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Biomedical subjects

S R Bates

Publications and source records attributed to S R Bates.

At least 37 records · Page 2Linked to original sources
PubMed1989

Convulsions in children undergoing renal transplantation.

We reviewed the records of 154 children who received 207 renal transplants for end-stage renal disease from 1965 to 1987, and discovered that 48 (31%) had had convulsive seizures, some before transplant surgery, others only after transplant, and some during both before and after transplantation. The majority of children had minimal long-term problems, and 60% of the children had only a single convulsion. In six of the patients, convulsions were a manifestation of more serious underlying conditions that produced significant morbidity. Seizures of differing clinical type occurred, with hypertension being the most significant etiologic factor. In children with renal failure, there are minimal symptoms heralding the hypertensive encephalopathy. Rapid resolution without recurrence of seizures after control of hypertension is a major sign that hypertension was the cause and that the long-term prognosis is good.

Child↗
PubMed1989

Phospholipids co-isolated with rat surfactant protein C account for the apparent protein-enhanced uptake of liposomes into lung granular pneumocytes.

Phosphatidylethanolamine (PE) and phosphatidylglycerol (PG) were co-isolated with the low molecular weight rat surfactant-associated protein C (SP-C) of Mr approximately equal to 6,000. The contribution of these phospholipids to the incorporation of 3H-labeled phosphatidylcholine (PC) liposomes into rat alveolar type II cells stimulated by SP-C was examined. PG showed a concentration-dependent enhancement in the uptake of PC liposomes by the pneumocytes. PE alone had no effect but could inhibit the incorporation of liposomal PC stimulated by PG depending on the concentration of PG and the PG to PE ratio. SP-C augmented the cellular uptake of the PC liposomes only when the SP-C preparation had a protein to phospholipid ratio greater than 1 and a PG to PE ratio greater than 2. The results with the isolated SP-C could be reproduced using mixtures of PG and PE which reflected the phospholipid composition of the SP-C in the absence of SP-C protein. Thus, the ability of SP-C to stimulate liposomal PC uptake by rat type II cells could be accounted for by its phospholipid composition.

Amino Acids↗
PubMed1988

Comparison of fatty acid and triacylglycerol metabolism of macrophages and smooth muscle cells.

The response of macrophages and smooth muscle cells to culture in free fatty acid has been compared. Because oleate and linoleate promoted triacylglycerol enrichment of smooth muscle cells, whereas palmitate had little effect, oleate was used for these studies. The kinetics of the accumulation of triacylglycerol produced by oleate was comparable between smooth muscle cells and macrophages. When grown in increasing concentrations of oleic acid at various fatty acid to albumin molar ratios, the extent of triacylglycerol accumulation in both cell types was dependent on the concentration of oleate, the concentration of albumin, and the oleate to albumin molar ratio. However, macrophages contained 2.6-fold more triacylglycerol than smooth muscle cells in the presence of oleate at 0.36 mM or greater and at levels of albumin higher than 0.15 mM. The cellular triacylglycerol content of macrophages was linearly related to the oleate to albumin molar ratio at both a constant albumin concentration and a constant oleate concentration, whereas the accumulation of triacylglycerol in smooth muscle cells showed a curvilinear relationship. When cells were preloaded with triacylglycerol, smooth muscle cells showed a greater loss of lipid when exposed to albumin than macrophages did. Over a two-hr time period, macrophages incorporated twice as much labeled fatty acid as smooth muscle cells. Thus, while smooth muscle cells and macrophages showed similar responses to exogenous fatty acid and albumin, there were also significant quantitative distinctions.

Animals↗
PubMed1988

Atherosclerosis and apoprotein E. An enigmatic relationship.

In this article, we consider the role of apoprotein E in lipoprotein metabolism and especially in the metabolism of potentially atherogenic lipoproteins. Particular consideration has been given to three features of apoprotein E involvement in lipid cell interactions. Evidence implicating free cholesterol as a mediator of apoprotein E biosynthesis in cholesterol-loaded macrophages is presented. Experiments pointing to apoprotein E as the ligand promoting the interaction of beta-very-low-density lipoprotein (beta-VLDL) with macrophages are summarized. Finally, we describe the influence of fat and cholesterol fed to rhesus monkeys and baboons on the generation of hepatogenous (from isolated liver perfusates) VLDL enriched in cholesterol ester and apoprotein E. These hepatic VLDLs, none of which exhibits beta-electrophoretic mobility, promote cholesterol esterification in macrophages in proportion to their apoprotein E content. The complex role of apoprotein E in the genesis and reversal of atherosclerosis is briefly discussed.

