1
40
5
-
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.nbd.2017.08.009" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.nbd.2017.08.009</a>
Pages
115–127
Volume
108
Dublin Core
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Title
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Alternative microglial activation is associated with cessation of progressive dopamine neuron loss in mice systemically administered lipopolysaccharide.
Publisher
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Neurobiology of disease
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-12
Subject
The topic of the resource
Animals; Astrocytes/immunology/pathology; Cell Death/physiology; Corpus Striatum/immunology/pathology; Cytokines/metabolism; Disease Progression; Dopaminergic Neurons/*immunology/pathology; Inbred C57BL; Inflammation/pathology/physiopathology; Lipopolysaccharides/*toxicity; Male; Messenger/metabolism; Mice; Microglia/*immunology/pathology; Nerve Degeneration/*immunology/pathology; Neurodegenerative Diseases/immunology/pathology; Neuroimmunomodulation/physiology; Random Allocation; RNA; Time Factors
Creator
An entity primarily responsible for making the resource
Beier Eric E; Neal Matthew; Alam Gelerah; Edler Melissa; Wu Long-Jun; Richardson Jason R
Description
An account of the resource
Inflammation arising from central and/or peripheral sources contributes to the pathogenesis of multiple neurodegenerative diseases including Parkinson's disease (PD). Emerging data suggest that differential activation of glia could lead to the pathogenesis and progression of PD. Here, we sought to determine the relationship between lipopolysaccharide (LPS) treatment, loss of dopaminergic neurons and differential activation of glia. Using a model of repeated injections with LPS (1mg/kg, i.p. for 4days), we found that LPS induced a 34% loss of dopamine neurons in the substantia nigra 19days after initiation of treatment, but no further cell loss was observed at 36days. LPS induced a strong pro-inflammatory response with increased mRNA expression of pro-inflammatory markers, including tumor necrosis factor-alpha (4.8-fold), inducible nitric oxide synthase (2.0-fold), interleukin-1 beta (8.9-fold), interleukin-6 (10.7-fold), and robust glial activation were observed at 1day after final dose of LPS. These pro-inflammatory genes were then reduced at 19days after treatment, when there was a rise in the anti-inflammatory genes Ym1 (1.8-fold) and arginase-1 (2.6-fold). Additionally, 36days after the last LPS injection there was a significant increase in interleukin-10 (2.1-fold) expression. The qPCR data results were supported by protein data, including cytokine measurements, western blotting, and immunofluorescence in brain microglia. Taken together, these data demonstrate that progressive neurodegeneration in the substantia nigra following LPS is likely arrested by microglia shifting to an anti-inflammatory phenotype. Thus, strategies to promote resolution of neuroinflammation may be a promising avenue to slow the progressive loss of dopamine neurons in PD.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.nbd.2017.08.009" target="_blank" rel="noreferrer noopener">10.1016/j.nbd.2017.08.009</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
Alam Gelerah
Animals
Astrocytes/immunology/pathology
Beier Eric E
Cell Death/physiology
Corpus Striatum/immunology/pathology
Cytokines/metabolism
Department of Pharmaceutical Sciences
Disease Progression
Dopaminergic Neurons/*immunology/pathology
Edler Melissa
Inbred C57BL
Inflammation/pathology/physiopathology
Lipopolysaccharides/*toxicity
Male
Messenger/metabolism
Mice
Microglia/*immunology/pathology
Neal Matthew
NEOMED College of Pharmacy
Nerve Degeneration/*immunology/pathology
Neurobiology of disease
Neurodegenerative Diseases/immunology/pathology
Neuroimmunomodulation/physiology
Random Allocation
Richardson Jason R
RNA
Time Factors
Wu Long-Jun
-
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/10.1186/s12974-018-1310-6" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/s12974-018-1310-6</a>
Pages
278–278
Issue
1
Volume
15
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
Genetically enhancing the expression of chemokine domain of CX3CL1 fails to prevent tau pathology in mouse models of tauopathy.
