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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    European radiology 8 (1998), S. 707-725 
    ISSN: 1432-1084
    Keywords: Key words: MRI ; Breast ; Breast carcinoma ; Indications
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Contrast-enhanced MRI of the breast is probably the most sensitive method to detect breast pathology. It is best used to improve the sensitivity of mammography and sonography in selected patient groups with high breast cancer prevalence, where conventional methods are known to be less sensitive. Despite the high sensitivity of MRI, 5–12 % of invasive carcinomas are not recognized during MRI, because of lack of the typical criteria of carcinoma. MRI is probably inferior to mammography in detecting ductal in-situ carcinoma or very small carcinomas (〈 3 mm), because the neo-angiogenesis induced by these small carcinomas is too faint to be detected by contrast-enhanced MRI. These tumours cannot be excluded by a normal MRI examination. MRI is non-specific as the distinction of benign and malignant breast lesions is unreliable. Only in selected cases (fat- or blood-containing lesions) may it improve the specificity of mammography and sonography. Mostly image-guided core biopsy is by far the most specific and least expensive method to establish a definitive diagnosis. For lesions exclusively detected by contrast-enhanced MRI, simple and reliable localisation devices are urgently needed. Presently accepted indications for MRI of the breast are: patients with silicone implants after mastectomy or augmentation mammoplasty (detection of recurrence/prothesis rupture/silicon leakage); patients whose breasts are difficult to evaluate by combined mammography and sonography, who have had breast conservation therapy (local recurrence), or who have proven carcinoma in one breast (multifocality/-centricity or contralateral breast carcinoma) or proven axillary lymph node metastases from an unknown primary tumor, especially when these are hormone receptor positive; patients with extensive postoperative scarring. In the future, genetically defined high breast cancer risk may become an indication.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 418 (1991), S. 238-247 
    ISSN: 1432-2013
    Keywords: Isolated cardiocytes ; Whole cell recording ; Reoxygenation ; Increased net current ; Transient inward current ; Ca current
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Single myocytes were isolated from ventricles of adult guinea-pig hearts. The patch-clamp technique in the whole-cell configuration was used to study ionic currents. Experiments were performed in an experimental chamber that allowed the cells to be exposed to a sufficiently low O2 pressure to cause metabolic inhibition after 4–35 min (mean 14.1 min, n=20), which was indicated by the appearance of a large time-independent K current. Reoxygenation about 1 min after the first extra outward current was observed caused this current to vanish completely within 2–6 s if the calcium inside the pipette was buffered to negligible values with 20 mmol/l EGTA. With only 10 μM EGTA in the pipette, reoxygenation was followed by an arrhythmogenic period of 10–150 s duration, which was dominated by three types of event: (a) transient inward currents (I ti) developed during the first 5–10 s (26 cells); (b) the net current was increased by a factor of 1.9±0.4 (mean±SD, n=17) yielding a reversal potential for the increased component of −77±4 mV (mean±SD, n=4); and (c) the Ca current decreased by 20%–100% within the first 5–10 s. At the end of the arrhythmogenic period, I ti vanished, the net current recovered completely, and the Ca current recovered partially. At −45 mV, increasing preceding depolarization enlarged the amplitude of both the I ti and the net current, Iti being about four times more increased than the net current. The suppression of the Ca current was independent of the phase of the preceding I ti. We conclude that in isolated cardiocytes, after the induction of an anoxia-induced K current, reoxygenation causes a period of up to 150 s of cytosolic Ca overload, during which I ti is triggered, the net current is enhanced, and the Ca current is suppressed.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 418 (1991), S. 248-260 
    ISSN: 1432-2013
    Keywords: Isolated cardiocytes ; Transient inward current ; Current-voltage relationship ; Kinetics ; Na/Ca exchanger
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Transient inward currents (I ti), activated by a rise in intracellular Ca concentration, are believed to trigger cardiac arrhythmias in reperfused hearts. In this report, I ti in isolated cardiocytes from the guinea-pig were evoked by reoxygenation following a period of anoxia of between 4 min and 35 min. Reoxygenation was performed 1 min after the full development of an anoxia-induced time-independent K current. This current disappeared within 2–6 s and in the following 10 s I ti developed to maximum amplitude. I ti were evoked using a constant pulse pattern (holding potential V h=−45 mV; test potential V t=+10 mV; pulse duration 350 ms; frequency 1 Hz). In more than 95% of the cells, I ti at the holding potential I ti (−45 mV) declined with a time constant of τ=670±240 ms (mean±SD, n=17). In two cells, undamped oscillatory currents were observed. The amplitude of I ti (-45 mV) was proportional to the amplitude and duration of the preceding depolarizing test pulse. Test pulses of long duration (500 ms and 1000 ms, mean ± SD) to potentials positive to +10 mV produced slowly decaying tail currents (τ=391±51 ms, mean ± SD), which superimposed with I ti (−45 mV). The current/voltage relationship of I ti peaked between −30 mV and −10 mV and approximated zero at the most positive potentials, i.e. no reversal of I ti was found up to +80 mV. Using double-pulse protocols (prepulse potential +40 mV), I ti were enhanced at potentials negative to −30 mV and were also present in the range of the normal resting potential of ventricular heart cells. The instantaneous current-voltage relationship was monotone between −50 mV and +40 mV. Because of the dependence of I ti on the preceding depolarization, the instantaneous current-voltage relationship provides more reliable information on the voltage dependence of I ti. The interval between two subsequent I ti (−45 mV) values was 237±35 ms (mean ± SD, n=27) and depended on the amplitude of I ti (−45 mV) to increase by 5.2±0.5% (mean ± SD) per 100 pA decrease in I ti (−45 mV). A simple noise analysis showed that if one assumes that ionic channels are responsible for the generation of I ti (−45 mV), their unitary conductance cannot exceed 0.36 pS. We conclude that reoxygenation-induced I ti are triggered by a cyclic release of Ca from the sarcoplasmic reticulum and provide evidence that they are mediated by the electrogenic Na/Ca exchanger. The arrhythmogenic potency of reoxygenation-induced I ti is demonstrated under current-clamp conditions.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 416 (1990), S. 207-209 
    ISSN: 1432-2013
    Keywords: Isolated cardiocytes ; Anoxia ; AP shortening ; K current ; Ca current
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Whole cell currents were measured in isolated cardiocytes of guinea pig under anoxic conditions (pO2 〈0.5 torr). After 2 to 32 (mean 11.2) minutes of anoxia, time independent outward currents developed gradually which had a linear current-voltage relation between -100 and +20 mV and reversed at the resting potential of the cells (-82 to -90 mV). After 20 to 170 (mean 38) seconds, the amplitude of these outward currents saturated (3.6±0.5 nA at +10 mV, n=23). Reoxygenation within one minute after the appearance of the first extra outward currents led in most cells (〉90%) to their complete disappearance in 2 to 4 (mean 2.87, n=15) seconds. Ca currents were not affected at the time when the first extra outward currents occurred. It is concluded that (i) the anoxia-induced outward current is carried by K+ ions probably through KATP channels which open at intracellular ATP concentrations below 1 mmol/l (Noma and Shibasaki 1985) and (ii) this degree of ATP depletion does not affect normal Ca channel function.
    Type of Medium: Electronic Resource
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