bluuebunny/crossref_metadata_2025_split huggingface dataset:
Helical silica nanotubes: Nanofabrication architecture, transfer of helix and chirality to silica nanotubes
Authors: Kim Tae , Jeong Euh , Oh Chae , Shin Min , Kim Jong-Pil , Jung Ok-Sang , Suh Hongsuk , Khan Fazlur , Hyun Myung , Jin Jong 
Published: August 2011

AbstractA series of neutral gelators and cationic amphiphiles derived from 1,2 diphenylethylenediamine (I) and 1,2-cyclohexanediamine (II) was synthesised. Helical silica nanotubes were prepared utilising these organic gelators through sol-gel polycondensation of tetraethoxy silane, (TEOS-silica source). Right- and left-handed helical nanotubes respectively were obtained from a 1: 1 mass mixture of optically active, (1S,2S)-III-(1S,2S)-V neutral gelator and (1S,2S)-IV-(1S,2S)-VI cationic amphiphile and a 1: 1 mass mixture of optically active, (1R,2R)-III-(1R,2R)-V neutral gelator and (1R,2R)-IV-(1R,2R)-VI cationic amphiphile, indicating that the handedness of the helical nanotubes varied with the change in the neutral gelator precursors used. The nanotubes were characterised by SEM images.
Investigation of multi-layered silicate ceramics using laser ablation optical emission spectrometry, laser ablation inductively coupled plasma mass spectrometry, and electron microprobe analysis
Authors: Zaoralkova Linda , Hrdlicka Ales , Otruba Vitezslav , Sulovsky Petr , Gilon Nicole , Günther Detlef , Kanicky Viktor 
Published: August 2011

AbstractThe applicability of laser ablation (LA) inductively coupled plasma (ICP) spectrometry for assessing elemental distributions in layered ceramics was investigated and compared with electron probe microanalysis (EPMA). Ordinary glazed wall tiles were employed as model specimens due to their defined structure and composition. They were used for calibration in the analysis of ancient pottery. A qualitative depth profile was acquired by single-spot laser drilling perpendicular to coatings with a Nd:YAG (1064 nm) laser coupled with an ICP optical emission spectrometer (OES). The lower lateral resolution associated with the laser spot diameter of 1.0 mm led to smoothing of the depth profile due to the averaging of local irregularities. In addition, transverse line scans by ablation across the tile section using an ArF* (193 nm) laser coupled with an ICP mass spectrometer (MS) were performed. LA-ICP-OES depth profiles and LA-ICP-MS transverse scans were validated by EPMA section scans and 2D back-scattered electrons images. The LA-ICP-OES acquisition was less dependent on sample surface and layer irregularities, whereas the transverse line scan over the tile section with the small-spot beam offered insight into the micromorphology of the individual layer. The combined approach revealed the occurrence of individual mineral grains, micro-heterogeneities and the character of interfaces between layers.
Becoming Empowered: A Grounded Theory Study of Aboriginal Women's Agency
Authors: Bainbridge Roxanne 
Published: August 2011

Objective: The study aim was to identify the process underlying the performance of agency for urban-dwelling Aboriginal women in contemporary Australian society with a view to promoting social change for Aboriginal people. Method: Grounded theory methods were used in the conduct of 20 life history narrative interviews with Aboriginal women from across fourteen different language groups. Results: Analysis identified a specific ecological model of Aboriginal women's empowerment, defined as “becoming empowered”. “Performing Aboriginality” was identified as the core category and encompassed the women's concern for carving out a fulfilling life and carrying out their perceived responsibilities as Aboriginal women. Conclusions: While confirming much of the extant literature on empowerment, the analysis also offered unique contributions – a spiritual sensibility, cultural competence and an ethics of care and morality. This sheds new light on the creative ways in which Aboriginal women “disrupt” discourses and create alternate modes of existence. The findings have implications for improving quality of life for Aboriginal people by informing the practical development and delivery of social and health policies and programs.
Indigenous Mental Health 2035: Future Takers, Future Makers and Transformational Potential
Authors: Durie Mason 
Published: August 2011

