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Article: Traitement des gonalgies en antalgie interventionnelle.

Choffat, Caroline / Chu Sin Chung, Paul / Cachemaille, Matthieu

2020 Volume 16, Issue 700, Page(s) 1342–1347

Abstract: Arthritis is the main cause of knee pain among adults over 50 years old. Prosthetic surgery is the ultimate treatment, however percutaneous interventional pain management is a good alternative treatment for patients who are not eligible for an operation ... ...

Title translation	Interventional pain management for knee pain.
Abstract	Arthritis is the main cause of knee pain among adults over 50 years old. Prosthetic surgery is the ultimate treatment, however percutaneous interventional pain management is a good alternative treatment for patients who are not eligible for an operation or for those who experiment persistent pain after surgery. Intra-articular corticosteroids or hyaluronic acid injections have a mild effect which is limited in time. Nerve ablation treatment using radiofrequency or cryotherapy may have longer lasting analgesic effects superior than 6 months. Finally, regenerative medicine, meaning platelet-rich plasma or mesenchymal stem cells, seems a very promising treatment by improving pain and mobility for a longer period.
MeSH term(s)	Adult ; Humans ; Injections, Intra-Articular ; Knee Joint ; Middle Aged ; Osteoarthritis, Knee ; Pain ; Pain Management ; Treatment Outcome
Language	French
Publishing date	2020-07-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2177010-4
ISSN	1660-9379
ISSN	1660-9379
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Article ; Online: Characterisation of GFAP-Expressing Glial Cells in the Dorsal Root Ganglion after Spared Nerve Injury.

Konnova, Elena A / Deftu, Alexandru-Florian / Chu Sin Chung, Paul / Pertin, Marie / Kirschmann, Guylène / Decosterd, Isabelle / Suter, Marc R

International journal of molecular sciences

2023 Volume 24, Issue 21

Abstract: Satellite glial cells (SGCs), enveloping primary sensory neurons' somas in the dorsal root ganglion (DRG), contribute to neuropathic pain upon nerve injury. Glial fibrillary acidic protein (GFAP) serves as an SGC activation marker, though its DRG ... ...

Abstract	Satellite glial cells (SGCs), enveloping primary sensory neurons' somas in the dorsal root ganglion (DRG), contribute to neuropathic pain upon nerve injury. Glial fibrillary acidic protein (GFAP) serves as an SGC activation marker, though its DRG satellite cell specificity is debated. We employed the hGFAP-CFP transgenic mouse line, designed for astrocyte studies, to explore its expression within the peripheral nervous system (PNS) after spared nerve injury (SNI). We used diverse immunostaining techniques, Western blot analysis, and electrophysiology to evaluate GFAP+ cell changes. Post-SNI, GFAP+ cell numbers increased without proliferation, and were found near injured ATF3+ neurons. GFAP+ FABP7+ SGCs increased, yet 75.5% of DRG GFAP+ cells lacked FABP7 expression. This suggests a significant subset of GFAP+ cells are non-myelinating Schwann cells (nmSC), indicated by their presence in the dorsal root but not in the ventral root which lacks unmyelinated fibres. Additionally, patch clamp recordings from GFAP+ FABP7-cells lacked SGC-specific K
MeSH term(s)	Animals ; Mice ; Ganglia, Spinal/metabolism ; Glial Fibrillary Acidic Protein/genetics ; Glial Fibrillary Acidic Protein/metabolism ; Neuroglia/metabolism ; Satellite Cells, Perineuronal/metabolism ; Neuralgia/metabolism ; Trauma, Nervous System/metabolism
Chemical Substances	Glial Fibrillary Acidic Protein
Language	English
Publishing date	2023-10-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms242115559
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Article ; Online: Potassium channel modulation in macrophages sensitizes dorsal root ganglion neurons after nerve injury.

Konnova, Elena A / Deftu, Alexandru-Florian / Chu Sin Chung, Paul / Kirschmann, Guylène / Decosterd, Isabelle / Suter, Marc R

Glia

2023 Volume 72, Issue 4, Page(s) 677–691

Abstract: Macrophages and satellite glial cells are found between injured and uninjured neurons in the lumbar dorsal root ganglia (DRG). We explored the mechanism of neuro-immune and neuron-glia crosstalk leading to hyperexcitability of DRG neurons. After spared ... ...

