bluuebunny/crossref_metadata_2025_split huggingface dataset:
Multiple roles of Id4 in developmental myelination: Predicted outcomes and unexpected findings
Authors: Marin‐Husstege Mireya , He Ye , Li Jiadong , Kondo Toru , Sablitzky Fred , Casaccia‐Bonnefil Patrizia 
Published: July 2006

AbstractMyelination in the central nervous system is a complex process requiring the integration of oligodendrocyte progenitor differentiation and the coordinate expression of myelin genes. This study addresses the role of the helix‐loop‐helix protein Id4 in these two events. Overexpression of Id4 in oligodendrocyte progenitors prevents differentiation and consequently decreases the endogenous expression of all myelin genes. Conversely, progenitors lacking Id4 display precocious differentiation both in vitro and in vivo, and this phenotype is partially compensated by increased apoptosis. Besides this role, Id4 also has the ability to decrease the activity of specific myelin promoters, since Id4 overexpression decreases the activity of luciferase reporter genes driven by the ceramide galactosyltransferase (CGT) or myelin basic protein (MBP) promoter, but not by a myelin proteolipid protein (PLP) promoter. Consistent with these results, the expression levels of MBP and CGT are greater in neonatal Id4 null mice when compared with wild‐type siblings and correlate with the early detection of MBP immunoreactive myelinated fibers. In contrast, the levels of other myelin proteins, such as PLP and myelin associated glycoprotein (MAG) are decreased in the Id4 null mice. MAG expression is localized to the soma rather than the fibers of immunoreactive cells in the neonatal brain and compensated at later developmental stages. These data support the role of Id4 as oligodendrocyte differentiation inhibitor with the ability to differentially regulate the expression and subcellular distribution of myelin gene products. © 2006 Wiley‐Liss, Inc.
The effect of temperature on viscoelastic properties of glass ionomer cements and compomers
Authors: Helvatjoglu‐Antoniades M. , Papadogiannis Y. , Lakes R. S. , Palaghias G. , Papadogiannis D. 
Published: July 2006

AbstractThe objective of this study was to determine the viscoelastic properties of different types of glass ionomer cements (GICs) and compomers under varying temperature conditions found in the mouth. The materials tested were a conventional GIC (Aqua Ionofil U), a resin modified GIC (Fuji II LC), a highly viscous GIC (Voco Ionofil Molar), and two polyacid modified composite resins/compomers (Glasiosite and Dyract Flow). Six groups of four specimens were prepared from each material. One group was stored dry for 24 h and was subsequently tested dry at 21°C. Each of the remaining five groups was stored for 24 h in distilled water at the temperatures 21, 30.5, 37, 43.5, and 50°C, respectively, and was subsequently tested at that temperature. Shear storage modulus and loss tangent were determined by conducting dynamic torsional loading. Static shear moduli were determined by applying a constant torque (below the proportional limit of the materials) for 10 s and recording the angular deformation of the specimens. Data were analyzed by ANOVA and Duncan's test (α= 0.05). It was found that the viscoelastic properties varied significantly (p < 0.05) across the different materials. The compomer Glasiosite, with the highest filler content, and the highly viscous GIC Voco Ionofil Molar exhibited the highest elastic moduli and lowest loss tangents. Viscoelastic properties varied also significantly (p < 0.05) with temperature levels, but changes in the tested region were not indicative of a glass transition. Dynamic shear storage moduli were highly correlated to the static ones. Storage in water lowered the values of elastic moduli. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2007
Biocompatibility of various formula root filling materials for primary teeth
Authors: Huang Tsui‐Hsien , Ding Shinn‐Jyh , Kao Chia‐Tze 
Published: July 2006

AbstractThe aim of this study was to compare the effects of different materials used in primary root canal fillings on the cell viability of human osteosarcoma cell lines. The experimental group contained six different types of root canal filling materials, including zinc oxide (ZnO) + eugenol + formocresol (FC), Ca(OH)2 + FC, Ca(OH)2 + Iodoform, Ca(OH)2 + Iodoform + camphorated parachlorophenol (CPC), Ca(OH)2 + CPC, and Vitapex. Cell viability tests were performed using tetrazolium bromide colorimetric (MTT) assay on human osteosacorma cell lines (U2OS). The results were analyzed using one‐way analysis of variance (ANOVA) and Student–Newman–Keul's test with p < 0.05 showed statistical differences. The ZnO + eugenol + FC group and Ca(OH)2 + FC group showed the lowest survival rates (p < 0.05). The Ca(OH)2 + Iodoform + CPC group and Ca(OH)2 + CPC group showed significantly lower survival rates at concentrations above 6 μL/mL (p < 0.05). The Ca(OH)2 + Iodoform group and Vitapex group showed the highest survival rates (p < 0.05). We concluded that the use of calcium hydroxide with iodoform as a root filling base material is a better option than other medications. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2007
Upregulation of matrix metalloproteinase (MMP)‐1 and its activator MMP‐3 of human osteoblast by uniaxial cyclic stimulation
Authors: Sasaki Kan , Takagi Michiaki , Konttinen Yrjö T. , Sasaki Akiko , Tamaki Yasunobu , Ogino Toshihiko , Santavirta Seppo , Salo Jari 
Published: July 2006