Publisher
An entity responsible for making the resource available
Journal of neuroinflammation
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-09
Subject
The topic of the resource
Alzheimer's disease; Animal; Animals; Antigens; Biological; Calcium Binding Proteins – Metabolism; Calcium-Binding Proteins/metabolism; Cells – Drug Effects; Cells – Metabolism; Cells – Pathology; Chemokine CX3CL1/*genetics/metabolism; Cognition Disorders – Etiology; Cognition Disorders/etiology; CX3CL1; CX3CR1; Cytokines; Cytokines – Metabolism; Cytokines/metabolism; Differentiation/genetics/metabolism; Disease Models; Gene Expression Regulation/drug effects/*genetics; Genes; Genes – Drug Effects; Learning; Lipopolysaccharides; Lipopolysaccharides/toxicity; Maze Learning; Mice; Microfilament Proteins – Metabolism; Microfilament Proteins/metabolism; Microglia; Microglia/drug effects/*metabolism/pathology; Models; Mutation; Mutation/genetics; Nerve Tissue Proteins; Nerve Tissue Proteins – Metabolism; Neurodegenerative Diseases; Neurodegenerative Diseases – Complications; Neurodegenerative Diseases – Pathology; Neuroinflammation; Surface; Surface – Metabolism; Tau; tau Proteins/genetics/metabolism; Tauopathies; Tauopathies/complications/genetics/*pathology; Transgenic
Creator
An entity primarily responsible for making the resource
Bemiller Shane M; Maphis Nicole M; Formica Shane V; Wilson Gina N; Miller Crystal M; Xu Guixiang; Kokiko-Cochran Olga N; Kim Ki-Wook; Jung Steffen; Cannon Judy L; Crish Samuel D; Cardona Astrid E; Lamb Bruce T; Bhaskar Kiran
Description
An account of the resource
BACKGROUND: Fractalkine (CX3CL1) and its receptor (CX3CR1) play an important role in regulating microglial function. We have previously shown that Cx3cr1 deficiency exacerbated tau pathology and led to cognitive impairment. However, it is still unclear if the chemokine domain of the ligand CX3CL1 is essential in regulating neuronal tau pathology. METHODS: We used transgenic mice lacking endogenous Cx3cl1 (Cx3cl1(-/-)) and expressing only obligatory soluble form (with only chemokine domain) and lacking the mucin stalk of CX3CL1 (referred to as Cx3cl1(105Delta) mice) to assess tau pathology and behavioral function in both lipopolysaccharide (LPS) and genetic (hTau) mouse models of tauopathy. RESULTS: First, increased basal tau levels accompanied microglial activation in Cx3cl1(105Delta) mice compared to control groups. Second, increased CD45(+) and F4/80(+) neuroinflammation and tau phosphorylation were observed in LPS, hTau/Cx3cl1(-/-), and hTau/Cx3cl1(105Delta) mouse models of tau pathology, which correlated with impaired spatial learning. Finally, microglial cell surface expression of CX3CR1 was reduced in Cx3cl1(105Delta) mice, suggesting enhanced fractalkine receptor internalization (mimicking Cx3cr1 deletion), which likely contributes to the elevated tau pathology. CONCLUSIONS: Collectively, our data suggest that overexpression of only chemokine domain of CX3CL1 does not protect against tau pathology.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1186/s12974-018-1310-6" target="_blank" rel="noreferrer noopener">10.1186/s12974-018-1310-6</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2018
Alzheimer's disease
Animal
Animals
Antigens
Bemiller Shane M
Bhaskar Kiran
Biological
Calcium Binding Proteins – Metabolism
Calcium-Binding Proteins/metabolism
Cannon Judy L
Cardona Astrid E
Cells – Drug Effects
Cells – Metabolism
Cells – Pathology
Chemokine CX3CL1/*genetics/metabolism
Cognition Disorders – Etiology
Cognition Disorders/etiology
Crish Samuel D
CX3CL1
CX3CR1
Cytokines
Cytokines – Metabolism
Cytokines/metabolism
Department of Pharmaceutical Sciences
Differentiation/genetics/metabolism
Disease Models
Formica Shane V
Gene Expression Regulation/drug effects/*genetics
Genes
Genes – Drug Effects
Journal of neuroinflammation
Jung Steffen
Kim Ki-Wook
Kokiko-Cochran Olga N
Lamb Bruce T
Learning
Lipopolysaccharides
Lipopolysaccharides/toxicity
Maphis Nicole M
Maze Learning
Mice
Microfilament Proteins – Metabolism
Microfilament Proteins/metabolism
Microglia
Microglia/drug effects/*metabolism/pathology
Miller Crystal M
Models
Mutation
Mutation/genetics
NEOMED College of Pharmacy
Nerve Tissue Proteins
Nerve Tissue Proteins – Metabolism
Neurodegenerative Diseases
Neurodegenerative Diseases – Complications
Neurodegenerative Diseases – Pathology
Neuroinflammation
Surface
Surface – Metabolism
Tau
tau Proteins/genetics/metabolism
Tauopathies
Tauopathies/complications/genetics/*pathology
Transgenic
Wilson Gina N
Xu Guixiang
-
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/10.1111/j.1478-3231.2010.02295.x" target="_blank" rel="noreferrer noopener">http://doi.org/10.1111/j.1478-3231.2010.02295.x</a>
Pages
1103–1114
Issue
8
Volume
30
Dublin Core
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Title
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Resveratrol and liver disease: from bench to bedside and community.
