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  • 1
    Electronic Resource
    Electronic Resource
    College Park, Md. : American Institute of Physics (AIP)
    The Journal of Chemical Physics 101 (1994), S. 1202-1218 
    ISSN: 1089-7690
    Source: AIP Digital Archive
    Topics: Physics , Chemistry and Pharmacology
    Notes: Evidence for the formation of NeMu*, an isotopic analog of the Rydberg molecule NeH*, has been obtained from the observation of chemiluminescent emission in the near-infrared region. This is the first spectroscopic detection of a muonium-containing molecule. NeMu* was formed by stopping a 4 MeV muon (μ+) beam in a target vessel containing 1–6 atm of Ne and ∼1 Torr Ar. The wavelength spectrum of the emission, from ∼680–1000 nm, was measured using a variable-wavelength filter, with a resolution of ±12.5 nm. Lower resolution spectra were also taken with a series of long pass filters. A complete histogram of photon events vs time was collected for each wavelength. Two strong transitions are observed, centered at 818 and 943 nm. Identification of NeMu* was made by a comparison of the experimental spectrum with a simulated spectrum based on detailed ab initio calculations, extended to higher excitation levels than had heretofore been reported. Both experimental and theoretical results are reported here. Although the mechanism by which the emitting states in NeMu* are formed remains unclear, radiolysis effects appear to play a dominant role, indicating that NeMu+ (the product of muon thermalization in Ne) undergoes charge exchange with metastable Ar* and/or is neutralized by a spur electron, both species produced during the slowing down of the high energy muon.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1572-9540
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract Near-infrared chemiluminescent emission from NeMu*, the analogue of the Rydberg molecule NeH, has been observed in Ne, Ar, and Ne/Ar gas mixtures. Three temporally distinct features were observed: First, a large sharp emission peak at time zero, observed in all gases (Ne, He, N2, Ar), is assigned to scintillation light during muon thermalization, probably caused by spur electrons. Second, a lowintensity broad region observed in all gases is attributed to e+ from muon decay. Finally, NeMu in 1–6 atm Ne with 0.1–2 torr Ar appeared as a high intensitydelayed emission, whose width and intensity depended linearly on the Ar concentration. Its wavelength spectrum from 680–960 nm was measured. Although questions remain as to how NeMu* is formed, the precursor is likely Neμ +. Possible electron donors include metastable Ar* (3 P 2 or3 P 0) and long-lived free (spur) electrons.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    BJOG 101 (1994), S. 0 
    ISSN: 1471-0528
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    BJOG 101 (1994), S. 0 
    ISSN: 1471-0528
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 57 (1991), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The incorporation of enkephalin-containing peptides (ECPs) derived from proenkephalin into chromaffin vesicles was examined in primary cultures of adrenal medullary chromaffin cells. Cells were pulse-labeled with [35S]methionine and chased for periods up to 24 h. Chromaffin vesicles in cell homogenates were then fractionated by density gradient centrifugation and the presence of [35S]Met-enkephalin sequences in gradient fractions determined. 35S-ECPs were incorporated into particles suggestive of immature vesicles within 1–2 h after radiolabeling. Vesicle maturation, measured by co-equilibration of 35S-ECPs and total ECPs in the gradients, was complete within 9–12 h and was unaffected by treatments that increase proenkephalin synthesis. Incorporation of [35S]chromogranin A into chromaffin vesicles followed a similar time course, but 35S-labeled dopamine β-hydroxylase was much more slowly incorporated, possibly reflecting differences in incorporation of membrane and soluble components. In summary, the data demonstrate that ECPs are rapidly sequestered in immature chromaffin vesicles, a process unaltered by changing rates of proenkephalin synthesis.