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  • 1
    Electronic Resource
    Electronic Resource
    Oxidation of ruthenium(II) and ruthenium(III) porphyrins. Crystal structures of .mu.-oxo-bis[(p-methylphenoxo)(meso-tetraphenylporphyrinato)ruthenium(IV)] and ethoxo(meso-tetraphenylporphyrinato)(ethanol)ruthenium(III)-bisethanol (1984)
    s.l. : American Chemical Society
    Journal of the American Chemical Society 106 (1984), S. 5151-5163 
    Details
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ja00330a020
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  • 2
    Electronic Resource
    Electronic Resource
    Expression of the mutant gene for L-gulono-γ-lactone oxidase in scurvy-prone rats (1989)
    Springer
    Cellular and molecular life sciences 45 (1989), S. 126-129 
    Details
    ISSN: 1420-9071
    Keywords: L-gulono-γ-lactone oxidase ; ascorbic acid deficiency ; enzyme defect ; rat ; nuclei acid hybridization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary A mutant strain of Wistar rats with L-gulono-γ-lactone oxidase deficiency has recently been established. To investigate this deficiency by DNA and RNA blot hybridization analyses, a fragment of a previously cloned cDNA encoding rat L-gulono-γ-lactone oxidase was used as a probe. When genomic DNA of the mutant rat was digested with several restriction enzymes, the probe hybridized to fragments of the same sizes as those produced from DNA of normal rats. Poly(A)+RNA from the liver of the mutant rat was found to contain an L-gulono-γ-lactone oxidase-specific mRNA of a normal size at a comparable level to that of normal rats. An in vitro translation experiment revealed that the mRNA programmed the synthesis of an enzyme protein which had the same molecular weight as that of the translational product of the normal mRNA, although the amount synthesized was markedly reduced as compared with that synthesized with the normal mRNA. In accordance with this observation, a very low but definite degree of L-gulono-γ-lactone oxidase activity was detected in the microsomes of the mutant rat by a newly developed, highly sensitive method.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01954844
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  • 3
    Electronic Resource
    Electronic Resource
    Decreased activity of cytochromec oxidase in the macular mottled mouse: an immuno-electron microscopic study (1989)
    Springer
    Acta neuropathologica 77 (1989), S. 465-471 
    Details
    ISSN: 1432-0533
    Keywords: Menkes kinky hair syndrome ; Macular mottled mouse ; Mitochondrion ; Cytochromec oxidase ; Gold-labeling immuno-electron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The macular mottled mouse is a murine model of the kinky hair syndrome, characterized by a deficiency in copper transport. Cytochromec oxidase (CCO), a respiratory enzyme, is located in the inner mitochondrial membrane and consists of seven subunits, along with copper and iron. Biochemical and histochemical findings indicated that CCO activity was decreased in the cerebellum of the macular mottled mice but not in that of the controls. Immunocytochemical analysis, using anti-CCO and anti-complex III rabbit sera, revealed that CCO in the macular mottled mice was stained more weakly than that in the controls. Immuno-electron microscopic examination of CCO and complex III, using a method of gold labeling, was also performed. In the control mice, a high concentration of gold particles present over CCO and complex III could be seen in the inner mitochondrial membrane. The number of CCO-labeled gold particles was remarkably less, however, in the macular mottled mice, while no significant difference was found in the labeling of complex III between the two groups. It may concluded that the very low CCO enzyme content in the macular mottled mouse results not only from a copper transport disorder but also from a CCO protein synthesis disorder which impairs the localization of CCO protein in the cerebellum.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687247
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  • 4
    Electronic Resource
    Electronic Resource
