bluuebunny/crossref_metadata_2025_split huggingface dataset:
The use of herbal remedies by adolescents with eating disorders
Authors: Trigazis Leo , Tennankore Dhenuka , Vohra Sunita , Katzman Debra K. 
Published: February 2004

AbstractObjectiveTo determine the frequency and type of herbal remedies and the reasons for herbal remedy use by adolescents with eating disorders.MethodsForty‐six female adolescent females (age range, 10–17 years; mean age, 15 ± 1.3 years) in a tertiary‐care pediatric eating disorder treatment center from May 1998 to July 2000 volunteered for this cross‐sectional study. They met the criteria for anorexia nervosa, bulimia nervosa, or eating disorder not otherwise specified. Participants completed a 92‐item self‐administered questionnaire. We summarized information on demographics, use of herbal remedies, knowledge of safety issues of herbal remedies, and trust in the health care system.ResultsOf these 46 subjects, 17 (37%) used herbal remedies. Of these 17 subjects, 35% (6 of 17) used herbal remedies to decrease their appetites and to induce vomiting, 41% (7 of 17) knew nothing about herbal remedies, despite their use of these products, and 24% (4 of 17) reported that their physicians asked whether they used herbal remedies. The participants did not use herbal remedies because of their dissatisfaction with allopathic medicine.DiscussionAdolescents with eating disorders frequently used herbal remedies for both weight control and non—weight control purposes. They did not regularly inform their physicians about their use of herbal remedies and physicians did not regularly inform their patients about this use. The generally high prevalence of herbal remedy use in this population suggests that health care providers need to be knowledgeable and should enquire about patients' use of these products. The perceived benefits, adverse effects, and herb‐drug interactions of self‐prescribed herbal remedies consumed by adolescents with eating disorders are unknown and further research is needed. © 2004 by Wiley Periodicals, Inc. Int J Eat Disord 35: 223–228, 2004.
Persistence of nutritional deficiencies after short‐term weight recovery in adolescents with anorexia nervosa
Authors: Castro Josefina , Deulofeu Ramón , Gila Araceli , Puig Josefina , Toro Josep 
Published: February 2004

AbstractObjectivesTo study nutritional abnormalities in adolescent anorexia nervosa and to establish whether certain abnormalities persist after short‐term refeeding.MethodSixty‐one patients (10–19 years old) admitted to a reference unit for eating disorders between 1999 and 2000 with a diagnosis of anorexia nervosa were evaluated at admission and at discharge. A range of biochemical, nutritional, and hormonal parameters were determined.ResultsAt admission, no protein or lipid deficiencies were found, although many patients presented with hormonal abnormalities and red blood cell folate and zinc deficiencies. Hormonal abnormalities reverted significantly (p < .000) after renutrition. There were decreases in erythrocytes and in levels of hemoglobin (p < .000) and folic acid (p < .05). Red blood cell folate and zinc increased but did not reach normal levels.ConclusionsIn a large proportion of adolescent anorexic patients, supplementation of folic acid and zinc is recommended although protein or hormonal replacement does not seem to be necessary. © 2004 by Wiley Periodicals, Inc. Int J Eat Disord 35: 169–178, 2004.
Undue influence of weight on self‐evaluation: A population‐based twin study of gender differences
Authors: Reichborn‐Kjennerud Ted , Bulik Cynthia M. , Kendler Kenneth S. , Roysamb Espen , Tambs Kristian , Torgersen Svenn , Harris Jennifer R. 
Published: February 2004