Abstract	Macrophages and satellite glial cells are found between injured and uninjured neurons in the lumbar dorsal root ganglia (DRG). We explored the mechanism of neuro-immune and neuron-glia crosstalk leading to hyperexcitability of DRG neurons. After spared nerve injury (SNI), CX3CR1
MeSH term(s)	Rats ; Mice ; Animals ; Ganglia, Spinal/metabolism ; Potassium Channels/metabolism ; Rats, Sprague-Dawley ; Neurons/metabolism ; Neuroglia
Chemical Substances	Potassium Channels
Language	English
Publishing date	2023-12-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.24496
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Article ; Online: Somatosensory profiling of patients undergoing alcohol withdrawal: Do neuropathic pain and sensory loss represent a problem?

Fernandez, Aurore / Graf, Guillaume / Lasserre, Aurélie / Daeppen, Jean-Bernard / Chu Sin Chung, Paul / Berna, Chantal / Suter, Marc R

Journal of the peripheral nervous system : JPNS

2023 Volume 28, Issue 3, Page(s) 490–499

Abstract: Introduction: Chronic heavy alcohol use is known to cause neurological complications such as peripheral neuropathy. Concerning the pathophysiology, few sural nerve and skin biopsy studies showed that small fibers might be selectively vulnerable to ... ...

Abstract	Introduction: Chronic heavy alcohol use is known to cause neurological complications such as peripheral neuropathy. Concerning the pathophysiology, few sural nerve and skin biopsy studies showed that small fibers might be selectively vulnerable to degeneration in alcohol-related peripheral neuropathy. Pain has rarely been properly evaluated in this pathology. The present study aims at assessing pain intensity, potential neuropathic characteristics as well as the functionality of both small and large nerve sensitive fibers. Methods: In this observational study, 27 consecutive adult patients, hospitalized for alcohol withdrawal and 13 healthy controls were recruited. All the participants underwent a quantitative sensory testing (QST) according to the standardized protocol of the German Research Network Neuropathic Pain, a neurological examination and filled standardized questionnaires assessing alcohol consumption and dependence as well as pain characteristics and psychological comorbidities. Results: Nearly half of the patients (13/27) reported pain. Yet, pain intensity was weak, leading to a low interference with daily life, and its characteristics did not support a neuropathic component. A functional impairment of small nerve fibers was frequently described, with thermal hypoesthesia observed in 52% of patients. Patients with a higher alcohol consumption over the last 2 years showed a greater impairment of small fiber function. Discussion: Patients report pain but it is however unlikely to be caused by peripheral neuropathy given the non-length-dependent distribution and the absence of neuropathic pain features. Chronic pain in AUD deserves to be better evaluated and managed as it represents an opportunity to improve long-term clinical outcomes, potentially participating to relapse prevention.
MeSH term(s)	Adult ; Humans ; Alcoholism/complications ; Alcoholism/pathology ; Substance Withdrawal Syndrome/complications ; Substance Withdrawal Syndrome/pathology ; Neuralgia/etiology ; Pain Measurement/adverse effects ; Pain Measurement/methods ; Skin/pathology
Language	English
Publishing date	2023-07-12
Publishing country	United States
Document type	Observational Study ; Case Reports
ZDB-ID	1364009-4
ISSN	1529-8027 ; 1085-9489
ISSN (online)	1529-8027
ISSN	1085-9489
DOI	10.1111/jns.12578
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Article ; Online: The Antidiabetic Drug Metformin Regulates Voltage-Gated Sodium Channel Na

Deftu, Alexandru-Florian / Chu Sin Chung, Paul / Laedermann, Cédric J / Gillet, Ludovic / Pertin, Marie / Kirschmann, Guylène / Decosterd, Isabelle

eNeuro

2022 Volume 9, Issue 2

Abstract: The antidiabetic drug metformin has been shown to reduce pain hypersensitivity in preclinical models of chronic pain and in neuropathic pain in humans. Multiple intracellular pathways have been described as metformin targets. Among them, metformin is an ... ...

