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Article ; Online: NeuroHeal Treatment Alleviates Neuropathic Pain and Enhances Sensory Axon Regeneration.

Romeo-Guitart, David / Casas, Caty

2020 Volume 9, Issue 4

Abstract: Peripheral nerve injury (PNI) leads to the loss of motor, sensory, and autonomic functions, and often triggers neuropathic pain. During the last years, many efforts have focused on finding new therapies to increase axonal regeneration or to alleviate ... ...

Abstract	Peripheral nerve injury (PNI) leads to the loss of motor, sensory, and autonomic functions, and often triggers neuropathic pain. During the last years, many efforts have focused on finding new therapies to increase axonal regeneration or to alleviate painful conditions. Still only a few of them have targeted both phenomena. Incipient or aberrant sensory axon regeneration is related to abnormal unpleasant sensations, such as hyperalgesia or allodynia. We recently have discovered NeuroHeal, a combination of two repurposed drugs; Acamprosate and Ribavirin. NeuroHeal is a neuroprotective agent that also enhances motor axon regeneration after PNI. In this work, we investigated its effect on sensory fiber regeneration and PNI-induced painful sensations in a rat model of spare nerve injury and nerve crush. The follow up of the animals showed that NeuroHeal treatment reduced the signs of neuropathic pain in both models. Besides, the treatment favored sensory axon regeneration, as observed in dorsal root ganglion explants. Mechanistically, the effects observed in vivo may improve the resolution of cell-protective autophagy. Additionally, NeuroHeal treatment modulated the P2X4-BDNF-KCC2 axis, which is an essential driver of neuropathic pain. These data open a new therapeutic avenue based on autophagic modulation to foster endogenous regenerative mechanisms and reduce the appearance of neuropathic pain in PNI.
MeSH term(s)	Acamprosate/pharmacology ; Acamprosate/therapeutic use ; Animals ; Autophagy/drug effects ; Axons/drug effects ; Axons/pathology ; Brain-Derived Neurotrophic Factor/metabolism ; Calcium-Binding Proteins/metabolism ; Drug Combinations ; Female ; Hyperalgesia/complications ; Hyperalgesia/drug therapy ; Hyperalgesia/physiopathology ; Male ; Microfilament Proteins/metabolism ; Motor Neurons/drug effects ; Motor Neurons/pathology ; Nerve Regeneration/drug effects ; Neuralgia/complications ; Neuralgia/drug therapy ; Neuralgia/physiopathology ; Neurites/drug effects ; Neurites/metabolism ; Neurogenesis/drug effects ; Peripheral Nerves/drug effects ; Peripheral Nerves/pathology ; Peripheral Nerves/physiopathology ; Rats, Sprague-Dawley ; Receptors, Purinergic P2X4/metabolism ; Ribavirin/pharmacology ; Ribavirin/therapeutic use ; Sensory Thresholds/drug effects ; Spinal Cord Dorsal Horn/drug effects ; Spinal Cord Dorsal Horn/metabolism ; Symporters/metabolism ; K Cl- Cotransporters
Chemical Substances	Aif1 protein, rat ; Brain-Derived Neurotrophic Factor ; Calcium-Binding Proteins ; Drug Combinations ; Microfilament Proteins ; Receptors, Purinergic P2X4 ; Symporters ; acamprosate, ribavirin drug combination ; Ribavirin (49717AWG6K) ; Acamprosate (N4K14YGM3J)
Language	English
Publishing date	2020-03-27
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9040808
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Network-centric medicine for peripheral nerve injury: Treating the whole to boost endogenous mechanisms of neuroprotection and regeneration.

Romeo-Guitart, David / Casas, Caty

Neural regeneration research

2019 Volume 14, Issue 7, Page(s) 1122–1128

Abstract: Peripheral nerve injuries caused by accidents may lead to paralysis, sensory disturbances, anaesthesia, and lack of autonomic functions. Functional recovery after disconnection of the motoneuronal soma from target tissue with proximal rupture of axons is ...