Animals↗
PubMed1988

Hepatic perfusate very low density lipoproteins obtained from fat-fed nonhuman primates stimulate cholesterol esterification in macrophages.

The livers of both baboons and rhesus monkeys fed a high fat, high cholesterol diet secreted very low density lipoproteins (VLDL) that were enriched in cholesteryl ester and apoe as compared to VLDL secreted by the livers of chow-fed animals. Stimulation of macrophage cholesterol esterification by the experimental VLDL was compared to that produced by the standard beta-VLDL obtained from the plasma of a rhesus monkey fed 25% coconut oil plus 2% cholesterol. This standard beta-VLDL stimulated 7- to 10-fold more esterification than did the bovine albumin control. Hepatic VLDL from fat-fed animals stimulated esterification in J774 macrophages 50 to 150% as well as did the standard beta-VLDL, even though hepatic VLDL did not display beta electrophoretic mobility on agarose gel electrophoresis. Plasma VLDL from lard-fed baboons did not exhibit beta electrophoretic mobility but did stimulate esterification in macrophages. Baboons were divided into high and low responders based on the change in plasma cholesterol levels in response to a high fat, high cholesterol diet. Both plasma and hepatic VLDL from high responders stimulated cholesterol esterification, whereas hepatic VLDL obtained from low responders or chow-fed baboons did not stimulate cholesterol esterification in macrophages. There was a strong positive correlation (r = 0.866) between the number of apoE molecules per VLDL particle in VLDL obtained from chow-fed, lard-fed, or coconut oil-fed primates and the rate of cholesterol esterification in macrophages. Our results show that hepatic perfusate VLDL obtained from fat- and cholesterol-fed primates have compositional and functional properties usually ascribed to circulating beta-VLDL, without displaying beta mobility, and indicate that the liver may be an important source of atherogenic lipoproteins.

Animals↗
PubMed1987

EEG monitoring during paroxysmal hyperpnea of tetralogy of Fallot: an epileptic or hypoxic phenomenon?

We describe a neurologically compromised infant with tetralogy of Fallot who was having multiple paroxysmal episodes of hypotonia, eye rolling, stiffening, and loss of consciousness. Simultaneous electroencephalography with video monitoring was used to determine if these episodes were a primary epileptic phenomenon or the result of hypoxic central nervous system involvement from paroxysms of hyperpnea and cyanosis. The findings would suggest that the paroxysmal episodes were not primarily epileptic. The electroencephalographic findings during the spell were similar to those found with hypoxia due to other causes. This may have physiological and therapeutic significance and be useful in following other infants with congenital heart disease who have similar episodes, especially when the infants have significant risk factors for seizures.

Diagnosis, Differential↗
PubMed1987

Cyclic AMP inhibits increased collagen production by cyclically stretched smooth muscle cells.

Rabbit arterial smooth muscle cells, grown on elastin membranes which were cyclically elongated and relaxed, responded by increasing their rates of synthesis of protein and, in particular, of collagen, compared to stationary controls. Raising intracellular cyclic AMP (cAMP) levels by adding theophylline or dibutyryl cAMP to the culture medium prevented the synthetic response to cyclic stretching, but did not alter the rates of protein or collagen synthesis by stationary controls. Both synthesis and degradation of collagen by cyclically stretched cells increased in parallel such that the proportion of synthesized collagen that was degraded was similar to that found in the stationary cultures. Collagen degradation was not affected by theophylline administration to stationary cell cultures but the drug increased degradation of collagen by cyclically stretched cells. We conclude that the net production of protein, and in particular of a structural protein, collagen, by arterial smooth muscle cells subjected to the mechanical force of stretching was inhibited when intracellular levels of cAMP were raised. The results suggest that cAMP may play a role in the modulation of structural protein content of artery walls in response to changes in tensile stress.

