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91.
CATHERINE C. AYOUB KURT W. FISCHER ERIN E. O'CONNOR 《Attachment & human development》2013,15(2):97-119
This article offers a developmental model of attachment theory rooted in dynamic skill theory. Dynamic skill theory is based on the assumption that people do not have integrated, fundamentally logical minds, but instead develop along naturally fractionated strands of a web. Contrary to traditional interpretations of attachment theory, dynamic skill theory proposes that individuals continue to modify their working models of attachments throughout the lifespan. In particular, working models of close relationships develop systematically through a series of skill levels such that the skills vary across strands in the web and will not automatically form a unified whole. The continual modification of working models is particularly pertinent for the consequences of hidden family violence for individuals' development. Dynamic skill theory shows how trauma can produce not developmental delay or fixation, as has been proposed previously, but instead the construction of advanced, complex working models. 相似文献
92.
HERBERT HÖNIGSMANN KURT F. JAENICKE WILHELM BRENNER† WALTRAUT RAUSCHMEIER JOHN A. PARRISH 《The British journal of dermatology》1981,105(5):491-501
The aim of this study was to measure unscheduled DNA synthesis (UDS) by autoradiography in normal htiman skin (1) after high dose UV-A, (2) after low dose UV-A applied before or after erythemogenic doses of UV-B, (3) after high dose PUVA and (4) after therapeutic doses of PUVA applied before and after erythemogenic doses of UV-B. Single high dose UV-A exposure induced rougbly 60% of the amount of UDS induced by equally erythemogenic doses of UV-B. Single low dose UV-A exposure did not induce UDS, nor did it significantly alter the amount of UV-B induced UDS when combined with UV-B exposure. Single high dose PUVA did not lead to UDS and had no influence on UV-B induced UDS when combined with UV-B exposure. Our findings indicate: (1) erythemogenic doses of UV-A induce a considerable DNA excision repair; (2) low dose UV-A neither augments UV-B induced DNA repair nor does it inhibit the repair process; (3) no UDS was shown to occur after either high or therapeutic doses of PUVA. This was unexpected since psoralen-DNA monoadducts have been shown to be repairable by a mechanism similar to excision repair of pyrimidine dimers. It is therefore assumed tbat PUVA as performed for therapeutic purposes either preferentially induced interstrand crosslinks not repairable via the classical repair mechanism or the repair of monoadducts was below resolution in this study; (4) therapeutic PUVA doses apparently do not interfere with excision repair of UV-B induced DNA lesions. 相似文献
93.
KURT LUSHINGTON LEON LACK DAVID J KENNAWAY NAOMI ROGERS CAMERON VAN DEN HEUVEL & DREW DAWSON 《Journal of sleep research》1998,7(2):75-83
The pineal hormone melatonin is thought to play a role in sleep initiation and maintenance. This was examined in a large sample of good sleeping controls ( n =52) and sleep maintenance insomniacs ( n =56), aged 55–80 y. Subjects collected 5 d of self-reported sleep diary measures, and 12-h urine samples (08.00–20.00 and 20.00–08.00 h) for analysis of the urinary melatonin metabolite, 6-sulphatoxymelatonin (aMT.6S). Insomniacs reported a significantly greater amount of wake after sleep onset, less sleep in total, less efficient sleep and poorer quality sleep compared to controls. However, no significant differences in melatonin excretion were observed between controls and insomniacs, with both groups showing similar mean (SEM) 12-h night-time [30.9 (2.9) vs. 30.6 (3.3) nmoles, respectively] as well as 24-h total [38.7 (3.4) vs. 36.7 (3.8)] aMT.6S excretion levels. No significant correlations were observed with any sleep parameters nor any effects of medication (anti-inflammatory agents, hormone replacement therapy, and an undifferentiated group of medications). The present results do not support a simple relationship between total melatonin production and self-reported sleep quality and duration in the aged. 相似文献
94.
BO ANGELIN KURT EINARSSON BARBRO LEIJD 《European journal of clinical investigation》1983,13(1):99-106
Bile acid kinetics and biliary lipid composition were determined in ten hypothyroid patients before and after treatment with L-thyroxine. Hypothyroid patients had normal synthesis rates of cholic acid and chenodeoxycholic acid. Hormone treatment, which lowered plasma cholesterol by about 35%, stimulated the formation of chenodeoxycholic acid by about 40% but did not significantly change the synthesis of cholic acid or total primary bile acids. The mean relative biliary concentration of deoxycholic acid was decreased from 30% to 19% and that of chenodeoxycholic acid was concomitantly increased. Cholesterol saturation of bile was decreased by treatment in six of the patients, but the mean value before treatment (135 +/- 13%) was not significantly different from that obtained after treatment (108 +/- 9%). It is suggested that the hypocholesterolaemic effect of thyroid hormones is not primarily due to an increased degradation of cholesterol to bile acids. Similar to what is observed in heterozygous familial hypercholesterolaemia, the defective receptor mediated degradation of plasma low density lipoproteins in hypothyroidism is thus apparently associated with a quantitatively normal catabolic rate of cholesterol to bile acids. 相似文献
95.
96.
