Multinational supermarket chains in developing countries: Does local agriculture benefit

There is no consensus in the empirical literature on how entry of multinational supermarket chains affects farmers in developing countries. We quantify the dynamic effects of supermarket expansion on agriculture within a structural framework that clarifies the adjustment mechanisms involved. The model specification takes the potential productivity linkage between supermarkets and local suppliers into account. While econometric analyses struggle with causality issues, we analyze the endogenous interaction between supermarkets’ choice of suppliers and agricultural productivity. Based on numerical simulations, two results emerge. First, we offer a possible understanding of the conflicting evidence in the empirical literature. Whether farmers benefit from supermarkets or get stuck in a low productivity trap depends on the extent of local constraints related to production capacity and market access. Second, supply chain development initiated by supermarkets can help farmers escape the low productivity trap. While supermarkets face a short run cost, they gradually gain from more productive local suppliers.

Resource Boom, Productivity Growth and Real Exchange Rate Dynamics - A dynamic general equilibrium analysis of South Africa.

We study the impact of a natural resource boom on structural change and real exchange rate dynamics, taking into account the indirect effect via relative sectoral productivity changes. Our contribution relative to the Dutch disease literature is threefold. First, the productivity specification is extended from simple learning by doing to include trade barriers and technology gap dynamics, consistent with the modern understanding of productivity growth. Second, we offer a dynamic general equilibrium model with imperfect substitution between domestic and foreign goods. Third, the model is applied to South Africa and analyzes the macroeconomic impact of the gold price increase in the 1970s. Political pressure for rapid domestic spending after a surge in resource rents tends to generate myopic government behavior with unsustainable high consumption spending. Such fiscal response to higher resource income is captured by the model specification. Numerical simulations show how the resource boom can help explain the structural change and real exchange rate path observed in South Africa. Due to productivity effects the initial real appreciation is followed by gradual depreciation of the real exchange rate.gold price boom;Dutch disease;trade barriers;fiscal response;deindustrialization

Productivity Growth in Backward Economies and the Role of Barriers to Technology Adoption

We offer a barrier model of growth with a broader understanding of the sources of productivity growth. Organizational change is suggested as an alternative to innovation and technology adoption. Domestic and international barriers (related to the level of human capital and the trade share) determine the timing and pace of technological catch-up, and as opposed to the catchingup hypothesis backward economies may get stuck in a poverty trap. Growth in lagging economies is not driven by adoption of foreign technology due to inappropriateness. The large technological distance forces the economy to rely more on own productivity improvements through organizational change. Trade liberalization in backward economies does not give the expected boost to productivity growth, because of low capability to take advantage of the frontier technology. Economies can escape the poverty trap by reducing trade barriers, but the benefits from an open economy is highest in middle-income economies, which have both the potential and capability to adopt foreign technology.Ramsey-model; sources of growth; trade barriers; poverty trap

Ramsey model of barriers to growth and skill-biased income distribution in South Africa

The paper integrates two mechanisms of economic growth, barriers to international spillovers and skill-biased effects on the income distribution. South Africa is an interesting case study because of dramatic changes in international barriers over time and policy focus to productivity and distribution. Barriers affect the balance between innovation and adoption in the productivity growth and thereby the skill-bias. The productivity dynamics and the distributional implications are investigated in an intertemporal Ramsey growth model. The model offers a calibrated tariff-equivalence measure of the sanction effect and allows for counterfactual analysis of no-sanctions. Increased openness is shown to reduce barriers to technology adoption leading to skill-biased economic growth and worsened income distribution. The result is consistent with the observation that economic growth under sanctions has been slow and with an increase in the relative wage of unskilled labor. The tradeoff between barriers and skill-bias, foreign spillover driven productivity growth and income distribution, obviously is a challenge for growth policy.

