LEADER 00898nam0 2200265 450 001 000025019 005 20090325131946.0 100 $a20090325d1981----km-y0itay50------ba 101 1 $aita$cger 102 $aIT 105 $ay-------001yy 200 1 $aSulla Russia$e1905-6/1917$fMax Weber$gtraduzione di Mauro Protti 210 $aBologna$cIl Mulino$dc1981 215 $a187 p.$d18 cm 225 2 $aUniversale paperbacks Il mulino$v128 410 0$12001$aUniversale paperbacks Il mulino 500 10$aZur Lage der burgelichen Demokratie in Russland$m$943780 610 1 $aRussia$aPolitica$a1905-1917 676 $a947$v18 700 1$aWeber,$bMax$f<1864-1920>$4070$032785 801 0$aIT$bUNIPARTHENOPE$c20090325$gRICA$2UNIMARC 912 $a000025019 951 $a060/10$b333$cNAVA2$d2009 996 $aZur Lage der burgelichen Demokratie in Russland$943780 997 $aUNIPARTHENOPE LEADER 04416nam 2200745z- 450 001 9910557382703321 005 20220111 035 $a(CKB)5400000000042072 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/76942 035 $a(oapen)doab76942 035 $a(EXLCZ)995400000000042072 100 $a20202201d2021 |y 0 101 0 $aeng 135 $aurmn|---annan 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 00$aCellular Senescence in Health, Disease and Aging: Blessing or Curse? 210 $aBasel, Switzerland$cMDPI - Multidisciplinary Digital Publishing Institute$d2021 215 $a1 online resource (112 p.) 311 08$a3-0365-2175-5 311 08$a3-0365-2176-3 330 $aDear Colleagues, When Hayflick and Moorhead coined the term "cellular senescence" (CS) almost 60 years ago, this phenomenon was understood as a mechanism, usually induced by activation of the DNA-repair machinery, to prevent uncontrolled proliferation. Meanwhile, additional beneficial roles for CS have been identified, such as embryonic development and wound healing. The senescence associated secretory phenotype (SASP) activated in most senescent cells (SC) signals to the immune system "come here and remove me". In organisms with young and functional immune systems, occurring SC are usually detected and removed. If SC remain in the tissue expressing the SASP, this will cause not just a damaging local inflammation but can also induce remodeling and regeneration of the surrounding tissue as well as spreading of senescence. Old organisms show reduced regenerative potential and immune function which leads to accumulation of SC. Accordingly, accumulation of SC was observed in tissues of aged individuals, but importantly also in the context of age-related disorders, neurodegenerative, or cardiovascular diseases and others. Because of its detrimental effect of the surrounding tissue, accumulation of SC is not just a consequence, but can rather been understood as a major driver of aging. In line with this, recent studies described that removal of SC showed beneficial effects on healthspan and lifespan. This exciting research led to the discovery of "senolytics", drugs which can kill SC. Given the heterogeneity of cell types that show senescence-like phenotypes, including heart muscle and post-mitotic neuronal cells, further research is required to unravel the molecular background that renders a cell type vulnerable to senesce. Additionally, it will be important to understand how senescence is cell type-specifically induced and which molecules serve as drug targets to prevent senescence and its spreading, or actively kill SC. This special issue will shed light on the molecular pathways of CS and inflammaging and on possible strategies to interfere with these processes. Dr. Markus Riessland Guest Editor 517 $aCellular Senescence in Health, Disease and Aging 606 $aBiology, life sciences$2bicssc 606 $aResearch and information: general$2bicssc 610 $aAIM2 inflammasome 610 $aAlzheimer's disease 610 $aamyotrophic lateral sclerosis 610 $abiology of aging 610 $abrain 610 $acancer 610 $acell-cycle 610 $acellular senescence 610 $achemotherapy resistance 610 $aDNA damage 610 $ageroscience 610 $ahomeostasis 610 $ainflammation 610 $amelanoma 610 $amild cognitive impairment 610 $an/a 610 $aneurodegeneration 610 $aneuronal senescence 610 $apancreatic adenocarcinoma 610 $aPOP3 610 $apost-mitotic 610 $aprostate 610 $aregeneration 610 $asecreted protein acidic and rich in cysteine 610 $asenescence 610 $asenescence-associated secretory phenotype (SASP) 610 $asenolytics 610 $astress response 610 $atauopathy 610 $atumor infiltration 610 $a?H2AX 615 7$aBiology, life sciences 615 7$aResearch and information: general 700 $aRiessland$b Markus$4edt$01327006 702 $aRiessland$b Markus$4oth 906 $aBOOK 912 $a9910557382703321 996 $aCellular Senescence in Health, Disease and Aging: Blessing or Curse$93037786 997 $aUNINA