8,301 research outputs found
The importance of glucocorticoid delivery in the development of atherosclerosis
No full textElevated circulating glucocorticoids are causally linked to increased cardiovascular
disease. Atherosclerosis is a key cardiovascular pathology, yet the contribution of
glucocorticoids to underlying atherogenesis is unclear. Corticosteroid binding globulin
(CBG) regulates glucocorticoid action by controlling systemic bioavailability, with only
unbound ‘free’ glucocorticoids able to enter tissue and exert biological effects.
Cleavage of CBG by neutrophil elastase (NE) is proposed to enhance bioavailability
by reducing its affinity for glucocorticoids, elevating local ‘free’ glucocorticoid levels.
Strikingly, Apoe-/- mice lacking NE display reduced atherosclerosis. This thesis
addresses the hypothesis that CBG mediates atherogenesis by facilitating
glucocorticoid action at sites of plaque development.
First, the role of glucocorticoids and their regulation by CBG in atherogenesis was
established in an adenovirus-induced murine model of atherosclerosis. Male C57Bl6/J
mice were injected with recombinant adeno-associated viral vector serotype 8
expressing the gain-of-function mutation of mouse proprotein convertase
subtilisin/kexin type 9 (AAV8-PCSK9) and fed a Western diet (21% fat; 0.21%
cholesterol) for up to 18 weeks. Control mice were fed the same Western diet in the
absence of AAV8-PCSK9. Brachiocephalic lesion development in AAV8-PCSK9-
treated mice was accompanied by reduced hepatic Serpina6 (CBG) mRNA levels, in
parallel with reduced circulating CBG binding capacity. Moreover, AAV8-PCSK9
treatment increased circulating NE protein levels, suggesting the ability of CBG to bind
glucocorticoids may also be reduced in this model because of increased cleavage.
Surprisingly, AAV8-PCSK9 treatment did not alter circulating total glucocorticoid levels.
These data provide the first evidence of CBG dysregulation in this model of
atherosclerosis.
The increase in circulating NE levels in the AAV8-PCSK9 overexpression model of
atherosclerosis resembles that seen in Apoe⁻/⁻ mice, which are resistant to
atherosclerotic plaque development in the absence of NE. This suggests that NE may
also play a role in atherogenesis in the PCSK9 overexpression model. To test this,
male NE deficient mice (Ela⁻/⁻) and WT littermates were administered AAV8-PCSK9
and fed Western diet for 18 weeks. In contrast to published data from Apoe⁻/⁻/Ela-⁻/⁻
double-knockout mice, NE deficiency did not alter brachiocephalic lesion incidence,
size, or composition (collagen, smooth muscle cell, and macrophage content),
suggesting that NE does not play an important role in the development of lesions in
this model of atherosclerosis. Additionally, deletion of NE did not alter total or free
glucocorticoid levels in the circulation, indicating that NE-mediated CBG cleavage
does not occur in the systemic circulation.
The importance of CBG itself in regulating atherogenesis was explored next. To test
the hypothesis that deletion of CBG will reduce lesion size through reduced
glucocorticoid action, AAV8-PCSK9 was administered to mice lacking CBG (Cbg⁻/⁻)
mice and wild type littermates which then received Western diet for 18 weeks. Total
and free glucocorticoid levels were decreased in Cbg-/- mice. There was an apparent
decrease in incidence of lesion development in the brachiocephalic artery of Cbg⁻/⁻
mice compared with WT controls; however, this did not achieve statistical significance
(p=0.1312). This suggests that although CBG regulates the bioavailability of
glucocorticoids this does not play an important role in the development of
brachiocephalic lesions in the AAV8-PCSK9 model. Furthermore, method
development of mass-spectrometry imaging (MSI) was able to detect and quantify
local corticosterone in an aortic root lesion (n=1).