Accumulation of education and regional income growth: Limited human capital effects in Norway

Accumulation of education and geographic concentration of educated people in cities are expected to generate urban income growth. New economic geography predicts income divergence across regions. We investigate the dynamic process of accumulating tertiary education and regional income growth in Norway during the past four decades. The expansion of smart cities goes along with catching up of education level in the periphery and overall the education levels converge. Income levels also are shown to converge in distribution analysis using Kernel functions and first order Markov chains. However, the movements in the income distribution are unrelated to the accumulation of education. The hypothesis of equal income transition probabilities across subgroups of regions with different increases in education cannot be rejected. We conclude that accumulation of education has not been important for the pattern of income growth. Catching up from low income is not driven by education and income growth has not taken off in cities with increasing education level.

Accumulation of education and regional income growth: Limited human capital effects in Norway

Accumulation of education and geographic concentration of educated people in cities are expected to generate urban income growth. New economic geography predicts income divergence across regions. We investigate the dynamic process of accumulating tertiary education and regional income growth in Norway during the past four decades. The expansion of smart cities goes along with catching up of education level in the periphery and overall the education levels converge. Income levels also are shown to converge in distribution analysis using Kernel functions and first order Markov chains. However, the movements in the income distribution are unrelated to the accumulation of education. The hypothesis of equal income transition probabilities across subgroups of regions with different increases in education cannot be rejected. We conclude that accumulation of education has not been important for the pattern of income growth. Catching up from low income is not driven by education and income growth has not taken off in cities with increasing education level.

Learning and Foreign Technology Spillover in Thailand: Empirical Evidence on Productivity Dynamics

Thailand has experienced annual average growth of GDP of remarkable 6.6% during the period 1950 – 2000. We analyze total factor productivity (TFP) growth in a modified Nelson-Phelps framework where foreign trade and foreign direct investment influence the adoption of technology. The econometric analysis separating between sources of productivity for agriculture and industry covers the period 1975 – 96. International spillovers are significant and important, and both sectors have been able to take benefit of openness. The analysis addresses the endogeneity issues involved in the estimation of TFP sources and investigates the dynamics of productivity. The effects during the period studied must be interpreted as transition growth, and endogenous growth effects are rejected.

Services trade and domestic regulation

This paper argues that regulatory measures affect the fixed cost of entering a market as well as the variable costs of servicing that market. Moreover, differences in regulation among countries often imply that firms have to incur entry costs in every new market. Indicators of regulatory intensity and heterogeneity are introduced in a gravity model and their impact on market entry and subsequent trade flows estimated for total services, business services and financial services. It is found that regulatory heterogeneity has a relatively large negative impact on both market entry and subsequent trade flows. Further, regulatory barriers have a negative effect on the local services sectors’ export performance. Finally it is found that regulations that aims at correcting market failure can have a positive impact on trade. It is concluded that services trade liberalization and regulatory reforms are complementary in creating competitive services markets.Trade in services; regulation; GATS; fixed trade costs

