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Jacobsson, Stig O. P.
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Publikasjoner (10 av 14) Visa alla publikasjoner
Gustafsson, S. & Jacobsson, S. O. (2019). Effects of cannabinoids on the development of chick embryos in ovo. Scientific Reports, 9, Article ID 13486.
Åpne denne publikasjonen i ny fane eller vindu >>Effects of cannabinoids on the development of chick embryos in ovo
2019 (engelsk)Inngår i: Scientific Reports, E-ISSN 2045-2322, Vol. 9, artikkel-id 13486Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

We have examined the effects of the synthetic cannabinoids HU 210 and HU 211, the plant-derived cannabidiol and the endogenous cannabinoid anandamide on the viability and development of chick embryos. Fertilized White Leghorn chicken eggs were injected with the test compounds or carrier vehicle, via a drilled small hole in the egg, directly into the egg yolk. After nine days of exposure, the embryonal viability, length and wet weight of embryos, and wet weight of brains were measured, and the development stages were assessed according to the Hamburger and Hamilton (HH) scale. The potent synthetic cannabinoid receptor agonist HU 210 and the non-psychotropic cannabidiol were embryotoxic at the highest concentrations examined (10µM and 50µM, respectively), with no viable embryos after the HU 210 injection, and 20% viability after the cannabidiol injections. The efects of HU 210 on the chick embryo were attenuated by α-tocopherol and the cannabinoid receptor antagonist AM251, whereas only α-tocopherol gave a statistically signifcant protection against the embryotoxic efects of cannabidiol. This study shows that exposure to plant-derived or synthetic cannabinoids during early embryonal development decreases embryonal viability. Extrapolation of data across species is of course difcult, but the data would argue against the use of cannabinoids, be it recreationally or therapeutically, during pregnancy

sted, utgiver, år, opplag, sider
Nature Publishing Group, 2019
Emneord
cannabinoids, chick embryo, viability, Hamburger-Hamilton scale, α-tocopherol
HSV kategori
Forskningsprogram
toxikologi
Identifikatorer
urn:nbn:se:umu:diva-51558 (URN)10.1038/s41598-019-50004-7 (DOI)000486140100032 ()31530885 (PubMedID)2-s2.0-85072268656 (Scopus ID)
Merknad

Originally included in thesis in manuscript form.

Tilgjengelig fra: 2012-01-31 Laget: 2012-01-26 Sist oppdatert: 2023-03-23bibliografisk kontrollert
Popova, D., Karlsson, J. & Jacobsson, S. O. P. (2017). Comparison of neurons derived from mouse P19, rat PC12 and human SH-SY5Y cells in the assessment of chemical- and toxin-induced neurotoxicity. BMC Pharmacology & Toxicology, 18, Article ID 42.
Åpne denne publikasjonen i ny fane eller vindu >>Comparison of neurons derived from mouse P19, rat PC12 and human SH-SY5Y cells in the assessment of chemical- and toxin-induced neurotoxicity
2017 (engelsk)Inngår i: BMC Pharmacology & Toxicology, E-ISSN 2050-6511, Vol. 18, artikkel-id 42Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background: Exposure to chemicals might be toxic to the developing brain. There is a need for simple and robust in vitro cellular models for evaluation of chemical-induced neurotoxicity as a complement to traditional studies on animals. In this study, neuronally differentiated mouse embryonal carcinoma P19 cells (P19 neurons) were compared with human neuroblastoma SH-SY5Y cells and rat adrenal pheochromocytoma PC12 cells for their ability to detect toxicity of methylmercury (MeHg), okadaic acid and acrylamide. Methods: Retinoic acid-treated P19 and SH-SY5Y cells and nerve growth factor-stimulated PC12 cells, allowed to differentiate for 6 days, were exposed to MeHg, okadaic acid and acrylamide for 48 h. Cell survival and neurite outgrowth were assessed with the calcein-AM assay and fluorescence detection of antibodies against the cytoskeletal neuron-specific protein beta III-tubulin, respectively. The effects of glutathione (GSH) and the potent inhibitor of GSH synthesis buthionine sulfoximine (BSO) on the MeHg induced-toxicity were assessed using the PrestoBlue (TM) cell viability assay and the TMRE mitochondrial membrane potential assay. Results: Differentiated P19 cells developed the most extensive neuronal network among the three cell models and were the most sensitive neuronal model to detect neurotoxic effects of the test compounds. MeHg produced a concentration-dependent toxicity in differentiated P19 cells and SH-SY5Y cells, with statistically significant effects at concentrations from 0.1 mu M in the P19 neurons and 1 mu M in the SH-SY5Y cells. MeHg induced a decrease in the cellular metabolic activity and mitochondrial membrane potential (Delta Psi m) in the differentiated P19 cells and SH-SY5Y cells, that were attenuated by GSH. Okadaic acid and acrylamide also showed statistically significant toxicity in the P19 neurons, but not in the SH-SY5Y cells or the P12 cells. Conclusions: P19 neurons are more sensitive to detect cytotoxicity of MeHg, okadaic acid and acrylamide than retinoic acid-differentiated SH-SY5Y cells and nerve growth factor-treated PC12 cells. P19 neurons are at least as sensitive as differentiated SH-SY5Y cells to detect the loss of mitochondrial membrane potential produced by MeHg and the protective effects of extracellular GSH on MeHg toxicity. P19 neurons may be a useful model to study neurotoxic effects of chemicals.

