bluuebunny/crossref_metadata_2025_split huggingface dataset:
Education in Sri Lanka: A Historical, Administrative, and Contemporary Overview with Emphasis on Secondary Schooling
Authors: Careemdeen Jalal Deen 
Published: January 2024

Aims: This research aims to comprehensively explore the historical evolution, administrative intricacies, and current state of secondary education in Sri Lanka, with a particular focus on the post-independence era. It seeks to provide valuable insights into the challenges, initiatives, and policy measures that have shaped the educational landscape in the country.
Study Design: The study adopts a historical research design, meticulously tracing the trajectory of education in Sri Lanka from ancient times through the colonial periods to the contemporary era. It places a particular emphasis on the post-independence period, scrutinizing administrative reforms, decentralization efforts, and the structure of secondary schooling.
Place and Duration of Study: The research is conducted in Sri Lanka, encompassing various regions and educational institutions across the country.
Methodology: Grey literature, including historical documents, archival records, and unpublished reports, serves as a pivotal source for this study. Government reports, policy documents, and contemporary educational sources are analyzed to provide a nuanced understanding of the challenges and initiatives in Sri Lanka's education system. Internal memos, working papers, and non-peer-reviewed literature are utilized to dissect administrative structures, policy measures, and curriculum development.
Results: The research reveals the intricate historical journey of education in Sri Lanka, highlighting the impact of colonial rulers on the traditional education system. Post-independence challenges and initiatives, such as decentralization efforts and administrative reforms, are scrutinized. The contemporary education system, including diverse school categories and the flow of education from preschool to tertiary levels, is comprehensively analyzed. Key policies, such as free education, medium of instruction, and compulsory education, are detailed to showcase the government's commitment to inclusive and accessible education.
Conclusion: In conclusion, this study provides a holistic understanding of the multifaceted dimensions of education in Sri Lanka. By examining historical roots, administrative intricacies, and the current state of the secondary education sector, the research sheds light on the enduring pursuit of knowledge and enlightenment in Sri Lanka's educational journey. The findings offer valuable insights for scholars, policymakers, and those interested in the dynamic evolution of education in the country.
Alefacept treatment in psoriatic arthritis: Reduction of the effector T cell population in peripheral blood and synovial tissue is associated with improvement of clinical signs of arthritis
Authors: Kraan Maarten C. , van Kuijk Arno W. R. , Dinant Huibert J. , Goedkoop Amber Y. , Smeets Tom J. M. , de Rie Menno A. , Dijkmans Ben A. C. , Vaishnaw Akshay K. , Bos Jan D. , Tak Paul P. 
Published: October 2002

AbstractObjectiveTo investigate whether alefacept (a fully human lymphocyte function–associated antigen 3 [LFA‐3]/IgG1 fusion protein that blocks the LFA‐3/CD2 interaction) is able to reduce the signs and symptoms of joint inflammation in patients with active psoriatic arthritis (PsA).MethodsEleven patients with active PsA were treated with alefacept for 12 weeks in an open‐label and explorative study. Clinical joint assessment and laboratory assessments were performed at baseline and after 4, 9, 12, and 16 weeks of treatment. Serial synovial tissue (ST) biopsy specimens from an inflamed index joint (knee, ankle, wrist, or metacarpophalangeal joint) were obtained by arthroscopy at baseline and after 4 and 12 weeks of treatment.ResultsAt the completion of treatment, 6 of 11 patients (55%) fulfilled the Disease Activity Score (DAS) response criteria. Nine patients (82%) fulfilled the DAS response criteria at any point during the study. There was a statistically significant reduction in CD4+ lymphocytes (P < 0.05), CD8+ lymphocytes (P = 0.05), and CD68+ macrophages (P < 0.02) in the ST after 12 weeks of treatment compared with baseline. The ST and peripheral blood of those patients fulfilling the DAS response criteria contained more CD45RO+ cells at baseline and displayed a significant reduction in these cells compared with nonresponding patients.ConclusionThe changes in ST, together with the improvement in clinical joint scores, after treatment with alefacept support the hypothesis that T cell activation plays an important role in this chronic inflammatory disease. Furthermore, since alefacept, a T cell–specific agent, led to decreased macrophage infiltration, the data indicate that T cells are highly involved in synovial inflammation in PsA.
Symptomatic macroglossia and tongue myositis in polymyositis: Treatment with corticosteroids and intravenous immunoglobulin
Authors: Chauvet E. , Sailler L. , Carreiro M. , Paoli J. R. , Arrue P. , Astudillo L. , Oksmann F. , Delisle M. B. , Arlet Ph. 
Published: October 2002

