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PubMed1977

Influence of isoproterenol and cholestyramine on acute gastric mucosal ulcerogenesis.

One thesis concerning the pathogenesis of "stress ulcer" states that the combination of (1) bile acid-induced H+ "back diffusion" and (2) gastric mucosal ischemia is acutely Hg) to induce ischemia, this thesis was further tested by selectively mitigating either the ischemic or the back diffusion components of the model. Vascularized wedges of proximal canine gastric wall mounted on Lucite chambers were studied. With the mucosa directly visualized, control group A (6 dogs) was subjected sequentially to (1) topical acid test solution alone (ATS), (2) ATS + S, and (3) ATS + S + topical 5 mM Na taurocholate (TC). Study group B (6 dogs): (1) ATS, (2) ATS + S + the beta adrenergic agonist, isoproterenol, 1.5 microng per kg-min infused into the splenic artery, and (3) ATS + S + TC + isoproterenol. Study group C (6 dogs): (1) ATS, (2) ATS + S + the bile acid binding resin, cholestyramine (C), 4 g per liter, and (3) ATS + S + TC + C. During each period the net flux of H+, the electrical potential difference, and the aminopyrine clearance (AC) were determined. Mucosal damage (intramucosal hemorrhage, erosions, and ulcers, graded 0 to 5) was assessed blindly by an independent observer using photographs. The results indicate (1) that, despite H+ back diffusion comparable to ATS + S + TC, intraarterial isoproterenol significantly protects against lesion formation by increasing AC, and (2) that, despite a reduction in AC comparable to ATS + S + TC, topical C significantly protects against lesion formation by preventing excessive back diffusion of H+.

Administration, Topical↗
PubMed1992

A proposed tolerance criterion for diffuse axonal injury in man.

The head injury criterion (HIC) is currently the government-accepted head injury indicator. The HIC is not injury-specific, does not relate to injury severity, nor does it take into account variations in the brain mass or load direction. This report focuses on one type of inertial brain injury, diffuse axonal injury (DAI), and utilizes animal studies, physical model experiments, and analytical model simulations to determine the kinematics of DAI in the subhuman primate and to scale these results to man. A human injury tolerance for moderate to severe DAI, which includes the influences of rotational loads and brain mass, is proposed.

Acceleration↗
PubMed1978

Nature of amorphous aluminum hydroxycarbonate.

The titration of sodium carbonate with aluminum nitrate is shown to produce amorphous aluminum hydroxycarbonate. This compound is not stoichiometric, although the maximum carbonate to aluminum ratio appears to be 0.5. The pH conditions for achieving the maximum carbonate content are concentration dependent. A model for the particle surface at the solution interface is proposed. This model accounts for the presence of carbonate directly coordinated to the aluminum and carbonate adsorbed by electrostatic forces. Sodium is present in the diffuse layer and is, therefore, not an integral part of the structure.

Aluminum↗
PubMedDate not supplied

Nuclear magnetic spin-lattice relaxation of water protons caused by metal cage compounds.

The nuclear magnetic spin-lattice relaxation rates of water protons are reported for solutions of manganese(II), copper(II), and chromium(III) cage complexes of the sarcophagine type. As simple aqueous solutions, the complexes are only modest magnetic relaxation agents, presumably because they lack protons on atoms in the first-coordination-sphere protons that are sufficiently labile to mix the large relaxation rate at the metal complex with that of the bulk solvent. The relaxation is approximately modeled using spectral density functions derived for translational diffusion of the interacting dipole moments with the modification that the electron spin relaxation rate is directly included as a contribution to the correlation time. In all cases studied, the electron spin relaxation rate is sufficiently large that it contributes directly to the water-proton spin relaxation process. The poor relaxation efficiency of the cage compound may, however, be improved dramatically by binding the complex to a protein. The efficiency is improved even further if the rotational motion of the protein is reduced drastically by an intermolecular cross-linking reaction. The relaxation efficiency of the cross-linked protein-cage complexes rivals that of the best first-coordination-sphere relaxation agents like [Gd(DTPA)(H2O)]2- and [Gd(DOTA)(H2O)]-.

Aza Compounds↗
PubMed1978

Estimation of dissolution rate of salicylamide in complexing media using a theoretical diffusion model.

Dissolution rates of salicylamide in water and caffeine solutions under perfect sink conditions were predicted by theoretical diffusion equations applicable to dissolution in complexing media. Experimental dissolution rates were measured using a compartmentalized rotating-basket apparatus under two sets of conditions. Agreement was found between experimental and predicted rates. Use of the theoretical equation for estimating dissolution rates involves simple calculations of diffusion coefficients and diffusion layer thickness under the operative dissolution conditions. The increase in dissolution rate caused by addition of the complexant can be calculated for diffusion-controlled dissolution directly if the stability constant and the drug solubility in water are known or measured.