sted, utgiver, år, opplag, sider
BIOMED CENTRAL LTD, 2017
Emneord
In vitro cytotoxicity, Neuronal cell cultures, Retinoic acid-treated P19 cells, Retinoic acid-treated SH-
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-137043 (URN)10.1186/s40360-017-0151-8 (DOI)000402970800002 ()28583171 (PubMedID)2-s2.0-85020229477 (Scopus ID)
Tilgjengelig fra: 2017-06-28 Laget: 2017-06-28 Sist oppdatert: 2023-03-23bibliografisk kontrollert
Popova, D., Forsblad, A., Hashemian, S. & Jacobsson, S. O. P. (2016). Non-Serotonergic Neurotoxicity by MDMA (Ecstasy) in Neurons Derived from Mouse P19 Embryonal Carcinoma Cells. PLOS ONE, 11(11), Article ID e0166750.
Åpne denne publikasjonen i ny fane eller vindu >>Non-Serotonergic Neurotoxicity by MDMA (Ecstasy) in Neurons Derived from Mouse P19 Embryonal Carcinoma Cells
2016 (engelsk)Inngår i: PLOS ONE, E-ISSN 1932-6203, Vol. 11, nr 11, artikkel-id e0166750Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

3,4-methylenedioxymethamphetamine (MDMA; ecstasy) is a commonly abused recreational drug that causes neurotoxic effects in both humans and animals. The mechanism behind MDMA-induced neurotoxicity is suggested to be species-dependent and needs to be further investigated on the cellular level. In this study, the effects of MDMA in neuronally differentiated P19 mouse embryonal carcinoma cells have been examined. MDMA produces a concentration-, time- and temperature-dependent toxicity in differentiated P19 neurons, as measured by intracellular MTT reduction and extracellular LDH activity assays. The P19-derived neurons express both the serotonin reuptake transporter (SERT), that is functionally active, and the serotonin metabolizing enzyme monoamine oxidase A (MAO-A). The involvement of these proteins in the MDMA-induced toxicity was investigated by a pharmacological approach. The MAO inhibitors clorgyline and deprenyl, and the SERT inhibitor fluoxetine, per se or in combination, were not able to mimic the toxic effects of MDMA in the P19-derived neurons or block the MDMA-induced cell toxicity. Oxidative stress has been implicated in MDMA-induced neurotoxicity, but pre-treatment with the antioxidants α-tocopherol or N-acetylcysteine did not reveal any protective effects in the P19 neurons. Involvement of mitochondria in the MDMA-induced cytotoxicity was also examined, but MDMA did not alter the mitochondrial membrane potential (ΔΨm) in the P19 neurons. We conclude that MDMA produce a concentration-, time- and temperature-dependent neurotoxicity and our results suggest that the mechanism behind MDMA-induced toxicity in mouse-derived neurons do not involve the serotonergic system, oxidative stress or mitochondrial dysfunction.

