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Biomedical subjects

K Scharnweber

Publications and source records attributed to K Scharnweber.

4 recordsLinked to original sources
PubMed2001

Kinetic modeling and simulation of in vitro transcription by phage T7 RNA polymerase.

This study provides a mathematical model of T7 RNA polymerase (T7 RNAP) kinetics under in vitro conditions targeted at application of this model to simulation of dynamic transcription performance. A functional dependence of transcript synthesis rate is derived based on: (a) essential reactant concentrations, including T7 RNAP and its promoter, substrate nucleotides, and the inhibitory byproduct inorganic pyrophosphate; (b) a distinction among vector characteristics such as recognition sequences regulating transcription initiation and termination, respectively; and (c) specific properties of the nucleotide sequence including both transcript length and nucleotide composition. Inactivation kinetics showed a half-life of T7 RNAP activity of 50 min under the conditions applied in vitro using the isolated enzyme. Model parameters and their precision are estimated using dynamic simulation and nonlinear regression analysis. The particular novelty of this model is its capability to incorporate linear genomic sequence information for simulation of nonlinear in vitro transcription kinetics.

Computer Simulation↗
PubMedDate not supplied

Alpha 1-antitrypsin deficiency and the impact of nursing interventions and treatment with intravenous therapy. An overview.

The primary function of alpha1-antitrypsin is to protect the alveoli in the lung from harmful destruction from proteolytic enzymes, which prevent optimal elastic recoil of the lungs and destroy the lungs. Insufficient serum levels of alpha1-antitrypsin eventually lead to early onset of emphysema in the third, fourth, or fifth decade of life. Treatment of alpha1-antitrypsin deficiency by intravenous administration of an enzyme inhibitor known as alpha1-proteinase inhibitor, a human-derived blood product, can be administered to help replace the enzymes required to maintain lung function. Early detection, nursing intervention, and clinical management slow the progression of this hereditary disease.

Disease Progression↗
PubMedDate not supplied

Recombinant human granulocyte colony-stimulating factor: an overview.

Recombinant granulocyte colony-stimulating factor (G-CSF) is a hematopoietic growth factor used for the reduction or prevention of cyclic neutropenia in cancer patients. Neutropenia is a major factor contributing to infection, morbidity, and mortality. Neutropenia also reduces the dosage of cytotoxic agents and often interrupts the course of treatment. The recent development of cloning G-CSF has been a major advancement in treating cyclic neutropenia. This article focuses on the mechanism of action, pharmacokinetics, and the clinical applications of G-CSF.

Granulocyte Colony-Stimulating Factor↗