AbstractSymptomatic macroglossia occurs in some rare congenital muscle diseases, such as Becker's and Duchenne's dystrophies or Pompe's disease. Herein we describe a case of symptomatic macroglossia with myositis of the tongue occurring in a patient with polymyositis. Tongue myositis was evidenced by dysarthria, frequent biting during mastication, swallowing difficulties without aspiration, and noisy breathing. Magnetic resonance imaging showed homogeneous hypertrophy of the tongue, especially the mouth's floor muscles. The diagnosis of tongue myositis was established by electromyography and biopsy. No other cause for the macroglossia was found. Symptoms resolved quickly with corticosteroid and intravenous immunoglobulin treatment. To our knowledge, this is the first reported case of symptomatic tongue myositis occurring in the course of polymyositis.
Association of autoantibodies to nuclear lamin B1 with thromboprotection in systemic lupus erythematosus: Lack of evidence for a direct role of lamin B1 in apoptotic blebs
Authors: Dieudé Mélanie , Senécal Jean‐Luc , Rauch Joyce , Hanly John G. , Fortin Paul , Brassard Nathalie , Raymond Yves 
Published: October 2002

AbstractObjectiveTo demonstrate the association between autoantibodies to nuclear lamin B1 (aLB1) and protection against thrombosis (“thromboprotection”) in patients with systemic lupus erythematosus (SLE), and to elucidate the mechanism by which aLB1 cause thromboprotection in vivo. Since a number of autoantigens in SLE have been localized specifically to the external surface of apoptotic blebs, it was hypothesized that circulating aLB1 may block the procoagulant effect of apoptotic blebs by binding to LB1 displayed at the external bleb surface.MethodsA cross‐sectional study was performed using serum samples obtained at first evaluation of 259 English Canadian and French Canadian patients from SLE registries at 3 hospitals. A case–control study was performed to analyze the relationship between aLB1 and lupus anticoagulant (LAC) status and thrombotic manifestations between onset of disease and last followup. Reactivity of aLB1 with Jurkat or endothelial cells, which had been induced to undergo apoptosis, was determined by indirect immunofluorescence. Localization of LB1 in apoptotic cells and blebs was analyzed by confocal microscopy and surface labeling of cell membrane proteins.ResultsHigh‐titer aLB1 was restricted to a subset of SLE patients (46 patients), with an overall frequency of 17.8% (range 11.6–24.3% in the 3 centers). LB1 antibodies were significantly associated with LAC but not with antibodies to cardiolipin (aCL) or β2‐glycoprotein I (anti‐β2GPI). The frequency of thrombosis differed markedly depending on aLB1 and LAC status, as follows: presence of LAC and absence of aLB1 50%, presence of both LAC and aLB1 22.7%, absence of both LAC and aLB1 25.5%, absence of LAC and presence of aLB1, 20.8%. Further subclassification of patients based on aCL and anti‐β2GPI status revealed that, in the presence of LAC but in the absence of aCL, anti‐β2GPI, and aLB1, the frequency of thrombosis was 40%, whereas in the presence of aLB1, it decreased strikingly, to 9.1%. LB1 was found to be translocated into surface membrane blebs during apoptosis and to be entirely enclosed within the apoptotic bleb plasma membrane of Jurkat and endothelial cells.ConclusionThe presence of aLB1 in SLE patients with LAC essentially nullifies the strong prothrombotic risk associated with LAC. Hence, aLB1 is associated with thromboprotection. Reactivity of aLB1 with apoptotic blebs does not seem to play a direct role in mediating this protection, since LB1 is buried within apoptotic blebs and inaccessible to circulating aLB1. The mechanism by which aLB1 confers thromboprotection in SLE remains to be elucidated.
Calcium‐independent phospholipase A2 through arachidonic acid mobilization is involved in Caco‐2 cell growth
Authors: Sanchez Teresa , Moreno Juan J. 
Published: October 2002

