Individual and population-level responses to ocean acidification

Ocean acidification is predicted to have detrimental effects on many marine organisms and ecological processes. Despite growing evidence for direct impacts on specific species, few studies have simultaneously considered the effects of ocean acidification on individuals (e.g. consequences for energy budgets and resource partitioning) and population level demographic processes. Here we show that ocean acidification increases energetic demands on gastropods resulting in altered energy allocation, i.e. reduced shell size but increased body mass. When scaled up to the population level, long-term exposure to ocean acidification altered population demography, with evidence of a reduction in the proportion of females in the population and genetic signatures of increased variance in reproductive success among individuals. Such increased variance enhances levels of short-term genetic drift which is predicted to inhibit adaptation. Our study indicates that even against a background of high gene flow, ocean acidification is driving individual- and population-level changes that will impact eco-evolutionary trajectories

Specific niche requirements underpin multidecadal range edge stability, but may introduce barriers for climate change adaptation

Aim: To investigate some of the environmental variables underpinning the past and present distribution of an ecosystem engineer near its poleward range edge. Location: >500 locations spanning >7,400 km around Ireland. Methods: We collated past and present distribution records on a known climate change indicator, the reef-forming worm Sabellaria alveolata (Linnaeus, 1767) in a biogeographic boundary region over 182 years (1836–2018). This included repeat sampling of 60 locations in the cooler 1950s and again in the warmer 2000s and 2010s. Using species distribution modelling, we identified some of the environmental drivers that likely underpin S. alveolata distribution towards the leading edge of its biogeographical range in Ireland. Results: Through plotting 981 records of presence and absence, we revealed a discontinuous distribution with discretely bounded sub-populations, and edges that coincide with the locations of tidal fronts. Repeat surveys of 60 locations across three time periods showed evidence of population increases, declines, local extirpation and recolonization events within the range, but no evidence of extensions beyond the previously identified distribution limits, despite decades of warming. At a regional scale, populations were relatively stable through time, but local populations in the cold Irish Sea appear highly dynamic and vulnerable to local extirpation risk. Contemporary distribution data (2013–2018) computed with modelled environmental data identified specific niche requirements which can explain the many distribution gaps, namely wave height, tidal amplitude, stratification index, then substrate type. Main conclusions: In the face of climate warming, such specific niche requirements can create environmental barriers that may prevent species from extending beyond their leading edges. These boundaries may limit a species’ capacity to redistribute in response to global environmental change

Oral abstracts 3: RA Treatment and outcomesO13. Validation of jadas in all subtypes of juvenile idiopathic arthritis in a clinical setting

Background: Juvenile Arthritis Disease Activity Score (JADAS) is a 4 variable composite disease activity (DA) score for JIA (including active 10, 27 or 71 joint count (AJC), physician global (PGA), parent/child global (PGE) and ESR). The validity of JADAS for all ILAR subtypes in the routine clinical setting is unknown. We investigated the construct validity of JADAS in the clinical setting in all subtypes of JIA through application to a prospective inception cohort of UK children presenting with new onset inflammatory arthritis. Methods: JADAS 10, 27 and 71 were determined for all children in the Childhood Arthritis Prospective Study (CAPS) with complete data available at baseline. Correlation of JADAS 10, 27 and 71 with single DA markers was determined for all subtypes. All correlations were calculated using Spearman's rank statistic. Results: 262/1238 visits had sufficient data for calculation of JADAS (1028 (83%) AJC, 744 (60%) PGA, 843 (68%) PGE and 459 (37%) ESR). Median age at disease onset was 6.0 years (IQR 2.6-10.4) and 64% were female. Correlation between JADAS 10, 27 and 71 approached 1 for all subtypes. Median JADAS 71 was 5.3 (IQR 2.2-10.1) with a significant difference between median JADAS scores between subtypes (p < 0.01). Correlation of JADAS 71 with each single marker of DA was moderate to high in the total cohort (see Table 1). Overall, correlation with AJC, PGA and PGE was moderate to high and correlation with ESR, limited JC, parental pain and CHAQ was low to moderate in the individual subtypes. Correlation coefficients in the extended oligoarticular, rheumatoid factor negative and enthesitis related subtypes were interpreted with caution in view of low numbers. Conclusions: This study adds to the body of evidence supporting the construct validity of JADAS. JADAS correlates with other measures of DA in all ILAR subtypes in the routine clinical setting. Given the high frequency of missing ESR data, it would be useful to assess the validity of JADAS without inclusion of the ESR. Disclosure statement: All authors have declared no conflicts of interest. Table 1Spearman's correlation between JADAS 71 and single markers DA by ILAR subtype ILAR Subtype Systemic onset JIA Persistent oligo JIA Extended oligo JIA Rheumatoid factor neg JIA Rheumatoid factor pos JIA Enthesitis related JIA Psoriatic JIA Undifferentiated JIA Unknown subtype Total cohort Number of children 23 111 12 57 7 9 19 7 17 262 AJC 0.54 0.67 0.53 0.75 0.53 0.34 0.59 0.81 0.37 0.59 PGA 0.63 0.69 0.25 0.73 0.14 0.05 0.50 0.83 0.56 0.64 PGE 0.51 0.68 0.83 0.61 0.41 0.69 0.71 0.9 0.48 0.61 ESR 0.28 0.31 0.35 0.4 0.6 0.85 0.43 0.7 0.5 0.53 Limited 71 JC 0.29 0.51 0.23 0.37 0.14 -0.12 0.4 0.81 0.45 0.41 Parental pain 0.23 0.62 0.03 0.57 0.41 0.69 0.7 0.79 0.42 0.53 Childhood health assessment questionnaire 0.25 0.57 -0.07 0.36 -0.47 0.84 0.37 0.8 0.66 0.4

Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes

Changing concentration in the New Zealand manufacturing sector

This paper seeks to trace and analyse changes in seller concentration in New Zealand manufacturing industries between 1973-74 and 1995. The primary motivation for this research topic is the substantial liberalisation of industry and commerce that occurred over this period, which is expected to have had an effect on concentration. This study will hopefully provide a basis for future work into the impact of recent economic reform on the economy, in particular, the manufacturing sector. The rational underlying interest in industry concentration measures is that they are often regarded as giving a significant dimension of market structure by indicating market power and subsequently business behaviour and performance (Curry and George 1983). Concentration measures are therefore widely employed by professional economic staff during the formulation and administration of competition policy (Baldwin and Gorecki 1994). According to Harper (1992), there are three main analytical frameworks which concentration measures are generally considered: the structure-conduct-performance paradigm (SCP); the efficient structure doctrine; and contestability theory. Under the SCP paradigm, high levels of concentration are thought to be conducive to firms being able to make supernormal profits by raising prices above production costs and engaging in anticompetitive behaviour (Ellis, 1976; Ratnayake, 1994). Such activities can lead to a misallocation of resources and poorer economic performance than would otherwise be the case (Madge et al, 1989). The SCP is supported by empirical evidence that suggests there is a critical concentration point where there is an abrupt change from competitive behaviour to oligopolistic co-operation (for example see Pickford and Haslett, 1996). United States studies have typically suggested this critical level to be between 45 and 60. Therefore, according to the SCP paradigm, changes in concentration over time are crucial for informed industrial and antitrust policy (Harper, 1992). In contrast to the SCP paradigm, the efficient structure doctrine suggests that high concentration and high profits are a result of greater efficiency of some large firms. Competitive forces are believed to operate for the emergence of a size distribution of firms that minimises costs, suggesting that higher returns and higher market shares are a result of increased efficiency. The theoretical linkage, therefore, is not from structure to performance, but from performance to structure, hence, high concentration may not be cause for concern. The efficient structure doctrine also implies that concentration levels may be important for a relatively small economy like that of New Zealand if it is to compete with larger trade partners. The third framework, contestability theory, also suggests that a high level of concentration does not imply a lack of competition (Harper, 1992). The crucial feature of a contestable market is its vulnerability to hit-and-run entry. Contestability theory claims that it is possible that the performance of some markets may be acceptable despite the presence of only a small number of large firms. The above analytical frameworks imply different approaches to market concentration. Whatever approach is ascribed to, by providing up to date data on concentration movements, this report may provide a basis for future research. Determining movements in concentration in the manufacturing sector is important since the manufacturing sector comprises a considerable proportion of the New Zealand economy, as is made evident by the graph below. The manufacturing sector contribution towards Gross Domestic Product has remained reasonably consistent over the last twenty years. This contrasts with Australia where the manufacturing sector has declined as a percentage of Gross Domestic Product (refer to Madge et al, 1989)UnpublishedBaldwin, J. and Gorecki, P., 1994, Concentration and mobility statistics in Canada's manufacturing sector, The Journal of Industrial Economics, Vol. XLII, No. 1. Baldwin, 3, Gorecki, P and Mc Vey, J, 1986, International trade, secondary output and concentration in Canadian manufacturing industries 1979, Applied Economics, 18(5), p. 529-543. Curry, B. and George, K. D., 1983, Industrial concentration: A survey, The Journal of Industrial Economics, Vol. XXXI, No. 3. Department of Statistics New Zealand, 'Economy wide census, Manufacturing 1987', Department of Statistics, Wellington New Zealand. Department of Statistics, Census of Manufacturing Bulletin, Series C, No 1-9, 1983-84, Department of Statistics. Ellis, J. A., 1976, Industrial concentration, New Zealand Institute of Economic Research, Research Paper No. 20. Gibson J. K. and Harris. I. D., 1996, Trade liberalisation and Plant exit in New Zealand manufacturing, The Review of Economics and Statistics, Vol. 78(3), p. 521-29. Hamilton, R. T., 1991, Diversification and concentration in New Zealand industry, New Zealand Economic Papers, 25 (2), p. 151-170. Hamilton, R. T., 1992, Diversification and concentration changes in a liberalised environment; The case of New Zealand Manufacturing industries, International Journal of Industrial Organisation, Vol. 10, pp 15-25. Hamilton R. T. and Shergill, G. S., 1993, The Logic of New Zealand Business; Strategy Structure and Performance, Oxford University Press. let Harper, D., 1992, Industrial Concentration in New Zealand, 1987-1990, NZ Institute of Economic Research, Occasional Paper No. 6, Nov 1992. Kwaok, J. E., 1981, Does the choice of concentration measure really matter? The Journal of industrial Economics, Vol. XXIX, No. 4, p. 445-53. Madge, A., Bennet, R., Robertson, R., 1989, Concentration in Australian Manufacturing 1972-73 to 1986-87, Bureau of Industry Economics, Canberra, Working Paper 57, Parket, S. C., 1991, Significantly concentrated markets; Theory and evidence from the U.K., International Journal of Industrial Organisation, Vol. 9, p. 585-590. Pickford, M. and Haslett, S., 1996, In search of the dominant firm, Massey University, School of Applied Economics, Vol. 96 (8). Pickford, M. and Wai, M., 1995, The profitability-concentration relationship in New Zealand manufacturing industry: Some preliminary findings using census data, Massey University, School ofApplied Economics, Vol. 95 (8). Ratnayake, R., 1994, Industry concentration-profitability relationship and competition policy: is the a critical concentration level?, Working Papers in Economics, University of Auckland. Ratnavake, R., 1993, Patterns and causes of industry concentration in New Zealand, Working Papers in Economics, University of Auckland. Saving, 1970 Scherer, F. M. and Ross, D., 1990, Industrial market structure and market performance, (3r( edition), Boston; Houghton Mifflin, Chapter 3. Schmalensee, R,. 1977, Using the H-index of concentration with published data, Review of' Economics and Statistics, LIX (2), p. 186-93

