bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monoclonal B‐cell lymphocytosis is closely related to chronic lymphocytic leukaemia and may be better classified as early‐stage CLL
Authors: Kern Wolfgang , Bacher Ulrike , Haferlach Claudia , Dicker Frank , Alpermann Tamara , Schnittger Susanne , Haferlach Torsten 
Published: January 2012

SummaryThe World Health Organization classification uses a cut‐off point of 5·0 × 109/l cells with a chronic lymphocytic leukaemia (CLL)‐phenotype in peripheral blood to discriminate between monoclonal B‐lymphocytosis (MBL) and B‐CLL. This study analysed 298 MBL patients by multi‐parameter flow cytometry, chromosome banding analysis (CBA)/fluorescence in situ hybridization (FISH), and IGHV mutation status and compared them with 356 CLL patients. In MBL, CBA more frequently revealed a normal karyotype and FISH identified less frequently del(6q), del(13q) (as sole alterations), and del(17)(p13). Within the MBL cohort, a shorter time to treatment (TTT) was found for ZAP‐70‐positivity, 14q32/IGH‐translocations (CBA), del(11)(q22·3) (FISH) and unmutated IGHV status. Higher CD38 and ZAP‐70 expression, del(11)(q22·3) (FISH), trisomy 12 (FISH), and 14q32/IGH‐translocations (CBA) were correlated with a shorter TTT in the combined cohort (MBL + CLL); a sole del(13)(q14) (FISH) correlated with longer TTT. Regarding overall survival, unmutated IGHV status and ‘other’ alterations (CBA) had an adverse impact. There was no correlation between the concentration of CLL‐cells and TTT or overall survival. Multivariate analysis confirmed a negative impact on TTT for del(11)(q22·3)/ATM, trisomy 12 (both by FISH), and 14q32/IGH‐translocations by CBA. These data emphasize a close relationship between MBL and CLL regarding clinically relevant parameters and provide no evidence to strictly separate these entities by a distinct threshold of clonal B‐cells.
Induction of GITRL expression in human keratinocytes by Th2 cytokines and TNF‐α: implications for atopic dermatitis
Authors: Byrne A. M. , Goleva E. , Chouiali F. , Kaplan M. H. , Hamid Q. A. , Leung D. Y.M. 
Published: January 2012

SummaryBackgroundGlucocorticoid‐induced TNF receptor‐related protein ligand (GITRL), a ligand for the T cell co‐stimulatory molecule GITR, is expressed by keratinocytes and involved in chemokine production. The expression of GITRL in skin inflammation remains unknown.ObjectivesThis study investigated cytokine regulation of keratinocyte GITRL expression.MethodsGlucocorticoid‐induced TNF receptor expression was evaluated in cytokine‐treated human epidermal keratinocytes (HEK)s, murine PAM 212 cell line, murine and human skin explants by real time PCR, flow cytometry and immunostaining. Functional responses to GITR fusion protein were examined by real time PCR and ELISA. GITRL expression in AD and psoriasis was studied by immunohistochemistry.ResultsSkin biopsies from STAT6VT transgenic mice, which develop spontaneous atopic skin inflammation, were found by immunofluoresence, to have increased keratinocyte GITRL expression. Exposure to Th2 cytokines augmented GITRL mRNA expression in the murine PAM 212 keratinocytic cell line and murine skin explants. In contrast, GITRL mRNA and protein expression was only increased in HEKs and human skin explants in the presence of the combination of TNF‐α and Th2 cytokines. A synergistic effect of Th2 cytokines and GITR fusion protein on production of CCL17, the Th2 chemokine, by murine keratinocytes was demonstrated. Immunohistochemical staining showed that acute AD lesions have increased expression of GITRL compared with normal skin, chronic AD lesions and psoriatic plaques.Conclusions and Clinical RelevanceOur studies demonstrate that GITRL expression is augmented by Th2 cytokines and TNF‐α in keratinocytes. Increased GITRL expression in acute AD skin lesions is shown. This observation suggests a link between cytokine‐regulated keratinocyte GITRL expression and its role in inflammatory responses in AD.
Priority effects among young‐of‐the‐year fish: reduced growth of bluegill sunfish (Lepomis macrochirus) caused by yellow perch (Perca flavescens)?
Authors: KAEMINGK MARK A. , JOLLEY JEFFREY C. , WILLIS DAVID W. , CHIPPS STEVEN R. 
Published: January 2012