Objective: The aims were to review progress in Indigenous mental health over the past 25 years and to identify possible directions for the next 25 years. Method: Māori involvement in health and health care was used to illustrate key Indigenous developments since 1984. Challenges in the decades ahead were discussed in the context of demographic transitions, life course epidemiology, global trends, technological innovations and health leadership. Results: Progress was measured by a range of indicators including Māori-referenced life expectancy, Māori agendas for health, strengthened cultural identity, the dissemination of health knowledge, and Māori participation in the health sector. In contrast to being ready to respond to change (future takers), active planning for the future (future makers) was seen as a better way of achieving Indigenous aspirations. One option for health advancement currently being developed in New Zealand involved an integrated approach premised on intersectoral delivery and a focus on families. Conclusions: Indigenous health will be advanced by dedicated approaches to family wellbeing that avoid fragmentation, focus on positive strengths, and lead to positive outcomes for family members and the family as a whole.
The Primary Determinants of Indigenous Household Information and Communication Technology Adoption: Remote, Rural and Urban
Authors: Radoll Peter 
Published: August 2011

Objective: This paper examines the factors affecting adoption of information and communication technologies (computers and the Internet) in Australian Indigenous households across three Indigenous communities, remote, rural and urban. Drawing on the sociological notion of structure and agency it is argued that being engaged in external fields influences Indigenous household ICT adoption. This paper develops a conceptual schema by drawing on Bourdieu's theory of habitus to explain the low uptake of ICTs in Indigenous households across Australia. Conclusions: Evidence suggests that there is more commonality across diverse communities than differences.
Mycophenolic Acid Differentially Impacts B Cell Function Depending on the Stage of Differentiation
Authors: Karnell Jodi L. , Karnell Fredrick G. , Stephens Geoffrey L. , Rajan Bhargavi , Morehouse Chris , Li Ying , Swerdlow Bonnie , Wilson Mildred , Goldbach-Mansky Raphaela , Groves Christopher , Coyle Anthony J. , Herbst Ronald , Ettinger Rachel 
Published: August 2011

Abstract
Production of pathogenic Abs contributes to disease progression in many autoimmune disorders. The immunosuppressant agent mycophenolic acid (MPA) has shown clinical efficacy for patients with autoimmunity. The goal of these studies was to elucidate the mechanisms of action of MPA on B cells isolated from healthy individuals and autoimmune patients. In this study, we show that MPA significantly inhibited both proliferation and differentiation of primary human B cells stimulated under various conditions. Importantly, MPA did not globally suppress B cell responsiveness or simply induce cell death, but rather selectively inhibited early activation events and arrested cells in the G0/G1 phase of the cell cycle. Furthermore, MPA blocked expansion of both naive and memory B cells and prevented plasma cell (PC) differentiation and Ab production from healthy controls and individuals with rheumatoid arthritis. Finally, whereas MPA potently suppressed Ig secretion from activated primary B cells, terminally differentiated PCs were not susceptible to inhibition by MPA. The target of MPA, IMPDH2, was found to be downregulated in PCs, likely explaining the resistance of these cells to MPA. These results suggest that MPA provides benefit in settings of autoimmunity by directly preventing activation and PC differentiation of B cells; however, MPA is unlikely to impact autoantibody production by preexisting, long-lived PCs.
Foxp3+-Inducible Regulatory T Cells Suppress Endothelial Activation and Leukocyte Recruitment
Authors: Maganto-García Elena , Bu De-xiu , Tarrio Margarite L. , Alcaide Pilar , Newton Gail , Griffin Gabriel K. , Croce Kevin J. , Luscinskas Francis W. , Lichtman Andrew H. , Grabie Nir 
Published: August 2011

Abstract
The ability of regulatory T cells (Treg) to traffic to sites of inflammation supports their role in controlling immune responses. This feature supports the idea that adoptive transfer of in vitro expanded human Treg could be used for treatment of immune/inflammatory diseases. However, the migratory behavior of Treg, as well as their direct influence at the site of inflammation, remains poorly understood. To explore the possibility that Treg may have direct anti-inflammatory influences on tissues, independent of their well-established suppressive effects on lymphocytes, we studied the adhesive interactions between mouse Treg and endothelial cells, as well as their influence on endothelial function during acute inflammation. We show that Foxp3+ adaptive/inducible Treg (iTreg), but not naturally occurring Treg, efficiently interact with endothelial selectins and transmigrate through endothelial monolayers in vitro. In response to activation by endothelial Ag presentation or immobilized anti-CD3ε, Foxp3+ iTreg suppressed TNF-α– and IL-1β–mediated endothelial selectin expression and adhesiveness to effector T cells. This suppression was contact independent, rapid acting, and mediated by TGF-β–induced activin receptor-like kinase 5 signaling in endothelial cells. In addition, Foxp3+ iTreg adhered to inflamed endothelium in vivo, and their secretion products blocked acute inflammation in a model of peritonitis. These data support the concept that Foxp3+ iTreg help to regulate inflammation independently of their influence on effector T cells by direct suppression of endothelial activation and leukocyte recruitment.
IL-7 Is Required for the Development of the Intrinsic Function of Marginal Zone B Cells and the Marginal Zone Microenvironment
Authors: Willems Leen , Li Shengqiao , Rutgeerts Omer , Lenaerts Caroline , Waer Mark , Billiau An D. 
Published: August 2011