Caffeine↗
PubMed1976

Studies on the human pharmacokinetics of isophosphamide (NSC-109724).

The pharmacokinetics of isophosphamide (IP) in man has been studied using 14C-labeled drug and differential extraction of unchanged drug from metabolites by CHCl3 extraction of plasma and urine. The plasma decay of IP is biphasic with a terminal half-life of 15.2 hours which is twice that reported for cyclophosphamide (CP). The fraction of drug metabolized is 49% for IP compared to 88% reported for CP. This is consistent with the six-times larger pseudometabolic pharmacokinetic rate constant reported for CP (0.26 hr-1) than found by us for IP (0.04 hr-1). The renal clearance for IP (21.3 ml/min) is two times that of CP (10.7 ml/min). In addition to an analysis of the kinetics of disposition and elimination of unchanged IP, an analysis of the pharmacokinetics of total metabolite of IP in plasma and urine was made. A nonlinear pharmacokinetic model which includes a term for biotransformation according to Michaelis and Menten revealed that the total metabolites do not diffuse from a small plasma space of 2.1 liters but are excreted directly via the urine. In contrast to the biexponential plasma decay of single, high-dose IP (5 g/m2), multiple-dose IP (2.4 g/m2/day X 3) shows a monoexponential decay with a half-life of 6.9 hours, a pseudometabolic rate constant of 0.08 hour-1, and a renal clearance of 18.7 ml/minute. The fraction of drug metabolized (79.7%) calculated from the pharmacokinetic parameters agrees with the fraction of drug recovered in urine as total metabolites (72.8%). This is distinctly different from high-dose IP (48.6%) but similar to the fraction of drug metabolized as reported for CP (88.0%). This suggests that the pharmacokinetic transfer constant for IP metabolism is dose dependent, an observation that may be useful in developing new IP regimens.

Cyclophosphamide↗
PubMed2026

Glymphatic dysfunction mediates inflammation-driven vascular burden and cognitive decline in cerebral small vessel disease.

BACKGROUND: Cerebral small vessel disease (CSVD) is increasingly recognized as a disorder involving microvascular dysfunction, impaired perivascular clearance, and inflammatory processes. However, how systemic inflammatory burden, neurovascular coupling (NVC), glymphatic MRI markers, vascular lesion burden, and cognition are interrelated remains unclear. MATERIALS AND METHODS: In this prospective study, 155 patients with CSVD and 70 healthy controls (HCs) underwent multimodal MRI. NVC was quantified using the cerebral blood flow/fractional amplitude of low-frequency fluctuations ratio. Glymphatic function was assessed via the diffusion tensor image analysis along the perivascular space (ALPS) index, choroid plexus volume (CPV), and perivascular space (PVS) fractions. Structural equation modeling (SEM) was employed to evaluate the direct and indirect effects of inflammatory markers on vascular burden and cognitive performance. RESULTS: Patients with CSVD exhibited significantly diminished NVC (specifically in the right median cingulate and left frontal gyri) and impaired glymphatic function (lower ALPS-index; higher CPV and PVS fractions) compared to HCs. SEM revealed that inflammatory biomarkers exerted both a direct effect on vascular burden and a substantial indirect effect (accounting for 66.3% of the total effect) mediated through two pathways: a single-mediation path via glymphatic function (42.8%) and a serial-mediation path via NVC and glymphatic function (23.5%). Increased vascular burden was significantly associated with poorer cognitive performance. CONCLUSION: Inflammation drives CSVD progression and cognitive decline primarily through the disruption of NVC and glymphatic clearance mechanisms. These findings highlight glymphatic dysfunction as a critical mediator of inflammation-related structural brain damage.

Humans↗
PubMed1979

Experimental glomerulonephritis induced by in situ formation of immune complexes in glomerular capillary wall.

An experimental model of glomerulonephritis was produced by the in situ formation of immune complexes directly in the glomerular capillary wall. Perfusing the lectin concanavalin A (Con A) into the left renal arteries of rats led to its binding diffusely to the glycoproteins of the glomerular capillary wall of only that kidney in each animal. The subsequent reaction with anti-Con A antibody (either administered systemically or actively induced) resulted in an exudative and proliferative glomerulonephritis confined to the Con A perfused kidney. Immunofluorescence disclosed the diffuse deposition of immunoglobulin, Con A, and C3 in the perfused, but not the unperfused kidney. The quantitative relationship between antigen and antibody binding and histologic outcome was determined. Since lectins have been found in mammalian tissues, as well as in infectious agents that are pathogenic in man, a series of events conceptually similar to this in situ model may occur in some cases of glomerulonephritis in man.

