bluuebunny/crossref_metadata_2025_split huggingface dataset:
Fear of Moving Outdoors and Development of Outdoor Walking Difficulty in Older People
Authors: Rantakokko Merja , Mänty Minna , Iwarsson Susanne , Törmäkangas Timo , Leinonen Raija , Heikkinen Eino , Rantanen Taina 
Published: April 2009

OBJECTIVES: To study which individual characteristics and environmental factors correlate with fear of moving outdoors and whether fear of moving outdoors predicts development of mobility limitation.DESIGN: Observational prospective cohort study and cross‐sectional analyses.SETTING: Community and research center.PARTICIPANTS: Seven hundred twenty‐seven community‐living people aged 75 to 81 were interviewed at baseline, of whom 314 took part in a 3.5‐year follow‐up.MEASUREMENTS: Fear of moving outdoors and its potential individual and environmental correlates were assessed at baseline. Perceived difficulties in walking 0.5 km and 2 km were assessed twice a year over a 3.5‐year period.RESULTS: At baseline, 65% of the women and 29% of the men reported fear of moving outdoors. Poor socioeconomic status; musculoskeletal diseases; slow walking speed; and the presence of poor street conditions, hills in the nearby environment, and noisy traffic correlated with fear of moving outdoors. At the first 6‐month follow‐up, participants with fear of moving outdoors had more than four times the adjusted risk (odds ratio (OR)=4.6, 95% confidence interval (CI)=1.92–11.00) of developing difficulties in walking 0.5 km and a three times greater adjusted risk (OR=3.10, 95% CI=1.49–6.46) for developing difficulty in walking 2 km compared with those without fear. The difference in the prevalence of walking difficulties remained statistically significant over the 3.5‐year follow‐up (P=.02 and P=.009, respectively).CONCLUSION: Fear of moving outdoors is common in older adults and increases the risk of developing self‐reported difficulties in walking 0.5 km and 2 km. Knowledge about individual and environmental factors underlying fear of moving outdoors and finding ways to alleviate fear of moving outdoors are important for community planning and prevention of disability.
EFFECT OF HYDROTHERMAL TREATMENT ON THE PHYSICOCHEMICAL, RHEOLOGICAL AND OIL‐RESISTANT PROPERTIES OF RICE FLOUR*
Authors: KIM DEOK NYUN , BAE IN YOUNG , INGLETT GEORGE E. , LEE SUYONG 
Published: April 2009

ABSTRACT Rice flour was thermomechanically modified by steam‐jet cooking and the physicochemical, rheological and oil‐resistant properties of the resulting product were characterized. Compared with native rice flour, the steam jet‐cooked rice flour exhibited significantly increased hydration properties. Its pasting properties were also characterized by cold initial viscosity, decreased setback and the lack of peak viscosity. The shear‐thinning behaviors of the steam jet‐cooked rice flour were satisfactorily fitted into the Carreau equation. In addition, dynamic viscoelastic measurements showed that the liquid‐like nature was more dominant over the solid‐like properties. When incorporated into frying batter formulations, the steam jet‐cooked rice flour increased the batter viscosity and pickup. The use of steam jet‐cooked rice flour also enabled fried batters to control the moisture loss effectively. Furthermore, the wheat flour replacement with 20% steam jet‐cooked rice flour in batters led to dramatic reduction of oil uptake by around 40%. PRACTICAL APPLICATIONSThis study introduces a hydrothermal treatment (steam‐jet cooking) as a new technique to impart better functional properties to rice flour. Specially, the steam jet‐cooked rice flour exhibited oil‐resisting properties when incorporated into frying batters, consequently producing fried foods with reduced content of oil and calorie.
Evaluation of the New Architect Cytomegalovirus Immunoglobulin M (IgM), IgG, and IgG Avidity Assays
Authors: Lagrou K. , Bodeus M. , Van Ranst M. , Goubau P. 
Published: April 2009

