bluuebunny/crossref_metadata_2025_split huggingface dataset:
Web Technology: A tool for social networking and resource sharing knowledge indicators towards community development
Authors: Kasirao V , Kumar R Santha , Rengaraj M 
Published: April 2012

Web Technology plays a vital role in library, information and documentation knowledge resource centres and as tool for social networking and resource sharing knowledge indicators towards community development. The Information Communication Technologies (ICTs) serve as a tool for knowledge indicators in Knowledge Organization Management for e-knowledge dissemination and access to service providers (i.e. Governments/Institutions) and service receivers (i.e. community people) for socio economic development. The social network programmes such as e-governance, e-communities, e-culture, e-health, e-business, e-learning etc. are promoting through ICTs applications for rural community development. In view of this, the present paper is related to the paper theme literature analysis on web under study. Outlines the information scientist’s effective role in content analysis and content management for knowledge dissemination for access towards community development. This paper emphasizes the need for knowledge access and sharing initiatives for rural community development. Highlights the key issues in relation to ICTs application sources in development context. Provides the guidelines for issues to consider developing the ICTs polices and implementation strategies for socio, economic and cultural development in the present knowledge based society.DOI: http://dx.doi.org/10.4038/sllim.v4i1-2.4251 Sri Lankan Journal of Librarianship and Information Management. Vol.4, Nos.1&2 (Jan. – June 2011) pp. 18-26
Sri Lanka's earliest libraries - Anuradhapura and Polonnuruwa periods
Authors: Bowden Russell 
Published: April 2012

DOI: http://dx.doi.org/10.4038/sllim.v4i3-4.4252 Sri Lankan Journal of Librarianship and Information Management. Vol.4, Nos.3&4 (Jan. – June 2011) pp. 1-58
Joint NOD2/RIPK2 Signaling Regulates IL-17 Axis and Contributes to the Development of Experimental Arthritis
Authors: Vieira Silvio M. , Cunha Thiago M. , França Rafael F. O. , Pinto Larissa G. , Talbot Jhimmy , Turato Walter M. , Lemos Henrique P. , Lima Jonilson B. , Verri Waldiceu A. , Almeida Sérgio C. L. , Ferreira Sergio H. , Louzada-Junior Paulo , Zamboni Dario S. , Cunha Fernando Q. 
Published: April 2012

Abstract
Intracellular pattern recognition receptors such as the nucleotide-binding oligomerization domain (NOD)-like receptors family members are key for innate immune recognition of microbial infection and may play important roles in the development of inflammatory diseases, including rheumatic diseases. In this study, we evaluated the role of NOD1 and NOD2 on development of experimental arthritis. Ag-induced arthritis was generated in wild-type, NOD1−/−, NOD2−/−, or receptor-interacting serine-threonine kinase 2−/− (RIPK2−/−) immunized mice challenged intra-articularly with methylated BSA. Nociception was determined by electronic Von Frey test. Neutrophil recruitment and histopathological analysis of proteoglycan lost was evaluated in inflamed joints. Joint levels of inflammatory cytokine/chemokine were measured by ELISA. Cytokine (IL-6 and IL-23) and NOD2 expressions were determined in mice synovial tissue by RT-PCR. The NOD2−/− and RIPK2−/−, but not NOD1−/−, mice are protected from Ag-induced arthritis, which was characterized by a reduction in neutrophil recruitment, nociception, and cartilage degradation. NOD2/RIPK2 signaling impairment was associated with a reduction in proinflammatory cytokines and chemokines (TNF, IL-1β, and CXCL1/KC). IL-17 and IL-17 triggering cytokines (IL-6 and IL-23) were also reduced in the joint, but there is no difference in the percentage of CD4+ IL-17+ cells in the lymph node between arthritic wild-type and NOD2−/− mice. Altogether, these findings point to a pivotal role of the NOD2/RIPK2 signaling in the onset of experimental arthritis by triggering an IL-17–dependent joint immune response. Therefore, we could propose that NOD2 signaling is a target for the development of new therapies for the control of rheumatoid arthritis.
Usp18 Promotes Conventional CD11b+ Dendritic Cell Development
Authors: Cong Xiu-Li , Lo Miao-Chia , Reuter Brian A. , Yan Ming , Fan Jun-Bao , Zhang Dong-Er 
Published: April 2012