    Functional respiratory chain studies in mitochondrial cytopathies. Support for mitochondrial DNA heteroplasmy in myoclonus epilepsy and ragged red fibers (MERRF) syndrome (1991)
    Springer
    Acta neuropathologica 81 (1991), S. 318-323 
    Details
    ISSN: 1432-0533
    Keywords: Mitochondrial disease ; Myoclonus epilepsy and ragged red fibers (MERRF) syndrome ; Mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) syndrome ; Polarographic studies ; Immunoblot studies
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Mitochondrial respiratory chain function was investigated with polarographic and enzymatic studies, and correlated with immunoblot studies using a battery of probes against respiratory chain holocomplexes in a series of patients with myoclonus epilepsy and ragged red fibers (MERRF) syndrome. State III respiration rates in intact skeletal muscle mitochondria were normal in two cases, suggested site I deficiency in one case and a midrespiratory defect in another. Immunological studies of complex I showed reduced levels of several subunits with the apparent absence of two bands (which at 45 and 42 kDa, coincide with the predicted electrophoretic mobility of the ND5 gene product) in one case. Complex I, III and IV composition was normal in the other three cases indicating no major disruption of complex assembly. A differing severity of skeletal muscle respiratory chain impairment in a group of unrelated patients with severe cerebral clinical involvement is best explained by uneven tissue distribution between brain and muscle of a heteroplasmic mtDNA mutation. The relationship between MERRF and mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) encephalopathies is reappraised by extension of this hypothesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00305874
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  • 5
    Electronic Resource
    Electronic Resource
    Intracellular pH regulation in the mouse lacrimal gland acinar cells (1988)
    Springer
    The journal of membrane biology 101 (1988), S. 73-81 
    Details
    ISSN: 1432-1424
    Keywords: intracellualr pH ; lacrimal gland ; amiloride ; DIDS ; Na+/H+ antiport ; Cl−/HCO 3 − ; antiport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Intracellular pH (pH i ) of the acinar cells of the isolated, superfused mouse lacrimal gland has been measured using pH-sensitive microelectrodes. Under nonstimulated condition pH i was 7.25, which was about 0.5 unit higher than the equilibrium pH. Alterations of the external pH by ±0.4 unit shifted pH i only by ±0.08 unit. The intracellular buffering value determined by applications of 25mm NH 4 + and bicarbonate buffer solution gassed with 5% CO2/95% O2 was 26 and 46mm/pH, respectively Stimulation with 1 μm acetylcholine (ACh) caused a transient, small decrease and then a sustained increase in pH i . In the presence of amiloride (0.1mm) or the absence of Na+, application of ACh caused a significant decrease in pH i and removal of amiloride or replacement with Na+-containing saline, respectively, rapidly increased the pH i . Pretreatment with DIDS (0.2mm) did not change the pH i of the nonstimulated conditions; however, it significantly enhanced the increase in pH i induced by ACh. The present results showed that (i) there is an active acid extrusion mechanism that is stimulated by ACh; (ii) stimulation with ACh enhances the rate of acid production in the acinar cells; and (iii) the acid extrusion mechanism is inhibited by amiloride addition to and Na+ removal from the bath solution. We suggest that both Na+/H+ and HCO 3 − /Cl− exchange transport mechanisms are taking roles in the intracellular pH regulation in the lacrimal gland acinar cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01872822
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  • 6
    Electronic Resource
    Electronic Resource
    Characterization of Ryanodine-sensitive Ca2+ Release from Microsomal Vesicles of Rat Parotid Acinar Cells: Regulation by Cyclic ADP-ribose (1997)
    Springer
    The journal of membrane biology 156 (1997), S. 231 -239 
    Details
    ISSN: 1432-1424