Changing concentration in the New Zealand manufacturing sector

This paper seeks to trace and analyse changes in seller concentration in New Zealand manufacturing industries between 1973-74 and 1995. The primary motivation for this research topic is the substantial liberalisation of industry and commerce that occurred over this period, which is expected to have had an effect on concentration. This study will hopefully provide a basis for future work into the impact of recent economic reform on the economy, in particular, the manufacturing sector. The rational underlying interest in industry concentration measures is that they are often regarded as giving a significant dimension of market structure by indicating market power and subsequently business behaviour and performance (Curry and George 1983). Concentration measures are therefore widely employed by professional economic staff during the formulation and administration of competition policy (Baldwin and Gorecki 1994). According to Harper (1992), there are three main analytical frameworks which concentration measures are generally considered: the structure-conduct-performance paradigm (SCP); the efficient structure doctrine; and contestability theory. Under the SCP paradigm, high levels of concentration are thought to be conducive to firms being able to make supernormal profits by raising prices above production costs and engaging in anticompetitive behaviour (Ellis, 1976; Ratnayake, 1994). Such activities can lead to a misallocation of resources and poorer economic performance than would otherwise be the case (Madge et al, 1989). The SCP is supported by empirical evidence that suggests there is a critical concentration point where there is an abrupt change from competitive behaviour to oligopolistic co-operation (for example see Pickford and Haslett, 1996). United States studies have typically suggested this critical level to be between 45 and 60. Therefore, according to the SCP paradigm, changes in concentration over time are crucial for informed industrial and antitrust policy (Harper, 1992). In contrast to the SCP paradigm, the efficient structure doctrine suggests that high concentration and high profits are a result of greater efficiency of some large firms. Competitive forces are believed to operate for the emergence of a size distribution of firms that minimises costs, suggesting that higher returns and higher market shares are a result of increased efficiency. The theoretical linkage, therefore, is not from structure to performance, but from performance to structure, hence, high concentration may not be cause for concern. The efficient structure doctrine also implies that concentration levels may be important for a relatively small economy like that of New Zealand if it is to compete with larger trade partners. The third framework, contestability theory, also suggests that a high level of concentration does not imply a lack of competition (Harper, 1992). The crucial feature of a contestable market is its vulnerability to hit-and-run entry. Contestability theory claims that it is possible that the performance of some markets may be acceptable despite the presence of only a small number of large firms. The above analytical frameworks imply different approaches to market concentration. Whatever approach is ascribed to, by providing up to date data on concentration movements, this report may provide a basis for future research. Determining movements in concentration in the manufacturing sector is important since the manufacturing