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Article ; Online: Fatty acid signaling: the new function of intracellular lipases.

Papackova, Zuzana / Cahova, Monika

International journal of molecular sciences

2015 Volume 16, Issue 2, Page(s) 3831–3855

Abstract: Until recently, intracellular triacylglycerols (TAG) stored in the form of cytoplasmic lipid droplets have been considered to be only passive "energy conserves". Nevertheless, degradation of TAG gives rise to a pleiotropic spectrum of bioactive ... ...

Abstract	Until recently, intracellular triacylglycerols (TAG) stored in the form of cytoplasmic lipid droplets have been considered to be only passive "energy conserves". Nevertheless, degradation of TAG gives rise to a pleiotropic spectrum of bioactive intermediates, which may function as potent co-factors of transcription factors or enzymes and contribute to the regulation of numerous cellular processes. From this point of view, the process of lipolysis not only provides energy-rich equivalents but also acquires a new regulatory function. In this review, we will concentrate on the role that fatty acids liberated from intracellular TAG stores play as signaling molecules. The first part provides an overview of the transcription factors, which are regulated by fatty acids derived from intracellular stores. The second part is devoted to the role of fatty acid signaling in different organs/tissues. The specific contribution of free fatty acids released by particular lipases, hormone-sensitive lipase, adipose triacylglycerol lipase and lysosomal lipase will also be discussed.
MeSH term(s)	Animals ; Fatty Acids/genetics ; Fatty Acids/metabolism ; Humans ; Lipase/metabolism ; Organ Specificity ; Signal Transduction ; Transcription Factors/metabolism
Chemical Substances	Fatty Acids ; Transcription Factors ; Lipase (EC 3.1.1.3)
Language	English
Publishing date	2015-02-10
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms16023831
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Article ; Online: Silymarin prevents acetaminophen-induced hepatotoxicity in mice.

Papackova, Zuzana / Heczkova, Marie / Dankova, Helena / Sticova, Eva / Lodererova, Alena / Bartonova, Lenka / Poruba, Martin / Cahova, Monika

PloS one

2018 Volume 13, Issue 1, Page(s) e0191353

Abstract: Acetaminophen or paracetamol (APAP) overdose is a common cause of liver injury. Silymarin (SLM) is a hepatoprotective agent widely used for treating liver injury of different origin. In order to evaluate the possible beneficial effects of SLM, Balb/c ... ...

Abstract	Acetaminophen or paracetamol (APAP) overdose is a common cause of liver injury. Silymarin (SLM) is a hepatoprotective agent widely used for treating liver injury of different origin. In order to evaluate the possible beneficial effects of SLM, Balb/c mice were pretreated with SLM (100 mg/kg b.wt. per os) once daily for three days. Two hours after the last SLM dose, the mice were administered APAP (300 mg/kg b.wt. i.p.) and killed 6 (T6), 12 (T12) and 24 (T24) hours later. SLM-treated mice exhibited a significant reduction in APAP-induced liver injury, assessed according to AST and ALT release and histological examination. SLM treatment significantly reduced superoxide production, as indicated by lower GSSG content, lower HO-1 induction, alleviated nitrosative stress, decreased p-JNK activation and direct measurement of mitochondrial superoxide production in vitro. SLM did not affect the APAP-induced decrease in CYP2E1 activity and expression during the first 12 hrs. Neutrophil infiltration and enhanced expression of inflammatory markers were first detected at T12 in both groups. Inflammation progressed in the APAP group at T24 but became attenuated in SLM-treated animals. Histological examination suggests that necrosis the dominant cell death pathway in APAP intoxication, which is partially preventable by SLM pretreatment. We demonstrate that SLM significantly protects against APAP-induced liver damage through the scavenger activity of SLM and the reduction of superoxide and peroxynitrite content. Neutrophil-induced damage is probably secondary to necrosis development.
MeSH term(s)	Acetaminophen/adverse effects ; Acetaminophen/pharmacology ; Animals ; Chemical and Drug Induced Liver Injury/prevention & control ; Drug Overdose/pathology ; Liver/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Necrosis/pathology ; Protective Agents/pharmacology ; Silymarin/metabolism ; Silymarin/pharmacology
Chemical Substances	Protective Agents ; Silymarin ; Acetaminophen (362O9ITL9D)
Language	English
Publishing date	2018
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0191353
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Article ; Online: Aberrant energy metabolism and redox balance in seizure onset zones of epileptic patients.

