bluuebunny/crossref_metadata_2025_split huggingface dataset:
Spatial and temporal variations of sedimentation rate in the Timah Tasoh Water Reservoir, Perlis, Malaysia
Authors: Rahaman Zullyadini , Ismail Wan 
Published: July 2010

Spatial and temporal variations of sedimentation rate in the Timah Tasoh Water Reservoir, Perlis, Malaysia
Human activities such as logging, land conservation, road construction and other disturbances in watersheds will increase erosion rate and thus the amount of sediment transported into the river that reaches lakes, reservoirs and sea. Accelerated sedimentation rate in the reservoir can significantly reduce a reservoir's surface area, eliminating wetland area surrounding the reservoir and shallow the areas near the shore of the reservoir. A study of sedimentation rate in the Timah Tasoh water reservoir was carried out from May 2001 to April 2002 by means of sediment traps. The aim of this study is to determine the spatial and temporal pattern of sedimentation rates in the reservoir. The sediment traps were installed at five different locations in the reservoir and replaced every month. Gross sedimentation rates measured in the sediment traps vary from about an average of 1.4 kg/m2/month or 16.3 kg/m2/yr in the deepest part of the reservoir to about 79.2 kg/m2/yr (monthly average of 6.6 kg/m2/month) and 47.1 kg/m2/yr (monthly average of 3.9 kg/m2/month) near the inlet of the Pelarit River and the Tasoh River respectively. The sedimentation rate near the Pelarit River and the Tasoh River inflow is correlated with the water and suspended sediment discharge in the river, owing to its proximity to the rivers and the flooding effect, mainly during the wet season. The sedimentation rate decreases southward along the reservoir, as a result of increasing distance from the river mouth. The total suspended sediment load of the Upper Pelarit River and the Jarum River flowing into the reservoir is 11.4 × 103 ton/year and 5.41 × 103 ton//year respectively.
Prediction of littoral drift with Adaptive Neuro-Fuzzy Inference System
Authors: Sabet Masumeh , Naseri Mehdi , Sabet Hosein 
Published: July 2010

Prediction of littoral drift with Adaptive Neuro-Fuzzy Inference System
The amount of sand moving parallel to a coastline forms a prerequisite for many harbor design projects. Such information is currently obtained through various empirical formulae. Despite so many works in the past, an accurate and reliable estimation of the rate of sand drift has still remained a problem. It is a non-linear process and can be described by chaotic time-series. The current study addresses this issue through the use of Adaptive Neuro-Fuzzy Inference System (ANFIS). ANFIS is about taking an initial fuzzy inference system (FIS) and tuning it with a back propagation algorithm based on the collection of input-output data. ANFIS was developed to predict the sand drift from a variety of causative variables. The structure and algorithm of ANFIS for predicting the rate of sand drift is described. The Adaptive Neuro-Fuzzy Inference System was validated by confirming its consistency with a database of specified physical process.
Cranial nerve injury after minor head trauma
Authors: Coello Alejandro Fernández , Canals Andreu Gabarrós , Gonzalez Juan Martino , Martín Juan José Acebes 
Published: July 2010

Object
There are no specific studies about cranial nerve (CN) injury following mild head trauma (Glasgow Coma Scale Score 14–15) in the literature. The aim of this analysis was to document the incidence of CN injury after mild head trauma and to correlate the initial CT findings with the final outcome 1 year after injury.

Methods
The authors studied 49 consecutive patients affected by minor head trauma and CN lesions between January 2000 and January 2006. Detailed clinical and neurological examinations as well as CT studies using brain and bone windows were performed in all patients. Based on the CT findings the authors distinguished 3 types of traumatic injury: no lesion, skull base fracture, and other CT abnormalities. Patients were followed up for 1 year after head injury. The authors distinguished 3 grades of clinical recovery from CN palsy: no recovery, partial recovery, and complete recovery.

Results
Posttraumatic single nerve palsy was observed in 38 patients (77.6%), and multiple nerve injuries were observed in 11 (22.4%). Cranial nerves were affected in 62 cases. The most affected CN was the olfactory nerve (CN I), followed by the facial nerve (CN VII) and the oculomotor nerves (CNs III, IV, and VI). When more than 1 CN was involved, the most frequent association was between CNs VII and VIII. One year after head trauma, a CN deficit was present in 26 (81.2%) of the 32 cases with a skull base fracture, 12 (60%) of 20 cases with other CT abnormalities, and 3 (30%) of 10 cases without CT abnormalities.

