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Degradation diffusant interaction

Another explanation for reduced biocide penetration into biofilms is the interaction between biocide and biofilm constituents, including cells and EPS a result would be depletion of the antimicrobial compound in the biofilm interior. The underlying mechanisms may be chemical reactions of the biocide with, or sorption to, the biofilm components or the enzymatic degradation of the biocide, resulting in a restricted penetration of the biocide into the biofilms (reaction-diffusion interaction mechanism). [Pg.98]

In this work we will focus on the use of the cubic phase as a delivery system for oligopeptides - Desmopressin, Lysine Vasopressin, Somatostatin and the Renin inhibitor H214/03. The amino acid sequences of these peptides are given in Table I. The work focuses on the cubic phase as a subcutaneous or intramuscular depot for extended release of peptide drugs, and as a vehicle for peptide uptake in the Gl-tract. Several examples of how the peptide drugs interact with this lipid-water system will be given in terms of phase behaviour, peptide self-diffusion, in vitro and in vivo release kinetics, and the ability of the cubic phase to protect peptides from enzymatic degradation in vitro. Part of this work has been described elsewhere (4-6). [Pg.250]

It was recognized very early that diffuse reflectance spectroscopy could be used to study the interactions of various compounds in a formulation, and the technique has been particularly useful in the characterization of solid state reactions [24]. Lach concluded that diffuse reflectance spectroscopy could also be used to verify the potency of a drug in its formulation. In addition, studies conducted under stress conditions would be useful in the study of drug-excipient interactions, drug degradation pathways, and alterations in bioavailability owing to chemisorption of the drug onto other components in the formulation [24]. [Pg.46]

The action of catecholamines released at the synapse is modulated by diffusion and reuptake into presynaptic nerve terminals. Catecholamines diffuse from the site of release, interact with receptors and are transported back into the nerve terminal. Some of the catecholamine molecules may be catabolized by MAO and COMT. The cate-cholamine-reuptake process was originally described by Axelrod [18]. He observed that, when radioactive norepinephrine was injected intravenously, it accumulated in tissues in direct proportion to the density of the sympathetic innervation in the tissue. The amine taken up into the tissues was protected from catabolic degradation, and studies of the subcellular distribution of catecholamines showed that they were localized to synaptic vesicles. Ablation of the sympathetic input to organs abolished the ability of vesicles to accumulate and store radioactive norepinephrine. Subsequent studies demonstrated that this Na+- and Cl -dependent uptake process is a characteristic feature of catecholamine-containing neurons in both the periphery and the brain (Table 12-2). [Pg.216]

Once synthesized, acetylcholine is stored in synaptic vesicles until time for its use. Once liberated into the synapse, acetylcholine diffuses across the synaptic cleft in about 100 microseconds (10 " seconds one ten-thousandth of a second), where it interacts with its receptor, and then dissociates from it in the next 1 or 2 milliseconds. Once liberated, acetylcholine is degraded by a second enzyme, acetylcholinesterase, a target for drug discovery (as I develop a bit later). [Pg.293]

After interaction of the aforementioned carriers with specific receptors, the carrier is then taken up by endocytosis and transported intracellularly to acidified endosomes and lyso-somes.The carrier is proteolytically degraded in the lysosomes and if a drug is coupled to the carrier, it is then released to diffuse into the cytoplasmic compartment. [Pg.101]

The unconventional applications of SEC usually produce estimated values of various characteristics, which are valuable for further analyses. These embrace assessment of theta conditions for given polymer (mixed solvent-eluent composition and temperature Section 16.2.2), second virial coefficients A2 [109], coefficients of preferential solvation of macromolecules in mixed solvents (eluents) [40], as well as estimation of pore size distribution within porous bodies (inverse SEC) [136-140] and rates of diffusion of macromolecules within porous bodies. Some semiquantitative information on polymer samples can be obtained from the SEC results indirectly, for example, the assessment of the polymer stereoregularity from the stability of macromolecular aggregates (PVC [140]), of the segment lengths in polymer crystallites after their controlled partial degradation [141], and of the enthalpic interactions between unlike polymers in solution (in eluent) [142], as well as between polymer and column packing [123,143]. [Pg.474]

Finally, the balance equation for the SMSL looks like Eq. 23-30, except for the reaction term which is not necessarily linear now. Note that Cssc depends also on z (the depth in the lake, not the depth in the sediment column). Every depth zone has its own SMSL, but it is assumed that these layers do not interact with each other. In fact, the distance between them is much too large for lateral molecular diffusion in the sediments to play any role. There is no equation for the particles in the SMSL. Their balance is indirectly included in the preservation factor (3(z). Remember that if total solids are used to describe the solid phase, (3 is about 1, whereas if particulate organic carbon (POC) is used, (3 is smaller than one because part of the POC is degraded in the SMSL. Finally, we get ... [Pg.1088]

CuO, and PbO react at temperatures >600-700 °C quite strongly with the grain boundary phase and accelerate the oxidation and degradation. At temperatures below the transition temperature Tg of the glassy phase this interaction can be neglected because of the low ion diffusion into the grain boundary. [Pg.125]


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Diffusion degradation

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