scholarly journals CENTRAL EFFECTS ON MINOR TREMOR

1963 ◽  
Vol 13 (5) ◽  
pp. 492-499
Author(s):  
Hisanobu SUGANO
Keyword(s):  
Central Effects ◽  
Minor Tremor

A brief review on the use of cannabis as a treatment option for local inflammation in peripheral tissue01

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Secondary Metabolites ◽  
Treatment Option ◽  
Cell Injury ◽  
Local Inflammation ◽  
Topical Formulations ◽  
Central Effects ◽  
Complex Process ◽  
Anti Inflammatory

Inflammation is a complex process which, ideally, comes about as a “mop up’ response to cell injury. Ithowever occasionally results in undesired effects that should otherwise be prevented or resolvedspeedily. There are available numerous medicines with varied modes of administration commerciallyavailable for the management of inflammation. With the growing evidence of cannabis’ therapeuticeffects, its anti-inflammatory properties being one of them, debates among proponents and opponents ofcannabis use are ever growing. These debates are centered on the undesired central effects of some of theplants secondary metabolites an argument that can be moderated by using the plant in a manner thatsteers clear of these effects. Effective topical formulations could very well be one avenue through whichnature can be allowed to heal with minimal negative repercussions.

Evaluation of Importance of Central Effects of Atenolol and Metoprolol Measured by Heart Rate Variability During Mental Performance Tasks, Physical Exercise, and Daily Life in Stable Postinfarct Patients

Circulation ◽  
1995 ◽  
Vol 92 (12) ◽  
pp. 3415-3423 ◽  
Author(s):  
Ype S. Tuininga ◽  
Harry J.G.M. Crijns ◽  
Jan Brouwer ◽  
Maarten P. van den Berg ◽  
Arie J. Man in’t Veld ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Physical Exercise ◽  
Daily Life ◽  
Mental Performance ◽  
Performance Tasks ◽  
Central Effects

Neuroimaging in Drug Discovery and Development: Paradigms for Accelerating New Drug Availability

2001 ◽  
Vol 14 (5) ◽  
pp. 407-415
Author(s):  
John T. Metz ◽  
Malcolm D. Cooper ◽  
Terry F. Brown ◽  
Leann H. Kinnunen ◽  
Declan J. Cooper
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Metabolism ◽  
Phase Ii ◽  
New Drugs ◽  
Central Effects ◽  
Drug Discovery And Development ◽  
Psychological Tasks ◽  
The Brain ◽  
Phase Iv

The process of discovering and developing new drugs is complicated. Neuroimaging methods can facilitate this process. An analysis of the conceptual bases and practical limitations of different neuroimaging modalities reveals that each technique can best address different kinds of questions. Radioligand studies are well suited to preclinical and Phase II questions when a compound is known or suspected to affect well-understood mechanisms; they are also useful in Phase IV to characterize effective agents. Cerebral blood flow studies can be extremely useful in evaluating the effects of a drug on psychological tasks (mostly in Phase IV). Glucose metabolism studies can answer the simplest questions about whether a compound affects the brain, where, and how much. Such studies are most useful in confirming central effects (preclinical and early clinical phases), in determining effective dose ranges (Phase II), and in comparing different drugs (Phase IV).

scholarly journals Correction: Paszkiewicz et al. A Peripheral CB1R Antagonist Increases Lipolysis, Oxygen Consumption Rate, and Markers of Beiging in 3T3-L1 Adipocytes Similar to RIM, Suggesting That Central Effects Can Be Avoided. Int. J. Mol. Sci. 2020, 21, 6639

2021 ◽  
Vol 22 (9) ◽  
pp. 4366
Author(s):  
Rebecca L. Paszkiewicz ◽  
Richard N. Bergman ◽  
Roberta S. Santos ◽  
Aaron P. Frank ◽  
Orison O. Woolcott ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Oxygen Consumption Rate ◽  
Consumption Rate ◽  
Central Effects

The authors wish to make the following corrections to this paper [...]

Toxicology and the vulnerable brain

1995 ◽  
Vol 7 (1) ◽  
pp. 1-6 ◽  
Author(s):  
D.R.A. Uges
Keyword(s):  
The Netherlands ◽  
Forensic Toxicology ◽  
Symptomatic Treatment ◽  
Environmental Toxicology ◽  
Clinical Toxicology ◽  
Suicidal Attempt ◽  
Central Effects ◽  
The Past ◽  
Cardio Vascular ◽  
The Brain

SummaryToxicology is one of the eldest areas of special attention in medicine and pharmacy. In the past, forensic toxicology was the most important part, but nowadays, at least in the Netherlands, the clinical, occupational and environmental toxicology have the centre of attention.The brain plays its own role in the clinical toxicology. There the intoxication can take place, it can be the basis of the peripheral symptoms of the intoxication or it can be the cause of the intoxication, e.g. at a suicidal attempt or the hospital addiction syndrome.The somatic treatment of an intoxicated patient includes in the first place the stabilization of the patient (cardio-vascular, ventilation and central effects); then the removal of the poison from the surroundings and out of the patient by different suitable methods and finally the symptomatic treatment, sometimes with antidotes.In the Netherlands, hardly any intoxication is fatal, when the patient arrives in the hospital in time, or euthanasia took place on purpose.

scholarly journals Acute Nicotine Reduces Brain Arachidonic Acid Signaling in Unanesthetized Rats

2009 ◽  
Vol 29 (3) ◽  
pp. 648-658 ◽  
Author(s):  
Lisa Chang ◽  
Stanley I Rapoport ◽  
Henry N Nguyen ◽  
Dede Greenstein ◽  
Mei Chen ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Brain Regions ◽  
Membrane Phospholipids ◽  
Dose Equivalent ◽  
Central Effects ◽  
Postsynaptic Receptors ◽  
Cytosolic Phospholipase ◽  
Presynaptic Release

Nicotine exerts its central effects by activating pre- and postsynaptic nicotinic acetylcholine receptors (nAChRs). Presynaptic nAChRs modulate the release of many neurotransmitters that bind to postsynaptic receptors. These may be coupled to the activation of cytosolic phospholipase A2 (cPLA2), which hydrolyzes arachidonic acid (AA) from membrane phospholipids. We hypothesized that nicotine would modify brain signaling involving AA by binding to nAChRs. Nicotine (0.1 mg/kg, subcutaneously) or saline was injected 2 or 10 mins before infusing [1-14C]AA in unanesthetized rats. The AA incorporation coefficient k∗ (a marker of the AA signal) was measured in 80 brain regions by quantitative autoradiography. Nicotine, compared to saline, when administrated 2 mins before [1-14C]AA infusion, significantly decreased k∗ for AA in 26 regions, including cerebral cortex, thalamus, and habenula—interpeduncular regions, by 13% to 45%. These decreases could be entirely prevented by pretreatment with mecamylamine (1.0 mg/kg, subcutaneously). When administered 10 mins before [1-14C]AA infusion, nicotine did not alter any value of k∗. In summary, nicotine given to unanesthetized rats rapidly reduces signaling involving AA in brain regions containing nAChRs, likely by modulating the presynaptic release of neurotransmitters. The effect shows rapid desensitization and is produced at a nicotine dose equivalent to smoking one cigarette in humans.

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