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

The effects of injection of n-3 polyunsaturated fatty acids (PUFAs) on the delayed-type hypersensitivity (DTH) response was investigated in mice. Mice were immunized with sheep red blood cells (SRBCs). Six days later 50 microliters of a 20% SRBC suspension was injected into the right hind footpad of each mouse. Just before the challenge of SRBCs, various amount of a trieicosapentaenoyl-glycerol emulsion (10%) was injected through tail veins (5 mice per each dose). Then 24 hr later the dorsoventral thickness of the right hind footpad was measured and compared with that of the left hind footpad. The difference in thickness between both footpads was regarded as the DTH response. The effect of the emulsion on DTH was dose-dependent; the DTH responses (in mm) in the control group (injected with 0.5 ml of a 2.5% glycerol solution through tail veins) and EPA-injected groups (with 5 mg, 10 mg, and 20 mg) were 1.53 +/- 0.16 (mean +/- SEM), 1.09 +/- 0.14, 0.43 +/- 0.07 (P less than 0.005), and 0.36 +/- 0.13 (P less than 0.005), respectively. The DTH response was also depressed by the injection of a tridocosahexaenoyl-glycerol emulsion. Consequently, n-3 PUFA emulsions have clinical implication in DTH-related diseases such as rejection of allografts.
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PMID:Reduction of delayed-type hypersensitivity by the injection of n-3 polyunsaturated fatty acids in mice. 141 31

This study was designed to compare changes in high-density lipoprotein (HDL)- and low-density lipoprotein (LDL)-cholesterol in normolipidaemic male insulin-dependent diabetics (IDD) following dietary supplementation with either the fish oil concentrate Max EPA or olive oil. The contribution of the small quantity of cholesterol in Max EPA to these changes was also examined. Twenty-seven subjects were matched in groups of three and randomly allocated to one of three treatment groups of nine subjects each. Subjects were given 15 1-g capsules of oil daily for 3 weeks, consisting of either Max EPA, olive oil, or olive oil to which was added the same amount of cholesterol as contained in Max EPA, respectively. There was a significant increase in eicosapentaenoic acid, and a decrease in arachidonic acid, in the platelet membrane phospholipids of subjects taking Max EPA. In this group, there was an approximately 30% increase in serum HDL2-cholesterol (0.59 +/- 0.07 to 0.77 +/- 0.11 mmol/L, mean +/- SEM; P less than .01) and a corresponding decrease in HDL3-cholesterol (0.79 +/- 0.03 to 0.71 +/- 0.03 mmol/L; P less than .05). Although total and LDL-cholesterol concentrations were also higher after Max EPA, the changes were not significant. Triglycerides were significantly decreased by Max EPA. There were no significant changes in lipids in the groups given olive oil. These results show that compared with olive oil, dietary supplementation with Max EPA substantially increases HDL2-cholesterol in insulin-dependent diabetics. This is most likely due to a selective effect of omega 3 fatty acids.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of diets supplemented with fish oil or olive oil on plasma lipoproteins in insulin-dependent diabetics. 200 36

