THE SIGNAL TRANSDUCTION PATHWAYS INVOLVED IN HEPATIC CYTOCHROME P450 REGULATION IN THE RAT DURING A LIPOPOLYSACCHARIDE-INDUCED MODEL OF CENTRAL NERVOUS SYSTEM INFLAMMATION

2005 ◽  
Vol 33 (10) ◽  
pp. 1521-1531 ◽  
Author(s):  
Dalya Abdulla ◽  
Kerry B. Goralski ◽  
Elena Garcia Del Busto Cano ◽  
Kenneth W. Renton
Keyword(s):  
Signal Transduction ◽  
Central Nervous System ◽  
Nervous System ◽  
Cytochrome P450 ◽  
Signal Transduction Pathways ◽  
Central Nervous System Inflammation ◽  
Hepatic Cytochrome

Efavirenz-induced neurological symptoms in rare homozygote CYP2B6 *2/*2 (C64T)

2007 ◽  
Vol 18 (8) ◽  
pp. 575-576 ◽  
Author(s):  
Osamu Usami ◽  
Yugo Ashino ◽  
Yuichi Komaki ◽  
Masafumi Tomaki ◽  
Toshiya Irokawa ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cytochrome P450 ◽  
Plasma Concentrations ◽  
Highly Active ◽  
P450 Isozymes ◽  
Cytochrome P450 Isozymes ◽  
Hiv 1 ◽  
Rare Homozygote ◽  
Hepatic Cytochrome

Some of the HIV-1-infected patients who were given highly active anti-retroviral therapy (HAART) including efavirenz (EFV) presented adverse central nervous system (CNS) symptoms such as fatigue and insomnia. The incidence of adverse CNS symptoms is associated with hepatic cytochrome P450 isozymes (CYP2B6) polymorphisms. For example, CYP2B6 *6 (G516T and A785G) and *7 (G516T, A785G and C1459T) prolonged the EFV half-life despite discontinuation of EFV. CYP2B6 *2/*2 (C64T) is extremely rare and there have been no data describing the EFV plasma concentrations in C64T homozygous patients, who developed adverse CNS symptoms. C64T homozygous possibly has some catalytic defects.

scholarly journals Interactions and Signal Transduction Pathways Involved during Central Nervous System Entry by Neisseria meningitidis across the Blood–Brain Barriers

2020 ◽  
Vol 21 (22) ◽  
pp. 8788
Author(s):  
Julia Borkowski ◽  
Horst Schroten ◽  
Christian Schwerk
Keyword(s):  
Signal Transduction ◽  
Central Nervous System ◽  
Nervous System ◽  
Neisseria Meningitidis ◽  
Severe Disease ◽  
Blood Stream ◽  
Brain Parenchyma ◽  
Host Cells ◽  
Signal Transduction Pathways ◽  
Blood Brain

The Gram-negative diplococcus Neisseria meningitidis, also called meningococcus, exclusively infects humans and can cause meningitis, a severe disease that can lead to the death of the afflicted individuals. To cause meningitis, the bacteria have to enter the central nervous system (CNS) by crossing one of the barriers protecting the CNS from entry by pathogens. These barriers are represented by the blood–brain barrier separating the blood from the brain parenchyma and the blood–cerebrospinal fluid (CSF) barriers at the choroid plexus and the meninges. During the course of meningococcal disease resulting in meningitis, the bacteria undergo several interactions with host cells, including the pharyngeal epithelium and the cells constituting the barriers between the blood and the CSF. These interactions are required to initiate signal transduction pathways that are involved during the crossing of the meningococci into the blood stream and CNS entry, as well as in the host cell response to infection. In this review we summarize the interactions and pathways involved in these processes, whose understanding could help to better understand the pathogenesis of meningococcal meningitis.

scholarly journals A cell-based drug delivery platform for treating central nervous system inflammation

2021 ◽  
Author(s):  
Oren Levy ◽  
Veit Rothhammer ◽  
Ivan Mascanfroni ◽  
Zhixiang Tong ◽  
Rui Kuai ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Central Nervous System ◽  
Nervous System ◽  
Central Nervous System Inflammation ◽  
Delivery Platform ◽  
A Cell
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