INT264244

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Context Info
Confidence 0.58
First Reported 2007
Last Reported 2010
Negated 4
Speculated 0
Reported most in Body
Documents 10
Total Number 24
Disease Relevance 3.24
Pain Relevance 1.09

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

proteinaceous extracellular matrix (Cpz)
Anatomy Link Frequency
brain 2
white matter 2
Cpz (Mus musculus)
Pain Link Frequency Relevance Heat
Hippocampus 120 96.68 Very High Very High Very High
cerebral cortex 30 94.72 High High
Demyelination 15 92.72 High High
agonist 24 84.92 Quite High
anesthesia 24 81.44 Quite High
Neurotransmitter 99 80.56 Quite High
Locus ceruleus 15 79.00 Quite High
Antihistamine 9 78.96 Quite High
Catecholamine 18 73.44 Quite High
Morphine 9 43.44 Quite Low
Disease Link Frequency Relevance Heat
Schizophrenia 399 99.80 Very High Very High Very High
Unconsciousness 9 99.16 Very High Very High Very High
Psychosis 66 97.00 Very High Very High Very High
Stress 60 94.08 High High
Death 39 93.12 High High
Demyelinating Disease 15 92.72 High High
Emergencies 9 92.24 High High
Surgical Shock 9 91.52 High High
Brain Disease 9 82.44 Quite High
Mental Disorders 18 81.24 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Introduction of CPZ was also instrumental in the development of neuropsychopharmacology, a new discipline that provided the necessary methodology for psychiatry to examine and change its theoretical framework.
Gene_expression (Introduction) of CPZ
1) Confidence 0.58 Published 2007 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2655089 Disease Relevance 0.48 Pain Relevance 0
Two years later, in 1957, the importance of CPZ was recognized by the scientific community with the presentation of the American public health association’s prestigious Albert Lasker Award to the three key players in the clinical development of the drug: Henri Laborit, for using CPZ as a therapeutic agent first and recognizing its potential for psychiatry; Pierre Deniker, for his leading role in introducing CPZ into psychiatry and demonstrating its influence on the clinical course of psychosis; and Heinz Lehmann, for bringing the full practical significance of CPZ to the attention of the medical community (Ban 1994).
Gene_expression (introducing) of CPZ associated with psychosis
2) Confidence 0.58 Published 2007 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2655089 Disease Relevance 0.10 Pain Relevance 0.04
But in spite of all the progress made in the understanding of signal transduction in the brain, and designing drugs which fit like keys in their locks, none of the newer antipsychotic drugs has surpassed the effectiveness of CPZ (Ban 2004; Lieberman et al 2005).
Gene_expression (effectiveness) of CPZ in brain
3) Confidence 0.58 Published 2007 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2655089 Disease Relevance 0.40 Pain Relevance 0
His paper, co-authored by Hanrahan and published in the Archives of Neurology and Psychiatry (USA), had a major impact on the introduction of CPZ in North America (Lehmann and Hanrahan 1954).
Gene_expression (introduction) of CPZ
4) Confidence 0.58 Published 2007 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2655089 Disease Relevance 0 Pain Relevance 0
By the end of 1955 there were reports on the effects of CPZ in psychiatric patients from Switzerland (Staehelin and Kielholz 1953; Staehelin 1954); England (Anton-Stephens 1954; Elkes and Elkes 1954); Canada (Lehmann 1954; Lehmann and Hanrahan 1954); Germany (Bente and Itil 1954); Hungary (Kardos and Pertorini 1954); Latin America (Saly y Rosas et al 1954), United States (Winkelman 1954); Australia (Webb 1955); and the USSR (Tarasov 1955).
Gene_expression (effects) of CPZ
5) Confidence 0.58 Published 2007 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2655089 Disease Relevance 0 Pain Relevance 0
The six publications of Delay and Deniker during the six months that followed (Delay and Deniker 1952a, 1952b, 1952c; Delay et al 1952a, 1952b, 1952c), set the stage for the introduction of CPZ in psychiatry (Olie 2004).
Gene_expression (introduction) of CPZ
6) Confidence 0.58 Published 2007 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2655089 Disease Relevance 0 Pain Relevance 0
He found that CPZ, in the dosage of 50 to 100 mg given intravenously, produced disinterest without loss of consciousness and with only a slight tendency to sleep.
