bluuebunny/crossref_metadata_2025_split huggingface dataset:
Refugees, Expellees and the Language Situation in Lusatia (1945–7)
Authors: Barker Peter 
Published: September 2004

AbstractThe first part of this article deals with the general situation of refugees and expellees in the Soviet Zone of Occupation immediately after 1945, concentrating in particular on Lusatia. It then goes on to consider the special conditions which existed in the bilingual areas of Upper and Lower Lusatia and the impact of the refugees on the language situation. The major source for the article is a research project based at the Sorbian Institute in Bautzen: in the original project a sociologist at the Institute, Ines Keller, examined the life stories of thirty refugee families, representing different generations, which formed part of a general study of German‐Sorbian families. A continuation of this project concentrated on the generation of refugees which came into Lusatia as children or young people, and then married into Sorbian families.1
Doppelte Erinnerung: Täter‐ und Opferidentitäten in Christa Wolfs Rekonstruktion Des Traumas Der Flucht
Authors: Jansen Odile 
Published: September 2004

AbstractAdornos Frage aus dem Jahre 1959 ‘Was bedeutet Aufarbeitung der Vergangenheit?’ hat im Licht der neuesten Erinnerungsdebatte nichts von ihrer Gültigkeit eingebüßt. Ist es möglich, die Erinnerung an deutsche Opferschaft mit der Erinnerung an deutsche Täterschaft zu vereinen? Verdrängt die Geschichte der deutschen Kriegstraumata nicht die Geschichte von Auschwitz? Aus diesem Konflikt gehen ethische und ästhetische Probleme hervor, wie in literarischen Darstellungen deutscher Leidenserfahrungen erkennbar wird. In diesem Artikel wird eben jene Problematik am Beispiel verschiedener Prosaarbeiten der ehemaligen DDR‐Autorin Christa Wolf (1929) dargestellt, in denen die in der DDR tabuisierten Themen Flucht und Vertreibung zur Sprache gebracht werden. Die Flucht vor der Sowjetarmee im Jahre 1945 bildet eine Erinnerungsspur in diesen Prosaarbeiten, die durch den Konflikt zwischen emotionaler und historischer Wahrheit gekennzeichnet werden, sowie durch den Versuch, eigene Leidenserfahrung in Einklang zu bringen mit der nachträglich gewonnenen Einsicht in die Umstände, die zu Flucht und Heimatsverlust führten. Die Aufarbeitung der Vergangenheit wird dabei begrenzt, einerseits durch den ideologisch und erinnerungspolitisch bedingten Rahmen, in dem die Autorin sich bewegt, andererseits durch eine Fesselung an die narrativ nicht integrierbare Erfahrung der Flucht. Dabei tut sich eine konflikthafte Selbstbestimmung über die Bilder der Vergangenheit hervor. Opfer‐ und Täteridentität verschmelzen in der Perspektive eines ‘schuldlosen Schuldigen’.
‘Gebranntes Kind’? W.G. Sebald's ‘Metaphysik Der Geschichte’
Authors: Jackman Graham 
Published: September 2004

AbstractThis essay investigates the relationship between Sebald's Luftkrieg und Literatur and the prose works on which his reputation primarily depends. Sebald's account of the bombing of German cities, particularly of Hamburg in 1943, reveals two significant intellectual affinities: first with Walter Benjamin, whose conception of history in Ursprung des deutschen Trauerspiels is linked through the ruins left by the bombing to Sebald's preoccupation with scenes of decay and dereliction in his fictional works, and secondly with Horkheimer and Adorno's critique of ‘progress’ in Dialektik der Aufklärung. Sebald sees the bombing campaign, along with the Holocaust, as part of the one great catastrophe of the Third Reich in which the history of ‘progress’ culminated – a history analysed at length in Sebald's Austerlitz. The ‘firestorm’ in Hamburg, emblematic of this destructive process, illustrates Sebald's recurrent use of the fire motif in his narrative works and is linked to comments on his own childhood in Nach der Natur. His entire oeuvre is at once an attempt to ‘memorialise’ individual victims of this destructive process and a critique of, and a resistance to, the tendency within post‐war German culture to complete the ‘liquidation’ of the past begun during the wartime bombing.
‘Weil Die Geschichte Nicht Aufhört’: Günter Grass's Im Krebsgang
Authors: Dye Elizabeth 
Published: September 2004