Abstract
The characteristic microarchitecture of the marginal zone (MZ), formed by locally interacting MZ-specific B cells, macrophages, and endothelial cells, is critical for productive marginal zone B cell (MZB cell) Ab responses. Reportedly, IL-7–deficient mice, although severely lymphopenic, retain small numbers of CD21highCD23low B cells consistent with MZB cell phenotype, suggesting that IL-7 signaling is not exclusively required for MZB cell lymphopoiesis. In this study, we investigated the function of IL-7−/− MZB cells and the IL-7−/− microenvironment using a model of hamster heart xenograft rejection, which depends exclusively on MZB cell-mediated production of T cell-independent IgM xenoantibodies (IgMXAb). C57BL/6-IL-7−/− mice accepted xenografts indefinitely and failed to produce IgMXAb, even after transfer of additional IL-7−/− or wild-type C57BL/6 MZB cells. Transfer of wild-type but not IL-7−/− B cells enabled SCID mice to produce IgMXAb. When transferred to SCID mice, wild-type but not IL-7−/− B cells formed B cell follicles with clearly defined IgM+, MOMA-1+, and MAdCAM-1+ MZ structures. Conversely, adoptively transferred GFP+ C57BL/6 B cells homed to the MZ area in a SCID but not an IL-7−/− environment. Naive IL-7−/− mice showed absent or aberrant splenic B cell structures. We provide evidence that IL-7 is critical for the development of the intrinsic function of MZB cells in producing rapidly induced IgM against T cell-independent type II Ags, for their homing potential, and for the development of a functional MZ microanatomy capable of attracting and lodging MZB cells.
Modulation of IL-7 Thresholds by SOCS Proteins in Developing B Lineage Cells
Authors: Corfe Steven A. , Rottapel Robert , Paige Christopher J. 
Published: August 2011

Abstract
During B lymphopoiesis, IL-7 induces survival, proliferation, and differentiation signals that are important during the pro-B to pre-B cell transition. We showed that murine small pre-B stage cells do not signal or proliferate in response to IL-7, yet they maintain IL-7R surface expression. Loss of proliferative responsiveness to IL-7 is mediated by suppressor of cytokine signaling protein 1 (SOCS-1), the expression of which is regulated during B lymphopoiesis, with the highest levels observed in small pre-B cells. SOCS-1 inhibits IL-7 responses in pre-B cell lines and ex vivo B lineage cells. SOCS-1 expression and, thus, responsiveness to IL-7, can be regulated by IL-7 itself, as well as IFN-γ and IL-21. Additionally, the transcriptional repressor Gfi-1b enhances the proliferative responsiveness of B cell lines to IL-7. We demonstrated that these molecules act together to form a SOCS-mediated “rheostat” that controls the level of IL-7R signaling in developing murine B lineage cells.
IFN-γ Acts on the Airway Epithelium To Inhibit Local and Systemic Pathology in Allergic Airway Disease
Authors: Mitchell Charlotte , Provost Karin , Niu Naiqian , Homer Robert , Cohn Lauren 
Published: August 2011

Abstract
Inhibiting allergic airway inflammation is the goal of therapy in persistent asthma. Administration of medication via the airways delivers drug directly to the site of inflammation and avoids systemic side effects but often fails to modulate systemic features of asthma. We have shown that Th1 cells, through production of IFN-γ, inhibit many Th2-induced effector functions that promote disease. Using a newly generated mouse that expresses IFN-γR only on airway epithelial cells, we show that the airway epithelium controls a range of pathological responses in asthma. IFN-γ acting only through the airway epithelium inhibits mucus, chitinases, and eosinophilia, independent of Th2 cell activation. IFN-γ signaling through the airway epithelium inhibits eosinophil generation in the bone marrow, indicating that signals on the airway mucosal surface can regulate distant functions to inhibit disease. IFN-γ actions through the airway epithelium will limit airway obstruction and inflammation and may be therapeutic in refractory asthma.
An Age-Specific CD8+ T Cell Pathway That Impairs the Effectiveness of Strategies To Prolong Allograft Survival
Authors: Du Wei , Shen Hua , Galan Anjela , Goldstein Daniel R. 
Published: August 2011