HSV kategori
Forskningsprogram
toxikologi
Identifikatorer
urn:nbn:se:umu:diva-128533 (URN)10.1371/journal.pone.0166750 (DOI)000388350300099 ()27861613 (PubMedID)2-s2.0-84995911753 (Scopus ID)
Tilgjengelig fra: 2016-12-06 Laget: 2016-12-06 Sist oppdatert: 2023-03-23bibliografisk kontrollert
Popova, D. & Jacobsson, S. O. P. (2014). A fluorescence microplate screen assay for the detection of neurite outgrowth and neurotoxicity using an antibody against βIII-tubulin. Toxicology in Vitro, 28(3), 411-418
Åpne denne publikasjonen i ny fane eller vindu >>A fluorescence microplate screen assay for the detection of neurite outgrowth and neurotoxicity using an antibody against βIII-tubulin
2014 (engelsk)Inngår i: Toxicology in Vitro, ISSN 0887-2333, E-ISSN 1879-3177, Vol. 28, nr 3, s. 411-418Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The majority of environmental and commercial chemicals have not been evaluated for their potential to cause neurotoxicity. We have investigated if neuron specific anti-βIII-tubulin antibodies are useful in a microplate assay of neurite outgrowth of retinoic acid-induced neurons from mouse P19 embryonal carcinoma cells. By incubating the P19-derived neurons with the primary anti-βIII-tubulin antibody and a secondary Alexa Fluor 488-conjugated antibody, followed by measuring the fluorescence in a microplate reader, a time-dependent increase in anti-βIII-tubulin immunofluorescence was observed. The relative fluorescence units increased by 4.3-fold from 2 to 10 days in culture. The results corresponded well with those obtained by semi-automatic tracing of neurites in fluorescence microscopy images of βIII-tubulin-labeled neurons. The sensitivity of the neurite outgrowth assay using a microplate reader to detect neurotoxicity produced by nocodazole, methyl mercury chloride and okadaic acid was significantly higher than for a cell viability assay measuring intracellular fluorescence of calcein-AM. The microplate-based method to measure toxicity targeting neurites using anti-βIII-tubulin antibodies is however less sensitive than the extracellular lactate dehydrogenase activity assay to detect general cytotoxicity produced by high concentrations of clomipramine, or glutamate-induced excitotoxicity. In conclusion, the fluorescence microplate assay for the detection of neurite outgrowth by measuring changes in βIII-tubulin immunoreactivity is a rapid and sensitive method to assess chemical- or toxin-induced neurite toxicity.

sted, utgiver, år, opplag, sider
Elsevier, 2014
Emneord
neurotoxicity, cell culture, βIII-tubulin, beta III-tubulin, calcein-AM, fluorescence, microplate assay
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-87628 (URN)10.1016/j.tiv.2013.12.009 (DOI)000332053800010 ()2-s2.0-84892491604 (Scopus ID)
Tilgjengelig fra: 2014-04-10 Laget: 2014-04-07 Sist oppdatert: 2023-03-24bibliografisk kontrollert
Björklund, E., Larsson, T. N. L., Jacobsson, S. O. P. & Fowler, C. J. (2014). Ketoconazole Inhibits the Cellular Uptake of Anandamide via Inhibition of FAAH at Pharmacologically Relevant Concentrations. PLOS ONE, 9(1), e87542
Åpne denne publikasjonen i ny fane eller vindu >>Ketoconazole Inhibits the Cellular Uptake of Anandamide via Inhibition of FAAH at Pharmacologically Relevant Concentrations
2014 (engelsk)Inngår i: PLOS ONE, E-ISSN 1932-6203, Vol. 9, nr 1, s. e87542-Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background: The antifungal compound ketoconazole has, in addition to its ability to interfere with fungal ergosterol synthesis, effects upon other enzymes including human CYP3A4, CYP17, lipoxygenase and thromboxane synthetase. In the present study, we have investigated whether ketoconazole affects the cellular uptake and hydrolysis of the endogenous cannabinoid receptor ligand anandamide (AEA). Methodology/Principal Findings: The effects of ketoconazole upon endocannabinoid uptake were investigated using HepG2, CaCo2, PC-3 and C6 cell lines. Fatty acid amide hydrolase (FAAH) activity was measured in HepG2 cell lysates and in intact C6 cells. Ketoconazole inhibited the uptake of AEA by HepG2 cells and CaCo2 cells with IC50 values of 17 and 18 mu M, respectively. In contrast, it had modest effects upon AEA uptake in PC-3 cells, which have a low expression of FAAH. In cell-free HepG2 lysates, ketoconazole inhibited FAAH activity with an IC50 value (for the inhibitable component) of 34 mu M. Conclusions/Significance: The present study indicates that ketoconazole can inhibit the cellular uptake of AEA at pharmacologically relevant concentrations, primarily due to its effects upon FAAH. Ketoconazole may be useful as a template for the design of dual-action FAAH/CYP17 inhibitors as a novel strategy for the treatment of prostate cancer.

HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-86616 (URN)10.1371/journal.pone.0087542 (DOI)000330288000212 ()2-s2.0-84899788593 (Scopus ID)
Tilgjengelig fra: 2014-04-29 Laget: 2014-03-03 Sist oppdatert: 2023-03-24bibliografisk kontrollert
Gustafsson, S., Wallenius, A., Zackrisson, H., Popova, D., Plym Forshell, L. & Jacobsson, S. O. (2013). Effects of cannabinoids and related fatty acids upon the viability of P19 embryonal carcinoma cells. Archives of Toxicology, 87(11), 1939-1951
Åpne denne publikasjonen i ny fane eller vindu >>Effects of cannabinoids and related fatty acids upon the viability of P19 embryonal carcinoma cells
Vise andre…
2013 (engelsk)Inngår i: Archives of Toxicology, ISSN 0340-5761, E-ISSN 1432-0738, Vol. 87, nr 11, s. 1939-1951Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Compounds acting on the cannabinoid (CB) receptors are involved in the control of cell fate, and there is an emerging consensus that CBs have anticancer effects. However, the CB-mediated effects are contradictory since some studies suggest stimulatory effects on cancer cell proliferation, and CBs have been shown to stimulate both proliferation and differentiation of other mitotic cells such as stem and progenitor cells. In this study, the concentration-dependent effects of synthetic and endogenous CBs on the viability of mouse P19 embryonal carcinoma (EC) cells have been examined by using fluorescence assays of cell membrane integrity, cell proliferation, oxidative stress, and detection of apoptosis and necrosis. All compounds examined produced a concentration-dependent decrease in cell viability in the micromolar range, with the potent CB receptor agonist HU 210 and the enantiomer HU 211(with no CB receptor activity) being the most potent compounds examined with apparent IC50 values of 1 µM and 0.6 µM, respectively. The endogenous CB anandamide showed similar potency and efficacy as structurally related polyunsaturated fatty acids with no reported activity at the CB receptors. The rapid (within hours) decrease in cell viability induced by the examined CBs suggests cytocidal rather than antiproliferative effects, and is dependent on the plating cell population density with the highest toxicity around 100 cells/mm2. The CB-induced cytotoxicity, that appears to involve CB receptors and the sphingomyelin-ceramide pathway, is a mixture of both apoptosis and necrosis that can be blocked by the antioxidants α-tocopherol and N-acetylcysteine. In conclusion, both synthetic and endogenous CBs, produce seemingly unspecific cytotoxic effects in the P19 EC cells.