AbstractW.G. Sebald's 1997 lectures, Luftkrieg und Literatur, sparked intense debate in the German media over the supposed taboo surrounding the literary depiction of German civilian victims of Allied attacks and the potential blurring of the already problematic ‘Täter’/‘Opfer’ complex. On its publication, Grass's most recent work Im Krebsgang either fuelled or became embroiled in this dispute and became front‐ page news. It is contended that such a media frenzy led to literary reviews at the time ignoring the aesthetic merits and failures of the novella and thus overlooking the complexities of its narratological structure, giving rise to over‐simplistic interpretations of Grass's contribution to the ‘Täter’/‘Opfer’ debate. The following article attempts to redress the journalistic imbalance by undertaking a detailed analysis of the various narrative strategies employed within the work and relating this to the generational and familial framework with which Grass addresses the issue of German suffering. This serves to illuminate further the topic of memory and memorialising the past which lies at the heart of Sebald's essay and of Grass's novella.
Kinetics of Ca2+ release by InsP3 in pig single aortic endothelial cells: evidence for an inhibitory role of cytosolic Ca2+ in regulating hormonally evoked Ca2+ spikes
Authors: Carter T. D. , Ogden D. 
Published: September 2004

The role of the InsP3 receptor and its interaction with Ca2+ in shaping endothelial Ca2+ spikes was investigated by comparing InsP3‐evoked intracellular Ca2+ release with hormonally evoked Ca2+ spikes in single endothelial cells.
Ins P3 was generated by flash photolysis of intracellular caged InsP3. InsP3 at 0.2 μM or higher released Ca2+ from stores with a time course comprising a well‐defined delay, a fast rise of free [Ca2+] to a peak where net flux into the cytosol is zero, and a slow decline to pre‐flash levels. InsP3‐evoked Ca2+ flux into unit cytosolic volume was measured as the rate of change of free [Ca2+]i during the fast rise, d[Ca2+]i/dt (mol s−1 l −1).
The mean delay decreased from 433 ms at 0.2 μM to 30 ms at 5 μM. At very high InsP3 concentrations, 78 μM, the delay was shorter, < 10 ms. At low InsP3 concentration the delay was reduced by ∼30% by prior elevation of free [Ca2+]i, supporting a co‐operative action of free [Ca2+] and InsP3 in activation.
Both Ca2+ flux and peak free [Ca2+]i increased with InsP3 concentration within each cell. Maximal activation was at > 5 μM, 50% maximum Ca2+ flux was at 1.6 μM InsP3 and the Hill coefficient was between 3.6 and 4.3. A large variation of Ca2+ flux and peak [Ca2+]i was found from cell to cell at the same InsP3 concentration.
Strong inhibition of InsP3‐evoked flux was produced by an immediately preceding response, with complete inhibition at peak free [Ca2+]i due to the first pulse. InsP3 sensitivity returned over 1–2 min, with 50% recovery at ∼25 s. The recovery of InsP3 sensitivity may determine the minimum interval between hormonally evoked spikes.
Ca2+ flux due to a pulse of InsP3 terminated rapidly, in the continued presence of InsP3, producing a well‐defined peak [Ca2+]. A reciprocal relation was found between the duration and the rate of Ca2+ flux, such that high Ca2+ flux was of brief duration. The rate of termination of flux measured as the reciprocal of the 10–90% rise time of free [Ca2+]i showed a linear correlation with Ca2+ flux over a large range in all cells. A systematic deviation from linearity at low InsP3 concentration showed a greater rate of termination at low InsP3 concentration than at high for the same flux.
Elevating cytosolic free [Ca2+] by 0.1–2.5 μ M strongly inhibited Ca2+ release by InsP3, and buffering free [Ca2+] to low levels greatly prolonged Ca2+ release. Both results support the idea that Ca2+ flux quickly produces locally high free [Ca2+] which inhibits the receptor and terminates Ca2+ release.
Hormonally evoked Ca2+ spikes showed a similar reciprocal relation between rise time and Ca2+ flux, seen in the initial Ca2+ spike evoked by extracellular ATP in porcine aortic endothelial cells and by acetylcholine in rat aortic endothelial cells in situ, supporting the idea that the same mechanism of cytosolic Ca2+ inhibition determines the duration of hormonally and InsP3‐evoked Ca2+ spikes.
Relationship of substance P to afferent characteristics of dorsal root ganglion neurones in guinea‐pig
Authors: Lawson S. N. , Crepps B. A. , Perl E. R. 
Published: September 2004

