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At least 1,351 records · Page 75Linked to original sources
PubMed1989

[Function-structural features of cardiac adaptation to static physical loads].

The cardiovascular system of 70 white rats was studied during adaptation to the physical static load by means of functional and morphometric techniques. The physical static loads induced variations of adaptive changes of the myocardium: right ventricle hypertrophy was mainly responsible for the cardiac mass increase in 47.1% of rats; 31.4% of the hearts revealed an equal proportional hypertrophy of both ventricles; the predominants increase of the left ventricle mass was found in 17.2% of the animals; no changes were found in 4.3%. The various adaptive rearrangements of the myocardium led to individual peculiarities of the cardiac rhythm regulation.

Adaptation, Physiological↗
PubMedDate not supplied

Structural features of saphenous vein and internal thoracic artery endothelium: correlates with susceptibility and resistance to graft atherosclerosis.

Examination of saphenous vein (SV) and internal thoracic artery (ITA) endothelium at the time of coronary bypass surgery has confirmed the known susceptibility of SV to endothelial cell loss during preparation for grafting. In contrast the ITA showed only minimal cell loss. An ultrastructural morphometric analysis of the abluminal surface of the endothelium of both vessels showed significant differences in the numbers and depth of penetration of cytoplasmic processes or folds. Whereas the SV, perfusion-fixed at 110 mmHg, possessed relatively few (15/100 micron) and shallow (less than 1 micron deep) processes the ITA had significantly more (27/100 micron) and deeper (18% greater than 1 micron) processes. The ITA endothelial cells were also smaller and thicker. We suggest that the differences in the numbers and depth of the processes, which are believed to play a role in endothelial attachment, may account for the differing susceptibility of the two vessels to endothelial damage during grafting. This in turn correlates with the known susceptibility of SV grafts and resistance of ITA grafts to atherosclerotic changes.

Adult↗
PubMed1988

Structural features of an antigen required for cellular interactions and for T cell activation in a MHC-restricted response.

The protein Ag, tobacco mosaic virus protein, (TMVP) and its tryptic peptide number 8 (residues 93-112 of the protein) exhibit cross-reactivity on the T cell level in some strains of mice (e.g., C3H.SW, C57BL/10); these strains are termed cross-reactive (CR). In other strains such as A/J or B10.BR, no cross-reactivity is exhibited; these strains are termed non-cross-reactive (NCR). Genetic experiments indicated that the cross-reactivity is dominant and that it is mapped to the I-A or I-E region of the MHC, with cross-reactivity exhibited by the I-Ab haplotype but not by I-Ak or I-Ek. Cell reconstitution experiments have indicated that the non-cross-reactivity is associated with the inability of the NCR APC to present Ag. Analysis of the area(s) on peptide 8 which serve(s) as epitope revealed that both strains recognize an overlapping area consisting of 11 amino acid residues in the middle of peptide 8 (residues 97-107), which by itself is nonstimulatory to TMVP- or peptide 8-immune T cells of the CR or the NCR strains. However, the addition of a few amino acid residues of the sequence of peptide 8 to this area converts it to a complete stimulatory epitope. Additivity experiments revealed that the CR strain contains two major T cell populations each recognizing this middle region of peptide 8 when elongated by a few amino acids N-terminally and C-terminally, respectively. In contrast, the NCR strain contains one major T cell population recognizing elongation only N-terminally. Because TMVP (but not peptide 8) requires processing before presentation to T cells, it is postulated that, during processing of TMVP, there occur alterations in the area of the proximal three or four N-terminal amino acids of the region consisting of peptide 8, destroying the only region containing the T cell epitope recognized by the NCR strain, hence TMVP and peptide 8 do not exhibit cross-reactivity in this strain. The same alterations of TMVP still leave intact an epitope consisting of amino acid residues C-terminal to the altered area which is recognized by the CR strain, hence the cross-reactivity exhibited by this strain. The results suggest that the difference in cross-reactivity on the T cell level between TMVP and peptide 8 exhibited by the strains may be due to differences in the orientation of presentation and the subsequent cell recognition of an epitope contained within peptide 8.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acid Sequence↗
PubMed1986

The characteristic structural features of the blood vessels of the Lewis lung carcinoma (a light microscopic and scanning electron microscopic study).