Abstract
Dendritic cells (DCs) represent the key cells linking innate and adaptive immune responses. It is critical to understand the molecular factors regulating DC differentiation. Usp18 is an IFN-inducible member of the ubiquitin-specific protease family, which deconjugates ubiquitin-like modifier ISG15 from target proteins and competitively inhibits IFN-α/β–induced JAK/STAT activation. This study demonstrates that the frequency of conventional CD11b+ DCs in the spleen of Usp18−/− mice was significantly reduced, whereas the frequencies of conventional CD8+ DCs and plasmacytoid DCs remained normal. In addition, Usp18−/− bone marrow (BM) cells generate DCs less efficiently in GM-CSF–supplemented culture, demonstrating a fundamental defect throughout the DC differentiation pathway. Usp18−/− BM cells were rescued by exogenous expression of either wild-type or deconjugation-inactive Usp18, and superimposition of an IFN-α/β receptor knockout returned in vivo DC populations to normal, clearly showing that the defect seen is due solely to Usp18’s effect on IFN signaling. Finally, Usp18−/− BM-derived DCs expressed high levels of SOCS1/SOCS3, known inhibitors of GM-CSF signaling, providing a mechanistic explanation for the phenotype. In conclusion, we have identified a novel role of Usp18 in modulating conventional CD11b+ DC development via its inhibitory effect on type I IFN signaling.
Elevation of Sema4A Implicates Th Cell Skewing and the Efficacy of IFN-β Therapy in Multiple Sclerosis
Authors: Nakatsuji Yuji , Okuno Tatsusada , Moriya Masayuki , Sugimoto Tomoyuki , Kinoshita Makoto , Takamatsu Hyota , Nojima Satoshi , Kimura Tetsuya , Kang Sujin , Ito Daisuke , Nakagawa Yukinobu , Toyofuku Toshihiko , Takata Kazushiro , Nakano Misa , Kubo Masato , Suzuki Sinobu , Matsui-Hasumi Akiko , Uto-Konomi Ayako , Ogata Atsushi , Mochizuki Hideki , Sakoda Saburo , Kumanogoh Atsushi 
Published: April 2012

Abstract
Multiple sclerosis (MS) is a demyelinating autoimmune disease of the CNS and a leading cause of lasting neurologic disabilities in young adults. Although the precise mechanism remains incompletely understood, Ag presentation and subsequent myelin-reactive CD4+ T cell activation/differentiation are essential for the pathogenesis of MS. Although semaphorins were initially identified as axon guidance cues during neural development, several semaphorins are crucially involved in various phases of immune responses. Sema4A is one of the membrane-type class IV semaphorins, which we originally identified from the cDNA library of dendritic cell (DC). Sema4A plays critical roles in T cell activation and Th1 differentiation during the course of experimental autoimmune encephalomyelitis, an animal model of MS; however, its pathological involvement in human MS has not been determined. In this study, we report that Sema4A is increased in the sera of patients with MS. The expression of Sema4A is increased on DCs in MS patients and shed from these cells in a metalloproteinase-dependent manner. DC-derived Sema4A is not only critical for Th1 but also for Th17 cell differentiation, and MS patients with high Sema4A levels exhibit Th17 skewing. Furthermore, patients with high Sema4A levels have more severe disabilities and are unresponsive to IFN-β treatment. Taken together, our results suggest that Sema4A is involved in the pathogenesis of MS by promoting Th17 skewing.
Improvement of Psoriasis after Tonsillectomy Is Associated with a Decrease in the Frequency of Circulating T Cells That Recognize Streptococcal Determinants and Homologous Skin Determinants
Authors: Thorleifsdottir Ragna Hlin , Sigurdardottir Sigrun Laufey , Sigurgeirsson Bardur , Olafsson Jon Hjaltalin , Sigurdsson Martin Ingi , Petersen Hannes , Arnadottir Sigurlaug , Gudjonsson Johann Eli , Johnston Andrew , Valdimarsson Helgi 
Published: April 2012

