Surgical treatment of obstructive sleep apnea.
Explore the source record for details and available documents.
Humans↗
Biomedical subjects
S B Smith
Publications and source records attributed to S B Smith.
The localization and timing of post-translational modifications of rat rhodopsin.
Rat retinas were labeled by incubation with, or intravitreal injection of, [14C]leucine along with tritiated palmitic acid, glucosamine or galactose. At selected intervals, subcellular fractions were prepared on linear sucrose gradients and rhodopsin was extracted and purified by affinity chromatography and gel electrophoresis. Time courses revealed that leucine rapidly and transiently labeled the rhodopsin in the rough endoplasmic reticulum (RER), with a maximum at 1.5 hr post-injection. Subsequently, the rod outer segments (ROS) contained the labeled rhodopsin, with the ROS labeling maximally at 6-12 hr. Palmitate labeling followed the same pattern but was subject to a delay, presumably because of a large intracellular pool of the fatty acid. With palmitate the RER rhodopsin was not maximally labeled until 12 hr. The acylation of rhodopsin takes place in the RER sometime after the polypeptide has been translated but before transport to the Golgi. Glucosamine labeling was also delayed because of intracellular pools of the sugar or its metabolic derivatives. But because of secondary glycosylation in the Golgi, the rhodopsin in the ROS also labeled maximally with glucosamine at about 6 hr. Administration of [3H]galactose resulted in the labeling of rhodopsin both in vivo and in vitro, in part possibly because of its conversion to mannose and subsequent insertion into the core oligosaccharide on the RER. However, in the ROS the ratio of tritium, derived from [3H]galactose, to [14C]leucine decreased by a factor of 2 between 6 and 24 hr post-injection. Moreover, between 6 and 12 hr post-injection, labeled rhodopsin molecules in the ROS underwent a shift in mobility on gels indicative of trimming to a lower molecular weight. Thus some sugar residues may be added to the rhodopsin in the inner segment and removed in the ROS.
Animals↗
Adipose tissue cellularity and muscle growth in young steers fed the beta-adrenergic agonist clenbuterol for 50 days and after 78 days of withdrawal.
Angus steers (n = 40; approximate weight = 300 kg) were administered the beta-adrenergic agonist clenbuterol for 50 d (7 mg.hd-1.d-1), followed by a 78-d withdrawal period. Carcass fatness variables did not differ (P greater than .05) between treated and control animals either after 50 d or after 128 d. Weights of the 9-10-11th rib longissimus muscle were 25% larger, and longissimus cross-sectional areas were 28% greater, in clenbuterol-fed steers relative to controls from 0 to 50 d (P less than .05). After withdrawal these measurements increased no further in the treated steers. Marbling scores were decreased (P less than .05) in clenbuterol-fed steers after 50 d of treatment; this effect persisted after 128 d of withdrawal from treatment. Shear force values were increased 19% (P less than .05) by feeding clenbuterol for 50 d and remained greater (P less than .05) in treated animals after 128 d. Subcutaneous adipocytes in clenbuterol-fed steers were smaller (P less than .05) than those of controls after 50 d, and this effect was still apparent after the 78-d withdrawal period. Rates of lipogenesis did not differ (P less than .05) between treated and control animals at any time. Perirenal (p.r.) adipocytes were smaller (P less than .05) in treated animals after 50 d, but this effect disappeared by the end of the experiment. There was no indication of a bimodal distribution of smaller s.c. or p.r. adipocytes in either of the treatment groups. Apparent hyperplasia of s.c. adipocytes occurred in the area of the 9-10-11th rib in both treated (P less than .10) and control animals (P less than .05) from 0 to 50 d on trial. Within treated animals there was a significant increase (P less than .05) in total adipocytes in this depot during the withdrawal period. Although the effects of clenbuterol on muscle growth generally were reversed after 78 d, the effects of the beta-adrenergic agonist on adipose tissue development were more permanent.
