bluuebunny/crossref_metadata_2025_split huggingface dataset:
Trends in weights, heights, BMI and comparison of their differences in urban and rural areas for Iranian children and adolescents 2–18‐year‐old between 1990–1991 and 1999
Authors: Hosseini M. , Taslimi SH. , Dinarvand P. , Jones M. E. , Mohammad K. 
Published: August 2010

AbstractBackground  Secular trends in height and weight are interesting because in middle‐ and low‐income countries they are a marker for changes in population health. The present study aims to evaluate the secular trend in height and weight and body mass index (BMI) of Iranian children and adolescents aged 2–18 years old between 1990–1991 and 1999 and compare the magnitude of urban–rural differences during this period for the first time in an Asian country.Methods  Data from two national health surveys in 1990–1991 and 1999, of 22 349 and 25 196 weight and height measures of Iranian children and adolescents were used to study the trend and compare its difference in urban and rural children. Logarithmic transformation of weight, height and BMI was modelled as a polynomial in age for urban and rural boys and girls in each survey separately. The trend in urban and rural growth indexes (weight, height and BMI) and also the comparisons of urban–rural differences between two national surveys were tested in logarithmic scale using a weighted form of Z statistic for comparison of two means adjusted for age groups.Results  Urban and rural boys and girls became taller and heavier (P≤ 0.02) with no change of BMI (P > 0.05) during the period. There was not any significant difference between the magnitudes of urban–rural difference between two surveys (P≥ 0.61).Conclusion  Although generally positive weight and height trend was observed among urban and rural residents, the magnitude of their differences was not changed.
Elevation of heat shock protein synthesis and hsp gene transcription during monocyte to macrophage differentiation of U937 cells
Authors: TWOMEY B M , McCALLUM S , ISENBERG D A , LATCHMAN D S 
Published: August 2010

SUMMARY
During the phorbol myristale acetate (PMA)-induccd differentiation of U937 cells to a macrophage-like phenotype, the levels of the heat shock proteins hsp90, hsp72 and hsp65 increased dramatically to a peak level following 24 h of treatment, and then declined. In contrast, no significant increase was observed in the level of the constitutive hsp73 protein in this process. The observed increases in hsp levels were preceded by an increase in the transcription of each of the genes encoding these hsps, including both of the two genes which encode hsp90. The mechanism of this effect and the possible role of the hsps in the function of differentiated macrophages and in the differentiation process are discussed.
CD8 lymphocytosis in primary cytomegalovirus (CMV) infection of allograft recipients: expansion of an uncommon CD8+ CD57− subset and its progressive replacement by CD8+CD57+ T cells
Authors: LABALETTE M , SALEZ F , PRUVOT F R , NOEL C , DESSAINT J P 
Published: August 2010

SUMMARYAllograft recipients undergoing eytomegalovirus infection present increased proportions of circulating CD8+ lymphocytes. A longitudinal study of 11 kidney and five liver allograft recipients with primary CMV infection but no other etiological factor of graft dysfunction revealed selective imbalances of peripheral blood CDS+ T cell subsets. Initially, CMV viraemia is associated with elevated CDS+ bright T cell numbers and T cell activation. Activation markers fall to normal when viral cultures become negative (before the end of the first month). During the second to sixth month, most (12/16) patients keep up high CD8+ T cell counts (1050-2900 CD8+ cells/mm3), comprising an uncommon CD8+ T cell subset, as 45-73% of CD8+bright lymphocytes were CD3+ and TCRαβ+, but were not stained by anti-CD28, CDIIb, CD16. CD56. and CD57 antibody. Unexpectedly, CD8+CD57+ T cells, a hallmark of CMV infection, do not appear until the second to sixth month of primary CMV infection, and their numbers increase progressively thereafter. They become the predominant CD8+ T cell subset after 6 months of infection and their persistence for several (up to 4) years is strongly correlated (r = 0-87) with expansion of CD8+ cells. By analysis with MoAbs, there was no bias towards the use of particular TCR-Vβ gene families al any time of primary CMV infection. Persistence of CD8 lymphocytosis is thus directly related to the rate of expansion of an uncommon CD8+ CD57- subset and its progressive replacement by CD8+ CD57+ T cells that are chronically elicited by CMV.
Anti-neutrophil cytoplasmic antibodies (ANCA) in inflammatory bowel disease: characterization and clinical correlates
Authors: MULDER A H L , BROEKROELOFS J , HORST G , LIMBURG P C , NELIS G F , KALLENBERG C G M 
Published: August 2010