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 56 (1991), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In some animal models of ischemia, neuronal degeneration can be prevented by the selective antagonism of the N-methyl-D-aspartate (NMDA) glutamate receptor sub-type, suggesting that glutamate released during ischemia causes injury by activating NMDA receptors. The rat hippocampal slice preparation was used as an in vitro model to study the pharmacology of glutamate toxicity and investigate why NMDA receptors are critical in ischemic injury. Acute toxicity was assessed by quantifying the inhibition of protein synthesis, which we confirmed by autoradiography to be primarily neuronal. The effect of NMDA was prevented by the specific antagonists MK-801 and ketamine, as well as by the less selective antagonist kynurenic acid. The less selective antagonists kynurenic acid and 6,7-dinitroquinoxaline-2,3-dione antagonized the effects of quisqualate and NMDA. In contrast to previous observations with dissociated neurons in tissue culture, the toxicity of glutamate was unaffected by antagonists, regardless of the glutamate concentration, the duration of exposure, or the presence of magnesium. The high concentration of glutamate required to inhibit protein synthesis and the inability of receptor antagonists to block the effect of glutamate suggest that either glutamate acts through a non-receptor-mediated mechanism, or that the receptor-mediated nature of glutamate effects are masked in the slice preparation, perhaps by the glial uptake of glutamate. The altered physiology induced by ischemia must potentiate the neurotoxicity of glutamate, because we observed with a brain slice preparation that only high concentrations of glutamate caused neurotoxicity in the presence of oxygen and glucose and that these effects were not reversed by glutamate receptor antagonists.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 60 (1993), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Several synaptic vesicle proteins including synap-tophysin and p65/synaptotagmin are expressed by the pheochromocytoma cell line PC12. Stimulation of these cells with nerve growth factor for 7 days induces morphologic neuronotypic differentiation, but the levels of synaptophysin are markedly reduced. Stimulation with cyclic AMP analogs also produces neuronotypic differentiation of PC12 cells, and the degree of morphologic differentiation induced by these agents parallels their ability to effect reduction in synaptophysin levels. By contrast, levels of p65/synaptotagmin are increased following neuronotypic differentiation. The contrasting effects of neuronotypic differentiation on levels of synaptophysin and p65/synaptotagmin indicate potential differences in the regulation of these proteins in PC12 cells. Immunocytochemical labeling of undifferentiated PC12 cells reveals concentrations of synaptophysin in the perinuclear region. After neuronotypic differentiation, there is reduction in perinuclear labeling and concentration of label in swellings along PC12 cell processes. At the ultra-structural level, synaptophysin labeling is found on similar organelles in both undifferentiated and nerve growth factor-stimulated PC12 cells. Although the highest labeling densities were seen on small clear vesicles, specific labeling was also seen on dense core vesicles. The presence of synaptophysin on both small clear vesicles and dense core vesicles indicates potential functional similarities in these vesicle types. The changes in the levels and immunocytochemical distribution of synaptophysin after neuronotypic differentiation suggest possible functional heterogeneity among morphologically similar populations of small clear vesicles.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1471-0528
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Objective To determine whether circulating levels of cell adhesion molecules, markers of endothelial damage and leucocyte activation, were increased in pre-eclampsia.Design Serum was prepared from peripheral venous blood and stored at –70°C. The cell adhesion molecules, VCAM-1, E-Selectin and ICAM-1, were measured by ELISA.Setting Department of Obstetrics and Gynaecology, Royal Infirmary, Glasgow.Subjects Sixteen primigravid women with pre-eclampsia were recruited for the study. The pre-eclampsia group were compared with 18 healthy primigravid women with uncomplicated pregnancies.Results The pre-eclamptic group had significantly higher serum levels of the cell adhesion molecule VCAM-1 (t= 3.673; P 〈 0.001). There were no significant differences in the adhesion molecules ICAM-1 or E-Selectin.Conclusions Endothelial damage and dysfunction are common to all the pathological features of pre-eclampsia. This study shows that concentrations of cell adhesion molecules, which indicate leucocyte-endothelial attachment and activation, are elevated in the serum of patients with pre-eclampsia. Such increases in soluble circulating cell adhesion molecules may reflect increased expression of these molecules on the endothelium and thereby explain the mechanism for leucocyte activation in pre-eclampsia.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1471-0528
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    BJOG 100 (1993), S. 0 
    ISSN: 1471-0528
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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