bluuebunny/crossref_metadata_2025_split huggingface dataset:
Specific cementum attachment protein enhances selectively the attachment and migration of periodontal cells to root surfaces
Authors: Pitaru S. , Narayanan S.A. , Olson S. , Savion N. , Hekmati H. , Alt I. , Metzger Z. 
Published: July 2006

SummaryA specific cementum attachment protein (CAP) was identified in human cementum and found to bind with high affinity to non‐demineralized root surfaces, hydroxyapatite and fibronectin. Attempting to elucidate the biological function of this protein and its possible role in cementogenesis the capacity of CAP to promote selective cell migration towards and attachment of various periodontal derived cell populations to root surfaces in vitro was assessed. Human gingival fibroblasts (HGF), periodontal ligament cells (HPC), and alveolar bone cells (HABC) were labeled with [3H]Thymidine during their exponential growth phase. Root slices, 300 μm thick, were incubated with increasing concentrations of CAR Untreated and fibronectin (FN) treated root slices served as negative and positive controls, respectively. Migration was assessed by placing root slices on confluent layers of labeled cells maintained in serum free medium and determining the number of cells migrated onto the root surface 3 days thereafter. Attachment was assessed by incubating root slices with labeled cell suspensions for 2 h and determining the number of attached cells. CAP promoted both cell migration and attachment dose dependently. HABC responded better than HPC and HGF to CAP treated root slices, and HPC response was higher than that of HGF. Cell attachment was dose dependently inhibited by synthetic RGD pep‐tides. FN did not affect the migration of HGF, barely enhanced that of HABC, and was less potent than CAP at enhancing the migration of HPC. FN was more effective than CAP in promoting the attachment of HGF to root slices, but it was as potent as CAP in supporting the attachment of HPC and HABC. The results indicate that CAP promotes preferential migration towards and attachment to root surfaces of HABC and HPC as compared to HGF and suggests that CAP might be effective in supporting cementogenesis.
Influence of periodontal bacteria and disease status on Vβ expression in T cells
Authors: Mathur A. , Michalowicz B. , Yang C. , Aeppli D. 
Published: July 2006

SummarySome bacterial antigens such as S. aureus enterotoxins can selectively stimulate T cells that express specific Vβ genes of the T cell antigen receptor (TCR). The purpose of this study was to investigate whether or not periodontal bacteria could similarly alter the expression of Vβ families within the TCR complex. Peripheral blood mononuclear cells (PBMNCs) were isolated from 12 patients with early onset periodontitis and 11 periodontally‐healthy controls. PBMNCs were incubated in media alone, or co‐cultured for 48 h with heat‐inactivated A. actinomycetemcomitans, P. gingivalis, and P. intermedia. Expression of five Vβ families (Vαβ2, Vβ5, Vβ6, Vβ8, and Vβ12) was determined by use of monoclonal antibodies. Mean unstimulated expression of Vαβ2 and Vβ8 was significantly higher (p<0.05) in patients than healthy controls. Co‐culture with the three bacteria resulted in significant changes (increases or decreases) in Vβ expression in 27% of the trials. There were no significant differences in the number or direction of changes in samples from patients and controls. When compared to unstimulated controls, 18 significant increases but no decreases in the percentage of cell expressing Vαβ2, Vβ5, or Vβ6 were noted following co‐culture with P. intermedia. Overall, co‐culture with P. intermedia significantly (p<0.05) upregulated expression of the five Vβ families studied. These data suggest that periodontal bacteria may alter Vβ expression within the T cell receptor complex.
Components of a randomized clinical trial
Authors: Dennison David K. 
Published: July 2006

