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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

University of California, Davis, line 200 and 206 chickens spontaneously develop an autoimmune syndrome that has many features analogous to human scleroderma, including dermal fibrosis, antinuclear antibodies and antibodies to type II collagen. These birds also have thymic subcapsular epithelial defects and an abnormality in T cell calcium influx and proliferation in response to both T cell receptor-dependent and -independent activators. To determine whether fibroblast activation is a contributing factor to development of skin fibrosis in line 200/206 chickens, as it is in human scleroderma, we studied the collagen, non-collagenous protein and glycosaminoglycan (GAG) production of 34 separate fibroblast lines derived from the normal and fibrotic skin of line 200 and 206 chickens and from the skin of control chicken lines 058 and 254. The mean +/- SEM 24-h incorporation of 3H-proline or 3H-glucosamine into extracellular collagen, non-collagenous protein or GAG by first passage fibroblast lines derived from the fibrotic skin of diseased birds was 1,526 +/- 136, 859 +/- 82 and 25.7 +/- 1.3 dpm/10(3) cells, respectively, while fibroblast lines derived from the skin of control birds produced only 341 +/- 36, 343 +/- 42 and 15.2 +/- 1.4 dpm/10(3) cells. Similar differences in results were recorded for cell-associated production, and when collagen and non-collagenous protein production were assessed using non-radioactive electrophoretic methods. The activated phenotype of the fibroblast lines derived from the fibrotic skin of diseased birds persisted through 10 cell doublings in tissue culture. However, the ratio of type I:III collagen and the profile of GAG types produced were similar in all fibroblast lines studied. These results suggest that fibroblast activation is responsible for the skin fibrosis observed in this avian model of scleroderma.
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PMID:Cultured fibroblasts in avian scleroderma, an autoimmune fibrotic disease, display an activated phenotype. 141 97

The tachykinins substance P (SP) and neurokinin A (NKA) were studied in human inferior turbinate nasal mucosa by radioimmunoassay, immunohistochemistry, and autoradiography and for their effect upon mucus release in an in vitro culture system in order to infer their potential functions in the upper respiratory tract. Similar amounts of SP (1.03 +/- 0.12 pmol/g wet weight; mean +/- SEM; n = 26) and NKA (0.76 +/- 0.23; n = 7) were found. NKA and SP immunoreactive nerve fibers were found in the walls of arterioles, venules, and sinusoids and as individual fibers in gland acini, near the basement membrane, and in the epithelium. [125I]SP bound to arterioles, venules, and glands. [125I]NKA bound only to arterioles. In short-term explant culture of fragments of human nasal mucosa, both 1 microM SP and 1 microM NKA stimulated release of [3H]glucosamine-labeled respiratory glycoconjugates. These results indicate that SP and NKA have similar distributions in nociceptive sensory nerves in human nasal mucosa. The distribution of [125I]SP binding sites is consistent with a role for SP as a vasodilator and mucous secretagogue. The presence of [125I] NKA binding sites on vessels suggests a primary role for NKA in regulating vasomotor tone.
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PMID:Substance P and neurokinin A in human nasal mucosa. 170 9

Gastrin-releasing peptide (GRP), the 27 amino acid mammalian form of bombesin, was studied in human inferior turbinate nasal mucosa. The GRP content of the mucosa measured by radioimmunoassay was 0.60 +/- 0.25 pmol/g tissue (n = 9 patients; mean +/- SEM). GRP-immunoreactive nerves detected by the immunogold method of indirect immunohistochemistry were found predominantly in small muscular arteries, arterioles, venous sinusoids, and between submucosal gland acini. 125I-GRP binding sites determined by autoradiography were exclusively and specifically localized to nasal epithelium and submucosal glands. There was no binding to vessels. The effects of GRP on submucosal gland product release were studied in short-term explant culture. GRP (10 microM) significantly stimulated the release of the serous cell-specific product lactoferrin, and [3H]glucosamine-labeled glycoconjugates which are products of epithelial goblet cells and submucosal gland cells. These observations indicate that GRP released from nerve fibers probably acts on glandular GRP receptors to induce glycoconjugate release from submucosal glands and epithelium and lactoferrin release from serous cells, but that GRP would probably not affect vascular permeability.
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PMID:Gastrin-releasing peptide in human nasal mucosa. 231 84