In conclusion, this thesis presents data demonstrating the first glucocorticoid profiling
of mice who develop inducible-atherosclerosis via AAV8-induced over-expression of
PCSK9. Despite the reported role of NE in lesion development in the Apoe⁻/⁻ model,
this thesis provides evidence that manipulation of CBG, either genetically or indirectly
via NE, does not alter the development of lesions in this model. This suggests that the
choice of model when investigating factors that influence atherogenesis should be
given careful consideration. Future work may involve investigating the effect of NE and
CBG deletion on alternative sites of lesion development, e.g., aortic root. Additionally,
while this work does not support a role for changes in systemic glucocorticoid
bioavailability in mediating plaque developing, advancement in steroid quantification
by MSI may allow assessment of local glucocorticoid levels within various regions of
atherosclerotic plaques to determine local glucocorticoid action
Art, Biography, Sexuality: Patrick Procktor and Keith Vaughan
No full textThis critical review forms a reflection on the research published within the following publications:
Patrick Procktor: Art and Life (Unicorn Press, 2010)
Keith Vaughan: The Mature Oils 1946-1977, (Sansom & Co., 2012)
The research is on two artists, Patrick Procktor (1936-2003), and Keith Vaughan (1912-1977). The monograph on Procktor – previously one of the least documented of the generation of artists who came to prominence in London in the Sixties – positions him in a history of art from which he had been notably absent. The research on Vaughan asserts a new reading of his work, one that is both deeper and more nuanced in its analysis of the ways in which personal experience and sexuality are encoded autobiographically within his work. Crucially, in both artists biography and work are symbiotically linked; the research therefore examines the links between life and art.
Revisionary in intent, the work examines trajectories of experience of gay British (or rather, English) artists in the twentieth century, artists who sought to express themselves and forge careers within the constraints of a heteronormative society, albeit one in which attitudes to sexuality were undergoing change. As gay men, both were constrained by the social mores of their times, and each used painting as a means to affirm personal and sexual identities. A key research interest is in the ways in which sexuality and persona are reflected in critical responses to the artist’s work: in Vaughan, Procktor and other gay male artists of the period. The writing on both Procktor and Vaughan examines the relationship between their personal and professional/artistic lives, framed within a broader socio-political and art historical context. It asserts the place of biography as a means to understand and form new readings of the work. The work adds substantially to the literature and wider discourse on post-war British painting and social history
Inhibition or deletion of 11Β-HSD1 does not increase angiogenesis in ischemic retinopathy
No full text11-Hydroxysteroid dehydrogenase type I (11-HSD1) regenerates active glucocorticoids (cortisol in humans, corticosterone in rodents) from inert 11-keto metabolites [1]. Selective 11-HSD1 inhibitors have been shown to be safe and effective in the treatment of type 2 diabetes [2], lowering intracellular glucocorticoid concentrations in liver and adipose tissue (and thereby enhancing insulin sensitivity) [3]. They also improve a number of features of the metabolic syndrome, including liver fat content [4], are potentially atheroprotective [5] and improve cognition [6]. Although no longer under development for blood glucose lowering alone, 11-HSD1 inhibitors are being re-profiled for additional indications and may yet be prescribed in patients with type 2 diabetes.11-HSD1 is also expressed in smooth muscle cells throughout the vasculature [7]. By acting directly through glucocorticoid receptors in the blood vessel wall, glucocorticoids tonically inhibit angiogenesis [8]. Loss of 11-HSD1, and the resulting reduction of glucocorticoid action in blood vessels, is associated with enhanced angiogenesis in multiple sites and has been shown to be beneficial in the myocardium after coronary artery occlusion and in skin following wound incision [9]. Angiogenesis can also contribute to pathology, as seen in solid tumour development and ischemic retinopathies such as retinal vein occlusions and proliferative diabetic retinopathy (PDR). If 11-HSD1 inhibitors are to be used for chronic treatment in patients with type II diabetes, then there is a concern that they may accelerate the progression of inappropriate blood vessel growth in the retina and exacerbate progression to sight-threatening PDR.This study tests the hypothesis that pharmacological inhibition or deletion of 11-HSD1 promotes pathological retinal neovascularisation. Retinal vascular remodelling was induced using the oxygen induced retinopathy (OIR) model [10] in which exposure of neonatal mice to hyperoxia from postnatal days 7 to 12 causes obliteration and cessation of development of central retinal capillary beds so that, on return to normoxia, a potent pre-retinal neovascular response is induced. Expression and localisation of 11β-HSD1 in the retina was also investigated by immunohistochemistry.<br/
