The Suspension of the Gold Standard as Sustainable Monetary Policy

This paper models the gold standard as a state contingent commitment technology that is only feasible during peace. Monetary policy during war, when the gold convertibility rule suspended, can still be credible, if the policy maker’s plan is to resume the gold standard in the future. The DGE model developed in this paper suggests that the resumption of the gold standard was a sustainable plan, which replaced the gold standard as a commitment technology and made monetary policy time consistent. Trigger strategies support the equilibrium: private agents retaliate if a policy maker defaults its plan to resume the gold standard.Time Consistency, Monetary Policy, Monetary Regimes.

Macroeconomic Implications of Gold Reserve Policy of the Bank of England during the Eighteenth Century

By imposing a simple adjustment cost on gold purchases the Bank of England was able to manage external drains of monetary gold while maintaining the convertibility of pound during the eighteenth century. This was a period during which constant political disturbances and external shocks on the market price of gold made monetary policy a challenging task. The implications of adjustment cost were not just limited to the gold reserves of the Bank, but stabilised consumption and the price level.Gold standard, Monetary policy, Monetary regimes, Adjustment Costs.

Kannustaako Euroopan talous- ja rahaliitto EMU työmarkkinareformeihin?

Only abstract. Paper copies of master’s theses are listed in the Helka database (http://www.helsinki.fi/helka). Electronic copies of master’s theses are either available as open access or only on thesis terminals in the Helsinki University Library.Vain tiivistelmä. Sidottujen gradujen saatavuuden voit tarkistaa Helka-tietokannasta (http://www.helsinki.fi/helka). Digitaaliset gradut voivat olla luettavissa avoimesti verkossa tai rajoitetusti kirjaston opinnäytekioskeilla.Endast sammandrag. Inbundna avhandlingar kan sökas i Helka-databasen (http://www.helsinki.fi/helka). Elektroniska kopior av avhandlingar finns antingen öppet på nätet eller endast tillgängliga i bibliotekets avhandlingsterminaler.Euroopassa työttömyys on tyypillisesti ollut pitkäkestoista rakenteellista työttömyyttä, joka ei alene taloudellisen tilanteen parannuttua. Rakennetyöttömyys on johtunut jäykistymästä (hysteris), jonka vaikutuksesta suhdannetyöttömyys on muuttunut rakennetyöttömyydeksi. Lisäksi mikrotaloustieteelliset tarkastelut tukevat näkemystä, että rakennetyöttömyyttä lisäävät työmarkkinainstituutiot kuten tehoton työn verotus tai korkeat työttömyyskorvaukset. Työmarkkinainstituutioiden rakenteellinen reformi on tehokkain keino alentaa rakenteellista työttömyyttä mutta niiden toteuttamista ovat estäneet reformien korkeat kustannukset. Tässä Pro gradu ?työssä tarkastellaan muodostaako Euroopan talous- ja rahaliitto EMU sellaisen instituution, joka kannustaa päättäjiä ja työmarkkinaosapuolia toteuttamaan reformeja. Tutkijat eivät ole yksimielisiä siitä, miten rahapoliittisen yhteistyön tiivistäminen vaikuttaa reformeihin. Tutkielman ensimmäisessä osassa käsiteltävän Barron ja Gordonin (1983) malliin perustuvan tarkastelun mukaan rahaliiton kaltainen inflaatiota alentava instituutio vähentää kannustusta reformeihin. Taloudessa on työmarkkinoista johtuvia vääristymiä, joiden seurauksena toteutuva tuotanto tai työllisyys on sosiaalista tuotantoa ja työllisyyttä alhaisempi. Päättäjä voi tilapäisesti parantaa tuotantoa ja työllisyyttä inflaatiolla, jota yksityinen sektori ei voi ennustaa eli päättäjällä on inflaatioharhaa. Korkeasta inflaatiosta aiheutuva tehottomuus lisää reformeja, jotka pienentävät inflaatioharhaa vähentämällä työmarkkinoiden vääristymiä. Alentamalla inflaatiota ja inflaatioharhaa EMU ei kannusta päättäjiä reformeihin. Samasta syystä Maastrichtin sopimuksessa mainitut rahaliiton pääsyehdot, esimerkiksi inflaatioehto, eivät lisää reformeja. Vaihtoehtoinen malli tarkastella rahaliiton vaikutusta reformeihin on työn toisessa osassa käsiteltävä Lucasin kritiikki (Lucas Critique of Economic Models), jonka mukaan politiikkaregiimin muutos muuttaa talouden toimijoiden odotuksia ja käyttäytymistä. EMUssa Lucasin kritiikin mukainen käyttäytymisen muuttuminen näkyy esimerkiksi siten, että yksityinen sektori alentaa inflaatioennustettansa Euroopan keskuspankin (EKP) uskottavan rahapolitiikan myötä. Lisäksi taloudellisen integraation syventyminen lisää pääoman liikkuvuutta työvoimakustannusten suhteen, jolloin yritykset voivat siirtää tuotantoaan jäsenmaihin, joissa kustannukset ovat alhaisimpia. Kilpailun kiristyminen ja itsenäisen rahapolitiikan menettäminen EMUssa tekee reformit jäsenmaille houkuttelevimmiksi kuin rahapolitiikan ollessa itsenäistä Työn tulosten tulkinnan tekee mielenkiintoiseksi se, että EMUn vaikutus reformeihin riippuu EKP:n politiikasta. Jos keskuspankki ei noudata ensisijaista tavoitettaan hintatason vakautta ja tukee rahapolitiikalla talouskasvua, kannustus reformeihin vähentyy. Reformit toteuttavat kansalliset päättäjät valitsevat aina reformeja vähemmän kustannuksia aiheuttavan keinon alentaa työttömyyttä tai lisätä tuotantoa. Jos taas EKP pysyy tavoitteessaan, EMU kannustaa reformeihin. Reformeilla jäsenmaa varmistaa kilpailukykynsä ylläpitämisen ja parantaa talouden sopeutumista sokkeihin. Viime kädessä vastuu reformien toteuttamisesta on kuitenkin jäsenmaiden hallituksilla, eikä EMUlla ole kuin välillisiä vaikutuksia reformeihin

