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  • 1
    Electronic Resource
    Electronic Resource
    An autopsy case of acute porphyria with a decrease of both uroporphyrinogen I synthetase and ferrochelatase activities (1984)
    Springer
    Acta neuropathologica 64 (1984), S. 6-11 
    Details
    ISSN: 1432-0533
    Keywords: Acute porphyria ; Porphyric neuropathy ; Axonal degeneration ; Uroporhyrinogen I synthetase ; Ferrochelatase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An autopsy case of a 37-year-old woman with acute porphyria is reported. The patient began to complain of severe menstrual pains, and later developed serious peripheral neuropathy and various autonomic nervous symptoms. The autopsy revealed a marked loss and degeneration of axons and myelin sheaths in the peripheral nervous system (PNS), and prominent central chromatolysis of the spinal anterior horn cells. The predominant process of the peripheral neuropathy appeared to be axonal degeneration. Biochemical analysis showed a marked increase of delta-aminolevulinic acid (ALA), porphobilinogen, uroporphyrin, and coproporphyrin in the urine, and an increase of coproporphyrin and protoporphyrin in the stools and blood. In the analysis of the enzymatic activities of the liver and bone narrow, the activity of ALA synthetase (ALA-S) was markedly increased, and the activities of both uroporphyrinogen I synthetase (URO-S) and ferrochelatase were decreased. It was characteristic in this case that the enzymatic abnormalities found in both acute intermittent porphyria (AIP) and variegate porphyria (VP) coexisted. Biochemical analysis of the sciatic nerve showed an increase of ALA-S activity and a decrease of both URO-S and ALA dehydrase activities. This was the first report that indicated the presence of abnormal activities of the heme biosynthetic enzymes in the peripheral nerves of porphyric patients. The possibility was discussed that these enzymatic abnormalities of the heme biosynthesis in the peripheral nerve itself might be strongly related to the pathogenesis of the porphyric neuropathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00695599
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  • 2
    Electronic Resource
    Electronic Resource
    The increase of thiobarbituric acid reacting substances in rats with experimental chronic hypoxia (1982)
    Springer
    Cellular and molecular life sciences 38 (1982), S. 312-313 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Feeding under conditions of reduced oxygen supply prompted an increase in serum, arterial and brain tissue levels of thiobarbituric acid (TBA)-reacting substances. These observations indicated the possibility that hypoxia might be one of the factors predisposing to the accumulation of lipid peroxide.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01949361
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  • 3
    Electronic Resource
    Electronic Resource
    Immunopetentiators and the protection they give against carbon tetrachloride hepatotoxicity (1982)
    Springer
    Cellular and molecular life sciences 38 (1982), S. 501-502 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Immunopotentiators such as BCG, levamisole, PS-K and OK-432 prevent carbon tetrachloride (CCl4) hepatotoxicity, and in spite of exposure to CCl4 the liver tissue levels of thiobarbituric acid (TBA) reactive substances were not increased in rats pretreated with such immunopotentiators.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01952661
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  • 4
    Electronic Resource
    Electronic Resource
    Inhibitory effects of interferon-γ on the heterologous desensitization of β-adrenoceptors by transforming growth factor-β1 in tracheal smooth muscle (2003)
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 33 (2003), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Transforming growth factor-β1 (TGF-β1) is generally considered to play an important role in the pathogenesis of chronic inflammation and fibrosis.Objective and methods This study was designed to determine mechanisms of reduced responsiveness of guinea-pig tracheal smooth muscle to β-adrenoceptor agonists by TGF-β1, using isometric tension records and tissue cAMP measurement. Moreover, we examined the involvement of the signal transduction processes of TGF-β superfamily in the desensitization of β-adrenoceptors.Results After exposure to 0.2–2000 pm TGF-β1 for 4–8 h, the inhibitory effects of 1 µm isoprenaline (ISO) and 10 µm forskolin on 1 µm MCh-induced contraction were markedly reduced in a concentration-dependent fashion. The desensitization by TGF-β1 was greater against ISO than for forskolin. The values of EC75 for the curves for ISO after exposure to the normal bathing solution and TGF-β1 were 0.039 ± 0.02 and 0.38 ± 0.28 µm, respectively. The values of EC50 for the curves for forskolin under these conditions were 0.50 ± 0.12 and 0.89 ± 0.21 µm, respectively. On the other hand, the inhibitory effects of phosphodiesterase inhibitors such as theophylline and rolipram were not attenuated after exposure to TGF-β1. Concentration–inhibition curve for ISO was shifted to the right after exposure to 2000 pm TGF-β1 for 8 h more than that curve for forskolin. In contrast, the curve for theophylline was not shifted to the right by TGF-β1. When the tissues were incubated with TGF-β1 in the presence of IFN-γ, an intracellular antagonist of TGF-β signalling, IFN-γ inhibited the reduced response to ISO and forskolin after exposure to TGF-β1 in a concentration-dependent fashion. After exposure to TGF-β1, the effects of cAMP accumulation of ISO was significantly reduced, however, neither forskolin-nor theophylline-induced cAMP accumulation was affected. IFN-γ had no significant effect on cAMP accumulation either to ISO or forskolin.Conclusions Impairment of the β-adrenoceptors/adenylyl cyclase pathway are involved in heterologous desensitization of β-adrenoceptors induced by TGF-β1 in airway smooth muscle. IFN-γ functionally suppresses this phenomenon via cAMP-independent processes. Phosphodiesterase is still intact under this condition.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2222.2003.01681.x