AbstractProper mechanical loading is essential for bone remodeling and maintenance of human skeletal system. Matrix metalloproteinases (MMPs) are secreted by mesenchymal stromal lining cells and osteoblasts to prepare the initiation sites for osteoclastic bone resorption at the beginning of the remodeling cycle. However, only a few studies have addressed the effect of mechanical stress on MMPs and their endogenous tissue inhibitors of matrix metalloproteinases (TIMPs) in osteoblasts. In this study, the response of human osteoblasts to uniaxial cyclic stretching was investigated to clarify this more in detail. Stretching affected the orientation of the osteoblasts, and quantitative reverse transcription‐polymerase chain reaction revealed coordinated upregulation of MMP‐1 and its activator MMP‐3 mRNA by cyclic 5% stretching at 3 h (p < 0.01). Upregulation of cyclooxygenase‐2 mRNA was also found in response to cyclic 1 and 5% stretchings at 1, 3, and 6 h (p < 0.01). No changes were found in MMP‐2, TIMP‐1, and ‐2. The mRNA expression of MMP‐9 was low and MMP‐13 was not detected. This study suggests that MMP‐1 and ‐3, enhanced by uniaxial cyclic mechanical stimulation of osteoblasts, are candidate key enzymes in the processing of collagen on bone surface, which might be necessary to allow osteoclastic recruitment leading to bone resorption. The strain might also play a role in cleaning of demineralized bone surface during the reversal phase, before bone formation starts. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2007
Evaluation of the growth of chondrocytes and osteoblasts seeded into precision scaffolds fabricated by fused deposition manufacturing
Authors: Hsu Shan‐hui , Yen Hung‐Jen , Tseng Ching‐Shiow , Cheng Chia‐Sheng , Tsai Ching‐Lin 
Published: July 2006

AbstractIn this study, fused deposition manufacturing (FDM) was utilized to fabricate the precision scaffolds for cartilage and bone regeneration. Cell seeding into such scaffolds was evaluated. For poly(D,l‐lactide) (PLA) scaffolds used for cartilage regeneration, the structure with larger inner space, four direction stacking (4D) and small interval of fibers were better. Chondrocyte proliferated well with matrix accumulation in precision scaffolds coated with type II collagen at 4 weeks of in vitro culture. The seeding efficiency of osteoblasts in most polycaprolactone (PCL) scaffolds used for bone regeneration could arrive 50% of original cell seeding density, and the amount of cells in scaffolds increased to double fold after 2 weeks of in vitro culture. The histological cross‐section also revealed proliferation and mineralization of osteoblasts among the PCL fibers. The results indicated that the highly porous and interconnected structure of precision scaffolds could benefit cell ingrowth. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2007
Revenge of the “Sit”: How lifestyle impacts neuronal and cognitive health through molecular systems that interface energy metabolism with neuronal plasticity
Authors: Vaynman Shoshanna , Gomez‐Pinilla Fernando 
Published: July 2006

AbstractExercise, a behavior that is inherently associated with energy metabolism, impacts the molecular systems important for synaptic plasticity and learning and memory. This implies that a close association must exist between these systems to ensure proper neuronal function. This review emphasizes the ability of exercise and other lifestyle implementations that modulate energy metabolism, such as diet, to impact brain function. Mechanisms believed to interface metabolism and cognition seem to play a critical role with the brain derived neurotrophic factor (BDNF) system. Behaviors concerned with activity and metabolism may have developed simultaneously and interdependently during evolution to determine the influence of exercise and diet on cognition. Alook into our evolutionary past indicates that our genome remains unchanged from the times of our hunter‐gatherer ancestors, whose active lifestyle predominated throughout almost 100% of humankind's existence. Consequently, the sedentary lifestyle and eating behaviors enabled by the comforts of technologic progress may be reaping “revenge” on the health of both our bodies and brains. In the 21st century we are confronted by the ever‐increasing incidence of metabolic disorders in both the adult and child population. The ability of exercise and diet to impact systems that promote cell survival and plasticity may be applicable for combating the deleterious effects of disease and ageing on brain health and cognition. © 2006 Wiley‐Liss, Inc.
Heat shock protein 27 is involved in neurite extension and branching of dorsal root ganglion neurons in vitro
Authors: Williams Kristy L. , Rahimtula Masuma , Mearow Karen M. 
Published: July 2006

