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  1. Article ; Online: Hydrogel spacers in prostate radiotherapy: a promising approach to decrease rectal toxicity.

    Padmanabhan, Ranjani / Pinkawa, Michael / Song, Daniel Y

    Future oncology (London, England)

    2017  Volume 13, Issue 29, Page(s) 2697–2708

    Abstract: High-dose radiation is a well-established method of treatment for prostate cancer. The main limiting structure for dose escalation is the rectum. The risk of rectal toxicity is related to dose received by the rectum. Several strategies for reducing dose ... ...

    Abstract High-dose radiation is a well-established method of treatment for prostate cancer. The main limiting structure for dose escalation is the rectum. The risk of rectal toxicity is related to dose received by the rectum. Several strategies for reducing dose to rectum have been explored; these include endorectal balloons as well as injection of rectal spacers like hydrogels. They create greater distance between rectal wall and prostate to confer a dosimetric advantage to the rectum. Early clinical studies with hydrogels have shown favorable outcomes. A low incidence of major procedural adverse effects with hydrogel use has been reported and it is well tolerated by patients. Hydrogel holds promise in establishing itself as an adjunct to standard of care in prostate radiation.
    MeSH term(s) Biocompatible Materials/chemistry ; Cost-Benefit Analysis ; Humans ; Hydrogel, Polyethylene Glycol Dimethacrylate/chemistry ; Male ; Polyethylene Glycols ; Prostatic Neoplasms/diagnosis ; Prostatic Neoplasms/radiotherapy ; Quality of Life ; Radiation Dosage ; Radiation Injuries/diagnosis ; Radiation Injuries/prevention & control ; Radiometry ; Radiosurgery/adverse effects ; Radiosurgery/methods ; Radiotherapy Planning, Computer-Assisted ; Radiotherapy, Intensity-Modulated/adverse effects ; Radiotherapy, Intensity-Modulated/methods ; Rectum/radiation effects ; Treatment Outcome
    Chemical Substances Biocompatible Materials ; Hydrogel, Polyethylene Glycol Dimethacrylate (25852-47-5) ; Polyethylene Glycols (30IQX730WE)
    Language English
    Publishing date 2017-11-23
    Publishing country England
    Document type Journal Article
    ZDB-ID 2184533-5
    ISSN 1744-8301 ; 1479-6694
    ISSN (online) 1744-8301
    ISSN 1479-6694
    DOI 10.2217/fon-2017-0073
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Identification of novel modulators of mitochondrial function by a genome-wide RNAi screen in Drosophila melanogaster.

    Chen, Jian / Shi, Xiaoying / Padmanabhan, Ranjani / Wang, Qiong / Wu, Zhidan / Stevenson, Susan C / Hild, Marc / Garza, Dan / Li, Hao

    Genome research

    2007  Volume 18, Issue 1, Page(s) 123–136

    Abstract: Mitochondrial dysfunction is associated with many human diseases. There has not been a systematic genetic approach for identifying regulators of basal mitochondrial biogenesis and function in higher eukaryotes. We performed a genome-wide RNA interference ...

    Abstract Mitochondrial dysfunction is associated with many human diseases. There has not been a systematic genetic approach for identifying regulators of basal mitochondrial biogenesis and function in higher eukaryotes. We performed a genome-wide RNA interference (RNAi) screen in Drosophila cells using mitochondrial Citrate synthase (CS) activity as the primary readout. We screened 13,071 dsRNAs and identified 152 genes that modulate CS activity. These modulators are involved in a wide range of biological processes and pathways including mitochondrial-related functions, transcriptional and translational regulation, and signaling pathways. Selected hits among the 152 genes were further analyzed for their effect on mitochondrial CS activity in transgenic flies or fly mutants. We confirmed a number of gene hits including HDAC6, Rpd3(HDAC1), CG3249, vimar, Src42A, klumpfuss, barren, and smt3 which exert effects on mitochondrial CS activities in vivo, demonstrating the value of Drosophila genome-wide RNAi screens for identifying genes and pathways that modulate mitochondrial function.
    MeSH term(s) Animals ; Chromosome Mapping ; Drosophila Proteins/genetics ; Drosophila Proteins/metabolism ; Drosophila melanogaster ; Genome, Insect/genetics ; Humans ; Mitochondria/enzymology ; Mitochondria/genetics ; Mitochondrial Diseases/enzymology ; Mitochondrial Diseases/genetics ; Protein Biosynthesis/genetics ; RNA Interference ; Signal Transduction/genetics ; Transcription, Genetic/genetics
    Chemical Substances Drosophila Proteins
    Language English
    Publishing date 2007-11-27
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1284872-4
    ISSN 1549-5469 ; 1088-9051 ; 1054-9803
    ISSN (online) 1549-5469
    ISSN 1088-9051 ; 1054-9803
    DOI 10.1101/gr.6940108
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3729: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 8: Show issues

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  3. Article ; Online: HDAC6 rescues neurodegeneration and provides an essential link between autophagy and the UPS.

