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G J Raugi

Publications and source records attributed to G J Raugi.

10 recordsLinked to original sources
PubMed1992

Dermatologic features of the superior vena cava syndrome.

BACKGROUND: The superior vena cava syndrome occurs when extrinsic compression or intraluminal occlusion impedes blood flow through this vessel. The most common underlying cause is a malignant neoplasm, especially a bronchogenic carcinoma. This article describes the cutaneous findings of this disorder. OBSERVATIONS: Among the earliest and most prominent features are numerous, dilated, vertically oriented, and tortuous cutaneous venules or veins above the rib cage margin. Recognition of this cutaneous sign allowed us to make a diagnosis of lung cancer in several patients. Other features include upper body edema and ruddiness or cyanosis, distended neck veins, proptosis, and conjunctival suffusion. CONCLUSIONS: Detecting the characteristic cutaneous features can lead to an early diagnosis of the superior vena cava syndrome. These skin changes usually represent indirect dermatologic signs of an underlying malignant neoplasm; for most patients, this syndrome is the initial manifestation of their cancer. The most common cause is a bronchogenic carcinoma, especially the small-cell variety, but others include lymphomas, primary mediastinal tumors, and metastases to the mediastinal lymph nodes from extrathoracic primary tumors, especially breast cancer. Treatment of the underlying malignant neoplasm and relief of the obstruction produce prompt improvement in the dermatologic findings.

Adult↗
PubMed1990

Thrombospondin deposition in rat carotid artery injury.

The balloon catheter injury model was used to determine the relative contributions of vascular smooth muscle cells (SMC) and platelets to thrombospondin (TSP) antigen deposition in the artery wall. Rat carotid arteries were denuded of endothelium, exposing the thrombogenic subendothelial extracellular matrix (ECM) to the circulation. Rats were killed after 1 hour, or 5, 10, or 20 days. Thrombospondin antigen deposition in the injured arteries was assessed using a specific polyclonal antiserum raised in rabbit against rat platelet TSP and a sensitive silver-enhanced immunogold staining method. Faint immunostaining for TSP antigen was detected, associated mostly with cells, in the media of the carotid artery of the nonoperated controls. One hour after balloon catheter injury, however, prominent cell-associated immunostaining was evident in the media; extracellular matrix staining was negligible. At this time, large foci of immunostaining were present on the lumenal surface of the vessel. Intimal proliferation was evident on most stained sections of tissue taken 5 days after balloon injury. Thrombospondin antigen immunostaining was markedly increased compared to nonoperated controls in all sections, regardless of the degree of intimal thickening. Thrombospondin immunostaining remained associated with cells in the neointima and media; extracellular matrix staining remained negligible. Ten days after endothelial injury, immunostaining for TSP antigen was detected in all layers of the artery, but was greater in the neointima and media. Reaction product was still associated only with cells. Thrombospondin antigen levels, as detected by this procedure, remained high in the injured tissue through 10 days of observation but appeared less prominent 20 days after injury. At this time extracellular matrix staining was obvious and cell-associated staining was reduced. These data support the hypotheses that thrombospondin (TSP) expression by vascular smooth muscle cells is an early response to injury and that the primary source of TSP antigen in injured artery is the vascular smooth muscle cells (SMC). These results support data derived from in vitro studies of TSP secretion.

Animals↗
PubMed1979

Photoallergic contact dermatitis to men's perfumes.

Three patients with photosensitive eruptions related to the use of different men's perfumes were evaluated. We found that they were photoallergic to musk ambrette, an inexpensive, readily available synthetic perfume ingredient. Studies of cross-reactivity with other perfumed colognes and after-shave lotions suggest that musk ambrette is present in clinically significant concentration in large numbers of other cosmetic products.

Allergens↗
PubMed1979

Necrotizing sialometaplasia. A condition simulating malignancy.

Necrotizing sialometaplasia occurred in a 55-year-old woman. The ulcerated lesion on the hard palate was treated conservatively and resolved spontaneously in about three months. The histology of the lesion consisted of coagulative necrosis of the salivary gland lobules and prominent squamous metaplasia within adjacent viable lobules. Since this benign lesion has frequently been mistaken for mucoepidermoid carcinoma or squamous cell carcinoma, recognition of it may spare the patient a radical surgical procedure.

Carcinoma, Squamous Cell↗
PubMed1976

Inhibition of P-enolpyruvate carboxykinase and of glyconeogenesis in Tetrahymena by 3-mercaptopicolinic acid.

