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  • 1
    Language: German
    Description: Paradoxerweise aktiviert Sorafenib in menschlichen polyklonal expandierten NK-Zellen den MAPK/ERK- Signaltransduktionsweg und führt zeit- und dosisabhängig zu einer Verstärkung der Effektorfunktionen. Polyklonal expandierte NK-Zellen von gesunden menschlichen Blutspendern wurden mit Sorafenib bzw. dem spezifischen RAF-Inhibitor ZM336372 in variierenden Konzentrationen und Expositionsdauern behandelt und die Effekte auf NK-Zell Effektorfunktionen sowie Signaltansduktion geprüft. Paradoxerweise führte die Behandlung mit Sorafenib sowie ZM336372 in einem bestimmten Konzentrationsbereich zeitabhängig zu einer Verstärkung der Effektorfunktionen. Diese Effekte waren mit einem erhöhten Phosphorylierungsniveau von ERK1/2 sowie CRAF verbunden, während keine Effekte auf AKT zu beobachten waren. Sorafenib paradoxically activates NK cell effector function in polyclonal expanded NK cells in a time- and dose dependent manner. Polyclonal NK cells from healthy blood donors were treated with with Sorafenib or ZM336372 with varying concentations and exposition duration. Treatment with Paradoxicall Sorafenib and the specific RAF Inhibitor ZM336372 led in a certain dosing range to an increase in NK cell effector function and increased phosphorylation Level of CRAF and ERK1/2. The phosphorylation level of AKT was not altered.
    Keywords: Paradoxe Craf-Aktivierung ; Sorafenib ; Nk-Zellen ; Zm336372 ; Ddc:610
    Source: Networked Digital Library of Theses and Dissertations
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  • 2
    In: Schneider, Constanze and Oellerich, Thomas and Baldauf, Hanna-Mari and Schwarz, Sarah-Marie and Thomas, Dominique and Flick, Robert and Bohnenberger, Hanibal and Kaderali, Lars and Stegmann, Lena and Cremer, Anjali and Martin, Margarethe and Lohmeyer, Julian and Michaelis, Martin and Hornung, Veit and Schliemann, Christoph and Berdel, Wolfgang E and Hartmann, Wolfgang and Wardelmann, Eva and Comoglio, Federico and Hansmann, Martin-Leo and Yakunin, Alexander F and Geisslinger, Gerd and Ströbel, Philipp and Ferreirós, Nerea and Serve, Hubert and Keppler, Oliver T and Cinatl, Jindrich (2016) SAMHD1 is a biomarker for cytarabine response and a therapeutic target in acute myeloid leukemia. Nature medicine, 23 (2). pp. 250-255.
    Description: The nucleoside analog cytarabine (Ara-C) is an essential component of primary and salvage chemotherapy regimens for acute myeloid leukemia (AML). After cellular uptake, Ara-C is converted into its therapeutically active triphosphate metabolite, Ara-CTP, which exerts antileukemic effects, primarily by inhibiting DNA synthesis in proliferating cells. Currently, a substantial fraction of patients with AML fail to respond effectively to Ara-C therapy, and reliable biomarkers for predicting the therapeutic response to Ara-C are lacking. SAMHD1 is a deoxynucleoside triphosphate (dNTP) triphosphohydrolase that cleaves physiological dNTPs into deoxyribonucleosides and inorganic triphosphate. Although it has been postulated that SAMHD1 sensitizes cancer cells to nucleoside-analog derivatives through the depletion of competing dNTPs, we show here that SAMHD1 reduces Ara-C cytotoxicity in AML cells. Mechanistically, dGTP-activated SAMHD1 hydrolyzes Ara-CTP, which results in a drastic reduction of Ara-CTP in leukemic cells. Loss of SAMHD1 activity-through genetic depletion, mutational inactivation of its triphosphohydrolase activity or proteasomal degradation using specialized, virus-like particles-potentiates the cytotoxicity of Ara-C in AML cells. In mouse models of retroviral AML transplantation, as well as in retrospective analyses of adult patients with AML, the response to Ara-C-containing therapy was inversely correlated with SAMHD1 expression. These results identify SAMHD1 as a potential biomarker for the stratification of patients with AML who might best respond to Ara-C-based therapy and as a target for treating Ara-C-refractory AML.
