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Biomedical subjects

F J Manasek

Publications and source records attributed to F J Manasek.

At least 37 records · Page 2Linked to original sources
PubMed1977

Anionic glycopeptides and glycosaminoglycans synthesized by embryonic neural tube and neural crest.

Anionic glycopeptides and glycosaminoglycans synthesized by embryonic neural tube (epithelium) and neural crest (mesenchymal outgrowth) developing in vitro were examined. The profile of surface glycopeptides is relatively simple (two major ones for neural crest; four major ones for neural tube). There is one major glycopeptide found in the medium which is present only in trace amounts on the cells. Both hyaluronate and chondroitin sulfate are synthesized. Hyaluronate is predominantly cell associated; chondroitin sulfate is found predominantly in the medium. It is suggested that independent sorting of these relatively few glycopeptides can result in qualitative surface differences. Morphological state (epithelial or mesenchymal) and differentiated state may be related to these differences as well as to quantitative differences in surface glycosaminoglycans.

Animals↗
PubMed1977

Direct effects of trypan blue on cardiac extracellular macromolecule synthesis.

The direct effects of the cardiac teratogen trypan blue on some parameters of embryonic chick heart metabolism were examined in vitro. Trypan blue inhibits chondroitin sulfate biosynthesis but stimulates incorporation of 3H-glucosamine into hyaluronate, heparin, and glycopeptides. 3H-fucose incorporation into glycoprotein is also stimulated. Total incorporation of 14C-labeled amino acids is elevated in the presence of trypan blue. Trypan blue does not cause qualitative changes in labeled end products; rather the metabolic alterations are quantitative. The possible exceptions are glucosamine-labeled glycoproteins since quantitative differences in glycopeptides could reflect qualitative differences in parent glycoproteins. These observations suggest that abnormal heart development, induced by trypan blue, may result from a multiplicity of metabolic alterations and not from any single chemical change.

Animals↗
PubMed1972

The sensitivity of developing cardiac myofibrils to cytochalasin-B (electron microscopy-polarized light-Z-bands-heartbeat).

Developing cardiac muscle cells of 11- to 13-somite chick embryos are sensitive to cytochalasin-B. In cultured chick embryos, ranging in development from 11 to 13 somites, hearts stop beating in the presence of this agent. Both polarized light and electron microscopic examination show that cytochalasin-B disrupts existing myofibrils and inhibits the formation of new ones. Discrete Z-bands are not present in treated heart cells and thick, presumably myosin, filaments are found in disarray. These effects are reversible; after cytochalasin-B is removed from the medium, heartbeat recovers and myofibrils with discrete Z-bands reappear. Fibrillar sensitivity appears to be a function of age since fibrils in hearts of embryos having from 22 to 28 pairs of somites are more resistant.

Animals↗
PubMed1971

Left ventricular performance and coronary flow after coronary embolization with plastic microspheres.

Coronary flow, left ventricular circumference, and left ventricular pressure were observed in the isovolumically contracting, isolated canine heart supported with arterial blood from a donor. Systolic pressure, heart rate, and coronary perfusion pressure were held constant while the coronary bed was progressively embolized with either large (average 865 mu) or small (average 10 mu) polystyrene microspheres. During embolization with large microspheres, coronary flow diminished progressively. After sufficient embolization, decreased ventricular performance was indicated by a rise in end-diastolic pressure. During embolization with small microspheres, coronary flow initially increased, which suggests the effective release of a vasodilator substance. Return of coronary flow to control levels occurred only after the end-diastolic pressure rose, on the average, to above 30 mm Hg. After embolization with both sizes of microspheres, ventricular diastolic pressure-volume relationships showed decreased ventricular compliance. This was attributed, in part, to edema of the ventricular wall and, in part, to focal shortening of the sarcomeres where the circulation was compromised. Embolization with both sizes of microspheres ultimately caused a decrease in ventricular performance, although when the systolic pressure was increased the usual relationship between peak developed wall stress, and end-diastolic pressure showed less of a descending limb than that found in the nonembolized, isolated heart. It is felt that the data summarized above have bearing on ventricular performance and coronary flow in clinical situations where hearts are perfused through pump oxygenator systems and are thereby subject to embolization from aggregated clumps of platelets and fibrin.

Animals↗