1
40
3
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/0306-4522(95)00221-4" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/0306-4522(95)00221-4</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
321-330
Issue
1
Volume
69
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Reduction In The Number Of Spinal Motor-neurons In Neurotrophin-3-deficient Mice
Publisher
An entity responsible for making the resource available
Neuroscience
Date
A point or period of time associated with an event in the lifecycle of the resource
1995
1995-11
Subject
The topic of the resource
bdnf; cell-death; cord; expression; fusimotor neurons; motoneurons; motor neurons; muscle spindles; nerve; Neurosciences & Neurology; neurotrophic factor; neurotrophins; proprioception; rat muscle-spindles; size; survival
Creator
An entity primarily responsible for making the resource
Kucera J; Ernfors P; Walro J; Jaenisch R
Description
An account of the resource
The effects of a deficiency of neurotrophin-3 on spinal motor neurons were assessed by determining the number of myelinated nerve fibers in lumbar ventral spinal roots of mice with a deletion in the neurotrophin-3 gene. Few or no small-caliber (fusimotor) nerve fibers were present in the L4 ventral root of homozygous mutant mice lacking both copies of the neurotrophin-3 gene, and approximately one-half of the normal complement of the fibers was present in heterozygous mice having one copy of the neurotrophin-3 gene relative to wild type mice at two weeks of age. Numbers of fusimotor nerve fibers paralleled numbers of muscle spindles, the target organs of fusimotor innervation, in hindlimb muscles. Muscle spindles and intrafusal fibers were absent in the soleus muscles of homozygous mutants, and were reduced by approximately 50% in heterozygous relative to wild type mice in accord with previous reports. Neurotrophin-3 might be generated by the intrafusal fibers and may provide a target-derived neurotrophic support for developing fusimotor neurons because in the absence of muscle spindles the neurons did not differentiate and/or survive. In contrast, a great majority of skeletomotor neurons that innervate extrafusal muscle fibers differentiated normally in the absence of neurotrophin-3. This study, analysed in conjunction with our previously reported data, suggests that neurotrophin-3 acts in a coordinated fashion to support, either directly or indirectly, the development of each of the three classes of cells-Ia and Ib sensory neurons, fusimotor neurons, and intrafusal muscle fibers-that comprise the limb proprioceptive system.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/0306-4522(95)00221-4" target="_blank" rel="noreferrer noopener">10.1016/0306-4522(95)00221-4</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
1995
BDNF
cell-death
cord
Ernfors P
expression
fusimotor neurons
Jaenisch R
Journal Article or Conference Abstract Publication
Kucera J
motoneurons
motor neurons
muscle spindles
nerve
Neuroscience
Neurosciences & Neurology
neurotrophic factor
neurotrophins
proprioception
rat muscle-spindles
size
Survival
Walro J
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.2174/0929867023368674" target="_blank" rel="noreferrer noopener">http://doi.org/10.2174/0929867023368674</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
2271-2285
Issue
24
Volume
9
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The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Potential therapeutic application of the association of vitamins C and K-3 in cancer treatment
Publisher
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Current Medicinal Chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2002
2002-12
Subject
The topic of the resource
oxidative stress; cancer; Biochemistry & Molecular Biology; Pharmacology & Pharmacy; apoptosis; cell-death; growth-invitro; synergistic antitumor-activity; ascorbic-acid; carcinoma-cells; autoschizis; induced apoptosis; ascorbate (vitamin C); caloric restriction; cycle arrest; menadione (vitamin K-3); programmed; tumor-specific expression
Creator
An entity primarily responsible for making the resource
Calderon P B; Cadrobbi J; Marques C; Hong-Ngoc N; Jamison J M; Gilloteaux J; Summers J L; Taper H S
Description
An account of the resource
The decision of stressed cells to die or to survive is made by integrating signals at different levels through multiple check points. However, initiation and continued progression toward cell death by apoptosis in cancer cells may be blocked by mutation of the tumor suppressor p53 or overexpression of members of the bcl-2 family of proteins. The existence of such mechanisms indicates that cancer cells lose the controls regulating their cell cycle. Therefore, the activation of their programmed cell death appears as a major therapeutic target. Oxidative stress can stimulate growth, trigger apoptosis, or cause necrosis depending upon the dose and the exposure time of the oxidizing agent. A large body of evidence supports the idea that oxidative stress induced by redox cycling of vitamins C and K-3 in association surpasses cancer cellular defense