Abstract	The antidiabetic drug metformin has been shown to reduce pain hypersensitivity in preclinical models of chronic pain and in neuropathic pain in humans. Multiple intracellular pathways have been described as metformin targets. Among them, metformin is an activator of the adenosine 5'-monophosphate protein kinase that can in turn modulate the activity of the E3 ubiquitin ligase NEDD4-2 and thus post-translational expression of voltage-gated sodium channels (Na
MeSH term(s)	Animals ; Ganglia, Spinal/metabolism ; Hypoglycemic Agents/pharmacology ; Metformin/metabolism ; Metformin/pharmacology ; Mice ; NAV1.8 Voltage-Gated Sodium Channel/metabolism ; Nedd4 Ubiquitin Protein Ligases/metabolism ; Ubiquitin/metabolism ; Ubiquitin/pharmacology ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism ; Voltage-Gated Sodium Channels/metabolism
Chemical Substances	Hypoglycemic Agents ; NAV1.8 Voltage-Gated Sodium Channel ; Ubiquitin ; Voltage-Gated Sodium Channels ; Metformin (9100L32L2N) ; Nedd4 Ubiquitin Protein Ligases (EC 2.3.2.26) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2022-03-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2800598-3
ISSN	2373-2822 ; 2373-2822
ISSN (online)	2373-2822
ISSN	2373-2822
DOI	10.1523/ENEURO.0409-21.2022
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Article ; Online: Cortico-autonomic local arousals and heightened somatosensory arousability during NREMS of mice in neuropathic pain.

Cardis, Romain / Lecci, Sandro / Fernandez, Laura Mj / Osorio-Forero, Alejandro / Chu Sin Chung, Paul / Fulda, Stephany / Decosterd, Isabelle / Lüthi, Anita

eLife

2021 Volume 10

Abstract: Frequent nightly arousals typical for sleep disorders cause daytime fatigue and present health risks. As such arousals are often short, partial, or occur locally within the brain, reliable characterization in rodent models of sleep disorders and in human ...

Abstract	Frequent nightly arousals typical for sleep disorders cause daytime fatigue and present health risks. As such arousals are often short, partial, or occur locally within the brain, reliable characterization in rodent models of sleep disorders and in human patients is challenging. We found that the EEG spectral composition of non-rapid eye movement sleep (NREMS) in healthy mice shows an infraslow (~50 s) interval over which microarousals appear preferentially. NREMS could hence be vulnerable to abnormal arousals on this time scale. Chronic pain is well-known to disrupt sleep. In the spared nerve injury (SNI) mouse model of chronic neuropathic pain, we found more numerous local cortical arousals accompanied by heart rate increases in hindlimb primary somatosensory, but not in prelimbic, cortices, although sleep macroarchitecture appeared unaltered. Closed-loop mechanovibrational stimulation further revealed higher sensory arousability. Chronic pain thus preserved conventional sleep measures but resulted in elevated spontaneous and evoked arousability. We develop a novel moment-to-moment probing of NREMS vulnerability and propose that chronic pain-induced sleep complaints arise from perturbed arousability.
MeSH term(s)	Animals ; Arousal/physiology ; Autonomic Nervous System ; Brain/physiology ; Cerebral Cortex/physiology ; Mice ; Neuralgia ; Sleep/physiology ; Sleep Initiation and Maintenance Disorders ; Sleep, REM/physiology ; Wakefulness/physiology
Language	English
Publishing date	2021-07-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.65835
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Article ; Online: Delta opioid receptors in brain function and diseases.

Chu Sin Chung, Paul / Kieffer, Brigitte L

Pharmacology & therapeutics

2013 Volume 140, Issue 1, Page(s) 112–120

Abstract: Evidence that the delta opioid receptor (DOR) is an attractive target for the treatment of brain disorders has strengthened in recent years. This receptor is broadly expressed in the brain, binds endogenous opioid peptides, and shows as functional ... ...