AbstractSeveral studies indicate that phospholipase A2 (PLA2) expression and/or activation account for the high levels of arachidonic acid (AA) detected in cancer and, together with the elevated expression of cyclooxygenase‐2, lead to cell proliferation and tumor formation. Using Caco‐2 cells, a human colorectal carcinoma cell, we studied the role of high‐molecular‐weight PLA2s, cytosolic PLA2 (cPLA2), and calcium‐independent PLA2 (iPLA2) in the AA cascade and in cell growth. Treatment with an antisense oligonucleotide against cPLA2α decreased [3H]AA release induced by ionophore A23187 or by a phorbol ester but did not affect the release of [3H]AA, [3H]thymidine incorporation, or Caco‐2 growth induced by fetal calf serum (FCS). However, these parameters were significantly modified by iPLA2 inhibitors and by an antisense oligonucleotide against iPLA2β. Our results show that iPLA2 was involved in AA release and the subsequent prostaglandin production induced by serum. Moreover, these data indicate that iPLA2 may be involved in the signaling pathways involved in the control of Caco‐2 proliferation. © 2002 Wiley‐Liss, Inc.
Inhibition of epidermal growth factor‐induced invasion by dexamethasone and AP‐1 decoy in human squamous cell carcinoma cell lines
Authors: Shiratsuchi Toru , Ishibashi Hiroaki , Shirasuna Kanemitsu 
Published: October 2002

AbstractInvasive squamous cell carcinoma (SCC) cells degrade extracellular matrix (ECM) via an extracellular protease cascade that includes urokinase‐type plasminogen activator (uPA), plasmin, and the metalloprotease (MMP) family of collagenases. In this study, treatment of oral SCC cells with epidermal growth factor (EGF) stimulated the cells to invade Matrigel (constructive basement membrane (BM) protein). EGF‐induced cell invasion was inhibited by antibodies to uPA and by synthetic uPA inhibitors. EGF also induced increased expression of uPA and uPA receptor (uPAR) proteins and mRNA, as well as transcription factor activator protein‐1 (AP‐1)–DNA binding. These EGF‐induced changes were inhibited by treatment with dexamethasone (DEX). DEX treatment also stimulated the production of plasminogen activator inhibitor type 1. Moreover, transfection of SCC cells with AP‐1 decoy oligodeoxynucleotides (ODNs) resulted in the suppression of EGF‐induced uPA and uPAR expression and Matrigel invasion. These results suggest that oral SCC cells invade Matrigel mainly through the uPA‐plasmin cascade, which is mediated by the transcription factor AP‐1. The uPA–uPAR interaction is essential for augmenting proteolytic activity and uPAR‐mediated signaling, which ultimately induce motility and invasion. Since DEX inhibits the expression of both uPA and uPAR, it may be a useful treatment for oral SCC. J. Cell. Physiol. 193: 340–348, 2002. © 2002 Wiley‐Liss, Inc.
Mobile IP route optimization method for next‐generation mobile networks
Authors: Takagi Yasushi , Ihara Takeshi , Ohnishi Hiroyuki 
Published: October 2002

AbstractMobile IP has gained attention as a technology that can provide mobility to universal users independently of the access network. The introduction of Mobile IP in mobile core networks is currently under investigation. This paper discusses route optimization methods when Mobile IP technology is applied to mobile core networks. More specifically, it discusses means of resolving the “Triangle Routing” problem, which occurs when communications from a correspondent node to a mobile node must be routed through a Home Agent (HA). This paper first describes the conventional route optimization method being investigated by the Internet Engineering Task Force (IETF) and indicates problems with that method. It then proposes a new Mobile IP Border Gateway (MBG) method for solving the problems of the conventional method. The MBG method enables packets that arrive from another network to be directly received at the mobile node by having a Border Gateway router maintain Binding Information consisting of the care‐of address and home address that were originally being maintained by the Home Agent for the communicating node. This paper also shows that introducing the MBG method enables the mean route length within the network to be shortened and the traffic volume routed through the Home Agent to be reduced. Finally, it shows methods of reducing the burden of registering Binding Information at the Mobile IP Border Gateway and indicates the applicability of the MBG method to large‐scale mobile communications networks. © 2002 Wiley Periodicals, Inc. Electron Comm Jpn Pt 1, 86(2): 31–41, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/ecja.1151
AGC output characteristics in broadband mobile communication systems
Authors: Taira Akinori , Ishizu Fumio , Miyake Makoto 
Published: October 2002