    Keywords: RM Therapeutics. Pharmacology
    ISSN: 1078-8956
    Source: University of Kent
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  • 3
    In: Nature Medicine, 2016
    Description: The nucleoside analog cytarabine (Ara-C) is an essential component of primary and salvage chemotherapy regimens for acute myeloid leukemia (AML). After cellular uptake, Ara-C is converted into its therapeutically active triphosphate metabolite, Ara-CTP, which exerts antileukemic effects, primarily by inhibiting DNA synthesis in proliferating cells1. Currently, a substantial fraction of patients with AML fail to respond effectively to Ara-C therapy, and reliable biomarkers for predicting the therapeutic response to Ara-C are lacking2, 3. SAMHD1 is a deoxynucleoside triphosphate (dNTP) triphosphohydrolase that cleaves physiological dNTPs into deoxyribonucleosides and inorganic triphosphate4, 5. Although it has been postulated that SAMHD1 sensitizes cancer cells to nucleoside-analog derivatives through the depletion of competing dNTPs6, we show here that SAMHD1 reduces Ara-C cytotoxicity in AML cells. Mechanistically, dGTP-activated SAMHD1 hydrolyzes Ara-CTP, which results in a drastic reduction of Ara-CTP in leukemic cells. Loss of SAMHD1 activity--through genetic depletion, mutational inactivation of its triphosphohydrolase activity or proteasomal degradation using specialized, virus-like particles7, 8--potentiates the cytotoxicity of Ara-C in AML cells. In mouse models of retroviral AML transplantation, as well as in retrospective analyses of adult patients with AML, the response to Ara-C-containing therapy was inversely correlated with SAMHD1 expression. These results identify SAMHD1 as a potential biomarker for the stratification of patients with AML who might best respond to Ara-C-based therapy and as a target for treating Ara-C-refractory AML.
    Keywords: Leukemia ; Chemotherapy ; Biomarkers ; Medical Prognosis ; Cytotoxicity;
    ISSN: 1078-8956
    E-ISSN: 1546-170X
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  • 4
    In: Nature Medicine, 2017, Vol.23(6), p.788
    Description: Corrigendum: SAMHD1 is a biomarker for cytarabine response and a therapeutic target in acute myeloid leukemia
    Keywords: Medicine ; Biology;
    ISSN: 1078-8956
    E-ISSN: 1546-170X
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  • 5
    Language: English
    In: Journal of Plastic, Reconstructive & Aesthetic Surgery, August 2012, Vol.65(8), pp.1119-1122
    Description: So far a few case reports about laptops causing burns have been published. Now for the first time, we report on a case, in which notebook-induced thermal injuries placed in a patient’s lap resulted in severe second- and third-degree burns. As a consequence, a partial amputation of the left foot had to be performed. Furthermore, we measured maximum temperatures of 12 popular laptops, which were running full load for 3 h. For this experiment air circulation underneath the device was blocked in order to simulate surrounding conditions, which were present when the patient got injured. Although this setting may be the reason for most of all notebook burns, this kind of test has not been part of any scientific publication until now. Patients with lower extremity sensation, altered consciousness or decreased peripheral sensitivity have a higher risk for thermal injuries.