AbstractExacerbation of chronic psoriasis can be associated with streptococcal throat infections, and T cells that respond to peptide sequences common to streptococcal M proteins and skin keratins have been detected in patients’ blood. To our knowledge, we have conducted the first blinded, prospective study to assess the impact of tonsillectomy on psoriasis. Twenty-nine patients with chronic psoriasis and history of exacerbation after sore throat were randomly assigned to tonsillectomy (n = 15) or control (n = 14) groups and monitored for 2 y clinically and by enumeration of circulating skin homing T cells that respond to short homologous M protein or keratin peptides. Thirteen patients (86%) showed sustained improvement after tonsillectomy ranging from 30 to 90% reduction in disease severity. Furthermore, there was a close correlation between the degree of clinical improvement in individual patients and reduction in the frequency of peptide-reactive skin-homing T cells in their circulation. No corresponding clinical or immunologic changes were observed among the controls. These findings indicate that tonsillectomy may have a beneficial effect on chronic psoriasis because the palatine tonsils generate effector T cells that recognize keratin determinants in the skin.
Complement Activation Product C5a Is a Selective Suppressor of TLR4-Induced, but Not TLR3-Induced, Production of IL-27(p28) from Macrophages
Authors: Bosmann Markus , Haggadone Mikel D. , Hemmila Mark R. , Zetoune Firas S. , Sarma J. Vidya , Ward Peter A. 
Published: April 2012

Abstract
There is accumulating evidence that the complement activation product, C5a, can orchestrate cellular immune functions. IL-27(p28/EBI3) is an emerging key player essential for regulating inflammatory responses and T cells. In this article, we report that C5a robustly suppressed IL-27(p28) gene expression and release in peritoneal macrophages. These cells from C57BL/6J mice abundantly produced IL-27(p28) after engagement of either the TLR3 (polyinosinic-polycytidylic acid) or TLR4 (LPS) receptor. Genetic deficiency of either TLR4 or LBP completely incapacitated the ability of macrophages to secrete IL-27(p28) in response to LPS. IL-27(p28)–producing macrophages also expressed the C5aR receptor, thus displaying an IL-27(p28)+F4/80+C5aR+ phenotype. C5a suppressed IL-27(p28) in LPS-stimulated macrophages via interactions with the C5aR receptor rather than the C5L2 receptor. After endotoxemia, C5aR−/− mice displayed higher plasma levels of IL-27(p28) compared with C57BL/6J mice. C5a did not affect the release of IL-27(p28) or the frequency of IL-27(p28)+F4/80+ macrophages after engagement of TLR3. Mechanistically, LPS activated both the NF-κB and the PI3K/Akt pathways, whereas C5a activated only the PI3K/Akt pathway. Engagement of PI3K/Akt was inhibitory for IL-27(p28) production, because PI3K/Akt pharmacologic blockade resulted in increased amounts of IL-27(p28) and reversed the suppressive effects of C5a. Blockade of PI3K/Akt in endotoxemic C57BL/6J mice resulted in higher generation of IL-27(p28). In contrast, the PI3K/Akt pathway was not involved in TLR3-mediated release of IL-27(p28). These data provide new evidence about how complement activation may selectively interfere with production of T cell regulatory cytokines by APCs in the varying contexts of either bacterial (TLR4 pathway) or viral (TLR3 pathway) infection.
Structural Analysis of a Dengue Cross-Reactive Antibody Complexed with Envelope Domain III Reveals the Molecular Basis of Cross-Reactivity
Authors: Midgley Claire M. , Flanagan Aleksandra , Tran Hai Bac , Dejnirattisai Wanwisa , Chawansuntati Kriangkrai , Jumnainsong Amonrat , Wongwiwat Wiyada , Duangchinda Thaneeya , Mongkolsapaya Juthathip , Grimes Jonathan M. , Screaton Gavin R. 
Published: April 2012

