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At least 1,189 records · Page 66Linked to original sources
PubMed2003

Film drainage between two captive drops: PEO-water in silicon oil.

An experimental study of the deformation and drainage of a Newtonian liquid film trapped between two drops is performed for the cases of a constant and slightly rising interaction force. Series of polyethylene oxide (PEO) water solutions are used for the dispersed and polydimethylsiloxane (PDMS) for the continuous phase. The film evolution is observed by an interferometric technique. Experimental data for the film thinning rate and for the film profile allow quantitative comparison with the available drainage models.

Journal Article↗
PubMed1999

Dark incoherent soliton splitting and "phase-memory" effects: Theory and experiment.

We report on an experimental observation of dark incoherent soliton Y splitting. The effects of incoherence on the evolution of incoherent dark soliton doublets are investigated both theoretically and experimentally. We show that the dynamics of these incoherent self-trapped entities are associated with strong "phase-memory" effects that are otherwise absent in the linear regime.

Journal Article↗
PubMed1980

Myocardial infarct size. Measurements and predictions.

Because patient prognosis is related in part to infarct size, therapies that could limit infarct size should be beneficial. The development of such therapies has been hampered by the lack of proven techniques to measure infarct size or to assess the effect of therapy in living patients. In addition, the evolution of ischemic cell death in human infarcts is not understood, and therefore the amount of ischemic myocardium that might be salvageable at various times after the onset of myocardial infarction is unknown. Experimental studies have contributed to our understanding of the evolution of acute myocardial infarcts. However, there is a continuing need for experimental and human anatomical studies to validate indirect in vivo techniques of estimating infarct size. In addition, reliable experimental models in which potential therapies can be tested are needed. In dogs, infarct size is predetermined in part by the amount of myocardium at risk and the amount of collateral flow in this risk region. Measuring these parameters should provide a framework within which the effects of therapy on infarct size can be assessed.

Animals↗
PubMed1981

A computer model of the evolution of specific maximum lifespan.

To answer the question of why organisms have evolved finite and specific maximum lifespans, I have built and experimentally studied a discrete-event simulation model of the evolution of lifespan. Through natural selection, the model evolves an apparent plateau in maximum lifespan, the height of which is a decreasing function of both the intensity of niche fluctuations and specific fecundity. Evolved lifespan is therefore finite (small and essentially constant over accessible time intervals) and specific. Experiments demonstrate that the plateau is not due to group selection. Instead, it occurs because the rate of increase of maximum lifespan by natural selection - in an environment presenting a finite probability that death will occur prior to reaching the genetically specified maximum - is a decreasing function of maximum lifespan itself and asymptotically approaches zero. This supports in part a class of existing hypotheses that finite lifespan is due to an equilibrium between weak selection, as in the model, and various lifespan-decreasing processes, which however were not simulated in the present experiments. Although the model shows that such counter processes are not strictly necessary for the evolution of finite and specific maximum lifespan, my interpretation of the model's correspondence to organic evolution does imply a counter process, a bias in random genetic drift toward shorter lifespan, that is more general than those previously hypothesized.

Biological Evolution↗
PubMed2004

Are residues in a protein folding nucleus evolutionarily conserved?

Protein is the working molecule of the cell, and evolution is the hallmark of life. It is important to understand how protein folding and evolution influence each other. Several studies correlating experimental measurement of residue participation in folding nucleus and sequence conservation have reached different conclusions. These studies are based on assessment of sequence conservation at folding nucleus sites using entropy or relative entropy measurement derived from multiple sequence alignment. Here we report analysis of conservation of folding nucleus using an evolutionary model alternative to entropy-based approaches. We employ a continuous time Markov model of codon substitution to distinguish mutation fixed by evolution and mutation fixed by chance. This model takes into account bias in codon frequency, bias-favoring transition over transversion, as well as explicit phylogenetic information. We measure selection pressure using the ratio omega of synonymous versus non-synonymous substitution at individual residue site. The omega-values are estimated using the PAML method, a maximum-likelihood estimator. Our results show that there is little correlation between the extent of kinetic participation in protein folding nucleus as measured by experimental phi-value and selection pressure as measured by omega-value. In addition, two randomization tests failed to show that folding nucleus residues are significantly more conserved than the whole protein, or the median omega value of all residues in the protein. These results suggest that at the level of codon substitution, there is no indication that folding nucleus residues are significantly more conserved than other residues. We further reconstruct candidate ancestral residues of the folding nucleus and suggest possible test tube mutation studies for testing folding behavior of ancient folding nucleus.