The nonestrogen receptor-mediated antiproliferative action of antiestrogen binding site (AEBS) ligands, including triphenylethylene antiestrogens and phenothiazines, has been linked to their ability to inhibit protein kinase C (PKC). Recent studies indicate that some diphenylmethane derivatives inhibit growth, are potent AEBS ligands, and antagonize histamine binding at an AEBS-related histamine site different from H1 and H2. Three novel diphenylmethane derivatives, N,N-diethyl-2-[4-(phenylmethyl)phenoxy]ethanamine.HCI (DPPE), 4-decanoyl-DPPE (dec-DPPE), and 4-benzylphenyl decanoate (BPD) were studied in an attempt to determine whether PKC or histamine interactions best correlate with their antiproliferative effects. Platelet aggregation and the phosphorylation of a platelet Mr 47,000 protein (p47) induced by phorbol-12-myristate-13-acetate (PMA) represent two processes mediated by PKC. DPPE inhibits PMA-induced aggregation [50% inhibitory concentration (IC50) = 31.2 +/- 2.4 (SEM) x 10(-6) M] but does not significantly inhibit either PMA-induced phosphorylation of Mr 47,000 protein (IC50 greater than 500 x 10(-6) M), or binding of [3H]phorbol dibutyrate to platelets. dec-DPPE is a more potent inhibitor of PMA-induced platelet aggregation (IC50 = 18.8 +/- 0.7 x 10(-6) M), a weak inhibitor of Mr 47,000 phosphorylation (IC50 = 80-200 x 10(-6) M), but is without effect on [3H]phorbol dibutyrate binding. BPD, which lacks the alkylaminoethoxy side chain necessary for binding to the AEBS/DPPE site, is devoid of anti-PMA effects. These results are compared to the inhibition of [3H]histamine binding in rat cortex membranes (Ki value for DPPE = 0.83 +/- 0.62 x 10(-6) M; Ki value for dec-DPPE = 6.6 +/- 3.5 x 10(-6) M; BPD is inactive) and growth inhibition of MCF-7 cells (IC50 value for DPPE = 4.5 x 10(-6) M; IC50 value for dec-DPPE = 1.5 x 10(-5) M; BPD is ineffective at all concentrations tested). Thus, while dec-DPPE is a more potent inhibitor of PKC-mediated phosphorylation, DPPE is a more potent inhibitor of histamine binding and is correspondingly more antiproliferative than dec-DPPE. The results support a relationship between antagonism of histamine binding and growth inhibition but argue against an association between the antiproliferative effects of DPPE and dec-DPPE and inhibition of PKC. The findings for DPPE suggest that platelet response to PMA, antagonized by diphenylmethane-type AEBS-ligands, may be mediated, at least in part, by mechanisms other than activation of protein kinase C-dependent phosphorylation.
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PMID:Correlation of the antiproliferative action of diphenylmethane-derivative antiestrogen binding site ligands with antagonism of histamine binding but not of protein kinase C-mediated phosphorylation. 316 53

Multiple potentially injurious agents are present in smoke but the importance of each of these agents in producing lung injury as well as the mechanisms by which the lung injury is produced are unknown. In order to study smoke inhalation injury, we developed a synthetic smoke composed of a carrier of hot carbon particles of known size to which a single known common toxic agent in smoke, in this case HCI, could be added. We then exposed rats to the smoke, assayed their blood for the metabolites of thromboxane and prostacyclin, and intervened shortly after smoke with the cyclooxygenase inhibitors indomethacin or ibuprofen to see if the resulting lung injury could be prevented. Smoke exposure produced mild pulmonary edema after 6 h with a wet-to-dry weight ratio of 5.6 +/- 0.2 SEM (n = 11) compared with the non-smoke-exposed control animals with a wet-to-dry weight ratio of 4.3 +/- 0.2 (n = 12), p less than 0.001. Thromboxane B, and 6-keto-prostaglandin F1 alpha rose to 1,660 +/- 250 pg/ml (p less than 0.01) and to 600 +/- 100 pg/ml (p greater than 0.1), respectively, in the smoke-injured animals compared with 770 +/- 150 pg/ml and 400 +/- 100 pg/ml in the non-smoke-exposed control animals. Indomethacin (n = 11) blocked the increase in both thromboxane and prostacyclin metabolites but failed to prevent lung edema.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ibuprofen prevents synthetic smoke-induced pulmonary edema. 353 56

Increased vascular collagen content is a major feature of pulmonary vascular remodeling. The functional role of excess collagen in decreasing pulmonary vascular compliance has not been established. We determined whether there was a correlation between hydroxyproline content of rat pulmonary artery segments and elastance (EPA) of the pulmonary artery bed during development of hypoxic pulmonary hypertension (10% O2, 10 d) and normoxic recovery. EPA was measured by air-filled pressure-volume curves. After 10 d of hypoxia, hydroxyproline content increased approximately 2-fold in large segments (1,200-250 microns in diameter) but not significantly in small segments (> 250 microns). Elastance increased from 87 +/- 6 (SEM) to 145 +/- 8 mm Hg/ml (p < 0.05) within 5 d of hypoxia and returned to control value 3 wk after recovery. There was a correlation between collagen content and EPA in large segments during development of hypertension; no correlation was found during recovery from hypoxia. The ratio of hydroxyproline to total protein was unchanged in large segments after recovery from hypoxia but was increased in small segments after recovery. We conclude that increased collagen in large pulmonary arteries directly influences EPA during the development of hypoxic pulmonary hypertension.
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PMID:Excess collagen in hypertensive pulmonary arteries decreases vascular distensibility. 817 73

