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  • 1
    Unknown
    Stuttgart : Kohlhammer
    (Die roten Hefte, 54)  
    Call number: Z060:40
    Keywords: Lifesaving ; Rescue work
    Pages: 57 p. : ill.
    Edition: 6., überarb. u. erw. Aufl.
    ISBN: 3-17-018750-3
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    Z060:40 departmental collection or stack – please contact the library
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  • 2
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    German Medical Science; Düsseldorf, Köln
    In:  122. Kongress der Deutschen Gesellschaft für Chirurgie; 20050405-20050408; München; DOC05dgch3036 /20050615/
    Publication Date: 2005-06-16
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 3
    Keywords: ORGANIC ANION TRANSPORTER ; TRANSPORTER ; EXPRESSION ; liver ; ACID ; BIOLOGY
    Type of Publication: Book chapter
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  • 4
    Keywords: Germany ; human ; CT ; IMAGES ; SURGERY ; validation ; TIME ; MR ; PERFORMANCE ; NUMBER ; REPRODUCIBILITY ; REGISTRATION ; LOCALIZATION ; HEAD ; SELECTION ; STANDARD ; FEATURES ; INCREASE ; TASK ; EXTRACTION ; intensity ; development ; SIZE ; 3D ; CT images ; ANATOMICAL POINT LANDMARKS ; differential approaches ; DIFFERENTIAL-OPERATORS ; landmark detection ; THIN-PLATE SPLINES
    Abstract: We introduce a novel multi-step approach to improved detection of 3D anatomical point landmarks in tomographic images. Such landmarks serve as important image features for a variety of 3D medical image analysis tasks (e.g. image registration). Existing approaches to landmark detection, however, often suffer from a rather large number of false detections. Our multi-step approach combines an existing robust 3D detection operator with two different novel approaches to the reduction of false detections, and is applied within a semi-automatic procedure allowing for interactive control by the user. Experimental results obtained for a number of different anatomical landmarks of the human head in 3D CT and MR images demonstrate that both automatic ROI size selection and incorporation of a priori knowledge of the intensity structure at a landmark significantly improve the detection performance. The applicability of semi-automatic landmark extraction is thus considerably improved. We also summarize the results of a validation study in which we compare the performance of semi-automatic landmark extraction with that of a (standard) manual procedure for landmark extraction. As an exemplary application, we consider rigid MR/CT registration. The main result of our study is that compared to a purely manual procedure, semi-automatic landmark extraction (a) significantly reduces the elapsed time for landmark extraction, (b) generally yields registration results of comparable quality, and (c) increases the reproducibility of the results. (c) 2005 Elsevier B.V. All rights reserved
    Type of Publication: Journal article published
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  • 5
  • 6
    Abstract: High polo-like kinase 1 (PLK1) expression has been linked to poor outcome in neuroblastoma (NB), indicating that it represents a relevant therapeutic target in this malignancy. Here, we identify a synergistic induction of apoptosis by the PLK1 inhibitor BI 2536 and vinca alkaloids in NB cells. Synergistic drug interaction of BI 2536 together with vincristine (VCR), vinblastine (VBL) or vinorelbine (VNR) is confirmed by calculation of combination index (CI). Also, BI 2536 and VCR act in concert to reduce long-term clonogenic survival. Importantly, BI 2536 significantly enhances the antitumor activity of VCR in an in vivo model of NB. Mechanistically, BI 2536/VCR co-treatment triggers prolonged mitotic arrest, which is necessary for BI 2536/VCR-mediated apoptosis, since pharmacological inhibition of mitotic arrest by the CDK1 inhibitor RO-3306 significantly reduces cell death. Prolonged mitotic arrest leads to phosphorylation-mediated inactivation of BCL-2 and BCL-XL as well as downregulation of MCL-1, since inhibition of mitotic arrest by RO-3306 also prevents phosphorylation of BCL-2 and BCL-XL and MCL-1 downregulation. This inactivation of antiapoptotic BCL-2 proteins promotes activation of BAX and BAK, cleavage of caspase-9 and -3 and caspase-dependent apoptosis. Engagement of the mitochondrial pathway of apoptosis is critically required for BI 2536/VCR-induced apoptosis, since ectopic expression of a non-degradable MCL-1 phospho-mutant, BCL-2 overexpression or BAK knockdown significantly reduce BI 2536/VCR-mediated apoptosis. Thus, PLK1 inhibitors may open new perspectives for chemosensitization of NB.