SUMMARY
ANCA were detected by indirect immunofluorescence in 34 out of 67 patients with ulcerative colitis (UC, 51%) and in 14 out of 35 patients with Crobn's disease (CD, 40%). All but one ANCA-positive sera produced a perinuclear pattern of fluorescence (P-ANCA) on ethanol-fixed neutrophils. On paraformaldehyde-fixed neutrophils 76% of P-ANCA-positive sera in UC and 50% of P-ANCA-positive sera in CD produced cytoplasmic fluorescenec, indicating that, indeed, cytoplasmie antigens are recognized by a considerable number of these sera. By Western blot analysis using whole neutrophil extract as a substrate 46% of sera from patients with UC and 32%, of sera from patients with CD showed reactivity with either lactolerrin, polypeptides occurring as a doublet of 66/67 kD mol. wt, or polypeptides occurring as a doublet of 63/54 kD mol. wt, respectively. Identical patterns of reactivity have been observed among P-ANCA-positive sera from patients with autoimmune liver disease and rheumatoid arthritis. These data suggest that ANCA of restricted specificities are not specific for inflammatory bowel disease (IBD), but are present in diverse conditions characterized by chronic idiopathie inflammation.
In vitrotreatment of monocytes with 8-methoxypsolaren and ultraviolet A light induces dendritic cells with a tolerogenic phenotype
Authors: Legitimo A , Consolini R , Failli A , Fabiano S , Bencivelli W , Scatena F , Mosca F 
Published: August 2010

SummaryExtracorporeal photopheresis (ECP) has been considered an efficient dendritic cell (DC) therapy, used for treating both T cell malignancy, as well as T cell-mediated diseases. During the ECP procedure leucocytes are exposed to photoactivable agent 8-methoxypsolaren (8-MOP) and ultraviolet (UV) A radiation (PUVA) prior to reinfusion. Despite its clinical efficacy the mechanism of action remains elusive. As it has been reported that ECP might promote the differentiation of monocytes into immature DCs, we investigated the effects of UVA light (2 J/cm2) and 8-MOP (100 ng/ml) on in vitro monocyte-to-DC differentiation from normal donors. DCs were generated from human purified CD14+ cells. Because monocytes are killed by PUVA and taking into account that only 5–10% of circulating mononuclear cells are exposed to PUVA during the ECP procedure, we developed an assay in which 10% of PUVA-treated monocytes were co-cultured with untreated monocytes. We first demonstrate that the presence of 10% apoptotic cells and monocyte activation were not enough to induce monocyte differentiation into DCs. Adding cytokines to our culture system, we obtained immature DCs characterized by significantly higher phagocytic activity and human leucocyte antigen D-related (HLA-DR) expression. These DCs preserved the capacity to be activated by lipopolysaccharide, but showed a reduced capacity to induce allogeneic T cell proliferation when first co-cultured with 10% of PUVA-treated cells. Our experimental design provides a novel insight into the real action of 8-MOP and UVA light on dendritic cell biology, suggesting an additional mechanism by which 8-MOP and UVA light exposure may influence immune responses.
Clonotypic analysis of T cell reconstitution after haematopoietic stem cell transplantation (HSCT) in patients with severe combined immunodeficiency
Authors: Okamoto H , Arii C , Shibata F , Toma T , Wada T , Inoue M , Tone Y , Kasahara Y , Koizumi S , Kamachi Y , Ishida Y , Inagaki J , Kato M , Morio T , Yachie A 
Published: August 2010

Summary
Haematopoietic stem cell transplantation (HSCT) is performed for treatment of a broad spectrum of illnesses. Reconstitution of an intact immune system is crucial after transplantation to avoid infectious complications, and above all, the establishment of T cell receptor (TCR) diversity is the most important goal in the procedure. Until recently, little has been known of the mechanism of T cell reconstitution in the very early period after HSCT. In this study, we analysed TCR repertoires sequentially in four patients with severe combined immunodeficiency (SCID) before and after HSCT. In all patients, the TCR repertoires were extremely abnormal before HSCT, whereas after transplantation there was progressive improvement in TCR diversity, based on analysis of the TCR Vβ repertoire and CDR3 size distributions. Somewhat unexpectedly, there was a significant but transient expansion of TCR diversity 1 month after transplantation in all cases. Clonotypic analysis of TCRs performed in one case showed that many T cell clones shared identical CDR3 sequences at 1 month and that the shared fraction decreased progressively. These results indicate that early expansion of TCR diversity may reflect transient expansion of pre-existing mature T cells from the donor blood, independent of de novo T cell maturation through the thymus.
Epithelial overexpression of interleukin-32α in inflammatory bowel disease
Authors: Shioya M , Nishida A , Yagi Y , Ogawa A , Tsujikawa T , Kim-Mitsuyama S , Takayanagi A , Shimizu N , Fujiyama Y , Andoh A 
Published: August 2010