Grove, Ryan A / Madhavan, Deepak / Boone, Cory H T / Braga, Camila Pereira / Papackova, Zuzana / Kyllo, Hannah / Samson, Kaeli / Simeone, Kristina / Simeone, Timothy / Helikar, Tomas / Hanson, Corrine K / Adamec, Jiri

Journal of proteomics

2020 Volume 223, Page(s) 103812

Abstract: Epilepsy is a disorder that affects around 1% of the population. Approximately one third of patients do not respond to anti-convulsant drugs treatment. To understand the underlying biological processes involved in drug resistant epilepsy (DRE), a ... ...

Abstract	Epilepsy is a disorder that affects around 1% of the population. Approximately one third of patients do not respond to anti-convulsant drugs treatment. To understand the underlying biological processes involved in drug resistant epilepsy (DRE), a combination of proteomics strategies was used to compare molecular differences and enzymatic activities in tissue implicated in seizure onset to tissue with no abnormal activity within patients. Label free quantitation identified 17 proteins with altered abundance in the seizure onset zone as compared to tissue with normal activity. Assessment of oxidative protein damage by protein carbonylation identified additional 11 proteins with potentially altered function in the seizure onset zone. Pathway analysis revealed that most of the affected proteins are involved in energy metabolism and redox balance. Further, enzymatic assays showed significantly decreased activity of transketolase indicating a disruption of the Pentose Phosphate Pathway and diversion of intermediates into purine metabolic pathway, resulting in the generation of the potentially pro-convulsant metabolites. Altogether, these findings suggest that imbalance in energy metabolism and redox balance, pathways critical to proper neuronal function, play important roles in neuronal network hyperexcitability and can be used as a primary target for potential therapeutic strategies to combat DRE. SIGNIFICANCE: Epileptic seizures are some of the most difficult to treat neurological disorders. Up to 40% of patients with epilepsy are resistant to first- and second-line anticonvulsant therapy, a condition that has been classified as refractory epilepsy. One potential therapy for this patient population is the ketogenic diet (KD), which has been proven effective against multiple refractory seizure types However, compliance with the KD is extremely difficult, and carries severe risks, including ketoacidosis, renal failure, and dangerous electrolyte imbalances. Therefore, identification of pathways disruptions or shortages can potentially uncover cellular targets for anticonvulsants, leading to a personalized treatment approach depending on a patient's individual metabolic signature.
MeSH term(s)	Anticonvulsants/therapeutic use ; Energy Metabolism ; Epilepsy/drug therapy ; Humans ; Oxidation-Reduction ; Seizures/drug therapy
Chemical Substances	Anticonvulsants
Language	English
Publishing date	2020-05-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2400835-7
ISSN	1876-7737 ; 1874-3919
ISSN (online)	1876-7737
ISSN	1874-3919
DOI	10.1016/j.jprot.2020.103812
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Article ; Online: The opposite effects of high-sucrose and high-fat diet on Fatty Acid oxidation and very low density lipoprotein secretion in rat model of metabolic syndrome.

Cahova, Monika / Dankova, Helena / Palenickova, Eliska / Papackova, Zuzana / Kazdova, Ludmila

Journal of nutrition and metabolism

2012 Volume 2012, Page(s) 757205

Abstract: Aims. To determine the effect of two different diets (high-sucrose (HS) and high-fat (HF)) on the main metabolic pathways potentially contributing to the development of steatosis: (1) activity of the liver lysosomal and heparin-releasable lipases; (2) ... ...