Publisher
An entity responsible for making the resource available
Liver international : official journal of the International Association for the Study of the Liver
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-09
Subject
The topic of the resource
Acetaminophen/metabolism; Anti-Inflammatory Agents; Antioxidants/therapeutic use; Carbon Tetrachloride/metabolism; Cytokines/metabolism; Ethanol/metabolism; Free Radicals/metabolism; Glutathione/metabolism; Hepatocytes/drug effects/pathology; Humans; Liver Diseases/*drug therapy/epidemiology; NF-kappa B/antagonists & inhibitors; Non-Steroidal/therapeutic use; Resveratrol; Stilbenes/pharmacokinetics/*pharmacology/therapeutic use/toxicity
Creator
An entity primarily responsible for making the resource
Bishayee Anupam; Darvesh Altaf S; Politis Themos; McGory Robb
Description
An account of the resource
Liver diseases incorporate several maladies, which can range from benign histological changes to serious life-threatening conditions. These may include inborn metabolic disease, primary and metastatic cancers, alcoholic cirrhosis, viral hepatitis and drug-induced hepatotoxicity. Liver disease remains a major cause of morbidity and mortality with significant economic and social costs. Several novel approaches are currently being studied which may provide a better therapeutic outcome. The use of naturally occurring phytochemicals, some of them obtained from dietary sources, in the amelioration of illness have recently gained considerable popularity. These agents, having anti-oxidant and anti-inflammatory properties, provide a safe and effective means of ameliorating chronic disease. Resveratrol, a grape polyphenol, has shown considerable promise as a therapeutic agent in the treatment of the aforementioned liver ailments. Several studies have highlighted the hepatoprotective properties of resveratrol. Resveratrol has been shown to prevent hepatic damage because of free radicals and inflammatory cytokines, induce anti-oxidant enzymes and elevate glutathione content. Resveratrol has also been shown to modulate varied signal transduction pathways implicated in liver diseases. This review critically examines the current preclinical in vitro and in vivo studies on the preventive and therapeutic effects of resveratrol in liver diseases. The review highlights the pharmacological mechanisms involved in mediating the aforementioned effects. Toxicity, pharmacokinetics and clinical bioavailability of resveratrol are also reviewed in this article. The challenges involved, future directions and novel approaches such as site-specific drug delivery in the use of resveratrol for the prevention and treatment of liver disease are also discussed.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1111/j.1478-3231.2010.02295.x" target="_blank" rel="noreferrer noopener">10.1111/j.1478-3231.2010.02295.x</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2010
Acetaminophen/metabolism
Anti-Inflammatory Agents
Antioxidants/therapeutic use
Bishayee Anupam
Carbon Tetrachloride/metabolism
Cytokines/metabolism
Darvesh Altaf S
Department of Pharmaceutical Sciences
Ethanol/metabolism
Free Radicals/metabolism
Glutathione/metabolism
Hepatocytes/drug effects/pathology
Humans
Liver Diseases/*drug therapy/epidemiology
Liver international : official journal of the International Association for the Study of the Liver
McGory Robb
NEOMED College of Pharmacy
NF-kappa B/antagonists & inhibitors
Non-Steroidal/therapeutic use
Politis Themos
Resveratrol
Stilbenes/pharmacokinetics/*pharmacology/therapeutic use/toxicity
-
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/10.1039/c6nr00398b" target="_blank" rel="noreferrer noopener">http://doi.org/10.1039/c6nr00398b</a>
Pages
6542–6554
Issue
12
Volume
8
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
Anti-atherogenic effect of trivalent chromium-loaded CPMV nanoparticles in human aortic smooth muscle cells under hyperglycemic conditions in vitro.