Gene_expression (produced) of CPZ associated with unconsciousness
7) Confidence 0.58 Published 2007 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2655089 Disease Relevance 0.29 Pain Relevance 0.08
The introduction of CPZ focused attention on the heterogeneity of schizophrenia in terms of responsiveness to treatment (Ban 1969, 1972, 1986).
Gene_expression (introduction) of CPZ associated with schizophrenia
8) Confidence 0.58 Published 2007 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2655089 Disease Relevance 0.34 Pain Relevance 0.11
Since the introduction of CPZ more than 50 years have passed; and pharmacotherapy has become the primary treatment in psychiatry.
Gene_expression (introduction) of CPZ
9) Confidence 0.58 Published 2007 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2655089 Disease Relevance 0.46 Pain Relevance 0
More interestingly, the CPZ-induced decrease in NE levels was blocked by the antipsychotics tested in this study (Figure 4).
Gene_expression (decrease) of CPZ-induced
10) Confidence 0.55 Published 2010 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2842101 Disease Relevance 0.07 Pain Relevance 0.22
When CPZ-exposure was extended for 42?
Gene_expression (extended) of CPZ-exposure
11) Confidence 0.55 Published 2010 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2842101 Disease Relevance 0 Pain Relevance 0
That is, CPZ decreases activities of cupric enzymes, such as SOD1 (Ljutakova and Russanov, 1985) and cytochrome oxidase (Wakabayashi et al., 1978), thus causes oxidative stress and leads to OLs death and demyelination in the brain (Mason et al., 2004; Copray et al., 2005).
Gene_expression (decreases) of CPZ in brain associated with stress, demyelination and death
12) Confidence 0.55 Published 2010 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2842101 Disease Relevance 0.42 Pain Relevance 0.09
Post hoc comparisons revealed significant differences between CNT and CPZ groups as well as between CNT and CPZ+CLZ groups.
Gene_expression (groups) of CPZ
13) Confidence 0.55 Published 2010 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2842101 Disease Relevance 0 Pain Relevance 0.03
Post hoc comparisons revealed significant differences between CNT and CPZ groups as well as between CNT and CPZ+CLZ groups.
Gene_expression (groups) of CPZ+CLZ
14) Confidence 0.55 Published 2010 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2842101 Disease Relevance 0 Pain Relevance 0.03
In our recent study, CPZ-exposed mice showed PPI deficits on 14th and 21st days after CPZ-exposure (Xu et al., 2009).
Gene_expression (showed) of CPZ-exposure
15) Confidence 0.55 Published 2010 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2842101 Disease Relevance 0 Pain Relevance 0
For high-performance liquid chromatography (HPLC) analysis, two additional experiments were performed, in which the same treatments (CPZ ingestion and antipsychotics administration) continued for 12 and 21?
Gene_expression (ingestion) of CPZ
16) Confidence 0.55 Published 2010 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2842101 Disease Relevance 0 Pain Relevance 0
In fact, C57BL/6 mice fed the CPZ-containing diet for 21?
Gene_expression (fed) of CPZ
17) Confidence 0.55 Published 2010 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2842101 Disease Relevance 0.08 Pain Relevance 0.21
This association between normalized DA levels and ameliorated MBP changes in PFC implies that high levels of DA may contribute to the CPZ-induced white matter damage in PFC.
Gene_expression (damage) of CPZ-induced in white matter
18) Confidence 0.55 Published 2010 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2842101 Disease Relevance 0.08 Pain Relevance 0.11
In summary, CPZ acts on cupric enzymes, including SOD1, cytochrome oxidase, and D?
Gene_expression (acts) of CPZ
19) Confidence 0.55 Published 2010 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2842101 Disease Relevance 0.51 Pain Relevance 0.11
And significant differences were also found in the comparisons of CNT and CPZ, CNT and HAL, as well as CPZ and CPZ+HAL (individual F and p values were not presented).
Neg (not) Gene_expression (presented) of CPZ+HAL
20) Confidence 0.55 Published 2010 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2842101 Disease Relevance 0 Pain Relevance 0.03

General Comments

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