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  • 1
    Electronic Resource
    Electronic Resource
    Overproduction of inhibitory hematopoietic cytokines by lipopolysaccharide-activated peripheral blood mononuclear cells in patients with aplastic anemia (1995)
    Springer
    Annals of hematology 71 (1995), S. 281-286 
    Details
    ISSN: 1432-0584
    Keywords: Aplastic anemia ; MIP-1α ; TNF-α ; TGF-β2 ; IFN-γ
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of this study was to measure the level of cytokines produced by peripheral blood mononuclear cells (PBMNC) in patients with aplastic anemia (AA) and to determine their effect on the clonal growth of normal bone marrow (BM) cells. Twenty-one patients with AA and 11 normal controls were enrolled in this study. Medium conditioned by PBMNC of AA patients in the presence of lipopolysaccharide (LPS) was found to be suppressive to the colony growth of normal BM cells. Thus, we further determined the presence in the PBMNC-conditioned medium (CM) of both inhibitory cytokines: macrophage inflammatory protein-1α (MIP-1α), tumor necrosis factor-α (TNF-α), transforming growth factor-β2 (TGF-β2), and interferon-γ (IFN-γ), and stimulatory cytokines: interleukin-3 (IL-3) and stem cell factor (SCF). Spontaneous production of MlP-1α was higher in the AA patients than the normal controls (1887±174 pg/ml vs 1643±93 pg/ml), but the difference was not significant. After LPS stimulation, the production of MIP-1α was markedly increased in the AA patients, and its level was significantly higher than that of the normal controls (2360±149 pg/ml vs 1517±92 pg/ml, p=0.0022). The level of TNFα was also higher in the AA patients. However, IFN-γ, TGF-β2, SCF, and IL-3 were not detectable in the PBMNC-CM of either AA patients or normals. The myelopoietic suppressing effect of AA-PBMNC-CM from each AA patient was significantly blocked by pretreatment with anti-TNF-α, resulting in a colony-forming enhancement of 174%±12%. A similar effect was noted in six of 11 AA patients by pretreatment with anti-MIP-1α. We conclude that TNFα and MIP-1α can be overproduced by the PBMNC of some AA patients, which may play a role in the progression of AA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01697980
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  • 2
    Electronic Resource
    Electronic Resource
    Primary transplantation of allogeneic peripheral blood stem cell for severe aplastic anemia (1997)
    Springer
    Annals of hematology 74 (1997), S. 191-192 
    Details
    ISSN: 1432-0584
    Keywords: Key words Allogeneic PBSCT ; Bone marrow transplantation ; Aplastic anemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Primary allogeneic peripheral blood stem cell transplantation (allo-PBSCT) has not been previously described in the treatment of severe aplastic anemia (SAA). We report a patient with SAA who underwent primary allo-PBSCT with cells from her HLA-identical sibling and achieved rapid bone marrow reconstitution. The patient has been in complete remission with normal blood counts for 9 months following allo-PBSCT. This suggests that primary allo-PBSCT is a safe and effective alternative in the treatment of SAA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002770050281
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  • 3
    Electronic Resource
    Electronic Resource
    Modification of cloned brain Na+ channels by batrachotoxin (1994)
    Springer
    Pflügers Archiv 427 (1994), S. 309-316 
    Details
    ISSN: 1432-2013
    Keywords: Na+ channel ; Batrachotoxin ; Tetrodotoxin ; Benzocaine ; NaIIA channel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of batrachotoxin (BTX) on cloned α-subunit Na+ channels were examined in CHO-K1 cells (a chinese hamster ovary cell line) transfected with rat brain NaIIA cDNA. Under whole-cell patch clamp conditions, BTX shifted the voltage dependence of the activation process by about 45 mV towards the hyperpolarizing direction and eliminated the inactivating phase of Na+ currents. Repetitive depolarizations greatly facilitated the binding of BTX with NaIIA channels while the membrane was held at −100 mV. In chloramine-T-pretreated cells, the association rate of BTX binding with the NaIIA channel was 6.5-fold faster than that in untreated cells. The estimated association rate constant for BTX binding with the open form of NaIIA channel was 1.11×106 mol−1·s−1 at room temperature. BTX-modified NaIIA channels were blocked by tetrodotoxin (TTX) in a complicated manner. First, the TTX binding to the closed state of BTX-modified NaIIA channels was not voltage dependent. The K D value of TTX was measured at 8.9 nM, which was similar to that of unmodified channels (K D=14.2 nM). Second, the block of the open state of BTX-modified NaIIA channels by TTX was voltage dependent; depolarization reduced the potency of TTX block between −20 mV to +50 mV. Below −30 mV, the TTX affinity began to level off, probably because of the increased presence of the closed state. Unexpectedly, steady-state inactivation of BTX-modified NaIIA channels was minimal as measured by the two-pulse protocol, a phenomenon distinctly different from that found in GH3 cells. Neutral local anesthetic benzocaine, however, drastically enhanced the steady-state inactivation of BTX-modified NaIIA channels, with its maximal effect around −60 mV. We conclude that BTX can bind and modify the NaIIA α-subunit. However, a specific subtype of α-subunits and/or an unidentified modulating process may be required for the optimal steady-state inactivation of BTX-modified Na+ channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374539
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  • 4
    Electronic Resource
    Electronic Resource
    Slow inactivation of muscle μ1 Na+ channels in permanently transfected mammalian cells (1996)
    Springer
    Pflügers Archiv 432 (1996), S. 692-699 
    Details
    ISSN: 1432-2013
    Keywords: Key words Na+ channel ; Slow inactivation ; μ1 channel ; Chloramine-T ; Batrachotoxin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The slow inactivation of cloned muscle α-subunit Na+ channels was investigated using a Chinese hamster ovary cell line permanently transfected with rat muscle μ1 cDNA. Expression of μ1 Na+ channels was found in cells maintained for more than 6 months after transfection; 〉 70% of cells expressed ≥ 3 nA of Na+ current at +30 mV under whole-cell patch-clamp conditions. As expected, Na+ currents in these cells were blocked by tetrodotoxin as well as by μ-conotoxin. After prolonged depolarization (10 s at +30 mV) to inactivate voltage-gated Na+ channels, Na+ currents slowly reappeared over a time course of several minutes, during which time the cell was repolarized to the holding potential of −100 mV. This recovery from slow inactivation was best fitted by a double exponential function with τ1 = 2.5 s (amplitude = 53%) and τ2 = 83.4 s (amplitude = 38%). In contrast, the development of slow inactivation at +30 mV was best fitted by a single exponential function, with τ = 3.0 s. Steady-state slow inactivation (s ∞) had a midpoint potential (s 0.5) of −52 mV and a slope factor (k) of 7.8 mV. Elimination of fast inactivation by treatment with chloramine-T accelerated the development of slow inactivation significantly (by ≈four fold) but had little effect on recovery or on steady-state slow inactivation. Finally, as in cloned brain NaIIA Na+ channels, batrachotoxin abolished both fast and slow inactivation of μ1 Na+ channels. These results together suggest that slow inactivation takes place in the α-subunit of μ1 muscle Na+ channels and is governed by a μl protein region different from that governing fast inactivation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050187
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    Paper (German National Licenses)
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