bluuebunny/crossref_metadata_2025_split huggingface dataset:
Enhanced osteolytic potential of monocytes/macrophages derived from bone marrow after particle stimulation
Authors: Tamaki Yasunobu , Sasaki Kan , Sasaki Akiko , Takakubo Yuya , Hasegawa Hiroshi , Ogino Toshihiko , Konttinen Yrjö T. , Salo Jari , Takagi Michiaki 
Published: May 2007

AbstractBackground: Total hip replacement can be complicated by periprosthetic osteolysis. Monocytes/macrophages play a major role in the formation of the foreign body granulomas induced by wear debris. We hypothesized that periprosthetic monocytes/macrophages do not only accelerate inflammatory and osteoclast‐mediated osteolytic processes, but also resorb periprosthetic bone directly by themselves. This study was designed to evaluate the osteolytic potential in vitro of monocytes/macrophages derived from bone marrow. Methods: Monocytes/macrophages were produced by filtration of rat bone marrow cells, followed by culture in the presence of macrophage‐colony stimulating factor (M‐CSF). Monocyte/macrophage properties were ascertained using immunocytochemistry and phagocytic activity. Osteolytic cytokines and extracellular matrix degrading proteinases were quantified at the mRNA level. Results: Adherent cell fraction was immunoreactive for the monocyte/macrophage specific marker CD68 and active in the phagocytosis of carbon particles up to 72 h. They also showed immunoreactivity to cathepsin K, IL‐1β, IL‐6, and M‐CSF, but mostly did not react to TRAP. mRNA levels of osteolytic cytokines and extracellular matrix degrading proteinases were enhanced, but that of RANKL were not. Monocytes/macrophages resorbed dentine discs and carbonated calcium phosphate was very actively resorbed after stimulation with titanium particles. Discussion: Harvested bone marrow cells expressed monocyte/macrophage phenotype, but not osteoclastic markers. The capacity of these cathepsin‐K–positive phagocytic cells to resorb dentine discs and carbonated calcium phosphate in vitro suggests a direct role of monocytes/macrophages in bone resorption and periprosthetic osteolysis. The finding supports our hypothesis and previous histomorphometric observations on the presence of such osteolytic macrophages in vivo around loosening prosthesis. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 2008
Oxidation of proteins adsorbed on hemodialysis membranes and model materials
Authors: Caillou Samuel , Boonaert Christophe J. P. , Dewez Jean‐Luc , Rouxhet Paul G. 
Published: May 2007

AbstractThe cleaning of cellulosic hemodialysis membrane Cuprophan and model materials (glass; polystyrene and polypropylene, as such and surface‐oxidized), conditioned by adsorption of blood plasma proteins (HSA, fibrinogen, IgG) was investigated in vitro. Sodium hypochlorite (NaClO) and Renalin, a product containing hydrogen peroxide and peroxyacetic acid, were used as cleaning reagents. X‐ray photoelectron spectroscopy and the use of radiolabeled fibrinogen demonstrated the presence of varying amounts of a polypeptidic residue, with sulfur brought to a high oxidation stage (sulfonate‐like). The trends were the same for the three proteins regarding the effectiveness of the oxidizer and the influence of the surface properties. NaClO was much more effective than Renalin to remove the adsorbed proteins. The proteins adsorbed on Cuprophan were more sensitive to the oxidizers, when compared with proteins adsorbed on other materials. This may be due to both the lower protein–surface affinity, as indicated by radiochemical measurements, and the sensitivity of the material itself to the oxidizer, as revealed by weight loss measurements. These results support the attribution of hemocompatibility improvement after regeneration of Cuprophan with Renalin to the masking of the activating surface by a residue from previously adsorbed proteins. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 2008
Human osteoblast‐like cells response to nanofunctionalized surfaces for tissue engineering
Authors: Soumetz Federico Caneva , Pastorino Laura , Ruggiero Carmelina 
Published: May 2007