Amino Acid Sequence↗
PubMed2000

Effects of environment on compensatory mutations to ameliorate costs of antibiotic resistance.

Most types of antibiotic resistance impose a biological cost on bacterial fitness. These costs can be compensated, usually without loss of resistance, by second-site mutations during the evolution of the resistant bacteria in an experimental host or in a laboratory medium. Different fitness-compensating mutations were selected depending on whether the bacteria evolved through serial passage in mice or in a laboratory medium. This difference in mutation spectra was caused by either a growth condition-specific formation or selection of the compensated mutants. These results suggest that bacterial evolution to reduce the costs of antibiotic resistance can take different trajectories within and outside a host.

Adaptation, Physiological↗
PubMedDate not supplied

The role of diffusion tensor imaging in the evaluation of ischemic brain injury - a review.

Water diffusion in brain tissue is affected by the presence of barriers to translational motion such as cell membranes and myelin fibers. The measured water apparent diffusion coefficient (ADC) value is therefore frequently anisotropic and varies depending upon the orientation of restricting barriers (such as white matter tracts) relative to the diffusion-sensitive-gradient direction. Anisotropic water diffusion can be specified using indices of diffusion anisotropy [e.g. standard deviation of the individual ADC values, fractional anisotropy (FA), lattice index (LI)], which are derived from measurements of the full diffusion tensor. The rotationally invariant nature of particular diffusion anisotropy indices (e.g. FA, LI) allows orientation-independent comparisons of these parameters between different subjects. Pathophysiological processes (such as cerebral ischemia) that modify the integrity of the tissue microstructure result in significant alterations in tissue anisotropy and make this metric a useful endpoint for characterizing the temporal evolution of the disease. Diffusion-tensor imaging (DTI) studies of both experimental and human stroke suggest that DTI may provide additional information about the evolution of the disease that is not available from diffusion-weighted MRI (DWI) alone. Acute reductions in the average diffusivity [ = (lambda(1) + lambda(2) + lambda(3))/3 where lambda(1), lambda(2), and lambda(3) are the eigenvalues of the diffusion tensor] following the onset of cerebral ischemia are often accompanied by increases in diffusion anisotropy. In the transition from acute to sub-acute and chronic stroke, renormalizes and subsequently increases whereas diffusion anisotropy measures (e.g. FA) decline and remained reduced in chronic infarcts. Overall isotropic ADC changes during infarct evolution have been observed to be greater in white matter (WM) than in gray matter (GM) lesions (although there have been conflicting reports on this issue) and GM lesions tend to renormalize prior to WM lesions as the infarct evolves. Ischemic WM exhibits a significant decrease in diffusion anisotropy (relative to normal WM) during ischemic evolution whereas that of ischemic GM remains statistically unchanged. Furthermore, the percentage decrease in ischemic WM is largely determined by reductions in lambda(1), the eigenvalue that coincides with the long axis of the WM fiber tract. Variations in unidirectional ADC or over the ischemic time course limit the usefulness of this parameter alone as a predictor of ischemic injury. Consequently, ADC information has been combined with that of other MR parameters (including DTI) to unambiguously stage and predict ischemic brain injury over its entire temporal evolution. Combined and diffusion anisotropy measurements have identified three phases of diffusion abnormality: (1) reduced and elevated anisotropy; (2) reduced and reduced anisotropy; and (3) elevated and reduced anisotropy. However, variations in the differential patterns of and diffusion anisotropy evolution have been observed by a number of investigators and more work is needed to clarify the role of these measurements in characterizing the severity of the ischemic insult as well as the potential outcome in response to the initial ischemic injury. The use of DTI, in combination with more sophisticated analysis methods for performing multiparametric segmentation, such as multispectral analysis, may enhance the use of MRI for accurate diagnosis and prognosis of stroke. Furthermore, these techniques may also play an important role in the clinical evaluation of new stroke treatments.

Animals↗
PubMed1992

Coronary vascular and myocardial lesions due to experimental constriction of the abdominal aorta.