Conclusions
Trivial head trauma that causes a minor head injury (Glasgow Coma Scale Score 14–15) can result in CN palsies with a similar distribution to moderate or severe head injuries. The CNs associated with the highest incidence of palsy in this study were the olfactory, facial, and oculomotor nerves. The trigeminal and lower CNs were rarely damaged. Oculomotor nerve injury can have a good prognosis, with a greater chance of recovery if no lesion is demonstrated on the initial CT scan.
Hazard of Incident and Progressive Knee and Hip Radiographic Osteoarthritis and Chronic Joint Symptoms in Individuals with and without Limb Length Inequality
Authors: GOLIGHTLY YVONNE M. , ALLEN KELLI D. , HELMICK CHARLES G. , SCHWARTZ TODD A. , RENNER JORDAN B. , JORDAN JOANNE M. 
Published: July 2010

Objective.To examine the hazard of incident and progressive radiographic osteoarthritis (rOA) and chronic joint symptoms at the hip and knee by limb length inequality (LLI) in a large, community-based sample.Methods.A longitudinal cohort completed baseline (1991–97) clinical evaluation and identical followup assessment (1999–2003) (median followup time 5.9 yrs, range 3.0–13.1 yrs). LLI was defined at baseline as a measured difference between limbs ≥ 2 cm. The study groups with LLI data comprised 1583 participants with paired (baseline and followup) knee radiographs and 1453 participants with paired hip radiographs. Multivariable Cox regression models were used to examine the hazard of incident and progressive knee and hip rOA and chronic joint symptoms, with adjustment for demographic and clinical factors.Results.The hazard of developing incident knee or hip rOA was 20%–30% higher and of developing progressive knee or hip rOA was 35%–83% higher among participants with LLI, but results were only statistically significant for progressive knee rOA (adjusted hazard ratio = 1.83, 95% CI 1.10–3.05). The hazards of progressive chronic knee symptoms and incident and progressive chronic hip symptoms were 13%–59% higher among participants with LLI, but were not statistically significant.Conclusion.LLI was associated with progressive knee rOA and was nonsignificantly associated with incident knee or hip rOA and progressive hip rOA, progressive chronic knee symptoms, and incident and progressive chronic hip symptoms. Longer studies may strengthen these associations and help determine whether LLI is a risk factor or marker of these outcomes.
Regulation of the IL-21 Gene by the NF-κB Transcription Factor c-Rel
Authors: Chen Guobing , Hardy Kristine , Bunting Karen , Daley Stephen , Ma Lina , Shannon M. Frances 
Published: July 2010

Abstract
IL-21 is a member of the common γ-chain–dependent cytokine family and is a key modulator of lymphocyte development, proliferation, and differentiation. IL-21 is highly expressed in activated CD4+ T cells and plays a critical role in the expansion and differentiation of the Th cell subsets, Th17 and follicular helper T (TFH) cells. Because of its potent activity in both myeloid and lymphoid cell immune responses, it has been implicated in a number of autoimmune diseases and has also been used as a therapeutic agent in the treatment of some cancers. In this study, we demonstrate that c-Rel, a member of the NF-κB family of transcription factors, is required for IL-21 gene expression in T lymphocytes. IL-21 mRNA and protein levels are reduced in the CD4+ cells of rel−/− mice when compared with rel+/+ mice in both in vitro and in vivo models. A c-Rel binding site identified in the proximal promoter of il21 is confirmed to bind c-Rel in vitro and in vivo and to regulate expression from the il21 promoter in T cells. Downstream of IL-21 expression, Th17, TFH, and germinal center B cell development are also impaired in rel−/− mice. The administration of IL-21 protein rescued the development of TFH cells but not germinal center B cells. Taken together, c-Rel plays an important role in the expression of IL-21 in T cells and subsequently in IL-21-dependent TFH cell development.
In Hepatic Fibrosis, Liver Sinusoidal Endothelial Cells Acquire Enhanced Immunogenicity
Authors: Connolly Michael K. , Bedrosian Andrea S. , Malhotra Ashim , Henning Justin R. , Ibrahim Junaid , Vera Valery , Cieza-Rubio Napoleon E. , Hassan Burhan U. , Pachter H. Leon , Cohen Steven , Frey Alan B. , Miller George 
Published: July 2010