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  • 5
    Electronic Resource
    Electronic Resource
    Passivation of oxygen-related donors in microcrystalline silicon by low temperature deposition (2001)
    Woodbury, NY : American Institute of Physics (AIP)
    Applied Physics Letters 78 (2001), S. 2330-2332 
    Details
    ISSN: 1077-3118
    Source: AIP Digital Archive
    Topics: Physics
    Notes: Low-temperature processing for high-performance solar cells based on hydrogenated microcrystalline silicon (μc-Si:H) has been developed using a conventional rf plasma-enhanced chemical vapor deposition (PECVD) technique at an excitation frequency of 13.56 MHz under a high deposition pressure condition. Among pin type solar cells, it is found that deposition temperature of i-layer at 140 °C is effective particularly for improving open circuit voltage (Voc), surprisingly without deteriorating short circuit current or fill factor. Carrier density of undoped μc-Si abruptly decreases for deposition temperatures lower than 180 °C, and the improvement of Voc is ascribed to a decrease of shunt leakage current arising from the oxygen-related donors. This implies that oxygen-related donors can be passivated at low deposition temperatures and that hydrogen plays an important role for the passivation. We propose a simple model for the hydrogen passivation of oxygen related donors. We apply this passivation technique to solar cells, and consequently a conversion efficiency of 8.9% (Voc=0.51 V, Jsc=25 mA/cm−1, FF=0.70) has been obtained in spite of an oxygen concentration of 2×1019 cm−3 in combination with device optimization such as a p-layer. Effect of deposition temperature of i-layer upon other solar cell parameter, short circuit current, and fill factor is also discussed. © 2001 American Institute of Physics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.1364657
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  • 6
    Electronic Resource
    Electronic Resource
    A new mechanism for anti-inflammatory actions of proton pump inhibitors – inhibitory effects on neutrophil–endothelial cell interactions (2000)
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 14 (2000), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: Neutrophil–endothelial cell interactions mediated by adhesion molecules may be involved in gastric mucosal inflammation associated with Helicobacter pylori or nonsteroidal anti-inflammatory drugs. Aim: To investigate the effects of proton pump inhibitors and histamine-2 receptor antagonists (HRA) on neutrophil-endothelial cell adhesive interactions induced by H. pylori water extract (HPE) or interleukin-1β (IL-1β). Methods: Human peripheral neutrophils and umbilical vein endothelial cells were incubated with either proton pump inhibitors (lansoprazole and omeprazole) or HRA (famotidine and ranitidine). Neutrophil surface expression of CD11b and CD18 and endothelial cell intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) were assessed by flow cytometry and an enzyme immunoassay, respectively. Neutrophil adherence was defined as the ratio of exogenous neutrophils that adhered to the endothelial monolayers. Results: The expression of CD11b and CD18 on neutrophils and neutrophil-dependent adhesion to endothelial cells elicited by HPE were inhibited by lansoprazole and omeprazole at clinical relevant doses, and the expression of ICAM-1 and VCAM-1 on endothelial cells and endothelial-dependent neutrophil adherence induced by IL-1β were also inhibited by lansoprazole and omeprazole at similar doses. Famotidine and ranitidine had no effect on neutrophil–endothelial cell interactions. Conclusions: These results indicate that proton pump inhibitors can attenuate neutrophil adherence to endothelial cells via inhibiting the expression of adhesion molecules, suggesting that proton pump inhibitors may have anti-inflammatory activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2000.014s1074.x
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  • 7
    Electronic Resource
    Electronic Resource
    Protective role of intracellular glutathione against nitric oxide-induced necrosis in rat gastric mucosal cells (2000)
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 14 (2000), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: Nitric oxide synthase activity is increased in the stomach in association with Helicobacter pylori infection and portal hypertension, but the mechanism by which nitric oxide contributes to mucosal damage remains unclear. Aim: To examine whether nitric oxide injures gastric mucosal cells and whether cellular glutathione affects nitric oxide-induced cytotoxicity. Methods: A confluent monolayer of RGM-1 gastric mucosal cells was exposed to nitric oxide donors (NOC5 or NOC12). Cell viability was determined by trypan blue dye exclusion, lactate dehydrogenase release and supravital staining with Hoechst 33342 and propidium iodide. The kinetics of the reduced/oxidized forms of glutathione were also measured, as well as the effect of glutathione-depletion or glutathione-precursor treatment on nitric oxide-induced cytotoxicity. Results: Excess exogenous nitric oxide produced by NOC5 or NOC12 induced necrosis in RGM-1 cells in a time- and concentration-dependent manner. The level of reduced glutathione drastically decreased prior to the loss of cell viability and remained low, but oxidized glutathione was not affected. Glutathione depletion increased necrosis of both NOCs in an NOC-concentration-related fashion, while pre-treatment with γ-glutamylcysteine ethyl ester reduced their necrotic susceptibility. Conclusion: Exogenous nitric oxide induced necrosis in gastric mucosal cells, and intracellular reduced glutathione protects gastric mucosal cells from damage by nitric oxide.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2000.014s1145.x