Abstract	Aims. To determine the effect of two different diets (high-sucrose (HS) and high-fat (HF)) on the main metabolic pathways potentially contributing to the development of steatosis: (1) activity of the liver lysosomal and heparin-releasable lipases; (2) fatty acid (FFA) oxidation; (3) FFA synthesis de novo; (4) VLDL output in vivo in a rat model of metabolic syndrome (MetS), hereditary hypertriglyceridemic (HHTg) rats fed HS or HF diets. Results. Both diets resulted in triacylglycerol (TAG) accumulation in the liver (HF > HS). The intracellular TAG lipolysis by lysosomal lipase was increased in both groups and positively correlated with the liver TAG content. Diet type significantly affected partitioning of intracellular TAG-derived fatty acids among FFA-utilizing metabolic pathways as HS feeding accentuated VLDL secretion and downregulated FFA oxidation while the HF diet had an entirely opposite effect. FFA de novo synthesis from glucose was significantly enhanced in the HS group (fed ≫ fasted) while being completely eradicated in the HF group. Conclusions. We found that in rats prone to the development of MetS associated diseases dietary-induced steatosis is not simply a result of impaired TAG degradation but that it depends on other mechanisms (elevated FFA synthesis or attenuated VLDL secretion) that are specific according to diet composition.
Language	English
Publishing date	2012-10-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	2573563-9
ISSN	2090-0732 ; 2090-0724
ISSN (online)	2090-0732
ISSN	2090-0724
DOI	10.1155/2012/757205
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Article ; Online: Nutritional regulation of adipose tissue lipoprotein lipase is blunted in insulin resistant rats

Cahova Monika / Papackova Zuzana / Palenickova Eliska / Dankova Helena / Zdychova Jana / Skop Vojtech / Kazdova Ludmila

Open Life Sciences, Vol 7, Iss 2, Pp 201-

2012 Volume 209

Keywords	adipose tissue ; hypertriglyceridemia ; glucose metabolism ; fatty acids ; angiopoietin-like protein 4 ; high-sucrose diet ; hhtg rats ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2012-04-01T00:00:00Z
Publisher	De Gruyter
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Kupffer cells ameliorate hepatic insulin resistance induced by high-fat diet rich in monounsaturated fatty acids: the evidence for the involvement of alternatively activated macrophages

Papackova, Zuzana / Palenickova, Eliska / Dankova, Helena / Zdychova, Jana / Skop, Vojtech / Kazdova, Ludmila / Cahova, Monika

Nutrition and metabolism. 2012 Dec., v. 9, no. 1

2012

Abstract: BACKGROUND: Resident macrophages (Kupffer cells, KCs) in the liver can undergo both pro- or anti-inflammatory activation pathway and exert either beneficiary or detrimental effects on liver metabolism. Until now, their role in the metabolically ... ...

Abstract	BACKGROUND: Resident macrophages (Kupffer cells, KCs) in the liver can undergo both pro- or anti-inflammatory activation pathway and exert either beneficiary or detrimental effects on liver metabolism. Until now, their role in the metabolically dysfunctional state of steatosis remains enigmatic. Aim of our study was to characterize the role of KCs in relation to the onset of hepatic insulin resistance induced by a high-fat (HF) diet rich in monounsaturated fatty acids. METHODS: Male Wistar rats were fed either standard (SD) or high-fat (HF) diet for 4 weeks. Half of the animals were subjected to the acute GdCl₃ treatment 24 and 72 hrs prior to the end of the experiment in order to induce the reduction of KCs population. We determined the effect of HF diet on activation status of liver macrophages and on the changes in hepatic insulin sensitivity and triacylglycerol metabolism imposed by acute KCs depletion by GdCl₃. RESULTS: We found that a HF diet rich in MUFA itself triggers an alternative but not the classical activation program in KCs. In a steatotic, but not in normal liver, a reduction of the KCs population was associated with a decrease of alternative activation and with a shift towards the expression of pro-inflammatory activation markers, with the increased autophagy, elevated lysosomal lipolysis, increased formation of DAG, PKCε activation and marked exacerbation of HF diet-induced hepatic insulin resistance. CONCLUSIONS: We propose that in the presence of a high MUFA content the population of alternatively activated resident liver macrophages may mediate beneficial effects on liver insulin sensitivity and alleviate the metabolic disturbances imposed by HF diet feeding and steatosis. Our data indicate that macrophage polarization towards an alternative state might be a useful strategy for treating type 2 diabetes.
Keywords	Kupffer cells ; high fat diet ; insulin resistance ; lipolysis ; liver ; monounsaturated fatty acids ; noninsulin-dependent diabetes mellitus ; rats ; triacylglycerols
Language	English
Dates of publication	2012-12
Size	p. 414.
Publishing place	Springer-Verlag
Document type	Article
ZDB-ID	2160376-5
ISSN	1743-7075
ISSN	1743-7075
DOI	10.1186/1743-7075-9-22
Database	NAL-Catalogue (AGRICOLA)