    Pandey, Udai Bhan / Nie, Zhiping / Batlevi, Yakup / McCray, Brett A / Ritson, Gillian P / Nedelsky, Natalia B / Schwartz, Stephanie L / DiProspero, Nicholas A / Knight, Melanie A / Schuldiner, Oren / Padmanabhan, Ranjani / Hild, Marc / Berry, Deborah L / Garza, Dan / Hubbert, Charlotte C / Yao, Tso-Pang / Baehrecke, Eric H / Taylor, J Paul

    Nature

    2007  Volume 447, Issue 7146, Page(s) 859–863

    Abstract: A prominent feature of late-onset neurodegenerative diseases is accumulation of misfolded protein in vulnerable neurons. When levels of misfolded protein overwhelm degradative pathways, the result is cellular toxicity and neurodegeneration. Cellular ... ...

    Abstract A prominent feature of late-onset neurodegenerative diseases is accumulation of misfolded protein in vulnerable neurons. When levels of misfolded protein overwhelm degradative pathways, the result is cellular toxicity and neurodegeneration. Cellular mechanisms for degrading misfolded protein include the ubiquitin-proteasome system (UPS), the main non-lysosomal degradative pathway for ubiquitinated proteins, and autophagy, a lysosome-mediated degradative pathway. The UPS and autophagy have long been viewed as complementary degradation systems with no point of intersection. This view has been challenged by two observations suggesting an apparent interaction: impairment of the UPS induces autophagy in vitro, and conditional knockout of autophagy in the mouse brain leads to neurodegeneration with ubiquitin-positive pathology. It is not known whether autophagy is strictly a parallel degradation system, or whether it is a compensatory degradation system when the UPS is impaired; furthermore, if there is a compensatory interaction between these systems, the molecular link is not known. Here we show that autophagy acts as a compensatory degradation system when the UPS is impaired in Drosophila melanogaster, and that histone deacetylase 6 (HDAC6), a microtubule-associated deacetylase that interacts with polyubiquitinated proteins, is an essential mechanistic link in this compensatory interaction. We found that compensatory autophagy was induced in response to mutations affecting the proteasome and in response to UPS impairment in a fly model of the neurodegenerative disease spinobulbar muscular atrophy. Autophagy compensated for impaired UPS function in an HDAC6-dependent manner. Furthermore, expression of HDAC6 was sufficient to rescue degeneration associated with UPS dysfunction in vivo in an autophagy-dependent manner. This study suggests that impairment of autophagy (for example, associated with ageing or genetic variation) might predispose to neurodegeneration. Morover, these findings suggest that it may be possible to intervene in neurodegeneration by augmenting HDAC6 to enhance autophagy.
    MeSH term(s) Animals ; Autophagy/genetics ; Autophagy/physiology ; Disease Models, Animal ; Drosophila Proteins/metabolism ; Drosophila melanogaster/genetics ; Drosophila melanogaster/metabolism ; Histone Deacetylase 6 ; Histone Deacetylases/metabolism ; Humans ; Muscular Disorders, Atrophic/genetics ; Muscular Disorders, Atrophic/metabolism ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism ; Peptides/genetics ; Peptides/metabolism ; Proteasome Endopeptidase Complex/genetics ; Proteasome Endopeptidase Complex/metabolism ; Receptors, Androgen/genetics ; Receptors, Androgen/metabolism ; Ubiquitin/metabolism
    Chemical Substances Drosophila Proteins ; Peptides ; Receptors, Androgen ; Ubiquitin ; polyglutamine (26700-71-0) ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; HDAC6 protein, Drosophila (EC 3.5.1.98) ; Histone Deacetylase 6 (EC 3.5.1.98) ; Histone Deacetylases (EC 3.5.1.98)
    Language English
    Publishing date 2007-06-14
    Publishing country England
    Document type Journal Article
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/nature05853
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 26: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 9: Show issues
    Zs.MO 244: Show issues

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