Plasminogen is activated into the fibrinolytic enzyme plasmin via: a tissue type activator and F-XII dependent and F-XII independent systems. The purpose of this study was extract and quantify the tissue-type plasminogen activator present in the salivary glands of rats. The extracted plasminogen activator-EPA- was obtained by homogenizing 1 vol of tissue with 1 vol of 2M KSCN solution. Solution with EPA was applied by triplicated in the standard plasminogen-rich and plasminogen-free fibrin plates. The degree of fibrinolytic activity was observed as areas of liquefaction and measured as the product (mm2) of the two perpendicular diameter of the lysed zones. The submaxillary's EPA produced a mean lytic area of 198 mm2 +/- 18 SEM only in the plasminogen-rich fibrin plate. This activity extrapolated into a standard dilution curve, represented the equivalent to a 50 mg/ml plasmin solution. No lysis was induced by EPA from parotid and sublingual glands. The antifibrinolytic drug E-ACA in a dose dependent inhibitory action, significantly reduced the lytic activity induced by submaxillary's EPA. The observation that EPA produced areas of liquefaction only in plasminogen-rich fibrin plate and that this activity was inhibited by E-ACA is clear indication that the zones of lysis was specific fibrinolysis -activation of plasminogen into plasmin- and not due to non-specific proteolysis.
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PMID:Extraction of plasminogen activator in the rat's submaxillary gland. 858 May 23

It has been reported that the presence of a smear layer on dentinal substrates can compromise bonding. Typically, smear layers are removed by acidic agents that selectively extract calcium salts from dentin surfaces to leave a collagen-rich substrate. Acid-conditioned dentin (i.e., demineralized) is then primed and an adhesive agent applied. In the present study, we removed smear layers by "polishing" dentin specimens with a hydroxyapatite paste and ultrasonication. Bonding procedures were carried out by means of an aqueous solution of 20% 2-methacryloyloxyethyl phenyl phosphoric acid (phenyl-P) and 30% 2-hydroxyethyl methacrylate, referred to as 2OP-30H, a "self-etching primer". The 20P-30H solution was applied to "intact" dentin (i.e., non-demineralized) for either 30 or 60 s. Control samples received no application (O s) of the self-etching primer. Mean tensile bond strengths (10 MPa) were similar in both the 30-second- and 60-second-primed groups. The widths of formed hybrid layers varied from 0.3 +/- 0.2 micron at O s application (control) to 2.1 +/- 0.3 micron for the 30-second group and 4.1 +/- 0.2 micron for the 60-second group. SEM and TEM observations revealed that the 20P-30H self-etching primer created diffusion channels into "intact" calcium-rich dentin which permitted monomer to infiltrate dentin substrates. Hybrid layers identified under microscopic examination demonstrated resistance to both HCI and NaOCI treatments, suggesting that the hybrid layer was not defective, and that bonding was stable.
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PMID:Bonding to intact dentin. 895 25