The relationship between the afferent properties and substance P‐like immunoreactivity (SP‐LI) of L6 and SI dorsal root ganglion (DRG) neuronal somata was examined in anaesthetized guinea‐pigs. Glass pipette microelectrodes filled with fluorescent dyes were used to make intracellular recordings and to label DRG somata. The dorsal root conduction velocity (CV) and the afferent receptive properties of each unit were categorized according to criteria established in other species. Categories included a variety of low threshold mechanoreceptive classes, innocuous thermoreceptive and several nociceptive classes. Nociceptive units were further subdivided on the basis of CV and the locus of the receptive field (superficial cutaneous, deep cutaneous or subcutaneous).
SP‐LI was determined using the avidin–biotin complex method and the relative staining intensity determined by image analysis. The possible significance of labelling intensity is discussed. Clear SP‐LI appeared in twenty‐nine of 117 dye‐labelled neurones. All SP‐LI positive units with identified receptive properties were nociceptive but not all categories of nociceptors were positive. The intensity of SP‐LI labelling varied, often systematically, in relation to afferent properties. There was a tendency for nociceptive neurones with slower CVs and/or smaller cell bodies to show SP‐LI.
Nineteen of fifty‐one C fibre neurones showed SP‐LI. Fewer than half the C polymodal nociceptors (CPMs) were positive. The most intensely labelled units were the deep cutaneous nociceptors and some of the CPMs in glabrous skin. C low threshold mechanoreceptors and cooling‐sensitive units did not show SP‐LI.
Ten of sixty‐six A fibre neurones exhibited SP‐LI, including eight of sixteen Aδ nociceptors and two of fifteen Aα/β nociceptors. A fibre neurones exhibiting SP‐LI included seven of eight deep cutaneous mechanical nociceptors and some superficial cutaneous mechano‐heat nociceptors of hairy skin. In contrast, none of twenty superficial cutaneous A high threshold mechanoreceptor units or the thirty‐five A fibre low threshold units (D‐hair and other units) showed detectable SP‐LI.
We conclude that SP‐LI labelling in guinea‐pig DRG neurones is related to (a) afferent receptive properties, (b) the tissue in which the peripheral receptive terminals are located, (c) the CV and (d) the soma size.
Glucose‐induced swelling in rat pancreatic β‐cells
Authors: Miley Helen E. , Sheader Elizabeth A. , Brown Peter D. , Best Leonard 
Published: September 2004

Changes in relative cell volume in response to hypotonic solutions and glucose were studied in single isolated rat pancreatic β‐cells using a video‐imaging technique, β‐cell electrical activity was recorded under similar conditions using the perforated patch technique.
Exposure of β‐cells to hypotonic solutions (10 and 33% hypotonicity) caused an immediate increase in cell volume to relative values of 1.09 and 1.33, respectively. This was followed by a gradual regulatory volume decrease.
Raising the concentration of glucose from 4 to 20 mm or 12 mm (with substitution of mannitol) increased β‐cell volume by 12 and 10%, respectively. This effect of glucose persisted when Co2+ was added to inhibit insulin release. Glucose‐induced volume increases were sustained for the duration of exposure to elevated hexose concentration. The addition of 16 mm 3‐O‐methylglucose, which is transported into the β‐cell but not metabolized, produced only a transient 5% increase in β‐cell volume.
Exposure of β‐cells to a 15% hypotonic solution resulted in a transient depolarization and electrical activity. Raising the glucose concentration to 20 or 12 mm caused a sustained depolarization and generation of electrical activity. However, the addition of 16 mm 3‐O‐methylglucose had no effect on β‐cell membrane potential. The glucose‐induced increase in volume and induction of electrical activity, when measured in single β‐cells simultaneously, showed comparable kinetics.
The secretion of insulin from intact pancreatic islets was stimulated by exposure to hypotonic solutions (10–33% hypotonicity). A 15% hypotonic solution stimulated insulin release to a peak value comparable to that elicited by raising the glucose concentration from 4 to 20 mm. Whereas hypotonic solutions caused a transient stimulation of insulin release, the effect of glucose was sustained.
It is suggested that glucose increases the volume in rat pancreatic β‐cells by a mechanism dependent upon metabolism of the sugar. The extent of cell swelling evoked by raised glucose concentrations is sufficient to depolarize the cells and induce electrical and secretory activity and may involve activation of a volume‐sensitive anion conductance.
Outward Currents in Smooth Muscle Cells Isolated from Sheep Mesenteric Lymphatics
Authors: Cotton K. D. , Hollywood M. A. , McHale N. G. , Thornbury K. D. 
Published: September 2004