Endothelial Cells' Activation and Apoptosis Induced by a Subset of Antibodies against Human Cytomegalovirus: Relevance to the Pathogenesis of Atherosclerosis

Human cytomegalovirus (hCMV) is involved in the pathogenesis of atherosclerosis. We have previously shown in patients with atherosclerosis that antibodies directed against the hCMV-derived proteins US28 and UL122 are able to induce endothelial cell damage and apoptosis of non-stressed endothelial cells through cross-rection with normally expressed surface molecules. Our aim was to dissect the molecular basis of such interaction and to investigate mechanisms linking innate immunity to atherosclerosis.We analysed the gene expression profiles in endothelial cells stimulated with antibodies affinity-purified against either the UL122 or the US28 peptides using the microarray technology. Microarray results were validated by quantitative PCR and by detection of proteins in the medium. Supernatant of endothelial cells incubated with antibodies was analysed also for the presence of Heat Shock Protein (HSP)60 and was used to assess stimulation of Toll-Like Receptor-4 (TLR4). Antibodies against UL122 and US28 induced the expression of genes encoding for adhesion molecules, chemokines, growth factors and molecules involved in the apoptotis process together with other genes known to be involved in the initiation and progression of the atherosclerotic process. HSP60 was released in the medium of cells incubated with anti-US28 antibodies and was able to engage TLR4.Antibodies directed against hCMV modulate the expression of genes coding for molecules involved in activation and apoptosis of endothelial cells, processes known to play a pivotal role in the pathogenesis of atherosclerosis. Moreover, endothelial cells exposed to such antibodies express HSP60 on the cell surface and release HSP60 in the medium able to activate TLR4. These data confirm that antibodies directed against hCMV-derived proteins US28 and UL122 purified from patients with coronary artery disease induce endothelial cell damage and support the hypothesis that hCMV infection may play a crucial role in mediating the atherosclerotic process

