherited defects in the gene for methylmalonyl-CoA mutase (EC 5.4.99.2) result in the mut forms of methylmalonic aciduria. mut- mutations lead to the absence of detectable mutase activity and are not corrected by excess cobalamin, whereas mut- mutations exhibit residual activity when exposed to excess cobalamin. Many of the mutations that cause methylmalonic aciduria in humans affect residues in the C-terminal region of the methylmalonyl-CoA mutase. This portion of the methylmalonyl-CoA mutase sequence can be aligned with regions in other B12 (cobalamin)-dependent enzymes, including the C-terminal portion of the cobalamin-binding region of methionine synthase. The alignments allow the mutations of human methylmalonyl-CoA mutase to be mapped onto the structure of the cobalamin-binding fragment of methionine synthase from Escherichia coli (EC 2.1.1.13), which has recently been determined by x-ray crystallography. In this structure, the dimethylbenzimidazole ligand to the cobalt in free cobalamin has been displaced by a histidine ligand, and the dimethylbenzimidazole nucleotide "tail" is thrust into a deep hydrophobic pocket in the protein. Previously identified mut0 and mut- mutations (Gly-623 --> Arg, Gly-626 --> Cys, and Gly-648 --> Asp) of the mutase are predicted to interfere with the structure and/or stability of the loop that carries His-627, the presumed lower axial ligand to the cobalt of adenosylcobalamin. Two mutants that lead to severe impairment (mut0) are Gly-630 --> Glu and Gly-703 --> Arg, which map to the binding site for the dimethylbenzimidazole nucleotide substituent of adenosylcobalamin. The substitution of larger residues for glycine is predicted to block the binding of adenosylcobalamin.
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"ONR Contract No. Nonr-1055(00)."
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"issued 7/83."
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