AbstractObjectiveTo explore the extent to which genetic and environmental factors contribute to liability to placing undue importance on weight as an indicator of self‐evaluation and to determine whether differences exist across genders in the nature and magnitude of these effects.MethodSelf‐report data were collected on 8,045 same‐sex and opposite‐sex twins, aged 18–31 years, from a population‐based registry of Norwegian twins. Structural equation modeling was utilized to estimate the relative contribution of genetic and environmental factors to liability for undue influence of weight on self‐evaluation, allowing for gender‐specific effects.ResultsIndividual variation in undue influence of weight on self‐evaluation was best explained by shared and individual environmental influences. No significant gender differences were found. Shared environmental factors accounted for 31% of the variance.DiscussionThese results raise the possibility that there may be distinct sources of familial resemblance for different symptoms of bulimia nervosa as codified in the 4th ed. of the Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association, 1994). © 2004 by Wiley Periodicals, Inc. Int J Eat Disord 35: 123–132, 2004.
The cost‐effectiveness of anorexia nervosa treatment
Authors: Crow Scott J. , Nyman John A. 
Published: February 2004

AbstractObjectiveAnorexia nervosa (AN) is an expensive‐to‐treat illness with a high mortality rate. Some health care systems have limited the amount of treatment provided for AN despite the lack of clearly documented efficacy for these limited‐intensity approaches. One method that can inform decisions about AN treatment is cost‐effectiveness analysis.MethodCost‐modeling analysis was used to estimate the incremental cost‐effectiveness of AN treatment. Modeling was chosen given the lack of primary data on costs and outcomes in AN treatment. Data for age of onset, life expectancy, and disease‐associated mortality were taken from the literature. The costs of treatment used in the analysis were those in use at the University of Minnesota.ResultsAssuming an approach consisting of inpatient weight restoration, followed by treatment of gradually diminishing intensity (partial hospitalization, then outpatient psychotherapy plus medication management), incremental cost‐effectiveness ratios were calculated and compared with a limited intensity, “usual care” model. These assumptions yielded a cost per year of life saved of $30,180.DiscussionRelative to many other medical interventions, the comprehensive treatment of AN appears to be quite cost‐effective in terms of cost per year of life saved. Such data may have an impact on payer decisions and underscore the serious nature of AN. © 2004 by Wiley Periodicals, Inc. Int J Eat Disord 35: 155–160, 2004.
Differential chemokine activation of CC chemokine receptor 1‐regulated pathways: ligand selective activation of Gα 14‐coupled pathways
Authors: Tian Yaji , New David C. , Yung Lisa Y. , Allen Rodger A. , Slocombe Patrick M. , Twomey Breda M. , Lee Maggie M. K. , Wong Yung H. 
Published: February 2004

AbstractChemokines regulate the chemotaxis, development, and differentiation of many cell types enabling the regulation of routine immunosurveillance and immunological adaptation. CC chemokine receptor 1 (CCR1) is the target of 11 chemokines. This promiscuity of receptor‐ligand interactions and the potential for functional redundancy has led us to investigate the selective activation of CCR1‐coupled pathways by known CCR1 agonists. Chemokines leukotactin‐1, macrophage inflammatory protein (MIP)‐1α, monocyte chemotactic peptide (MCP)‐3, RANTES, and MIP‐1δ all inhibited adenylyl cyclase activity in cells transiently transfected with CCR1. In contrast, only MIP‐1δ was unable to signal via G14‐, G16‐ or chimeric 16z44‐coupled pathways. In a stable cell line expressing CCR1 and Gα14, all of these five chemokines along with hemofiltrate CC chemokine (HCC)‐1 and myeloid progenitor inhibitory factor (MPIF)‐1 were able to stimulate Gi/o‐coupled pathways, but MIP‐1δ, HCC‐1 and MPIF‐1 were unable to activate G14‐mediated stimulation of phospholipase Cβ activity. In addition, MIP‐1δ was unable to promote the phosphorylation of extracellular signal‐regulated kinase and c‐Jun N‐terminal kinase. This suggests that different chemokines are able to selectively activate CCR1‐coupled pathways, probably because of differentintrinsic ligand efficacies. CCR1 and Gα14 or Gα16 are co‐expressed in several cell types and we hypothesize that selective activation of chemokine receptors provides a mechanism by which chemokines are able to fine‐tune intracellular signaling pathways.
Expression and function of 4‐1BB during CD4 versus CD8 T cell responses in vivo
Authors: Dawicki Wojciech , Watts Tania H. 
Published: February 2004