Patrick Chamoiseau Recovering Memory
No full textThis timely new book skillfully examines the work of the award-winning writer Patrick Chamoiseau. Considered by many as one of the most innovative writers to hit the French literary scene in over 40 years, Chamoiseau made his name with his book Texaco (published in 1992 and winner of the highest literary prize in France, the Prix Goncourt). His books have gone on to sell millions and his work has been translated by a number of academic presses. McCusker sets the author in context, providing a valuable contribution to 'memory studies' by looking at literary representation of memory in Martinique, a society founded on slavery but now politically assimilated to the metropolitan centre, France.Title Page -- Contents -- Introduction -- 1: Beginnings: The Enigma of Origin -- 2: 'Une tracée de survie': Autobiographical Memory -- 3: Memory Re-collected: Witnesses and Words -- 4: Memory Materialized: Traces of the Past -- 5: Flesh Made Word: Traumatic Memory in Biblique des derniers gestes -- Afterword -- Notes -- Bibliography -- IndexThis timely new book skillfully examines the work of the award-winning writer Patrick Chamoiseau. Considered by many as one of the most innovative writers to hit the French literary scene in over 40 years, Chamoiseau made his name with his book Texaco (published in 1992 and winner of the highest literary prize in France, the Prix Goncourt). His books have gone on to sell millions and his work has been translated by a number of academic presses. McCusker sets the author in context, providing a valuable contribution to 'memory studies' by looking at literary representation of memory in Martinique, a society founded on slavery but now politically assimilated to the metropolitan centre, France.Description based on publisher supplied metadata and other sources.Electronic reproduction. Ann Arbor, Michigan : ProQuest Ebook Central, YYYY. Available via World Wide Web. Access may be limited to ProQuest Ebook Central affiliated libraries
11β-Hydroxysteroid Dehydrogenase Type 1: a new therapeutic target post-myocardial infarction?
No full textGlucocorticoids can reduce infarct size when given immediately after myocardial infarction (MI) but are detrimental when administration is continued into the post-infarct healing phase. A number of experimental studies have shown that reduction of infarct expansion by enhancing blood supply to the infarct border reduces remodelling and improves heart function post-MI. Previous experiments from this laboratory have shown that mice unable to locally regenerate corticosterone due to deficiency in 11β-hydroxysteroid dehydrogenase type 1 (11HSD1) have an enhanced angiogenic response during myocardial infarct healing that is associated with improved cardiac function. We hypothesized that the enhanced angiogenic response in 11HSD1 knock out (-/-) mice would be preceded by augmented inflammation. Moreover this would be associated with improved cardiac function.
This thesis aimed firstly to establish that murine cardiac phenotype was not influenced by 11HSD1 deficiency. 11HSD1-/- and C57Bl6 control mice had comparable cardiac structure and function. 11HSD1 expression was localised to fibroblasts and vascular smooth muscle cells in the myocardium.
The second aim of this thesis was to characterise the healing response after MI in 11HSD1-/- mice compared to C57Bl6 mice. Neutrophil infiltration peaked 2 days after MI and was significantly enhanced in the 11HSD1-/- mice relative to C57Bl6 mice, despite comparable infarct size in both groups. This was followed by increased macrophage accumulation in the infarct border. Furthermore, in the 11HSD1-/- mice a greater proportion of macrophages were of the alternatively activated phenotype. Left ventricular expression of pro-angiogenic IL-8, but not VEGF, was increased. Cellular proliferation and vessel density at 7 days were greater in 11HSD1-/- compared to C57Bl6 hearts. This was associated with improved cardiac function 7 days post-MI.
The third aim of this thesis was to determine whether the enhancement in vessel density and cardiac function was maintained beyond the initial wound healing phase. 11HSD1-/- mice retained the increased vessel density compared to C57Bl6 mice and these vessels were smooth muscle coated suggesting vessel maturation. This was associated with sustained improvement in cardiac function and modification of the scar characteristics.
The final aim of this thesis was to establish whether the effect of the knock out could be recapitulated by administration of a small molecule inhibitor of 11HSD1 after MI. Oral administration of the 11HSD1 inhibitor had no effect on inflammation, angiogenesis and heart function as determined at 7 days post-MI relative to vehicle treated animals.