AbstractAlteration of the cytoskeleton in response to growth factors and extracellular matrix proteins is necessary for neurite growth. The cytoskeletal components, such as actin and tubulin, can be modified through interaction with other cellular proteins, including the small heat shock protein Hsp27. Our previous work suggested that Hsp27 influences neurite growth, potentially via its phosphorylation state interactions with actin. To investigate further the role of Hsp27 in neurite outgrowth of adult dorsal root ganglion (DRG) neurons, we have both down‐regulated endogenous Hsp27 and expressed exogenous Hsp27. Down‐regulation of Hsp27 with Hsp27 siRNA resulted in a decrease of neuritic tree length and complexity. In contrast, expression of exogenous Hsp27 in these neurons resulted in an increase in neuritic tree length and branching. Collectively, these results demonstrate that Hsp27 may play a role in neuritic growth via modulation of the actin cytoskeleton. © 2006 Wiley‐Liss, Inc.
Amyloid β up‐regulates brain‐derived neurotrophic factor production from astrocytes: Rescue from amyloid β‐related neuritic degeneration
Authors: Kimura Nobuyuki , Takahashi Masaki , Tashiro Tomoko , Terao Keiji 
Published: July 2006

AbstractAstrocytes, the most abundant type of glia in the brain, are considered to play a key role in Alzheimer's disease (AD) pathologies. In a cell culture study, we have previously shown that astroglial responses against amyloid β (Aβ) occur before obvious neuronal damage could be detected, suggesting the possibility that astrocytes might be an attractive therapeutic target for treating AD. In the present study, we investigated astroglial gene expression changes in response to Aβ to elucidate further the role of astrocytes in Aβ toxicity. By using real‐time PCR and ELISA analyses, we found that Aβ rapidly induced astrocytes to produce brain‐derived neurotrophic factor (BDNF). Aβ42 was more effective than Aβ40 in increasing astroglial BDNF production. Moreover, BDNF treatment rescued the neuronally differentiated human neuroblastoma cells from neuritic degeneration caused by Aβ toxicity. This is the first study to demonstrate that astrocytes are capable of increasing the production of a particular neurotrophic factor in response to Aβ. Our findings also identify BDNF as a potential therapeutic agent for preventing Aβ‐related neuritic degeneration. © 2006 Wiley‐Liss, Inc.
Effects of huperzine A on amyloid precursor protein processing and β‐amyloid generation in human embryonic kidney 293 APP Swedish mutant cells
Authors: Peng Ying , Jiang Liying , Lee David Y.W. , Schachter Steven C. , Ma Zhongze , Lemere Cynthia A. 
Published: July 2006

AbstractThe amyloid precursor protein (APP) is cleaved enzymatically by nonamyloidogenic and amyloidogenic pathways. α‐Secretase (α‐secretase), cleaves APP within the β‐amyloid (Aβ) sequence, resulting in the release of a secreted fragment of APP (αAPPs) and precluding Aβ generation. In this study, we investigated the effects of an acetylcholinesterase inhibitor, huperzine A (Hup A), on APP processing and Aβ generation in human embryonic kidney 293 cells transfected with human APP bearing the Swedish mutation (HEK293 APPsw). Hup A dose dependently (0–10 μM) increased αAPPs release and membrane‐coupled APP CTF‐C83, suggesting increased APP metabolism toward the nonamyloidogenic α‐secretase pathway. The metalloprotease inhibitor TAPI‐2 inhibited the Hup A‐induced increase in αAPPs release, further suggesting a modulatory effect of Hup A on α‐secretase activity. The synthesis of full‐length APP and cell viability were unchanged after Hup A incubation, whereas the level of AβTotalwas significantly decreased, suggesting an inhibitory effect of Hup A on Aβ production. Hup A‐induced αAPPs release was significantly reduced by the protein kinase C (PKC) inhibitors GF109203X and Calphostin C. These data, together with the finding that the PKCα level was enhanced prior to the increase of αAPPs secretion, indicate that PKC may be involved in Hup A‐induced αAPPs secretion by HEK293 APPsw cells. Our data suggest alternative pharmacological mechanisms of Hup A relevant to the treatment of Alzheimer's disease. © 2006 Wiley‐Liss, Inc.
Production of nerve growth factor by β‐amyloid‐stimulated astrocytes induces p75NTR‐dependent tau hyperphosphorylation in cultured hippocampal neurons
Authors: Sáez Estefanía T. , Pehar Mariana , Vargas Marcelo R. , Barbeito Luis , Maccioni Ricardo B. 
Published: July 2006