Abstract	Peripheral nerve injuries caused by accidents may lead to paralysis, sensory disturbances, anaesthesia, and lack of autonomic functions. Functional recovery after disconnection of the motoneuronal soma from target tissue with proximal rupture of axons is determined by several factors: motoneuronal soma viability, proper axonal sprouting across inhibitory zones and elongation toward specific muscle, effective synapse contact rebuilding, and prevention of muscle atrophy. Therapies, such as adjuvant drugs with pleiotropic effects, that promote functional recovery after peripheral nerve injury are needed. Toward this aim, we designed a drug discovery workflow based on a network-centric molecular vision using unbiased proteomic data and neural artificial computational tools. Our focus is on boosting intrinsic capabilities of neurons for neuroprotection; this is in contrast to the common approach based on suppression of a pathobiological pathway known to be associated with disease condition. Using our workflow, we discovered neuroheal, a combination of two repurposed drugs that promotes motoneuronal soma neuroprotection, is anti-inflammatory, enhances axonal regeneration after axotomy, and reduces muscle atrophy. This drug discovery workflow has thus yielded a therapy that is close to its clinical application.
Language	English
Publishing date	2019-02-25
Publishing country	India
Document type	Journal Article
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.251187
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Article ; Online: Endogenous Mechanisms of Neuroprotection: To Boost or Not to Boost.

Marmolejo-Martínez-Artesero, Sara / Casas, Caty / Romeo-Guitart, David

Cells

2021 Volume 10, Issue 2

Abstract: Postmitotic cells, like neurons, must live through a lifetime. For this reason, organisms/cells have evolved with self-repair mechanisms that allow them to have a long life. The discovery workflow of neuroprotectors during the last years has focused on ... ...

Abstract	Postmitotic cells, like neurons, must live through a lifetime. For this reason, organisms/cells have evolved with self-repair mechanisms that allow them to have a long life. The discovery workflow of neuroprotectors during the last years has focused on blocking the pathophysiological mechanisms that lead to neuronal loss in neurodegeneration. Unfortunately, only a few strategies from these studies were able to slow down or prevent neurodegeneration. There is compelling evidence demonstrating that endorsing the self-healing mechanisms that organisms/cells endogenously have, commonly referred to as cellular resilience, can arm neurons and promote their self-healing. Although enhancing these mechanisms has not yet received sufficient attention, these pathways open up new therapeutic avenues to prevent neuronal death and ameliorate neurodegeneration. Here, we highlight the main endogenous mechanisms of protection and describe their role in promoting neuron survival during neurodegeneration.
MeSH term(s)	Animals ; Apoptosis ; Autophagy/drug effects ; Caloric Restriction ; Humans ; Neuroprotection/drug effects ; Neuroprotective Agents/pharmacology ; Unfolded Protein Response/drug effects
Chemical Substances	Neuroprotective Agents
Language	English
Publishing date	2021-02-10
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10020370
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Article ; Online: SIRT2 Inhibition Improves Functional Motor Recovery After Peripheral Nerve Injury.

Romeo-Guitart, David / Leiva-Rodríguez, Tatiana / Casas, Caty

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics

2019 Volume 17, Issue 3, Page(s) 1197–1211

Abstract: Sirtuin-2 (Sirt2) is a member of the NAD (+)-dependent protein deacetylase family involved in neuroprotection, cellular metabolism, homeostasis, and stress responses after injury of the nervous system. So far, no data have been published describing the ... ...

Abstract	Sirtuin-2 (Sirt2) is a member of the NAD (+)-dependent protein deacetylase family involved in neuroprotection, cellular metabolism, homeostasis, and stress responses after injury of the nervous system. So far, no data have been published describing the role of SIRT2 in motor functional recovery after damage. We found that SIRT2 expression and deacetylase activity were increased within motoneurons after axotomy. To shed light onto the biological relevance of this change, we combined in vitro and in vivo models with pharmacological and genetic ablation approaches. We found that SIRT2 KO (knockout) mice exhibited improved functional recovery after sciatic nerve crush. SIRT2 activity blockage, using AK7, increased neurite outgrowth and length in organotypic spinal cord cultures and human cell line models. SIRT2 blockage enhanced the acetyltransferase activity of p300, which in turn increased the levels of an acetylated form of p53 (Ac-p53 k373), histone 3 (Ac-H3K9), and expression of GAP43, a downstream marker of regeneration. Lastly, we verified that p300 acetyltransferase activity is essential for these effects. Our results suggest that bolstering an epigenetic shift that promotes SIRT2 inhibition can be an effective therapy to increase functional recovery after peripheral nerve injury.
MeSH term(s)	Animals ; Cell Line, Tumor ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Peripheral Nerve Injuries/genetics ; Peripheral Nerve Injuries/metabolism ; Peripheral Nerve Injuries/therapy ; Rats ; Rats, Sprague-Dawley ; Recovery of Function/physiology ; Sirtuin 2/antagonists & inhibitors ; Sirtuin 2/deficiency ; Sirtuin 2/genetics ; Spinal Cord/metabolism
Chemical Substances	Sirt2 protein, mouse (EC 3.5.1.-) ; Sirtuin 2 (EC 3.5.1.-)
Language	English
Publishing date	2019-05-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2316693-9
ISSN	1878-7479 ; 1933-7213
ISSN (online)	1878-7479
ISSN	1933-7213
DOI	10.1007/s13311-020-00860-3
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Article ; Online: Is it the time of autophagy fine-tuners for neuroprotection?