Glucose phosphorylation was studied in a pure capillary preparation obtained from the rete mirabile of the eel swimbladder. In the 3000g supernatant of capillary homogenates, the glucose phosphorylating activity did not reach the maximum at low glucose concentration (1 mmole/liter), as it occurs in most tissues, but increased with the increase in glucose concentration and approached the maximum at very high (300 mmole/liter) glucose levels, with values (mean +/- SEM, n = 10) of 5.85 +/- 0.94 nmole.min-1.mg-1 protein and 19.97 +/- 1.89 at 1 and 300 mmole/liter glucose, respectively. The apparent Km value for glucose was about 50 mmole/liter, i.e., at supraphysiological glucose concentration, like the enzyme glucokinase, typically present in the liver but absent from most other tissues. This new enzyme did not phosphorylate fructose (similar to glucokinase from liver, which is rather specific for glucose) but was not inhibited by N-acetyl-glucosamine (in contrast to hepatic glucokinase). Thus, capillaries phosphorylate glucose in a concentration-dependent manner, which suggests that they are equipped with a glucokinase-like enzyme. This may explain the reported increase in glucose uptake during capillary exposure to high glucose concentrations and would suggest that the hyperglycemia of the diabetic state may be associated with increased glucose utilization, which may play a role in the development of microangiopathy.
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PMID:Capillaries phosphorylate glucose in a concentration-dependent manner through a glucokinase-like enzyme: a study in the eel. 238 26

IM-9 cultured human lymphocytes were treated with N-linked glycosylation inhibitors, N-linked oligosaccharide processing inhibitors, or neuraminidase to study the effect of glycosylation modification on human growth hormone binding and molecular weight of surface hGH receptor. One mg/l tunicamycin and 20 mmol/l glucosamine decreased 125I-hGH binding to the cells to 46.3 +/- 2.4% (mean +/- SEM) and 21.9 +/- 0.2% of the controls, respectively. The hGH binding was 33.0 +/- 18.4% of the control value in the cells treated with monensin. The inhibition of binding was due to a decrease in the hGH receptor number without any affinity changes in these cells. Neither 1 mg/l swainsonine nor 100 mg/l castanospermine had any effect on the hGH binding. On the other hand, 125I-hGH binding to neuraminidase-treated cells was significantly enhanced with accompanying affinity changes. When 125I-hGH was cross-linked to IM-9 cells, there were no differences in the molecular weight of hGH receptor complexes (140 K) between untreated cells and cells treated with tunicamycin, glucosamine, monensin, or castanospermine. However, the 128 K hGH-receptor complex appeared in swainsonine-treated cells; this complex was sensitive to endoglycosidase H. These data show that the altered carbohydrate moiety changed hGH binding and the size of surface hGH receptor and suggest that glycosylation of receptor is important for the binding of hGH and for its physiological action.
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PMID:Effects of glycosylation inhibitors on human growth hormone receptor in cultured human lymphocytes. 314 7

The high incidence of clinical remission after faecal diversion for Crohn's colitis suggests the faecal stream may play a part in the inflammatory mechanism. The effect of faecal diversion (n = 22) and restoration of intestinal continuity (n = 10) was assessed in patients with Crohn's colitis and compared with controls. Faecal diversion produced significant improvement in the disease activity index mean (SEM) (before 176 (9); after 114 (9), p < 0.01) and serum albumin concentrations (before 33 (3.0); after 38 (3.0), p < 0.05) in all patients with Crohn's colitis. The crypt cell production rate (CCPR) was maintained after faecal diversion for Crohn's colitis but fell in the control group (before = 3.6 (0.8)), at two (1.4 (0.4), p < 0.02), and six weeks (1.6 (0.4), p < 0.05). Mucosal glucosamine synthetase activity, reflecting glycoprotein synthesis, was significantly lower in patients with Crohn's colitis (analysis of variance p < 0.05) after diversion but was maintained in the control group. Restoration of intestinal continuity failed to produce reciprocal changes. The sustained cellular proliferation and fall in glycoprotein synthesis in Crohn's colitis after faecal diversion may represent the end of an exaggerated protective response and regenerative hyperplasia after exclusion of the faecal stream. This study suggests the faecal stream may participate in the inflammatory process in Crohn's colitis. The underlying mechanism is unknown.
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PMID:Faecal diversion for Crohn's colitis: a model to study the role of the faecal stream in the inflammatory process. 830 75

