PubMed Health⌕ Search

Biomedical subjects

L Terracio

Publications and source records attributed to L Terracio.

83 records · Page 5Linked to original sources
PubMed1980

Human diploid fibroblast-like cells (CF-3) as a model system for the study of Golgi biogenesis.

Human diploid fibroblast-like cells were maintained in an arrested, essentially non-mitotic state for extended periods of time in culture by lowering the serum concentration in the medium from 10 to 0.5%. These arrested cells re-entered the proliferative state when subcultivated in medium containing 10% serum. The morphological distribution and enzyme activities associated with the Golgi complex were examined during growth, arrest, and recovery. Cells grown in medium containing 10% serum possessed a well-developed Golgi complex consisting of parallel arrays of membranes and associated vesicles. Galactosyl transferase activity was highest after 3 days growth (17.5 +/- 5.0 nmol galactose transferred/45 min/mg protein) and declined to 9.8 +/- 3.0 at day 7. When the serum concentration was reduced to 0.5%, Golgi complexes were rarely observed by electron microscopy and galactosyl transferase activity was further reduced into medium containing 10% serum recovered from the arrested state and ultrastructurally resembled cells continuously cultured at the higher serum level. Numerous Golgi complexes reappeared and galactosyl transferase activity increased to 13.0 +/- 3.34 days after subcultivation. These results indicate that the Golgi complex can be experimentally manipulated in human diploid fibroblast-like cells in a manner which may be useful for the study of the biogenesis of this organelle.

Cell Cycle↗
PubMed1979

Increased coronary collateral blood flow. A possible mechanism of action for betahistine-HCl.

beta-Histine-HCl has been shown to be effective in modifying the size of developing myocardial infarcts. In the present study the hypothesis that beta-histine increases the flow of blood through collateral channels and thus supplies blood to ligated areas of the myocardium was investigated in the dog. The methods used were measurement of retrograde coronary blood flow and angiography after coronary artery ligation. beta-Histine administration for 6 h increased retrograde blood flow 68.2--91.0% over controls. Coronary angiography demonstrated the existence of collateral channels 200--400 micrometer in diameter within the myocardium after ligation and 4 h of beta-histine administration.

Angiography↗
PubMed1978

Modification of the size of developing infarcts in the ligated dog heart by betahistine-HCL.

The effectiveness of beta-histine-HCL in modifying the size of developing myocardial infarcts was tested in the surgically ligated dog. Branches of the left coronary artery were ligated and a 6-hour continuous intravenous infusion of 0.24 mg/kg/min of beta-histine was administered from 0 to 120 min after ligation. The effect of this treatment was evaluated histologically in studies on acute ischemia by the use of the hematoxylin-basic fuchsin-picric acid stain for early myocardial ischemia. The treatment was also evaluated grossly in a study on chronic ischemia where the dogs were permitted to survive for 30 days before sacrifice. In these experiments the size of infarcts found in the beta-histine-treated animals was compared with those found in the saline controls. Both studies showed that the control ligations produced a large uniform area of ischemia or infarction that was greatly reduced or prevented by immediate treatment with beta-histine. Also, beta-histine was capable of significantly reducing the size of developing infarcts for up to 120 min after ligation.

Animals↗
PubMed1977

Preparation of biological tissues for electron microscopy by freeze-drying.

A dependable method for freeze-drying tissues for electron microscopy has been developed. Thin slices of fresh tissue were frozen by bringing them into direct contact with a polished copper bar at liquid nitrogen temperature. The tissue was transferred to a copper specimen block equipped with a thermocouple and heating circuit for accurate control of the environmental temperature of the tissue, and evacuated in a glass freeze-drier using clean high vacuum techniques for keeping the system free of hydrocarbons. The tissue was dried by increasing the temperature of the specimen block 10 degrees C each hour while monitoring the rate of water removal from the tissue with a partial pressure analyzer. The dry tissue was fixed with OsO4 vapor, vacuum embedded in a low viscosity epoxy resin, sectioned, stained, and viewed with the electron microscope. Tissue processed in this manner exhibits excellent morphological preservation at both cellular and organellar levels without prefixation or the use of cryoprotective agents. The results of the experiments using the partial pressure analyzer indicate that small blocks of tissue can be dried in a short time at low temperature.

Animals↗
PubMedDate not supplied

Altered expression of tropomodulin in cardiomyocytes disrupts the sarcomeric structure of myofibrils.

Tropomodulin is a tropomyosin-binding protein that terminates "pointed-end" actin filament polymerization. To test the hypothesis that regulation of tropomodulin:actin filament stoichiometry is critical for maintenance of actin filament length, tropomodulin levels were altered in cells by infection with recombinant adenoviral expression vectors, which produce either sense or antisense tropomodulin mRNA. Neonatal rat cardiomyocytes were infected, and sarcomeric actin filament organization was examined. Confocal microscopy indicated that overexpression of tropomodulin protein shortened actin filaments and caused myofibril degeneration. In contrast, decreased tropomodulin content resulted in the formation of abnormally long actin filament bundles. Despite changes in myofibril structure caused by altered tropomodulin expression, total protein turnover of the cardiomyocytes was unaffected. Biochemical analyses of infected cardiomyocytes indicated that changes in actin distribution, rather than altered actin content, accounted for myofibril reorganization. Ultrastructural analysis showed thin-filament disarray and revealed the presence of leptomeres after tropomodulin overexpression. Tropomodulin-mediated effects constitute a novel mechanism to control actin filaments, and our findings demonstrate that regulated tropomodulin expression is necessary to maintain stabilized actin filament structures in cardiac muscle cells.

Actins↗