Summary
Interleukin (IL)-32 is a recently described proinflammatory cytokine, characterized by induction of nuclear factor (NF)-κB activation. We studied IL-32α expression in the inflamed mucosa of inflammatory bowel disease (IBD). We also investigated mechanisms regulating IL-32α expression. Tissue samples were obtained endoscopically or surgically from patients with ulcerative colitis (UC) (n = 10), Crohn's disease (CD) (n = 10), ischaemic colitis (n = 4) and normal colorectal tissues (n = 10). IL-32α expression was evaluated by standard immunohistochemical procedure. IL-32 mRNA expression was analysed by Northern blot. IL-32α was expressed weakly by colonic epithelial cells from normal individuals and subjects with ischaemic colitis. In the inflamed mucosa of IBD patients, epithelial IL-32α expression was increased markedly. In UC and CD patients, IL-32α expression was enhanced in affected mucosa compared to non-affected mucosa. In intestinal epithelial cell lines, expression of IL-32α mRNA and protein was enhanced by IL-1β, interferon (IFN)-γ and tumour necrosis factor (TNF)-α. A combination of TNF-α plus IFN-γ exerted synergistic effects. IL-32α induction by IL-1β and/or TNF-α was mediated by NF-κB activation. Epithelial IL-32α expression was increased in IBD patients, and in CD patients in particular. IL-32α might be involved in the pathophysiology of IBD as a proinflammatory cytokine and a mediator of innate immune response.
Impairment of circulating myeloid dendritic cells in immunosuppressed liver transplant recipients
Authors: Bosma B M , Metselaar H J , Tra W M W , Mancham S , Kuipers E J , Tilanus H W , Kwekkeboom J 
Published: August 2010

SummaryThe aim of the present study was to elucidate the impact of liver transplantation (LTX) on myeloid dendritic cell (MDC) homeostasis. We observed a threefold reduction of circulating CD1c+ MDC immediately after LTX (n = 16; P &lt; 0·01), and normalization between 3 and 12 months after LTX. This decline was not due to recruitment of MDC into the liver graft, as numbers of MDC in post-LTX liver graft biopsies were not increased compared to pre-LTX biopsies (n = 7). Moreover, no change in chemokine receptor expression on circulating MDC was observed, suggesting that their homing properties were not altered. Normalization of circulating MDC was associated with withdrawal of corticosteroid therapy, and not with changes in calcineurin inhibitor intake, indicating that corticosteroids are responsible for the observed changes in numbers of circulating MDC. During high-dose corticosteroid treatment early after LTX, circulating MDC showed a lowered maturation status with decreased expression of human leucocyte antigen D-related (HLA-DR) and CD86 compared to pre-LTX values (P &lt; 0·01). However, when MDC from blood of LTX recipients were matured ex vivo, they up-regulated HLA-DR and co-stimulatory molecules to a comparable extent as MDC from healthy individuals. In addition, ex vivo matured MDC from both groups had equal allogeneic T cell stimulatory capacity. In conclusion, during the first months after LTX numbers and maturational status of circulating MDC are impaired significantly, probably due to a suppressive effect of corticosteroids on MDC. However, corticosteroid therapy does not imprint MDC with an intrinsic resistance to maturation stimuli.
Antibodies to selected minor target antigens in patients with anti-neutrophil cytoplasmic antibodies (ANCA)
Authors: Talor M V , Stone J H , Stebbing J , Barin J , Rose N R , Burek C L 
Published: August 2010