AbstractAt present, there are increasing demands for transmission and reception of multimedia information, and various broadband communication systems are being considered in order to respond to these requests. In these systems, frequency‐selective fading due to the delayed wave is one of the most important problems. One of the properties of the frequency‐selective fading environment is the phenomenon that the received power depends on the transmitted data pattern. Thus, there can arise a problem that the AGC output deviates from the reference value when there is a difference of patterns between the data part and the AGC part. This paper investigates the relation between the transmitted pattern and the received power distribution in the frequency‐selective fading environment, and calculates the probability distribution under the condition that there is no fading fluctuation. Then, the AGC output characteristics are examined by computer simulation for the case in which there is a pattern difference between the data part and the AGC part. It is shown that the output distribution greatly depends on the selection of the pattern in ordinary environments in broadband mobile communication. © 2002 Wiley Periodicals, Inc. Electron Comm Jpn Pt 1, 86(2): 42–50, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/ecja.1152
Polarized glucose transporters and mRNA expression properties in newly developed rat syncytiotrophoblast cell lines, TR‐TBTs
Authors: Kitano Tomohide , Iizasa Hisashi , Terasaki Tetsuya , Asashima Tomoko , Matsunaga Noriko , Utoguchi Naoki , Watanabe Yoshiteru , Obinata Masuo , Ueda Masatsugu , Nakashima Emi 
Published: October 2002

AbstractIn this study, we have established new syncytiotrophoblast cell lines (TR‐TBTs) from the recently developed transgenic rat harboring temperature‐sensitive simian virus 40 large T‐antigen gene (Tg‐rat). Four conditionally immortalized syncytiotrophoblast cell lines (TR‐TBT 18d‐1∼4) were obtained from pregnant Tg‐rats at gestational day 18. These cell lines had a syncytium‐like morphology, could be prepared as monolayers, expressed cytokeratins and rat syncytiotrophoblast markers, and exhibited apical or basal GLUT1 localizations and apical GLUT3 localizations. TR‐TBTs express large T‐antigen and grow well at 33°C with a doubling time of about 30 h. TR‐TBTs have processes for the uptake of dehydroepiandrosteron‐3‐sulfate (DHEAS) and these are predominantly located on the basal side, and this is the first report of an in vitro model of blood placental barrier (BPB) able to incorporate DHEAS. Therefore, TR‐TBTs are an appropriate in vitro model for investigating carrier‐mediated transport functions at the BPB. Moreover, TR‐TBTs express betaine/GABA transporter (GAT‐2/BGT‐1), concentrative nucleoside transporter 2 (CNT2), equilibrative nucleoside transporter 1 (ENT1), and ENT2 and the expression of these transporters has been reported in blood–brain barrier (BBB). Thus, the expression patterns of nucleoside and neurotransmitter transporters examined are quite similar in both the BPB and BBB. © 2002 Wiley‐Liss, Inc.
CD14+,CD16+ blood monocytes and joint inflammation in rheumatoid arthritis
Authors: Kawanaka Norikuni , Yamamura Masahiro , Aita Tetsushi , Morita Yoshitaka , Okamoto Akira , Kawashima Masanori , Iwahashi Mitsuhiro , Ueno Akiko , Ohmoto Yasukazu , Makino Hirofumi 
Published: October 2002

AbstractObjectiveCD14+,CD16+ monocytes, identified as a minor population of monocytes in human peripheral blood (PB), have been implicated in several inflammatory diseases. We undertook this study to investigate the relevance of this phenotype to joint inflammation in rheumatoid arthritis (RA).MethodsThe expression of CD14, CD16, CC chemokine receptor 1 (CCR1), CCR5, and intercellular adhesion molecule 1 (ICAM‐1) on monocytes was measured by flow cytometric analysis. Concentrations of the cytokines known to induce CD16 (including transforming growth factor β1 [TGFβ1], macrophage colony‐stimulating factor [M‐CSF], and interleukin‐10 [IL‐10]) and concentrations of the soluble form of CD14 (sCD14) in plasma and synovial fluid (SF) samples were measured by enzyme‐linked immunosorbent assay. The induction of CD16 on RA blood monocytes cultured for 18 hours with 1 or with all 3 cytokines was determined.ResultsThe mean ± SD frequency of CD14+,CD16+ blood monocytes was significantly increased in RA patients (11.7 ± 5.6%; n = 105) compared with healthy controls (9.5 ± 2.2%; n = 15) (P < 0.01), and the patient group with an increased frequency of CD16+ monocytes (≥13.9%) had active disease, as defined by increased counts of tender and swollen joints, levels of acute‐phase reactants, and titers of rheumatoid factor. The response to drug therapy correlated with changes in the frequency of this phenotype. The expression of CD16 on SF monocytes from RA patients was markedly elevated compared with the expression on PB monocytes. CD16 expression on RA blood monocytes was augmented in vitro by IL‐10, M‐CSF, and TGFβ1. Plasma concentrations of these cytokines and of sCD14 were significantly higher in RA patients with high CD16+ monocyte frequencies than in those with low CD16+ monocyte frequencies or in healthy controls. CD14+,CD16+ monocytes expressed higher levels of CCR1, CCR5, and ICAM‐1 than did regular CD14++,CD16− monocytes, particularly in active RA.ConclusionThese results indicate that the maturation of blood monocytes into tissue‐infiltrative CD16+ cells before entry into the joint, induced by cytokine spillover from the inflamed joint, may contribute to the persistent joint inflammation of RA.
Significant increases in serum and plasma concentrations of matrix metalloproteinases 3 and 9 in patients with rapidly destructive osteoarthritis of the hip
Authors: Masuhara Kensaku , Nakai Tsuyoshi , Yamaguchi Katsuyuki , Yamasaki Satoshi , Sasaguri Yasuyuki 
Published: October 2002