Abstract
The normal liver is characterized by immunologic tolerance. Primary mediators of hepatic immune tolerance are liver sinusoidal endothelial cells (LSECs). LSECs block adaptive immunogenic responses to Ag and induce the generation of T regulatory cells. Hepatic fibrosis is characterized by both intense intrahepatic inflammation and altered hepatic immunity. We postulated that, in liver fibrosis, a reversal of LSEC function from tolerogenic to proinflammatory and immunogenic may contribute to both the heightened inflammatory milieu and altered intrahepatic immunity. We found that, after fibrotic liver injury from hepatotoxins, LSECs become highly proinflammatory and secrete an array of cytokines and chemokines. In addition, LSECs gain enhanced capacity to capture Ag and induce T cell proliferation. Similarly, unlike LSECs in normal livers, in fibrosis, LSECs do not veto dendritic cell priming of T cells. Furthermore, whereas in normal livers, LSECs are active in the generation of T regulatory cells, in hepatic fibrosis LSECs induce an immunogenic T cell phenotype capable of enhancing endogenous CTLs and generating potent de novo CTL responses. Moreover, depletion of LSECs from fibrotic liver cultures mitigates the proinflammatory milieu characteristic of hepatic fibrosis. Our findings offer a critical understanding of the role of LSECs in modulating intrahepatic immunity and inflammation in fibro-inflammatory liver disease.
Identification of Regulatory Foxp3+ Invariant NKT Cells Induced by TGF-β
Authors: Monteiro Marta , Almeida Catarina F. , Caridade Marta , Ribot Julie C. , Duarte Joana , Agua-Doce Ana , Wollenberg Ivonne , Silva-Santos Bruno , Graca Luis 
Published: July 2010

Abstract
Invariant NKT (iNKT) cells were shown to prevent the onset of experimental autoimmune encephalomyelitis in mice following administration of their specific TCR agonist α-galactosylceramide. We found that this protection was associated with the emergence of a Foxp3+ iNKT cell population in cervical lymph nodes. We demonstrate that the differentiation of these cells is critically dependent on TGF-β in both mice and humans. Moreover, in vivo generation of Foxp3+ iNKT cells was observed in the TGF-β–rich environment of the murine gut. Foxp3+ iNKT cells displayed a phenotype similar to that of Foxp3+ regulatory T cells, and they suppress through a contact-dependent, glucocorticoid-induced TNFR-mediated mechanism. Nevertheless, Foxp3+ iNKT cells retain distinctive NKT cell characteristics, such as promyelocytic leukemia zinc finger protein expression and preferential homing to the liver following adoptive transfer, where they stably maintained Foxp3 expression. Our data thus unveil an unexpected capacity of iNKT cells to acquire regulatory functions that may contribute to the establishment of immunological tolerance.
P2X7 Receptor-Mediated Release of Cathepsins from Macrophages Is a Cytokine-Independent Mechanism Potentially Involved in Joint Diseases
Authors: Lopez-Castejon Gloria , Theaker Jill , Pelegrin Pablo , Clifton Andrew D. , Braddock Martin , Surprenant Annmarie 
Published: July 2010

AbstractThe ATP-gated P2X7 receptor (P2X7R) is a promising therapeutic target in chronic inflammatory diseases with highly specific antagonists currently under clinical trials for rheumatoid arthritis. Anti-inflammatory actions of P2X7R antagonists are considered to result from inhibition of P2X7R-induced release of proinflammatory cytokines from activated macrophages. However, P2X7Rs are also expressed in resting macrophages, suggesting that P2X7R may also signal via cytokine-independent mechanisms involved in joint disease. In this study, we examined P2X7R function in resting human lung macrophages and mouse bone marrow-derived macrophages and found that ATP induced rapid release of the lysosomal cysteine proteases cathepsin B, K, L, and S and that was independent of the presence of the proinflammatory cytokines IL-1β and IL-18. Cathepsins released into the medium were effective to degrade collagen extracellular matrix. ATP-induced cathepsin release was abolished by P2X7R antagonists, absent from P2X7R−/− mouse macrophages, and not associated with cell death. Our results suggest P2X7R activation may play a novel and direct role in tissue damage through release of cathepsins independently of its proinflammatory actions via IL-1 cytokines.
Inhibitory Role for d-Alanylation of Wall Teichoic Acid in Activation of Insect Toll Pathway by Peptidoglycan of Staphylococcus aureus
Authors: Tabuchi Yukichika , Shiratsuchi Akiko , Kurokawa Kenji , Gong Ji Hee , Sekimizu Kazuhisa , Lee Bok Luel , Nakanishi Yoshinobu 
Published: July 2010