Summary
In patients with anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis, indirect immunofluorescence (IF) distinguishes between cytoplasmic (C-ANCA) and perinuclear (P-ANCA) neutrophil staining patterns. In patients with primary systemic vasculitis such as Wegener's granulomatosis, microscopic polyangiitis and Churg–Strauss syndrome, these IF staining patterns correspond broadly with antibodies to the two major antigens: the C-ANCA pattern is associated generally with antibodies to serine protease 3 (PR3) and the P-ANCA pattern with antibodies to myeloperoxidase (MPO). However, some sera positive for ANCA by IF are negative for anti-PR3 and anti-MPO antibodies, suggesting the presence of antibodies to minor antigens of PMN granules. We tested sera from a previously well-defined clinical cohort of patients for antibodies to four possible minor antigens: bactericidal permeability increasing protein, elastase, cathepsin G and lactoferrin. IF-positive (+) sera had significantly higher antibody frequencies to the minor antigens than did the IF-negative (–) sera (P &lt; 0·01). Patients with IF+ PR3-MPO- sera showed the most varied reactivity to the minor antigens. Among the IF+ groups, the IF+ PR3+/MPO- sera showed the lowest reactivity to the minor antigens. Patients with well-defined ANCA specificities, e.g. the PR3-ANCA response associated with Wegener's granulomatosis, are less likely than are other patient subsets to have antibodies to minor antigen targets. Autoantibodies to these minor antigens contribute to the overall pattern of ANCA identified by IF and help to explain why the correlation between IF and enzyme immunoassays show discrepancies. While the pathophysiological significance of antibodies to minor target antigens needs further evaluation, they may be markers of inflammation associated with disease processes.
Translational Mini-Review Series on Immunodeficiency:&#x2028;Molecular defects in common variable immunodeficiency
Authors: Bacchelli C , Buckridge S , Thrasher A J , Gaspar H B 
Published: August 2010

Summary
Common variable immunodeficiency (CVID) is a primary immunodeficiency that typically affects adults and is characterized by abnormalities of quantative and qualitative humoral function that are heterogeneous in their immunological profile and clinical manifestations. The recent identification of four monogenic defects that result in the CVID phenotype also demonstrates that the genetic basis of CVID is highly variable. Mutations in the genes encoding the tumour necrosis factor (TNF) superfamily receptors transmembrane activator and calcium-modulating ligand interactor (TACI) and B cell activation factor of the TNF family receptor (BAFF-R), CD19 and the co-stimulatory molecule inducible co-stimulator molecule (ICOS) all lead to CVID and illustrate the complex interplay required to co-ordinate an effective humoral immune response. The molecular mechanisms leading to the immune defect are still not understood clearly and particularly in the case of TACI, where a number of heterozygous mutations have been found in affected individuals, the molecular pathogenesis of disease requires further elucidation. Together these defects account for perhaps 10–15% of all cases of CVID and it is highly likely that further genetic defects will be identified.
A murine model of appendicitis and the impact of inflammation on appendiceal lymphocyte constituents
Authors: Watson Ng W S , Hampartzoumian T , Lloyd A R , Grimm M C 
Published: August 2010

Summary
Data indicate that appendicectomy for intra-abdominal inflammation protects against inflammatory bowel disease (IBD). This suggests an important role for the appendix in mucosal immunity. There is no established model of appendicitis. We therefore developed a murine model of appendicitis and examined the effect of inflammation on appendiceal lymphocyte constituents. The caecal patch of specific pathogen-free (SPF)-Balb/c mice was transformed into an obstructed ‘appendiceal pouch’ by standardized suction and band ligation. Mice were killed and ‘pouches’ removed for histology and phenotypic analysis of leucocytes by flow cytometry. Serum C-reactive protein (CRP) was determined by enzyme-linked immunosorbent assay. All ‘pouches’ developed features resembling human appendicitis – mucosal ulceration, transmural inflammation with neutrophils, lymphocytes and occasional eosinophils, and serositis. These changes were most evident between days 7 and 10. There was significant elevation of serum CRP (8·0 ± 0·3 ng/ml to 40·0 ± 3·1 ng/ml; P &lt; 0·01), indicating systemic inflammation. Following the initial neutrophil-predominant response, there was an increase in CD4+ (15·3% ± 1·2% to 31·0 ± 2·0%; P &lt; 0·01) and CD8+ T lymphocytes (3·7% ± 0·6% to 9·2 ± 0·8%; P &lt; 0·01). CD25+ forkhead box P3 (FoxP3)+ regulatory T lymphocytes were increased by 66% (P &lt; 0·01). Furthermore, significant increases in CD8+ FoxP3+ regulatory T lymphocytes were restricted to younger mice (age &lt; 10 weeks, P &lt; 0·003). This is the first description of a murine model of appendicitis. Inflammation resulted in T lymphocyte accumulation associated with an increase in regulatory T lymphocytes, which might explain the age-dependent protective phenomenon. Further exploration will provide insights into the mechanisms of intestinal immune homeostasis and the immunopathogenesis of IBD.
Anti-tumour necrosis factor-α therapy for severe enteropathy in patients with common variable immunodeficiency (CVID)
Authors: Chua I , Standish R , Lear S , Harbord M , Eren E , Raeiszadeh M , Workman S , Webster D 
Published: August 2010