Abstract
Dengue virus infections are still increasing at an alarming rate in tropical and subtropical countries, underlying the need for a dengue vaccine. Although it is relatively easy to generate Ab responses to dengue virus, low avidity or low concentrations of Ab may enhance infection of FcR-bearing cells with clinical impact, posing a challenge to vaccine production. In this article, we report the characterization of a mAb, 2H12, which is cross-reactive to all four serotypes in the dengue virus group. Crystal structures of 2H12-Fab in complex with domain III of the envelope protein from three dengue serotypes have been determined. 2H12 binds to the highly conserved AB loop of domain III of the envelope protein that is poorly accessible in the mature virion. 2H12 neutralization varied between dengue serotypes and strains; in particular, dengue serotype 2 was not neutralized. Because the 2H12-binding epitope was conserved, this variation in neutralization highlights differences between dengue serotypes and suggests that significant conformational changes in the virus must take place for Ab binding. Surprisingly, 2H12 facilitated little or no enhancement of infection. These data provide a structural basis for understanding Ab neutralization and enhancement of infection, which is crucial for the development of future dengue vaccines.
PD-1 Protects against Inflammation and Myocyte Damage in T Cell-Mediated Myocarditis
Authors: Tarrio Margarite L. , Grabie Nir , Bu De-xiu , Sharpe Arlene H. , Lichtman Andrew H. 
Published: April 2012

Abstract
PD-1, a member of the CD28 family of immune regulatory molecules, is expressed on activated T cells, interacts with its ligands, PD-L1/B7-H1 and PD-L2/B7-DC, on other cells, and delivers inhibitory signals to the T cell. We studied the role of this pathway in modulating autoreactive T cell responses in two models of myocarditis. In a CD8+ T cell-mediated adoptive transfer model, we found that compared with Pd1+/+ CD8+ T cells, Pd1−/− CD8+ T cells cause enhanced disease, with increased inflammatory infiltrate, particularly rich in neutrophils. Additionally, we show enhanced proliferation in vivo and enhanced cytotoxic activity of PD-1–deficient T lymphocytes against myocardial endothelial cells in vitro. In experimental autoimmune myocarditis, a disease model dependent on CD4+ T cells, we show that mice lacking PD-1 develop enhanced disease compared with wild-type mice. PD-1–deficient mice displayed increased inflammation, enhanced serum markers of myocardial damage, and an increased infiltration of inflammatory cells, including CD8+ T cells. Together, these studies show that PD-1 plays an important role in limiting T cell responses in the heart.
Fine needle aspiration cytology of primary sphenoid sinus esthesioneuroblastoma metastatic to the skin
Authors: Akinfolarin Josephine , Jazaerly Tarek , Jones Kia , Abu-Hamdan Maher , Lonardo Fulvio , Folbe Adam , Giorgadze Tamar 
Published: April 2012

AbstractEsthesioneuroblastoma (ENB) is a rare tumor derived from olfactory neuroepithelium. ENB in a site outside of where olfactory epithelium exists is exceedingly rare with only five cases of ENB isolated to the sphenoid sinuses described in the literature to date. To the best of our knowledge, a skin metastasis of ENB outside the head and neck region has not been reported. We present an unusual case of a 33-year-old male diagnosed with primary sphenoid sinus ENB, who underwent surgical resection of the tumor followed by chemoradiation. About 5 months later, the patient developed a dermal mass in the sternal region, clinically suspicious for metastasis. Fine needle aspiration (FNA) revealed a tumor with morphological features and immunophenotype consistent with the metastasis from patient′s known primary sphenoid sinus ENB. Our case demonstrates that the skin may be a rare site of a metastatic ENB, and FNA is a cost-effective and reliable diagnostic method of a suspected cutaneous metastasis.
Monodisperse Hollow Supraparticles via Selective Oxidation
Authors: Xia Yunsheng , Tang Zhiyong 
Published: April 2012