AbstractAge-related decline in immunity can impair cell-mediated responses during an infection, malignancy, and acute allograft rejection. Although much research has been allocated to understand the immune responses that impact the former two conditions, the cellular mechanisms by which aging impacts the immune acceptance of organ allografts are not completely clear. In this study, we examined how recipient age impacts the efficacy of therapies that modulate immune recognition of allografts using an immunogenic murine skin transplant model. We found that costimulatory blockade-based treatment failed to extend allograft survival in older recipients to the same extent as that observed in younger recipients. CD8+ T cells were critical for the inability of aged recipients to achieve maximal allograft survival. Although aged mice displayed a larger number of effector memory T cells prior to transplantation, these cells did not exhibit enhanced alloreactivity compared with young memory T cells. In contrast, naive aged CD8+ T cells exhibited enhanced IFN-γ production to allostimulation compared with young naive T cells. Our results provide evidence that aging enhances CD8+ T cell alloreactivity. This could impair the ability of costimulatory blockade-based therapies to prolong allograft survival. Thus, targeting CD8+ T cells in humans may be a way to improve outcomes in older patients requiring immune modulatory therapy.
Host Immunity and Pathogen Strain Contribute to Intestinal Disaccharidase Impairment following Gut Infection
Authors: Solaymani-Mohammadi Shahram , Singer Steven M. 
Published: August 2011

Abstract
Infection or other inflammatory insults in the small intestine often result in reduced disaccharidase enzyme levels. Using a mouse model of giardiasis, we examined the role of host immunity and pathogen virulence in mediating disaccharidase deficiency postinfection (p.i.). C57BL/6J mice were infected with two strains, WB and GS, of the human parasite Giardia duodenalis. The levels of sucrase, maltase, and lactase decreased in wild-type mice p.i. with the GS strain but not with the WB strain. Both CD4-deficient and SCID mice failed to eliminate the infection and did not exhibit disaccharidase deficiency. β2-Microglobulin knockout animals controlled infections similar to wild-type mice but exhibited no decrease in disaccharidase activity. Analysis of cytokine production by spleen and mesenteric lymph node cells showed production of IL-4, IL-10, IL-13, IL-17, IL-22, TNF-α, and IFN-γ p.i. with both WB and GS, with IFN-γ being the dominant cytokine for both parasite strains. Mesenteric lymph node cells produced lower levels of cytokines compared with splenocytes in response to parasite extract, although the overall pattern was similar. These data suggest that T cell responses mediate parasite clearance whereas also contributing to pathogenesis. They also demonstrate that differences in pathogen strain can also determine the outcome of infection and further our understanding of the clinical variation seen in human giardiasis.
Glycogen Synthase Kinase-3 Facilitates Con A-Induced IFN-γ–Mediated Immune Hepatic Injury
Authors: Tsai Cheng-Chieh , Huang Wei-Ching , Chen Chia-Ling , Hsieh Chia-Yuan , Lin Yee-Shin , Chen Shun-Hua , Yang Kao-Chi , Lin Chiou-Feng 
Published: August 2011

Abstract
Immune hepatic injury induced by Con A results primarily from IFN-γ–mediated inflammation, followed by hepatic cell death. Glycogen synthase kinase (GSK)-3, which acts proapoptotically and is proinflammatory, is also important for facilitating IFN-γ signaling. We hypothesized a pathogenic role for GSK-3 in Con A hepatic injury. Con A stimulation caused GSK-3 activation in the livers of C57BL/6 mice. Inhibiting GSK-3 reduced Con A hepatic injury, including hepatic necrosis and apoptosis, inflammation, infiltration of T cells and granulocytes, and deregulated expression of adhesion molecule CD54. Con A induced hepatic injury in an IFN-γ receptor 1-dependent manner. Con A/IFN-γ induced activation and expression of STAT1 in a GSK-3–dependent manner. GSK-3 facilitated IFN-γ–induced inducible NO synthase, but had limited effects on CD95 upregulation and CD95-mediated hepatocyte apoptosis in vitro. Notably, inhibiting GSK-3 decreased Con A-induced IFN-γ production in both wild-type and IFN-γ receptor 1-deficient C57BL/6 mice. In Con A-activated NKT cells, GSK-3 was also activated and was required for nuclear translocation of T-box transcription factor Tbx21, a transcription factor of IFN-γ, but it was not required for CD95 ligand expression or activation-induced cell death. These results demonstrate the dual and indispensable role of GSK-3 in Con A hepatic injury by facilitating IFN-γ–induced hepatopathy.
Differential Expression of the Adaptor Protein HSH2 Controls the Quantitative and Qualitative Nature of the Humoral Response
Authors: King R. Glenn , Herrin Brantley R. , Justement Louis B. 
Published: August 2011