Romeo-Guitart, David / Marmolejo-Martínez-Artesero, Sara / Casas, Caty

Autophagy

2020 Volume 16, Issue 11, Page(s) 2108–2109

Abstract: Cells and organisms are intrinsically prepared to effectively deal with damage caused by insults and heal themselves by triggering a plethora of stress responses including macroautophagy/autophagy. However, autophagy may become malfunctional during aging, ...

Abstract	Cells and organisms are intrinsically prepared to effectively deal with damage caused by insults and heal themselves by triggering a plethora of stress responses including macroautophagy/autophagy. However, autophagy may become malfunctional during aging, neurodegeneration, and neurotrauma. We aimed to overcome autophagy dysfunction by refining therapeutics using multi-target approaches. Thus, we have demonstrated that modulation of autophagy with the multitarget drug NeuroHeal is neuroprotective in several neurodegeneration models in which previous autophagy modulators have failed. The key element of success is the coordinated activation of opposing forces that modulate autophagy with NeuroHeal, probably leading to the autophagy-dependent degradation of death executors such as PARP1. The precise tuning of autophagy thus allows the neuron to adapt to insults, survive and repair itself. These findings support the advent a new era of neuroprotectants that counteract neuronal damage by targeting in unison different pathways of the self-repair process, including autophagy.
MeSH term(s)	Acamprosate ; Autophagy ; Drug Combinations ; Motor Neurons ; Neuroprotection ; Ribavirin
Chemical Substances	Drug Combinations ; acamprosate, ribavirin drug combination ; Ribavirin (49717AWG6K) ; Acamprosate (N4K14YGM3J)
Language	English
Publishing date	2020-07-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2020.1794355
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Article ; Online: Improved Motor Nerve Regeneration by SIRT1/Hif1a-Mediated Autophagy.

Romeo-Guitart, David / Leiva-Rodriguez, Tatiana / Forés, Joaquim / Casas, Caty

Cells

2019 Volume 8, Issue 11

Abstract: Complete restoring of functional connectivity between neurons or target tissue after traumatic lesions is still an unmet medical need. Using models of nerve axotomy and compression, we investigated the effect of autophagy induction by genetic and ... ...

Abstract	Complete restoring of functional connectivity between neurons or target tissue after traumatic lesions is still an unmet medical need. Using models of nerve axotomy and compression, we investigated the effect of autophagy induction by genetic and pharmacological manipulation on motor nerve regeneration. ATG5 or NAD
MeSH term(s)	Animals ; Autophagy ; Autophagy-Related Protein 5/genetics ; Autophagy-Related Protein 5/metabolism ; Cells, Cultured ; Female ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Mice ; Mice, Inbred C57BL ; Motor Neurons/cytology ; Motor Neurons/physiology ; Nerve Regeneration ; Neuroblastoma/genetics ; Neuroblastoma/metabolism ; Neuroblastoma/pathology ; Rats ; Rats, Sprague-Dawley ; Sirtuin 1/genetics ; Sirtuin 1/metabolism
Chemical Substances	ATG5 protein, human ; Autophagy-Related Protein 5 ; HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; SIRT1 protein, human (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2019-10-30
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells8111354
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Article ; Online: Slc20a1 and Slc20a2 regulate neuronal plasticity and cognition independently of their phosphate transport ability.

