scholarly journals Role of anoxia, euxinia and microbes in seafloor hydrothermal sulphide (VMS and SEDEX) deposit formation

2017 ◽  
Author(s):  
J M Peter ◽  
M G Gadd ◽  
D Layton-Matthews ◽  
S E Jackson ◽  
B E Taylor ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Donita L. Garland ◽  
Eric A. Pierce ◽  
Rosario Fernandez-Godino

AbstractThe complement system plays a role in the formation of sub-retinal pigment epithelial (RPE) deposits in early stages of age-related macular degeneration (AMD). But the specific mechanisms that connect complement activation and deposit formation in AMD patients are unknown, which limits the development of efficient therapies to reduce or stop disease progression. We have previously demonstrated that C3 blockage prevents the formation of sub-RPE deposits in a mouse model of EFEMP1-associated macular degeneration. In this study, we have used double mutant Efemp1R345W/R345W:C5-/- mice to investigate the role of C5 in the formation of sub-RPE deposits in vivo and in vitro. The data revealed that the genetic ablation of C5 does not eliminate the formation of sub-RPE deposits. Contrarily, the absence of C5 in RPE cultures promotes complement dysregulation that results in increased activation of C3, which likely contributes to deposit formation even in the absence of EFEMP1-R345W mutant protein. The results also suggest that genetic ablation of C5 alters the extracellular matrix turnover through an effect on matrix metalloproteinases in RPE cell cultures. These results confirm that C3 rather than C5 could be an effective therapeutic target to treat early AMD.



1991 ◽  
Vol 14 (1) ◽  
pp. 21-28 ◽  
Author(s):  
Jane M. Abbott ◽  
Roderick W.J. Bowers ◽  
Valerie J. Franklin ◽  
Brian J. Tighe
Keyword(s):  


2014 ◽  
Vol 87 ◽  
pp. 71-79 ◽  
Author(s):  
Fabio Scenini ◽  
Gaetano Palumbo ◽  
Nicholas Stevens ◽  
Anthony Cook ◽  
Andrew Banks


2005 ◽  
Vol 14 (1) ◽  
pp. 109-116 ◽  
Author(s):  
D. Zhang ◽  
P.H. Shipway ◽  
D.G. McCartney


2021 ◽  
Author(s):  
Donita Garland ◽  
Eric Pierce ◽  
Rosario Fernandez-Godino

Abstract The complement system plays a role in the formation of sub-retinal pigment epithelial (RPE) deposits in early stages of age-related macular degeneration (AMD). But the specific mechanisms that connect complement activation and deposit formation in AMD patients are unknown, which limits the development of efficient therapies to reduce or stop disease progression. We have previously demonstrated that C3 blockage prevents the formation of sub-RPE deposits in a mouse model of EFEMP1-associated macular degeneration. In this study, we have used double mutant Efemp1R345W/R345W:C5-/- mice to investigate the role of C5 in the formation of sub-RPE deposits in vivo and in vitro. The data revealed that the genetic ablation of C5 does not eliminate the formation of sub-RPE deposits. Contrarily, the absence of C5 in RPE cultures promotes complement dysregulation that results in increased activation of C3, which likely contributes to deposit formation even in the absence of EFEMP1-R345W mutant protein. The results also suggest that genetic ablation of C5 alters the extracellular matrix turnover through an effect on matrix metalloproteinases in RPE cell cultures. These results confirm that C3 rather than C5 could be an effective therapeutic target to treat early AMD.



2013 ◽  
Vol 76 ◽  
pp. 92-97 ◽  
Author(s):  
Feng-e Zhang ◽  
Yanhong Wang ◽  
Zhe Wang ◽  
Ping Li ◽  
Sheng Zhang ◽  
...  


2020 ◽  
Author(s):  
Donita L. Garland ◽  
Eric A. Pierce ◽  
Rosario Fernandez-Godino

ABSTRACTThe complement system plays a role in the formation of sub-retinal pigment epithelial (RPE) deposits in early stages of age-related macular degeneration (AMD). But the specific mechanisms that connect complement activation and deposit formation in AMD patients are unknown, which limits the development of efficient therapies to reduce or stop disease progression. We have previously demonstrated that C3 blockage prevents the formation of sub-RPE deposits in a mouse model of EFEMP1-associated macular degeneration. In this study, we have used double mutant Efemp1R345W/R345W:C5-/- mice to investigate the role of C5 in the formation of sub-RPE deposits in vivo and in vitro. The data revealed that the genetic ablation of C5 does not eliminate the formation of sub-RPE deposits in vivo or in vitro. Contrarily, the absence of C5 in RPE cultures promotes complement dysregulation that results in increased activation of C3, which likely contributes to deposit formation even in the absence of EFEMP1-R345W mutant protein. The results also suggest that genetic ablation of C5 alters the extracellular matrix turnover through an effect on matrix metalloproteinases in RPE cell cultures. These results confirm that C3 rather than C5 could be an effective therapeutic target to treat early AMD.



Author(s):  
T L Chou ◽  
G H Priestman

Most previous laboratory-scale deposit simulator studies have considered mainly fuel or lubricant composition and properties, with no consideration of possible effects of NOx, which may affect initiation of the deposit formation process and the overall rate at which deposition occurs. In this study a laboratory-scale deposit simulator was developed which produced thin deposit films by spraying gasoline on to a heated aluminium sleeve to investigate the effects of temperature, NO2 and possible gasoline blending components, on deposit formation. The amount of deposit collected is indicative of the deposit-forming tendency of the test fuel. The deposit film composition was analysed using Fourier transform infrared (FTIR) spectroscopy. The results of the experiments indicate that deposit formation is indeed sensitive to NO2, in addition to the effects of temperature and the molecular structure of the hydrocarbons. Thus the effect of NOx in deposit-related studies is important and should not be ignored. The FTIR analyses showed that when using NO2 the deposits are of a very similar structure to those produced in a real engine test. The analyses also gave some insight into the role of NO2 in the deposit formation mechanism.



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