The purpose of this paper is to discuss a number of components associated with the design, development and conduct of a randomized clinical trial (RCT). In a RCT, a patient is entered into a protocol in which therapy is randomly assigned. Thus, neither the patient nor the care provider have active roles in deciding treatment. The elements of informed consent were developed to ensure that the patient's interests are protected. The informed consent document serves as the cornerstone of a clinical study by introducing patients to the research protocol, informing them of their role as participants in the study, and educating them of their rights. Questions regarding ethics arise during all phases of a study. A study designed with insufficient sample size will provide inconclusive data, thus making participation in the study of limited to no value. Conversely, having patients enrolled in a RCT after data has proved superiority of an arm of the study postpones beneficial therapy for patients and society. Other ethical conflicts arise when subjects are recruited for clinical trials. Special care must be taken to avoid coercion in protected populations such as students, employees, the mentally challenged, and the indigent. Careful planning with adequate attention to consent form development can minimize problems and optimize patient care and research integrity.The role of the RCT in the future is unclear. The logistics of conducting a multicentered trial has escalated the costs of new agents in terms of both time and money. In many cases, the decision to conduct a RCT is made on the potential profitability of the product/agent under test. Whatever the reasons credited for conducting an RCT, the research must be adequately designed to protect both the subjects involved in the study, as well as humankind from erroneous data.
Responses to Fire in Selected Tropical Dry Forest Trees1
Authors: Otterstrom Sarah M. , Schwartz Mark W. , Velázquez‐Rocha Ileana 
Published: July 2006

ABSTRACTFire is a frequent disturbance in the tropical dry forests of Central America, yet very little is known about how native species respond to such events. We conducted an experimental burn in a tropical dry forest of western Nicaragua to evaluate plant responses to fire with respect to survivorship and recruitment. Measurements of woody vegetation of all size classes were carried out prior to the prescribed burn and three successive years post fire. We selected the 15 most abundant species <10 cm DBH to assess percent survivorship and sprouting responses post fire. Changes in seedling densities for these 15 most abundant species and the 15 least abundant species were analyzed using a repeated measure ANOVA. We also assessed changes in seedling densities for three species of international conservation concern. We found three major fire‐coping strategies among common dry forests plants: resisters (low fire‐induced mortality), resprouters (vigorous sprouting), and recruiters (increased seeding post‐fire). While survivorship was generally high relative to tropical moist forest species, those species with lower survivorship used either seeding or sprouting as an alternative strategy for persisting in the forest community. Seed dispersal mechanisms, particularly wind dispersal, appear to be an important factor in recruitment success post‐fire. Burn treatment led to a significant increase in the density of seedlings for two species of conservation concern: Guaiacum sanctum and Swietenia humilis. Results of this study suggest that common dry forest species in western Nicaragua are fire tolerant. Further study of individual species and their fire responses is merited.
Mangrove Seedling Net Photosynthesis, Growth, and Survivorship are Interactively Affected by Salinity and Light1
Authors: López‐Hoffman Laura , DeNoyer Jeanne L. , Monroe Ian E. , Shaftel Rebecca , Anten Niels P. R. , Martínez‐Ramos Miguel , Ackerly David D. 
Published: July 2006

ABSTRACTWe hypothesized that salinity and light interactively affect mangroves, such that net photosynthesis, growth, and survivorship rates increase more with increase in light availability at low than high salinity. Using greenhouse and field experiments, we determined that net photosynthesis, growth rates, and size increased more with light at low than high salinity. At high salinity, the ratio of leaf respiration to assimilation increased fourfold, suggesting that salinity may have contributed to declines in net photosynthesis. Stomatal conductance, leaf‐level transpiration, and internal CO2 concentrations were lower at high salinity. Ratios of root mass to leaf mass were higher at high salinity. Stomatal limitations and increased respiratory costs may explain why at high salinity, the seedlings did not respond to increased light availability with increased net photosynthesis. Increased root mass relative to leaf mass suggests that at high salinity, either water or nutrient limitations may have prevented the seedlings from increasing growth with increasing light availability. At both low‐ and high‐salinity zones in the field, seedling survivorship increased with light availability, and the effect of light was stronger at low salinity. However, at low light, survivorship was higher at high than low salinity, indicating that there may be a trade‐off between survivorship and growth. The interactive effects observed in the greenhouse were robust in the field, despite the presence of other factors in the field such as inundation and nutrient gradients and herbivory. This study provides a robust test of the hypothesis that salinity and light interactively effect mangrove seedling performance.
Cockscomb Revisited: Jaguar Diet in the Cockscomb Basin Wildlife Sanctuary, Belize1
Authors: Weckel Mark , Giuliano William , Silver Scott 
Published: July 2006