AbstractA novel and general strategy to fabricate monodisperse hollow supraparticles (SPs) via selective chemical oxidation is developed. Core‐shell SPs made of semiconductor nanocrystals (NCs) are first obtained by an in situ assembly method. Subsequently, the cores can be selectively removed by preferential oxidation with dilute H2O2, resulting in formation of monodisperse hollow SPs. The structural parameters of the products, such as size, shell thickness, and composition, are tailored easily. The hollow structures achieved from CdSe/CdS core‐shell SPs possess high fluorescence quantum yields and a large Stokes shift, the latter is remarkably different from that of conventional organic dyes and quantum dots. In addition to simple hollow structures, rattle‐type nanostructures composed of semiconductor SPs or noble metal‐semiconductor hybrids are also prepared, exemplifying the versatility of the proposed strategy.
Structure‐Reactivity Studies of Simple 4‐Hydroxyprolinamide Organocatalysts in the Asymmetric Michael Addition Reaction of Aldehydes to Nitroolefins
Authors: Watts John , Luu Lien , McKee Vickie , Carey Ed , Kelleher Fintan 
Published: April 2012

AbstractA series of simple 4‐hydroxyprolinamides was synthesised and they were found to act as organocatalysts for the asymmetric conjugate addition of aldehydes to nitroolefins in excellent yields (98%), with complete diastereoselectivity (99:1, syn:anti) and enantioselectivity (98% ee for syn). Furthermore, the use of low catalyst loadings (5 mol%) and a low aldehyde molar excess (1.5 equivalents) were achieved.
Platinum(II) Diphosphinamine Complexes for the Efficient Hydration of Alkynes in Micellar Media
Authors: Trentin Francesco , Chapman Andrew M. , Scarso Alessandro , Sgarbossa Paolo , Michelin Rino A. , Strukul Giorgio , Wass Duncan F. 
Published: April 2012

AbstractHighly active monomeric bis‐cationic platinum(II) catalysts bearing small bite angle diphosphinamine [N,N‐bis(diarylphosphino)amine] ‘PNP’ ligands efficiently catalyze Markovnikov hydration of terminal and internal alkynes to the corresponding ketones in water. Catalyst solubilization in water is achieved via ion pairing with anionic micelles formed by surfactant addition. The micelles ensure dissolution of apolar alkynes and promote the intimate contact between reagents and catalyst, while in organic‐water media in the absence of surfactants the reaction is sluggish. Hydration products can be isolated by means of extraction with an apolar solvent and the catalyst, that remains confined in the aqueous phase, can be recycled up to four times without loss of catalytic activity.
Palladium‐Catalyzed Heck‐Type Reactions of Allylic Esters with Arylboronic Acids or Potassium Aryltrifluoroborates
Authors: Yao Bo , Liu Yan , Wang Meng‐Ke , Li Jin‐Heng , Tang Ri‐Yuan , Zhang Xing‐Guo , Deng Chen‐Liang 
Published: April 2012