AbstractObjectiveRapidly destructive osteoarthritis (OA) of the hip is an uncommon subset of OA that affects mainly elderly women. Previous studies indicate that elevated levels of matrix metalloproteinases (MMPs) are produced within the tissue of patients with the condition. In the present study, we sought to determine whether serum and plasma levels of MMPs and tissue inhibitors of metalloproteinases (TIMPs) are also elevated.MethodsBlood samples were obtained from 16 patients with rapidly destructive hip OA and from 20 patients with OA before total hip arthroplasty was performed. Synovial specimens were obtained during surgery. Synovial fibroblasts that had migrated sufficiently from explants were subcultured in vitro for 72 hours after confluency, and harvested supernatants were collected. Blood, tissue samples, and fibroblasts were assayed for MMPs 1, 2, 3, and 9, and TIMPs 1 and 2 by sandwich enzyme immunoassay.ResultsIn blood samples, the levels of MMP‐3 and MMP‐9 in the group with rapidly destructive hip OA were significantly higher than the normal range and were also significantly higher than those in the OA group. In tissue samples, the levels of MMP‐1, MMP‐3, MMP‐9, and TIMP‐1 in the group with rapidly destructive hip OA were significantly higher than those in the OA group.ConclusionThe results of this study show that serum and plasma levels of MMP‐3 and MMP‐9 are significantly increased in patients with rapidly destructive hip OA. Significantly large amounts of these MMPs produced in synovial tissues within the hip joint could contribute in part to elevation of blood levels. Detection of increased levels of MMP‐3 and MMP‐9 in patients with painful, disabling hip OA may be of diagnostic value for rapidly destructive hip OA.
Evidence for linkage of HLA loci in juvenile idiopathic oligoarthritis: Independent effects of HLA–A and HLA–DRB1
Authors: Zeggini Eleftheria , Donn Rachelle P. , Ollier William E. R. , Thomson Wendy ,   The British Paediatric Rheumatology Study Group
Published: October 2002

AbstractObjectiveAlthough multiple associations between HLA loci and juvenile oligoarthritis have previously been documented, evidence for linkage of HLA loci in oligoarthritis in UK Caucasians with juvenile idiopathic arthritis (JIA) has not been described. The aim of this study was to investigate linkage of HLA–A, B, and DRB1 in UK Caucasian JIA patients with oligoarthritis.MethodsOne hundred forty‐two families comprising affected offspring and their parents (45 with one parent available and 97 with both parents available) were typed for HLA–A, B, and DRB1 by polymerase chain reaction–sequence‐specific oligonucleotide probe. Single‐point and multipoint analyses were performed using various modifications of the extended transmission disequilibrium test. Linkage disequilibrium (LD) analysis was performed using the EH‐Plus system.ResultsLinkage to HLA–A and HLA–DRB1 was seen in oligoarthritis and in the International League of Associations for Rheumatology–defined subgroups of persistent oligoarthritis and extended oligoarthritis. Linkage to HLA–A, B, and DRB1 was also observed in female patients with oligoarthritis. Linkage of the HLA loci seemed to be attributable to maternal preferential transmission of alleles. Furthermore, LD patterns between the HLA–A, B, and DRB1 loci were investigated. HLA–A and HLA–DRB1 were confirmed as independent susceptibility loci for oligoarthritis.ConclusionThis is the first study to establish linkage of HLA–A and HLA–DRB1 in oligoarthritis and to show that the 2 loci contribute independently to disease. Further studies are being performed to determine whether it is these loci or other genes in LD with them that are responsible for susceptibility to oligoarthritis in UK Caucasian patients with JIA.