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Article: Nutritional regulation of adipose tissue lipoprotein lipase is blunted in insulin resistant rats

Cahova, Monika / Papackova, Zuzana / Palenickova, Eliska / Dankova, Helena / Zdychova, Jana / Skop, Vojtech / Kazdova, Ludmila

Central European journal of biology. 2012 Apr., v. 7, no. 2

2012

Abstract: BACKGROUND: Hypertriglyceridemia is a common lipid abnormality accompanying insulin resistance. This study was designed to assess the contribution of dysregulation of adipose tissue lipoprotein lipase (LPL) activity to the hypertriglyceridemia in a rat ... ...

Abstract	BACKGROUND: Hypertriglyceridemia is a common lipid abnormality accompanying insulin resistance. This study was designed to assess the contribution of dysregulation of adipose tissue lipoprotein lipase (LPL) activity to the hypertriglyceridemia in a rat model of insulin resistance. METHODOLOGY: Hereditary hypertriglyceridemic (HHTg) rats were challenged for two weeks on a high sucrose diet and LPL activity, angptl-4 expression and FFA utilisation in vitro were determined in adipose tissue. RESULTS: Compared to control rats (Wistar), HHTg rats exhibited hyperinsulinemia, impaired fatty acid storage in adipose tissue and elevated LPL activity both in fasting and after refeeding. The expression of angiopoietin-like protein 4 (angptl4), a fastinginduced control protein for LPL activity, was not increased in adipose tissue of fasted HHTg rats as it was in the control rats. CONCLUSION: We conclude that LPL remains in its active form to a higher extent in HHTg rat adipose tissue due to the low expression of angptl4 on fasting. This is a possible consequence of the hyperinsulinemia. In combination with the impaired storage of fatty acids as triglycerides in adipose tissue in HHTg rats, the inflexibility of angptl4 expression may contribute to the establishment of hypertriglyceridemia in the insulin-resistant animals.
Keywords	adipose tissue ; animal models ; diet ; fasting ; fatty acids ; hyperinsulinemia ; hypertriglyceridemia ; insulin ; insulin resistance ; lipoprotein lipase ; rats ; refeeding ; sucrose ; triacylglycerols
Language	English
Dates of publication	2012-04
Size	p. 201-209.
Publishing place	Springer-Verlag
Document type	Article
ISSN	1895-104X
DOI	10.2478/s11535-012-0002-y
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Kupffer cells ameliorate hepatic insulin resistance induced by high-fat diet rich in monounsaturated fatty acids: the evidence for the involvement of alternatively activated macrophages.

Papackova, Zuzana / Palenickova, Eliska / Dankova, Helena / Zdychova, Jana / Skop, Vojtech / Kazdova, Ludmila / Cahova, Monika

Nutrition & metabolism

2012 Volume 9, Page(s) 22

Abstract: Background: Resident macrophages (Kupffer cells, KCs) in the liver can undergo both pro- or anti-inflammatory activation pathway and exert either beneficiary or detrimental effects on liver metabolism. Until now, their role in the metabolically ... ...