Animals↗
PubMed1987

Apoprotein E mediates the interaction of beta-VLDL with macrophages.

beta-Very low density lipoproteins (beta-VLDL) isolated from cholesterol-fed rhesus monkeys stimulated cholesteryl ester synthesis and accumulation in mouse peritoneal macrophages. The apoprotein specificity and requirement for the cell surface uptake of beta-VLDL was investigated by treating the beta-VLDL with trypsin (beta-VLDL (T], incubating the beta-VLDL (T) with other lipoproteins or apoproteins, reisolating the beta-VLDL (T) and measuring its biological activity which, for this study, is defined as the ability of the lipoprotein to stimulate cholesterol esterification in the macrophages. Trypsin treatment of beta-VLDL abolished its biological activity. Apoprotein analysis of the beta-VLDL (T) demonstrated the absence of intact apoproteins B-100, B-48, and E. The J774 macrophage-like cell line and mouse peritoneal macrophages responded similarly with respect to cholesterol esterification following incubation with inactive and treated beta-VLDL. The J774 macrophage-like cell line was used to establish the conditions necessary for the restoration of biologic activity to the trypsinized beta-VLDL. The loss of biological activity of beta-VLDL (T) could be reversed by restoring apoprotein E-containing LDL from hyperlipemic monkeys or purified apoprotein E. Apoprotein A-I had no such effect. The restored biological activity of the beta-VLDL (T) was proportional to the amount of apoprotein E acquired by the lipoprotein. beta-VLDL particles composed of apoprotein E and either intact or degraded apoprotein B-100 had comparable biological activity. Thus, intact apoprotein E, without intact apoprotein B, is a sufficient mediator for the biological activity and metabolism of beta-VLDL by macrophages and plays a major role in receptor-lipoprotein interaction.

Animals↗
PubMed1986

Paucifascicular congenital sensory neuropathy in identical twins.

A male infant had sensory and autonomic dysfunction, and his identical twin had a similar clinical finding. One twin was extensively studied, utilizing sural nerve, skin, and conjunctival biopsy specimens, to evaluate the status of peripheral sensory axons. The results support an antenatal neurodevelopmental disturbance in axonal growth that affects sensory neurons and limits their distal extension. Neuropathologic studies of this patient closely resemble findings in hereditary sensory neuropathy type II; clinically, however, this patient resembles patients with congenital autonomic dysfunction and universal pain loss. Investigation of proximal and distal sural nerve, skin, and/or conjunctival biopsy specimens is recommended in patients with sensory and autonomic dysfunction to help differentiate these patients to assist in genetic counselling, treatment, and prognosis. It is possible that clinical overlap in such patients may result from a common neuropathic process, but with varying degrees of involvement.

Conjunctiva↗
PubMed1986

Migraine in children: association with primary and familial dyslipoproteinemias.

We studied lipids and lipoprotein cholesterols in 39 children (26 boys, 13 girls) with severe migraine, to examine the hypothesis that primary and familial lipoprotein abnormalities might be associated with or predispose children to the migraine syndrome. Each of the children, 4 to 20 years of age, had severe migraine, leading to pediatric neurologic referral and therapy. Twenty-five of the 39 probands (64%) had a first degree relative with severe migraine, and 18% had a second degree relative with severe migraine. In 11 of the 39 kindreds (28%), there was a family history of premature myocardial infarction and/or cerebral vascular accident (less than age 55 years), involving one grandparent from each of ten kindreds and one parent in the 11th kindred. In nine of the 26 boys, low-density lipoprotein cholesterol (LDL-C) levels were greater than or equal to the age-, sex-, race-specific 90th percentile, and in three of these nine children, there was at least one additional first degree relative also having a primary top decile LDL-C level, consistent with the presumptive diagnosis of familial hypercholesterolemia. The finding of more than three times as many boys with migraine headache having top decile LDL-C than expected (9 v 2.6) was significant (chi 2 = 17.5, P less than .01). Also, there were six boys having bottom decile levels of high-density lipoprotein cholesterol (HDL-C); all six came from kindreds with at least one first degree relative also having bottom decile HDL-C.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

Macrophage interaction with very-low-density lipoproteins results in triacylglycerol-enriched smooth muscle cells.