Summary1. When available, Daphnia spp. are often preferred by age‐0 yellow perch and bluegill sunfish because of energetic profitability. We hypothesised that predation by age‐0 yellow perch could lead to a midsummer decline (MSD) of Daphnia spp. and that priority effects may favour yellow perch because they hatch before bluegill, allowing them to capitalise on Daphnia spp. prior to bluegill emergence.2. Data were collected from 2004 to 2010 in Pelican Lake, Nebraska, U.S.A. The lake experienced a prolonged MSD in all but 1 year (2005), generally occurring within the first 2 weeks of June except in 2008 and 2010 when it occurred at the end of June. MSD timing is not solely related to seasonal patterns of age‐0 yellow perch consumption. Nevertheless, when Daphnia spp. biomass was low during 2004 and 2006–2010 (<4 mg wet weight L−1), predation by age‐0 yellow perch seems to have suppressed Daphnia spp. biomass (i.e. <1.0 mg wet weight L−1). The exception was 2005 when age‐0 yellow perch were absent.3. Growth of age‐0 bluegill was significantly faster in 2005, when Daphnia spp. were available in greater densities (>4 mg wet weight L−1) compared with the other years (<0.2 mg wet weight L−1).4. We conclude that age‐0 yellow perch are capable of reducing Daphnia biomass prior to the arrival of age‐0 bluegill, ultimately slowing bluegill growth. Thus, priority effects favour age‐0 yellow perch when competing with age‐0 bluegill for Daphnia. However, these effects may be minimised if there is a shorter time between hatching of the two species, higher Daphnia spp. densities or lower age‐0 yellow perch densities.
Tooth bioengineering leads the next generation of dentistry
Authors: WANG YING , PRESTON BRIAN , GUAN GUOQIANG 
Published: January 2012

International Journal of Paediatric Dentistry 2012; 22: 406–418Background.  As a result of numerous rapid and exciting developments in tissue engineering technology, scientists are able to regenerate a fully functional tooth in animal models, from a bioengineered tooth germ. Advances in technology, together with our understanding of the mechanisms of tooth development and studies dealing with dentally derived stem cells, have led to significant progress in the field of tooth regeneration.Aim and design.  This review focuses on some of the recent advances in tooth bioengineering technology, the signalling pathways in tooth development, and in dental stem cell biology. These factors are highlighted in respect of our current knowledge of tooth regeneration.Results and conclusion.  An understanding of these new approaches in tooth regeneration should help to prepare clinicians to use this new and somewhat revolutionary therapy while also enabling them to partake in future clinical trials. Tooth bioengineering promises to be at the forefront of the next generation of dental treatments.
Consequences of frugivore‐mediated seed dispersal for the spatial and genetic structures of a neotropical palm
Authors: CHOO J. , JUENGER T. E. , SIMPSON B. B. 
Published: January 2012

AbstractThe idiosyncratic behaviours of seed dispersers are important contributors to plant spatial associations and genetic structures. In this study, we used a combination of field, molecular and spatial studies to examine the connections between seed dispersal and the spatial and genetic structures of a dominant neotropical palm Attalea phalerata. Field observation and genetic parentage analysis both indicated that the majority of A. phalerata seeds were dispersed locally over short distances (<30 m from the maternal tree). Spatial and genetic structures between adults and seedlings were consistent with localized and short‐distance seed dispersal. Dispersal contributed to spatial associations among maternal sibling seedlings and strong spatial and genetic structures in both seedlings dispersed near (<10 m) and away (>10 m) from maternal palms. Seedlings were also spatially aggregated with juveniles. These patterns are probably associated with the dispersal of seeds by rodents and the survival of recruits at specific microsites or neighbourhoods over successive fruiting periods. Our cross‐cohort analyses found palms in older cohorts and cohort pairs were associated with a lower proportion of offspring and sibling neighbours and exhibited weaker spatial and genetic structures. Such patterns are consistent with increased distance‐ and density‐dependent mortality over time among palms dispersed near maternal palms or siblings. The integrative approaches used for this study allowed us to infer the importance of seed dispersal activities in maintaining the aggregated distribution and significant genetic structures among A. phalerata palms. We further conclude that distance‐ and density‐dependent mortality is a key postdispersal process regulating this palm population.
Temporal trends in sudden infant death syndrome in Canada from 1991 to 2005: contribution of changes in cause of death assignment practices and in maternal and infant characteristics
Authors: Gilbert Nicolas L. , Fell Deshayne B. , Joseph K. S. , Liu Shiliang , León Juan Andrés , Sauve Reg ,   for the Fetal and Infant Health Study Group of the Canadian Perinatal Surveillance System
Published: January 2012