Adipose Tissue↗
Effect of postmortem treatments on the tenderness of meat from Hereford, Brahman and Brahman-cross beef cattle.
The effect of postmortem aging (7, 14, 21 or 28 d), high-voltage electrical stimulation (stimulated or not stimulated) and blade tenderization (none or once; crossbreds only) on the sensory and cooking properties of meat from four beef breeds or breed-types (purebred Hereford, purebred Brahman, Hereford x Brahman and Brahman x Hereford) was determined. The meat from purebred Brahman cattle that was not electrically stimulated was less tender and more variable in tenderness than that from other breed-types but electrical stimulation reduced these differences in tenderness. The Brahman crossbred steers produced meat that was not different in tenderness or variability in tenderness from that of purebred Hereford steers, although all were only judged "slightly tender." Electrical stimulation reduced the length of postmortem aging needed to reach a given level of tenderness regardless of breed or breed-type. Meat from crossbred animals that was blade-tendernized was not different in tenderness from meat that was electrically stimulated. The results of this investigation indicate that purebred Brahman muscle was inherently less tender, but postmortem tenderization procedures produced meat that was similar tenderness to that of the other breed-types used in this study.
Animals↗
Mechanisms associated with the variation in tenderness of meat from Brahman and Hereford cattle.
To study possible mechanisms for differences in meat tenderness, 10 purebred Hereford and 10 American Grey Brahman steers were fed a typical feedlot diet and slaughtered when ultrasound measurements indicated that they had approximately 1 cm of fat thickness at the 12th rib. Longissimus muscle from Brahman cattle was less (P less than .05) tender after 7, 14, 21, 28 and 35 d postmortem than muscle from Hereford cattle, but muscle from Hereford cattle showed greater improvement in tenderness from 7 to 14 d postmortem than muscle from Brahman cattle (interaction P less than .05). Cathepsin B or cathepsin B+L activities and the myofibrillar response to elevated ionic strength were not different between breeds, but both could be related to the postmortem increase in tenderness of both breeds. Calcium-dependent protease activity, as modulated by calcium-dependent protease inhibitor, seems to play a major role in the inherent tenderness differences between breeds.
Adipose Tissue↗
Lean beef: impetus for lipid modifications.
Health-conscious consumers want lean beef. The beef industry has responded by physically removing much of the adipose tissue from retail products and by initiating attempts to produce--genetically and environmentally--cattle with more muscle, less external fat, and less seam fat, without sacrificing the quality dependent on the amount of marbling present. Offering lean beef that is closely or completely trimmed of external fat has improved retail beef sales. Impetus for modification of the lipid composition of bovine muscle and adipose tissue, including marbling, has resulted from the following: (a) diet/health concerns of consumers and demands for leaner beef, (b) research clarifying effects of dietary fatty acids and cholesterol on serum cholesterol levels, (c) dietary guidelines and recommendations from health organizations, and (d) dietary recommendations by physicians and dietitians to reduce beef consumption. Analysis of cholesterol content of marbling dissected from the rib (longissimus dorsi) muscle revealed that marbling contributes little to total cholesterol content. Cholesterol content of marbling was 117 mg/100 gm intramuscular adipose tissue (equivalent to about a 2 mg cholesterol contribution to a 100-gm serving of uncooked meat). The difference in fatty acid composition of lean meat and of adipose tissue is primarily in the percentage of polyunsaturated fatty acids, which is higher in lean meat. The most prevalent fatty acids in adipose tissue including marbling were: palmitic acid (24.1%), stearic acid (13.5%), and oleic acid (37.7%).
Adipose Tissue↗
Observation of individual DNA molecules undergoing gel electrophoresis.
Individual DNA molecules undergoing agarose gel electrophoresis were viewed with the aid of a fluorescence microscope. Molecular shape and orientation were studied in both steady and pulsed electric fields. It was observed that (i) DNA macromolecules advanced lengthwise through the gel in an extended configuration, (ii) the molecules alternately contracted and lengthened as they moved, (iii) the molecules often became hooked around obstacles in a U-shape for extended periods, and (iv) the molecules displayed elasticity as they extended from both ends at once. A computer model has been developed that simulates the migration of the molecules in a rotating-field gel electrophoresis experiment.