Randomly and Non-Randomly Missing Renal Function Data in the Strong Heart Study: A Comparison of Imputation Methods

We gratefully acknowledge Rachel Schaperow, MedStar Health Research Institute, for editing the manuscript.Disclaimer: The opinions expressed in this paper are those of the authors and do not necessarily reflect the views of the Indian Health Service.Kidney and cardiovascular disease are widespread among populations with high prevalence of diabetes, such as American Indians participating in the Strong Heart Study (SHS). Studying these conditions simultaneously in longitudinal studies is challenging, because the morbidity and mortality associated with these diseases result in missing data, and these data are likely not missing at random. When such data are merely excluded, study findings may be compromised. In this article, a subset of 2264 participants with complete renal function data from Strong Heart Exams 1 (1989–1991), 2 (1993–1995), and 3 (1998–1999) was used to examine the performance of five methods used to impute missing data: listwise deletion, mean of serial measures, adjacent value, multiple imputation, and pattern-mixture. Three missing at random models and one non-missing at random model were used to compare the performance of the imputation techniques on randomly and non-randomly missing data. The pattern-mixture method was found to perform best for imputing renal function data that were not missing at random. Determining whether data are missing at random or not can help in choosing the imputation method that will provide the most accurate results.Yeshttp://www.plosone.org/static/editorial#pee

Hyperoxemia and excess oxygen use in early acute respiratory distress syndrome : Insights from the LUNG SAFE study

Publisher Copyright: © 2020 The Author(s). Copyright: Copyright 2020 Elsevier B.V., All rights reserved.Background: Concerns exist regarding the prevalence and impact of unnecessary oxygen use in patients with acute respiratory distress syndrome (ARDS). We examined this issue in patients with ARDS enrolled in the Large observational study to UNderstand the Global impact of Severe Acute respiratory FailurE (LUNG SAFE) study. Methods: In this secondary analysis of the LUNG SAFE study, we wished to determine the prevalence and the outcomes associated with hyperoxemia on day 1, sustained hyperoxemia, and excessive oxygen use in patients with early ARDS. Patients who fulfilled criteria of ARDS on day 1 and day 2 of acute hypoxemic respiratory failure were categorized based on the presence of hyperoxemia (PaO2 > 100 mmHg) on day 1, sustained (i.e., present on day 1 and day 2) hyperoxemia, or excessive oxygen use (FIO2 ≥ 0.60 during hyperoxemia). Results: Of 2005 patients that met the inclusion criteria, 131 (6.5%) were hypoxemic (PaO2 < 55 mmHg), 607 (30%) had hyperoxemia on day 1, and 250 (12%) had sustained hyperoxemia. Excess FIO2 use occurred in 400 (66%) out of 607 patients with hyperoxemia. Excess FIO2 use decreased from day 1 to day 2 of ARDS, with most hyperoxemic patients on day 2 receiving relatively low FIO2. Multivariate analyses found no independent relationship between day 1 hyperoxemia, sustained hyperoxemia, or excess FIO2 use and adverse clinical outcomes. Mortality was 42% in patients with excess FIO2 use, compared to 39% in a propensity-matched sample of normoxemic (PaO2 55-100 mmHg) patients (P = 0.47). Conclusions: Hyperoxemia and excess oxygen use are both prevalent in early ARDS but are most often non-sustained. No relationship was found between hyperoxemia or excessive oxygen use and patient outcome in this cohort. Trial registration: LUNG-SAFE is registered with ClinicalTrials.gov, NCT02010073publishersversionPeer reviewe

Cyclooxygenases and the cardiovascular system.

