bluuebunny/crossref_metadata_2025_split huggingface dataset:
Trade policy and wage inequality: evidence from Indian manufacturing
Authors: Sen Kunal 
Published: October 2008

PurposeThere has been a period of slow but a steady increase in wage inequality in the Indian manufacturing sector since the mid‐1980s, which has gone hand‐in‐hand with an increase in the relative employment of skilled workers across all industries in the same period. The purpose of this paper is to investigate whether the co‐movement of relative employment and wages of skilled workers can be attributed to the changes in trade policy that has occurred in the Indian economy since the mid‐1980s.Design/methodology/approachThe two dominant theoretical perspectives on why trade reforms lay lead to wage inequality are Heckscher–Ohlin theory and trade‐induced skill‐biased technological change (SBTC). The paper evaluates the applicability of these theoretical perspectives to the Indian case using disaggregated industry data from Annual Survey of Industries from 1973 to 1997.FindingsEvidence was found of the validity of both the two dominant theoretical perspectives on wage inequality to explain the co‐movement in wage inequality and relative skill intensity in Indian manufacturing, with both variables increasing in the 1990s. Trade‐induced technological progress has led to an increase in relative skill intensity and wage inequality within industries. At the same time, the decline in protection that seems to have occurred more in unskilled labour‐intensive industries has led to a relative fall in the economy‐wide return to unskilled labour relative to skilled labour. Therefore, trade reforms have led to a widening of wage gap between skilled and unskilled workers, and an increase in relative skill intensity in Indian manufacturing.Originality/valueThe paper contributes to support of the trade‐induced SBTC hypothesis which may provide a consistent explanation of why many countries in the south experienced increases in wage inequality with the onset of trade liberalisation.
Transaction costs, information technology and development
Authors: Singh Nirvikar 
Published: October 2008

PurposeThe purpose of this paper is to examine the impact of transaction costs on economic welfare and development, and the role of information technology (IT) in reducing transaction costs.Design/methodology/approachThe paper extends the static model of Romer, in which transaction costs reduce welfare by reducing the equilibrium number of intermediate goods, and estimate the welfare losses in the case of domestic transaction costs. The main analysis of the paper extends a dynamic model of Ciccone and Matsuyama to incorporate transaction costs. Also described are case studies of the use of IT in rural India.FindingsIn the static model, it is shown that domestic transaction costs have a substantial welfare impact when the number of goods is endogenous. In the dynamic model, it is shown that high transaction costs reduce the long‐run level of development, and may arrest development completely in the extreme case. Some preliminary, qualitative evidence from rural India is offered to illustrate how these reductions may occur through the use of IT.Originality/valueThe treatment of transaction costs in a dynamic model is novel, and the use of such a model provides a new theoretical underpinning for understanding the potential impacts of IT on development.
The total factor productivity in China and India: new measures and approaches
Authors: Nin Pratt Alejandro , Yu Bingxin , Fan Shenggen 
Published: October 2008

PurposeThis paper aims to measure and compare agricultural total factor productivity (TFP) growth in China and India and relates TFP growth in each country to policy milestones and investment in agricultural research.Design/methodology/approachTFP is measured using a non‐parametric Malmquist index which allows the decomposition of TFP growth into its components: efficiency and technical change.FindingsComparing TFP growth in China and India it is found that efficiency improvement played a dominant role in promoting TFP growth in China, while technical change has also contributed positively. In India, the major source of productivity improvement came from technical change, as efficiency barely changed over the last three decades, which explains lower TFP growth than in China. Agricultural research has significantly contributed to improve agricultural productivity in both China and India. Even today, returns to agricultural R&D investments are very high, with benefit/cost ratios ranging from 20.7 to 9.6 in China and from 29.6 to 14.8 in India.Originality/valueThe applied methodology and the comparison between TFP growth patterns contribute to a better understanding of the consequences that the different approaches to agricultural reform followed by China and India had on the performance of agriculture in both countries.
Correlation of faecal calprotectin and lactoferrin with an endoscopic score for Crohn’s disease and histological findings
Authors: SIPPONEN T. , KÄRKKÄINEN P. , SAVILAHTI E. , KOLHO K.‐L. , NUUTINEN H. , TURUNEN U. , FÄRKKILÄ M. 
Published: October 2008