AbstractA selective and general route to (E)‐1,3‐diaryl‐prop‐1‐enes and (E)‐3‐arylallyl acetates has been developed by palladium‐catalyzed Heck‐type reactions of allylic esters with arylboronic acids or potassium aryltrifluoroborates. The present method selectively proceeds including β‐OAc elimination or β‐H elimination on the basis of the boronic acids. Whereas a variety of allylic esters were reacted with arylboronic acids, palladium(II) acetate [Pd(OAc)2], tetra(n‐butyl)ammonium chloride [(n‐Bu)4NCl] and postassium dihydrogen phosphate (KH2PO4) to afford the corresponding diarylation products in moderate to good yields, treatment of allylic esters with potassium aryltrifluoroborates furnished the corresponding monoarylation products.
Somatic mosaicism and the phenotypic expression of COL2A1 mutations
Authors: Nagendran Sonali , Richards Allan J. , McNinch Annie , Sandford Richard N. , Snead Martin P. 
Published: April 2012

AbstractMutations in COL2A1, the gene for type II‐collagen, can result in a wide variety of phenotypes depending upon the nature of the mutation. Dominant negative mutations tend to result in severe and often lethal skeletal dysplasias such as achondrogenesis type 2, Kniest dysplasia, and spondyloepiphyseal dysplasia congenita. Stickler syndrome, a condition characterized by ophthalmological and orofacial features, deafness and arthritis, usually, but not exclusively, results from haploinsufficiency. Overlapping features of all these disorders can also be seen in the same family. Rare reports have demonstrated that phenotypic variability can be explained in some families by somatic mosaicism. Here, we describe five further examples of somatic mosaicism of COL2A1 mutations illustrating the importance of detailed clinical evaluation and molecular testing even in clinically normal parents of affected individuals. © 2012 Wiley Periodicals, Inc.
Cytological and epidemiological findings in trisomies 13, 18, and 21: England and Wales 2004–2009
Authors: Alberman Eva , Mutton David , Morris Joan K. 
Published: April 2012

AbstractThis study describes the cytological and epidemiological findings in 985 trisomy 13 and 2512 trisomy 18 compared with 10,255 trisomy 21 diagnoses between 2004 and 2009 included in the National Down Syndrome Cytogenetic Register of England and Wales. The frequency of occurrence, proportions diagnosed prenatally, sex ratios, mean maternal age, and proportions of mothers with recurrences were analyzed. Ninety‐seven, 98%, and 92% were free karyotypes for trisomy 21, 18, and 13, respectively; 3% of 21, 1% of 18, and 8% of trisomy 13 were translocations; and under 1% of trisomies 21 and 18 were double or triple aneuploids. Overall 1% of each trisomy had mosaicism, but 48% of the trisomy 21 double aneuploids, and 10% of trisomy 18 multiple aneuploids had mosaicism. The proportion of livebirths was 40% of trisomy 21, 11% of 18, and 13% of 13, respectively. Free trisomies 21 and 13 had an excess of males, and 18 had an excess of females, as did mosaic free trisomies 21 and 18. Mean maternal ages were 35.9 years in trisomy 21, 36.4 years in 18, and 34.6 years in 13. During the 6 years of data collection 1% of the mothers had recurrences, most recurrent trisomy 21 or 18 were identical translocations, but hetero‐trisomic recurrences included 21 and 18, and 21 and 13. There are significant differences between the trisomic karyotypes and attributes, possibly related to their variable origins. Notable are the relative excess of trisomy 13 translocations, mosaicism in cases with multiple aneuploidy, and the types of homo‐ and hetero‐recurrences. © 2012 Wiley Periodicals, Inc.
Working up autism: The practical role of medical genetics
Authors: Gurrieri Fiorella 
Published: April 2012

AbstractThe autism spectrum disorders (ASD) comprise a group of neurobehavioral phenotypes of heterogeneous etiology. In spite of a worldwide extensive research effort to unravel the genetic mystery of autism, medical geneticists are still facing an embarrassing lack of knowledge in dealing with the diagnosis, and consequently prognosis, of a child with autism. However, some lessons can be learned from accumulating experience in the clinical and molecular genetic evaluation of children with this condition. Patient evaluation, indications for molecular testing and counseling are the three aspects that will be discussed in this review. © 2012 Wiley Periodicals, Inc.