sted, utgiver, år, opplag, sider
Springer Berlin/Heidelberg, 2013
Emneord
cannabinoids, polyunsaturated fatty acids, embryonal carcinoma cells, cytotoxicity, oxidative stress
HSV kategori
Forskningsprogram
biokemisk farmakologi
Identifikatorer
urn:nbn:se:umu:diva-51550 (URN)10.1007/s00204-013-1051-3 (DOI)000325700300005 ()2-s2.0-84885950944 (Scopus ID)
Tilgjengelig fra: 2012-01-31 Laget: 2012-01-26 Sist oppdatert: 2023-03-24bibliografisk kontrollert
Popova, D., Forsblad, A. N. P. & Jacobsson, S. O. P. (2013). In vitro studies on the neurotoxic effects of piperazine-derived designer drugs and 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy"). Paper presented at 49th Congress of the European-Societies-of-Toxicology (EUROTOX), SEP 01-04, 2013, Interlaken, SWITZERLAND. Toxicology Letters, 221(Suppl. S), S151-S151
Åpne denne publikasjonen i ny fane eller vindu >>In vitro studies on the neurotoxic effects of piperazine-derived designer drugs and 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy")
2013 (engelsk)Inngår i: Toxicology Letters, ISSN 0378-4274, E-ISSN 1879-3169, Vol. 221, nr Suppl. S, s. S151-S151Artikkel i tidsskrift, Meeting abstract (Annet vitenskapelig) Published
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-81008 (URN)10.1016/j.toxlet.2013.05.310 (DOI)000323865800463 ()
Konferanse
49th Congress of the European-Societies-of-Toxicology (EUROTOX), SEP 01-04, 2013, Interlaken, SWITZERLAND
Tilgjengelig fra: 2013-10-01 Laget: 2013-09-30 Sist oppdatert: 2018-06-08bibliografisk kontrollert
Rodriguez-Gaztelumendi, A., Alvehus, M., Andersson, T. & Jacobsson, S. (2011). Comparison of the effects of nicotine upon the transcellular electrical resistance and sucrose permeability of human ECV304/rat C6 co-cultures and human CaCo2 cells. Toxicology Letters, 207(1), 1-6
Åpne denne publikasjonen i ny fane eller vindu >>Comparison of the effects of nicotine upon the transcellular electrical resistance and sucrose permeability of human ECV304/rat C6 co-cultures and human CaCo2 cells
2011 (engelsk)Inngår i: Toxicology Letters, ISSN 0378-4274, E-ISSN 1879-3169, Vol. 207, nr 1, s. 1-6Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

It is now well established that nicotine adversely affects the integrity of the blood–brain barrier (BBB). In contrast, nicotine has been reported to increase the transendothelial electrical resistance (TEER) of CaCo2 colon cancer cells. In the present study, the effects of nicotine upon the TEER and sucrose permeability of ECV304/C6 co-cultures and, for comparative purposes, CaCo2 cells has been investigated. Neither ECV304 nor C6 cells were found to express measurable membrane levels of nicotinic acetylcholine receptors, as assessed by [3H]–epibatidine binding. Nicotine treatment (0.01–1 µM) for up to 48 h had little or no effect upon the TEER or sucrose permeability of either ECV304/C6 co-cultures or CaCo2 cells. It is concluded that in contrast to the situation for the BBB, ECV304 cells lack nicotinic acetylcholine receptors and the barrier properties of ECV304/C6 co-cultures are not affected to any important extent by nicotine. This study underlines the conclusions made by other authors that the ECV304/C6 co-culture system is of limited validity as a model of the BBB.

sted, utgiver, år, opplag, sider
Elsevier Ireland Ltd., 2011
Emneord
Nicotine, In vitro blood–brain barrier model, TEER, Sucrose permeability
HSV kategori
Forskningsprogram
toxikologi
Identifikatorer
urn:nbn:se:umu:diva-47573 (URN)10.1016/j.toxlet.2011.08.014 (DOI)21889975 (PubMedID)2-s2.0-80052746624 (Scopus ID)
Tilgjengelig fra: 2011-09-23 Laget: 2011-09-23 Sist oppdatert: 2023-03-24bibliografisk kontrollert
Gustafsson, S. B., Palmqvist, R., Henriksson, M. L., Dahlin, A. M., Edin, S., Jacobsson, S. O., . . . Fowler, C. J. (2011). High tumour cannabinoid CB(1) receptor immunoreactivity negatively impacts disease-specific survival in stage II microsatellite stable colorectal cancer. PLOS ONE, 6(8), 1-11
Åpne denne publikasjonen i ny fane eller vindu >>High tumour cannabinoid CB(1) receptor immunoreactivity negatively impacts disease-specific survival in stage II microsatellite stable colorectal cancer
Vise andre…
2011 (engelsk)Inngår i: PLOS ONE, E-ISSN 1932-6203, Vol. 6, nr 8, s. 1-11Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background: There is good evidence in the literature that the cannabinoid system is disturbed in colorectal cancer. In the present study, we have investigated whether CB(1) receptor immunoreactive intensity (CB(1)IR intensity) is associated with disease severity and outcome.