ABSTRACT
A panel of new cytomegalovirus (CMV) assays for use on the Architect instrument has been developed, including a CMV avidity assay based on a new technology. The purpose of this study was to compare the performance characteristics of the fully automated CMV immunoglobulin M (IgM), IgG, and IgG avidity tests on the Architect instrument with those of other available assays. A total of 503 consecutive fresh patient serum specimens (routine serum specimens) and 96 serum specimens from 33 pregnant women with a recent CMV primary infection (seroconversion serum specimens) were tested for CMV IgM and IgG by the Architect (Abbott), Vidas (BioMérieux), and Enzygnost (Siemens) assays. The seroconversion sera and 100 preselected serum specimens IgM negative and IgG positive by the AxSYM assay were also tested by the IgG avidity tests on the Architect and Vidas instruments. The relative agreements for CMV IgM determination with routine sera between the Architect assay and the Vidas, Enzygnost, and AxSYM assays were 97%, 94%, and 93%, respectively, for the CMV IgM tests and 99%, 98%, and 98%, respectively, for the CMV IgG tests. The specificities of the CMV IgG avidity test were 98% for the Architect assay and 76% for the Vidas assay. No high CMV IgG avidity test results were found within the first 3 months after seroconversion by either of those assays. The correlation between the results of the newly developed CMV IgM and IgG tests on the Architect instrument with the Vidas and Enzygnost assays was excellent (≥94%). The CMV IgG avidity test reliably excluded patients with recent infections and showed an excellent specificity (98%).
Quantitative Drug Susceptibility Testing of
Mycobacterium tuberculosis
by Use of MGIT 960 and EpiCenter Instrumentation
Authors: Springer Burkhard , Lucke Katja , Calligaris-Maibach Romana , Ritter Claudia , Böttger Erik C. 
Published: April 2009

ABSTRACT

Since numbers of drug-resistant
Mycobacterium tuberculosis
strains are on the rise, the simple classification into “susceptible” and “resistant” strains based on susceptibility testing at “critical concentrations” has to be reconsidered. While future studies have to address the correlation of phenotypic resistance levels and treatment outcomes, a prerequisite for corresponding investigations is the ability to exactly determine levels of quantitative drug resistance in clinical
M. tuberculosis
isolates. Here we have established the conditions for quantitative drug susceptibility testing for first- and second-line agents using MGIT 960 instrumentation and EpiCenter software equipped with the TB eXiST module. In-depth comparative analysis of a range of well-characterized susceptible and resistant clinical isolates has allowed us to propose conditions for testing and to develop criteria for interpretation.
The Virological Synapse Facilitates Herpes Simplex Virus Entry into T Cells
Authors: Aubert Martine , Yoon Miri , Sloan Derek D. , Spear Patricia G. , Jerome Keith R. 
Published: April 2009

ABSTRACTThe virological synapse (VS) is a specialized molecular structure that facilitates the transfer of certain lymphotropic viruses into uninfected T cells. However, the role of the VS in the transfer of nonlymphotropic viruses into T cells is unknown. Herpes simplex virus (HSV) has been shown in vitro to infect T cells and modulate T-cell receptor function, thereby suppressing T-cell antiviral function. However, whether such infection of T cells occurs in vivo is unknown. Here, we examined whether T-cell infection could be observed in human HSV disease and investigated the mechanism of HSV entry into T cells. We found that HSV-infected T cells were readily detectable during human disease, suggesting that infection and modulation of T-cell function plays a role in human immunopathology. HSV infection of both CD4+and CD8+T cells occurred much more efficiently via direct cell-to-cell spread from infected fibroblasts than by cell-free virus. Activation of T cells increased their permissivity to HSV infection. Cell-to-cell spread to T cells did not require HSV glycoproteins E and I (gE and gI), which are critical for cell-to-cell spread between epithelial cells. Transfer of HSV to T cells required gD, and the four known entry receptors appear to be contributing to viral entry, with a dominant role for the herpesvirus entry mediator and nectin-1. VS-like structures enriched in activated lymphocyte function-associated antigen 1 (LFA-1) were observed at the point of contact between HSV-infected fibroblasts and T cells. Consistent with spread occurring via the VS, transfer of HSV was increased by activation of LFA-1, and cell-to-cell spread could be inhibited by antibodies to LFA-1 or gD. Taken together, these results constitute the first demonstration of VS-dependent cell-to-cell spread for a predominantly nonlymphotropic virus. Furthermore, they support an important role for infection and immunomodulation of T cells in clinical human disease. Targeting of the VS might allow selective immunopotentiation during infections with HSV or other nonlymphotropic viruses.
Identification of novel transcriptional regulators involved in macrophage differentiation and activation in U937 cells
Authors: Baek Young-Sook , Haas Stefan , Hackstein Holger , Bein Gregor , Hernandez-Santana Maria , Lehrach Hans , Sauer Sascha , Seitz Harald 
Published: April 2009

Abstract

Background
Monocytes and macrophages play essential role in innate immunity. Understanding the underlying mechanism of macrophage differentiation and the identification of regulatory mechanisms will help to find new strategies to prevent their harmful effects in chronic inflammatory diseases and sepsis.

