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At least 415 records · Page 23Linked to original sources
PubMed1984

[CT volumetry of intrathoracic space-occupying processes].

Preoperative CT volumetry was performed in 39 patients with intrathoracic neoplasms. The results are compared to postoperative volume measures of the surgical preparation. The correlation of both measuring series was very high (p = .94). The estimated influence of systematic and stochastic errors was only 10 to 15%. The authors outline the consequences for clinical practice: by means of the better quantification in the T category of the TNM system, the surgeon is in a position to make a more precise preoperative planning. The reliable numeric in vivo determination of regression and growth velocity of tumors and/or metastases allows for the first time an exact quantification of control examinations during and after radiotherapy or chemotherapy. This will possibly lead to a more precise individual prognosis. In experimental radiotherapy a more detailed description of the evolution of experimental tumors in the living animal will be possible by this procedure.

Humans↗
PubMed2003

The ecology, genetics and evolution of bacteria in an experimental setting.

Richard Lenski is the John Hannah Distinguished Professor of Microbial Ecology at Michigan State University. He studies the ecology, genetics and evolution of bacteria in an experimental setting that enables him to observe the dynamical processes and outcomes across many generations. One of his experiments with Escherichia coli has passed 30,000 generations and is still on-going. A few years ago, he also began studying artificial life in the form of 'digital organisms' - computer programs that replicate, mutate, compete, and therefore evolve and adapt.

Bacteria↗
PubMed2006

Mating system and the evolution of quantitative traits: an experimental study of Mimulus guttatus.

The mating system of a population profoundly influences its evolution. Inbreeding alters the balance of evolutionary forces that determine the amount of genetic variation within a population. It redistributes that variation among individuals, altering heritabilities and genetic correlations. Inbreeding even changes the basic relationships between these genetic statistics and response to selection. If populations differing only in mating system are exposed to the same selection pressures, will they respond in qualitatively different ways? Here, we address this question by imposing selection on an index of two negatively correlated traits (flower size and development rate) within experimental populations that reproduce entirely by outcrossing, entirely by self-fertilizing, or by a mixture of outcrossing and selfing. Entirely selfing populations responded mainly by evolving larger flowers whereas outcrossing populations also evolved more rapid development. Divergence occurred despite an equivalent selection regime and no direct effect of mating system on fitness. The study provides an experimental demonstration of how the interaction of selection, genetic drift, and mating system can produce dramatic short-term changes in trait means, variances, and covariances.

Crosses, Genetic↗
PubMed1989

[Evolution of autologous graft interface in rats: experimental study].

With purpose to study the evolution of autologous venous graft interface, an experimental model utilizing an autologous venous patch to repair an infrarenal abdominal aortic defect in rats was developed. A small piece of both the jugular vein and the aorta were first excised. After implantation and reestablishment of blood flow, the animals were subsequently sacrificed in groups of 3 at the following intervals: 10 seconds, 1 minute, 10 minutes, 30 minutes, 1 hour, 6 hours, 12 hours, 24 hours, 7 days, 30 days and 90 days. All the patches and adjacent aortae were collected and studied using scanning electron microscopy, with the following results: 1) the endothelial lining of both the autologous vein patch and the adjacent aorta is destroyed before implantation due to operative manipulation; 2) after blood flow reestablishment, the patch and adjacent aortic interfaces are reactive to platelets and other blood cells; 3) New endothelial lining begins to appear from the 7th day after implantation, but the regeneration is not complete at 3 months. From the model, it is deducted that the endothelial repair of autologous venous patch and its adjacent aorta involves a very slow process.

Animals↗
PubMed1975

Experimental bacterial endocarditis. IV. Structure and evolution of very early lesions.

The vegetations of experimental sterile and bacterial endocarditis in rabbits were studied using light, immunofluorescent and electron microscopy. At an early stage, both lesions were composed chiefly of masses of platelets supported in a scaffolding of fibrin strands. In previous studies, this structure has often been described merely as "fibrin". After i.v. injection of Thorotrast, sterile vegetations showed remarkable accumulations of mononuclear phagocytes containing this substance, on surfaces projecting into the bloodstream. Sections fixed 30 min. after i.v. injection of streptococci also showed these phagocytes, which contained large numbers of bacteria. The possibility that BE is initiated by phagocytosis of circulating bacteria has been raised. Smaller numbers of circulating streptococci reached the vegetation by direct adhesion to exposed surfaces. In contrast, a majority of Proteus and Staphylococcus albus adhered directly to vegetations, without phagocytosis. Subsequently, these first settlers multiplied rapidly to form rounded colonies surrounded by capsules of fibrin, which apparently provided protection from phagocytosis. The vegetations grew by accretion of layers of fibrin and platelets, with colonies sandwiched between them. This suggested that a cycle of thrombosis and reseeding by circulating bacteria was a factor in their growth. Colonies showed morphological changes consistent with ageing after two days. Healing occurred by endothelialisation and organisation, and was greatly accelerated by penicillin treatment.