ABSTRACTThe Cockscomb Basin Wildlife Sanctuary, Belize was established in 1986 following Rabinowitz and Nottingham's 1986 study on jaguar diet and distribution. In 2002, we reexamined jaguar diet following two decades of mitigated human hunting of jaguar prey. We observed high overlap between historical and current jaguar diet constructs. Nine‐banded armadillo remained the most frequently consumed prey item. However, collared peccary consumption increased by nearly 20 percent while dietary breadth decreased by 60 percent presumably reflecting increased prey availability following reduced human hunting pressure.
Biological activity of rainbow trout Ea4‐peptide of the pro‐insulin‐like growth factor (pro‐IGF)‐I on promoting attachment of breast cancer cells (MDA‐MB‐231) via α2‐ and β1‐integrin
Authors: Siri Sineenat , Chen Maria J. , Chen Thomas T. 
Published: July 2006

AbstractE‐peptide of pro‐IGF‐I was considered as biologically inactive. We have demonstrated that rainbow trout (rt) Ea4‐peptide exerted biological activities in several established tumor cell lines [Chen et al., 2002; Kuo and Chen, 2002]. Here we report the activity of rtEa4‐peptide in promoting attachment of human breast cancer cells (MDA‐MB‐231). While rtEa2‐, rtEa3‐, and rtEa4‐peptides enhanced the attachment of MDA‐MB‐231 cells in a dose dependent manner, rtEa4‐peptide possessed the highest activity. Antibodies specific to α2 and β1 integrins significantly inhibited the attachment of cells to rtEa4‐peptide coated‐plates by 40%. In addition, rtEa4‐peptide induced the expression of fibronectin 1 and laminin receptor genes in MDA‐MB‐231 cells. Blocking new protein synthesis by cycloheximide significantly reduced the attachment of MDA‐MB‐231 cells to rtEa4‐peptide coated wells by 50%. These results suggest that rtEa4‐peptide may promote cell attachment by interacting with α2/β1 integrin receptors at the cell surface and by inducing the expression of fibronectin 1 and laminin receptor genes. Expression of fibronectin 1 gene induced by rtEa4‐peptide in MDA‐MB‐231 cells was abolished by inhibitors of PI3K, PKC, Mek1/2, JNK1/2, and p38 MAPK signaling transduction molecules. These results suggested that induction of fibronectin 1 gene expression in MDA‐MB‐231 cells by rtEa4‐peptide may be mediated via PI3K, PKC, Mek1/2, JNK1/2, and p38 MAPK signal transduction molecules. J. Cell. Biochem. 99: 1524–1535, 2006. © 2006 Wiley‐Liss, Inc.
Functional analysis of CBP/p300 in embryonic orofacial mesenchymal cells
Authors: Warner D.R. , Pisano M.M. , Greene R.M. 
Published: July 2006