Results
Maturation of blood monocytes into tissue macrophages and subsequent inflammatory response was mimicked in U937 cells of human histocytic lymphoma origin. Whole genome array analysis was employed to evaluate gene expression profile to identify underlying transcriptional networks implicated during the processes of differentiation and inflammation. In addition to already known transcription factors (i.e. MAFB, EGR, IRF, BCL6, NFkB, AP1, Nur77), gene expression analysis further revealed novel genes (i.e. MEF2, BRI, HLX, HDAC5, H2AV, TCF7L2, NFIL3) previously uncharacterized to be involved in the differentiation process. A total of 58 selected genes representing cytokines, chemokines, surface antigens, signaling molecules and transcription factors were validated by real time PCR and compared to primary monocyte-derived macrophages. Beside the verification of several new genes, the comparison reveals individual heterogeneity of blood donors.

Conclusion
Up regulation of MEF2 family, HDACs, and H2AV during cell differentiation and inflammation sheds new lights onto regulation events on transcriptional and epigenetic level controlling these processes. Data generated will serve as a source for further investigation of macrophages differentiation pathways and related biological responses.
Effects of hip joint position and intra-capsular volume on hip joint intra-capsular pressure: a human cadaveric model
Authors: Yen Chi-Hung , Leung Hon-Bong , Tse Paul Yun-Tin 
Published: April 2009

AbstractBackgroundIncrease in hip intra-capsular pressure has been implicated in various hip pathologies, such as avascular necrosis complicating undisplaced femoral neck fracture. Our study aimed at documenting the relationship between intra-capsular volume and pressure in various hip positions.MethodsFifty-two cadaveric hips were studied. An electronic pressure-monitoring catheter recorded the intra-capsular hip pressure after each instillation of 2 ml of normal saline and in six hip positions.ResultsIn neutral hip position, the control position for investigation, intra-capsular pressure remained unchanged when its content was below 10 ml. Thereafter, it increased exponentially. When the intra-capsular volume was 12 ml, full abduction produced a 2.1-fold increase (p = 0.028) of the intra-capsular hip joint pressure; full external rotation and full internal rotation increased the pressure by at least 4-fold (p < 0.001). Conversely, there was a 19% (p = 0.046) and 81% (p = 0.021) decrease in intra-capsular hip joint pressure with flexion of the hip joint to 90-degree and 45-degree, respectively.ConclusionIntra-capsular pressure increases with its volume, but with a wide variation with different positions. It would be appropriate to recommend that hips with haemarthrosis or effusion should be positioned in 45-degree flexion.
Enrichment of Human CD4+ Vα24/Vβ11 Invariant NKT Cells in Intrahepatic Malignant Tumors
Authors: Bricard Gabriel , Cesson Valerie , Devevre Estelle , Bouzourene Hanifa , Barbey Catherine , Rufer Nathalie , Im Jin S. , Alves Pedro M. , Martinet Olivier , Halkic Nermin , Cerottini Jean-Charles , Romero Pedro , Porcelli Steven A. , MacDonald H. Robson , Speiser Daniel E. 
Published: April 2009

