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排序方式: 共有564条查询结果,搜索用时 15 毫秒
1.
2.
AG Nettetal 《MedR Medizinrecht》2007,25(11):664-666
Abstrakt 1. Nimmt ein Patient einen ihm von seinem (Zahn-)Arzt einger?umten Exklusiv-Termin nicht wahr, obwohl er auf dessen Eigenschaft
ausdrücklich hingewiesen wurde, so hat er dem (Zahn-)Arzt den Behandlungsausfall abzüglich eines angemessenen Eigenanteils
des (Zahn-)Arztes zu ersetzen.
2. Die Ersatzpflicht tritt auch dann ein, wenn der Patient den Termin nicht in der in dem Behandlungsvertrag vorgesehenen
Frist absagt. Eine hierfür seitens des (Zahn-)Arztes bestimmte Frist von zwei Tagen vor Behandlungsbeginn stellt sich für
den Patienten grunds?tzlich auch nicht als unangemessene Benachteiligung i.S. des § 307 BGB dar.
3. Ein Anspruch des Arztes entf?llt auch bei nur mündlicher Vereinbarung nicht unter dem Gesichtspunkt des § 4 Abs. 5b BMV-Z,
denn diese Vorschrift ist teleologisch dahin zu reduzieren, dass nur zahn?rztliche Honoraransprüche aus erfolgten Behandlungen
schriftlich vereinbart werden müssen. Soweit es jedoch um einen vertraglichen Anspruch wegen einer Leistungsst?rung geht,
vermag das Schriftformerfordernis des § 4 Abs. 5b BMV-Z grunds?tzlich nicht einzugreifen. (Leits?tze des Bearbeiters) 相似文献
3.
4.
Early during rat thymus ontogeny, an important proportion of thymocytes
expresses IL-2R and contains IL-2 mRNA. To investigate the role of the
IL-2-IL-2R complex in rat T cell maturation, we supplied either recombinant
rat IL-2 or blocking anti-CD25 mAb to rat fetal thymus organ cultures
(FTOC) under several experimental conditions. The IL-2 treatment initially
stimulated the growth of thymocytes and, as a result, induced T cell
differentiation, but the continuous addition of IL-2 to rat FTOC, as well
as the anti-CD25 administration, resulted in cell number decrease and
inhibition of thymocyte maturation. These results indicate that immature
rat thymocytes bear functional high- affinity IL-2R and that IL-2 promotes
T cell differentiation as a consequence of its capacity to stimulate cell
proliferation. Modifications in TCR alpha beta repertoire and increased
numbers of NKR- P1+ cells, largely NK cells, were also observed in
IL-2-treated FTOC. Furthermore, IL-2-responsiveness of different thymocyte
subsets changed throughout thymic ontogeny. Immature CD4-CD8-cells
responded to IL-2 in two stages, early in thymus development and around
birth, in correlation with the maturation of two distinct waves of thymic
cell progenitors. Mature CD8+ thymocytes maximally responded to IL-2 around
birth, supporting a role for IL-2 in the increased proliferation of mature
thymocytes observed in vivo in the perinatal period. Taken together, these
findings support a role for IL-2 in rat T cell development.
相似文献
5.
6.
Life expectancy in British Marfan syndrome populations 总被引:2,自引:0,他引:2
JR Gray AB Bridges RR West L. McLeish AG Stuart JCS Dean MEM Porteous M. Boxer SJ Davies 《Clinical genetics》1998,54(2):124-128
A total of 206 patients with Marfan syndrome were ascertained throughout genetic clinics in Wales and Scotland during the period 1970–1990. There were 45 deaths representing 22% of the cohort. Mean age at death was 45.3 ± 16.5 years. 50% median cumulative survival in the total cohort (n = 206) was 53 years for males and 72 years for females. Multivariate analysis confirmed severity as the best independent indicator of survival. These findings and survival curves will assist in the counselling of British families and individuals with Marfan syndrome. 相似文献
7.