sector comprises a considerable proportion of the New Zealand economy, as is made evident by the graph below. The manufacturing sector contribution towards Gross Domestic Product has remained reasonably consistent over the last twenty years. This contrasts with Australia where the manufacturing sector has declined as a percentage of Gross Domestic Product (refer to Madge et al, 1989)UnpublishedBaldwin, J. and Gorecki, P., 1994, Concentration and mobility statistics in Canada's manufacturing sector, The Journal of Industrial Economics, Vol. XLII, No. 1. Baldwin, 3, Gorecki, P and Mc Vey, J, 1986, International trade, secondary output and concentration in Canadian manufacturing industries 1979, Applied Economics, 18(5), p. 529-543. Curry, B. and George, K. D., 1983, Industrial concentration: A survey, The Journal of Industrial Economics, Vol. XXXI, No. 3. Department of Statistics New Zealand, 'Economy wide census, Manufacturing 1987', Department of Statistics, Wellington New Zealand. Department of Statistics, Census of Manufacturing Bulletin, Series C, No 1-9, 1983-84, Department of Statistics. Ellis, J. A., 1976, Industrial concentration, New Zealand Institute of Economic Research, Research Paper No. 20. Gibson J. K. and Harris. I. D., 1996, Trade liberalisation and Plant exit in New Zealand manufacturing, The Review of Economics and Statistics, Vol. 78(3), p. 521-29. Hamilton, R. T., 1991, Diversification and concentration in New Zealand industry, New Zealand Economic Papers, 25 (2), p. 151-170. Hamilton, R. T., 1992, Diversification and concentration changes in a liberalised environment; The case of New Zealand Manufacturing industries, International Journal of Industrial Organisation, Vol. 10, pp 15-25. Hamilton R. T. and Shergill, G. S., 1993, The Logic of New Zealand Business; Strategy Structure and Performance, Oxford University Press. let Harper, D., 1992, Industrial Concentration in New Zealand, 1987-1990, NZ Institute of Economic Research, Occasional Paper No. 6, Nov 1992. Kwaok, J. E., 1981, Does the choice of concentration measure really matter? The Journal of industrial Economics, Vol. XXIX, No. 4, p. 445-53. Madge, A., Bennet, R., Robertson, R., 1989, Concentration in Australian Manufacturing 1972-73 to 1986-87, Bureau of Industry Economics, Canberra, Working Paper 57, Parket, S. C., 1991, Significantly concentrated markets; Theory and evidence from the U.K., International Journal of Industrial Organisation, Vol. 9, p. 585-590. Pickford, M. and Haslett, S., 1996, In search of the dominant firm, Massey University, School of Applied Economics, Vol. 96 (8). Pickford, M. and Wai, M., 1995, The profitability-concentration relationship in New Zealand manufacturing industry: Some preliminary findings using census data, Massey University, School ofApplied Economics, Vol. 95 (8). Ratnayake, R., 1994, Industry concentration-profitability relationship and competition policy: is the a critical concentration level?, Working Papers in Economics, University of Auckland. Ratnavake, R., 1993, Patterns and causes of industry concentration in New Zealand, Working Papers in Economics, University of Auckland. Saving, 1970 Scherer, F. M. and Ross, D., 1990, Industrial market structure and market performance, (3r( edition), Boston; Houghton Mifflin, Chapter 3. Schmalensee, R,. 1977, Using the H-index of concentration with published data, Review of' Economics and Statistics, LIX (2), p. 186-93

Pericardial fluid analysis in diagnosis and prognosis of patients who underwent pericardiocentesis

