No Observable Correlation between Central Nervous System Side Effects and EFV Plasma Concentrations in Japanese HIV Type 1-Infected Patients Treated with EFV Containing HAART

2007 ◽  
Vol 23 (8) ◽  
pp. 983-987 ◽  
Author(s):  
Masaaki Takahashi ◽  
Shiro Ibe ◽  
Yuichi Kudaka ◽  
Naoya Okumura ◽  
Atsushi Hirano ◽  
...  
2013 ◽  
Vol 29 (2) ◽  
pp. 365-370 ◽  
Author(s):  
Lachlan R. Gray ◽  
Daniel Cowley ◽  
Emma Crespan ◽  
Casey Welsh ◽  
Charlene Mackenzie ◽  
...  

Author(s):  
Abdullah Alkattan ◽  
Eman Alsalameen ◽  
Amr Ahmed

Objectives: The mechanism of action of drugs that depress the central nervous system (CNS) was unknown until molecular pharmacology discovered each drug's exact role. The benefit of knowing the mechanism of action is to design a new drug that could have the same efficacy as the prototype drug but with fewer side effects. Some of the available CNS depressant drugs that were abused or illegally used could be modified to make them used medically. Methods: We reviewed various published articles in PubMed and Google Scholar that focused on CNS depressants' molecular pharmacology.Results: It was clear that at specific plasma concentrations of ethyl alcohol showed almost same mode of action of propofol by targeting the extrasynaptic GABA-A receptors, which causes tonic GABAergic inhibition. Besides, the High affinity of some benzodiazepines (e.g., midazolam) to α1 subunit of GABA-A receptor causes sedative, hypnotic, amnesic, and some antiepileptic effects; however, some other benzodiazepines (e.g., diazepam) have high affinity to α3 subunits, which causes anxiolytic, muscle relaxant, and strong antiepileptic effects. The CB1 receptor partial agonism effect of tetrahydrocannabinol has a sedative advantage over full agonism due to desensitization of CB1 receptors. Conclusion: From the molecular pharmacology prospect, it is possible to design new drugs with more specific CNS depressants effect and fewer side effects by targeting particular receptors with a precise reaction.


2000 ◽  
Vol 16 (15) ◽  
pp. 1491-1502 ◽  
Author(s):  
David W. Haas ◽  
Lisa A. Clough ◽  
Benjamin W. Johnson ◽  
Victoria L. Harris ◽  
Paul Spearman ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1831
Author(s):  
Camilla Russo ◽  
Carmela Russo ◽  
Daniele Cascone ◽  
Federica Mazio ◽  
Claudia Santoro ◽  
...  

Neurofibromatosis type 1 (NF1), the most frequent phakomatosis and one of the most common inherited tumor predisposition syndromes, is characterized by several manifestations that pervasively involve central and peripheral nervous system structures. The disorder is due to mutations in the NF1 gene, which encodes for the ubiquitous tumor suppressor protein neurofibromin; neurofibromin is highly expressed in neural crest derived tissues, where it plays a crucial role in regulating cell proliferation, differentiation, and structural organization. This review article aims to provide an overview on NF1 non-neoplastic manifestations of neuroradiological interest, involving both the central nervous system and spine. We also briefly review the most recent MRI functional findings in NF1.


2012 ◽  
Vol 101 (7) ◽  
pp. 2048-2050 ◽  
Author(s):  
Takahiko Murata ◽  
Masahiro Kawashima ◽  
Yasuo Terayama

2005 ◽  
Vol 136A (2) ◽  
pp. 218-218 ◽  
Author(s):  
Margareta Holub ◽  
Lorraine Potocki ◽  
Olaf A. Bodamer

1927 ◽  
Vol 23 (11) ◽  
pp. 1183-1183

The adverse side effects of salvarsan injections include bleeding from the nose, gums, kidney, lung, etc. The reason for this is the permeability of the capillary walls to red blood cells due to irritation of the central nervous system in persons who are too sensitive to salvarsan. They are caused by the permeability of the capillary walls to red blood cells, caused by irritation of the central nervous system in persons over-sensitive to salvarsan.


2018 ◽  
Vol 69 (8) ◽  
pp. 1345-1352 ◽  
Author(s):  
Sarah B Joseph ◽  
Laura P Kincer ◽  
Natalie M Bowman ◽  
Chris Evans ◽  
Michael J Vinikoor ◽  
...  

Abstract Background Human immunodeficiency virus type 1 (HIV-1) populations are detected in cerebrospinal fluid (CSF) of some people on suppressive antiretroviral therapy (ART). Detailed analysis of these populations may reveal whether they are produced by central nervous system (CNS) reservoirs. Methods We performed a study of 101 asymptomatic participants on stable ART. HIV-1 RNA concentrations were cross-sectionally measured in CSF and plasma. In participants with CSF HIV-1 RNA concentrations sufficient for analysis, viral populations were genetically and phenotypically characterized over multiple time points. Results For 6% of participants (6 of 101), the concentration of HIV-1 RNA in their CSF was ≥0.5 log copies/mL above that of plasma (ie, CSF escape). We generated viral envelope sequences from CSF of 3 participants. One had a persistent CSF escape population that was macrophage-tropic, partially drug resistant, genetically diverse, and closely related to a minor macrophage-tropic lineage present in the blood prior to viral suppression and enriched for after ART. Two participants (1 suppressed and 1 not) had transient CSF escape populations that were R5 T cell-tropic with little genetic diversity. Conclusions Extensive analysis of viral populations in 1 participant revealed that CSF escape was from a persistently replicating population, likely in macrophages/microglia, present in the CNS over 3 years of ART. CSF escape in 2 other participants was likely produced by trafficking and transient expansion of infected T cells in the CNS. Our results show that CNS reservoirs can persist during ART and that CSF escape is not exclusively produced by replicating CNS reservoirs.


2007 ◽  
Vol 18 (8) ◽  
pp. 575-576 ◽  
Author(s):  
Osamu Usami ◽  
Yugo Ashino ◽  
Yuichi Komaki ◽  
Masafumi Tomaki ◽  
Toshiya Irokawa ◽  
...  

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.


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