    Keywords: Key words:45Ca2+ efflux — Caffeine — Ruthenium red — Heparin — Endoplasmic reticulum — Thapsigargin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract. We have measured ryanodine (caffeine)-sensitive 45Ca2+ release from isolated microsomal vesicles of endoplasmic reticulum prepared from rat parotid acinar cells. After a steady state of ATP-dependent 45Ca2+ uptake, the addition of caffeine (40 mm), ryanodine (10∼500 μm) or an NAD+ metabolite, cyclic ADP-ribose (cADPR, 4 μm) released about 10% of the 45Ca2+ that had been taken up. The 45Ca2+ release was not inhibited by heparin, an antagonist of IP3 receptor. The effects of caffeine, ryanodine and cADPR on 45Ca2+ release were also tested in the presence of thapsigargin (TG), an inhibitor of microsomal Ca2+-ATPase. When caffeine (10∼40 mm), ryanodine (10 μm) or cADPR (1∼10 μm) was added in the medium with 100 nm TG, a significant 45Ca2+ release was seen, while higher concentrations of ryanodine (〉100 μm) did not cause any 45Ca2+ release in the presence of TG. The initial rate of caffeine (40 mm)-induced 45Ca2+ release was increased by a pretreatment with 10 μm ryanodine, whereas the caffeine-induced 45Ca2+ release was strongly inhibited by the presence of a higher concentration (500 μm) of ryanodine. cADPR-induced 45Ca2+ release was also inhibited by 500 μm ryanodine. Caffeine (40 mm)- or cADPR (4 μm)-induced 45Ca2+ release was abolished by a presence of ruthenium red (50∼100 μm). The presence of a low concentration (0.5 μm) of cADPR shifted the dose-response curve of caffeine-induced 45Ca2+ release to the left. These results indicate the presence of a ryanodine sensitive Ca2+ release mechanism in the endoplasmic reticulum of rat parotid acinar cells that is distinct from the IP3-sensitive Ca2+ channel and is activated by caffeine, cADPR and a low concentration (10 μm) of ryanodine, but is inhibited by higher concentrations (〉100 μm) of ryanodine and ruthenium red. The properties of the ryanodine-sensitive mechanism are similar to that of the ryanodine receptor as described in muscle cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002329900203
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  • 7
    Electronic Resource
    Electronic Resource
    Characterization of two different Ca2+ uptake and IP3-sensitive Ca2+ release mechanisms in microsomal Ca2+ pools of rat pancreatic acinar cells (1995)
    Springer
    The journal of membrane biology 144 (1995), S. 111-120 
    Details
    ISSN: 1432-1424
    Keywords: Thapsigargin ; Vanadate ; Ca2+ pump ; Ca2+ ATPase ; SERCA ; Endoplasmic reticulum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract We have examined the effect of the Ca2+ (Mg2+)-ATPase inhibitors thapsigargin (TG) and vanadate on ATP-dependent 45Ca2+ uptake into IP3-sensitive Ca2+ pools in isolated microsomes from rat pancreatic acinar cells. The inhibitory effect of TG was biphasic. About 40–50% of total Ca2+ uptake was inhibited by TG up to 10 nm (apparent Ki≈4.2 nm, Ca2+ pool I). An additional increase of inhibition up to 85–90% of total Ca2+ uptake could be achieved at 15 to 20 nm of TG (apparent Ki≈12.1 nm, Ca2+ pool II). The rest was due to TG-insensitive contaminating plasma membranes and could be inhibited by vanadate (apparent Ki≈10 μm). In the absence of TG, increasing concentrations of vanadate also showed two phases of inhibition of microsomal Ca2+ uptake. About 30–40% of total Ca2+ uptake was inhibited by 100 μm of vanadate (apparent Ki≈18 μm, Ca2+ pool II). The remaining 60–70% could be inhibited either by vanadate at concentrations up to 1 mm (apparent Ki≈300 μm) or by TG up to 10 nm (Ca2+ pool I). The amount of IP3-induced Ca2+ release was constant at ≈25% over a wide range of Ca2+ filling. About 10–20% remained unreleasable by IP3. Reduction of IP3 releasable Ca2+ in the presence of inhibitors showed similar dose-response curves as Ca2+ uptake (apparent Ki≈ 3.0 nm for IP3-induced Ca2+ release as compared to ≈4.2 nm for Ca2+ uptake at TG up to 10 nm) indicating that the highly TG-sensitive Ca2+ pump fills the IP3-sensitive Ca2+ pool I. At TG concentrations 〉10 nm which blocked Ca2+ pool II the apparent Ki values were ≈11.3 and ≈12.1 nm, respectively. For inhibition by vanadate up to 100 μm the apparent Ki values were ≈18 μm for Ca2+ uptake and ≈7 μm for Ca2+ release (Ca2+ pool II). At vanadate concentrations up to 1 mm the apparent