Tetrahymena grown overnight in deep cultures were incubated for 1 hr with [1-14C]labeled substrates in the presence or absence of 3-mercaptopicolinic acid (3MPA). 3-MPA inhibited appearance of label in glycogen from bicarbonate, acetate, pentanoate, octanoate, and succinate, but not from glycerol or glucose. In vitro assays of phosphoenolpyruvate carboxylase and phosphoenolpyruvate carboxykinase activity showed that both enzymes were about equally distributed between the particulate and cytosol fractions. 3-MPA inhibited phosphoenolpyruvate carboxykinase from both the cytoplasmic and particulate fractions, but had no effect on phosphoenolpyruvate carboxylase from either location. These results suggest that the in vivo effects of this drug are due to inhibition of glyconeogenesis at this site.

Acetates↗
PubMed1976

Effect of 4-pentenoic acid on intermediate metabolism of Tetrahymena.

The growth of Tetrahymena pyriformis strain HSM was strongly inhibited by 4-pentenoic acid. Supplementing the medium acetate reversed the growth inhibition, but pyruvate was ineffective. Glycogen content was much lower in cells grown with 4-pentenoic acid than in controls; this effect was not reversed by acetate or by pyruvate. There was little effect of 4-penteonic acid on the in incorporation of label from [1-14C]acetate, [2-14C]glycerol, [1-14C]ribose, [U-14C]fructose, or [1-14C]glucose into CO2 but incorporation of label into glycogen was inhibited, the strongest inhibition being on acetate and the weakest approximately 20%) on ribose, fructose, and glucose. A 3-compartment model for quantitation of labeled acetyl CoA fluxes was shown to be applicable to Tetrahymena grown in the presence of 4-pentenoic acid, and experiments were performed to establish the flux of [1-14C]acetyl CoA into glycogen, lipids, CO2, glutamate, and alanine. It was evident from the results of these experiments that 4-pentenoic acid did not appreciably inhibit beta-oxidation or lipogenesis, but markedly decreased the glyconeogenic flux of labeled acetyl-CoA from the peroxismal and outer mitochondrial compartments.

Acetates↗
PubMed1975

A quantitative analysis of metabolite fluxes along some of the pathways of intermediary metabolism in Tetrahymena pyriformis.

A detailed model of intermediary metabolism has been constructed which is consistent with all known information on the compartmental structure of metabolism in Tetrahymena, on the enzyme complement of this cell, and on the localization of the enzymes. The model allows computation of the specific activity of every carbon atom of all metabolites and thus of the flux of carbon along the major pathways of metabolism under steady state conditions. To test the model, data were required from cells grown under standard conditions and then suspended in a dilute salt solution and incubated for 1 hour in a mixture of acetate, pyruvate, hexanoate, bicarbonate, and glutamate labeled in a total of 10 positions, but with only one substrate labeled in any given flask. Twenty-seven measurements of label incorporation into CO2, lipids, glycogen, glutamate, and alanine were made, plus measurements of label distribution into fatty acid and glycerol moieties for 4 of the substrates and of oxygen consumption and of glycogenolysis, yielding 33 independent measurements. These, plus about 18 "limit" measurements which also constrain any possible solutions, were in sufficient excess of the 23 independent parameters to permit a stringent assessment of the model. Equations derived directly from the structure of the model and from the known stereochemistry of the reactions were programmed on a PDP-15 computer and values of the Qo2 and of label expected to be incorporated into the various products actually measured were computed for any given set of flux rates. A set of flux rates was found which yielded an excellent fit to the observed data. The ability to achieve a fit to the data for an overdetermined system constitutes strong support for this structural model of intermediary metabolism and the computed flux rates therefore provide a quantitative description of metabolite flow in the intact cell. Despite the redundancy of measurements relative to parameters to be determined, it was not possible to define a unique set of values for the flux through phosphoenolpyruvate carboxylase and phosphoenolpyruvate carboxykinase, although the relationship between these fluxes is specified by the model. The analysis allows estimation of the recycling of phosphoenopyruvate through pyruvate kinase under conditions of net glyconeogenesis and an apparently futile exchange of acetyl-CoA between the inner and outer mitochondrial compartments. Carbon flow through the glyoxylate bypass under these conditions is about one-third of that through the Krebs cycle. The analysis also shows a net transport of malate from the peroxisomes to the mitochondria, consistent with the anaplerotic role of the peroxisomal glyoxylate bypass in Tetrahymena.