Abstract4‐1BBL–/– mice have a defect in recall CD8+ T cell responses to viruses, whereas CD4+ T cell responses to virus are unimpaired in these mice. In contrast, both CD4+ and CD8+ T cells respond to 4‐1BB ligand (4‐1BBL) in vitro. To clarify the role of 4‐1BB/4‐1BBL in CD4+ versus CD8+ T cell responses in vivo, wecompared CD4 (OT‐II) and CD8 (OT‐I) TCR transgenic T cells responding to the same antigen in an in vivo adoptive transfer model in 4‐1BBL+/+ versus 4‐1BBL–/– mice. Duringprimary and secondary responses, expression of 4‐1BB on in vivo‐activated TCR transgenic T cells was earlier and more transient than previously observed in vitro, correlating withexpression of the early activation antigen CD69 and preceding the transition to the CD44hi state. Although 4‐1BB is expressed early in the primary response, there was no effect of 4‐1BBL deficiency on initial CD8 T cell expansion and only a minor effect on initial CD4 T cell expansion. The major effect of 4‐1BB/4‐1BBL interaction is on the T cell recall response. This is due to effects of 4‐1BBL on maintenance of T cell numbers at the end of the primary response with additional effects of 4‐1BBL on secondary expansion of T cells.
The human antibody response to pneumococcal capsular polysaccharides is dependent on the CD40‐CD40 ligand interaction
Authors: Jeurissen Axel , Wuyts Greet , Kasran Ahmad , Ramdien‐Murli Seema , Blanckaert Norbert , Boon Louis , Ceuppens Jan L. , Bossuyt Xavier 
Published: February 2004

AbstractProtection against infections with Streptococcus pneumoniae is mediated by antibodies against the capsular polysaccharides (caps‐PS). Here we show that in in vitro experiments CD4+ T lymphocytes stimulate and CD8+ T lymphocytes inhibit the human anti‐caps‐PS antibody response. Using antagonistic anti‐CD40 and antagonistic anti‐CD40 ligand (CD40L) monoclonal antibodies, we showed that the CD4+ T lymphocyte‐mediated stimulation is dependent on the CD40‐CD40L interaction. The role of CD40L was further illustrated by the observation that CD4+ T lymphocytes obtained from a patient with hyper‐IgM syndrome were unable to enhance the immune response to caps‐PS. Furthermore, CD4+ T lymphocytes from cord blood, which did not express CD40L in response to stimulation with caps‐PS, failed to stimulate the antibody response of adult B lymphocytes to caps‐PS.
These in vitro findings were confirmed by in vivo experiments in which SCID/SCID mice were reconstituted with human mononuclear cells. Furthermore, we showed that caps‐PS induce production of IL‐4, IL‐6, IL‐10, and IFN‐γ, and that thisenhanced production was inhibited by blocking the CD40‐CD40L interaction. This is the first demonstration that the human immune response to caps‐PS, which is markedly regulated by T lymphocytes, is dependent on the CD40‐CD40L interaction.
Two waves of antigen‐containing dendritic cells in vivo in experimental Leishmania major infection
Authors: Misslitz Ana Clara , Bonhagen Kerstin , Harbecke Dorothee , Lippuner Christoph , Kamradt Thomas , Aebischer Toni 
Published: February 2004