Abstract
Pathogenic bacteria mitigate host immunity to establish infections, but the mechanism of this bacterial action has not been fully elucidated. To search for cell wall components that modulate innate immune responses in host organisms, we examined Staphylococcus aureus mutants, which were deficient in components of the cell wall, for pathogenicity in Drosophila. A mutation of dltA, which is responsible for the d-alanylation of teichoic acids, brought about an increase in the survival rate of adult flies that had received a septic infection with the bacteria. The growth of dltA-deficient S. aureus in adult flies was less efficient than that of the parental strain. The level of mRNA of Toll pathway-dependent antimicrobial peptides was higher in flies infected with the dltA mutant than that observed after the infection with the parental strain. The defective phenotype associated with the mutation of dltA, reduced pathogenicity and growth, was not evident in flies lacking the Toll pathway. Finally, a fraction of peptidoglycan prepared from the dltA mutant induced the expression of mRNA of a Toll-dependent antimicrobial peptide in flies and was bound by peptidoglycan recognition protein-SA in vitro more effectively than that obtained from the parental strain, and this difference was lost after the removal of wall teichoic acid from peptidoglycan. Taken together, we conclude that d-alanylated wall teichoic acid of S. aureus mitigates a Toll-mediated humoral response in Drosophila interfering with the recognition of peptidoglycan by a pattern recognition receptor.
B7-H1 (Programmed Cell Death Ligand 1) Is Required for the Development of Multifunctional Th1 Cells and Immunity to Primary, but Not Secondary, Salmonella Infection
Authors: Lee Seung-Joo , O’Donnell Hope , McSorley Stephen J. 
Published: July 2010

Abstract
Robust Ab and CD4 T cell responses are required for the resolution of Salmonella infection in susceptible mice. In this study, we examined the role of B7-H1 (programmed cell death ligand 1) in resistance to primary Salmonella infection. Infected B7-H1–deficient mice had significantly higher bacterial burdens at day 21 and day 35 postinfection compared with wild-type mice, demonstrating that B7-H1 plays an important role in immunity to Salmonella. B7-H1–deficient and wild-type mice both generated Salmonella-specific IgM and IgG2c Ab responses to infection, and clonal expansion of endogenous and adoptively transferred Salmonella-specific CD4 T cells was similar in both groups. However, although Salmonella-specific IFN-γ–producing Th1 CD4 T cells were generated in Salmonella-infected B7-H1–deficient mice, these cells did not expand to the level observed in wild-type mice. Furthermore, fewer multifunctional Th1 cells that simultaneously secreted IFN-γ, TNF-α, and IL-2 were detected in Salmonella-infected B7-H1–deficient mice. Together, these data demonstrate that B7-H1 is required for the generation of multifunctional Th1 responses and optimal protective immunity to primary Salmonella infection.
Qualitatively Different Memory CD8+ T Cells Are Generated after Lymphocytic Choriomeningitis Virus and Influenza Virus Infections
Authors: Mueller Scott N. , Langley William A. , Li Guimei , García-Sastre Adolfo , Webby Richard J. , Ahmed Rafi 
Published: July 2010

Abstract
Viral infections often induce robust T cell responses that are long-lived and protective. However, it is unclear to what degree systemic versus mucosal infection influences the generation of effector and memory T cells. In this study, we characterized memory CD8+ T cells generated after respiratory influenza virus infection and compared the phenotypic and functional qualities of these cells with memory T cells generated after systemic infection with lymphocytic choriomeningitis virus (LCMV). Using a recombinant influenza virus expressing the LCMV gp33–41 epitope and TCR transgenic CD8+ T cells with a fixed TCR, we compared responses to the same Ag delivered by mucosal or systemic viral infection. Memory cells generated postinfection with either virus showed only a few phenotypic differences. Yet, influenza memory T cells produced lower amounts of effector cytokines upon restimulation and displayed reduced proliferation compared with LCMV-induced memory cells. Strikingly, we observed reduced expansion of spleen- and, in particular, lung-derived influenza memory cells after recall in vivo, which correlated with reduced early protection from secondary infection. These findings suggest that qualitatively different memory CD8+ T cells are generated after respiratory or systemic virus infections.
Twins with omphalocele in Denmark (1970–1989)
Authors: Bugge Merete 
Published: July 2010