Ramos-Brossier, Mariana / Romeo-Guitart, David / Lanté, Fabien / Boitez, Valérie / Mailliet, François / Saha, Soham / Rivagorda, Manon / Siopi, Eleni / Nemazanyy, Ivan / Leroy, Christine / Moriceau, Stéphanie / Beck-Cormier, Sarah / Codogno, Patrice / Buisson, Alain / Beck, Laurent / Friedlander, Gérard / Oury, Franck

Cell death & disease

2024 Volume 15, Issue 1, Page(s) 20

Abstract: In recent years, primary familial brain calcification (PFBC), a rare neurological disease characterized by a wide spectrum of cognitive disorders, has been associated to mutations in the sodium (Na)-Phosphate (Pi) co-transporter SLC20A2. However, the ... ...

Abstract	In recent years, primary familial brain calcification (PFBC), a rare neurological disease characterized by a wide spectrum of cognitive disorders, has been associated to mutations in the sodium (Na)-Phosphate (Pi) co-transporter SLC20A2. However, the functional roles of the Na-Pi co-transporters in the brain remain still largely elusive. Here we show that Slc20a1 (PiT-1) and Slc20a2 (PiT-2) are the most abundant Na-Pi co-transporters expressed in the brain and are involved in the control of hippocampal-dependent learning and memory. We reveal that Slc20a1 and Slc20a2 are differentially distributed in the hippocampus and associated with independent gene clusters, suggesting that they influence cognition by different mechanisms. Accordingly, using a combination of molecular, electrophysiological and behavioral analyses, we show that while PiT-2 favors hippocampal neuronal branching and survival, PiT-1 promotes synaptic plasticity. The latter relies on a likely Otoferlin-dependent regulation of synaptic vesicle trafficking, which impacts the GABAergic system. These results provide the first demonstration that Na-Pi co-transporters play key albeit distinct roles in the hippocampus pertaining to the control of neuronal plasticity and cognition. These findings could provide the foundation for the development of novel effective therapies for PFBC and cognitive disorders.
MeSH term(s)	Cognition ; Ion Transport ; Neuronal Plasticity/genetics ; Phosphates ; Symporters
Chemical Substances	Phosphates ; Symporters
Language	English
Publishing date	2024-01-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-023-06292-z
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Article ; Online: NeuroHeal Reduces Muscle Atrophy and Modulates Associated Autophagy.

Marmolejo-Martínez-Artesero, Sara / Romeo-Guitart, David / Mañas-García, Laura / Barreiro, Esther / Casas, Caty

Cells

2020 Volume 9, Issue 7

Abstract: Muscle wasting is an unmet medical need which leads to a reduction of myofiber diameter and a negative impact on the functional performance of daily activities. We previously found that a new neuroprotective drug called NeuroHeal reduced muscle atrophy ... ...

Abstract	Muscle wasting is an unmet medical need which leads to a reduction of myofiber diameter and a negative impact on the functional performance of daily activities. We previously found that a new neuroprotective drug called NeuroHeal reduced muscle atrophy produced by transient denervation. Aiming to decipher whether NeuroHeal has a direct role in muscle biology, we used herein different models of muscle atrophy: one caused by chronic denervation, another caused by hindlimb immobilization, and lastly, an in vitro model of myotube atrophy with Tumor Necrosis Factor-α (TNFα). In all these models, we observed that NeuroHeal reduced muscle atrophy and that SIRT1 activation seems to be required for that. The treatment downregulated some critical markers of protein degradation: Muscle Ring Finger 1 (MuRF1), K48 poly-Ub chains, and p62/SQSTM1. Moreover, it seems to restore the autophagy flux associated with denervation. Hence, we envisage a prospective use of NeuroHeal at clinics for different myopathies.
MeSH term(s)	Acamprosate/therapeutic use ; Animals ; Autophagy/drug effects ; Cell Line ; Drug Combinations ; Immunoblotting ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/metabolism ; Muscular Atrophy/drug therapy ; Muscular Atrophy/metabolism ; Prospective Studies ; Proteasome Endopeptidase Complex/drug effects ; Proteasome Endopeptidase Complex/metabolism ; Ribavirin/therapeutic use ; Sirtuin 1/metabolism
Chemical Substances	Drug Combinations ; acamprosate, ribavirin drug combination ; Ribavirin (49717AWG6K) ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Sirtuin 1 (EC 3.5.1.-) ; Acamprosate (N4K14YGM3J)
Keywords	covid19
Language	English
Publishing date	2020-06-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9071575
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Article ; Online: NeuroHeal Improves Muscle Regeneration after Injury.