SummaryGilbert NL, Fell DB, Joseph KS, Liu S, León JA, Sauve R, for the Fetal and Infant Health Study Group of the Canadian Perinatal Surveillance System. Temporal trends in sudden infant death syndrome in Canada from 1991 to 2005: contribution of changes in cause of death assignment practices and in maternal and infant characteristics. Paediatric and Perinatal Epidemiology 2012; 26: 124–130.The rate of sudden infant death syndrome (SIDS) declined significantly in Canada and the US between the late 1980s and the early 2000s. In the US, this decline was shown to be due in part to a shift in diagnosis, as deaths from accidental suffocation and strangulation in bed and from other ill‐defined and unspecified cause increased concurrently. This study was undertaken to determine whether there was such a shift in diagnosis from SIDS to other causes of death in Canada, and to quantify the true temporal decrease in SIDS. Cause‐specific infant death rates were compared across three periods: 1991–95, 1996–2000 and 2001–05 using the Canadian linked livebirth‐infant death file. The temporal decline in SIDS was estimated after adjustment for maternal and infant characteristics such as maternal age and small‐for‐gestational age using logistic regression. Deaths from SIDS decreased from 78.4 [95% confidence interval (CI) 73.4, 83.4] per 100 000 livebirths in 1991–95, to 48.5 [95% CI 44.3, 52.7] in 1996–2000 and to 34.6 [95% CI 31.0, 38.3] in 2001–05. Mortality rates from other ill‐defined and unspecified causes and accidental suffocation and strangulation in bed remained stable. The temporal decline in SIDS between 1991–95 and 2001–05 did not change substantially after adjustment for maternal and infant factors. It is unlikely that the temporal decline of SIDS in Canada was due to changes in cause‐of‐death assignment practices or in maternal and infant characteristics.
Trichinella spiralis‐secreted products modulate DC functionality and expand regulatory T cells in vitro
Authors: ARANZAMENDI C. , FRANSEN F. , LANGELAAR M. , FRANSSEN F. , Van Der LEY P. , Van PUTTEN J.P.M. , RUTTEN V. , PINELLI E. 
Published: January 2012

SummaryHelminths and their products can suppress the host immune response which may benefit parasite survival. Trichinella spiralis can establish chronic infections in a wide range of mammalian hosts including humans and mice. Here, we aim at studying the effect of T. spiralis muscle larvae excretory/secretory products (TspES) on the functionality of DC and T cell activation. We found that TspES suppress in vitro DC maturation induced by both S‐ and R‐form lipopolysaccharide(LPS) from enterobacteria. Using different toll‐like receptor (TLR) agonists, we show that the suppressive effect of TspES on DC maturation is restricted to TLR4. These helminth products also interfere with the expression of several genes related to the TLR‐mediated signal transduction pathways. To investigate the effect of TspES on T cell activation, we used splenocytes derived from OVA‐TCR transgenic D011.10 that were incubated with OVA and TspES‐pulsed DC. Results indicate that the presence of TspES resulted in the expansion of CD4+ CD25+ Foxp3+ T cells. These regulatory T (Treg) cells were shown to have suppressive activity and to produce TGF‐β. Together these results suggest that T. spiralis secretion products can suppress DC maturation and induce the expansion of functional Treg cells in vitro.
Excretory–secretory products of Giardia lamblia induce interleukin‐8 production in human colonic cells via activation of p38, ERK1/2, NF‐κB and AP‐1
Authors: LEE H.‐Y. , HYUNG S. , LEE N. Y. , YONG T.‐S. , HAN S.‐H. , PARK S.‐J. 
Published: January 2012