    Keywords: Severe Burns ; Thermal Injuries ; Laptop ; Notebook ; Foot Amputation ; Portable Computer
    ISSN: 1748-6815
    E-ISSN: 1878-0539
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  • 6
    Language: English
    In: Journal of Plastic, Reconstructive & Aesthetic Surgery, August, 2012, Vol.65(8), p.e223-e225
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.bjps.2012.03.017 Byline: Felix Julian Paprottka, Hans-Gunther Machens, Jorn Andreas Lohmeyer Abstract: Dysfunction of the lower limb's muscles can cause severe impairment and immobilisation of the patient. As one of the leg's major motor and sensory nerves, the deep peroneal nerve (synonym: deep fibular nerve) plays a very important role in muscle innervation in the lower extremities. We report the case of a 19-year-old female patient, who suffered from a brace-like exostosis 6-cm underneath her left fibular head causing a partially irreversible paresis of her deep peroneal nerve. This nerve damage resulted in complete atrophy of her extensor digitorum longus and extensor hallucis longus muscle, and in painful sensory disturbance at her left shin and first web space. The tibialis anterior muscle stayed intact because its motor branch left the deep peroneal nerve proximal to the nerve lesion. Diagnosis was first verified 6 years after the onset of symptoms by a magnetic resonance imaging (MRI) scan of her complete left lower leg. Subsequently, the patient was operated on in our clinic, where a neurolysis was performed and the 4-cm-long osteocartilaginous exostosis was removed. Paralysis was already irreversible but sensibility returned completely after neurolysis. The presented case shows that an osteocartilaginous exostosis can be the cause for partial deep peroneal nerve paresis. If this disorder is diagnosed at an early stage, nerve damage is reversible. Typical for an exostosis is its first appearance during the juvenile growth phase. Author Affiliation: Department of Plastic Surgery and Hand Surgery, Klinikum rechts der Isar, Technische Universitat Munchen, Ismaninger Str. 22, 81675 Munich, Germany Article History: Received 23 January 2012; Accepted 8 March 2012 Article Note: (footnote) [star] The following case report was so far not presented at any meeting.
    Keywords: Paralysis ; Plastic Surgery
    ISSN: 1748-6815
    Source: Cengage Learning, Inc.
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  • 7
    Language: English
    In: Antiviral therapy, 10 June 2019
    Description: Patients with chronic hepatitis C virus (HCV) infection are at increased risk to develop B-cell non-Hodgkin lymphoma (B-NHL). Regression of HCV-associated B-NHL (HCV-NHL) can be achieved through HCV eradication using interferon (IFN). However, only about two thirds of patients with sustained virologic response (SVR) also had a consecutive lymphoma response. MiRNA-26b is associated with HCV-NHL response to antiviral therapy. Recent data suggest that IFN-free direct acting antiviral (DAA) regimens also have anti-lymphoma activity in this patient population. We report four patients with HCV-NHL who were treated with different interferon-free DAA regimens as oncological monotherapy in our center between 2015 and 2016. We analyzed the virological and lymphoproliferative disease response. Moreover, we analyzed miRNA-26b expression in peripheral blood mononuclear cells at different time points during antiviral therapy for all included patients as well as for a total of ten controls with (n=5) and without (n=5) chronic HCV infection. All patients had marginal zone lymphoma subtype and received different DAA regimens for 12-24 weeks. All four patients achieved SVR, but only 3 patients also had lymphoma response (1 complete response 2 partial responses). One patient showed progression to a high-grade lymphoma subtype after SVR. MiRNA-26b expression was generally decreased in patients with HCV-NHL. Moreover, miRNA-26b expression was restored in those HCV-NHL patients with lymphoma response after 6 months (p=0.009). We could demonstrate that IFN-free DAA treatment of HCV can improve or even cure NHL. MiRNA-26b-levels could be a potentially useful biomarker to predict lymphoma response in HCV-NHL patients.