AbstractCREB binding protein (CBP) and the close structural homolog, p300, are nuclear coactivators of multiple signaling pathways that play important roles in embryonic development and cellular homeostasis. TGFβ regulates the proliferation rate of many cell types and has been demonstrated to inhibit the growth rate of mouse embryonic maxillary mesenchymal (MEMM) cells. The role of CBP and p300 in TGFβ‐mediated control of proliferation of MEMM cells was thus investigated using an in vitro gene knockdown approach. TGFβ reporter assays demonstrated that p300 mRNA knockdown via targeted siRNAs led to a reduction in the response to TGFβ, whereas knockdown of CBP by the same approach had an insignificant effect. In MEMM cell proliferation assays, siRNA‐mediated knockdown of CBP and/or p300 had little impact upon TGFβ‐mediated growth inhibition; however, the basal rate of proliferation was increased. Inhibition of p300 activity via overexpression of a dominant‐negative mutant (p300ΔC/H3) led to significant inhibition of TGFβ‐mediated activation of p3TP‐lux. As with the siRNA knockdown approach, p300ΔC/H3 also increased the basal rate of cell proliferation of MEMM cells. CBP/p300 siRNA knockdown had a significant but incomplete inhibition of TGFβ‐induction of matrix metalloproteinase‐9 (gelatinase B) expression. These data demonstrate that p300 is involved in Smad‐mediated transcription of p3TP‐lux, however, its role (and that of CBP) in biological processes such as the control of cell proliferation and extracellular matrix metabolism is more complex and may be mediated via mechanisms beyond coactivator recruitment. J. Cell. Biochem. 99: 1374–1379, 2006. © 2006 Wiley‐Liss, Inc.
Differential effects of matrix and growth factors on endothelial and fibroblast motility: Application of a modified cell migration assay
Authors: van Horssen Remco , Galjart Niels , Rens Joost A.P. , Eggermont Alexander M.M. , ten Hagen Timo L.M. 
Published: July 2006

AbstractCell migration is crucial in virtually every biological process and strongly depends on the nature of the surrounding matrix. An assay that enables real‐time studies on the effects of defined matrix components and growth factors on cell migration is not available. We have set up a novel, quantitative migration assay, which enables unharmed cells to migrate along a defined matrix. Here, we used this so‐called barrier‐assay to define the contribution of fibronectin (FN) and Collagen‐I (Col‐I) to vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and lysophosphatidic acid (LPA)‐induced cell migration of endothelial cells (EC) and fibroblasts. In EC, both FN and Col‐I stimulated migration, but FN‐induced motility was random, while net movement was inhibited. Addition of bFGF and VEGF overcame the effect of FN, with VEGF causing directional movement. In contrast, in 3T3 fibroblasts, FN stimulated motility and this effect was enhanced by bFGF. This motility was more efficient and morphologically completely different compared to LPA stimulation. Strikingly, directional migration of EC was not paralleled by higher amounts of stable microtubules (MT) or an increased reorientation of the microtubule‐organizing centre (MTOC). For EC, the FN effect appeared concentration dependent; high FN was able to induce migration, while for fibroblasts both low and high concentrations of FN induced motility. Besides showing distinct responses of the different cells to the same factors, these results address contradictive reports on FN and show that the interplay between matrix components and growth factors determines both pattern and regulation of cell migration. J. Cell. Biochem. 99: 1536–1552, 2006. © 2006 Wiley‐Liss, Inc.
Centrosome function in normal and tumor cells
Authors: Sankaran Satish , Parvin Jeffrey D. 
Published: July 2006

AbstractCentrosomes nucleate microtubules that form the mitotic spindle and regulate the equal division of chromosomes during cell division. In cancer, centrosomes are often found amplified to greater than two per cell, and these tumor cells frequently have aneuploid genomes. In this review, we will discuss the cellular factors that regulate the proper duplication of the centrosome and how these regulatory steps can lead to abnormal centrosome numbers and abnormal mitoses. In particular, we highlight the newly emerging role of the Breast Cancer 1 (BRCA1) ubiquitin ligase in this process. J. Cell. Biochem. 99: 1240–1250, 2006. © 2006 Wiley‐Liss, Inc.
Phosphatidylinositol 3‐kinase/Akt auto‐regulates PDGF‐BB‐stimulated interleukin‐6 synthesis in osteoblasts
Authors: Hanai Yoshiteru , Tokuda Haruhiko , Ohta Toshiki , Matsushima‐Nishiwaki Rie , Takai Shinji , Kozawa Osamu 
Published: July 2006