Vascular corrosion casts of Lewis lung carcinomas (LLC) grown subcutaneously in C57BL/6-mice are correlated with histological sections and with tumor tissue prepared for scanning electron microscopy (SEM). By making low, medium and high pressure cast preparations we studied the influence of perfusion and injection pressure on the resulting cast sample. Three types of vascular proliferations are distinguishable in LLC: Small globular outgrowths on sinusoidal dilated tumor capillaries, caused by proliferation of their endothelial cells. New sprouts on surrounding host vessels, invading the small, still avascular implant. Superficially located, centrifugally running sprouts in peripheral regions of large tumors. They invade the surrounding host tissue. Vascular sprouts are of venous origin, have a fragmentary endothelium and are rather "leaky" if casted. High pressure preparations of large tumors reveal central avascular cavities surrounded by centripetally running, compressed and blind ending tumor vessels. Irrespective of the applied injection pressure, the casts always exhibit extravasal channels caused by degeneration of the endothelium of central tumor vessels. We show that SEM of vascular corrosion casts combined with histology not only demonstrates such contrary processes as the development of tumor blood vessels and the simultaneously occurring vascular degeneration, but also elucidates all other morphological characteristics of the tumor vascular system.

Animals↗
PubMed1985

Structural features of 4-amino antifolates required for substrate activity with mammalian folylpolyglutamate synthetase.

The activity of a series of folic acid analogues as substrates for partially purified mouse liver folylpolyglutamate synthetase was determined and the effects of substituents on the binding to, and catalytic processes of, this enzyme were inferred. A 4-amino group improved substrate activity primarily by decreasing the apparent Km while N10-methyl substitution substantially diminished utilization as a substrate, again, by effects on Km. Isosteric replacement of N-10 altered substrate activity. A free alpha-carboxyl group in the amino acid side chain was required for catalysis as was the presence of the side chain amide carbonyl group. Modification of the amino acid side chain length profoundly affected activity. Several observations were made that may be relevant to chemotherapy with folate antimetabolites: 1) 7-hydroxymethotrexate was a substrate for this enzyme; 2) substrate activity and substrate inhibition were observed with CB 3717, a potent inhibitor of thymidylate synthase; 3) potent classical dihydrofolate reductase inhibitors were identified that were either not substrates for mouse liver folylpolyglutamate synthetase (e.g., 4-amino-4-deoxy-N10-methylpteroyl-L-alpha-aminoadipate) or were much better substrates than methotrexate for this enzyme (e.g., aminopterin); and 4) leucovorin and methotrexate appeared to be substrates for the same synthetase, but leucovorin saturated the reaction at much lower concentrations. These results have implications for the design of folylpolyglutamate synthetase inhibitors and for the selection of dihydrofolate reductase inhibitors that are either not polyglutamated or are efficiently polyglutamated in vivo.

Amines↗
PubMed1985

Structural features of endotoxin required for stimulation of endothelial cell tissue factor production; exposure of preformed tissue factor after oxidant-mediated endothelial cell injury.

Cultured human umbilical vein endothelial cells synthesize the procoagulant, tissue factor, after exposure to bacterial endotoxin. Wild-type lipopolysaccharide from Escherichia coli 0127:B8 stimulates a five- to 20-fold increase in cellular tissue factor. Similarly, rough or incomplete lipopolysaccharide subunits from mutant bacterial strains, or lipid A prepared by mild acid hydrolysis of whole endotoxin, are also stimulatory. In addition, a lipid A biosynthetic precursor, consisting of a phosphorylated glucosamine disaccharide substituted with four beta-hydroxymyristoyl residues, is stimulatory at nanomolar concentrations. Endothelial cell tissue factor is not detectable on the surface of undisrupted cells, but can activate clotting on the cell surface after oxidant-mediated cell injury. The procoagulant, tissue factor, is synthesized by endothelial cells after stimulation mediated by a moiety contained within the lipid A region of lipopolysaccharide. Exposure of clotting factors at the endothelial cell surface after cell injury suggests a mechanism for the microvascular thrombosis associated with disseminated intravascular coagulation with sepsis.

Cells, Cultured↗