The medieval Calvary group in Norway: context and functions

Flere av triumfkrusifiksene som er bevart fra perioden ca. 1150-1350 i Norge tilhørte en såkalt kalvariegruppe, hvor Kristus på korset er flankert av Maria og apostelen Johannes. Krusifikset uttrykker sentrale dogmer, og har dermed også en klar tilknytning til liturgien. Hvilke funksjoner Maria og Johannes har hatt ved korset i en liturgisk sammenheng i middelalderen er mindre opplagt. Denne artikkelen diskuterer Marias og Johannesââ¬â¢ betydning ved krusifikset, og hvilke funksjoner kalvariegruppen som helhet kan ha hatt i det norske kirkerommet i middelalderen. Kalvariegruppens ikonografi og dens sannsynlige plassering i kirken tyder på at disse gruppene må ha tjent liturgien først og fremst gjennom de funksjonene Staale Sinding-Larsen kaller auxiliary functions (hjelpefunksjoner). Dette betyr at gruppen ikke kan defineres som et liturgisk bilde i streng forstand, men at den først og fremst ble brukt illustrativt uten en formell liturgisk tilknytning.<p>I artikkelen kommer det frem at det sannsynligvis er ulike årsaker til at flere kirker, særlig fra 1200-tallet og utover, foretrakk korsfestelsesikonografien med Maria og Johannes fremfor et enkelt krusifiks. Blant annet fungerte trolig kalvariegruppen både som et fokus og som en illustrasjon av liturgiens hovedpoeng. Gruppen kan også ha fungert som en introduksjon av disse hovedpoengene til menigheten. Maria og Johannes, de to sentrale øyenvitnene, aksentuerer triumfkrusifiksets sentrale dogme; troen på Kristus oppstandelse og frelse av menneskene, muliggjort gjennom hans menneskelige lidelse og død på korset. Det er også sannsynlig at kalvariegruppen fungerte som et ikke-formelt andaktsbilde, både under og etter messen. Helgenskulpturene minnet menigheten om Marias og Johannesââ¬â¢ sorg og deres nære forhold til Kristus, både på jorden og etter deres himmelfart. De var viktige forbilder i tillegg til å være sentrale formidlere av den enkeltes empati, andakt og bønn. Kalvariegruppen som helhet kan også, i likhet med annen kirkeutsmykking, ha hatt en positiv distraksjonsfunksjon for menigheten under messen

Virkningen av lav doserate ioniserende stråling : studier av molekylære responser og transgenerasjonell genomisk ustabilitet gjort i mus