SummaryBackground  Faecal calprotectin and lactoferrin increasingly serve as surrogate markers of disease activity in IBD. Data on the correlation of these markers with simple endoscopic score for Crohn’s disease (SES‐CD) and with histological findings are as yet limited.Aim  To study the correlation of faecal calprotectin and lactoferrin with SES‐CD and histology.Methods During 87 consecutive ileocolonoscopies, SES‐CD was calculated and biopsy specimens were obtained from the ileum, colon and rectum. Faecal calprotectin and lactoferrin were measured.Results  In ileocolonic or colonic disease, both faecal calprotectin and lactoferrin correlated significantly with colon SES‐CD (P < 0.001) and colon histology (P < 0.001). In patients with normal calprotectin or lactoferrin levels, endoscopic and histology scores were significantly lower than in those with elevated concentrations (P < 0.001). In ileal CD, ileal SES‐CD correlated with histology (P < 0.001), but not with faecal calprotectin (P = 0.161) or lactoferrin (P = 0.448).Conclusion  In ileocolonic and colonic disease, endoscopic score SES‐CD and histological findings correlated significantly with faecal calprotectin and lactoferrin. A normal faecal‐marker concentration was a reliable surrogate marker for endoscopically and histologically inactive CD. Ileal endoscopic score and histological findings failed, however, to correlate with faecal markers.
A model of the long‐term cost effectiveness of scheduled maintenance treatment with infliximab for moderate‐to‐severe ulcerative colitis
Authors: TSAI H. H. , PUNEKAR Y. S. , MORRIS J. , FORTUN P. 
Published: October 2008

SummaryBackground  Infliximab (IFX) has been shown to be efficacious in moderate‐severe ulcerative colitis (UC).Aim  To evaluate the cost‐effectiveness of a scheduled maintenance treatment (SMT) with IFX in moderate‐severe UC patients.Methods  A Markov model was constructed to simulate the progression of a cohort of moderate‐severe UC patients treated with IFX (5 mg/kg) SMT. Transitions were estimated from two phase III trials of IFX (ACT I and ACT II). Standard care, comprising immunomodulators and/or corticosteroids was used as a comparator. Two separate treatment strategies were evaluated – continued treatment in IFX responders and continued treatment in IFX patients achieving remission. The dose of IFX was estimated for a 73 kg typical UC patient in the UK. The results were calculated over 10 years using a discount rate of 3.5% for costs and outcomes. The outcome measure was quality‐adjusted life years (QALYs) estimated using EQ‐5D. Sensitivity analyses explored the uncertainty around the results.Results  The incremental cost effectiveness ratio (ICER) for IFX was £27 424 in the responder strategy and £19 696 in the remission strategy at 10 years. In sensitivity analysis, the ICER for IFX in the responder strategy ranged from £21 066 to £86 322 and in the remission strategy ranged from £14 728 to £46 765. The model time horizon and patient body weight were important factors affecting results.Conclusion  Eight‐week SMT with IFX appears to be a cost‐effective treatment option for adult patients suffering from moderate to severe UC.
Anti-calreticulin immunoglobulin A (IgA) antibodies in refractory coeliac disease
Authors: Sánchez D , Palová-Jelínková L , Felsberg J , Šimšová M , Pekáriková A , Pecharová B , Swoboda I , Mothes T , Mulder C J J , Beneš Z , Tlaskalová-Hogenová H , Tučková L 
Published: October 2008