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  • 8
    Electronic Resource
    Electronic Resource
    Quantification of bone volume on radiographs using NIH Image (2000)
    Springer
    Modern rheumatology 10 (2000), S. 220-224 
    Details
    ISSN: 1439-7609
    Keywords: Key words Radiograph ; Rheumatoid arthritis ; Bone volume ; NIH Image ; Computer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We attempted to quantify periarticular bone atrophy from radiographs of the proximal phalanx in patients with rheumatoid arthritis (RA) by means of the National Institutes of Health (NIH) Image computer program. The degree of brightness or darkness in four squares, each 20 × 20 pixels, in the right third proximal phalanx was measured using NIH Image, and the mean value of the 400 pixels was defined as the brightness/darkness index (BDI). The BDI was used to express bone volume. The BDI value was set at zero for an area of complete darkness and at 255 for an area of maximum brightness. The mean coefficient of variation in our hospital was 2.28%. The BDI was measured in 54 RA patients and 146 normal volunteers. The mean BDI at the midpoint of the diaphysis was 100 in RA patients and 176 in normal volunteers, while at the medial side of the proximal end it was 75 and 145, respectively. The difference between normal volunteers and RA patients was greatest in younger people. In some young RA patients, the BDI was significantly low at the medial side of the proximal end, clearly demonstrating periarticular bone atrophy. Periarticular bone atrophy can be quantified using the NIH Image computer program.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s101650070006
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  • 9
    Electronic Resource
    Electronic Resource
    Increase of δ-Aminolevulinic Acid Dehydratase (ALAD) in rat erythrocytes in lead poisoning (1983)
    Springer
    Archives of toxicology 52 (1983), S. 1-11 
    Details
    ISSN: 1432-0738
    Keywords: Lead poisoning ; Erythrocytes ; δ-Aminolevulinic acid dehydratase(ALAD) ; Rat ; Porphyrins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The well known fact that the activity of δ-aminolevulinic acid dehydratase (ALAD: EC 4.2.1.24) is reduced in red cells of animals with lead poisoning was found to be upset, by using a modified method of Gibson's original procedure, for determination of activated ALAD activity. The modified method involves addition of 0.2 mM Zn2+ and then preheating the enzyme solution at 60° C for 5 min before following Gibson's original procedure. With this methodological modification, the ALAD activity of erythrocytes of rats poisoned with lead was found increased. Furthermore, the enzyme was purified from the peripheral blood of lead-poisoned rats. ALAD protein in peripheral blood was also determined by single radial immuno diffusion using rabbit anti-serum raised against rat liver ALAD. As the result, the ALAD activity obtained from the modified method was found to be directly proportional to the absolute amount of enzyme proteins determined both by chemically and immunochemically. The modified method for measuring true ALAD content in blood cells in lead poisoning is more reliable than previous ones.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00317977
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  • 10
    Electronic Resource
    Electronic Resource
    Effect of a protein-bound polysaccharide PS-K on the complement system (1983)
    Springer
    Research in experimental medicine 182 (1983), S. 85-94 
    Details
    ISSN: 1433-8580
    Keywords: Protein-bound polysaccharide ; PS-K ; Complement
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A protein-bound polysaccharide from mycelia ofCoriolus versicolor PS-K, clinically used as an immunomodulator, has been shown to restore the decreased cellular immune response and to exhibit host-mediated antitumor activity. In this experiment, PS-K was found to increase serum complement level in guinea pig and in human without malignancy, when hemolytic assay of complement was performed using sensitized sheep erythrocytes for the classical pathway activity and unsensitized rabbit erythrocytes for the alternative pathway activity. Assay of complement components revealed increase in C3 level in guinea pig, but no significant changes in Clq, C4, C3, properdin, C3 activator, and C $$\bar 1$$ -inhibitor in human, while C5 and C9 were depressed. Conversion ofβ1C toβ1A was observed in the 7th day's plasma of these patients by crossed immunoelectrophoresis. Biosynthesis of guinea pig C3 was accelerated by administration of PS-K, but that of C4 was not affected. These evidences suggested that PS-K might potentiate immune response of the host by elevating serum complement level, in addition to the activation of the complement system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01851114
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