Animals↗
PubMed1991

Kinetic evaluation of pharmacological effects based on allosteric coupling of the benzodiazepine/gamma-aminobutyric acidA receptor in the brain.

A mathematical allosteric coupling model has been proposed to describe the process by which binding to the benzodiazepine/gamma-aminobutyric acid (GABA) receptor complex initiates a biological response. The model states that the first receptors (benzodiazepine receptors) can diffuse independently in the plane of the membrane and reversibly associate with the second receptors (GABA receptors) to regulate their activity (induction of increased chloride ion flux due to the opening of the chloride ion channel). The ratio of agonist-bound to total GABA receptor density was defined to be directly proportional to the biological response in the model. The analysis makes the following assumptions: i) the binding affinity of agonists (muscimol or benzodiazepine) to the benzodiazepine receptor/GABA receptor complex is much greater than that to each receptor alone; ii) the double receptor-single agonist (benzodiazepine, muscimol or GABA) ternary complex binds to the other agonist with a high binding affinity as compared with that of each agonist to an agonist-free receptor complex; iii) benzodiazepine receptor-GABA receptor interaction is enhanced in the presence of each agonist; iv) the GABA receptor is desensitized after the binding of GABA agonist (GABA or muscimol) to the receptor. The modeling exercise shows that the benzodiazepine concentration required for half-maximal biological response is lower than that required for half-maximal receptor binding. In the case of the GABA agonist, a linear relationship between receptor occupancy and biological response was observed. The degree of discrepancy between the two profiles (receptor occupancy and biological response) concerning benzodiazepine concentration dependency and time dependency increased with a decrease in the dissociation constants based on the benzodiazepine receptor-GABA receptor interaction.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain↗
PubMed1975

Free energy and the kinetics of biochemical diagrams, including active transport.

In earlier papers on muscle contraction it was found very useful to relate the actual (not standard) free energy levels of the different states in the biochemical diagram of the myosin cross-bridge to the first-order rate constants governing transitions between these states and to the details of the conversion of ATP free energy into mechanical work. This same approach is applied here to other macromolecular biochemical systems, for example, carriers in active transport, and simple enzyme reactions. With the definition of free energy changes between states of diagram used here (and in the muscle papers), the rate constants of the diagram are firat order, the macromolecular transitions are effectively isomeric, the equilibrium constants are dimensionless, the free energy changes are directly related to first-order rate constant ratios, and the ratio of products of forward and backward rate constants around any cycle of the diagram is related to operational free energy changes (e.g. the in vivo free energy of ADP HYDROLYSIS). These general points are illustrated by means of particular arbitrary models, especially transport models. In contrast to the muscle case, the free energy conversion question in other biochemical systems can be handled at the less detailed, complete-cycle level rather than at the elementary transition level. There is a corresponding complete-cycle kinetics, with composite first-order rate constants for the different possible cycles (in both directions). An introductory stochastic treatment of cycle kinetics is included.

Adenosine Triphosphatases↗
PubMed1975

Airborne infection in a fully air-conditioned hospital. II. Transport of gaseous and airborne particulate material along ventilated passageways.

A mathematical model is described for the transport of gaseous or airborne particulate material between rooms along ventilated passageways. Experimental observations in three hospitals lead to a value of about 0.06 m.2/sec. for the effective diffusion constant in air without any systematic directional flow. The 'constant' appears to increase if there is any directional flow along the passage, reaching about 0.12 m. 2/sec. at a flow velocity of 0.04 m./sec. Together with previously published methods the present formulae make it possible to calculate the expected average amounts of gaseous or particulate material that will be transported from room to room in ventilated buildings in which the ventilation and exchange airflows can be calculated. The actual amounts transported in occupied buildings, however, vary greatly from time to time.

Air Conditioning↗
PubMed1978

Kinetics of D-histidine diffusion across rat intestine in vitro.

A five-compartment linear model for diffusion in vitro across rat jejunum has been proposed for the study of the kinetic constants of D-histidine transport. Once preliminary experiments using 2,4-dinitrophenol and L-methionine have proved that D-histidine gives rise to passive transport only, the validity of the model was tested and its parameters estimated through a best-fitting procedure by using experimental data concerning D-histidine transport. D-Histidine diffusion was studied in everted and unreverted loops mounted in an oxygenated bath system. Both mucosa to serosa and seroa to mucosa movements of D-histidine (3-30 mM) were evaluated by measuring chemically the amount of D-histidine transported into intestinal lumen every 5 min for 60 min. Results obtained proved that D-histidine transport in each direction (mucosa to seroa or seroa to mucosa) was dependent-concentration process. Nevertheless different values of gain and time constants were estimated for the transport in the two directions.

Animals↗
PubMed1992

Formation of a regular dissipative structure: a bifurcation and non-linear analysis.