AbstractIt has been reported that platelet‐derived growth factor (PDGF)‐BB stimulates the synthesis of interleukin (IL)‐6 in osteoblasts. In the present study, we investigated whether the phosphatidylinositol 3‐kinase (PI3K)/Akt is involved in the PDGF‐BB‐induced IL‐6 synthesis in osteoblast‐like MC3T3‐E1 cells. PDGF‐BB markedly induced the phosphorylation of Akt and GSK‐3β. Akt inhibitor, 1L‐6‐hydroxymethyl‐chiro‐inositol 2‐(R)‐2‐O‐methyl‐3‐O‐octadecylcarbonate, significantly amplified the synthesis of IL‐6 by PDGF‐BB. The PDGF‐BB‐induced GSK‐3β phosphorylation was suppressed by the Akt inhibitor. The IL‐6 synthesis stimulated by PDGF‐BB was markedly enhanced by LY294002 and wortmannin, inhibitors of PI3K. Wortmannin and LY294002 suppressed the PDGF‐BB‐induced phosphorylation of Akt and GSK‐3β. Taken together, these results strongly suggest that PI3K/Akt negatively regulates the PDGF‐BB‐stimulated IL‐6 synthesis in osteoblasts. J. Cell. Biochem. 99: 1564–1571, 2006. © 2006 Wiley‐Liss, Inc.
Mechanism of 24,25‐dihydroxyvitamin D3‐mediated inhibition of rapid, 1,25‐dihydroxyvitamin D3‐induced responses: Role of reactive oxygen species
Authors: Nemere Ilka , Wilson Cody , Jensen Wendy , Steinbeck Marla , Rohe Ben , Farach‐Carson Mary C. 
Published: July 2006

AbstractIn intestine, 24,25(OH)2D3, which is made under conditions of calcium‐, phosphate‐, and 1,25(OH)2D3 sufficiency, inhibits the stimulatory actions of 1,25(OH)2D3 on phosphate and calcium absorption. In the current work, we provide evidence that 24,25(OH)2D3‐mediated signal transduction occurs mechanistically through increased H2O2 production which involves binding of 24,25(OH)2D3 to catalase and resultant decreases in enzyme activity. Physiological levels of H2O2 mimicked the action of 24,25(OH)2D3 on inhibiting 1,25(OH)2D3‐stimulated phosphate uptake in isolated enterocytes. Moreover, the molecular basis of such inhibition was suggested by the presence of two thioredoxin domains in the 1,25D3‐MARRS protein/ERp57: Exposure of cells to either 24,25(OH)2D3 or H2O2 gradually reduced 1,25(OH)2D3 binding to 1,25D3‐MARRS protein, between 10 and 20 min of incubation, but not to VDR. Feeding studies with diets enriched in the antioxidants vitamins C and E showed that net phosphate absorption in vivo nearly doubled relative to chicks on control diet. Antioxidant diets also resulted in increased [3H]1,25(OH)2D3 binding to both 1,25D3‐MARRS and VDR, suggesting benefits to both transcription‐ and membrane‐initiated signaling pathways. Intriguingly, phosphorous content of bones from birds on antioxidant diets was reduced, suggesting increased osteoclast activity. Because mature osteoclasts lack VDR, we analyzed a clonal osteoclast cell line by RT‐PCR and found it contained the 1,25D3‐MARRS mRNA. The combined data provide mechanistic details for the 1,25(OH)2D3/24,25(OH)2D3 endocrine system, and point to a role for the 1,25D3‐MARRS protein as a redox‐sensitive mediator of osteoclast activity and potential therapeutic target. J. Cell. Biochem. 99: 1572–1581, 2006. © 2006 Wiley‐Liss, Inc.
The effects of a mutant p53 protein on the proliferation and differentiation of PC12 rat phaeochromocytoma cells
Authors: Fábián Zsolt , Vecsernyés Mónika , Pap Marianna , Szeberényi József 
Published: July 2006