In conclusion, the data confirm the enhancement in vessel density and cardiac function in 11HSD1-/- mice and demonstrate that this was preceded by enhanced inflammation. This was not due to an underlying cardiac phenotype or modification of the infarct size. Increased infiltration of alternatively activated macrophages may have been the source of pro-angiogenic factor, IL-8, which was also increased at the time of angiogenesis. Importantly the enhanced vessel density was retained 4 weeks after MI, these vessels were mature suggesting longevity and the improvement in cardiac function was retained. While pharmacological inhibition did not recapitulate the effect of the knock out this may have been due to route of administration. The data provides compelling evidence that further development and use of small molecule inhibitors of 11HSD1 may be of benefit post-MI
Investigating the role of endothelin receptor subtypes in the response to vascular injury
No full textNeointimal hyperplasia, the proliferative growth of the innermost layer of the blood
vessel wall, is a key process in the response to vascular injury, underlying conditions
such as post-interventional restenosis and vein/arterial graft disease. One of the many
mediators implicated in this process is endothelin-1 (ET-1), a potent vasoconstrictor
with pro-inflammatory and pro-mitogenic actions, which acts through ETA and ETB
receptor subtypes. It is well established that ET-1 increases, and ETA blockade
reduces, neointima formation following vascular injury. The role of ETB is less clear
because these receptors mediate potentially beneficial actions in endothelial cells
(EC; such as nitric oxide production, and ET-1 clearance) but detrimental effects
elsewhere (such as vascular smooth muscle) and it has been recently reported that
non-cell-specific ETB deficiency is associated with increased neointimal lesion size
following injury. The work described in this thesis addressed the hypothesis that
endogenous ET-1 contributes to neointimal hyperplasia by activation of the ETA
receptor, and that this action is moderated by concurrent activation of the ETB
receptor expressed in EC.
The role of ET receptors in neointimal lesion development was assessed using two
models of femoral arterial injury in the mouse: (i) an established method of intraluminal
wire-injury, and (ii) adaptation of a model of ligation injury that induces
robust neointimal lesion formation without physical damage to the endothelium.
Lesion development was assessed using standard histological techniques and this
was augmented by development of quantitative optical projection tomography (OPT)
to allow three-dimensional analysis of lesions.
The role of ETA and ETB receptors in these models was addressed using suitable
pharmacological ET receptor antagonists. Following wire-injury, selective ETB
blockade (A192621; 30mg.kg-1.day-1; 35 days) increased lesion size and blood
pressure without significant altering lesion composition. In contrast, selective ETA
blockade (atrasentan; 10mg.kg-1.day-1; 35 days) reduced lesion size and blood
pressure. Combined ETA+ETB antagonism had no effect on lesion size, despite reducing blood pressure, and reducing collagen content of the lesions. In the ligation
model, neither ETA selective, ETB selective nor ETA+ETB blockade altered lesion
size as assessed by standard histology but analysis by OPT indicated that ETA
blockade, with or without concurrent ETB blockade, reduced lesion volume.
The influence of ETB receptors expressed by ECs on lesion formation was addressed
using EC-specific ETB knockout mice. Small vessel myography indicated that
endothelium-dependent relaxation was unaltered in femoral arteries from these mice.
In addition, no effect on lesion size or rate of development was observed in either
wire- or ligation-injury models of neointima formation (although subtle effects on
lesion and medial composition were apparent after intra-luminal injury).
These results indicate that ETB receptor activation can moderate the detrimental
actions of the ETA receptor on neointimal lesion progression, and that this role is
dependent on the mode of vascular injury. Furthermore, in this setting, this beneficial
action is not primarily mediated by ETB expressed by EC, suggesting that ETB in
other cell types can reduce lesion development through another, unidentified
mechanism. Therefore, while both ETA selective and non-selective ETA/B
antagonists are currently in clinical use, in conditions where similar arterial
remodelling processes occur, selective ETA receptor antagonists might be preferred
Mechanisms of actions and roles of 5α-reduced glucocorticoids during inflammation and wound repair
No full textTopical inflammatory diseases are most commonly treated with
glucocorticoids, such as hydrocortisone, which have debilitating side effects including
a range of systemic metabolic side effects as well as local effects such as to thin the
skin and delay wound healing. Safer anti-inflammatory therapies are required and this
thesis investigates a novel drug called 5α-tetrahydrocorticosterone (5α-THB) as a safer
topical anti-inflammatory treatment. The main foci of this thesis are to assess the
effects of 5αTHB on wound repair, as well as to characterise its mechanisms of action.
