Modification of the brain proteome of Africanized honeybees (Apis mellifera) exposed to a sub‐lethal doses of the insecticide fipronil

Ecotoxicology ◽  
2014 ◽  
Vol 23 (9) ◽  
pp. 1659-1670 ◽  
Author(s):  
T. C. Roat ◽  
J. R. A. dos Santos-Pinto ◽  
L. D. dos Santos ◽  
K. S. Santos ◽  
O. Malaspina ◽  
...  
PROTEOMICS ◽  
2012 ◽  
Vol 12 (23-24) ◽  
pp. 3610-3620 ◽  
Author(s):  
Joanna Gawinecka ◽  
Franco Cardone ◽  
Abdul R. Asif ◽  
Angela De Pascalis ◽  
Wiebke M. Wemheuer ◽  
...  

2020 ◽  
Vol 16 (S3) ◽  
Author(s):  
Thomas Kukar ◽  
Meixiang Huang ◽  
Erica S Modeste ◽  
Eric B Dammer ◽  
Christopher J Holler ◽  
...  

2020 ◽  
Vol 6 (43) ◽  
pp. eaaz9360 ◽  
Author(s):  
Lenora Higginbotham ◽  
Lingyan Ping ◽  
Eric B. Dammer ◽  
Duc M. Duong ◽  
Maotian Zhou ◽  
...  

Alzheimer’s disease (AD) lacks protein biomarkers reflective of its diverse underlying pathophysiology, hindering diagnostic and therapeutic advancements. Here, we used integrative proteomics to identify cerebrospinal fluid (CSF) biomarkers representing a wide spectrum of AD pathophysiology. Multiplex mass spectrometry identified ~3500 and ~12,000 proteins in AD CSF and brain, respectively. Network analysis of the brain proteome resolved 44 biologically diverse modules, 15 of which overlapped with the CSF proteome. CSF AD markers in these overlapping modules were collapsed into five protein panels representing distinct pathophysiological processes. Synaptic and metabolic panels were decreased in AD brain but increased in CSF, while glial-enriched myelination and immunity panels were increased in brain and CSF. The consistency and disease specificity of panel changes were confirmed in >500 additional CSF samples. These panels also identified biological subpopulations within asymptomatic AD. Overall, these results are a promising step toward a network-based biomarker tool for AD clinical applications.


2010 ◽  
Vol 100 (1) ◽  
pp. 51-65 ◽  
Author(s):  
Karin Berg ◽  
Pål Puntervoll ◽  
Stig Valdersnes ◽  
Anders Goksøyr

2009 ◽  
Vol 44 (3) ◽  
pp. 403-411 ◽  
Author(s):  
Shogo Nomura ◽  
Jun-ichi Takahashi ◽  
Tetsuhiko Sasaki ◽  
Tadaharu Yoshida ◽  
Masami Sasaki

2001 ◽  
Vol 75 (24) ◽  
pp. 12039-12046 ◽  
Author(s):  
Katherine R. Spindler ◽  
Lei Fang ◽  
Martin L. Moore ◽  
Gwen N. Hirsch ◽  
Corrie C. Brown ◽  
...  

ABSTRACT Mouse adenovirus type 1 (MAV-1) targets endothelial and monocyte/macrophage cells throughout the mouse. Depending on the strain of mouse and dose or strain of virus, infected mice may survive, become persistently infected, or die. We surveyed inbred mouse strains and found that for the majority tested the 50% lethal doses (LD50s) were >104.4 PFU. However, SJL/J mice were highly susceptible to MAV-1, with a mean LD50 of 10−0.32 PFU. Infected C3H/HeJ (resistant) and SJL/J (susceptible) mice showed only modest differences in histopathology. Susceptible mice had significantly higher viral loads in the brain and spleen at 8 days postinfection than resistant mice. Infection of primary macrophages or mouse embryo fibroblasts from SJL/J and C3H/HeJ mice gave equivalent yields of virus, suggesting that a receptor difference between strains is not responsible for the susceptibility difference. When C3H/HeJ mice were subjected to sublethal doses of gamma irradiation, they became susceptible to MAV-1, with an LD50 like that of SJL/J mice. Antiviral immunoglobulin G (IgG) levels were measured in susceptible and resistant mice infected by an early region 1A null mutant virus that is less virulent that wild-type virus. The antiviral IgG levels were high and similar in the two strains of mice. Taken together, these results suggest that immune response differences may in part account for differences in susceptibility to MAV-1 infection.


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