Abstract	Background: Resident macrophages (Kupffer cells, KCs) in the liver can undergo both pro- or anti-inflammatory activation pathway and exert either beneficiary or detrimental effects on liver metabolism. Until now, their role in the metabolically dysfunctional state of steatosis remains enigmatic. Aim of our study was to characterize the role of KCs in relation to the onset of hepatic insulin resistance induced by a high-fat (HF) diet rich in monounsaturated fatty acids. Methods: Male Wistar rats were fed either standard (SD) or high-fat (HF) diet for 4 weeks. Half of the animals were subjected to the acute GdCl3 treatment 24 and 72 hrs prior to the end of the experiment in order to induce the reduction of KCs population. We determined the effect of HF diet on activation status of liver macrophages and on the changes in hepatic insulin sensitivity and triacylglycerol metabolism imposed by acute KCs depletion by GdCl3. Results: We found that a HF diet rich in MUFA itself triggers an alternative but not the classical activation program in KCs. In a steatotic, but not in normal liver, a reduction of the KCs population was associated with a decrease of alternative activation and with a shift towards the expression of pro-inflammatory activation markers, with the increased autophagy, elevated lysosomal lipolysis, increased formation of DAG, PKCε activation and marked exacerbation of HF diet-induced hepatic insulin resistance. Conclusions: We propose that in the presence of a high MUFA content the population of alternatively activated resident liver macrophages may mediate beneficial effects on liver insulin sensitivity and alleviate the metabolic disturbances imposed by HF diet feeding and steatosis. Our data indicate that macrophage polarization towards an alternative state might be a useful strategy for treating type 2 diabetes.
Language	English
Publishing date	2012-03-22
Publishing country	England
Document type	Journal Article
ISSN	1743-7075
ISSN (online)	1743-7075
DOI	10.1186/1743-7075-9-22
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Article ; Online: Epinephrine-dependent control of glucose metabolism in white adipose tissue: the role of α- and β-adrenergic signalling.

Cahova, Monika / Palenickova, Eliska / Papackova, Zuzana / Dankova, Helena / Skop, Vojtech / Kazdova, Ludmila

Experimental biology and medicine (Maywood, N.J.)

2012 Volume 237, Issue 2, Page(s) 211–218

Abstract: Epinephrine controls many important and sometimes opposite processes. This pleiotropic effect is achieved via coupling to different receptor/effector systems. In epididymal white adipose tissue (EWAT) of Wistar rats, we showed that epinephrine stimulated ...

Abstract	Epinephrine controls many important and sometimes opposite processes. This pleiotropic effect is achieved via coupling to different receptor/effector systems. In epididymal white adipose tissue (EWAT) of Wistar rats, we showed that epinephrine stimulated protein kinase B (PKB) phosphorylation on Ser(473). Epinephrine further increased the glucose incorporation into glyceride-glycerol without decreasing glucose availability for other metabolic pathways (i.e. lactate production). Wortmannin (phosphatidylinositol 3-kinase inhibitor) treatment significantly decreased glucose incorporation into glyceride-glycerol and elevated the epinephrine-induced release of free fatty acids (FFA) from the adipose tissue without any change in the intensity of lipolysis measured as glycerol release. Using specific cyclic adenosine monophosphate (cAMP) analogs we demonstrated that cAMP-protein kinase A (PKA) signalling resulted in a strong PKB dephosphorylation and significantly lowered the glucose availability in EWAT. Specific activation of the Epac (exchange protein activated by cAMP)-dependent pathway had only a moderately negative effect on PKB phosphorylation and glucose metabolism. In contrast, α(1) agonist methoxamine increased PKB phosphorylation and lactate production. This effect of methoxamine was additive to the effect of insulin and it was abolished by wortmannin treatment. In EWAT of spontaneously dyslipidemic hereditary hypertriglyceridemic (HHTg) rats, we demonstrated significantly lower epinephrine-induced glucose utilization but higher sensitivity to its lipolytic effect. We conclude that in EWAT, epinephrine controls two opposite processes (FFA release and FFA retention) via two different effector systems. The impairment of α(1)-dependent, epinephrine-stimulated, glycolysis-dependent FFA esterification may contribute to the establishment of dyslipidemia in insulin resistance.
MeSH term(s)	Adipose Tissue/metabolism ; Animals ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Epinephrine/metabolism ; Fatty Acids, Nonesterified/blood ; Fatty Acids, Nonesterified/metabolism ; Glucose/metabolism ; Male ; Metabolic Syndrome/metabolism ; Models, Biological ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Receptors, Adrenergic, alpha/metabolism ; Receptors, Adrenergic, beta/metabolism ; Signal Transduction
Chemical Substances	Fatty Acids, Nonesterified ; Receptors, Adrenergic, alpha ; Receptors, Adrenergic, beta ; Cyclic AMP (E0399OZS9N) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11) ; Glucose (IY9XDZ35W2) ; Epinephrine (YKH834O4BH)
Language	English
Publishing date	2012-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	4015-0
ISSN	1535-3699 ; 1525-1373 ; 0037-9727
ISSN (online)	1535-3699 ; 1525-1373
ISSN	0037-9727
DOI	10.1258/ebm.2011.011189
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Article ; Online: Autophagy inhibition in early but not in later stages prevents 3T3-L1 differentiation: Effect on mitochondrial remodeling.