Defective angiogenesis accounts for impaired wound healing brought about by
steroids in many cases. 5αTHB suppressed vessel growth in a mouse ex vivo model of
angiogenesis, but was less potent in this action than hydrocortisone, suggesting a safer
therapeutic profile. To understand the underlying mechanisms, the effect of 5αTHB
on gene expression in the mouse aorta during angiogenesis was compared with that of
dexamethasone (a selective GR agonist) and hydrocortisone. Whereas dexamethasone
and hydrocortisone caused differential expression of genes involved in inflammatory
signalling and extracellular matrix remodelling, 5αTHB did not and instead selectively
regulated Pecam1, involved in vasculature remodelling. This suggested that 5αTHB
suppresses angiogenesis through different mechanisms of action in comparison to
dexamethasone, and thus may not act through GR. Supporting this, dexamethasone
increased the abundance of GR responsive transcripts (Per1, Hsd11b1, Fkbp51)
whereas 5αTHB only increased the abundance of Per1. Furthermore, whereas the GR
antagonist RU486 attenuated dexamethasone-regulation of genes, it had no effect on
gene regulation by 5αTHB.
To assess GR-mediation of 5αTHB effects, model systems were used to investigate
whether 5αTHB is able to bind GR, stimulate its nuclear translocation, and initiate
changes in its interaction with co regulator peptides. In a competitive binding assay,
dexamethasone and hydrocortisone both decreased the fluorescence polarisation of a
GR specific ligand, consistent with GR binding. In contrast, 5αTHB only displaced the
specific GR ligand at very high concentrations. In terms of nuclear translocation,
5αTHB also did not have an effect on the ratio of GR in the nucleus and cytoplasm
(N/C) of A549 cells, suggesting that GR remained predominantly in the cytoplasm
after 5αTHB treatment and did not translocate into the nucleus, whereas
dexamethasone increased the N/C ratio at three different time points. Likewise,
whereas dexamethasone stimulated changes in the interaction between GR and many
co regulator peptides, 5αTHB had no effect. Collectively these results from model
systems suggest that 5αTHB does not work through the conventional GR mechanism
of action.
Finally, a hypothesis generating approach was taken in order to gain hints into how
5αTHB may be working. A microarray was performed to compare the effects of
5αTHB and dexamethasone on gene expression in human peripheral blood derived
macrophages. Both dexamethasone and 5αTHB were able to cause differential
expression of genes in these cells. However unexpectedly, out of the 350 genes
regulated by dexamethasone, and the 165 genes regulated by 5αTHB, only 35 genes
were commonly regulated by both steroids. This suggested that 5αTHB mainly acts
through different mechanisms to dexamethasone also in macrophages. In an
enrichment analysis of the differentially expressed genes, whereas the NFκB signalling
pathway was the top enriched pathway in genes only regulated by dexamethasone,
enriched pathways in genes only regulated by 5αTHB included those related to
phagocytosis, the TGF-beta signalling pathway, and Th1-Th2 cell differentiation.
This thesis therefore provides evidence to suggest that 5αTHB may provide a safer
topical anti-inflammatory steroid, less harmful to wound repair processes. In addition,
the mechanisms underlying the action of 5αTHB differ from those of classical GCs,
consistent with its reduced side-effect profile. Other potential mechanisms, such as
actions through the mineralocorticoid receptor, must now be explored
Regulation of angiogenesis through the efficient delivery of microRNAs into endothelial cells using polyamine-coated carbon nanotubes
No full textMicroRNAs (miRNAs) directly regulate gene expression at a post-transcriptional level and represent an attractive therapeutic target for a wide range of diseases. Here, we report a novel strategy for delivering miRNAs to endothelial cells (ECs) to regulate angiogenesis, using polymer functionalized carbon nanotubes (CNTs). CNTs were coated with two different polymers, polyethyleneimine (PEI) or polyamidoamine dendrimer (PAMAM), followed by conjugation of miR-503 oligonucleotides as recognized regulators of angiogenesis. We demonstrated a reduced toxicity for both polymer-coated CNTs, compared with pristine CNTs or polymers alone. Moreover, polymer-coated CNT stabilized miR-503 oligonucleotides and allowed their efficient delivery to ECs. The functionality of PAMAM-CNT-miR-503 complexes was further demonstrated in ECs through regulation of target genes, cell proliferation and angiogenic sprouting and furthermore, in a mouse model of angiogenesis. This comprehensive series of experiments demonstrates that the use of polyamine-functionalized CNTs to deliver miRNAs is a novel and effective means to regulate angiogenesis
Non-invasive imaging of fibrosis with positron emission tomography in a rat model with systemic hypertension and myocardial fibrosis
No full textHeart failure is one of the leading causes of death worldwide. Hypertension can initiate myocardial remodelling processes which, often via fibrotic triggers through the renin-angiotensin-aldosterone system, can lead to the development of heart failure. A main contributor of these pathways is angiotensin II, increased levels of which can induce volume and pressure overload in the cardiovascular system, making it an important factor in both hypertension and associated cardiovascular disease. A main process during cardiac remodelling is fibrosis which can be divided into two types: reactive and replacement fibrosis. The latter refers to the changes via scar formation at an injury site while the former (interstitial or perivascular fibrosis) can happen as a response to changes in the physical or chemical environment within the tissue such as hypertension or inflammation. Fibrillary collagen is an important extracellular matrix component and abundantly deposited during fibrosis. Collagen can have various subtypes based on its structure which can add different characteristics to the tissue. During collagen biosynthesis, cis- or trans-proline containing pro-α chains can be integrated into the protein, where chains containing cis isomer are associated with more distensible and abnormal collagen and those with trans isomer with more rigid triple helix collagen. Other factors can also influence the development of heart failure via the myocardial remodelling processes, such as inflammatory and angiogenic pathways.