Methodology/Principal Findings: CB(1)IR was assessed in formalin-fixed, paraffin-embedded specimens collected with a consecutive intent during primary tumour surgical resection from a series of cases diagnosed with colorectal cancer. Tumour centre (n = 483) and invasive front (n = 486) CB(1)IR was scored from 0 (absent) to 3 (intense staining) and the data was analysed as a median split i.e. CB(1)IR <2 and >= 2. In microsatellite stable, but not microsatellite instable tumours (as adjudged on the basis of immunohistochemical determination of four mismatch repair proteins), there was a significant positive association of the tumour grade with the CB1IR intensity. The difference between the microsatellite stable and instable tumours for this association of CB(1)IR was related to the CpG island methylation status of the cases. Cox proportional hazards regression analyses indicated a significant contribution of CB(1)IR to disease-specific survival in the microsatellite stable tumours when adjusting for tumour stage. For the cases with stage II microsatellite stable tumours, there was a significant effect of both tumour centre and front CB(1)IR upon disease specific survival. The 5 year probabilities of event-free survival were: 8565 and 66+/-8%; tumour interior, 86+/-4% and 63+/-8% for the CB(1)IR<2 and CB(1)IR >= 2 groups, respectively.

Conclusions/Significance: The level of CB(1) receptor expression in colorectal cancer is associated with the tumour grade in a manner dependent upon the degree of CpG hypermethylation. A high CB(1)IR is indicative of a poorer prognosis in stage II microsatellite stable tumour patients.

sted, utgiver, år, opplag, sider
San Francisco, CA: Public Library of Science, 2011
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-47396 (URN)10.1371/journal.pone.0023003 (DOI)2-s2.0-80052069061 (Scopus ID)
Tilgjengelig fra: 2011-09-23 Laget: 2011-09-20 Sist oppdatert: 2023-03-23bibliografisk kontrollert
Fowler, C. J., Gustafsson, S. B., Chung, S. C., Persson, E., Jacobsson, S. O. & Bergh, A. (2010). Targeting the endocannabinoid system for the treatment of cancer: a practical view. Current Topics in Medicinal Chemistry, 10(8), 814-827
Åpne denne publikasjonen i ny fane eller vindu >>Targeting the endocannabinoid system for the treatment of cancer: a practical view
Vise andre…
2010 (engelsk)Inngår i: Current Topics in Medicinal Chemistry, ISSN 1568-0266, E-ISSN 1873-4294, Vol. 10, nr 8, s. 814-827Artikkel, forskningsoversikt (Fagfellevurdert) Published
Abstract [en]

In recent years, considerable interest has been generated by findings that cannabinoids not only have useful palliative effects, but also can affect the viability and invasivity of a variety of different cancer cells. In the present review, the potential of targeting the cannabinoid system for the treatment of cancer is considered from a practical, rather than a mechanistic viewpoint, addressing questions such as whether human tumour cells express CB receptors; whether the potencies of action of cannabinoids in vitro match the potencies expected on the base of receptor theory; what is known about the in vivo effects of cannabinoids and cancer, and how relevant the experiments undertaken are to the clinical situation; and finally, what approaches can be taken to minimise unwanted effects of cannabinoid treatment. It is concluded that cannabinoids (or agents modulating the endogenous cannabinoid system) are an attractive target for drug development in the cancer area, but that more in vivo studies, particularly those investigating the potential of cannabinoids as an addition to current treatment strategies, are needed.

sted, utgiver, år, opplag, sider
Bentham Science Publishers, 2010
Emneord
Cannabinoid, anandamide, 2-arachidonoylglycerol, fatty acid amide hydrolase, monoacylglycerol lipase, cancer, glioma, prostate cancer
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-35626 (URN)10.2174/156802610791164201 (DOI)000277157100005 ()20370711 (PubMedID)2-s2.0-77954378342 (Scopus ID)
Tilgjengelig fra: 2010-08-26 Laget: 2010-08-26 Sist oppdatert: 2023-03-23bibliografisk kontrollert
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