Computer Simulation↗
The antioxidant butylated hydroxytoluene can retard cerebellar degeneration induced transplacentally by a single low dosage of N-methyl-N-nitrosourea.
Late-onset cerebellar degeneration can be induced transplacentally in mice by a single low-dose (1 mg/kg) injection of the direct-acting DNA alkylating agent N-methyl-N-nitrosourea (MNU) on day 16 of pregnancy. The offspring develop a mild ataxia that manifests by 12-16 weeks of age postnatally when the animals are challenged with a motor coordination task. Morphological evidence of degeneration includes pyknosis of Purkinje cells and abnormal foliation patterns. Additionally, these animals demonstrate a progressive retinopathy characterized by thinning of the nuclear and plexiform layers of the retina. Efforts to retard the cerebellar degeneration were undertaken in the present study. MNU-exposed and control animals were fed a standard mouse chow diet supplemented with 0.75% butylated hydroxytoluene (BHT), an antioxidant. This supplementation commenced 24 h following exposure to the teratogen and continued throughout the life of the offspring. A second group of MNU-exposed and control mice were fed a non-BHT-supplemented, standard Purina mouse chow diet. Quantitative histological evaluation of cerebellar coronal sections indicated that by 4 weeks of age BHT-fed, MNU-exposed mice had significantly fewer pyknotic Purkinje cells than non-BHT-fed, MNU-exposed animals. This was true for the vermal, paravermal, and lateral areas of the cerebellum. The findings suggest the usefulness of teratogenic models of degenerative diseases for the testing of potential intervention strategies.
Animals↗
Addition of the chromophore to rat rhodopsin is an early post-translational event.
Rat retinas were labeled either by intravitreal injection of [14C]leucine or by incubation with [3H]-leucine or [35S]-methionine. Subcellular fractions were prepared on linear sucrose gradients and rhodopsin was extracted with detergent and purified by chromatography on ConA-Sepharose. A fraction enriched in rough endoplasmic reticulum (RER) and substantially free of rod outer segments (ROS) was found to contain a light-sensitive protein exhibiting the properties of rhodopsin on ConA-Sepharose or Agarose chromatography and on SDS-polyacrylamide gel electrophoresis, as well as immunologically. Intravitreal injection of [3H]-retinol also labeled the rhodopsin in the RER under conditions in which the rhodopsin in the ROS was not heavily labeled. Thus the chromophore appears to be attached to opsin shortly after the apoprotein is translated in the RER.
Animals↗
Elevation of a specific mRNA in longissimus muscle of steers fed ractopamine.
To address the hypothesis that some classes of growth promoters stimulate muscle protein synthesis in growing cattle, 23 crossbred steers were fed diets containing the phenethanolamine growth promoter ractopamine in a 140-d feeding trial. Steers received either no ractopamine, .18 or .36 mg.kg BW-1.d-1 ractopamine for 140 d or .36 or .72 mg.kg BW-1.d-1 ractopamine for 56 d. Longissimus muscle was obtained at slaughter and frozen in liquid N2. RNA was extracted by homogenization of pulverized frozen muscle in guanidinium isothiocyanate and centrifugation through cesium chloride. Polyadenylated mRNA was extracted by capture on oligo-dT columns. Ractopamine had no effect on total RNA or mRNA concentrations (P greater than .25). Hybridization of the RNA to a putative myosin light chain-1/3 (MLC-1/3) cDNA clone in a Northern blot indicated one heavy band (approximately 1 kb) with no evidence of extensive destruction of the RNA. A second, minor band (approximately 3 kb) also was observed in some samples. The MLC-1/3 cDNA clone was hybridized to 1- or 5-micrograms samples of total RNA, and the intensity of the resultant autoradiographs was quantified by laser densitometry. There was a statistical correlation between MLC-1/3 mRNA-micrograms RNA-1 and longissimus cross-sectional area (P less than .05) and average daily gain (P less than .025). The results suggest that ractopamine either increased the transcription of the putative MLC-1/3 gene and(or) increased the stability of MLC-1/3 mRNA in bovine longissimus muscle, either of which could result in an increase in specific myofibrillar protein synthesis.