SummaryGiardia lamblia, a pathogen causing diarrhoeal outbreaks, is interesting how it triggers immune response in the human epithelial cells. This study defined the crucial roles of signalling components involved in G. lamblia‐induced cytokine production in human epithelial cells. Incubation of the gastrointestinal cell line HT‐29 with G. lamblia GS trophozoites triggered production of interleukin (IL)‐1β, IL‐8 and tumour necrosis factor (TNF)‐α. IL‐8 production was not significantly decreased by physically separating the HT‐29 cells and G. lamblia GS trophozoites. Indeed, treatment of HT‐29 with G. lamblia excretory–secretory products (ESP) induced IL‐8 production. Electrophoretic mobility gel shift and transfection assays using mutagenized IL‐8 promoter reporter plasmids indicated that IL‐8 production by G. lamblia ESP occurs through activation of two transcriptional factors, nuclear factor kappaB (NF‐κB) and activator protein 1 (AP‐1) in HT‐29 cells. In addition, activation of two mitogen‐activated protein kinases (MAPKs), p38 and ERK1/2, was also detected in the HT‐29 cells stimulated with G. lamblia ESP. Selective inhibition of these MAPKs resulted in decreased production of ESP‐induced IL‐8. These results indicate that activation of p38, ERK1/2 MAPK, NF‐κB and AP‐1 comprises the signalling pathway responsible for IL‐8 production by G. lamblia ESP.
Increased levels of angiopoietins 1 and 2 in sputum supernatant in severe refractory asthma
Authors: Tseliou E. , Bakakos P. , Kostikas K. , Hillas G. , Mantzouranis K. , Emmanouil P. , Simoes D. , Alchanatis M. , Papiris S. , Loukides S. 
Published: January 2012

AbstractBackground:Airway and vascular remodeling may play a prominent role in the clinical severity of severe refractory asthma (SRA). Angiopoietin‐1 (Ang‐1) is an essential mediator of angiogenesis by establishing vascular integrity, whereas angiopoietin‐2 (Ang‐2) acts as its natural inhibitor.Objective:We aimed to determine the levels of angiopoietins in sputum supernatants of patients with SRA and to investigate the possible associations with mediators and cells involved in both the inflammatory and the vascular remodeling processes.Methods:Thirty‐eight patients with SRA, 35 patients with moderate asthma, and 20 healthy subjects were studied. All participants underwent lung function tests, bronchial hyperresponsiveness assessment and sputum induction for cell count identification and Ang‐1, Ang‐2, VEGF, TGF‐β1, Cys‐LTs, MMP‐2, IL‐13, ECP, and IL‐8 measurement in supernatants. Airway vascular permeability (AVP) index was also assessed.Results:Ang‐1 (ng/ml) and Ang‐2 (pg/ml) levels were significantly elevated in patients with SRA compared with patients with moderate asthma and control subjects [median, interquartile ranges: 30 (17–39) vs 7.5 (5–11) vs 4.7 (3.8–5.9) respectively, P < 0.001; and 506 (400–700) vs 190 (146–236) vs 96 (89–120) respectively, P < 0.001]. Regression analysis showed a significant positive association between Ang‐2 and AVP index, MMP‐2, Ang‐1, and VEGF in SRA. A weak association was also observed between Ang‐1 and sputum eosinophils% in SRA.Conclusion:Our results indicate that both angiopoietins levels are higher in SRA compared with moderate asthma and healthy subjects. In SRA, Ang‐2 is associated with mediators involved in both the inflammatory and the vascular remodeling processes.
Extracellular matrix in airway smooth muscle is associated with dynamics of airway function in asthma
Authors: Yick C. Y. , Ferreira D. S. , Annoni R. , von der Thüsen J. H. , Kunst P. W. , Bel E. H. , Lutter R. , Mauad T. , Sterk P. J. 
Published: January 2012