AbstractDendritic cells (DC) can induce Th1 cell differentiation by producing IL‐12. In experimental infection with Leishmania major, DC could differently respond to infection and induce Th1 cells in C57BL/6 but not BALB/c mice, and thus determine the resistance or susceptibility of these mice. We characterized L. major antigen‐containing DC in vivo in draining lymph nodes of both strains. Conventional experimental infection is shown to result in two waves of these DC and our data argue against a relevant genetic difference in the DC initiating the anti‐parasite Th cell response in these mice. In both strains the first wave of DC presented L. major antigens but was not infected, produced IL‐12 but induced disease‐mediating Th2 cells upon adoptive transfer. In contrast to current belief, this response was therefore not initiated by infected DC, which were only detected in the second wave. The kinetics of the two waves suggests that DC turnoverhas an important impact on antigen presentation during infections with complex pathogens.
Regulation of human IL‐18 gene expression: interaction of PU.1 with GC‐box binding protein is involved in human IL‐18 expression in myeloid cells
Authors: Koyama Noriko , Hoelzer Dieter , Ottmann Oliver G. 
Published: February 2004

AbstractInterleukin‐18 (IL‐18) is a pro‐inflammatory cytokine which participates in host defense against a variety of infections as well as in chronic inflammation including autoimmune diseases. However, little is known about human IL‐18 regulation at the gene level. We have previously demonstrated that sodium butyrate, a bacterial fermentation product, induces IL‐18 production via the proximal region of the promoter. In this study we investigated the molecular mechanisms for basal and sodium butyrate‐induced expression of IL‐18 in human myeloid cells. Two regulatory regions, a consensus binding site for PU.1 and a GC‐rich region, are required for basal IL‐18 promoter activity in human myeloid cells. PU.1 bound to the PU.1 consensus binding site in electrophoretic mobility shift assays, and overexpression of PU.1 led to activation of the IL‐18 promoter through this site. Mutation analysis revealed that the GC‐rich region, but not PU.1 site, participates in sodium butyrate‐induced transactivation. Furthermore, DNA pull‐down experiments and the critical spacing of the two binding sites suggest that formation of a protein complex involving both cis elements and the respective binding proteins might be crucial for human IL‐18 expression.
IgD+IgM– B cells mount immune responses that exhibit altered antibody repertoire
Authors: Han Shuhua , Zhang Xuejun , Xu Renling , Finkelman Fred D. , Brombacher Frank , Zheng Biao 
Published: February 2004

AbstractIgM and IgD expression during B cell development and differentiation is strictly and developmentally controlled. Although studies have suggested subtle differences in B cell activation, tolerance, and affinity maturation when antigens ligate cell membrane IgM or IgD, the mechanisms that may explain these differences remain unknown and no drastic differences in immune responses have been reported in mice whose B cells selectively lack IgM or IgD. We now show that the antibody repertoire in IgM–/– mice is dramatically altered during the primary response to phosphorylcholine.In IgM–/– mice, B cells that are activated and differentiate into antibody‐forming cells and germinal center B cells express VH genes other than the T15 genes that dominate in wild‐type mice. The kinetics of the antigen‐specific IgD primary antibody response in IgM–/– mice appears similar to that of IgG, but not to that of IgM in wild‐type mice. Thus, our studies demonstrate that differences in the roles played by IgM and IgD in regulating the responsiveness and differentiation of B lymphocytes can have major biological consequences during adaptive immune responses.
NKp46 defines a subset of bovine leukocytes with natural killer cell characteristics
Authors: Storset Anne K. , Kulberg Siri , Berg Ingvild , Boysen Preben , Hope Jayne C. , Dissen Erik 
Published: February 2004