In this study, we aimed to examine the diagnostic yield of pericardial fluid biochemistry and cytology and their prognostic significance in patients with percutaneously drained pericardial effusions, with and without malignancy. This is a single-center, retrospective study of patients who underwent pericardiocentesis between 2010 and 2020. Data were extracted from electronic patient records, including procedural information, underlying diagnosis, and laboratory results. Patients were grouped into those with and without underlying malignancy. A Cox proportional hazards model was used to analyze the association of variables with mortality. The study included 179 patients; 50% had an underlying malignancy. There were no significant differences in pericardial fluid protein and lactate dehydrogenase between the 2 groups. Diagnostic yield from pericardial fluid analysis was greater in the malignant group (32% vs 11%, p = 0.002); 72% of newly diagnosed malignancies had positive fluid cytology. The 1-year survival was 86% and 33% in nonmalignant and malignant groups, respectively (p &lt;0.001). Of 17 patients who died within the nonmalignant group, idiopathic effusions were the largest group (n = 6). In malignancy, lower pericardial fluid protein and higher serum C-reactive protein were associated with increased risk of mortality. In conclusion, pericardial fluid biochemistry has limited value in determining the etiology of pericardial effusions; fluid cytology is the most important diagnostic test. Mortality in malignant pericardial effusions may be associated with lower pericardial fluid protein levels and a higher serum C-reactive protein. Nonmalignant pericardial effusions do not have a benign prognosis and close follow-up is required

Pericardial fluid analysis in diagnosis and prognosis of patients who underwent pericardiocentesis

In this study, we aimed to examine the diagnostic yield of pericardial fluid biochemistry and cytology and their prognostic significance in patients with percutaneously drained pericardial effusions, with and without malignancy. This is a single-center, retrospective study of patients who underwent pericardiocentesis between 2010 and 2020. Data were extracted from electronic patient records, including procedural information, underlying diagnosis, and laboratory results. Patients were grouped into those with and without underlying malignancy. A Cox proportional hazards model was used to analyze the association of variables with mortality. The study included 179 patients; 50% had an underlying malignancy. There were no significant differences in pericardial fluid protein and lactate dehydrogenase between the 2 groups. Diagnostic yield from pericardial fluid analysis was greater in the malignant group (32% vs 11%, p = 0.002); 72% of newly diagnosed malignancies had positive fluid cytology. The 1-year survival was 86% and 33% in nonmalignant and malignant groups, respectively (p &lt;0.001). Of 17 patients who died within the nonmalignant group, idiopathic effusions were the largest group (n = 6). In malignancy, lower pericardial fluid protein and higher serum C-reactive protein were associated with increased risk of mortality. In conclusion, pericardial fluid biochemistry has limited value in determining the etiology of pericardial effusions; fluid cytology is the most important diagnostic test. Mortality in malignant pericardial effusions may be associated with lower pericardial fluid protein levels and a higher serum C-reactive protein. Nonmalignant pericardial effusions do not have a benign prognosis and close follow-up is required

Specific niche requirements underpin multidecadal range edge stability, but may introduce barriers for climate change adaptation

Aim To investigate some of the environmental variables underpinning the past and present distribution of an ecosystem engineer near its poleward range edge. Location >500 locations spanning >7,400 km around Ireland. Methods We collated past and present distribution records on a known climate change indicator, the reef‐forming worm Sabellaria alveolata (Linnaeus, 1767) in a biogeographic boundary region over 182 years (1836–2018). This included repeat sampling of 60 locations in the cooler 1950s and again in the warmer 2000s and 2010s. Using species distribution modelling, we identified some of the environmental drivers that likely underpin S. alveolata distribution towards the leading edge of its biogeographical range in Ireland. Results Through plotting 981 records of presence and absence, we revealed a discontinuous distribution with discretely bounded sub‐populations, and edges that coincide with the locations of tidal fronts. Repeat surveys of 60 locations across three time periods showed evidence of population increases, declines, local extirpation and recolonization events within the range, but no evidence of extensions beyond the previously identified distribution limits, despite decades of warming. At a regional scale, populations were relatively stable through time, but local populations in the cold Irish Sea appear highly dynamic and vulnerable to local extirpation risk. Contemporary distribution data (2013–2018) computed with modelled environmental data identified specific niche requirements which can explain the many distribution gaps, namely wave height, tidal amplitude, stratification index, then substrate type. Main conclusions In the face of climate warming, such specific niche requirements can create environmental barriers that may prevent species from extending beyond their leading edges. These boundaries may limit a species’ capacity to redistribute in response to global environmental change