Summary
We present three common variable immunodeficiency (CVID) patients with severe inflammatory bowel disease of unknown aetiology, resistant to steroid treatment, treated with infliximab. After exclusion of any infection, infliximab was given at a dose of 5 mg/kg every 4 weeks for a 3 month induction followed by every 4–8 weeks depending on clinical response. Two of these patients had predominantly small bowel disease; they both showed clinical response to infliximab with weight gain and improvement of quality of life scores. The third patient had large bowel involvement with profuse watery diarrhea; this patient improved dramatically within 48 hours of having infliximab treatment. All three patients have been maintained on infliximab treatment for between 5 and 53 months (mean 37 months) with no evidence of increased susceptibility to infections in the patients with small bowel disease, although the third patient developed two urinary tract infections and a herpes zoster infection following therapy. This is the first small case series to show that infliximab is a useful addition to current therapy in this rare group of patients with potentially life threatening enteritis.
Antibody responses to deamidated gliadin peptide show high specificity and parallel antibodies to tissue transglutaminase in developing coeliac disease
Authors: Ankelo M , Kleimola V , Simell S , Simell O , Knip M , Jokisalo E , Tarkia M , Westerlund A , He Q , Viander M , Ilonen J , Hinkkanen A E 
Published: August 2010

Summary
Coeliac disease (CD) is an enteropathy induced in genetically susceptible individuals by gluten components, gliadin, hordein and secalin, polypeptides present in cereals such as wheat, barley and rye, respectively. Although the disease starts as intolerance to gliadins, antibodies to tissue transglutaminase (tTG) in the gut epithelium are characteristic of the disease. Whereas serum autoantibodies against tTG (tTGA) are highly specific for CD, antibodies to gliadin are less informative as they can also be detected in other enteropathies, and even in healthy individuals. However, it was shown recently that antibodies to certain gliadin peptides occur with high specificity in CD patient sera. We developed a solid phase lanthanide-based immunofluorometric assay for simultaneous detection of serum IgA and IgG antibodies to a synthetic peptide derived from gamma gliadin of wheat comprising amino acids 86–103. Three glutamine residues of this native 18-mer peptide were replaced by glutamic acids and the peptide was biotinylated. Sera from 87 individuals who had undergone duodenal biopsy and were diagnosed with CD and from 81 healthy individuals were analysed for the presence of both IgA and IgG anti-gliadin peptide antibodies. The performance of the peptide AGA assay was excellent, showing a specificity and sensitivity of 90% and 92% for IgA, and 98% and 75% for IgG, respectively. The corresponding values for conventional anti-gliadin antibody (AGA) enzyme-linked immunosorbent assay (ELISA) tests were 72% specificity and 87% sensitivity for IgA, and 64% specificity and 78% sensitivity for IgG. In a prospective study, almost all the tTGA-positive sera drawn from children who later developed CD were also positive for gliadin peptide antibodies.
The immunodominant T helper 2 (Th2) response elicited in BALB/c mice by theLeishmaniaLiP2a and LiP2b acidic ribosomal proteins cannot be reverted by strong Th1 inducers
Authors: Iborra S , Abánades D R , Parody N , Carrión J , Risueño R M , Pineda M A , Bonay P , Alonso C , Soto M 
Published: August 2010

SummaryThe search for disease-associated T helper 2 (Th2) Leishmania antigens and the induction of a Th1 immune response to them using defined vaccination protocols is a potential strategy to induce protection against Leishmania infection. Leishmania infantum LiP2a and LiP2b acidic ribosomal protein (P proteins) have been described as prominent antigens during human and canine visceral leishmaniasis. In this study we demonstrate that BALB/c mice infected with Leishmania major develop a Th2-like humoral response against Leishmania LiP2a and LiP2b proteins and that the same response is induced in BALB/c mice when the parasite P proteins are immunized as recombinant molecules without adjuvant. The genetic immunization of BALB/c mice with eukaryotic expression plasmids coding for these proteins was unable to redirect the Th2-like response induced by these antigens, and only the co-administration of the recombinant P proteins with CpG oligodeoxynucleotides (CpG ODN) promoted a mixed Th1/Th2 immune response. According to the preponderance of a Th2 or mixed Th1/Th2 responses elicited by the different regimens of immunization tested, no evidence of protection was observed in mice after challenge with L. major. Although alterations of the clinical outcome were not detected in mice presensitized with the P proteins, the enhanced IgG1 and interleukin (IL)-4 response against total Leishmania antigens in these mice may indicate an exacerbation of the disease.