Mye av det vi vet om risiko for helseeffekter etter å ha blitt usatt for ioniserende stråling er kunnskap lært fra de som overlevde atombombene i Hiroshima og Nagasaki. Imidlertid er denne kunnskapen basert på effekter etter høye strålingsnivåer som skjedde over kort tid. Nyere forskningen viser i økende grad at lavere konsentrasjon av stråling (lav doserate), hvor eksponeringen skjer over lengre tid, påvirker cellene våre på andre måter enn stråling med høy konsentrasjon, slik som stråling fra en atombombe. Forandringene som skjer i genene, er antatt å være en viktig bidragsyter til responsene som oppstår ved lav doserate bestråling. Man antar at endringer i såkalte epigenetiske markører kan føre til langvarige forandringer av genuttrykket. De fleste som har studert dette har i all hovedsak undersøkt responsene kort tid etter bestrålingen. Det er derfor et behov for studier som undersøker om endringene er målbare også lenge etter bestrålingen. Dersom langvarige endringer i genuttrykket oppstår, er det videre viktig med kunnskap om hvilke mekanismer som har bidratt til dette. Formålet med dette doktorgradsprosjektet har derfor vært å bidra med å tette kunnskapshullene knyttet til betydningen av bestrålingsfaktoren «doserate», som beskriver hvor mye man bestråles per tidsenhet. Dette er blitt gjort ved å studere effektene i musemodeller. To strålingsstudier ble gjennomført i FIGARO kilden som driftes av NMBU. Studiene hadde ulike doserater, (1,5 mGy/t til 1,5 Gy (Eksperiment A), og 2,5, 10 og 100 mGy/t til 3 Gy (Eksperiment B)) gitt med gamma stråling fra en kobolt-60 (60Co) kilde. Et viktig aspekt med prosjektet var å studere betydningen av lav doserate stråling som gis over lengre tid ved å undersøke responsene på tre ulike tidspunkter etter bestråling; kort (én dag), lang (>100 dager (3 måneder)), og over to generasjoner. I musene som ble direkte bestrålt (F0) fokuserte vi på å undersøke endringer i genprofilene. I tillegg ble det undersøkt om tilgjengeligheten til DNAet, hvor genene er kodet, som blant annet endres av epigenetisk markører (epigenomet), også endret seg etter bestrålingen. For å studere om effekter også var målbare to generasjoner etter mus-bestefar (F2) var blitt bestrålt, ble det brukt metoder som måler DNA-skader som kan føre til mutasjoner, og skader som oppstår i kromosomene når cellene deler seg (dannelse av mikrokjerner). Disse metodene ble benyttet for å finne ut om noe hadde endret seg i muse-barnebarna (F2) som kunne fører til ustabilitet i prosesser som omhandler genomet. For at prosjektet skulle kunne måle dette ble det etablert en meget sensitiv metode for å undersøke effekter på blodceller med mikrokjerner, i tillegg til å optimalisere metoden som måler DNA-skader i hvite blodceller («komet metoden») slik at tellingen av celler ble automatisert. Resultatene én dag etter bestrålingen viste store endringer i både genuttrykket og i tilgjengeligheten av DNAet. Endringene var større jo høyere doseraten var, selv om alle hadde fått samme totale dose, altså så vi en doserate-spesifikk respons. Det viste seg også at genene var knyttet til biologiske signalveier koblet til kreft, fettmetabolisme og inflammasjon, for alle de målte doseratene. På de ulike tidspunktene var det stor forskjell på genekspresjon og DNA tilgjengelighet mellom lav og høy doserate. Vi brukte to ulike muselinjer i studien og det var store forskjeller mellom disse muselinjene, noe som viser at hvilken muselinje som benyttes har en stor effekt på de molekylære responsene man undersøker. Selv tre måneder etter bestråling ble det funnet endret genuttrykk, men antall endrede gener var betraktelig færre sammenlignet med én dag etter bestråling. Det er vanskelig å vite den biologiske betydningen av at disse få genene var endret. Når det gjelder tilgjengeligheten til DNAet fant vi ingen endringer tre måneder etter lav doserate bestråling. Derimot, viste det seg at etter bestråling med akutt høy doserate ble det funnet reduserte tilgjengeligheten til gener, viktige for strålingsinduserte effekter, som blant annet har funksjoner i reparasjon av DNA-skader. I muse-barnebarna av bestrålte muse-bestefedre undersøkte vi genomisk ustabilitet som er mål på nedarvede effekter. Det var ønskelig å studere effekter i muse-barnebarna da disse musene var de første som ble fertilisert av sædceller som ikke hadde vært påvirket av bestrålingen. I tillegg utsatte vi å avle neste generasjon av musene en periode slik at vi kunne være sikre på at sædcellene hadde oppstått fra en bestrålt stamcelle, og ikke blitt bestrålt selv. I blodprøver fra muse-barnebarna målte vi hvor mye DNA- og kromosom-skader som oppsto av seg selv, hvor mye skade som oppsto rett etter en akutt dose røntgenstråler (betydelig høyere dose enn de vi får ved medisinsk undersøkelse), og i tillegg hvor fort noen typer DNA-skader ble reparert. Resultatene viste at musene som hadde en bestrålt bestefar hadde høyere endogent nivå av DNA-skader (DNA-skade som oppstår «av seg selv»). Denne økningen var veldig lav, og det er vanskelig å konkludere om dette er et biologisk funn eller om det skyldes metodologiske aspekter. Det ble ikke funnet noen holdepunkter for endringer i genomisk ustabilitet etter en akutt dose med røntgenstråler, ei heller på evnen til å reparere DNA-skade. Hovedfunnene fra dette doktorgradsprosjektet er at doserate har modulerende virkning på type og grad av effekt etter bestråling, og at doserate burde bli tatt med i betraktningen når man vurderer strålingseffekter. Når det gjelder overføring