Analysis of Variance↗
Glycerolipid biosynthesis in porcine adipose tissue in vitro: effect of adiposity and depot site.
To compare genetic differences in glycerolipid biosynthesis, rates were determined in s.c. adipose tissue of lean and obese pigs at 28, 60 and 110 d of age. To compare depot-specific differences, glycerolipid biosynthetic rates were determined in outer s.c., middle s.c., perirenal and omental adipose tissues obtained from 105-kg contemporary pigs. Rates were determined with a 700 x g infranatant fraction of an adipose tissue homogenate by measuring glycerophosphate incorporation into total lipids (mostly phosphatidic acid) during 4 min. This assay represents entrance of substrates into the glycerolipid synthesis pathway or glycerophosphate acyltransferase (GPAT) activity. Rates measured for 60 min represent maximal synthesis of glycerolipid (more triacylglycerol than phosphatidic acid) or lipid synthesis capacity (LSC). Adipocyte diameter and volume were greater for adipose tissue of obese than of lean pigs both at 60 and 110 d. When expressed per cell, activity of GPAT and LSC were similar for lean and obese pigs at 28 d. At 60 d and 110 d, LSC was greater for obese than for lean pigs; GPAT activity was greater at 60 but not at 110 d in obese than in lean pigs. Expressed on a cell basis, GPAT activity was highest in omental and outer s.c., intermediate in perirenal and lowest in middle s.c. adipose tissue depots. Lipid synthesis capacity was highest in perirenal and lowest in outer and middle s.c. depots. Our results indicate that the LSC assay was more closely related to the accretion of fat in vivo than to GPAT activity.
Adipose Tissue↗
Acute and long-term lipogenic response to insulin and clenbuterol in bovine intramuscular and subcutaneous adipose tissues.
The present study was conducted to determine whether insulin and clenbuterol affected either short-term (2-h) incubations or long-term (48-h) tissue cultures of i.m. and s.c. adipose tissue explants. Samples were taken from control steers and steers fed 7 mg.head-1.d-1 clenbuterol for 50 d, after which time the drug was withdrawn from the diet for 90 d prior to slaughter. Neither short-term incubations nor long-term explant cultures contained bovine serum albumin (BSA). Insulin (6.67 x 10(-9) M) had no effect (P greater than .05) on lipogenesis in s.c. and i.m. adipose tissue in 2-h tissue incubations of fresh adipose tissue. There was a substantial decrease in activity during the culture period, which was ameliorated somewhat in s.c. adipose tissue by the presence of insulin in the culture media. Clenbuterol exposure for 48 h in vitro decreased the production of lipids from acetate in both adipose tissue depots but had no effect in short-term adipose tissue incubations. Results from the present study confirm that omitting BSA from incubation media does not enhance the responsiveness of bovine s.c. adipose tissue or the less mature i.m. adipose tissue to insulin. Insulin may maintain greater cell viability in 48-h explant cultures.
Adipose Tissue↗
Ionophores alter hepatic concentrations of intermediary carbohydrate metabolites in steers.
