Hearing loss and cochlear damage in experimental pneumococcal meningitis, with special reference to the role of neutrophil granulocytes

2006 ◽  
Vol 23 (2) ◽  
pp. 300-311 ◽  
Author(s):  
C.T. Brandt ◽  
P. Cayé-Thomasen ◽  
S.P. Lund ◽  
L. Worsøe ◽  
C. Østergaard ◽  
...  
1993 ◽  
Vol 167 (3) ◽  
pp. 675-683 ◽  
Author(s):  
S. M. Bhatt ◽  
A. Lauretano ◽  
C. Cabellos ◽  
C. Halpin ◽  
R. A. Levine ◽  
...  

2007 ◽  
Vol 195 (8) ◽  
pp. 1189-1193 ◽  
Author(s):  
Matthias Klein ◽  
Caroline Schmidt ◽  
Stefan Kastenbauer ◽  
Robert Paul ◽  
Carsten J. Kirschning ◽  
...  

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Lukas Muri ◽  
Ngoc Dung Le ◽  
Jonas Zemp ◽  
Denis Grandgirard ◽  
Stephen L. Leib

1986 ◽  
Vol 1 (1) ◽  
pp. 15-32 ◽  
Author(s):  
Elaine Tuomanen ◽  
Bruno Hengstler ◽  
Oto Zak ◽  
Alexander Tomasz

1995 ◽  
Vol 14 (2) ◽  
pp. 93-96 ◽  
Author(s):  
SAMIR M. BHATT ◽  
CARMEN CABELLOS ◽  
JOSEPH B. NADOL ◽  
CHRIS HALPIN ◽  
ARTHUR LAURETANO ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Lingjun Zhang ◽  
Zhengde Du ◽  
Shusheng Gong

Mitochondrial dysfunction has been suggested to be a risk factor for sensorineural hearing loss (SNHL) induced by aging, noise, ototoxic drugs, and gene. Reactive oxygen species (ROS) are mainly derived from mitochondria, and oxidative stress induced by ROS contributes to cochlear damage as well as mitochondrial DNA mutations, which may enhance the sensitivity and severity of hearing loss and disrupt ion homeostasis (e.g., Ca2+ homeostasis). The formation and accumulation of ROS further undermine mitochondrial components and ultimately lead to apoptosis and necrosis. SIRT3–5, located in mitochondria, belong to the family of sirtuins, which are highly conserved deacetylases dependent on nicotinamide adenine dinucleotide (NAD+). These deacetylases regulate diverse cellular biochemical activities. Recent studies have revealed that mitochondrial sirtuins, especially SIRT3, modulate ROS levels in hearing loss pathologies. Although the precise functions of SIRT4 and SIRT5 in the cochlea remain unclear, the molecular mechanisms in other tissues indicate a potential protective effect against hearing loss. In this review, we summarize the current knowledge regarding the role of mitochondrial dysfunction in hearing loss, discuss possible functional links between mitochondrial sirtuins and SNHL, and propose a perspective that SIRT3–5 have a positive effect on SNHL.


1999 ◽  
Vol 179 (1) ◽  
pp. 264-268 ◽  
Author(s):  
Jamie M. Rappaport ◽  
Samir M. Bhatt ◽  
Robert F. Burkard ◽  
Saumil N. Merchant ◽  
Joseph B. Nadol, Jr.

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