Acetates↗
PubMed1975

Effects of pentanoic acid and 4-pentenoic acid on the intracellular fluxes of acetyl coenzyme A in Tetrahymena.

Cultures of Tetrahymena pyriformis were incubated for 1 hour with a mixture of acetate, pyruvate, and pentanoate with only one substrate labeled at a time and with the position of the label chosen so that [1-14-C]acetyl coenzyme A was an early product of the metabolism of each substrate. The appearance of label in CO2, lipids, glycogen, glutamate, and alanine were measured and results interpreted in terms of a previously developed three-compartment model of metabolism, which was found to quantitatively describe the data even when two of the flux rates (the flux of acetyl-CoA from the peroxisomal to the outer mitochondrial compartment and from the outer mitrochondrial to the inner mitochondrial compartment) were set equal to zero. This reduction in the number of independent parameters leads to the model being overdetermined and to a probably unique fit of the three-compartment model tof the present data and to previous data when octanoate was the fatty acid substrate. Pentanoate was metabolized to a greater extent than octanoate and did not inhibit growth. Pentanoate inhibited acetate utilization in both the inner mitochondrial and peroxisomal compartments as indicated by a reduction in the incorporation of label from [1-14-C]acetate into lipids and into CO2, but there was no difference in oxidation of [2-14-C]pyruvate when pentanoate was the fatty acid substrate as compared to octanoate. Glyconeogenesis was inhibited when pentanoate was substituted for octanoate. Similar experiments were performed on cells treated with 4-pentenoic acid. The effects of 4-pentenoic acid were essentially the same whether octanoate or pentanoate was the fatty acid substrate, i.e. inhibition of glyconeogenesis from all labeled substrates and inhibition of [2-14-C]pyruvate oxidation. The results indicate that the effects of pentanoate are largely confined to the peroxisomal and the inner mitochondrial compartments whereas the effects of 4-pentenoic acid are confined to the peroxisomal and outer mitochondrial compartments.

Acetates↗
PubMed1975

Effect of oxygen on the regulation of intermediate metabolism in Tetrahymena.

Tetrahymena grown in poorly aerated cultures have a greater capacity to utilize oxygen than cells grown in relatively well aerated cultures. Paradoxically, the oxidation of (1-14C)-glucose was inhibited, while oxidation of (2-14C)pyruvate and (2-14C)glyoxylate was enhanced in cells grown under relatively anaerobic conditions. Total glycogen content measured after 17 hours of growth was increased 30 to 60% in cells grown partially anaerobically. In 1-hour incubations at the end of this time, the capacity to incorporate label into glycogen from (1-14C)pyruvate and (2-14C)glyoxylate was increased several fold. The ratio of adenosine di- and triphosphates was nearly identical in the cells grown under different conditions of oxygenation, indicating that this ratio may not play a major role in regulating these changes. After 17 hours of growth in cultures of different depths, cells were also incubated with a mixture of acetate, pyruvate, and octanoate, with one substrate labeled at a time in such a way that (1-14C)-acetyl-CoA is generated at the initial step in the metabolism of each. These results were interpreted in terms of a previously developed three-compartment model of acetyl-CoA metabolism. Glyconeogenesis from peroxisomal and mitochondrial precursors was increased in cells grown in low oxygen tension, with the greater contribution coming from the peroxisomes. Oxidation of acetate and pyruvate was increased under these conditions, but appearance of (1-14C)-acetate label in glutamate was decreased. Lipogenesis from labeled peroxisomal precursors was also increased in cells grown under relatively low oxygen tension. After a shift down in O2 tension there is a rapid rise in glyconeogenesis from the peroxisomes which levels off after about 4 hours, whereas the rate of oxidation in the Krebs cycle increases steadily for at least 8 hours following the transition to relatively anaerobic conditions. In response to a shift up in O2 tension there is a decline in peroxisomal glyconeogenesis which continues for 8 hours, whereas the rate of oxidation in the Krebs cycle does not begin decreasing until about 4 hours after the increase in O2 tension. Thus the flux of (1-14C)acetyl-CoA changes according to a different temporal pattern in mitochondria as compared to peroxisomes, and in each compartment the sequence of changes in response to a shift up in O2 tension is not the mirror image of the sequence in response to a shift down.

Acetyl Coenzyme A↗