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Biomedical subjects

R J Rodriguez

Publications and source records attributed to R J Rodriguez.

52 records · Page 3Linked to original sources
PubMed1984

Microsurgical anatomy of the deep venous system of the brain.

The microsurgical anatomy of the deep venous system of the brain was examined in 20 cerebral hemispheres. The deep venous system is composed of the internal cerebral, basal, and great veins and their tributaries. This system drains the deep white and gray matter surrounding the lateral and 3rd ventricles and the basal cisterns. The deep veins are divided into a ventricular group composed of the veins converging on the walls of the lateral ventricles and a cisternal group that includes the veins draining the walls of the basal cisterns. The internal cerebral vein is included in the ventricular group because it is predominantly related to the ventricles, and the basal and great veins are reviewed with the cisternal group because they course through the basal cisterns. The choroidal veins are included with the ventricle veins because they arise on the choroid plexus in the ventricles. The thalamic veins appear in both the ventricular and the cisternal groups because some course on the ventricular surfaces and others course in the basal cisterns. The operative approaches to the major trunks in this system are reviewed.

Brain↗
PubMed1983

Structural and physiological features of sterols necessary to satisfy bulk membrane and sparking requirements in yeast sterol auxotrophs.

A variety of sterols and stanols have been analyzed for their ability to satisfy bulk membrane and high-specificity (sparking) functions in three yeast sterol auxotrophs. While many sterols and stanols satisfied bulk membrane requirements, only those possessing a C-5,6 unsaturation or capable of being desaturated at C-5 fulfilled the high-specificity sparking requirement. Unsaturation of the A-ring or beta-saturation of a C-5,6 double bond rendered both sterol and stanol unsuitable for either function. The C-28 methyl group of ergosterol, while not required for growth, allowed for greater ease of desaturation at C-5 in vivo. As a result some sterols and stanols lacking the C-28 methyl were incapable of satisfying the sparking requirement while identical compounds possessing the C-28 methyl were able to fulfill the sparking function(s). These data are extended to hypothesize a role for the C-28 methyl group of ergosterol in yeast.

Cholestanols↗
PubMed1983

Relationship between antifungal activity and inhibition of sterol biosynthesis in miconazole, clotrimazole, and 15-azasterol.

The availability of Saccharomyces cerevisiae mutants which are defective in sterol biosynthesis makes it possible to determine whether the ability of several antifungal agents to inhibit cell growth is due to their effect on sterol production. 15-Aza-24-methylene-8,14-cholestadien-3 beta-ol (15-azasterol) is known to block the reduction of the sterol delta 14 bond following C-14 demethylation. This agent inhibits the growth of wild-type S. cerevisiae but does not inhibit the growth of a strain that is defective in the removal of the C-14 methyl group of lanosterol and in the introduction of the 5,6 double bond. 15-Azasterol does not inhibit the growth of a sterol auxotrophic strain growing on an exogenous supply of sterol. Therefore, the effect of 15-azasterol on sterol biosynthesis is clearly the cause of its ability to inhibit growth. On the other hand, growth inhibition by two imidazole antifungal agents, clotrimazole and miconazole, cannot be ascribed to their ability to prevent the removal of the C-14 methyl group of lanosterol, because they inhibit the growth of the sterol auxotrophic strain as well as that of the demethylase mutant.

Antifungal Agents↗
PubMed1983

Requirement for a second sterol biosynthetic mutation for viability of a sterol C-14 demethylation defect in Saccharomyces cerevisiae.

Genetic analysis of a nystatin-resistant sterol mutant (strain JR4) of Saccharomyces cerevisiae defective in C-14 demethylation revealed the presence of a second mutation in 5,6-desaturation. It appeared from complementation tests that a defect in delta 5-desaturase enzyme activity was required for the viability of the C-14 demethylation mutant. Growth studies with a sterol auxotrophic strain indicated that the major sterol of strain JR4, 14 alpha-methyl-ergosta-8,24(28)-dien-3 beta-ol, could satisfy "bulk" membrane requirements but not the second, structurally specific, sterol function that we defined previously (Rodriguez et al., Biochem. Biophys. Res. Commun. 106:435-441, 1982). Leakiness in the sterol mutations in strain JR4 provided a small amount of ergosterol which could satisfy this second function.

Cytochrome P-450 Enzyme System↗
PubMed1981

Physiological response of Saccharomyces cerevisiae to 15-azasterol-mediated growth inhibition.

We studied 15-aza-24-methylene-8,14-cholestadiene-3 beta-ol (15-azasterol) inhibition of Saccharomyces cerevisiae growth. Exposure to sublethal concentrations of this drug caused S. cerevisiae cells to undergo a transient period of inhibition at midlog phase. During growth inhibition the turbidity of each culture remained constant, as did the total cell number. Although the proportion of viable cells in cultures decreased from 90 to 12% during inhibition, methylene blue staining showed that less than 40% of the cells underwent metabolic inactivation. We monitored adenosine triphosphate levels throughout the inhibition cycle, and these levels followed kinetics identical to cell growth kinetics. After overcoming inhibition, cellular lipid extracts revealed the presence of a modified form of 15-azasterol. It appeared that the yeast cells were able to overcome 15-azasterol inhibition by an inactivating transmethylation reaction involving S-adenosylmethionine.