AbstractReactive astrocytes surround amyloid depositions and degenerating neurons in Alzheimer's disease (AD). It has been previously shown that β‐amyloid peptide induces inflammatory‐like responses in astrocytes, leading to neuronal pathology. Reactive astrocytes up‐regulate nerve growth factor (NGF), which can modulate neuronal survival by signaling through TrkA or p75 neurotrophin receptor (p75NTR). Here, we analyzed whether soluble Aβ peptide 25–35 (Aβ) stimulated astrocytic NGF expression, modulating the survival of cultured embryonic hippocampal neurons. Hippocampal astrocytes incubated with Aβ up‐regulated NGF expression and release to the culture medium. Aβ‐stimulated astrocytes increased tau phosphorylation and reduced the survival of cocultured hippocampal neurons. Neuronal death and tau phosphorylation were reproduced by conditioned media from Aβ‐stimulated astrocytes and prevented by caspase inhibitors or blocking antibodies to NGF or p75NTR. Moreover, exogenous NGF was sufficient to induce tau hyperphosphorylation and death of hippocampal neurons, a phenomenon that was potentiated by a low steady‐state concentration of nitric oxide. Our findings show that Aβ‐activated astrocytes potently stimulate NGF secretion, which in turn causes the death of p75‐expressing hippocampal neurons, through a mechanism regulated by nitric oxide. These results suggest a potential role for astrocyte‐derived NGF in the progression of AD. © 2006 Wiley‐Liss, Inc.
Suppression of astroglial scar formation and enhanced axonal regeneration associated with functional recovery in a spinal cord injury rat model by the cell cycle inhibitor olomoucine
Authors: Tian Dai‐Shi , Yu Zhi‐Yuan , Xie Min‐Jie , Bu Bi‐Tao , Witte Otto W. , Wang Wei 
Published: July 2006

AbstractIt is well established that axons of the adult mammalian CNS are capable of regrowing only a limited amount after injury. Astrocytes are believed to play a crucial role in the failure to regenerate, producing multiple inhibitory proteoglycans, such as chondroitin sulphate proteoglycans (CSPGs). After spinal cord injury (SCI), astrocytes become hypertrophic and proliferative and form a dense network of astroglial processes at the site of lesion constituting a physical and biochemical barrier. Down‐regulations of astroglial proliferation and inhibitory CSPG production might facilitate axonal regeneration. Recent reports indicated that aberrant activation of cell cycle machinery contributed to overproliferation and apoptosis of cells in various insults. In the present study, we sought to determine whether a cell cycle inhibitior, olomoucine, would decrease neuronal cell death, limit astroglial proliferation and production of inhibitory CSPGs, and eventually enhance the functional compensation after SCI in rats. Our results showed that up‐regulations of cell cycle components were closely associated with neuronal cell death and astroglial proliferation as well as the production of CSPGs after SCI. Meanwhile, administration of olomoucine, a selective cell cycle kinase (CDK) inhibitor, has remarkably reduced the up‐regulated cell cycle proteins and then decreased neuronal cell death, astroglial proliferation, and accumulation of CSPGs. More importantly, the treatment with olomoucine has also increased expression of growth‐associated proteins‐43, reduced cavity formation, and improved functional deficits. We consider that suppressing astroglial cell cycle in acute SCIs is beneficial to axonal growth. In the future, therapeutic strategies can be designed to achieve efficient axonal regeneration and functional compensation after traumatic CNS injury. © 2006 Wiley‐Liss, Inc.
On double shearing in frictional materials
Authors: Teunissen J. A. M. 
Published: July 2006