av effektene over generasjoner (transgenerasjonell arvelighet) er det vanskelig å konkludere, gitt de eksperimentelle forholdene, om resultatene skyldes reelle biologiske effekter eller metodologiske aspekter. Resultatene må derfor verifiseres i andre studier.Most of our epidemiological knowledge about radiation-induced health effects originates from atomic bomb survivors. However, the exposure from the atomic bombs was received over a short period and at high dose rates. An increasing number of studies suggest that low dose rate irradiation induces biological effects that differ from responses observed after acute high dose/high dose rate exposures. The modulation of gene expression constitutes an essential part of radiation-induced biological responses, while epigenetic changes have the ability to cause long-term changes in transcriptional programs. In most studies, responses are analysed shortly after exposure. Hence, there is a need to employ longer post-radiation timelines to investigate how (and if) perturbations in gene expression persist post-exposure. The objectives of this PhD project have been to address research gaps concerning the impact of dose rate using mice models. The experiments were designed to gain information about the impact of low dose rate at three different post-irradiation timepoints; early- (one day), long-term (>100 days (three months)), and across generations. The design was strengthened by including high dose rate exposure groups to compare gene expression profiles and chromatin accessibility in directly exposed mice when all dose rate groups received the same total dose. Two mouse experiments were conducted using different dose rates of gamma radiation from a 60Co source. These spanned from low to high dose rates: 1.5 mGy/h to 1.5 Gy (Experiment A), and 2.5, 10 and 100 mGy/h to 3 Gy (Experiment B). The induced responses were evaluated by profiling the transcriptional activity and chromatin accessibility, in liver tissue using RNA-sequencing and the Assay for Transposase Accessible Chromatin (ATAC)-sequencing in directly exposed mice at the two post-radiation timepoints; early (one day) and later (three months). Effects manifested across generations were evaluated using DNA- and cytogenic damage to assess transgenerational inherited genomic instability through the paternal germline. The comet assay and a highly sensitive MN-assay were used for this purpose. One day post-radiation, the expression of genes and the accessibility to the chromatin were perturbed in a dose rate-specific manner when irradiated to a total dose of 3 Gy. The enrichment of functional pathways indicated that the affected genes were linked to lipid metabolism and inflammation, in addition to cancer, for all dose rate exposures. The overall results suggest a dose-rate-specific response and that prolonged exposure to low dose rates could be assumed to introduce lower level of cellular stress per time inflicting other mechanisms than high dose rate exposures. Furthermore, as the design included the use of two strains of mice, the results displayed that the choice of mouse strain is highly relevant for the molecular outcomes. Differentially expressed genes were present three months after both low and high dose rate, although to a lesser extent when compared to one day post-radiation. Concerning the long-term (three months after exposure) epigenomic profile, there was no evidence that low dose rate irradiation introduced epigenetic changes affecting the chromatin accessibility. This indicate that the differentially changed chromatin regions present one day after low dose rate irradiation were reverted to a profile comparable with controls. The impact of a high dose rate on the epigenome long-term was clearly different to that seen following low dose rate. Here, the accessibility of the chromatin was almost exclusively reduced, occurring in transcriptional start sites (promoter regions) adjacent to genes relevant for radiation-induced damage, like the repair of DNA double-strand breaks and activation of p53-related responses. In addition, accessibility was also reduced in promoter regions to genes linked to transcriptional regulation. Paternal transgenerational (F2) genomic instability was used to investigate inheritance across generations, where F2 represents the first unexposed generation. The low dose rate irradiated (1,5 mGy/h) F0 generation was exposed for 45 days to a cumulative total dose of 1.5 Gy. Genomic instability was assessed in the blood samples from male F2 mice before and after a challenging dose of X-ray. Changes in the rate of repair of induced DNA lesions were also evaluated. The results did display statistically significant increased endogenously occurring DNA lesions. However, due to a low effect size, it is challenging to conclude whether the results represent a true biological finding or that it relates to methodological aspects. There was further no evidence that F0 low dose rate irradiation affected the level of DNA damage directly after X-ray, the rate of repair of the DNA lesions, or the formation of micronuclei in reticulocytes. The overall findings of this PhD project suggest that low dose rate should be considered a significant dose-effect modulating irradiation factor after direct exposure. Concerning transgenerational inheritance, given the experimental conditions a conclusion is elusive. The significance of these results upon the risk for human health needs to be addressed in appropriate epidemiological studies