Kappa light chain nephropathy

1983 ◽  
Vol 50 (2) ◽  
pp. 243-246
Author(s):  
W. R. Hart ◽  
G. N. Gephardt
1982 ◽  
Vol 2 (5) ◽  
pp. 276-281 ◽  
Author(s):  
Robert M. Gipstein ◽  
Arthur H. Cohen ◽  
Donald A. Adams ◽  
Thompson Adams ◽  
Morris T. Grabie

2019 ◽  
Vol 18 (2) ◽  
pp. 176-182
Author(s):  
Chen Weiyan ◽  
Deng Wujian ◽  
Chen Songwei

Acute lung injury is a clinical syndrome consisting of a wide range of acute hypoxemic respiratory failure disorders. Sepsis is a serious complication caused by an excessive immune response to pathogen-induced infections, which has become a major predisposing factor for acute lung injury. Taxifolin is a natural flavonoid that shows diverse therapeutic benefits in inflammation- and oxidative stress-related diseases. In this study, we investigated the role of taxifolin in a mouse model of cecal ligation and puncture-induced sepsis. Cecal ligation and puncture-operated mice presented damaged alveolar structures, thickened alveolar walls, edematous septa, and hemorrhage compared to sham-treated controls. Cecal ligation and puncture mice also showed increased wet-to-dry (W/D) lung weight ratio and elevated total protein concentration and lactate dehydrogenase level in bronchoalveolar lavage fluid. Taxifolin treatment protected animals against sepsis-induced pulmonary damage and edema. Septic mice presented compromised antioxidant capacity, whereas the administration of taxifolin prior to cecal ligation and puncture surgery decreased malondialdehyde concentration and enhanced the levels of reduced glutathione and superoxide dismutase in mice with sepsis-induced acute lung injury. Moreover, cecal ligation and puncture-operated mice showed markedly higher levels of proinflammatory cytokines relative to sham-operated group, while taxifolin treatment effectively mitigated sepsis-induced inflammation in mouse lungs. Further investigation revealed that taxifolin suppressed the activation of the nuclear factor kappa-light-chain-enhancer of activated B cells signaling pathway in cecal ligation and puncture-challenged mice by regulating the phosphorylation of p65 and IκBα. In conclusion, our study showed that taxifolin alleviated sepsis-induced acute lung injury via the inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells signaling pathway, suggesting the therapeutic potential of taxifolin in the treatment sepsis-induced acute lung injury.


1980 ◽  
Vol 255 (11) ◽  
pp. 5291-5295
Author(s):  
T. Kataoka ◽  
M. Ono ◽  
M. Kawakami ◽  
Y. Ikawa ◽  
M. Aida ◽  
...  

1994 ◽  
Vol 39 (1) ◽  
pp. 107-110 ◽  
Author(s):  
W. MAHANA ◽  
F. JACQUEMART ◽  
M. ERMONVAL

1992 ◽  
Vol 26 (2) ◽  
pp. 207-209 ◽  
Author(s):  
Muhammad Yaqoob ◽  
Gordon M. Bell ◽  
John M. Davies ◽  
Ian W. McDicken

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