Publisher
An entity responsible for making the resource available
Nanoscale
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-03
Subject
The topic of the resource
*Comovirus; Aorta/*metabolism; Atherosclerosis/*drug therapy/therapy; Azo Compounds/chemistry; Cell Proliferation; Cells; Chlorides/*chemistry; Chromium Compounds/*chemistry; Cultured; Cytokines/metabolism; Drug Delivery Systems; Electron; Fluorescence; Glucose/chemistry; Humans; Hyperglycemia/*metabolism; Lipids/chemistry; Microscopy; Myocytes; Nanoparticles/chemistry; NF-kappa B/metabolism; Proliferating Cell Nuclear Antigen/chemistry; Smooth Muscle/*metabolism; Spectrophotometry; Transforming Growth Factor beta/metabolism; Transmission; Ultraviolet
Creator
An entity primarily responsible for making the resource
Ganguly Rituparna; Wen Amy M; Myer Ashley B; Czech Tori; Sahu Soumyadip; Steinmetz Nicole F; Raman Priya
Description
An account of the resource
Atherosclerosis, a major macrovascular complication associated with diabetes, poses a tremendous burden on national health care expenditure. Despite extensive efforts, cost-effective remedies are unknown. Therapies for atherosclerosis are challenged by a lack of targeted drug delivery approaches. Toward this goal, we turn to a biology-derived drug delivery system utilizing nanoparticles formed by the plant virus, Cowpea mosaic virus (CPMV). The aim herein is to investigate the anti-atherogenic potential of the beneficial mineral nutrient, trivalent chromium, loaded CPMV nanoparticles in human aortic smooth muscle cells (HASMC) under hyperglycemic conditions. A non-covalent loading protocol is established yielding CrCl3-loaded CPMV (CPMV-Cr) carrying 2000 drug molecules per particle. Using immunofluorescence microscopy, we show that CPMV-Cr is readily taken up by HASMC in vitro. In glucose (25 mM)-stimulated cells, 100 nM CPMV-Cr inhibits HASMC proliferation concomitant to attenuated proliferating cell nuclear antigen (PCNA, proliferation marker) expression. This is accompanied by attenuation in high glucose-induced phospho-p38 and pAkt expression. Moreover, CPMV-Cr inhibits the expression of pro-inflammatory cytokines, transforming growth factor-beta (TGF-beta) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB), in glucose-stimulated HASMCs. Finally glucose-stimulated lipid uptake is remarkably abrogated by CPMV-Cr, revealed by Oil Red O staining. Together, these data provide key cellular evidence for an atheroprotective effect of CPMV-Cr in vascular smooth muscle cells (VSMC) under hyperglycemic conditions that may promote novel therapeutic ventures for diabetic atherosclerosis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1039/c6nr00398b" target="_blank" rel="noreferrer noopener">10.1039/c6nr00398b</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Comovirus
2016
Aorta/*metabolism
Atherosclerosis/*drug therapy/therapy
Azo Compounds/chemistry
Cell Proliferation
Cells
Chlorides/*chemistry
Chromium Compounds/*chemistry
Cultured
Cytokines/metabolism
Czech Tori
Department of Integrative Medical Sciences
Drug Delivery Systems
Electron
Fluorescence
Ganguly Rituparna
Glucose/chemistry
Humans
Hyperglycemia/*metabolism
Lipids/chemistry
Microscopy
Myer Ashley B
Myocytes
Nanoparticles/chemistry
Nanoscale
NEOMED College of Medicine
NF-kappa B/metabolism
Proliferating Cell Nuclear Antigen/chemistry
Raman Priya
Sahu Soumyadip
Smooth Muscle/*metabolism
Spectrophotometry
Steinmetz Nicole F
Transforming Growth Factor beta/metabolism
Transmission
Ultraviolet
Wen Amy M
-
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.expneurol.2017.06.020" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.expneurol.2017.06.020</a>
Pages
1–15
Volume
296
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
Injury-induced gp130 cytokine signaling in peripheral ganglia is reduced in diabetes mellitus.