This study was conducted to determine whether interferon-alpha-2b (IFN-alpha-2b) can be encapsulated in liposomes without compromising its anti-fibrogenic effects on human dermal fibroblasts. The rationale for this approach is that systemic administration of IFN-alpha-2b by injection for treatment of dermal fibrosis is uncomfortable, requires a large quantity of the cytokine, and cannot be easily used in children. Liposomes are potentially useful as vehicles for the topical delivery of drugs if they can be encapsulated without loss of biologic activity. Empty sonicated vesicles composed of dioleoyl-phosphatidylcholine:dioleoyl-phosphatidylglycerol at a molar ratio of 7:3 were mixed with various concentrations of IFN-alpha-2b and then dried and rehydrated. An enzyme-linked immunosorbent assay (ELISA) was used to determine the efficiency of encapsulation and the stability of the preparation under experimental conditions. Greater than 80% of added IFN-alpha-2b became associated with the liposomes and remained encapsulated for up to 5 d at 4 degrees C. The rate of release increased markedly at 37 degrees C. Liposome-encapsulated IFN-alpha-2b (2000 units per ml) significantly reduced the proliferation of dermal fibroblasts (60 +/- 8.8 vs. 100 +/- 8, mean +/- SEM, p < 0.05, n = 8) and the levels of mRNA for type I (41.5 +/- 8.7% vs 100 +/- 18, p < 0.05, n = 4) and type III (68 +/- 8.4% vs 100 +/- 4.9%, p < 0.05, n = 3) procollagen, as analyzed on northern blots. This was consistent with the reduction found in collagen in conditioned medium from treated fibroblasts. In contrast, treatment increased levels of mRNA for collagenase (241 +/- 42% vs 100 +/- 3.4, p < 0.05, n = 3) and collagenase activity (289 +/- 5.8% vs 100 +/- 10.9%, p < 0.05, n = 9) in conditioned medium. This last effect was probably not due to a reduction in TIMP-1 (tissue inhibitor of metalloproteinase-1) because levels of mRNA for this inhibitor were not lower in treated cells. The efficacy of liposome-associated IFN-alpha-2b in vitro supports the concept of the topical use of this anti-fibrogenic agent for treatment of fibroproliferative disorders.
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PMID:Liposome-associated interferon-alpha-2b functions as an anti-fibrogenic factor for human dermal fibroblasts. 920 55

In an attempt to determine if there is any overlap in local and general anaesthetic binding sites, we have examined the effects of thiopental, phenobarbital, pentobarbital, propofol, ketamine (racemic and R(+)/S(-)), alfaxalone, etomidate and halothane on [3H]tetracaine binding to rat cerebrocortical membranes. Membranes were prepared in Tris HCI 50 mmol litre-1, pH 7.4, by homogenization and centrifugation. Binding assays were performed in 1-ml volumes of Tris HCI buffer at room temperature or 37 degrees C for halothane. Binding of [3H]tetracaine was displaced dose-dependently by unlabelled tetracaine with a mean pIC50 value of 6.91 (SEM 0.07) (123 nmol litre-1). With the exception of propofol (at high concentrations), all i.v. anaesthetic agents failed to displace the binding of [3H]tetracaine. In contrast, halothane produced a dose-dependent and statistically significant reduction in total [3H]tetracaine binding at clinically achievable concentrations (0.289, 0.885 and 1.484 mmol litre-1 equivalent to 1.0, 3.1 and 5.1 rat MAC) without markedly affecting the pIC50. Collectively these data may suggest some overlap in the binding sites for [3H]tetracaine and volatile but not i.v. general anaesthetic agents.
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PMID:Effects of i.v. anaesthetic agents and halothane on [3H]tetracaine binding to rat cerebrocortical membranes. 950 82

The present study demonstrates the in vitro and in vivo adsorption of peroxidase onto titanium surfaces. Titanium foils (mean +/- SEM: 365 +/- 2 mm(2), n = 114) were incubated during 30 min with lactoperoxidase (4 mg in 5 mL 100 mM phosphate buffer pH 7). After 15 washings by H(2)O, titanium foils were incubated with o-phenylenediamine (6 mg/mL) and H(2)O(2) (7 mM) during 30 min. The reaction was then stopped by the addition of HCI 1M and the absorbance of the liquid phase was read on a spectrophotometer at 492 nm. In vitro adsorbed lactoperoxidase onto titanium surfaces was 0.70 +/- 0.05 ng/mm(2) (mean +/- SEM, n = 30). X-ray photoelectron spectroscopy confirmed the incorporation of protein nitrogen onto titanium surfaces: the nitrogen atomic percentage increased from 0.9 +/- 0.3 to 12.7 +/- 0.2% (n = 3) and from 3.7 +/- 0.1 to 14.4 +/- 0. 4% (n = 5) when titanium foils were incubated in the lactoperoxidase solution during 30 min and 24 h respectively. In vivo, oral peroxidases adsorbed on titanium healing abutments from 0.01 to 0.58 ng/mm(2) (n = 19) after 2 weeks in the oral environment.
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PMID:Adsorption of peroxidase on titanium surfaces: A pilot study. 1100 26


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