The development and evolution of arterial and myocardial lesions were morphologically evaluated in Wistar rats submitted to constriction of the abdominal aorta. The control (sham-operated) and operated groups were evaluated 1, 2, 4 and 6 weeks after surgery. The aorta-constricted groups developed arterial hypertension followed by myocardial hypertrophy evidenced from the first week onwards by the increase in ventricular weight and in the diameters of left and right ventricular myofibers. The histopathologic study of the myocardium revealed in aorta-constricted groups, since the first week, widespread necrotizing changes of the intramural coronary branches surrounded by multifocal areas of myofiber degeneration and necrosis. The lesions were more extensive in the wall of the right ventricle and were gradually replaced by scar tissue. At the 6th week patchy focal fibrotic scars were found scattered in the myocardium of both ventricles. There were no systemic lesions in aorta-constricted or sham-operated groups. The close association between the arterial and myocardial lesions shows that muscle necrosis and scars are due to ischemia. They may influence the contractile performance of the myocardium in this model of pressure-induced hypertrophy of the heart.

Animals↗
PubMed1985

Possible role of endothelium in the orientation of smooth muscle cells in experimental neointima.

Myointimal cells (MIC) orientation and intimal thickening evolution, induced by grafting an autogenous venous patch onto the rat common carotid artery, were studied with light microscopy at different times until 14 months after surgery. Intimal thickenings in the venous patch were most prominent at an intermediate postoperative period, after which their mean size did not change significantly. In host artery neointima, the greatest MIC proliferation was observed at a late stage of evolution. MIC arrangement was predominantly circumferential to the blood stream in venous patch neointima, whereas it was mostly axial in the host artery. The interaction between MIC orientation and endothelial regeneration in the operated vessel is discussed.

Animals↗
PubMedDate not supplied

[Character of changes in protease inhibitory capacity of blood in experimental osteoarticular tuberculosis].

All the steps of osteoarticular tuberculosis evolution were accompanied by an increase in proteolytic activity in rabbit blood serum, which was compensated by activation of alpha 1-inhibitor of proteinases at the initial steps of osteitis. The system "proteinases-inhibitors" was imbalanced during the severe phases of arthritis independently on the rate of its development as follows: predominance of proteolytic potential over inhibitory activity, dissimilar activity of alpha 1-inhibitor of proteinases simultaneously with equal rate of alpha 2-macroglobulin content decrease. Dissimilar alterations in the system studied enabled to suggest that differential application of proteinases is suitable for treatment of inflammation with respect to the step of osteoarticular tuberculosis development.

Animals↗
PubMed1990

Experimental obstructive coronary atherosclerosis in the hyperlipidemic hamster.

The evolution of coronary atherosclerotic lesions induced by a hyperlipidemic diet was examined in male hamsters subjected for up to 40 weeks to a standard chow supplemented with 3% cholesterol and 15% butter. Control animals were fed standard chow only. Five to seven hamsters were monthly sacrificed and investigated for serum lipids and coronary artery lesions. As compared with control animals, the hamsters fed the fat diet showed a progressive increase in serum cholesterol which reached maximum values up to 17 fold in the 10th month. The serum of the hyperlipidemic hamster examined by agarose electrophoresis, Laurell immunoelectrophoresis and cross-immunoelectrophoresis showed at most a 14 fold increase in low density lipoproteins after 10 months diet. The examination of coronary arteries revealed morphologic changes already detectable at 2 weeks of diet. The earliest modifications observed were characterized by proliferation of the subendothelial matrix or/and the appearance of liposome-like structures in the intima. After 2-3 weeks of diet, smooth muscle cells appeared occasionally in the intima and monocytes adhered and penetrated through the endothelium. Later on, smooth muscle cells and macrophage displayed lipid deposits. Focally, in areas of intimal proliferation and foam cells, endothelial cells were also lipid-loaded. Like in human atherosclerotic plaque, in the late stages of hamster coronary lesions, there was a progressive accumulation of extracellular unesterified cholesterol, calcium deposition and necrosis. Lesions evolved to a progressive narrowing of the coronary branches affected, with complete obstruction of some small arterial ramifications. Hamster appears to be a suitable model for studying the molecular and cellular events leading to obstructive coronary atherosclerosis.

Animals↗
PubMedDate not supplied

Experimental patterns related to multiple sclerosis pathology.

In the history of experimental demyelination, allergic encephalomyelitis (EAE) is the most impressive experimental demyelinating disease based on an immunological mechanism. The evolution of the neuropathological process of chronic EAE is very close to that of chronic Multiple Sclerosis. On the other hand experimental inoculation of different viruses can induce various types of demyelination depending on the main target of the virus and the host response, this latter being conditioned by the age, the mechanism of immunity and the persistence of the virus in the brain. The demyelination can be induced by a viral persistent infection primarily affecting oligodendrocytes (CDV, JHM hepatitis virus) or acting through an immunomediate response against myelin (Visna, Theiler virus, human conventional viruses). The experimental demyelinating models show that also in Multiple Sclerosis a viral etiology could be the starting point of a demyelinating process based on a immunologically mediated mechanism.