Heart failure can be diagnosed and assessed in the clinic via blood tests and imaging techniques such as ultrasound, magnetic resonance imaging (MRI), computerised tomography (CT), and single-photon emission computed tomography (SPECT) / positron emission tomography (PET). This thesis aimed to investigate the effect of increased angiotensin II and subsequent hypertension on the levels of myocardial collagen synthesis and to test PET radiotracers cis-4-18F-fluoro-L-proline and trans-4-18F-fluoro-L-proline for the detection of myocardial fibrosis and potential differentiation of the types of collagen fibers. The overarching hypothesis of the project was that myocardial fibrosis can be imaged non-invasively with PET in a rat pressure overload model with via persistent hypertension resulting in end-organ damage.
A hypertensive rat model with myocardial remodelling was established via angiotensin II infusion using osmotic mini-pumps. Treatment length and dosage were tested and the optimal protocol was chosen to induce myocardial fibrosis. The model was assessed for myocardial collagen content as well as markers of inflammation and vasculature. On a separate set of experiments, the performance of PET radiotracers, cis-4-18F-fluoro-L-proline and trans-4-18F-fluoro-L-proline, was assessed in naïve rats to understand their in vivo metabolism and kinetics. Then, the optimised animal model of hypertensive heart failure and PET imaging protocols were used to investigate whether the new imaging probes could visualise areas if increased collagen synthesis and whether the uptake was related to the type of collagen involved.
Using 500 ng/kg/min angiotensin II dose for 4 weeks duration was adequate to induce myocardial fibrosis and hypertension in the rat model. The fibrosis pattern was mainly perivascular in nature. Immunostaining also showed increased CD68 in the myocardium of rats on 250 ng/kg/min but not with the higher dose. The highest percentage of cells stained positive for all three of CD68, TSPO and isolectin B4 was found in the atria of animals on the higher angiotensin II dose, which area also showed the most fibrosis overall.
Both radiotracers were successfully assessed in naïve rats, showing no metabolism and favourable kinetics in vivo, allowing for simplified quantification of radiotracer uptake. Myocardial radiotracer uptake in the angiotensin II treated cohort showed increased myocardial signal with the trans-4-18F-fluoro-L-proline radiotracer but no significant differences with cis-4-18F-fluoro-L-proline compared to vehicle treated animals. Animals undergoing the imaging experiment showed increased myocardial fibrosis similarly to rats in the model development experiments.
Myocardial fibrosis develops during hypertension induced via angiotensin II treatment, and this change can be measured with PET imaging targeting collagen biosynthesis. Further investigation into the types of collagens involved and how they contribute to pathology needs to be carried out to characterise the underlying biological processes in more detail. Fluoroproline radiotracer PET imaging can become a valuable tool for the assessment of fibrosis pathology both in terms of early detection and disease progression
Replication Data for: Endogenous Price Commitment, Sticky and Leadership Pricing: Evidence from the Italian Petrol Market
No full textThe do-file contains the code to replicate "Endogenous Price Commitment, Sticky and Leadership Pricing: Evidence from the Italian Petrol Market", published in the International Journal of Industrial Organization, vol. 40(C), pages 32-48, by Patrick Andreoli-Versbach and Jens-Uwe Franck.
Contact author is Patrick Andreoli-Versbach. E-Mail: [email protected]
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