Cyclooxygenase (COX)-1 and COX-2 are centrally important enzymes within the cardiovascular system with a range of diverse, sometimes opposing, functions. Through the production of thromboxane, COX in platelets is a pro-thrombotic enzyme. By contrast, through the production of prostacyclin, COX in endothelial cells is antithrombotic and in the kidney regulates renal function and blood pressure. Drug inhibition of COX within the cardiovascular system is important for both therapeutic intervention with low dose aspirin and for the manifestation of side effects caused by nonsteroidal anti-inflammatory drugs. This review focuses on the role that COX enzymes and drugs that act on COX pathways have within the cardiovascular system and provides an in-depth resource covering COX biology and pharmacology. The review goes on to consider the role of COX in both discrete cardiovascular locations and in associated organs that contribute to cardiovascular health. We discuss the importance of, and strategies to manipulate the thromboxane: prostacyclin balance. Finally within this review the authors discuss testable COX-2-hypotheses intended to stimulate debate and facilitate future research and therapeutic opportunities within the field

Adding 6 months of androgen deprivation therapy to postoperative radiotherapy for prostate cancer: a comparison of short-course versus no androgen deprivation therapy in the RADICALS-HD randomised controlled trial

Background Previous evidence indicates that adjuvant, short-course androgen deprivation therapy (ADT) improves metastasis-free survival when given with primary radiotherapy for intermediate-risk and high-risk localised prostate cancer. However, the value of ADT with postoperative radiotherapy after radical prostatectomy is unclear. Methods RADICALS-HD was an international randomised controlled trial to test the efficacy of ADT used in combination with postoperative radiotherapy for prostate cancer. Key eligibility criteria were indication for radiotherapy after radical prostatectomy for prostate cancer, prostate-specific antigen less than 5 ng/mL, absence of metastatic disease, and written consent. Participants were randomly assigned (1:1) to radiotherapy alone (no ADT) or radiotherapy with 6 months of ADT (short-course ADT), using monthly subcutaneous gonadotropin-releasing hormone analogue injections, daily oral bicalutamide monotherapy 150 mg, or monthly subcutaneous degarelix. Randomisation was done centrally through minimisation with a random element, stratified by Gleason score, positive margins, radiotherapy timing, planned radiotherapy schedule, and planned type of ADT, in a computerised system. The allocated treatment was not masked. The primary outcome measure was metastasis-free survival, defined as distant metastasis arising from prostate cancer or death from any cause. Standard survival analysis methods were used, accounting for randomisation stratification factors. The trial had 80% power with two-sided α of 5% to detect an absolute increase in 10-year metastasis-free survival from 80% to 86% (hazard ratio [HR] 0·67). Analyses followed the intention-to-treat principle. The trial is registered with the ISRCTN registry, ISRCTN40814031, and ClinicalTrials.gov, NCT00541047. Findings Between Nov 22, 2007, and June 29, 2015, 1480 patients (median age 66 years [IQR 61–69]) were randomly assigned to receive no ADT (n=737) or short-course ADT (n=743) in addition to postoperative radiotherapy at 121 centres in Canada, Denmark, Ireland, and the UK. With a median follow-up of 9·0 years (IQR 7·1–10·1), metastasis-free survival events were reported for 268 participants (142 in the no ADT group and 126 in the short-course ADT group; HR 0·886 [95% CI 0·688–1·140], p=0·35). 10-year metastasis-free survival was 79·2% (95% CI 75·4–82·5) in the no ADT group and 80·4% (76·6–83·6) in the short-course ADT group. Toxicity of grade 3 or higher was reported for 121 (17%) of 737 participants in the no ADT group and 100 (14%) of 743 in the short-course ADT group (p=0·15), with no treatment-related deaths. Interpretation Metastatic disease is uncommon following postoperative bed radiotherapy after radical prostatectomy. Adding 6 months of ADT to this radiotherapy did not improve metastasis-free survival compared with no ADT. These findings do not support the use of short-course ADT with postoperative radiotherapy in this patient population