Specific high-affinity binding of 125I-labeled mouse interferon to interfevon resistant embryonal carcinoma cells in vitro 总被引:7,自引:0,他引:7
Multipotential mouse embryonal carcinoma cells are resistant to several biologic effects of mouse interferon: inhibition of viral multiplication and inhibition of cell division. Nevertheless using 125I-labeled highly purified mouse interferon we have shown that these embryonal carcinoma cells express specific interferon receptors in similar number and of the same affinity as interferon sensitive differentiated embryonal carcinoma cells. Thus, mechanisms of interferon resistance are probably multiple: some cells are resistant because they lack specific binding sites for interferon (interferon resistant mouse L1210 cells) and other cells, as shown herein, are resistant to some of the effects of interferon despite binding of interferon to specific receptor sites. Furthermore, these binding sites may be considered functional, since interferon does induce an increase in 2-5A synthetase in these cells. 相似文献
8.
Paulo CJL Santos Renata AG Soares Diogo BG Santos Raimundo M Nascimento George LLM Coelho José C Nicolau José G Mill José E Krieger Alexandre C Pereira 《BMC medical genetics》2011,12(1):13
Background
Recent studies have reported the clinical importance of CYP2C19 and ABCB1 polymorphisms in an individualized approach to clopidogrel treatment. The aims of this study were to evaluate the frequencies of CYP2C19 and ABCB1 polymorphisms and to identify the clopidogrel-predicted metabolic phenotypes according to ethnic groups in a sample of individuals representative of a highly admixtured population. 相似文献9.
Purification and partial characterization of a cellular inhibitor of the interferon-induced protein kinase of Mr 68,000 from influenza virus-infected cells. 总被引:14,自引:5,他引:14
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T G Lee J Tomita A G Hovanessian M G Katze 《Proceedings of the National Academy of Sciences of the United States of America》1990,87(16):6208-6212
A number of eukaryotic viruses have evolved mechanisms to downregulate activity of the interferon-induced, double-stranded RNA-activated protein kinase (referred to as P68 based on its Mr of 68,000 in human cells). This control is essential because once activated, the P68 kinase phosphorylates its natural substrate, the alpha subunit of the eukaryotic protein synthesis initiation factor 2 (eIF-2), limiting functional eukaryotic protein synthesis initiation factor 2 available for protein synthesis initiation. We have previously shown that influenza virus encoded a specific mechanism to repress the autophosphorylation and activity of P68. Using in vitro assays for P68 inhibition, we now have purified, to near homogeneity, the P68 repressor from influenza virus-infected cells. The purified product inhibited both the autophosphorylation of P68 as well as phosphorylation of the alpha subunit of eukaryotic protein synthesis initiation factor 2 by the kinase. We tested for both protease and phosphatase activity but found neither activity associated with the purified inhibitor. Surprisingly we found the purified repressor, which had an apparent Mr of approximately 58,000, was a cellular and not a viral-encoded protein. Possible mechanisms by which influenza virus activates this cellular regulator of the protein kinase, thereby minimizing potential antiviral effects of interferon, are discussed. 相似文献
10.
Zielinsky A; Hirsh J; Straumanis G; Carter CJ; Gent M; Sackett DL; Hull R; Kelton JG; Powers P; Turpie AG 《Blood》1982,59(2):346-350
We have evaluated the fibrinogen/fibrin fragment E antigen assay as a diagnostic test in patients with clinically suspected venous thrombosis by comparing the results of this assay with venography in 272 patients. The result of the fragment E antigen assay was elevated in 79 of 80 patients with positive venograms for recent venous thrombosis (sensitivity 99%) and within the normal range in 161 of 192 patients with normal venograms (specificity 84%). The fragment E assay was also evaluated in 130 medical and surgical controls without evidence of venous thrombosis by leg scanning and the test was found to be relatively nonspecific. However, in the patient group under study, a correct clinical diagnosis of no thrombosis, based on a normal fragment E result, was made in 161 of 162 cases (negative predictive value of 99%). Therefore, a normal test result effectively excludes a diagnosis of venous thrombosis in clinically symptomatic patients. The assay, as currently performed, is technically demanding and takes 24 hr to complete. Therefore, it will have to be simplified before it can be applied to clinical practice. 相似文献