Damage to the gastrointestinal tract mucous layer may render underlying cells susceptible to intraluminal toxins or carcinogens. Our aim was to determine the effect of bile acids on mucin, the primary constituent of mucous. Differentiated Caco-2 and HT29 cells were used as models of human colonic epithelial cells. Mucin was measured by [3H]-glucosamine labeling. Short term (30 min) incubations with 1-5 mM unconjugated bile acids or taurodeoxycholic acid induced mucin release relative to bile acid hydrophobicity. Longer incubations were cytotoxic. Long term (7 days) incubation at nontoxic concentrations (0.1 mM) of deoxycholic acid (DC) decreased total mucin by 36 +/- 2% (SEM, P = 0.0003) in differentiated HT29 cells and by 57.2 +/- 2% (P < 0.05) in Caco-2 cells. Tauroursodeoxycholic acid (TUDC) or ursodeoxycholic acid (0.1-0.5 mM) did not alter mucin levels. Simultaneous incubation of 0.1 mM DC and 0.1-0.5 mM TUDC or 2.5 mM TDC and TUDC did not change mucin levels. Differentiated HT29 and Caco-2 cells contained high levels of intestinal mucin MUC3 mRNA while undifferentiated HT29 cells did not possess a MUC3 message. Deoxycholic acid (0.1 mM) did not alter the MUC3 mRNA level. Neither cell type showed detectable expression of intestinal MUC2 or gastric MUC6. Thus, cytotoxic concentrations of bile acids induce mucin release, presumably due to detergent effects. Nontoxic concentrations of DC reduce mucin levels in differentiated enterocyte-like cells, which can be prevented by coincubation with TUDC. The bile acid-induced alterations in mucin production by enterocytes observed in vitro may influence intestinal cytoprotection in vivo.
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PMID:Bile acid-induced alterations of mucin production in differentiated human colon cancer cell lines. 872 6

An enzyme with properties similar to rat liver glucokinase (Hexokinase IV or D) is present in salmon liver in addition to low-Km hexokinase(s). The specific activity of this enzyme increases about 1.6 fold, comparing activities after feeding diets with 25% and 0% digestive energy from starch. The enzyme has a low affinity for glucose, S0.5 = 25.2-26.8 mM (95% confidence interval) and a low activity with fructose, approximately 8% of the activity with glucose. Its molecular mass was estimated to 50.7 +/- 0.6 kDa (SEM. n = 3) by gel filtration, and it displays positive cooperativity with respect to glucose. The Hill constant = 1.73-1.81 (95% confidence interval). The enzyme is competitively inhibited by N-acetyl glucosamine, K(i) approximately 0.28 mM.
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PMID:A glucokinase-like-enzyme in the liver of Atlantic salmon (Salmo salar). 875 98

The apical surface of the guinea-pig organ of Corti was examined with SEM after WGA-lectin histochemistry which has a binding specificity for sialic acid and N-acetyl-glucosamine. The contrast of colloidal gold markers were particularly enhanced by back-scattered electron imaging. WGA lectin showed remarkable preference for the microvilli as well as flat surface areas in the supporting cells. Stereociliary surfaces and interstereociliary connections of the sensory hair cell were strongly labelled, whilst only rarely the markers were found in the flat areas of the apical surface of the hair cell. The connections, which are known to be involved in the initiation of the mechanoelectrical transduction, should consist of sialic acid and/or N-acetyl-glucosamine.
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PMID:WGA lectin binding sites of the apical surface of corti epithelium: enhancement by back-scattered electron imaging in guinea-pig inner ear. 876 16

The cytotoxicity of the most common alloys used in orthodontic appliances was determined by cell culture testing. Human gingival fibroblasts were cultured on 304 and 316 stainless steel, on brazing alloy composed of palladium (Pd), copper (Cu), and silver (Ag), and on plastic substrate (control). Studies were carried out with SEM and radiolabeled precursor incorporation. Cells were cultured in MEM without serum but with the addition of (3)H-thymidine to evaluate cell proliferation and (3)H-glucosamine to evaluate glycosaminoglycan (GAG) synthesis and secretion in the culture medium. Moreover, gingival fibroblasts were cultured in the presence of some metal ions generally released by orthodontic appliances to evaluate the cytotoxic effects of single ions. Morphologic observations with SEM and radiolabeled incorporation studies showed that 304 and 316 stainless steel were more biocompatible than the brazing alloy. Among the metal ions tested, Ag and Pd, constituents of the brazing alloy, showed the highest cytotoxicity.
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PMID:Biocompatibility of alloys used in orthodontics evaluated by cell culture tests. 1088 Jan 3


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