    Type of Publication: Journal article published
    PubMed ID: 26046302
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  • 7
    Keywords: brain ; Germany ; human ; MODEL ; MODELS ; IMAGES ; imaging ; INFORMATION ; TISSUE ; TISSUES ; CONTRAST ; PERFORMANCE ; REGISTRATION ; TRANSFORMATION ; BEHAVIOR ; DEFORMATION ; STANDARD ; SOFTWARE ; human brain ; DEFORMATIONS ; elastic registration ; Navier equation ; spline interpolation
    Abstract: We introduce a new point-based elastic registration scheme for medical images which is based on elastic body splines (EBS). Since elastic body splines result from a physical model in form of analytical solutions of the Navier equation these splines describe elastic deformations of physical objects. This property is advantageous in medical registration applications, in which the geometric differences between the images are often caused by physical deformations of human tissue due to surgical interventions or pathological processes. In this contribution we introduce a new class of elastic body splines which is based on Gaussian forces (GEBS). By varying the standard deviation of the Gaussian forces our new approach is well suited to cope with local as well as global differences in the images. This is in contrast to the previous EBS approach where polynomial and rational forces have been used. We demonstrate the performance of our new approach by presenting two different kinds of experiments. First, we demonstrate that this approach well approximates deformations given by an analytic solution of the Navier equation. Second, we apply our approach to pre- and postsurgical tomographic images of the human brain. It turns out that the new EBS approach well models the physical deformation behavior of tissues and in the case of local deformations performs significantly better than the previous EBS
    Type of Publication: Journal article published
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  • 8
    Keywords: EXPRESSION ; Germany ; IN-VIVO ; MICROSCOPY ; liver ; RISK ; PROTEIN ; PROTEINS ; transcription ; DRUG ; METABOLISM ; FAMILY ; RAT ; RATS ; CONTRAST ; TRANSPORT ; RAT-LIVER ; resistance ; POLYPEPTIDE ; POLYMERASE-CHAIN-REACTION ; MULTIDRUG-RESISTANCE PROTEIN ; PHARMACOKINETICS ; rat liver ; MULTIDRUG-RESISTANCE ; MRP2 ; SUBSTRATE-SPECIFICITY ; ORGANIC ANION TRANSPORTER ; multidrug resistance ; INCREASE ; secretion ; polymerase chain reaction ; TRANSPORTER ; regulation ; POLYPEPTIDES ; FEMALE RATS ; GENDER ; EVENTS ; immunofluorescence ; multidrug resistance protein ; DEHYDROEPIANDROSTERONE-SULFATE ; MRP3 ; MRP ; CONSTITUTIVE ANDROSTANE RECEPTOR ; DHEA-S ; MRP FAMILY ; PREGNANE X-RECEPTOR ; SEX-DIFFERENCES
    Abstract: Background Sex differences in drug pharmacokinetics have been well recognized and gender has been considered a risk factor for adverse events to medications. The aim of this study was to investigate the effect of gender on the expression of hepatocellular transport proteins involved in uptake and secretion of organic anions in rat. Materials and methods Expression of the rat liver organic anion transporting polypeptides (Oatps) and multidrug resistance proteins (Mrps) was analysed by reverse transcription polymerase chain reaction (RT-PCR), immunoblot analysis and immunofluorescence microscopy in male and female rats. Regulation of these transport proteins in response to the steroid dehydroepiandrosterone (DHEA) was investigated. Results In untreated rats, protein expression significantly differed between genders being higher (Mrp2, Mrp3), comparable [Oatp1a1 (Oatp1); Oatp1b2 (Oatp4)] or lower [Oatp1a4 (Oatp2)] in female than in male rat. DHEA treatment over 3 days (100 mg d(-1)) led to a further increase in Mrp3 expression only in female rats. Mrp2 expression was not influenced by DHEA treatment. Oatp1a1 and Oatp1b2 were significantly down-regulated after DHEA treatment in both male and female rats. In contrast, Oatp1a4 was down-regulated in male rats only. Conclusions In rat, liver transport proteins of the Oatp and Mrp family are expressed and regulated in a gender-specific manner according to sexual differences in the hepatic metabolism of steroids and drugs. These findings may partly explain the well-known sex differences in hepatic handling of organic anions
    Type of Publication: Journal article published
    PubMed ID: 16178883
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  • 9