AbstractSeven pairs of twins, two monozygotic (MZ), two dizygotic (DZ), and three like‐sex pairs of unknown zygosity are described. The twin pairs were all discordant for omphalocele except for one pair of conjoined twins. The 8 infants with omphalocele represent 3.1% of the 253 infants with omphalocele, ascertained in an almost complete nationwide data set of live‐ and stillborn infants with abdominal wall defects in two decades in Denmark (1970–1989). The occurrence of twins with omphalocele was not significantly different from the occurrence of twins in the Danish population in the same period. To our knowledge this is the first report of the occurrence of twins with omphalocele in a systematic nationwide epidemiological study. © 2010 Wiley‐Liss, Inc.
Giuffrè–Tsukahara syndrome: Evidence for X‐linked dominant inheritance and review
Authors: Dalal Ashwin B. , Sarkar Anujit , Priya T. Padma , Nandineni Madhusudan R. 
Published: July 2010

AbstractWe report on a girl with Giuffrè–Tsukahara syndrome manifesting microcephaly, mental retardation, radio‐ulnar synostosis, short stature and scoliosis. Skewed X‐inactivation was not observed in our patient. We reviewed previous reports and provide evidence in support of X‐linked dominant inheritance of this condition. © 2010 Wiley‐Liss, Inc.
Double‐blind therapeutic trial in Angelman syndrome using betaine and folic acid
Authors: Peters Sarika U. , Bird Lynne M. , Kimonis Virginia , Glaze Daniel G. , Shinawi Lina M. , Bichell Terry Jo , Barbieri‐Welge Rene , Nespeca Mark , Anselm Irina , Waisbren Susan , Sanborn Erica , Sun Qin , O'Brien William E. , Beaudet Arthur L. , Bacino Carlos A. 
Published: July 2010

AbstractAngelman syndrome (AS) is caused by reduced or absent expression of the maternally inherited ubiquitin protein ligase 3A gene (UBE3A), which maps to chromosome 15q11–q13. UBE3A is subject to genomic imprinting in neurons in most regions of the brain. Expression of UBE3A from the maternal chromosome is essential to prevent AS, because the paternally inherited gene is not expressed, probably mediated by antisense UBE3A RNA. We hypothesized that increasing methylation might reduce expression of the antisense UBE3A RNA, thereby increasing UBE3A expression from the paternal gene and ameliorating the clinical phenotype. We conducted a trial using two dietary supplements, betaine and folic acid to promote global levels of methylation and attempt to activate the paternally inherited UBE3A gene. We performed a number of investigations at regular intervals including general clinical and developmental evaluations, biochemical determinations on blood and urine, and electroencephalographic studies. We report herein the data on 48 children with AS who were enrolled in a double‐blind placebo‐controlled protocol using betaine and folic acid for 1 year. There were no statistically significant changes between treated and untreated children; however, in a small subset of patients we observed some positive trends. © 2010 Wiley‐Liss, Inc.
Investigation of 90 patients referred for molecular cytogenetic analysis using aCGH uncovers previously unsuspected anomalies of imprinting
Authors: Poole Rebecca L. , Baple Emma , Crolla John A. , Temple I. Karen , Mackay Deborah J.G. 
Published: July 2010

AbstractThis study was an investigation of 90 patients referred to the Wessex Regional Genetics Laboratory for and negative by molecular cytogenetic analysis using array comparative genomic hybridization. This patient cohort represents typical referrals to a regional genetic centre. Methylation analysis was performed at 13 imprinted loci [PLAGL1, IGF2R, MEST, GRB10, H19, IGF2 DMR2 (IGF2P0), KCNQ1OT1 (KvDMR), MEG3, SNRPN, PEG3, GNAS (GNAS exon 1a and NESP55) and GNASAS]. In total 6/90 (6.67%) were shown to have a methylation defect, 2 of which were associated with known imprinting disorders: 1 patient had isolated hypomethylation at IGF2P0, an atypical epigenotype associated with Russell–Silver syndrome, and 1 showed hypomethylation at KvDMR consistent with a diagnosis of Beckwith–Wiedemann syndrome. A further 4 patients, 3 exhibiting complete hypermethylation, and 1 partial hypomethylation, had aberrations at IGF2R, the clinical significance of which remains unclear. This study demonstrates the potential utility of epigenetic investigation in routine diagnostic testing. © 2010 Wiley‐Liss, Inc.