AbstractNatural killer (NK) cells have not previously been precisely identified or characterized in cattle or any other ruminant species. We have generated a monoclonal antibody against bovine NKp46, which is expressed exclusively by NK cells in man. NKp46+ cells comprised 1–10% of blood mononuclear cells in cattle, and did not stain with antibodies against CD3, CD4, TCR1, B cell or granulocyte markers. The majority of the NKp46+ cells expressed CD2, and a variable fraction also expressed CD8. The tissue distribution of NKp46+ cells in cattle was compatible with the tissue distribution of NK cells in other species. Bovine NKp46+ cells had typical, large granular lymphocyte morphology, and proliferated vigorously in response to bovine IL‐2 for a limited number of cell divisions. IL‐2‐activated NKp46+ cells killed the bovine kidney cell line MDBK. This cytotoxicity was inhibited by preincubation with antibody against NKp46. In a redirected lysis assay, IL‐2‐activated NKp46+ cells killed the FcγR+ target cell line P815 after preincubation with antibody against NKp46. Together, these data indicate that bovine NKp46 is anactivating receptor and demonstrate the existence of a subset of leukocytes in cattle that, in terms of surface markers, morphology and function, represent NK cells.
Generation of Vα14 NKT cells in vitro from hematopoietic precursors residing in bone marrow and peripheral blood
Authors: Shimamura Michio , Kobayashi Kumi , Watanabe Hiroko , Huang Yi‐Ying , Okamoto Naoki , Kanie Osamu , Goji Hiroshi , Kobayashi Masumi 
Published: February 2004

AbstractWe previously reported the generation of Vα14 invariant TCR+ (Vα14i) NK1.1+ natural killer T (NKT) cells in the cytokine‐activated suspension culture of murine fetal liver cells. In this study, we attempted to apply this finding to the induction of Vα14i NKT cell differentiation in the culture of hematopoietic precursors residing in bone marrow or peripheralblood. Preferential generation of NKT cells was found in the culture of Thy‐1+‐depleted bone marrow cells in the presence of culture supernatant from Con A‐stimulated spleen T cells and a combination of recombinant IL‐3, IL‐4, IL‐7 and GM‐CSF. NKT cell development from peripheral blood hematopoietic precursors was induced when they were cultured on stromal cell monolayers prepared from Thy‐1+‐depleted bone marrow or fetal liver cells, suggesting that certain environments derived from hematopoietic organs are required for the induction of NKT cells from precursors in vitro. A significant fraction of NKT cells generated in the culture were positive for staining with CD1–α‐galactosylceramide tetramer, indicating that Vα14i NKT cells were the major subset among the NKT cells. The present methods for obtaining NKT cells in the culture of bone marrow or peripheral blood cells are applicable to the treatment of patients suffering from diseases with numerical and functional disorders of NKT cells.
Chemokine production during hypersensitivity pneumonitis
Authors: Nance Stephanie , Cross Richard , Fitzpatrick Elizabeth 
Published: February 2004

AbstractHypersensitivity pneumonitis (HP) is an interstitial lung disease that develops following repeated exposure to inhaled particulate antigens. Individuals with HP develop lymphocytic alveolitis,granuloma formation, and fibrosis. HP is categorized as a Th1 disease, and granuloma formation is dependent on T cells and the Th1 cytokine IFN‐γ. We therefore hypothesized that the IFN‐γ‐inducible chemokines IP‐10, Mig, and I‐TAC, which are frequently associated with Th1 diseases, would play an important role in the pathogenesis of disease. We analyzed the expression of multiple chemokines in the lungs of wild‐type (WT) and IFN‐γ‐knockout (GKO) mice exposed to the particulate antigen Saccharopolyspora rectivirgula (SR). Our results demonstrate the production of IP‐10, Mig, and I‐TAC in WT mice during the development of HP, whereas GKO mice have reduced levels of IP‐10 and no Mig or I‐TAC mRNA in the lungs in response to SR exposure. The production of these chemokines is associated with an influx of CXCR3+/CD4+ T cells into lungs of WT mice, which is reduced in GKO mice. These results suggest that IFN‐γ mediates the recruitment of CXCR3+/CD4+ T cells into the lung via production of the chemokines IP‐10, Mig, and I‐TAC, resulting in granuloma formation.
Natural killer cell receptors in the horse: evidence for the existence of multiple transcribed LY49 genes
Authors: Takahashi Tomoko , Yawata Makoto , Raudsepp Terje , Lear Teri L. , Chowdhary Bhanu P. , Antczak Douglas F. , Kasahara Masanori 
Published: February 2004