Abstract
Endogenous expression of the adaptor protein hematopoietic Src homology 2-containing adaptor protein (HSH2) is regulated in a dynamic manner during B cell maturation and differentiation. Developing B cells lack detectable HSH2, whereas transitional 1 and 2 B cells in the periphery exhibit increasing levels of expression. Mature follicular B cells exhibit decreased expression of HSH2 compared with transitional 2 B cells, and expression is further downregulated in germinal center B cells. In contrast, marginal zone B cells and B1a/b B cells exhibit high-level HSH2 expression. Regulation of HSH2 expression plays a critical role in determining the outcome of the humoral immune response as demonstrated using HSH2 transgenic (Tg) mice. Constitutive expression of HSH2 in the B lineage at levels comparable to B1a/b B cells results in decreased serum Ig titers for all subclasses with the exception of IgA. HSH2 Tg mice immunized with T-dependent or T-independent Ags exhibit a moderate decrease in the production of Ag-specific IgM, whereas class-switched isotypes are decreased by ∼80–90% compared with control mice. Analysis of HSH2 Tg B cell activation in vitro demonstrated that HSH2 selectively regulates the B cell response to TNF family receptors (i.e., CD40 and BAFF-R), but not BCR- or TLR-dependent signals. These data demonstrate that changes in HSH2 expression have profound effects on the humoral immune response.
Virus-Specific CD8+ T Cells Upregulate Programmed Death-1 Expression during Acute Friend Retrovirus Infection but Are Highly Cytotoxic and Control Virus Replication
Authors: Zelinskyy Gennadiy , Myers Lara , Dietze Kirsten K. , Gibbert Kathrin , Roggendorf Michael , Liu Jia , Lu Mengji , Kraft Anke R. , Teichgräber Volker , Hasenkrug Kim J. , Dittmer Ulf 
Published: August 2011

Abstract
It was recently reported that inhibitory molecules such as programmed death-1 (PD-1) were upregulated on CD8+ T cells during acute Friend retrovirus infection and that the cells were prematurely exhausted and dysfunctional in vitro. The current study confirms that most activated CD8+ T cells upregulated expression of PD-1 during acute infection and revealed a dichotomy of function between PD-1hi and PD-1lo subsets. More PD-1lo cells produced antiviral cytokines such as IFN-γ and TNF-α, whereas more PD-1hi cells displayed characteristics of cytotoxic effectors such as production of granzymes and surface expression of CD107a. Importantly, CD8+ T cells mediated rapid in vivo cytotoxicity and were critical for control of acute Friend virus replication. Thus, direct ex vivo analyses and in vivo experiments revealed high CD8+ T cell functionality and indicate that PD-1 expression during acute infection is not a marker of T cell exhaustion.
Mutagenesis of Beryllium-Specific TCRs Suggests an Unusual Binding Topology for Antigen Recognition
Authors: Bowerman Natalie A. , Falta Michael T. , Mack Douglas G. , Kappler John W. , Fontenot Andrew P. 
Published: August 2011

Abstract
Unconventional Ags, such as metals, stimulate T cells in a very specific manner. To delineate the binding landscape for metal-specific T cell recognition, alanine screens were performed on a set of Be-specific TCRs derived from the lung of a chronic beryllium disease patient. These TCRs are HLA-DP2–restricted and express nearly identical TCR Vβ5.1 chains coupled with different TCR α-chains. Site-specific mutagenesis of all amino acids comprising the CDRs of the TCRA and TCRB genes showed a dominant role for Vβ5.1 residues in Be recognition, with little contribution from the TCR α-chain. Solvent-exposed residues along the α-helices of the HLA-DP2 α- and β-chains were also mutated to alanine. Two β-chain residues, located near the proposed Be binding site of HLA-DP2, played a dominant role in T cell recognition with no contribution from the HLA-DP2 α-chain. These findings suggest that Be-specific T cells recognize Ag using an unconventional binding topology, with the majority of interactions contributed by TCR Vβ5.1 residues and the HLA-DP2 β1-chain. Thus, unusual docking topologies are not exclusively used by autoreactive T cells, but also for the recognition of unconventional metal Ags, such as Be.