AbstractPC12 rat phaeochromocytoma cells show neuronal differentiation upon NGF treatment. NGF induces prolonged activation of the Ras/Raf/MEK/ERK pathway in which the 42/44 kDa mitogen‐activated protein kinases (MAPKs), ERK 1 and 2 are thought to be the key mediators of the differentiation signals. Activation of ERKs leads to the increased transcription of early response genes resulting in cell cycle arrest. Upon NGF treatment the p53 protein, the most commonly mutated tumor suppressor in human cancers, translocates to the nucleus and may play a role in the mediation of NGF‐induced cell cycle arrest and neuronal differentiation. Here we demonstrate that in PC12 cells expressing both wild‐type and V143A mutant p53 proteins (p143p53PC12 cells), p53‐mediated biological responses are critically influenced. p143p53PC12 cells are not able to cease their proliferation and begin their neuronal differentiation program upon NGF treatment. The presence of mutant p53 also reduces the DNA‐binding activity of endogenous p53 and disturbs the regulatory machinery of p53 including both the phosphorylation of ERK 1/2, p38 and SAPK/JNK MAP kinases and itself. J. Cell. Biochem. 99: 1431–1441, 2006. © 2006 Wiley‐Liss, Inc.
In vivo modulation of epidermal growth factor receptor phosphorylation in mice expressing different gangliosides
Authors: Daniotti Jose L. , Crespo Pilar M. , Yamashita Tadashi 
Published: July 2006

AbstractWe studied in this work the in vivo phosphorylation of the epidermal growth factor receptor (EGFr) in skin from knockout mice lacking different ganglioside glycosyltransferases. Results show an enhancement of EGFr phosphorylation, after EGF stimulation, in skin from Sial‐T2 knockout and Sial‐T2/GalNAc‐T double knockout mice as compared with wild‐type and Sial‐T1 knockout mice. Qualitative analysis of ganglioside composition in mice skin suggest that the increase of EGFr phosphorylation observed in skin from Sial‐T2 knockout and Sial‐T2/GalNAc‐T double knockout mice in response to EGF might not be primary attributed to the expression of GD3 or a‐series gangliosides in mice skin. These studies provide, for the first time, an approach for studying the molecular mechanisms involved in the in vivo regulation of EGFr function by gangliosides. J. Cell. Biochem. 99: 1442–1451, 2006. © 2006 Wiley‐Liss, Inc.
Alpha1‐Antitrypsin Single Dose Adjuvant Therapy for Acute Otitis Media
Authors: Patrick J. Antonelli , Gregory S. Schultz , David J. Sundin , Philip A. Pemberton , Philip J. Barr 
Published: July 2006

OBJECTIVESProteases have been shown to play a role in the pathogenesis of otitis media. Inhibition of these proteases can improve treatment outcomes in certain conditions. The goal of this study was to determine if intratympanic administration of a single dose of the protease inhibitor, recombinant alpha 1‐antitrypsin (rAAT), can facilitate resolution of acute otitis media (AOM) in the chinchilla.METHODS AND MEASURESPneumococcus was injected into both middle ears of 12 chinchillas. After 3 to 4 days, middle ears were cultured, systemic antibiotics were initiated, and rAAT or its vehicle was administered into the middle ears of all animals. Serial tympanic membrane (TM) scoring, tympanometry, and auditory‐evoked brain stem response testing were performed. Animals were sacrificed at varying timepoints and temporal bones studied for objective measures of OM.RESULTSAlthough not reaching statistical significance, there was a trend to more rapid resolution of AOM in rAAT‐treated ears. Tympanometry, auditory thresholds, and quantitative histologic parameters did not differ between rAAT and vehicle treated ears.CONCLUSIONSA single dose of intratympanic rAAT likely does not facilitate the resolution of antibiotic‐treated pneumococcal AOM in the chinchilla model. Serial administration of this protease inhibitor may be necessary to see a significant treatment effect.