    Keywords: Germany ; DEATH ; DISEASE ; liver ; POPULATION ; DISTINCT ; GENE ; GENES ; PATIENT ; FAMILY ; MEMBERS ; polymorphism ; single nucleotide polymorphism ; ACID ; TRANSPORT ; AGE ; LINKAGE ANALYSIS ; MUTATION ; etiology ; DAMAGE ; genotyping ; MUTATIONS ; FAILURE ; fibrosis ; ADULT ; ADULTS ; CHILDHOOD ; SIBLINGS ; FAMILIES ; CANDIDATE GENES ; TRANSPORTER ; BILE ; hepatobiliary transport ; MUTATIONAL ANALYSIS ; analysis ; single-nucleotide polymorphism ; PREGNANCY ; USA ; MDR3 GENE ; CANDIDATE ; LIVER-DISEASE ; URSODEOXYCHOLIC ACID ; FAMILY-MEMBERS ; GENOME-WIDE ; BILIARY-CIRRHOSIS ; CHOLELITHIASIS ; FAMILIAL INTRAHEPATIC CHOLESTASIS ; SCLEROSING CHOLANGITIS
    Abstract: Cholestatic liver disease (CLD) is a major cause of progressive liver damage and liver failure. Several forms of biliary cirrhosis are caused by mutations in specific genes. We sought to identify a genetic defect in a family with CLD impossible to assign to a distinct pathogenic entity. Clinical and histopathological characterization of the family members, microarray-based single-nucleotide polymorphism genotyping, and analysis of candidate genes were performed. Among six of I I siblings severely affected by idiopathic CLD in a family from a population isolate in Transylvania, three died of cirrhosis (aged 5, 7, and 43 years) and three had adult-onset disease with small duct cholangiopathy, including ductopenia. Others were mildly affected and experienced intrahepatic cholestasis of pregnancy, miscarriages, or stillbirth. Pedigree studies revealed distant parental consanguinity. Genome-wide linkage analysis and autozygosity mapping yielded a single maximal lod-score of 3.88 on chromosome 7q21.1-7q22, excluding other genomic loci. Sequencing of ABCB4 at this locus revealed a novel missense mutation c.2362C〉T (p.Arg788Trp) which cosegregated with severity of disease. Bile from a mutation homozygote showed a reduced phosphatidylcholine/bile acid ratio, consistent with reduced ABCB4 phosphatidylcholine transport activity. Conclusion: We show that a missense mutation in ABCB4 is a cause for ductopenic CLD in adulthood. Allelic status correlated with severity of liver disease ranging from intrahepatic cholestasis of pregnancy through fibrosis to cirrhosis and death in childhood and adulthood. Mutational analysis of ABCB4 should be generally considered in all patients with cholestatic liver disease of unknown etiology regardless of age and onset of disease
    Type of Publication: Journal article published
    PubMed ID: 18781607
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  • 10
    Abstract: In patients with acute myeloid leukemia and low percentages of aldehyde-dehydrogenase-positive cells, non-leukemic hematopoietic stem cells can be separated from leukemic cells. By relating hematopoietic stem cell frequencies to outcome we detected poor overall- and disease-free survival of patients with low hematopoietic stem cell frequencies. Serial analysis of matched diagnostic and follow-up samples further demonstrated that hematopoietic stem cells increased after chemotherapy in patients who achieved durable remissions. However, in patients who eventually relapsed, hematopoietic stem cell numbers decreased dramatically at the time of molecular relapse demonstrating that hematopoietic stem cell levels represent an indirect marker of minimal residual disease, which heralds leukemic relapse. Upon transplantation in immune-deficient mice cases with low percentages of hematopoietic stem cells of our cohort gave rise to leukemic or no engraftment, whereas cases with normal hematopoietic stem cell levels mostly resulted in multi-lineage engraftment. Based on our experimental data, we propose that leukemic stem cells have increased niche affinity in cases with low percentages of hematopoietic stem cells. To validate this hypothesis, we developed new mathematical models describing the dynamics of healthy and leukemic cells under different regulatory scenarios. These models suggest that the mechanism leading to decreases in hematopoietic stem cell frequencies before leukemic relapse must be based on expansion of leukemic stem cells with high niche affinity and the ability to dislodge hematopoietic stem cells. Thus, our data suggest that decreasing numbers of hematopoietic stem cells indicate leukemic stem cell persistence and the emergence of leukemic relapse.
    Type of Publication: Journal article published
    PubMed ID: 28550184
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