Animals↗
PubMed1995

Chronic hepatitis in experimental schistosomiasis.

Histological features of chronic active and chronic persistent hepatitis were observed in mice, rabbits and non-human primates infected with either Schistosoma mansoni and Schistosoma japonicum. In early infection hepatitis appeared as a reactive change due to liver damage caused by the deposition of schistosome eggs, but portal and septal cellular infiltrations tended to remain long after parasite aggression had diminished or disappeared, either spontaneously with time or after chemotherapy. In rabbits, and to a lesser degree in monkeys, a picture of chronic active hepatitis was present, with evolution to cirrhosis in the former. The experimental findings indicate that schistosomiasis has the potential to induce chronic hepatitis and suggest that the current assumption that chronic hepatitis seen in humans with schistosomiasis is always due to concomitant viral infection should be reviewed.

Animals↗
PubMed2005

Divergent selection and the evolution of signal traits and mating preferences.

Mating preferences are common in natural populations, and their divergence among populations is considered an important source of reproductive isolation during speciation. Although mechanisms for the divergence of mating preferences have received substantial theoretical treatment, complementary experimental tests are lacking. We conducted a laboratory evolution experiment, using the fruit fly Drosophila serrata, to explore the role of divergent selection between environments in the evolution of female mating preferences. Replicate populations of D. serrata were derived from a common ancestor and propagated in one of three resource environments: two novel environments and the ancestral laboratory environment. Adaptation to both novel environments involved changes in cuticular hydrocarbons, traits that predict mating success in these populations. Furthermore, female mating preferences for these cuticular hydrocarbons also diverged among populations. A component of this divergence occurred among treatment environments, accounting for at least 17.4% of the among-population divergence in linear mating preferences and 17.2% of the among-population divergence in nonlinear mating preferences. The divergence of mating preferences in correlation with environment is consistent with the classic by-product model of speciation in which premating isolation evolves as a side effect of divergent selection adapting populations to their different environments.

Adaptation, Biological↗
PubMedDate not supplied

The evolution and maintenance of virulence in microparasites.

In recent years, population and evolutionary biologists have questioned the traditional view that parasite-mediated morbidity and mortality¿virulence¿is a primitive character and an artifact of recent associations between parasites and their hosts. A number of hypotheses have been proposed that favor virulence and suggest that it will be maintained by natural selection. According to some of these hypotheses, the pathogenicity of HIV, Vibrio cholerae, Mycobacterium tuberculosis,theShigella,as well as Plasmodium falciparum,and many other microparasites, are not only maintained by natural selection, but their virulence increases or decreases as an evolutionary response to changes in environmental conditions or the density and/or behavior of the human population. Other hypotheses propose that the virulence of microparasites is not directly favored by natural selection; rather, microparasite-mediated morbidity and mortality are either coincidental to parasite-expressed characters (virulence determinants that evolved for other functions) or the product of short-sighted evolution in infected hosts. These hypotheses for the evolution and maintenance of microparasite virulence are critically reviewed, and suggestions are made for testing them experimentally.

Animals↗
PubMed1987

The evolution of morphologic and biomechanical changes in reversed and in-situ vein grafts.

A comparative study of experimental reversed (RV) and in-situ (INS) vein grafts with respect to the evolution of morphologic and compliance characteristics was done in a canine model. In addition, the compliance characteristics in a series of human INS vein grafts were recorded as a function of time after operation. At 6 months after implantation, all experimental grafts displayed well-developed intimal hyperplasia. There was no significant difference in either absolute intimal thickness (INS 0.133 +/- 0.09 mm vs. RV 0.085 +/- 0.06 mm; NS) nor in the percentage of the total wall thickness occupied by the intima when experimental INS grafts were compared with RV grafts after 6 months. Similarly, compliance values of INS and RV vein grafts were similar at all time intervals examined up to 6 months after operation. Thirty-three human INS vein grafts had a mean compliance value of 1.74 +/- 0.72 (percent radial changes per mmHg X 10(-2) at a median postoperative interval of 14 weeks. This value did not differ significantly from those measured in the INS vein grafts. Although all vein grafts examined retained their native viscoelastic properties, this study suggests that functioning human INS vein grafts are less compliant than previously suspected on the basis of prior ex-vivo and clinical studies of RV saphenous vein grafts. The purported clinical superiority of the INS vein graft cannot be explained on the basis of superior biomechanical performance or failure to develop intimal hyperplasia.

Animals↗