    E-ISSN: 2040-2058
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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  • 8
    Language: English
    In: Journal of Plastic, Reconstructive & Aesthetic Surgery, August 2012, Vol.65(8), pp.e223-e225
    Description: Dysfunction of the lower limb's muscles can cause severe impairment and immobilisation of the patient. As one of the leg's major motor and sensory nerves, the deep peroneal nerve (synonym: deep fibular nerve) plays a very important role in muscle innervation in the lower extremities. We report the case of a 19-year-old female patient, who suffered from a brace-like exostosis 6-cm underneath her left fibular head causing a partially irreversible paresis of her deep peroneal nerve. This nerve damage resulted in complete atrophy of her extensor digitorum longus and extensor hallucis longus muscle, and in painful sensory disturbance at her left shin and first web space. The tibialis anterior muscle stayed intact because its motor branch left the deep peroneal nerve proximal to the nerve lesion. Diagnosis was first verified 6 years after the onset of symptoms by a magnetic resonance imaging (MRI) scan of her complete left lower leg. Subsequently, the patient was operated on in our clinic, where a neurolysis was performed and the 4-cm-long osteocartilaginous exostosis was removed. Paralysis was already irreversible but sensibility returned completely after neurolysis. The presented case shows that an osteocartilaginous exostosis can be the cause for partial deep peroneal nerve paresis. If this disorder is diagnosed at an early stage, nerve damage is reversible. Typical for an exostosis is its first appearance during the juvenile growth phase.
    Keywords: Deep Peroneal Nerve ; Partial Paresis ; Osteocartilaginous Exostosis ; Weakness of Toe Dorsiflexion ; Sensory Disturbance ; Extensor Hallucis Longus and Digitorum Longus Muscle
    ISSN: 1748-6815
    E-ISSN: 1878-0539
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  • 9
    In: Plastic and Reconstructive Surgery Global Open, 2014, Vol.2(3), pp.e114-e114
    Description: SUMMARY:: Skin cancer formation is on the rise. Only a few case reports, which focus on skin cancer being caused by tattoos, have been published so far. Our aim is to determine whether skin cancer occurrence can be triggered by tattoos. In our presented case, a squamous-cell carcinoma developed inside of the red areas of a multicolored tattoo within months. Furthermore, surgical removal of the cancerously mutated skin area without mutilating the design of the tattoo was challenging. Due to widespread skin alterations in other red areas of the tattoo, those affected skin regions were surgically removed and split-skin grafting was performed. After 1-year follow-up period, the patient has been tumor free. Squamous-cell carcinoma is an unusual reaction that can occur in tattoos. Nevertheless, this skin cancer should be included in the list of cutaneous complications related to tattooing.
    ISSN: 2169-7574
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  • 10
    Language: English
    In: Biomaterials, October 2009, Vol.30(30), pp.5918-5926
    Description: Clinical success in tissue regeneration requires improvements in vascularization capacity of scaffolds. Several efforts have been made in this field including cellular and acellular technologies. In this work we combined the use of stem cells derived from pancreas or submandibular glands expressing green fluorescent protein (GFP ) with a commercially available scaffold for dermal regeneration. Cells were isolated, characterized and seeded in a scaffold for dermal regeneration. Scaffolds containing cells were used to induce dermal regeneration in a full skin defect model. After 3 weeks of regeneration, tissues were harvested and vascularization was analyzed. Results showed that gland-derived stem cells displayed stem cell features and presented multipotential differentiation capacity because they were able to differentiate in cell types representing the 3 different germ layers. After seeding, cells were homogeneously distributed and formed focal adhesions with the scaffold. Metabolic assays showed that cells can be cultured for at least 3 weeks in the scaffold. , the presence of pancreatic or submandibular stem cells significantly enhanced the vascularization compared to empty scaffolds. Presence of gland-derived stem cells in the regenerating tissue was confirmed by the detection of GFP expression in the wound area. In order to explore the possible mechanisms behind the improvement in vascular regeneration, experiments were performed, showing that gland-derived stem cells could contribute by angiogenic and vasculogenic mechanisms to this process. Our results suggest that the combined use of stem cells derived from glands and scaffold for dermal regeneration could be a rational alternative to improve vascularization in scaffold-mediated dermal regeneration.
    Keywords: Tissue Engineering ; Tissue Regeneration ; Stem Cells ; Dermis ; Vascularization ; Medicine ; Engineering
    ISSN: 0142-9612
    E-ISSN: 1878-5905
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