The patch‐clamp technique was used to measure membrane currents in isolated smooth muscle cells dispersed from sheep mesenteric lymphatics. Depolarizing steps positive to −30 mV evoked rapid inward currents followed by noisy outward currents.
Nifedipine (1 μM) markedly reduced the outward current, while Bay K 8644 (1 μM) enhanced it. Up to 90% of the outward current was also blocked by iberiotoxin (Kd= 36 nM).
Large conductance (304 ±15 pS, 7 cells), Ca2+‐ and voltage‐sensitive channels were observed during single‐channel recordings on inside‐out patches using symmetrical 140 mM K+ solutions (at 37 °C). The voltage required for half‐maximal activation of the channels (V½) shifted in the hyperpolarizing direction by 146 mV per 10‐fold increase in [Ca2+]i.
In whole‐cell experiments a voltage‐dependent outward current remained when the Ca2+‐activated current was blocked with penitrem A (100 nM). This current activated at potentials positive to −20 mV and demonstrated the phenomenon of voltage‐dependent inactivation (V½=−41 ± 2 mV, slope factor = 18 ± 2 mV, 5 cells).
Tetraethylammonium (TEA; 30 mM) reduced the voltage‐dependent current by 75% (Kd= 3.3 mM, 5 cells) while a maximal concentration of 4‐aminopyridine (4‐AP; 10 mM) blocked only 40% of the current. TEA alone had as much effect as TEA and 4‐AP together, suggesting that there are at least two components to the voltage‐sensitive K+ current.
These results suggest that lymphatic smooth muscle cells generate a Ca2+‐activated current, largely mediated by large conductance Ca2+‐activated K+ channels, and several components of voltage‐dependent outward current which resemble ‘delayed rectifier’ currents in other smooth muscle preparations.
Small event Ca2+ release: a probable precursor of Ca2+ sparks in frog skeletal muscle
Authors: Shirokova Natalia , Ríos Eduardo 
Published: September 2004

Fluo‐3 fluorescence associated with Ca2+ release was recorded with confocal microscopy in single muscle fibres. Clamp depolarization to −65 or −60 mV elicited Ca2+ sparks with amplitudes and spatial widths distributed approximately normally, with mean values of 0.79 of resting fluorescence and 0.8 μm (S.D., 0.17 and 0.2 μm; n= 193), respectively. Given these distributions, events of amplitude less than 0.45 or width less than 0.4 μm are unlikely to be sparks.
Low voltage depolarization (−72 mV) elicited only one spark per triad every 6 s, but generated a relative increase in fluorescence at triads of 0.05. This increase must therefore have been due to events smaller than sparks.
The variance/mean ratio of triadic fluorescence gradients averaged 0.11 at low voltages and increased severalfold at the higher voltages at which sparks appeared, indicating the existence of at least two event amplitudes.
Tetracaine (200 μm) reversibly abolished sparks and the early peak of Ca2+ release at all voltages. In its presence, discrete events were smaller than the spark criterion, and triadic gradients had a variance/mean ratio of 0.11.
The phenylalkylamine D600 (2 μm) reduced release at all voltages, abolishing sparks and the peak of Ca2+ release at low but not at high voltages.
The parallel abolition of all sparks and the peak of Ca2+ release indicates that both phenomena are activated by Ca2+. The restoration of sparks by voltage in D600 suggests that release in small events provides the trigger Ca2+ for activation of sparks.
Calcium Sparks and Excitation–Contraction Coupling in Phospholamban‐Deficient Mouse Ventricular Myocytes
Authors: Santana L. F. , Kranias E. G. , Lederer W. J. 
Published: September 2004

We examined [Ca2+]i and L‐type Ca2+ channel current (ICa) in single cardiac myocytes to determine how the intracellular protein phospholamban (PLB) influences excitation‐contraction (E–C) coupling in heart. Wild type (WT) and PLB‐deficient (KO) mice were used. Cells were patch clamped in whole–Cell mode while [Ca2+]i was imaged simultaneously using the Ca2+ indicator fluo‐3 and a confocal microscope.
Although ICa was similar in magnitude, the decay of ICa was faster in KO than in WT cells and the [Ca2+]i transient was larger and decayed faster. Furthermore, the E–C coupling ‘gain’ (measured as Δ[Ca2+]i/ICa) was larger in KO cells than in WT cells.
Spontaneous Ca2+ sparks were three times more frequent and larger in KO cells than in WT myocytes but, surprisingly, the time constants of decay were similar.
SR Ca2+ content was significantly greater in KO than in WT cells. When the SR Ca2+ content in KO cells was reduced to that in WT cells, Ca2+ sparks in these ‘modified’ (KO') cells decayed faster. E–C coupling gain, [Ca2+]i transient amplitude and the kinetics of decay of ICa were similar in KO' and WT cells.
We conclude that SR Ca2+ content influences (1) ICa, (2) the amplitude and kinetics of Ca2+ sparks and [Ca2+]i transients, (3) the sensitivity of the RyRs to triggering by [Ca2+]i, (4) the amount of Ca2+ released, (5) the magnitude of the E–C coupling ‘gain’ function, and (6) the rate of Ca2+ re‐uptake by the SR Ca2+‐ATPase. In KO cells, the larger [Ca2+]i transients and Ca2+ sparks speed up ICa inactivation. Finally, we conclude that PLB plays an important regulatory role in E–C coupling by modulating SR Ca2+‐ATPase activity, which establishes the SR Ca2+ content and consequently influences the characteristics of local and global Ca2+ signalling.
The Relationship between Cutaneous C Fibre Type and Antidromic Vasodilatation in the Rabbit and the Rat
Authors: Gee M. D. , Lynn B. , Cotsell B. 
Published: September 2004