Marmolejo-Martínez-Artesero, Sara / Romeo-Guitart, David / Venegas, Vanesa / Marotta, Mario / Casas, Caty

Cells

2020 Volume 10, Issue 1

Abstract: Musculoskeletal injuries represent a challenging medical problem. Although the skeletal muscle is able to regenerate and recover after injury, the process engaged with conservative therapy can be inefficient, leading to a high re-injury rate. In addition, ...

Abstract	Musculoskeletal injuries represent a challenging medical problem. Although the skeletal muscle is able to regenerate and recover after injury, the process engaged with conservative therapy can be inefficient, leading to a high re-injury rate. In addition, the formation of scar tissue implies an alteration of mechanical properties in muscle. There is still a need for new treatments of the injured muscle. NeuroHeal may be one option. Published studies demonstrated that it reduces muscle atrophy due to denervation and disuse. The main objective of the present work was to assess the potential of NeuroHeal to improve muscle regeneration after traumatic injury. Secondary objectives included characterizing the effect of NeuroHeal treatment on satellite cell biology. We used a rat model of sport-induced injury in the gastrocnemius and analyzed the effects of NeuroHeal on functional recovery by means of electrophysiology and tetanic force analysis. These studies were accompanied by immunohistochemistry of the injured muscle to analyze fibrosis, satellite cell state, and fiber type. In addition, we used an in vitro model to determine the effect of NeuroHeal on myoblast biology and partially decipher its mechanism of action. The results showed that NeuroHeal treatment advanced muscle fiber recovery after injury in a preclinical model of muscle injury, and significantly reduced the formation of scar tissue. In vitro, we observed that NeuroHeal accelerated the formation of myotubes. The results pave the way for novel therapeutic avenues for muscle/tendinous disorders.
Language	English
Publishing date	2020-12-24
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10010022
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Article ; Online: Boosted Regeneration and Reduced Denervated Muscle Atrophy by NeuroHeal in a Pre-clinical Model of Lumbar Root Avulsion with Delayed Reimplantation.

Romeo-Guitart, David / Forés, Joaquim / Navarro, Xavier / Casas, Caty

Scientific reports

2017 Volume 7, Issue 1, Page(s) 12028

Abstract: The "gold standard" treatment of patients with spinal root injuries consists of delayed surgical reconnection of nerves. The sooner, the better, but problems such as injury-induced motor neuronal death and muscle atrophy due to long-term denervation mean ...

Abstract	The "gold standard" treatment of patients with spinal root injuries consists of delayed surgical reconnection of nerves. The sooner, the better, but problems such as injury-induced motor neuronal death and muscle atrophy due to long-term denervation mean that normal movement is not restored. Herein we describe a preclinical model of root avulsion with delayed reimplantation of lumbar roots that was used to establish a new adjuvant pharmacological treatment. Chronic treatment (up to 6 months) with NeuroHeal, a new combination drug therapy identified using a systems biology approach, exerted long-lasting neuroprotection, reduced gliosis and matrix proteoglycan content, accelerated nerve regeneration by activating the AKT pathway, promoted the formation of functional neuromuscular junctions, and reduced denervation-induced muscular atrophy. Thus, NeuroHeal is a promising treatment for spinal nerve root injuries and axonal regeneration after trauma.
MeSH term(s)	Acamprosate/pharmacology ; Animals ; Disease Models, Animal ; Drug Combinations ; Female ; Lumbar Vertebrae ; Muscle Denervation ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/physiopathology ; Muscle, Skeletal/surgery ; Muscular Atrophy/drug therapy ; Muscular Atrophy/physiopathology ; Nerve Regeneration/drug effects ; Nerve Regeneration/physiology ; Neuroprotective Agents/pharmacology ; Radiculopathy/drug therapy ; Radiculopathy/physiopathology ; Rats, Sprague-Dawley ; Recovery of Function ; Replantation ; Ribavirin/pharmacology ; Spinal Nerve Roots/drug effects ; Spinal Nerve Roots/physiopathology ; Spinal Nerve Roots/surgery
Chemical Substances	Drug Combinations ; Neuroprotective Agents ; acamprosate, ribavirin drug combination ; Ribavirin (49717AWG6K) ; Acamprosate (N4K14YGM3J)
Language	English
Publishing date	2017-09-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-11086-3
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