Animals↗
PubMed2025

Reproductive Isolation due to Divergent Ecological Selection Is Accompanied by Vast Genomic Instability in Experimentally Evolved Yeast Populations.

Populations evolving independently in divergent environments accumulate genetic differences and potentially evolve reproductive isolation as a by-product of divergence. The speed and mechanisms underlying this process are difficult to investigate because we rarely get the opportunity to witness them in natural settings, and histories of selection and gene flow between populations are often unknown. Here, we experimentally evolved yeast for 1000 generations of evolution in both divergent and parallel environments. At regular time points during experimental evolution, we made crosses between parallel- and divergent-evolving populations to measure postzygotic reproductive isolation (gamete viability). We used whole genome population sequencing to determine the mutational load, the number and types of structural variation, and other genomic features of the parent, F1 and F2 intraspecific hybrids. We found evidence for large-scale phenotypic and genome-wide differentiation in response to divergent laboratory selection. Divergent-selected populations produced hybrids with reduced gamete viability-a classic signature of postzygotic reproductive isolation in the form of hybrid breakdown. Parallel-selected populations, on the other hand, remained more reproductively compatible (with exceptions). We found that F2 hybrid genomes contained vast genomic instability, that is, new structural variants (especially insertions, deletions and interchromosomal translocations) that were not observed in parent and F1 genomes, which is likely a result of chromosome missegregation and recombination errors in hybrid meiosis. Our results provide phenotypic and genomic evidence that partial reproductive isolation evolved due to adaptation to divergent environments, consistent with predictions of ecological speciation theory.

Reproductive Isolation↗
PubMed1977

Study of two different subpopulations of anti-acetylcholine receptor antibodies in a rabbit with experimental auto-immune myasthenia gravis.

Two different subpopulations of anti-acetylcholine receptor antibodies were studied during the evolution of experimental autoimmune myasthenia in one rabbit immunized with Torpedo acetylcholine receptor. The results show that the subpopulation of antibodies directed against the toxin-binding site of the receptor might play a role in the appearance of the paralysis observed in this particular case.

Acetylcholine↗
PubMed2005

IgE expression on the surface of B1 and B2 lymphocytes in experimental murine schistosomiasis.

In a previous study we monitored the distribution and phenotype expression of B1 cells during the evolution of experimental murine schistosomiasis mansoni and we proposed that the B1 cells were heterogeneous: a fraction which originated in the spleen and followed the migratory pathway to mesenteric ganglia, while the other was the resident peritoneal B1-cell pool. In the present study, we have addressed the question of whether these two B1-lymphocyte populations are involved in the production of the late Ig isotype IgE, which is present in high levels in schistosomal infection. Lymphocyte expression of surface markers and immunoglobulins were monitored by immunofluorescence flow cytometry. Both in the spleen and mesenteric ganglia, the B1 and B2 cells were induced to switch from IgM to IgE in the early Th2-dominated phase of the disease, with an increase of IgE in its later phases. Conversely, peritoneal B1-IgM+ switched to the remaining IgE+ present in high numbers in the peritoneal cavity throughout the disease. We correlated the efficient induction of the expression of late Ig isotypes by B1 cells with high levels of inflammatory cytokines due to the intense host response to the presence of worms and their eggs in the abdominal cavity. In conclusion, B1 cells have a different switch behavior from IgM to IgE indicating that these cell sub-populations depend on the microenvironment.

Animals↗
PubMed1975

[Histochemical and histoenzymatic study of experimental myocardial infarction in the rat by temporary and permanent ligation of the left coronary artery (author's transl)].