Abstract
Invariant NKT cells (iNKT cells) recognize glycolipid Ags via an invariant TCR α-chain and play a central role in various immune responses. Although human CD4+ and CD4− iNKT cell subsets both produce Th1 cytokines, the CD4+ subset displays an enhanced ability to secrete Th2 cytokines and shows regulatory activity. We performed an ex vivo analysis of blood, liver, and tumor iNKT cells from patients with hepatocellular carcinoma and metastases from uveal melanoma or colon carcinoma. Frequencies of Vα24/Vβ11 iNKT cells were increased in tumors, especially in patients with hepatocellular carcinoma. The proportions of CD4+, double negative, and CD8α+ iNKT cell subsets in the blood of patients were similar to those of healthy donors. However, we consistently found that the proportion of CD4+ iNKT cells increased gradually from blood to liver to tumor. Furthermore, CD4+ iNKT cell clones generated from healthy donors were functionally distinct from their CD4− counterparts, exhibiting higher Th2 cytokine production and lower cytolytic activity. Thus, in the tumor microenvironment the iNKT cell repertoire is modified by the enrichment of CD4+ iNKT cells, a subset able to generate Th2 cytokines that can inhibit the expansion of tumor Ag-specific CD8+ T cells. Because CD4+ iNKT cells appear inefficient in tumor defense and may even favor tumor growth and recurrence, novel iNKT-targeted therapies should restore CD4− iNKT cells at the tumor site and specifically induce Th1 cytokine production from all iNKT cell subsets.
Trimolecular Complex Formation of IgE, FcεRI, and a Recombinant Nonanaphylactic Single-Chain Antibody Fragment with High Affinity for IgE
Authors: Lupinek Christian , Roux Kenneth H. , Laffer Sylvia , Rauter Ingrid , Reginald Kavita , Kneidinger Michael , Blatt Katharina , Ball Tanja , Pree Ines , Jahn-Schmid Beatrice , Allam Jean-Pierre , Novak Natalija , Drescher Anja , Kricek Franz , Valent Peter , Englund Hakan , Valenta Rudolf 
Published: April 2009

Abstract
IgE is a central molecule in allergic disease. We have isolated cDNAs coding for the heavy and light chains of a murine mAb specific to human IgE and expressed a recombinant single-chain variable fragment (ScFv) derived thereof in Escherichia coli. The purified recombinant ScFv has a molecular mass of 28 kDa as measured by mass spectrometry and shows a β-sheet fold as determined by circular dichroism. In biosensor-based studies it was demonstrated that the ScFv rapidly and stably binds to human IgE with an affinity of KD of 1.52 × 10−10 M, which is almost as high as the affinity of IgE for FcεRI, and that the ScFv is able to recognize FcεRI-bound IgE and to prevent IgE binding to FcεRI. The ScFv reacts specifically with IgE but not with other isotypes, allows the measurement of allergen-specific IgE in serum samples, and specifically targets cells that contain FcεRI- or FcεRII-bound IgE or that secrete IgE. Using negative-stain electron microscopy we demonstrated the formation of bimolecular complexes consisting of two ScFv molecules and one IgE and trimolecular complexes consisting of IgE, FcεRI, and ScFv in which only one ScFv is able to bind to IgE. Accordingly, we found that the ScFv does not cross-link basophil-bound IgE and hence does not induce histamine release or activation of basophils as demonstrated by FACS analysis of CD203c expression and by histamine release experiments. In vivo skin testing confirmed the lack of allergenic activity of the ScFv. The recombinant ScFv may represent a universal tool for the IgE-targeted treatment of allergies.
The NF-κB RelA Subunit Confers Resistance toLeishmania majorby Inducing Nitric Oxide Synthase 2 and Fas Expression but Not Th1 Differentiation
Authors: Mise-Omata Setsuko , Kuroda Etsushi , Sugiura Tsutomu , Yamashita Uki , Obata Yuichi , Doi Takahiro S. 
Published: April 2009

AbstractAlthough the NF-κB transcription factors participate in both innate and adaptive immune responses, little is known about the role of the RelA subunit because mice lacking the rela gene die at embryonic day 14. To elucidate the role of RelA in Leishmania major infection, we prepared fetal liver chimeric mice by adoptively transferring embryonic day 13.5 rela−/− or rela+/+ fetal liver into lethally irradiated host mice. About 90% of the peripheral lymphocytes of the chimeric mice had differentiated from rela fetal liver cells. The rela−/− fetal liver chimeric mice were highly sensitive to infection with L. major and died within 11 wk after infection. Despite the severity of the disease, parasite Ag-reactive Th1 cells developed normally. The rela−/− macrophages were less able to control intracellular parasite replication than rela+/+ macrophages, despite showing equally efficient phagocytosis. Both in vitro NO production of macrophages and in vivo expression of NO synthase 2 in the lesions and draining lymph nodes was reduced in rela−/− fetal liver chimeric mice. Moreover, up-regulation of Fas in rela−/− macrophages was impaired both after in vitro stimulation with LPS and after in vivo infection with L. major, implying a defect in their ability to eliminate infected cells. Thus, RelA is necessary for macrophages to be resistant to intracellular parasite infection.
Early Infection Termination Affects Number of CD8+ Memory T Cells and Protective Capacities in Listeria monocytogenes-Infected Mice upon Rechallenge
Authors: Tseng Kuo-En , Chung Cheng-Yu , H’ng Weng Siong , Wang Shih-Lien 
Published: April 2009