AbstractBackgroundAltered deposition of extracellular matrix (ECM) in the airway smooth muscle (ASM) layer as observed in asthma may influence ASM mechanical properties. We hypothesized that ECM in ASM is associated with airway function in asthma. First, we investigated the difference in ECM expression in ASM between asthma and controls. Second, we examined whether ECM expression is associated with bronchoconstriction and bronchodilation in vivo.MethodsOur cross‐sectional study comprised 19 atopic mild asthma patients, 15 atopic and 12 nonatopic healthy subjects. Spirometry, methacholine responsiveness, deep‐breath‐induced bronchodilation (ΔRrs) and bronchoscopy with endobronchial biopsies were performed. Positive staining of elastin, collagen I, III and IV, decorin, versican, fibronectin, laminin and tenascin in ASM was quantified as fractional area and mean density. Data were analysed using Pearson's or Spearman's correlation coefficient.ResultsExtracellular matrix expression in ASM was not different between asthma and controls. In asthmatics, fractional area and mean density of collagen I and III were correlated with methacholine dose–response slope and ΔRrs, respectively (r = 0.71, P < 0.01; r = 0.60, P = 0.02). Furthermore, ASM collagen III and laminin in asthma were correlated with FEV1 reversibility (r = −0.65, P = 0.01; r = −0.54, P = 0.04).ConclusionIn asthma, ECM in ASM is related to the dynamics of airway function in the absence of differences in ECM expression between asthma and controls. This indicates that the ASM layer in its full composition is a major structural component in determining variable airways obstruction in asthma.
Prenatal allergen exposures prevent allergen‐induced sensitization and airway inflammation in young mice
Authors: Gerhold K. , Avagyan A. , Reichert E. , Seib C. , Van D. V. , Luger E. O. , Hutloff A. , Hamelmann E. 
Published: January 2012

AbstractBackground:Immune‐modulation such as tolerance induction appears to be an upcoming concept to prevent development of atopic diseases. Pregnancy might present a critical period for preventing allergic sensitization of the progeny. We investigated the effect of maternal allergen exposures during pregnancy on allergen‐induced sensitization and airway inflammation in the offspring in a murine model.Methods:BALB/c mice were exposed to aerosolized ovalbumin (OVA) three times per week from day 7 of pregnancy until delivery (day 0). Offspring were systemically sensitized by six intraperitoneal injections with OVA between postnatal days 21 and 35, prior to airway allergen challenges on days 48, 49, and 50. Analyses were performed on day 52. To examine long‐lasting effects of maternal OVA exposures some offspring were sensitized between days 115 and 129; analyses took place on day 147.Results:Compared to maternal placebo exposures, maternal OVA exposures suppressed OVA‐specific IgE serum levels and inhibited development of allergen‐induced airway inflammation in the OVA‐sensitized offspring on both days 52 and 147. This protective effect was associated with a shift from a predominant Th2 immune response toward a predominant production of the cytokines IFN‐γ and IL‐10. Further, maternal OVA exposures were associated with development of CD25+Foxp3+ regulatory T cells (Tregs) in the OVA‐sensitized offspring. Depletion of Tregs or neutralization of IL‐10 prior to allergen sensitization re‐established OVA‐induced sensitization and eosinophilic airway inflammation in the OVA‐sensitized offspring.Conclusions:In our model, maternal allergen exposures during pregnancy prevented later allergen‐mediated sensitization and airway inflammation by allergen‐specific tolerance induction in the offspring.
Negative impact of occupational exposure on surgical outcome in patients with rhinosinusitis
Authors: Hox V. , Delrue S. , Scheers H. , Adams E. , Keirsbilck S. , Jorissen M. , Hoet P. H. , Vanoirbeek J. A. , Nemery B. , Hellings P. W. 
Published: January 2012

AbstractBackgroundChronic rhinosinusitis (CRS) is a frequent condition that is treated by functional endoscopic sinus surgery (FESS) when medical treatment fails. Endogenous as well as exogenous factors may be responsible for persisting symptoms after FESS. The role of occupational exposures on success of FESS has never been investigated.MethodsIn this case–control study, we tested the hypothesis that the outcome of FESS procedures is related to exposures at work. Questionnaires were sent to 890 patients who had undergone one or more FESS procedures and to 182 controls. Three independent experts assessed blindly the reported work exposures to inhaled agents. The relationship between exposure and the number of FESS procedures was analyzed.ResultsRelevant occupational exposure was reported by 25% of all responding patients undergoing FESS (n = 467) and 12% of controls (n = 69). The prevalence of occupational exposures increased linearly with the number of FESS procedures from 21% in those who had one FESS to 44% in those who had four or more FESS (χ2 = 12.74, P < 0.001). Logistic regression analysis with adjustments for potential confounders, including smoking, atopy, and asthma, confirmed that the odds ratio (OR) for reporting occupational exposures was significantly higher in those needing more than one FESS (OR = 1.64) or more than two FESS (OR = 1.97). These results were mainly driven by exposure to low molecular weight agents.ConclusionExposure at work appears to be a risk factor for the occurrence of CRS and for its recurrence or persistence, as evidenced by the need for revision surgery.