The effects of ionophores on liver weight and function were determined in finishing steers (n = 24; avg weight 440 kg). Steers were group-fed one of three treatments (control, lasalocid or monensin at 33 mg/kg feed) for 46 d prior to slaughter. Three days prior to slaughter, blood was collected for the determination of serum Ca and Mg. At slaughter, the liver was removed, weighed, sampled, frozen in liquid nitrogen and subsequently analyzed for concentrations of carbohydrate metabolites and minerals. Liver weight (5.9 kg) was unaffected by treatment. Serum and hepatic Ca and Mg were not affected by ionophore treatment. Hepatic glycogen levels in steers fed ionophores were unaffected by treatment. Fructose 1,6-bisphosphate was 21% lower (P less than .10) in hepatic tissue of steers fed ionophores, whereas dihydroxyacetone phosphate was 15 to 37% greater in hepatic tissue of steers fed monensin (P less than .20) or lasalocid (P less than .10). Glyceraldehyde 3-phosphate was elevated more extensively by lasalocid than by monensin with increases of 72 (P less than .05) and 132% (P less than .001), respectively, over controls. Glycerol 3-phosphate levels were 37% (P less than .05) and 12% (NS) greater with these ionophores. Hepatic levels of pyruvate were elevated 12 (NS) to 36% (P less than .17) for monensin and lasalocid. Fructose 2,6-bisphosphate levels were 25% lower (P less than .25) in hepatic tissue of steers fed ionophores than in hepatic tissue from control steers. Other metabolites of carbohydrate metabolism in hepatic tissue were not altered appreciably. Changes in levels of intermediary metabolites of carbohydrate metabolism suggest alterations in hepatic carbohydrate metabolism favoring gluconeogenesis in steers fed ionophores.
Animals↗
Effects of the antioxidant butylated hydroxytoluene (BHT) on retinal degeneration induced transplacentally by a single low dosage of N-methyl-N-nitrosourea (MNU).
A 1 mg/kg dose of the DNA alkylating agent, N-methyl-N-nitrosourea (MNU), when administered on day 16 of gestation provokes a progressive retinal degeneration in CD-1 albino mice reared under standard fluorescent lighting conditions (12 hr light: 12 hr dark); this degeneration begins at about 4 weeks post-natally and worsens with age. It is accelerated by constant fluorescent light exposure but is retarded greatly by constant darkness, suggesting the importance of secondary insults in the post-natal period for development of the degenerative disease. To determine whether the secondary photochemical damage might be specifically blocked, MNU-exposed and control animals in the present study were fed an antioxidant-enriched diet of Purina mouse chow supplemented with 0.75% butylated hydroxytoluene (BHT). A second group of MNU-exposed and control animals were fed a non-BHT supplemented standard Purina mouse chow diet. Systematic measurements of the number of rows of photoreceptor cell nuclei, the thickness of the inner/outer segment layer, and the thickness of the whole retina were made, to quantify and degenerative changes in animals 2, 4, 6, and 8 weeks of age. By 8 weeks, retinas of BHT-fed, MNU-exposed animals were significantly thicker and had more rows of photoreceptor cell nuclei than regular-diet, MNU-exposed animals. Moreover, the retinas of BHT-fed animals, both for MNU-exposed and controls, demonstrated sporadic morphologic changes in the form of circular configurations composed of ganglion cells, arcades of nuclear and plexiform layers, and, in one control animal, a hyperplastic nodule. These experiments suggested that MNU-induced retinal degeneration may be retarded by a BHT-enriched diet; however, continuous high doses of this compound pre- and postnatally may induce other retinal abnormalities.
Animals↗
Toxicity of six heterocyclic nitrogen compounds to Daphnia pulex.
Explore the source record for details and available documents.
Animals↗
Biochemical characterization of retinal protein and phospholipid synthesis in mice exposed transplacentally to N-methyl-N-nitrosourea.