Adenosine Triphosphate↗
PubMed1980

Growth and antifungal homoazasterol production in Geotrichum flavo-brunneum.

The growth cycle and production of 15-aza-24-methylene-8, 14-cholestadiene-3 beta-ol (15-azasterol) in Geotrichum flavo-brunneum strain NRRL28804 have been studied. During the growth cycle of this organism, morphological changes were noted which corresponded to changes in the pH of the culture medium. A physiological shift from acid to base production also occurred during the growth cycle. Concomitant with this physiological shift was the synthesis of 15-azasterol. Upon synthesis of this azasterol, variations in the sterol pool were observed. These variations are identical to sterol alterations in susceptible yeast cells exposed to this drug (P. R. Hays, W. D. Neal, and L. W. Parks, Antimicrob. Agents Chemother. 12: 185-191, 1977.) It appears that NRRL28804 avoids growth inhibition from 15-azasterol by confining its production to late in the growth cycle.

Antifungal Agents↗
PubMed1979

Receptor-mediated binding and internalization of leukocyte elastase by alveolar macrophages in vitro.

Radioiodinated leukocyte elastase was found to bind rapidly and specifically to alveolar macrophages in vitro. In contrast to the binding of pancreatic and bacterial proteases, leukocyte elastase binding did not require the presence of alpha 2 macroglobulin. The binding was inhibited by an excess of unlabeled enzyme and was saturable by increasing elastase concentrations. Leukocyte elastase binding thus met criteria for receptor-mediated binding, with and estimated association constant of 4.97 x 10(5) M-1 and an estimated total of 640 x 10(6) binding sites/cell. It differed from the previously described binding of lysosomal glycosidases to macrophages in that it was insensitive to trypsin pretreatment, did not require calcium ions, and was not inhibited by yeast mannan. High-resolution autoradiography indicated that the cell-associated radiolabeled leukocyte elastase was rapidly incorporated into phagolysosomes. Macrophage binding may have a role in clearance of leukocyte elastase from tissue sites where alpha 2 macroglobulin is absent or present in low concentration. Thus, enzyme uptake by alveolar macrophages may be an important factor in the amelioration of lung tissue injury by extracellular leukocyte elastase.

Autoradiography↗
PubMed1977

Directional coronary collateral growth with chronic circumflex occlusion in the dog.

The object of this study was to determine whether coronary collateral resistances were dependent on the direction of perfusion and to investigate whether a pattern of collateral growth with gradual circumflex occlusion could be discerned. In 12 dogs an Ameroid occluder was placed on the circumflex for 1 month, and six dogs for 3 months; 12 dogs served as controls. The circumflex, left anterior descending, and right coronary arteries were separately but simultaneously perfused in an isolated heart preparation in which the vasculature was maximally dilated with dipyridamole. Collateral flows were determined by measuring retrograde flows for two vessels simultaneously. The results showed that collateral flows from the right to the left coronaries in control dogs were 3.5-fold larger than when these collateral beds were perfused in the opposite direction. This difference in the 1- and 3-month Ameroid groups was approximately 20-fold. Relative to the control group, the collateral resistances from right to left coronary vessels were an average of 10-fold less in the 1- and 3-month groups, but there was no significant differences in resistance in the collaterals perfused from the left to the right. The results strongly suggest that collateral proliferation occurs in response to hypoxia rather than to a pressure gradient, and that collateral development is toward the hypoxid area.

Animals↗
PubMed1976

Changes in coronary and collateral flows and adequacy of perfusion in the dog following one and three months of circumflex occlusion.

We investigated changes in circumflex, left anterior descending (LAD), and right coronary artery flows as well as changes in collateral flows to these vessels after long-term circumflex occlusion. Coronary and collateral flows of each vessel were determined simultaneously in an isolated heart preparation in which the vasculature was maximally dilated with dipyridamole. The resistances as related to total heart weight of the circumflex, LAD, and right coronary arteries of 16 control dogs were found to be 0.59 +/- 0.06, 0.93 +/- 0.09, and 2.37 +/- 0.17 (mean +/- SEM) mm Hg/[(ml/min)/100 g], respectively. Total minimal coronary resistance was 0.21 +/- 0.01. In 10 dogs subjected to occlusion for 1 month no significant change in circumflex coronary resistance was observed, but the resistance of the unimpaired vessels decreased significantly. The resistances of the LAD and right coronary arteries were 0.66 +/-0.04 and 1.72 +/- 0.13, respectively. Both values were considerably less (P less than 0.01) than control. In nine dogs subjected to occlusion for 3 months the resistance of the unimpaired LAD and right arteries, as well as the circumflex coronary resitance, were not significantly different from control. We also found that retrograde flows for all vessels increased 7-fold after 1 month and 10.5-fold (relative to control) after 3 months of occlusion. From these data we conclude that vascular adaptations, which occurred in response to an ischemic stimulus, are responsible for the long-term regulation of the metabolic needs of the myocardium.

Animals↗