A non-linear reaction diffusion model of a negative feedback epigenetic control system is presented. The model involves synthesis of the mitotic inducing and inhibiting proteins, simultaneously with intercellular self-diffusion and cross-diffusion of the latter only. The importance of negative cross-diffusion for creating a regular dissipative structure is shown. A bifurcation analysis of the non-linear diffusive system has been performed and it is concluded that bifurcation is supercritical. Lastly, using Liapunov's direct method, it is shown that the pattern evolved by the system is globally asymptotically stable.

Cell Differentiation↗
PubMed1992

Dentin as inhibitor of bacterial toxicity on pulpal cells in vitro.

Many studies have shown that the major cause of pulpal disease is the presence of bacteria or their by-products in the dentinal tubules. The purpose of this investigation was to develop an in vitro model, simulating the pulp chamber, that would permit the study of the transport of bacterial by-products through dentin and their effect on pulpal cells. Human pulpal cells were cultured in a modified Sykes-Moore chamber and exposed through dentin to sonicated extracts of Porphyromonas gingivalis ATCC 33277. The cell response was evaluated with the thymidine incorporation method. The results were compared with the cell response obtained after direct exposure to the same irritant. It was found that dentin significantly restricts the diffusion of bacterial proteins in a 24-h experimental period. The time needed for the first bacterial protein molecule to cross the dentin barrier was 6 h. The "diffusion velocity" of the bacterial proteins was 0.023 microns/s. The proposed model has further applications in biocompatibility and microleakage research.

Bacterial Proteins↗
PubMed1992

Mutation of serine residue 318 in the class C beta-lactamase of Enterobacter cloacae 908R.

The involvement of the serine residue 318 in the specificity of a class C beta-lactamase was investigated. Multiple site-directed mutants at this position were generated using a polymerase chain reaction technique. These mutants were then probed for their activity towards various beta-lactam compounds. One mutant, S318G was further purified and its physico-chemical and catalytic properties determined. It was shown that the observed minimal inhibitory concentration values of this mutant could be correlated to its kinetic properties using a 'diffusion-hydrolysis' model. However, the data showed that residue 318 has little influence on the specificity of class C beta-lactamases.

Base Sequence↗
PubMed1992

Extending the stochastic two-stage model of carcinogenesis to include self-regulation of the nonmalignant cell population.

One of the challenges of introducing greater biological realism into stochastic models of cancer induction is to find a way to represent the homeostatic control of the normal cell population over its own size without complicating the analysis too much to obtain useful results. Current two-stage models of carcinogenesis typically ignore homeostatic control. Instead, a deterministic growth path is specified for the population of "normal" cells, while the population of "initiated" cells is assumed to grow randomly according to a birth-death process with random immigrations from the normal population. This paper introduces a simple model of homeostatically controlled cell division for mature tissues, in which the size of the nonmalignant population remains essentially constant over time. Growth of the nonmalignant cell population (normal and initiated cells) is restricted by allowing cells to divide only to fill the "openings" left by cells that die or differentiate, thus maintaining the constant size of the nonmalignant cell population. The fundamental technical insight from this model is that random walks, rather than birth-and-death processes, are the appropriate stochastic processes for describing the kinetics of the initiated cell population. Qualitative and analytic results are presented, drawn from the mathematical theories of random walks and diffusion processes, that describe the probability of spontaneous extinction and the size distribution of surviving initiated populations when the death/differentiation rates of normal and initiated cells are known. The constraint that the nonmalignant population size must remain approximately constant leads to much simpler analytic formulas and approximations, flowing directly from random walk theory, than in previous birth-death models.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Death↗
PubMed1979

Two-carrier influx of neutral amino acids into rabbit ileal mucosa.

1. The influx of serine, alanine and methionine across the brush border membrane of the rabbit ileal mucosa has been measured during short periods of incubation. 2. A kinetic analysis of the uptake data, assuming one mediated entry mechanism or one mediated entry mechanism plus a diffusion component to be present, does not provide an adequate explanation for the results obtained. Methionine inhibition of serine uptake provided direct evidence that the diffusive entry of serine into the rabbit ileum was small or non-existent. 3. Data taken from amino acid inhibition and substrate-uptake experiments, fitted simultaneously to a double hyperbolic model of amino acid uptake, give good agreement between predicted and experimental results. There is also good quantitative agreement between computer-derived kinetic constants in the present work and similar constants obtained previously using a different method of analysis. 4. Present work supports the general hypothesis that neutral amino acids use two mediated pathways to enter the rabbit ileal mucosa. The possible physiological significance of these results and their probable effect on currently held concepts of how amino acids cross the brush border membrane of the rabbit intestinal mucosa is discussed.

Alanine↗