Abstract	Evidence that the delta opioid receptor (DOR) is an attractive target for the treatment of brain disorders has strengthened in recent years. This receptor is broadly expressed in the brain, binds endogenous opioid peptides, and shows as functional profile highly distinct from those of mu and kappa opioid receptors. Our knowledge of DOR function has enormously progressed from in vivo studies using pharmacological tools and genetic approaches. The important role of this receptor in reducing chronic pain has been extensively overviewed; therefore this review focuses on facets of delta receptor activity relevant to psychiatric and other neurological disorders. Beneficial effects of DOR agonists are now well established in the context of emotional responses and mood disorders. DOR activation also regulates drug reward, inhibitory controls and learning processes, but whether delta compounds may represent useful drugs in the treatment of drug abuse remains open. Epileptogenic and locomotor-stimulating effects of delta agonists appear drug-dependent, and the possibility of biased agonism at DOR for these effects is worthwhile further investigations to increase benefit/risk ratio of delta therapies. Neuroprotective effects of DOR activity represent a forthcoming research area. Future developments in DOR research will benefit from in-depth investigations of DOR function at cellular and circuit levels.
MeSH term(s)	Animals ; Brain/physiology ; Brain Ischemia/physiopathology ; Emotions/physiology ; Epilepsy/physiopathology ; Humans ; Hypoxia/physiopathology ; Motor Activity ; Opioid-Related Disorders/physiopathology ; Receptors, Opioid, delta/physiology ; Reward
Chemical Substances	Receptors, Opioid, delta
Language	English
Publishing date	2013-06-10
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	194735-7
ISSN	1879-016X ; 0163-7258
ISSN (online)	1879-016X
ISSN	0163-7258
DOI	10.1016/j.pharmthera.2013.06.003
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Zs.A 1183: Show issues

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Article ; Online: Peripheral nerve injury induces a transitory microglial reaction in the rat infralimbic cortex.

Chu Sin Chung, Paul / Panigada, Tania / Cardis, Romain / Decosterd, Isabelle / Gosselin, Romain-Daniel

Neuroscience letters

2017 Volume 655, Page(s) 14–20

Abstract: Undeniable evidence shows that microglia in the spinal cord undergo marked reactions following peripheral injuries. However, only rare studies have investigated the possible short and long term microglial reaction in brain regions following peripheral ... ...

Abstract	Undeniable evidence shows that microglia in the spinal cord undergo marked reactions following peripheral injuries. However, only rare studies have investigated the possible short and long term microglial reaction in brain regions following peripheral nerve injury and its interspecies specificities. In the present study we examined microglia in subdivisions of the prefrontal cortex in mice and rats, 7days and 42days after spared nerve injury (SNI) of the sciatic nerve. We show that a bilateral increase of microglial density takes place in the infralimbic cortex in rats 7days post-injury (sham vs. SNI, n=5: ipsilateral 35.4% increase of the median, p=0.0317; contralateral 24.9% increase of the median, p=0.0079), without any detectable change in the other investigated regions, namely the anterior cingulate, prelimbic and agranular insular cortices. In mice, no observable difference could be found in any region at both time points, neither using Iba-1 immunostaining nor with CX3CR1-eGFP animals. Our results indicate that a transitory, species-specific and highly regionalized microglial reaction takes place in the prefrontal cortex following peripheral nerve injury.
Language	English
Publishing date	2017-08-10
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2017.06.037
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Article: Delta opioid receptors in brain function and diseases

Chu Sin Chung, Paul / Kieffer, Brigitte L

Pharmacology and therapeutics. 2013 Oct., v. 140, no. 1

2013

Abstract	Evidence that the delta opioid receptor (DOR) is an attractive target for the treatment of brain disorders has strengthened in recent years. This receptor is broadly expressed in the brain, binds endogenous opioid peptides, and shows as functional profile highly distinct from those of mu and kappa opioid receptors. Our knowledge of DOR function has enormously progressed from in vivo studies using pharmacological tools and genetic approaches. The important role of this receptor in reducing chronic pain has been extensively overviewed; therefore this review focuses on facets of delta receptor activity relevant to psychiatric and other neurological disorders. Beneficial effects of DOR agonists are now well established in the context of emotional responses and mood disorders. DOR activation also regulates drug reward, inhibitory controls and learning processes, but whether delta compounds may represent useful drugs in the treatment of drug abuse remains open. Epileptogenic and locomotor-stimulating effects of delta agonists appear drug-dependent, and the possibility of biased agonism at DOR for these effects is worthwhile further investigations to increase benefit/risk ratio of delta therapies. Neuroprotective effects of DOR activity represent a forthcoming research area. Future developments in DOR research will benefit from in-depth investigations of DOR function at cellular and circuit levels.
Keywords	agonistic behavior ; agonists ; brain ; drug abuse ; drug therapy ; drugs ; emotions ; in vivo studies ; learning ; nervous system diseases ; neuroprotective effect ; opioid peptides ; pain ; receptors ; relative risk
Language	English
Dates of publication	2013-10
Size	p. 112-120.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	194735-7
ISSN	1879-016X ; 0163-7258
ISSN (online)	1879-016X
ISSN	0163-7258
DOI	10.1016/j.pharmthera.2013.06.003
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Distinct mu, delta, and kappa opioid receptor mechanisms underlie low sociability and depressive-like behaviors during heroin abstinence.