Transplacental exposure to the DNA alkylating agent N-methyl-N-nitrosourea on day 16 of gestation in CD-1 albino mice induces a degeneration of the retina, the severity of which depends upon the dosage level of the drug. A 1 mg kg-1 dose provokes a progressive retinal degeneration in the offspring which begins at about 4-6 weeks of age and is characterized by gradual thinning of the retinal layers. A 15 mg kg-1 dosage of MNU provokes severe retinal dysplasia characterized morphologically by rosettes in the outer nuclear layer and loss of rod outer segments (ROS). In the present biochemical experiments, retinal protein synthesis was examined in mice 2-, 4-, and 6 weeks of age exposed to 1 mg kg-1 MNU and 2- and 5 weeks of age exposed to 15 mg kg-1 MNU. Phospholipid synthesis was examined in mice 2-, 4-, 6- and 12 weeks of age exposed to 1 mg kg-1 MNU and at 2 weeks in mice exposed to 15 mg kg-1 MNU. Retinas were incubated for 2 hr at 37 degrees C in media supplemented with either [3H]leucine for protein synthesis studies or [3H]glycerol for phospholipid synthesis experiments. Aliquots of crude ROS and the retinal debris were taken for protein determination, scintillation counting, SDS-PAGE separation of labeled opsin, phosphorus determination and TLC separation of phospholipids. Results indicated that mice exposed to 1 mg kg-1 MNU did not differ significantly from age-matched controls in these measurements, whereas mice exposed to 15 mg kg-1 MNU were significantly different from controls. These results suggest that even as early as 2 weeks of age protein and lipid metabolism are adversely affected in mice exposed to the higher dose of the alkylating agent at a critical time in retinal development, but general protein and lipid synthesis is not affected in animals exposed to 1 mg kg-1 MNU at least up to 12 weeks of age. These studies suggest further investigation of more subtle derangement in the retinal function in animals exposed to low levels of MNU.
Animals↗
Retinal degeneration in the mouse induced transplacentally by N-methyl-N-nitrosourea: effects of constant illumination or total darkness.
The DNA alkylating agent, N-methyl-N-nitrosourea (MNU), when administered prenatally (on day 16 of gestation) provokes a progressive retinal degeneration in CD-1 albino mice reared in standard fluorescent lighting conditions (12 L: 12 D). This degeneration begins at about 4 weeks postnatally and worsens with age. To determine whether light was essential to the development of this lesion, animals in the present study were maintained in either constant light or constant darkness. Systematic measurement of the inner and outer segment lengths, the number of rows of photoreceptor cells and the thicknesses of the outer nuclear layer and whole retina were made to quantify degenerative changes in animals at 2-, 4-, 6-, 8-, 12-, and 16 weeks of age. The constant light caused a drastic reduction in thickness of the retinas of MNU-treated and control mice. The MNU-exposed animals reared in the dark did not demonstrate this reduction in retinal thickness, at least up to 16 weeks of age. Rather, measurements from this group were much like those for dark-reared control mice. The results of the present study suggest that the retinopathy induced by this dose of MNU may require secondary insults such as light, to amplify the lesions induced in utero by the drug.
Aging↗
Adipose tissue, longissimus muscle and anterior pituitary growth and function in clenbuterol-fed heifers.
The present study was conducted to determine the effects of feeding clenbuterol on adipose tissue and longissimus muscle growth in heifers. For 50 d, 14 heifers were fed either a sucrose-based, clenbuterol supplement or a placebo in which the clenbuterol had been omitted. The heifers were slaughtered in two groups, based on initial weight. Adipose tissue from several anatomical sites and longissimus muscle (depending on slaughter group) were obtained fresh at slaughter. Changes in carcass characteristics elicited by clenbuterol were similar to those reported by others for steers and sheep. Subcutaneous (sc) and intramuscular (im), but not perirenal, adipocytes were smaller and there were more cells per g tissue in the adipose tissue depots of the clenbuterol-fed heifers. Clenbuterol decreased lipogenic enzyme activities, fatty acid-binding protein activity, basal lipolysis and acetate incorporation into glyceride-fatty acids (P less than .05) in sc adipose tissue, but had no effect (P greater than .05) on lipogenesis or lipolysis in im adipose tissue. Clenbuterol elicited a 20% increase in type II myofiber diameters (P less than .05) but had no effect on type I myofiber diameters. In vitro growth hormone release by perifused anterior pituitaries was not affected significantly by long-term in vivo exposure to clenbuterol. These data indicate that a depression in lipogenesis is the mechanism by which clenbuterol decreases subcutaneous fat accretion in cattle.
Adipose Tissue↗