systems and results in cell death. The molecular mechanisms underlying such a process are, however, still unknown. Indeed, several types of cell death may be produced, namely autoschizis, apoptosis and necrosis. Combined vitamin C and K-3 administration in vitro and in vivo produced tumor growth inhibition and increased the life-span of tumor-bearing mice. CK3-treatment selectively potentiated tumor chemotherapy, produced sensitization of tumors resistant to some drugs, potentiated cancer radiotherapy and caused inhibition of the development of cancer metastases without inducing toxicity in the host. We propose the association of vitamins C and K-3 as an adjuvant cancer therapy which may be introduced into human cancer therapy without any change in the classical anticancer protocols, and without any supplementary risk for patients.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.2174/0929867023368674" target="_blank" rel="noreferrer noopener">10.2174/0929867023368674</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2002
Apoptosis
ascorbate (vitamin C)
ascorbic-acid
autoschizis
Biochemistry & Molecular Biology
Cadrobbi J
Calderon P B
caloric restriction
Cancer
carcinoma-cells
cell-death
Current medicinal chemistry
cycle arrest
Gilloteaux J
growth-invitro
Hong-Ngoc N
induced apoptosis
Jamison J M
Journal Article or Conference Abstract Publication
Marques C
menadione (vitamin K-3)
Oxidative Stress
Pharmacology & Pharmacy
programmed
Summers J L
synergistic antitumor-activity
Taper H S
tumor-specific expression
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.psyneuen.2010.12.007" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.psyneuen.2010.12.007</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
955-969
Issue
7
Volume
36
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Sex differences in methamphetamine toxicity in mice: Effect on brain dopamine signaling pathways
Publisher
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Psychoneuroendocrinology
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-08
Subject
The topic of the resource
dopamine; mice; Psychiatry; Akt; 3; 2; 1-methyl-4-phenyl-1; Neurosciences & Neurology; Endocrinology & Metabolism; cell-death; activation; neurotoxicity; induced; rat striatum; kinase; striatum; Methamphetamine; evoked striatal dopamine; neurotoxicity; cd-1; element-binding protein; Sex difference; transporter function; 6-tetrahydropyridine mice
Creator
An entity primarily responsible for making the resource
Bourque M; Liu B; Dluzen D E; Di Paolo T
Description
An account of the resource
Mate mice were reported to display greater methamphetamine-induced neurotoxicity than females. The present study evaluated the involvement of phosphatidylinositol-3 kinase (PI3K)/Akt and extracellular signal-regulated kinase (ERK1/2) pathways in this sex-dependent methamphetamine toxicity. Intact female and male mice were administered methamphetamine (20 or 40 mg/kg) and euthanized a week later. Dopamine transporter (DAT) and vesicular monoamine transporter 2 (VMAT2) autoradiography in the lateral striatum showed a greater sensitivity in male mice treated with 20 mg/kg methamphetamine compared to female mice. Striatal dopamine concentration and DAT autoradiography showed a more extensive depletion in male mice given 40 mg/kg methamphetamine compared to female mice. Mice administered 40 mg/kg methamphetamine showed no sex difference in striatal VMAT2 autoradiography. In the substantia nigra, DAT specific binding was decreased only in male mice treated with 40 mg/kg methamphetamine and DAT mRNA levels decreased in methamphetamine-treated female and male mice. Methamphetamine-treated male mice presented a dose-dependent decrease of VMAT2 mRNA levels. Methamphetamine reduced insulin-like growth factor 1 receptor levels in females at both methamphetamine doses tested whereas it elevated G protein-coupled estrogen receptor 1 (GPER1) only in male mice. Phosphorylated Akt levels decreased only in male mice treated with 40 mg/kg methamphetamine. Glycogen synthase kinase 30 levels were reduced in male mice at both methamphetamine doses tested and in females receiving 40 mg/kg. Bcl-2 Levels were increased in male mice treated with methamphetamine, whereas ERK1/2 and BAD levels were unchanged. These results implicate some of the signaling pathways associated with the sex differences in methamphetamine-induced toxicity. (C) 2011 Elsevier Ltd. All rights reserved.
Identifier
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<a href="http://doi.org/10.1016/j.psyneuen.2010.12.007" target="_blank" rel="noreferrer noopener">10.1016/j.psyneuen.2010.12.007</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
1-Methyl-4-phenyl-1
2
2011
3
6-tetrahydropyridine mice
activation
Akt
Bourque M
cd-1
cell-death
Di Paolo T
Dluzen D E
Dopamine
element-binding protein
Endocrinology & Metabolism
evoked striatal dopamine
Induced
Journal Article or Conference Abstract Publication
Kinase
Liu B
Methamphetamine
Mice
Neurosciences & Neurology
Neurotoxicity
Psychiatry
Psychoneuroendocrinology
rat striatum
Sex difference
striatum
transporter function