Publisher
An entity responsible for making the resource available
Experimental neurology
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-10
Subject
The topic of the resource
*Axon regeneration; *Axotomy; *Diabetes; *Neuropathy; *Peripheral nervous system; Animal; Animals; Antibiotics; Antineoplastic/toxicity; Blood Glucose/drug effects; Body Weight/drug effects; Cytokine Receptor gp130/genetics/*metabolism; Cytokines/metabolism; Diabetes Mellitus; Disease Models; Experimental/chemically induced/complications/*pathology; Fasting/blood; Gene Expression Regulation/*physiology; Hyperalgesia/etiology; Hyperglycemia/etiology; Inbred C57BL; Male; Mice; Nerve Degeneration/*etiology/pathology; Nerve Tissue Proteins/metabolism; Pain Measurement; Signal Transduction/drug effects/*physiology; Streptozocin/toxicity; Superior Cervical Ganglion/drug effects/*metabolism; Sweating/drug effects
Creator
An entity primarily responsible for making the resource
Niemi Jon P; Filous Angela R; DeFrancesco Alicia; Lindborg Jane A; Malhotra Nisha A; Wilson Gina N; Zhou Bowen; Crish Samuel D; Zigmond Richard E
Description
An account of the resource
Neuropathy is a major diabetic complication. While the mechanism of this neuropathy is not well understood, it is believed to result in part from deficient nerve regeneration. Work from our laboratory established that gp130 family of cytokines are induced in animals after axonal injury and are involved in the induction of regeneration-associated genes (RAGs) and in the conditioning lesion response. Here, we examine whether a reduction of cytokine signaling occurs in diabetes. Streptozotocin (STZ) was used to destroy pancreatic beta cells, leading to chronic hyperglycemia. Mice were injected with either low doses of STZ (5x60mg/kg) or a single high dose (1x200mg/kg) and examined after three or one month, respectively. Both low and high dose STZ treatment resulted in sustained hyperglycemia and functional deficits associated with the presence of both sensory and autonomic neuropathy. Diabetic mice displayed significantly reduced intraepidermal nerve fiber density and sudomotor function. Furthermore, low and high dose diabetic mice showed significantly reduced tactile touch sensation measured with Von Frey monofilaments. To look at the regenerative and injury-induced responses in diabetic mice, neurons in both superior cervical ganglia (SCG) and the 4th and 5th lumbar dorsal root ganglia (DRG) were unilaterally axotomized. Both high and low dose diabetic mice displayed significantly less axonal regeneration in the sciatic nerve, when measured in vivo, 48h after crush injury. Significantly reduced induction of two gp130 cytokines, leukemia inhibitory factor and interleukin-6, occurred in diabetic animals in SCG 6h after injury compared to controls. Injury-induced expression of interleukin-6 was also found to be significantly reduced in the DRG at 6h after injury in low and high dose diabetic mice. These effects were accompanied by reduced phosphorylation of signal transducer and activator of transcription 3 (STAT3), a downstream effector of the gp130 signaling pathway. We also found decreased induction of several gp130-dependent RAGs, including galanin and vasoactive intestinal peptide. Together, these data suggest a novel mechanism for the decreased response of diabetic sympathetic and sensory neurons to injury.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.expneurol.2017.06.020" target="_blank" rel="noreferrer noopener">10.1016/j.expneurol.2017.06.020</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Axon regeneration
*Axotomy
*Diabetes
*Neuropathy
*Peripheral nervous system
2017
Animal
Animals
Antibiotics
Antineoplastic/toxicity
Blood Glucose/drug effects
Body Weight/drug effects
Crish Samuel D
Cytokine Receptor gp130/genetics/*metabolism
Cytokines/metabolism
DeFrancesco Alicia
Department of Pharmaceutical Sciences
Diabetes Mellitus
Disease Models
Experimental neurology
Experimental/chemically induced/complications/*pathology
Fasting/blood
Filous Angela R
Gene Expression Regulation/*physiology
Hyperalgesia/etiology
Hyperglycemia/etiology
Inbred C57BL
Lindborg Jane A
Male
Malhotra Nisha A
Mice
NEOMED College of Pharmacy
Nerve Degeneration/*etiology/pathology
Nerve Tissue Proteins/metabolism
Niemi Jon P
Pain Measurement
Signal Transduction/drug effects/*physiology
Streptozocin/toxicity
Superior Cervical Ganglion/drug effects/*metabolism
Sweating/drug effects
Wilson Gina N
Zhou Bowen
Zigmond Richard E