Summary
Refractory coeliac disease (RCD) is a very rare and dangerous form of CD, in which gluten-free diet loses its therapeutic effect and the damage of intestinal mucosa persists. Because of the adherence to the diet, serological markers of CD [immunoglobulin A (IgA) antibodies against gliadin, tissue transglutaminase (tTG) and endomysium] are often missing in RCD patients. We found substantially elevated levels of IgA anti-calreticulin (CRT) antibodies in the sera of almost all RCD patients tested. These sera were negative for IgA antibodies to gliadin and tTG and only some of them showed IgA antibodies to enterocytes. Analysis of patients' IgA reactivity to CRT fragments (quarters and halves) by Western blotting revealed differences in the specificity of IgA antibodies between RCD and CD patients. We therefore used the Pepscan technique with synthetic overlapping decapeptides of CRT to characterize antigenic epitopes recognized by serum IgA antibodies of RCD patients. Employing this method we demonstrated several dominant antigenic epitopes recognized by IgA antibodies of RCD patients on the CRT molecule. Epitope GVTKAAEKQMKD was recognized predominantly by serum IgA of RCD patients. Our results suggest that testing for serum IgA antibodies against CRT and its selected peptide could be a very useful tool in RCD differential diagnosis.
Membrane water permeability related to antigen-presenting function of dendritic cells
Authors: Wang G F , Dong C L , Tang G S , Shen Q , Bai C X 
Published: October 2008

SummaryAquaporin 5 (AQP5) is one of the water channel proteins which participate in a wide array of physiological processes and are primary determinants of membrane osmotic water permeability. The AQP5 gene is located in human chromosome 12q, the same region as the location of the major asthma susceptibility loci. In this study we try to determine whether the AQP5 knock-out has some effect on allergen-induced asthma. With a mouse asthma model induced by ovalbumin (OVA), we found that deletion of AQP5 reduced some major characteristic features of asthma, such as less inflammation cell infiltration in lung tissues, lower cytokine expression and fewer inflammation cells in bronchoalveolar lavage fluids compared with those from wild-type (WT) mice. Because it was found that mice injected intratracheally with OVA-pulsed dendritic cells (DCs), the AQP5 gene knock-out (AQP5−/−) ones presented fewer inflammation cells. Because DCs are major antigen-presenting cells that play an important role in antigen-induced asthma, we also probed into the possible effect of gene knock-out on DCs. Surprisingly, reverse transcription–polymerase chain reaction and fluorescence activated cell sorter analysis showed high levels of AQP5 on the surface of DCs from in vivo or bone marrow monocyte-derived DCs (mDC) in vitro. Immature mDC from AQP5 knock-out mice (AQP5−/−) showed decreased expression of CD80 and CD86 and endocytosis ability compared with that from WT, but the difference disappeared after mDCs matured with lipopolysaccharide. AQP5-mediated water transmembrane may play some role in the function of DCs. However, the mechanism of the effect of AQP5 on the DCs' function needs to be investigated further.
T cell cytokine polarity as a determinant of immunoglobulin A (IgA) glycosylation and the severity of experimental IgA nephropathy
Authors: Chintalacharuvu S R , Yamashita M , Bagheri N , Blanchard T G , Nedrud J G , Lamm M E , Tomino Y , Emancipator S N 
Published: October 2008

SummaryImmunoglobulin A (IgA) glycosylation, recognized as an important pathogenic factor in IgA nephropathy (IgAN), is apparently controlled by the polarity of T helper (Th) cytokine responses. To examine the role of cytokine polarity in IgAN, inbred mice were immunized by intraperitoneal priming with inactivated Sendai virus (SeV) emulsified in either complete Freund's adjuvant (CFA) or incomplete Freund's adjuvant (IFA), which promote Th1- or Th2-immune response, respectively, and then boosted identically twice orally with aqueous suspensions of inactivated virus. Next, some mice were challenged intranasally with infectious SeV. Mice primed with CFA or IFA had equal reductions in nasal viral titre relative to non-immune controls, and equally increased serum levels of SeV-specific IgA antibody. Mice primed with CFA showed higher SeV-specific IgG than those with IFA. Splenocytes from mice primed with IFA produced copious amounts of interleukin (IL)-4 and IL-5, but little interferon-γ and IL-2; those primed with CFA had reciprocal cytokine recall responses. Total serum IgA and especially SeV-specific IgA from mice primed with IFA showed a selective defect in sialylation and galactosylation. Although the frequency and intensity of glomerular deposits and haematuria did not differ, glomerulonephritis in mice primed with IFA and challenged with infectious virus was more severe than in those given CFA, as judged by serum creatinine level. We conclude that the polarity of T cell cytokines controls the pattern of IgA glycosylation and exerts direct or indirect effects on functional glomerular responses to immune complex deposition.
Influx of recent thymic emigrants into autoimmune thyroid disease glands in humans
Authors: Armengol M P , Sabater L , Fernández M , Ruíz M , Alonso N , Otero M J , Martínez-Cáceres E , Jaraquemada D , Pujol-Borrell R 
Published: October 2008