Macrophage-conditioned medium containing very-low-density lipoproteins (VLDL) and its effects on smooth muscle cell triacylglycerol metabolism was investigated. Macrophages exposed to VLDL from normolipemic rats accumulated high levels of intracellular triacylglycerol, while similarly treated smooth muscle cells showed only slight changes. Medium, initially composed of VLDL and albumin, contained substantial levels of free fatty acids after exposure to macrophages. In the presence of albumin, the loss of VLDL triacylglycerol from the medium and the appearance of medium free fatty acids was consistent with a precursor-product relationship. The extent of medium fatty acid accumulation was dependent on the length of time of incubation with macrophages and was proportional to the concentration of VLDL and albumin added to the culture dish. This macrophage-conditioned medium, when given to smooth muscle cells, promoted a 6-12-fold increase in smooth muscle cell triacylglycerol levels over that produced by fresh VLDL and albumin. Similar increases in cell triacylglycerol levels could be produced using fresh medium approximating the oleate concentration and the fatty acid to albumin molar ratios found in macrophage-conditioned medium. In macrophage-conditioned medium with VLDL but without albumin, little free fatty acid was found. Other factors produced by macrophages did not seem to affect the metabolism of VLDL by smooth muscle cells since, in the absence of albumin, media with VLDL caused comparable responses in smooth muscle cell triacylglycerol accumulation whether or not the medium was previously exposed to macrophages. Thus, the minor changes in triacylglycerol content in smooth muscle cells promoted by medium containing VLDL and albumin were substantially enhanced by a prior exposure of the medium to macrophages, primarily due to the free fatty acids present in the macrophage-conditioned medium.

Animals↗
PubMed1983

Prevention of the hyperlipidemic serum or LDL-induced cellular cholesterol ester accumulation by 22-hydroxycholesterol and its analogue.

Incubation of monkey arterial smooth muscle cells with hyperlipidemic serum or low-density lipoproteins (LDL) produces intracellular cholesterol ester accumulation. Increased esterification of free cholesterol within the cell may account for this effect. To examine such a possibility, oxygenated sterols were used to block cholesterol esterification. The increased esterification of free cholesterol by smooth muscle cells and human skin fibroblasts, through their exposure to hyperlipidemic lipoproteins, was inhibited by 22-hydroxycholesterol and its analogue, SC-32561 (22-hydroxy-25-fluorocholesterol). The hyperlipidemic LDL-stimulated elevation in the cholesterol ester content of the smooth muscle cells was also prevented by these sterols. This reduction in cellular cholesterol ester did not coincide with an increase in free cholesterol. 22-Hydroxycholesterol also blocked the stimulation of the esterification of cholesterol due to 25-hydroxycholesterol. In the absence of lipoproteins, 22-hydroxycholesterol and SC-32561 had a minor effect on the incorporation of [14C]oleate into cholesterol esters, and efficiently reduced sterol synthesis in fibroblasts and smooth muscle cells. 22-Hydroxycholesterol and SC-32561 had the additional effect of lowering the number of cell-surface LDL receptors to a greater extent than did hyperlipidemic LDL. The presence of 22-hydroxycholesterol did not alter the interaction of normal LDL with the receptor. Oxygenated sterols recovered in the cell represented 4-21% of the total sterol content. The level of intracellular oxygenated sterols was significantly reduced by the presence of lipoproteins in the culture media. Due to the multiple effects of the oxysterols, they were not effective as tools in determining the contribution of acyl-coenzyme A:cholesterol acyltransferase enzyme activity to the intracellular pool of cholesterol esters. These results indicated that 22-hydroxycholesterol and SC-32561 effectively blocked the hyperlipidemic LDL-stimulated increase in smooth muscle cell cholesterol ester content by lowering cholesterol esterification, reducing cholesterol synthesis and down-regulating LDL cell-surface receptors.

Animals↗
PubMed1983

A recording viscometer for assaying mammalian collagenase.

A recording viscometer for monitoring the action of mammalian collagenase on soluble collagen is described. For this system, where only one peptide bond is cleaved per subunit, it is shown theoretically that the decrease in viscosity is proportional to the fraction of molecules cleaved. Experimental confirmation was obtained by parallel monitoring of hydrolysis by using the fluorescamine assay of liberated amino groups. The initial velocity of reaction is proportional to substrate concentration and enzyme concentration.

Collagen↗
PubMed1982

Reproductive failure in women who practice weight control.

Forty-seven women (29 with unexplained infertility and 18 with menstrual dysfunction) practiced weight control by caloric restriction in order to maintain a fashionable body habitus. All of these women were below ideal body weight (IBW) when compared with Metropolitan Life Insurance Company tables for height and weight. When 36 of these women followed a dietary regimen designed to increase their weight to predicted IBW, 19 of 26 infertile women (73%) conceived spontaneously; 9 of 10 women (90%) with secondary amenorrhea resumed menstruation. Eleven women (23%) would not accept their practice of weight control as the cause of reproductive failure and did not participate in the study. Differences in the serum gonadotropin luteinizing hormone:follicle-stimulating hormone (LH:FSH) ratio were found to be significantly related to differences in the percentage of IBW. The practice of weight control may be a cause of unexplained infertility and menstrual disorders in otherwise healthy women.

Adolescent↗