17 research outputs found

    The value of different resistance parameters in distinguishing biopsy-proved dysfunction of renal allografts

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    The data concerning the value of duplex sonography in diagnosing parenchymatous renal allograft dysfunction are controversial. Most early studies did not take into consideration the many factors influencing resistance parameters. We therefore performed a prospective, biopsy-controlled study with exclusion of all known sources of error regarding resistance parameters. Furthermore we investigated the value of a new resistance parameter, the systolic deceleration percentage. Forty-seven duplex sonographic studies were performed on 43 patients (30 male, 13 female, median age 47 years, range 7-70). Fourteen studies were done on normally functioning grafts (control group) an average of 33 days after transplantation. Thirty-three studies were performed on dysfunctional grafts immediately prior to biopsy. Grafts which had been transplanted more than a year previously or with vascular findings or any other clinical or sonographic pathology probably explaining function deterioration were excluded. In all patients, the resistive index (RI), pulsatility index (PI) and systolic deceleration percentage (DP) were calculated in the main renal artery and in the interlobar artery. Of the 33 grafts with dysfunction, nine had vascular rejection (VR), 11 interstitial rejection (IR), 11 cyclosporin A toxicity (CAT) and two other histologies (OR). The mean RI in normal grafts (NO) was 0.71±0.06 in the main artery and 0.68±0.06 in the interlobar artery, in VR 0.86±0.12 and 0.80±0.18, in IR 0.72±0.05 and 0.70±0.07, in CAT 0.67±0.06 and 0.65±0.07 and in OR 0.64±0.07 and 0.60±0.01. For PI, the values were 1.45±0.23 and 1.41±0.28 (NO), 3.5±2.13 and 2.92±2.16 (VR), 1.55±0.26 and 1.46±0.33 (IR), 1.32±0.25 and 1.27±0.26 (CAT) and 1.30±0.34 and 1.13±0.04 (OR). For DP we calculated 28±5% and 29±6% (NO), 43±14% and 36±6% (VR), 29±9% and 27±9% (IR), 31±8% and 32±7% (CAT ) and 32±4% and 28±3% (OR). The sensitivity/specificity for VR with a cutoff mean+2 SD was 0.44/1 for RI, 0.55/0.97 for PI and 0.33/0.89 for DP. It was concluded that:(1) despite the high selection of our patient group, diagnostic accuracy of duplex sonography for diagnosing parenchymatous function disorder in renal allograft remains insufficient; (2) in vascular rejection only, the resistance parameters differ significantly from the values of normal allografts; (3) the higher the cutoff of resistance parameters, the better the specificity and the worse the sensitivity for diagnosing vascular rejection; (4) of all investigated resistance parameters, the RI is the most practical due to a simple measurement techniqu

    Early renal transplant dysfunction due to arterial kinking stenosis

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    The main differential diagnoses of early renal trans-plant dysfunction include ischaemic damage, cyclospo-rin toxicity, and rejection [1]. Rarer causes include bleeding, ureteral obstruction, urinary leak, venou

    Структура іншомовної професійно зорієнтованої мовленнєвої компетентності

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    Розгляд та аналіз структури професійно зорієнтованої іншомовної мовленнєвої компетентності у порівнянні зі структурою загальної мовленнєвої компетентності, враховуючи особливості їх компонентів

    Monitoring of Oral Anticoagulation by an Amidolytic Factor X Assay

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    PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours

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    The adult mouse mammary epithelium contains self-sustained cell lineages that form the inner luminal and outer basal cell layers, with stem and progenitor cells contributing to its proliferative and regenerative potential. A key issue in breast cancer biology is the effect of genomic lesions in specific mammary cell lineages on tumour heterogeneity and progression. The impact of transforming events on fate conversion in cancer cells of origin and thus their contribution to tumour heterogeneity remains largely elusive. Using in situ genetic lineage tracing and limiting dilution transplantation, we have unravelled the potential of PIK3CA(H1047R), one of the most frequent mutations occurring in human breast cancer, to induce multipotency during tumorigenesis in the mammary gland. Here we show that expression of PIK3CA(H1047R) in lineage-committed basal Lgr5-positive and luminal keratin-8-positive cells of the adult mouse mammary gland evokes cell dedifferentiation into a multipotent stem-like state, suggesting this to be a mechanism involved in the formation of heterogeneous, multi-lineage mammary tumours. Moreover, we show that the tumour cell of origin influences the frequency of malignant mammary tumours. Our results define a key effect of PIK3CA(H1047R) on mammary cell fate in the pre-neoplastic mammary gland and show that the cell of origin of PIK3CA(H1047R) tumours dictates their malignancy, thus revealing a mechanism underlying tumour heterogeneity and aggressiveness
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