scholarly journals Assessment of Drug-Induced Toxicity Biomarkers in the Brain Microphysiological System (MPS) Using Targeted and Untargeted Molecular Profiling

2019 ◽  
Vol 2 ◽  
Author(s):  
Sara G. Mina ◽  
Begum Alaybeyoglu ◽  
William L. Murphy ◽  
James A. Thomson ◽  
Cynthia L. Stokes ◽  
...  
Keyword(s):  
Molecular Profiling ◽  
Drug Induced ◽  
Toxicity Biomarkers ◽  
The Brain

Drug-induced xenogenization of tumors: A possible role in the immune control of malignant cell growth in the brain?

2018 ◽  
Vol 131 ◽  
pp. 1-6 ◽  
Author(s):  
Ornella Franzese ◽  
Fiorenzo Battaini ◽  
Grazia Graziani ◽  
Lucio Tentori ◽  
Maria Luisa Barbaccia ◽  
...  
Keyword(s):  
Cell Growth ◽  
Malignant Cell ◽  
Immune Control ◽  
Drug Induced ◽  
The Brain

A ZEBRAFISH MODEL OF CLOZAPINE EXPOSURE: DRUG-INDUCED TRANSCRIPTOMIC CHANGES IN THE BRAIN

2019 ◽  
Vol 29 ◽  
pp. S782
Author(s):  
Joana Viana ◽  
Eilis Hannon ◽  
Ronny van Aerle ◽  
Emma Dempster ◽  
Gregory Paull ◽  
...  
Keyword(s):  
Drug Induced ◽  
Zebrafish Model ◽  
Transcriptomic Changes ◽  
The Brain

SU103A ZEBRAFISH MODEL OF CLOZAPINE EXPOSURE: DRUG-INDUCED TRANSCRIPTOMIC CHANGES IN THE BRAIN

2019 ◽  
Vol 29 ◽  
pp. S1321
Author(s):  
Joana Viana ◽  
Nick Wildman ◽  
Eilis Hannon ◽  
Audrey Farbos ◽  
Paul O'Neill ◽  
...  
Keyword(s):  
Drug Induced ◽  
Zebrafish Model ◽  
Transcriptomic Changes ◽  
The Brain

Central vasopressin V1-blockade prevents salicylate but not acetaminophen antipyresis

1990 ◽  
Vol 68 (5) ◽  
pp. 1793-1798 ◽  
Author(s):  
M. F. Wilkinson ◽  
N. W. Kasting
Keyword(s):  
Rat Brain ◽  
Core Temperature ◽  
Mechanism Of Action ◽  
Arginine Vasopressin ◽  
Sodium Salicylate ◽  
Septal Area ◽  
Receptor Blockade ◽  
Drug Induced ◽  
Normal Core ◽  
The Brain

Recent evidence has suggested that the endogenous antipyretic arginine vasopressin (AVP) may participate in drug-induced antipyresis. This study sought to further those investigations by comparing the effects of two other antipyretic drugs, sodium salicylate and acetaminophen, administered intraperitoneally, during AVP V1-receptor blockade within the ventral septal area (VSA) of the rat brain. During endotoxin-evoked fever, V1-receptor blockade within the VSA of the conscious unrestrained rat significantly antagonized the antipyretic effects of salicylate. The effects of the V1-antagonist on salicylate-induced antipyresis were dose related. In contrast, the antipyresis elicited by acetaminophen was unaffected by VSA V1-antagonist pretreatment. Neither saline nor the V1-antagonist microinjected into the VSA of febrile or nonfebrile rats had any significant effects on the normal progression of endotoxin fever or normal core temperature, respectively. These data suggest that the mechanism of action of salicylate-induced antipyresis includes activation of AVP V1-type receptors within the VSA, as has been shown for indomethacin. However, the lack of effect of the V1-antagonist on antipyresis induced by acetaminophen indicates that not all antipyretic drugs act through the same mechanism in the brain.

Neurochemical effects of choline supplementation

1986 ◽  
Vol 64 (3) ◽  
pp. 329-333 ◽  
Author(s):  
Lynn Wecker
Keyword(s):  
Brain Tissue ◽  
Neuronal Activity ◽  
Cholinergic Neurons ◽  
Lipid Phosphorus ◽  
Drug Induced ◽  
Pharmacological Agents ◽  
Physiological Conditions ◽  
Free Choline ◽  
Drug Challenge ◽  
The Brain

Whether or not the brain can use supplemental choline to enhance the synthesis of acetylcholine (ACh) is an important consideration for assessing the merits of using choline or phosphatidylcholine (lecithin) for the treatment of neuropsychiatric disorders postulated to involve hypocholinergic activity. While it is well documented that administered choline is incorporated into ACh, the ability of supplemental choline to increase the synthesis and release of ACh has been questionable. Studies in my laboratory have demonstrated that acute or chronic choline supplementation does not, by itself, enhance the levels of ACh in brain under normal biochemical and physiological conditions. However, supplemental choline prevents the depletion of ACh in brain induced by numerous pharmacological agents that increase the firing of cholinergic neurons. Since the levels of free choline in brains from supplemented rats were not different from controls prior to drug challenge, evidence suggested that the observed effects of choline were mediated by alterations in the mobilization of choline from choline-containing compounds. Studies investigating the release of choline from brain indicated that more choline was released per unit time in tissues from choline-supplemented rats than from controls. In addition, brain tissue from choline-supplemented rats had increased concentrations of total lipid phosphorus as compared with controls. Hence, although choline supplementation does not alter the levels of ACh in brain under normal conditions, it does appear to support ACh synthesis during drug-induced increases in neuronal activity, an effect most likely mediated by alterations in the metabolism of choline-containing phospholipids.

scholarly journals Suspected phenobarbital-induced fever in a cat

2019 ◽  
Vol 5 (1) ◽  
pp. 205511691983021
Author(s):  
Dylan M Djani ◽  
William E Draper
Keyword(s):  
Fever Of Unknown Origin ◽  
Clinical Signs ◽  
Unknown Origin ◽  
Drug Induced ◽  
Fluid Analysis ◽  
Diagnostic Work ◽  
Phenobarbital Administration ◽  
Work Up ◽  
The Brain ◽  
Diagnostic Work Up

Case summary A 3-year-old spayed female domestic shorthair cat developed a fever 1 week after starting the anticonvulsant phenobarbital. A diagnostic work-up for seizures and subsequent onset of fever of unknown origin, consisting of MRI of the brain, cerebrospinal fluid analysis and infectious disease testing, was unremarkable. The cat was switched from phenobarbital onto pregabalin with complete resolution of the fever within 24 h, consistent with a drug-induced fever following phenobarbital administration. Relevance and novel information While anticonvulsant hypersensitivities have been reported and studied in veterinary medicine, phenobarbital-induced fever outside of the context of systemic clinical signs has not been documented in the veterinary scientific literature. Drug-induced fever secondary to anticonvulsants should be considered in patients that develop a fever after starting anticonvulsant therapy with an unrewarding diagnostic work-up for fever of unknown origin.

Molecular profiling of cancer and drug-induced toxicity using new proteomic technologies

2001 ◽  
Vol 62 (11) ◽  
pp. 803-819 ◽  
Author(s):  
Ali M. Ardekani ◽  
Ali M. Ardekani ◽  
Eugene H. Herman ◽  
Frank D. Sistare ◽  
Lance A. Liotta ◽  
...  
Keyword(s):  
Molecular Profiling ◽  
Drug Induced
Sign in / Sign up

Export Citation Format

Share Document