Ki values were ≈300 and ≈200 μm, respectively (Ca2+ pool I). Both Ca2+ pools I and II also showed different sensitivities to IP3. Dose-response curves for IP3 in the absence of inhibitors (control) showed an apparent Km value for IP3 at 0.6 μm. In the presence of TG (inhibition of Ca2+ pool I) the curve was shifted to the left with an apparent Km for IP3 at 0.08 μm. In the presence of vanadate (inhibition of Ca2+ pool II), the apparent Km for IP3 was 2.1 μm. These data allow the conclusion that there are at least three different Ca2+ uptake mechanisms present in pancreatic acinar cells: TG- and IP3 insensitive but highly vanadate-sensitive Ca2+ uptake occurs into membrane vesicles derived from plasma membranes. Two Ca2+ pools with different TG-, vanadate- and IP3-sensitivities are most likely located in the endoplasmic reticulum at different cell sites, which could have functional implications for hormonal stimulation of pancreatic acinar cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00232797
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  • 8
    Electronic Resource
    Electronic Resource
    Immunological and haematological changes during high-dose immunoglobulin therapy in an infant with autoimmune neutropenia (1987)
    Springer
    European journal of pediatrics 146 (1987), S. 412-415 
    Details
    ISSN: 1432-1076
    Keywords: Autoimmune neutropenia ; High-dose immunoglobulin therapy ; Antineutrophil autoantibodies ; Flow cytometry neutrophil-bound IgG
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract High-dose immunoglobulin (HD-Ig) therapy was given to an infant with autoimmune neutropenia (AIN), and antineutrophil autoantibodies (ANAA). The patient's absolute neutrophil count in peripheral blood increased from 300/ mm3 to 3000–4000/mm3 7 days after treatment. Although the neutrophil count gradually decreased thereafter, transient increases were observed after each single booster infusion repeated at 3-week intervals. By continuing this treatment, clinical symptoms were markedly alleviated, and the patient's susceptibility to infection was reduced. The increase in neutrophils showed a positive correlation with the increase in serum IgG, and with the increase in the ratio of T helper/T suppressor cells. The neutrophil-bound IgG level and serum lysozyme level were decreased after HD-Ig therapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00444951
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  • 9
    Electronic Resource
    Electronic Resource
    Emergency Evacuation of Expanding Intracerebral Haemorrhage in Parahaemophilia (Coagulation Factor V Deficiency) (1999)
    Springer
    Acta neurochirurgica 141 (1999), S. 667-668 
    Details
    ISSN: 0942-0940
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007010050359
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  • 10
    Electronic Resource
    Electronic Resource
    Surgical experience with massive lobar haemorrhage caused by cerebral amyloid angiopathy (1995)
    Springer
    Acta neurochirurgica 132 (1995), S. 48-52 
    Details
    ISSN: 0942-0940
    Keywords: Intracerebral haemorrhage ; spontaneous cerebral haemorrhage ; amyloid angiopathy ; surgery
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Nineteen patients with massive lobar haemorrhage without angiographic lesions received direct or stereotactic surgery, and biopsy specimens were examined histologically. Ten patients (53%) were found to have vessels positive for Congo-red staining, and demonstrating amyloid angiopathy. In the patients with amyloid angiopathy, CT scan and surgical findings were investigated. Subarachnoid haemorrhage (9/10), irregularly shaped haematoma (9/10) and fluid-blood density level in the haematoma cavity (7/10) were frequently found on CT scan. The characteristic surgical findings in patients treated by direct surgery were subarachnoid haemorrhage adjacent to intracerebral haematoma (8/8) and the existence of a tangle of vessels in the haematoma cavity (4/8). Evacuation of haematomas was relatively easy, and difficulty of haemostasis was not encountered during surgery.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01404847
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