SummaryAutoimmune thyroid diseases (AITD) are considered as prototypic organ-specific autoimmune diseases, yet their underlying aetiology remains poorly understood. Among the various pathophysiological mechanisms considered, a failure of central tolerance has received little attention. Here we present evidence in favour of dysregulated thymic function playing a role in AITD. Flow-cytometric analyses conducted in peripheral blood lymphocytes from 58 AITD patients and 48 age- and-sex-matched controls showed that AITD patients have significantly higher blood levels of CD4+CD45RA+, CD4+CD31+ and CD4/CD8 double-positive T lymphocytes, all markers of recent thymic emigrants (RTE). In addition, the α-signal joint T cell receptor excision circles (TRECs) content (a molecular marker of RTEs) was higher in the group of AITD patients older than 35 years than in age-matched controls. This was independent from peripheral T cell expansion as assessed by relative telomere length. Comparisons of TREC levels in peripheral blood lymphocytes and intrathyroidal lymphocytes in paired samples showed higher levels within the thyroid during the initial 30 months of the disease, indicating an influx of RTE into the thyroid during the initial stages of AITD. Additionally, a lack of correlation between TREC levels and forkhead box P3 expression suggests that the intrathyroidal RTE are not natural regulatory T cells. These results uncover a hitherto unknown correlation between altered thymic T cell export, the composition of intrathyroidal T cells and autoimmune pathology.
Appearance of B220low autoantibody-producing B-1 cells at neonatal and older stages in mice
Authors: Tachikawa S , Kawamura T , Kawamura H , Kanda Y , Fujii Y , Matsumoto H , Abo T 
Published: October 2008

SummaryIn this study, normal adult mice carried B220high conventional B cells in the spleen and liver, but carried both B220high and B220low in the bone marrow. However, at the neonatal stage, only B220low unconventional B cells were found in all these organs. This pattern continued up to 2 weeks after birth, and at this stage autoantibodies were detected in the sera. This phenomenon was seen in all tested young mice (1–2 weeks), irrespective of their gender. Furthermore, at older stages (more than 20 weeks), B220low cells reappeared in the spleen and liver, and these B220low cells became dominant in the bone marrow. Autoantibodies also reappeared in the sera of these older mice. Cell-sorting experiments revealed that B220low cells were able to produce autoantibodies upon lipopolysaccharide stimuli in vitro. These results suggest that B220low cells appear at both neonatal and older stages as physiological responses and eventually produce autoantibodies.
Allergy as an organ and a systemic disease
Authors: Pucci S , Incorvaia C 
Published: October 2008

Summary
Allergic disorders are viewed generally as organ diseases and thus referred to organ specialists, such as the ear, nose and throat specialist for rhinitis, the pulmonologist for asthma, the dermatologist for dermatitis, and so on. Indeed, the systemic nature of allergy is made evident by the fact that the same individual may develop during the life different manifestations to a given allergen. This is true for example in sensitisation to house dust mites, which may start in childhood as atopic dermatitis and later express as asthma or rhinitis.
The major player in driving the immune response is the T lymphocyte, and the T helper subpopulations – Th1 and Th2 – as well as the T regulatory cells, are involved in orienting tolerance or reactivity to allergens. Interesting observations on the systemic or organ-specific actions of T cells were obtained by transplantations from allergic donors to non-allergic recipients. Bone marrow is able to transfer all allergic manifestations, while lung transplantation transfers only asthma. A number of factors are involved in the expression of allergy as a systemic or organ disease and deserve deeper investigations. They include the antigen presenting cells, the homing of T cells, the cytokine and chemokine pattern, and the adhesion molecules.
Allergy and the lung
Authors: Passalacqua G , Ciprandi G 
Published: October 2008