The evolution of experimental myocardial infarction in the Rat with or without revascularization has been studied histochemically and histoenzymatically in 56 animals sacrified after 1, 6, 12, 24, 48 hrs and 7 days. Following permanent ischemis (14 animals), there appeared an extended transversal infarction marked by the complete disappearance of all phosphorylase activity (P-ase) after the first hour. During the first 6 hrs, changes appeared in succinodeshydrogenase (SHD) and cytochrome oxydase (Cyt-Ox). Glucose-6-phosphodeshydrogenase (G6PDH) presisted until lysis of the necrotic focus. It was possible to define a perinecrotic marginal area in which Pase activity is absent and SDH is granular "G3 in nature, characterized by continuous remodeling in the first 48 hrs. Following temporary ischemia (42 animals) the evolution was marked by rapid tissue reactions and early regression of the marginal zones. After 48 hrs and 7 days of survival, the planimetric evaluation of the infarcted area shows a definite reduction in the size of the infarctus in 50% of cases following removal of the ligature after 6 hrs, and in 66% of cases following removal of the ligature after 1 hr. It would appear probable that the revitalization of certain myocardial areas may extend from the marginal zones as is suggested by the reappearance in these zones several hrs after revascularization of P-ase and SDH activity. On the other hand, it is also true that the early restoration of blood flow does not always prevent the occurrence of an extended infarction. Certain recent observations have shown microcirculatory changes which are secondary to anoxia and should be studied further.

Animals↗
PubMed1986

Electrophysiological and sleep alterations in experimental mouse rabies.

Changes in the spontaneous brain electrical activity and sleep organization were investigated in 5 mice strains during the evolution of experimental fixed rabies infection. Cortical electrodes were chronically implanted for continuous EEG recording and spectral analysis until death. Three evolutionary phases were individualized. The initial phase exhibited alterations of sleep stages, REM sleep disappearance, pseudoperiodic facial myoclonus and first clinical signs. The mature phase was characterized by a generalized EEG slowing (2-4 cycles/s). The terminal phase occurring with extinction of hippocampal rhythmic slow activity showed a flattening of cortical activity. The brain electrical activity ceased about 30 min before the cardiac arrest. Paroxysmal activities appeared during the course of the disease as bursts of rhythmic slow waves, pseudoperiodic spikes or occasionally ictal epileptic discharges. Spectral analysis revealed a progressive and characteristic clustering of the EEG frequency band power values. The spread of infection in the CNS was monitored by specific immunofluorescence studies which revealed the presence of rabies virus antigen in the pons, the cerebellum, the thalamus and the cortex during the initial phase. The pyramidal field of the hippocampus was infected during the mature phase but the gyrus dentatus was never infected even at the terminal phase. These studies show that particular neuronal functions are impaired during rabies virus infection suggesting that neuronal alterations may be involved in the pathogenic mechanisms leading to lethality.

Animals↗
PubMed2002

Fitness evolution and the rise of mutator alleles in experimental Escherichia coli populations.

We studied the evolution of high mutation rates and the evolution of fitness in three experimental populations of Escherichia coli adapting to a glucose-limited environment. We identified the mutations responsible for the high mutation rates and show that their rate of substitution in all three populations was too rapid to be accounted for simply by genetic drift. In two of the populations, large gains in fitness relative to the ancestor occurred as the mutator alleles rose to fixation, strongly supporting the conclusion that mutator alleles fixed by hitchhiking with beneficial mutations at other loci. In one population, no significant gain in fitness relative to the ancestor occurred in the population as a whole while the mutator allele rose to fixation, but a substantial and significant gain in fitness occurred in the mutator subpopulation as the mutator neared fixation. The spread of the mutator allele from rarity to fixation took >1000 generations in each population. We show that simultaneous adaptive gains in both the mutator and wild-type subpopulations (clonal interference) retarded the mutator fixation in at least one of the populations. We found little evidence that the evolution of high mutation rates accelerated adaptation in these populations.

Adenosine Triphosphatases↗
PubMed1984

Evolution and host-dependent lesions in autoimmune thyroiditis: experimental study in inbred mice.

The evolution of thyroid pathology in experimental autoimmune thyroiditis was studied in several inbred strains of mice. The disease was induced by immunization with mouse thyroglobulin emulsified in Freund's complete adjuvant. In addition to the common lymphoid/mononuclear cell infiltration seen in other animal species with experimental autoimmune thyroiditis, several distinct thyroid lesions occurred only in certain strains of mice, suggesting a strain-dependency of these lesions. These lesions appeared often at the peak of the common lesion of autoimmune thyroiditis. These findings suggest that the thyroid pathology in murine autoimmune thyroiditis varies during its course and that some lesions occurring in this disease are strain-dependent. A genetic influence on the morphology of thyroid in chronic thyroiditis of man is postulated.

Animals↗