In vivo LPS administration alters S100B protein content in cerebrospinal fluid, but not in serum

2012 ◽  
Vol 18 (2) ◽  
pp. 54-55
Author(s):  
Lucas Silva Tortorelli ◽  
Maria Cristina Guerra ◽  
Fabiana Galland ◽  
Carollina Da Ré ◽  
Elisa Negri ◽  
...  
2000 ◽  
Vol 12 (10) ◽  
pp. 3721-3728 ◽  
Author(s):  
K. Q. Do ◽  
A. H. Trabesinger ◽  
M. Kirsten-Krüger ◽  
C. J. Lauer ◽  
U. Dydak ◽  
...  

2000 ◽  
Vol 52 (3) ◽  
pp. 281-288 ◽  
Author(s):  
TAKEO KITAZAWA ◽  
KEN-ICHI HOSOYA ◽  
TAKEO TAKAHASHI ◽  
YUICHI SUGIYAMA ◽  
TETSUYA TERASAKI

Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1833
Author(s):  
Shannon Morgan McCabe ◽  
Ningning Zhao

Manganese (Mn) is a trace nutrient necessary for life but becomes neurotoxic at high concentrations in the brain. The brain is a “privileged” organ that is separated from systemic blood circulation mainly by two barriers. Endothelial cells within the brain form tight junctions and act as the blood–brain barrier (BBB), which physically separates circulating blood from the brain parenchyma. Between the blood and the cerebrospinal fluid (CSF) is the choroid plexus (CP), which is a tissue that acts as the blood–CSF barrier (BCB). Pharmaceuticals, proteins, and metals in the systemic circulation are unable to reach the brain and spinal cord unless transported through either of the two brain barriers. The BBB and the BCB consist of tightly connected cells that fulfill the critical role of neuroprotection and control the exchange of materials between the brain environment and blood circulation. Many recent publications provide insights into Mn transport in vivo or in cell models. In this review, we will focus on the current research regarding Mn metabolism in the brain and discuss the potential roles of the BBB and BCB in maintaining brain Mn homeostasis.


1963 ◽  
Vol 117 (1) ◽  
pp. 105-125 ◽  
Author(s):  
Manuel E. Kaplan ◽  
James H. Jandl

Studies were undertaken in man and in the rat comparing the effects of rheumatoid factors and immune antiglobulins on red cells sensitized with incomplete antibodies. The interaction of immune antiglobulins with sensitized red cells produced (a) agglutination in vitro and (b) an accelerated sequestration of the sensitized cells in vivo. In contrast, rheumatoid macroglobulins, although capable of agglutinating Rh-sensitized red cells in vitro, did not modify their destruction in vivo. The failure of rheumatoid factors to function as antiglobulins in vivo appears to reflect their non-reactivity with sensitized cells in whole serum. It is suggested: (a) that the native (7S) gamma globulins of plasma competitively inhibit rheumatoid factors from reacting with fixed antibody in the blood stream; (b) that if these macroglobulins do indeed have pathogenetic activity, this may be limited to body fluids of low protein content.


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