Skin blood flow was monitored during antidromic stimulation of identified cutaneous C fibres in fine filaments dissected from the saphenous nerve of anaesthetized rabbits and rats. The techniques used to monitor skin blood flow were laser Doppler perfusion imaging and laser Doppler flowmetry.
In the rabbit filaments a total of thirty‐three C fibres were tested for their ability to produce antidromic vasodilatation. The only C fibres found to have vasodilator actions were of the polymodal nociceptor afferent class, and fourteen (50%) of the twenty‐eight polymodal nociceptor units tested were vasoactive. The afferent receptive fields of polymodal nociceptor afferents were mapped carefully using suprathreshold mechanical stimuli, and there was a good correlation between afferent receptive field area and area of vasodilatation.
In the rat, eleven of the fifty‐four C fibres antidromically stimulated had vasodilator actions. All eleven vasoactive C fibres were nociceptive and comprised seven polymodal nociceptor units, two heat nociceptor units and two incompletely classified nociceptor units. The area of increased blood flow was always coincident with the afferent field of the stimulated unit.
In the rat the vasodilator units were not evenly distributed over the saphenous nerve receptive field. Nine of the eleven vasoactive C fibres had receptive fields located on the foot or the digits, and only two were on the ankle or lower leg. Overall, the population of nociceptive C fibres was evenly distributed over the saphenous nerve receptive field.
In both the rabbit and the rat, a subclass of polymodal nociceptor afferents form the majority of the vasoactive units and will make the main contribution to axon reflex flare and other neurogenic inflammatory responses involving vasodilatation. The vasoactive polymodal nociceptor units tend to have relatively low mechanical sensitivity, although they have typical heat thresholds. In the rat heat nociceptor units also have vasodilator actions. However, such heat nociceptor units form a minor functional class of afferent C fibre in the rat saphenous nerve, and are not found in the rabbit saphenous nerve.
The findings from this study in the rabbit and the rat are compared with the situation in pig skin. The close relationship between afferent receptive field area and spread of flare across species is noted, and the way these measures increase with body size is discussed.
Electrogenic K+ transport by the Na+–K+ pump in rat cardiac ventricular myocytes
Authors: Peluffo R. Daniel , Berlin Joshua R. 
Published: September 2004

The involvement of electrogenic reaction steps in K+ transport by the Na+,K+‐ATPase was determined in rat cardiac ventricular myocytes using whole‐cell patch clamp techniques.
Under K+–K+ exchange conditions and in the presence of extracellular K+ or Tl+ at concentrations that stimulated submaximal levels of steady‐state Na+,K+‐ATPase activity, ouabain‐sensitive transient currents were observed during (‘on’) and after (‘off’) step changes in membrane potential (Vm).
The quantity of charge moved during the transient currents depended, in a saturable manner, on the magnitude of the voltage step. Maximal ouabain‐sensitive ‘on’ and ‘off’ charges were calculated to be 9.6 ± 0.9 and 9.1 ± 0.4 fC pF−1 (n= 4), respectively, with an effective valency of 0.48 ± 0.07 (n= 7).
Kinetics of the transient currents were independent of Vm and Tlo+ at positive potentials, but became more rapid at increasingly negative Vm values in an ion concentration‐dependent fashion.
These data demonstrate that electrogenic steps participate in K+ transport by the Na+,K+‐ATPase and that the electrogenic step is extracellular ion binding.
The temperature‐and Vm‐dependent properties of transient charge movements were compared under K+–K+ and Na+–Na+ exchange conditions. The data suggest that extracellular K+ and Na+ binding occur at different sites in the enzyme or to different enzyme conformations. The sum of the effective valencies, 1.14 ± 0.12, demonstrates that the electrogenicity of extracellular ion binding can explain the Vm dependence of ion transport by the Na+,K+‐ATPase.