Lutz, Pierre-Eric / Ayranci, Gulebru / Chu-Sin-Chung, Paul / Matifas, Audrey / Koebel, Pascale / Filliol, Dominique / Befort, Katia / Ouagazzal, Abdel-Mouttalib / Kieffer, Brigitte L

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2014 Volume 39, Issue 11, Page(s) 2694–2705

Abstract: Addiction is a chronic disorder involving recurring intoxication, withdrawal, and craving episodes. Escaping this vicious cycle requires maintenance of abstinence for extended periods of time and is a true challenge for addicted individuals. The ... ...

Abstract	Addiction is a chronic disorder involving recurring intoxication, withdrawal, and craving episodes. Escaping this vicious cycle requires maintenance of abstinence for extended periods of time and is a true challenge for addicted individuals. The emergence of depressive symptoms, including social withdrawal, is considered a main cause for relapse, but underlying mechanisms are poorly understood. Here we establish a mouse model of protracted abstinence to heroin, a major abused opiate, where both emotional and working memory deficits unfold. We show that delta and kappa opioid receptor (DOR and KOR, respectively) knockout mice develop either stronger or reduced emotional disruption during heroin abstinence, establishing DOR and KOR activities as protective and vulnerability factors, respectively, that regulate the severity of abstinence. Further, we found that chronic treatment with the antidepressant drug fluoxetine prevents emergence of low sociability, with no impact on the working memory deficit, implicating serotonergic mechanisms predominantly in emotional aspects of abstinence symptoms. Finally, targeting the main serotonergic brain structure, we show that gene knockout of mu opioid receptors (MORs) in the dorsal raphe nucleus (DRN) before heroin exposure abolishes the development of social withdrawal. This is the first result demonstrating that intermittent chronic MOR activation at the level of DRN represents an essential mechanism contributing to low sociability during protracted heroin abstinence. Altogether, our findings reveal crucial and distinct roles for all three opioid receptors in the development of emotional alterations that follow a history of heroin exposure and open the way towards understanding opioid system-mediated serotonin homeostasis in heroin abuse.
MeSH term(s)	Animals ; Antidepressive Agents, Second-Generation/pharmacology ; Depression/metabolism ; Disease Models, Animal ; Dorsal Raphe Nucleus/drug effects ; Dorsal Raphe Nucleus/metabolism ; Fluoxetine/pharmacology ; Heroin/pharmacology ; Heroin Dependence/physiopathology ; Heroin Dependence/psychology ; Male ; Memory Disorders/physiopathology ; Memory, Short-Term/drug effects ; Memory, Short-Term/physiology ; Mice, 129 Strain ; Mice, Inbred C57BL ; Mice, Knockout ; Narcotics/pharmacology ; Receptors, Opioid, kappa/genetics ; Receptors, Opioid, kappa/metabolism ; Receptors, Opioid, mu/genetics ; Receptors, Opioid, mu/metabolism ; Social Behavior ; Spatial Memory/drug effects ; Spatial Memory/physiology ; Substance Withdrawal Syndrome/drug therapy ; Substance Withdrawal Syndrome/physiopathology ; Substance Withdrawal Syndrome/psychology
Chemical Substances	Antidepressive Agents, Second-Generation ; Narcotics ; Receptors, Opioid, kappa ; Receptors, Opioid, mu ; Fluoxetine (01K63SUP8D) ; Heroin (70D95007SX)
Language	English
Publishing date	2014-05-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/npp.2014.126
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