Abstract
Here, we reevaluate the effects of early termination of infection on primary T cell expansion, subsequent memory cell development, and protective immunity. Using a murine Listeria monocytogenes (LM) infection model, we found the primary expansions of both CD4+ and CD8+ T cells were affected even when ampicillin was given as late as 60 h postinfection (p.i.). Subsequent development of CD8+ memory T cells was also impaired, although to a lesser extent, and only mice that received ampicillin at 24 h p.i. revealed a significant decrease in memory CD8+ T cells. Upon rechallenge with 1 × 105 CFU of LM, all ampicillin-treated mice cleared LM as effectively, and they generated similar amounts of Ag-specific CD8+ T cells as with untreated mice. However, mice that received ampicillin at 24 h p.i. lost their protective abilities when rechallenged with 7.5 × 105 CFU of LM. Ampicillin treatment also revealed early down-regulation of B7.1 and B7.2, but not CD40, on dendritic cells 72 h p.i. Our results have several important implications: 1) they argue against the hypothesis that brief exposure of T cells to an Ag is sufficient for full-fledged primary T cell responses and subsequent memory T cell development in vivo; 2) they suggest the existence of a reservoir of memory T cells, more than the immune system can possibly expand during secondary infection; and 3) they suggest that protective capacity is correlated with the number of preexisting memory T cells and that secondary expanding T cells play a limited role, at least in murine LM infection.
Early Hematopoietic Zinc Finger Protein Prevents Tumor Cell Recognition by Natural Killer Cells
Authors: La Rocca Rosanna , Fulciniti Mariateresa , Lakshmikanth Tadepally , Mesuraca Maria , Ali Talib Hassan , Mazzei Valerio , Amodio Nicola , Catalano Lucio , Rotoli Bruno , Ouerfelli Ouathek , Grieco Michele , Gulletta Elio , Bond Heather M. , Morrone Giovanni , Ferrone Soldano , Carbone Ennio 
Published: April 2009

Abstract
Early hematopoietic zinc finger/zinc finger protein 521 (EHZF/ZNF521) is a novel zinc finger protein expressed in hematopoietic stem and progenitor cells and is down-regulated during their differentiation. Its transcript is also abundant in some hematopoietic malignancies. Analysis of the changes in the antigenic profile of cells transfected with EHZF cDNA revealed up-regulation of HLA class I cell surface expression. This phenotypic change was associated with an increased level of HLA class I H chain, in absence of detectable changes in the expression of other Ag-processing machinery components. Enhanced resistance of target cells to NK cell-mediated cytotoxicity was induced by enforced expression of EHZF in the cervical carcinoma cell line HeLa and in the B lymphoblastoid cell line IM9. Preincubation of transfected cells with HLA class I Ag-specific mAb restored target cell susceptibility to NK cell-mediated lysis, indicating a specific role for HLA class I Ag up-regulation in the NK resistance induced by EHZF. A potential clinical significance of these findings is further suggested by the inverse correlation between EHZF and MHC class I expression levels, and autologous NK susceptibility of freshly explanted multiple myeloma cells.
Evolution of the Ikaros Gene Family: Implications for the Origins of Adaptive Immunity
Authors: John Liza B. , Yoong Simon , Ward Alister C. 
Published: April 2009

Abstract
Members of the Ikaros family of transcription factors are important for immune system development. Analysis of Ikaros-related genes from a range of species suggests the Ikaros family derived from a primordial gene, possibly related to the present-day protostome Hunchback genes. This duplicated before the divergence of urochordates to produce two distinct lineages: one that generated the Ikaros factor-like (IFL) 2 genes of urochordates/lower vertebrates and the Pegasus genes of higher vertebrates, and one that generated the IFL1 genes of urochordates/lower vertebrates, the IKFL1 and IKFL2 genes of agnathans and the remaining four Ikaros members of higher vertebrates. Expansion of the IFL1 lineage most likely occurred via the two intervening rounds of whole genome duplication. A proposed third whole genome duplication in teleost fish produced a further increase in complexity of the gene family with additional Pegasus and Eos members. These findings question the use of IFL sequences as evidence for the existence of adaptive immunity in early chordates and vertebrates. Instead, this study is consistent with a later emergence of adaptive immunity coincident with the appearance of the definitive lymphoid markers Ikaros, Aiolos, and Helios.