AbstractIn rodents, the Ly49 family encodes natural killer (NK) receptors interacting with classical MHC class I molecules, whereas the corresponding receptors in primates are members of the killer cell immunoglobulin‐like receptor (KIR) family. Recent evidence indicates that the cattle, domestic cat, dog, and pig have a single LY49 and multiple KIR genes, suggesting that predominant NK receptors in most non‐rodent mammals might be KIR. Here, we show that the horse has at least six LY49 genes, five with an immunoreceptor tyrosine‐based inhibition motif (ITIM) and one with arginine in the transmembrane region. Interestingly, none of the horse KIR‐like cDNA clones isolated by library screening encoded molecules likely to function asNK receptors; four types of clones were KIR‐Ig‐like transcript (KIR‐ILT) hybrids and contained premature stop codons and/or frameshift mutations, and two putative allelic sequences predicting KIR3DL molecules had mutated ITIM. To our knowledge, this is the first report suggesting that non‐rodent mammals may use LY49 as NK receptors for classical MHC class I. We also show that horse spleen expresses ILT‐like genes with unique domain organizations. Radiation hybrid mapping and fluorescence in situ hybridization localized horse LY49 and KIR/ILT genes to chromosomes 6q13 and 10p12, respectively.
p53 regulates thymic Notch1 activation
Authors: Laws Amy M. , Osborne Barbara A. 
Published: February 2004

AbstractNotch is crucial for multiple stages of T cell development, including the CD4+CD8+ double positive (DP)/CD8+ single positive (SP) transition, but regulation of Notchactivation is not well understood. p53 regulates Presenilin1 (PS1) expression, and PS1 cleaves Notch, releasing its intracellular domain (NIC), leading to the expression of downstream targets, e.g. the HES1 gene. We hypothesize that p53 regulates Notch activity during T cell development. We found that Notch1 expression and activation were negatively regulated by p53in several thymoma lines. Additionally, NIC was elevated in Trp53–/– thymocytes as compared to Trp53+/+ thymocytes. To determine if elevated Notch1 activation in Trp53–/– thymocytes had an effect on T cell development, CD4 and CD8 expression were analyzed. The CD4+ SP/CD8+ SP T cell ratio was decreased in Trp53–/– splenocytes and thymocytes. This alteration in T cell development correlated with the increased Notch1 activation observed in the absence of p53. These data indicate that p53 negatively regulates Notch1 activation during T cell development. Skewing of T cell development toward CD8+SP T cells in Trp53–/– mice is reminiscent of the phenotype of NIC‐overexpressing mice. Thus, we suggest that p53 plays a role in T cell development, in part by regulating Notch1 activation.
Frontline: Neuropilin‐1: a surface marker of regulatory T cells
Authors: Bruder Dunja , Probst‐Kepper Michael , Westendorf Astrid M. , Geffers Robert , Beissert Stefan , Loser Karin , von Boehmer Harald , Buer Jan , Hansen Wiebke 
Published: February 2004

AbstractCD4+CD25+ regulatory T cells (Treg cells) control immune responsiveness to a large variety of antigens. The isolation and therapeutic manipulation of Treg cells requires the use of reliable surface receptors that are selectively up‐regulated in Treg cells. On the basis of global gene expression studies, we identified neuropilin‐1 (Nrp1) as a specific surface marker for CD4+CD25+ Treg cells. Nrp1, a receptor involved in axon guidance, angiogenesis, and the activation of T cells, is constitutively expressed on the surface of CD4+CD25+ Treg cells independently of their activation status. In contrast, Nrp1 expression is down‐regulated in naive CD4+CD25– T cells after TCR stimulation. Furthermore, CD4+Nrp1high T cells express high levels of Foxp3 and suppress CD4+CD25– T cells. Thus, Nrp1 constitutes a useful surface marker to distinguish Treg cells from both naive and recently activated CD4+CD25+ non‐regulatory T cells.