SummaryAmong the ‘allergic’ conditions involving the lung, asthma is the more frequent and the most extensively investigated, although asthma itself may be caused by different disorders. The triggering event in allergic subjects is the reaction allergen-specific immunoglobulin E (IgE) that activates mast cells and initiates a complex and redundant inflammatory process, where cells, cytokines and adhesion molecules are involved at different stages. In fact, mucosal eosinophilic inflammation is one of the distinctive features of asthma and the particular T helper type 2 (Th2) phenotype of allergic patients favours it. In general, the clinical severity of asthma correlates well with the degree of inflammation. None the less, other phenomena such as non-specific bronchial hyperresponsiveness and remodelling intervene in the pathophysiology of allergic asthma. These phenomena are only partially inflammation-related. In particular, the remodelling of the bronchial wall seems to start very early in life and also seems to be a distinctive histological feature of the asthmatic bronchus. The recent introduction of biological treatments (monoclonal antibodies) has allowed elucidation of some of the pathogenic features of allergic asthma.
Alteration of the immunological synapse in lung cancer: a microenvironmental approach
Authors: Derniame S , Vignaud J-M , Faure G C , Béné M C 
Published: October 2008

Summary
This study was designed to investigate the immunological properties of stroma reaction T cells and tumoral cells by comparison with non-tumoral lung tissue and local lymph nodes in order to explore interactions between tumour cells and the immune system. Immunodetection of major histocompatibility complex (MHC) molecules, CD3/T cell receptor (TCR) complex and T cell subsets markers was carried out in situ on frozen sections, and the semi-quantitative expression of CD3, CD4 and CD8 was examined in flow cytometry on lymphocytes of nodal, tumoral and healthy lung tissue from 62 patients with non-small cell lung cancer. This study showed alterations on lymphocytes and tumour cells in lung cancer, consistent with an impairment of T cell activation. CD3, TCRαβ and accessory molecules expression is down-modulated on peri- or intra-tumoral lymphocytes. MHC class I and class II molecules are down-modulated significantly on tumour cells. Other differences were noted, such as the reversed CD4/CD8 ratio of tumour infiltrating cells, compared to healthy lung tissues, consistent with the development of cytotoxic anti-tumoral responses. This study reports on the presence of a strong in vivo immunomodulating effect of tumour cells in human non-small cell lung cancer, likely to impair proper formation of the immunological synapse.
CD8 chemokine receptors in chronic obstructive pulmonary disease
Authors: Smyth L J C , Starkey C , Gordon F S , Vestbo J , Singh D 
Published: October 2008

SummaryIncreased lung CD8 cells and their expression of chemokine receptors CXCR3 and CCR5 have been previously reported in chronic obstructive pulmonary disease (COPD). Alterations of CD8-CCR3 and -CCR4 expression and their ligands in COPD patients have not been fully investigated. The objective of this study was to assess in COPD patients: (i) broncho-alveolar lavage (BAL) CD8 CCR3 and CCR4 expression in COPD patients; and (ii) airway levels of the CCR3 ligands, CCL11 and CCL5. Multi-parameter flow cytometric anlaysis was used to assess BAL CD3 and CD8-chemokine receptor expression in COPD patients, smokers and healthy non-smokers (HNS). CCL5 and CCL11 levels were measured in BAL, and from the supernatants of lung resection explant cultures. CD8-CCR3 and -CCR5 expression (means) were increased in COPD patients (22% and 46% respectively) and smokers (20% and 45%) compared with HNS (3% and 22%); P &lt; 0·05 for all comparisons. CD3CXCR3 expression was raised in smokers and COPD while CD8CXCR3 and CD3 and CD8 CCR4 expression was similar between groups. CD8CCR5 expression correlated to smoking pack years (r = 0·42, P = 0·01). COPD explants released more CCL5 compared with smokers (P = 0·02), while there was low level CCL11 production. CD8CCR3 and CCR5 expression appear to be regulated by cigarette smoke exposure. We show that COPD lung tissue released more CCL5, suggesting a role for CCL5–CCR3 signalling in pulmonary CD8 recruitment in COPD.