Die folgenden Links führen aus den jeweiligen lokalen Bibliotheken zum Volltext:
Alternativ können Sie versuchen, selbst über Ihren lokalen Bibliothekskatalog auf das gewünschte Dokument zuzugreifen.
Bei Zugriffsproblemen kontaktieren Sie uns gern.
34 Ergebnisse
Sortierung:
SSRN
Working paper
SSRN
In: Community development journal, Band 58, Heft 4, S. 719-723
ISSN: 1468-2656
SSRN
SSRN
In: Waste management: international journal of integrated waste management, science and technology, Band 146, S. 119-129
ISSN: 1879-2456
In: World development: the multi-disciplinary international journal devoted to the study and promotion of world development, Band 36, Heft 4, S. 706-726
In: World development: the multi-disciplinary international journal devoted to the study and promotion of world development, Band 36, Heft 4, S. 706-726
ISSN: 0305-750X
World Affairs Online
In: European Accounting Review, forthcoming
SSRN
In: Reproductive sciences: RS : the official journal of the Society for Reproductive Investigation, Band 30, Heft 4, S. 1065-1073
ISSN: 1933-7205
In: Environmental sciences Europe: ESEU, Band 32, Heft 1
ISSN: 2190-4715
Abstract
Background
Exposure to airborne fine particulate matter (PM2.5) has been declared to be harmful to human kidney. However, whether activation of the autophagic pathway plays key roles in the nephrotoxicity caused by PM2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of kidney damage after PM2.5 exposure in vivo and in vitro.
Results
In the present study, statistically significant alterations in water intake, urine flow rate and mean blood pressure were observed between the concentrated PM2.5 (PM2.5) group and the filtered air (FA) group. Exposed animals showed severe edema of renal tubular epithelial cells, capillary congestion, reduction of the glomerular urinary space and early pro-fibrotic state. Moreover, significant increases in the levels of early kidney damage markers were observed in the exposed rats and these animals exhibited more apoptosis rate in kidney cells. In addition, PM2.5 exposure activated the autophagic pathway, as evidenced by LC3-I to LC3-II conversion, activation of P62 and beclin-1. All of these effects are in concurrence with the presence of more autophagosomes both in vivo and in vitro after PM2.5 exposure.
Conclusions
Taken together, our findings indicated that PM2.5 induced renal function impairment via the activation of the autophagic pathway in renal tubular epithelial cells.
In: Environmental science and pollution research: ESPR, Band 27, Heft 34, S. 43246-43261
ISSN: 1614-7499
In: Environmental science and pollution research: ESPR, Band 25, Heft 1, S. 153-162
ISSN: 1614-7499
In: Australian Journal of Agricultural and Resource Economics, Band 64, Heft 1, S. 126-149
SSRN
In: Environmental science and pollution research: ESPR, Band 30, Heft 26, S. 68191-68205
ISSN: 1614-7499