AbstractThis paper evaluates the mechanical behaviour of yielding frictional geomaterials. The general Double Shearing model describes this behaviour. Non‐coaxiality of stress and plastic strain increments for plane strain conditions forms an important part of this model. The model is based on a micro‐mechanical and macro‐mechanical formulation. The stress–dilatancy theory in the model combines the mechanical behaviour on both scales.It is shown that the general Double Shearing formulation comprises other Double Shearing models. These models differ in the relation between the mobilized friction and dilatancy and in non‐coaxiality. In order to describe reversible and irreversible deformations the general Double Shearing model is extended with elasticity.The failure of soil masses is controlled by shear mechanisms. These shear mechanisms are determined by the conditions along the shear band. The shear stress ratio of a shear band depends on the orientation of the stress in the shear band. There is a difference between the peak strength and the residual strength in the shear band. While peak stress depends on strength properties only, the residual strength depends upon the yield conditions and the plastic deformation mechanisms and is generally considerably lower than the maximum strength. It is shown that non‐coaxial models give non‐unique solutions for the shear stress ratio on the shear band. The Double Shearing model is applied to various failure problems of soils such as the direct simple shear test, the biaxial test, infinite slopes, interfaces and for the calculation of the undrained shear strength. Copyright © 2006 John Wiley & Sons, Ltd.
Influence of low‐energy laser in the prevention of oral mucositis in children with cancer receiving chemotherapy
Authors: Cruz Luciane B. , Ribeiro Anelise S. , Rech Angela , Rosa Lauro G.N. , Castro Cláudio G. , Brunetto Algemir L. 
Published: July 2006

AbstractBackgroundThis study assessed the use of low‐energy laser in the prevention or reduction of the severity of oral mucositis.ProcedureA randomized clinical trial was carried out. Patients from 3 to 18 years of age treated with chemotherapy or hematopoietic stem‐cell transplantation between May, 2003 and February, 2005 were elegible. The intervention group received laser application for 5 days following the start of chemotherapy. The grade of oral mucositis was assessed by the WHO per NCI‐CTC common toxicity criteria and the assessments were made on days 1, 8 and 15 by a trained examiner blind to the intervention.ResultsSixty patients were evaluable for analysis; thirty‐nine (65%) were males, 35 (58%) patients had a diagnosis of leukemia or lymphoma, and 25 (42%) had solid tumors. The mean age was 8.7 ± 4.3 years. Twenty‐nine patients were randomized in the laser group and 31 in the control group. On day 1, no patients presented with mucositis. On day 8, of 20 patients (36%) who developed mucositis, 13 of them were from the laser group and 7 from the control group. On day 15, of 24 patients (41%) who developed mucositis, 13 of them were from the laser group and 11 from the control group. There was no significant difference between groups concerning the grades of mucositis on day 8 (P = 0.234) or on day 15 (P = 0.208).ConclusionsThis study showed no evidence of benefit from the prophylactic use of low‐energy laser in children and adolescents with cancer treated with chemotherapy when optimal dental and oral care was provided. Pediatr Blood Cancer © 2006 Wiley‐Liss, Inc.
Enzyme‐catalyzed synthesis of natural and unnatural polysaccharides
Authors: Ohmae Masashi , Fujikawa Shun‐Ichi , Ochiai Hirofumi , Kobayashi Shiro 
Published: July 2006

AbstractSynthesis of natural and unnatural polysaccharide was achieved via “enzymatic polymerization” by utilizing a glycoside hydrolase as catalyst. Particularly, hyaluronan, chondroitin, and their derivatives belonging to glycosaminoglycans have been prepared using sugar oxazoline monomers designed on the basis of the concept “transition‐state analogue substrate”. The oxazoline derivatives of N‐acetylhyalobiuronate [GlcAβ(1→3)GlcNAc] and N‐acetylchondrosine [GlcAβ(1→3)GalNAc], which have the repeating disaccharide structures of hyaluronan and chondroitin, respectively, were successfully polymerized by the catalysis of hyaluronidase, giving rise to synthetic hyaluronan and chondroitin. Their 2‐substituted oxazoline derivatives were also polymerized to the corresponding N‐acylated hyaluronan and chondroitin derivatives. Furthermore, N‐acetylchondrosine oxazoline derivatives sulfated at the C4, the C6, and both the C4 and C6 of the GalNAc unit were catalyzed by hyaluronidase; the monomer sulfated at the C4 was polymerized to chondroitin 4‐sulfate with well‐defined structure, whereas the other two monomers were exclusively hydrolyzed to the corresponding disaccharides. These different kinds of natural and unnatural polysaccharides having relatively high molecular weights were produced in all cases by the catalysis of hyaluronidase. © 2006 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 44: 5014–5027, 2006