ULRICH DUHRSEN GABRIELE KNIELING WOLF BEECKEN STEFAN NEUMANN DIETER KURT HOSSFELD 《British journal of haematology》1995,90(3):502-511
Summary. PGM-1 is a transplantable C3H/HeJ leukaemia which is not viable in unstimulated in vitro culture, differentiates into mature granulocytes and macrophages in response to soluble cytokines, and undergoes self-renewing cell divisions in coculture with selected human bone marrow stromal cell lines. When PGM-1 cells were cultured on pre-established adherent layers from primary human marrow samples, their fate depended on the source of the human marrow. Adherent layers from healthy marrow donors or patients with reactive marrow alterations had no or very little capacity to maintain PGM-1 cells in an immature colony-forming state. However, in coculture with adherent layers from patients with myeloid leukaemia or, to a lesser extent, lymphoblastic leukaemia or marrow-infiltrating lymphoma the colony-forming potential was retained. There was no correlation between the remission status of the patient and the PGM-1 activity of the adherent layer. Consistent morphological differences between active and inactive stromal layers were not observed.
The PGM-1 coculture system enables the detection of a hitherto undescribed regulatory abnormality in bone marrow malignancies. Whether the PGM-1 supporting activity is mediated through differences in the production of a cytokine with close homology to complement factor Bb which has recently been shown to induce self-renewal in immature PGM-1 cells, requires further investigation. 相似文献
The PGM-1 coculture system enables the detection of a hitherto undescribed regulatory abnormality in bone marrow malignancies. Whether the PGM-1 supporting activity is mediated through differences in the production of a cytokine with close homology to complement factor Bb which has recently been shown to induce self-renewal in immature PGM-1 cells, requires further investigation. 相似文献
97.
ANDREAS HIRT VLADAN ANTIC EUGENIA WANG ANNETTE RIDOLFI LU¨THY KURT LEIBUNDGUT NICOLAS VON DER WEID ANDREAS TOBLER & HANS-PETER WAGNER 《British journal of haematology》1997,96(2):366-368
The percentage of non-cycling blast cells in children with untreated acute lymphoblastic leukaemia (ALL) was investigated by staining smears for statin, a nuclear protein specifically present in non-growing resting cells. Results were compared with purified normal CD34-positive progenitors. A low fraction of ALL and CD34-positive cells expressed statin (2.0 ± 3.8% and 2.8 ±3.1%, respectively), the growth fraction assessed by staining for the nucleolar antigen p120 was 94% in both ALL and CD34-positive cell samples. From this analysis it can be concluded that the compartment of non-replicating cells in ALL as well as in normal CD34-positive precursor cells collected from peripheral blood is very small and that most cells are cycling. 相似文献
98.
Atrial Fibrillation and Embolic Complications in Paced Patients 总被引:5,自引:0,他引:5
HEINER LANGENFELD WOLFRAM GRIMM BERNHARD MAISCH KURT KOCHSIEK 《Pacing and clinical electrophysiology : PACE》1988,11(11):1667-1672
Atrial fibrillation (AF) and thromboembolism are discussed to he complications of the WI mode. We reinvestigated the spontaneous ECG and the anamnesis of 246 pacemaker patients with the indications second and third degree atrioventricular block (AV block, n = III), sick sinus syndrome (SSS, n - 101) and other indications (n = 34), all had shown sinus rhythm at implantation. The mean implantation time was 63 ± 45 months (203 VVI and 43 dual chamber pacemkers). The results: (1) Atrial fibrillation was found in 63 patients (26%). Only one of them had a DDD pacemaker inserted, the implantation time of dual chamber devices being shorter, however, (2) The incidence of AF in patients with SSS (37%) was significantly higher (P < 0.01) than in patients with AV block (19%). (3) Three patients suffered from strokes or transitory ischemic attacks in the follow-up, only one of them had AF at control. Conclusions: Our results confirm that VVI stimulation favors AF long-term which is most likely due to irritation of the atrial rhythm by retrograde conduction. In our patients the incidence of thromboembolic complications was not higher in the group of patients with AF. However, from this study in surviving patients, we cannot exclude that we Jost some patients due to severe stroke. 相似文献
99.
KURT OELKE 《International reviews of immunology》2013,32(3-4):315-331
T cells from patients with active lupus have multiple biochemical abnormalities. One of these is DNA hypomethylation, which in model systems alters gene expression and induces lupus-like autoimmunity. Recent reports indicate that DNA methylation is regulated in part by the ERK pathway, and that ERK pathway signaling is diminished in lupus T cells. This suggests a model in which defective T cell ERK pathway signaling contributes to the development of autoimmunity by decreasing DNA methyltransferase expression, modifying DNA methylation patterns and altering gene expression. This mechanism could contribute to idiopathic and drug-induced lupus. 相似文献
100.
Gülnaz CULHA Isin AKYAR Fadile YILDIZ ZEYREK ?zgür KURT Cumhur GüNDüZ Seray ?ZENSOY T?Z Ipek ?STAN Ibrahim CAVUS Burcu Gülkan Tanil Kocag?z Yusuf ?zbel Ahmet ?zbilgin 《Iranian Journal of Parasitology》2014,9(2):239-248