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RISS 인기검색어
- 검색키워드
- 저자 : Multhaupt, Hinke A. B. (검색결과 3 건)
- 무료
- 기관 내 무료
- 유료
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Eichler, Christian,Pia, Multhaupt,Sibylle, Multhaupt,Sauerwald, Axel,Friedrich, Wolff,Warm, Mathias Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.3
Background: Tumor associated fatigue (TAF) or cancer related fatigue (CRF) is not a new concept. Nonetheless, no real headway has been made in the quantitative analysis of its successful treatment via cognitive behavioral therapy. Since 20 to 30% of all breast cancer patients suffer from anxiety and/or depression within the first year of their diagnosis, this issue needs to be addressed and a standard treatment protocol has to be developed. This study focused on developing a simple, reproducible and short (8 weeks) protocol for the cognitive behavioral therapy support of tumor associated fatigue patients. Materials and Methods: Between the year 2011 and 2012, 23 breast cancer patients fulfilled the diagnosis TAF requirements and were introduced into this study. Our method focused on a psycho-oncological support group using a predetermined, highly structured and reproducible, cognitive behavioral therapy treatment manual. Eight weekly, 90 minute sessions were conducted and patients were evaluated before and after this eight session block. Tumor fatigue specific questionnaires such as the multidimensional fatigue inventory (MFI) as well as the hospital anxiety and depression scale (HADS) were used in order to quantitatively evaluate patient TAF. Results: Of the 23 patients enrolled in the study, only 7 patients fulfilled the TAF diagnostic criteria after the psycho-oncological group treatment. This represents a 70% reduction in diagnosable tumor associated fatigue. The HADS analysis showed a 33% reduction in patient anxiety as well as a 57% reduction in patient depression levels. The MFI scores showed a significant reduction in 4 of the 5 evaluate categories. With the exception of the "mental fatigue" MFI category all results were statistically significant. Conclusions: This study showed that a highly structured, cognitive behavioral therapy group intervention will produce significant improvements in breast cancer patient tumor associated fatigue levels after only 8 weeks.
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Chung, Heesung,Jung, Hyejung,Jho, Eek-hoon,Multhaupt, Hinke A.B.,Couchman, John R.,Oh, Eok-Soo Elsevier 2018 Biochemical and biophysical research communication Vol.503 No.2
<P><B>Abstract</B></P> <P>In human skin, melanocytes and their neighboring keratinocytes have a close functional interrelationship. Keratinocytes, which represent the prevalent cell type of human skin, regulate melanocytes through various mechanisms. Here, we use a keratinocyte and melanoma co-culture system to show for the first time that keratinocytes regulate the cell surface expression of N-cadherin through cell-cell contact. Compared to mono-cultured human melanoma A375 cells, which expressed high levels of N-cadherin, those co-cultured with the HaCaT human keratinocyte cell line showed reduced levels of N-cadherin. This reduction was most evident in areas of A375 cells that underwent cell-cell contact with the HaCaT cells, whereas HaCaT cell-derived extracellular matrix and conditioned medium both failed to reduce N-cadherin levels. The intracellular level of calcium in co-cultured A375 cells was lower than that in mono-cultured A375 cells, and treatment with a cell-permeant calcium chelator (BAPTA) reduced the N-cadherin level of mono-cultured A375 cells. Furthermore, co-culture with HaCaT cells reduced the expression levels of transient receptor potential cation channel (TRPC) 1, −3 and −6 in A375 cells, and siRNA-mediated multi-depletion of TRPC1, -3 and -6 reduced the N-cadherin level in these cells. Taken together, these data suggest that keratinocytes negatively regulate the N-cadherin levels of melanoma cells via cell-to-cell contact-mediated calcium regulation.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Human keratinocyte cells reduce the N-cadherin levels of co-cultured melanoma cells. </LI> <LI> Cell-to-cell contact is necessary for this keratinocyte-mediated N-cadherin reduction. </LI> <LI> Keratinocytes reduce intracellular calcium in co-cultured melanoma cells. </LI> <LI> Keratinocytes reduce the expression of TRPCs in contacting melanoma cells. </LI> </UL> </P>
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Dovas, Athanassios,Choi, Youngsil,Yoneda, Atsuko,Multhaupt, Hinke A. B.,Kwon, Seung-Hae,Kang, Dongmin,Oh, Eok-Soo,Couchman, John R. American Society for Biochemistry and Molecular Bi 2010 The Journal of biological chemistry Vol.285 No.30
<P>Conventional protein kinase C (PKC) isoforms are essential serine/threonine kinases regulating many signaling networks. At cell adhesion sites, PKCα can impact the actin cytoskeleton through its influence on RhoGTPases, but the intermediate steps are not well known. One important regulator of RhoGTPase function is the multifunctional guanine nucleotide dissociation inhibitor RhoGDIα that sequesters several related RhoGTPases in an inactive form, but it may also target them through interactions with actin-associated proteins. Here, it is demonstrated that conventional PKC phosphorylates RhoGDIα on serine 34, resulting in a specific decrease in affinity for RhoA but not Rac1 or Cdc42. The mechanism of RhoGDIα phosphorylation is distinct, requiring the kinase and phosphatidylinositol 4,5-bisphosphate, consistent with recent evidence that the inositide can activate, localize, and orient PKCα in membranes. Phosphospecific antibodies reveal endogenous phosphorylation in several cell types that is sensitive to adhesion events triggered, for example, by hepatocyte growth factor. Phosphorylation is also sensitive to PKC inhibition. Together with fluorescence resonance energy transfer microscopy sensing GTP-RhoA levels, the data reveal a common pathway in cell adhesion linking two essential mediators, conventional PKC and RhoA.</P>
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