Skop, Vojtech / Cahova, Monika / Dankova, Helena / Papackova, Zuzana / Palenickova, Eliska / Svoboda, Petr / Zidkova, Jarmila / Kazdova, Ludmila

Differentiation; research in biological diversity

2014 Volume 87, Issue 5, Page(s) 220–229

Abstract: Autophagy is essential for successful white adipocyte differentiation but the data regarding the timing and relevance of autophagy action during different phases of adipogenesis are limited. We subjected 3T3-L1 preadipocytes to a standard differentiation ...

Abstract	Autophagy is essential for successful white adipocyte differentiation but the data regarding the timing and relevance of autophagy action during different phases of adipogenesis are limited. We subjected 3T3-L1 preadipocytes to a standard differentiation protocol and inhibited the autophagy within time-limited periods (days 0-2; 2-4; 4-6; 6-8) by asparagine or 3-methyladenine. In the normal course of events, both autophagy flux and the mRNA expression of autophagy related genes (Atg5, Atg12, Atg16, beclin 1) is most intensive at the beginning of differentiation (days 0-4) and then declines. The initiation of differentiation is associated with a 50% reduction of the mitochondrial copy number on day 2 followed by rapid mitochondrial biogenesis. Preadipocytes and differentiated adipocytes differ in the mRNA expression of genes involved in electron transport (Nufsd1, Sdhb, Uqcrc1); ATP synthesis (ATP5b); fatty acid metabolism (CPT1b, Acadl); mitochondrial transporters (Hspa9, Slc25A1) and the TCA cycle (Pcx, Mdh2) as well as citrate synthase activity. Autophagy inhibition during the first two days of differentiation blocked both phenotype changes (lipid accumulation) and the gene expression pattern, while having no or only a marginal effect over any other time period. Similarly, autophagy inhibition between days 0-2 inhibited mitotic clonal expansion as well as mitochondrial network remodeling. In conclusion, we found that autophagy is essential and most active during an initial stage of adipocyte differentiation but it is dispensable during its later stages. We propose that the degradation of preadipocyte cytoplasmic structures, predominantly mitochondria, is an important function of autophagy during this phase and its absence prevents remodeling of the mitochondrial gene expression pattern and mitochondrial network organization.
MeSH term(s)	3T3-L1 Cells ; Adipocytes/cytology ; Adipocytes/drug effects ; Adipogenesis/drug effects ; Adipogenesis/genetics ; Animals ; Asparagine/pharmacology ; Autophagy/drug effects ; Autophagy/genetics ; Cell Differentiation/drug effects ; Cell Differentiation/genetics ; Gene Expression Regulation, Developmental/drug effects ; Gene Expression Regulation, Developmental/genetics ; Mice ; Mitochondria/drug effects ; Mitochondria/metabolism
Chemical Substances	Asparagine (7006-34-0)
Language	English
Publishing date	2014-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	184540-8
ISSN	1432-0436 ; 0301-4681
ISSN (online)	1432-0436
ISSN	0301-4681
DOI	10.1016/j.diff.2014.06.002
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