AbstractCells are sensitive both to the micro/nanotopographic and chemical features of their surrounding environment. The engineering of the surface properties of biomaterials is then critical to develop bioactive devices with which to elicit appropriate cellular responses. To this regard, the layer by layer (LBL) self assembly technique represents a simple and versatile method to modify surface properties by the deposition of ultrathin films with specific and predetermined properties. In this work biomimetic coatings containing fibronectin, an adhesive glycoprotein of the extracellular matrix, were assembled by means of the LBL technique, and tested for the growth of MG63 human osteoblast‐like cells, in order to evaluate their potential for the treatment of materials employed in bone‐tissue engineering. As a first step the assembly process was optimized by quartz crystal microbalance measurements and subsequently was repeated on nickel/titanium, silicon and glass samples. The results obtained from the investigation of cell response to the modified surfaces, put in evidence that the deposited nanostructured ultrathin films are effective in promoting cell proliferation. Our results show the high potential of the developed bioactive coatings for the engineering of biomimetic implants and for the optimization of their integration with the surrounding tissues. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 2008
Effect of serum metabolites of Pueraria lobata in rats on peripheral nerve regeneration: In vitro and in vivo studies
Authors: Chen Hsien‐Tung , Yao Chun‐Hsu , Chao Pei‐Dawn Lee , Hou Yu‐Chi , Chiang Hsiu‐Mei , Hsieh Chang‐Chi , Ke Cherng‐Jyh , Chen Yueh‐Sheng 
Published: May 2007

AbstractThis study provides in vitro and in vivo evaluation of rat serum metabolites of the Pueraria lobata (SMP) on peripheral nerve regeneration. In the in vitro study, we found that the SMP caused a marked enhancement of the nerve growth factor (NGF)‐mediated neurite outgrowth and the expression of synapsin I from PC12 cells. In the in vivo study, silicone rubber chambers filled with the SMP were used to bridge a 10‐mm sciatic nerve defect in rats. At the conclusion of 8 weeks, animals from the groups treated with the SMP had a relatively more mature structure with larger mean values of myelinated axon number, endoneurial area, and total nerve area when compared with those in the controls receiving the saline only. These results suggest that the serum metabolites of Pueraria lobata can be a potential nerve growth‐promoting factor. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 2008
Multiple roles of M‐CSF in human osteoclastogenesis
Authors: Hodge Jason M. , Kirkland Mark A. , Nicholson Geoffrey C. 
Published: May 2007

AbstractAlthough the critical role of M‐CSF in osteoclastogenesis is well documented, there has been no detailed analysis of how it regulates human osteoclast formation and function in vitro. We used a human osteoclastogenesis model employing CFU‐GM osteoclast precursors cultured for 14 days on dentine with RANKL, with varying exposure to exogenous human M‐CSF. Short‐term treatment of precursors with M‐CSF (10–100 ng/mL) resulted in increased proliferation with or without RANKL. Treatment with M‐CSF (1–100 ng/mL) for 14 days caused a biphasic concentration‐dependent stimulation of formation, fusion, and resorption peaking at 10–50 ng/mL and almost complete abolition of resorption at 100 ng/mL. Time‐course studies using M‐CSF (25 ng/mL) showed that osteoclast size, nuclei/cell, and resorption increased with longer duration of M‐CSF treatment. When treatment was restricted to the first 4 days, M‐CSF (25–100 ng/mL) stimulated formation of normal numbers of osteoclasts that resorbed less. Blockade of endogenous M‐CSF signaling with neutralizing M‐CSF antibody during the first week of culture extensively inhibited osteoclastogenesis, whereas blockade during the second week produced only a small reduction in resorption. Treatment with M‐CSF during the second week of culture caused a small increase in osteoclast number and a concentration‐dependent increase in cytoplasmic spreading with inhibition of resorption. We have shown that M‐CSF modulates multiple steps of human osteoclastogenesis, including proliferation, differentiation and fusion of precursors. In the later stages of osteoclastogenesis, M‐CSF modulates osteoclast‐resorbing activity, but is not required for survival. Modulation of M‐CSF signaling is a potential therapeutic target for conditions associated with excess bone resorption. J. Cell. Biochem. 102: 759–768, 2007. © 2007 Wiley‐Liss, Inc.
Development and iron‐dependent expression of hephaestin in different brain regions of rats
Authors: Qian Zhong‐Ming , Chang Yan‐Zhong , Zhu Li , Yang Lei , Du Jun‐Rong , Ho Kwok‐Ping , Wang Qin , Li Lian‐Zhi , Wang Chen‐Yuen , Ge Xiaohu , Jing Niu Li , Li Lin , Ke Ya 
Published: May 2007

AbstractIt has been suggested that Hephaestin (Heph), a newly discovered ceruloplasmin homologue, is necessary for iron egress from the enterocytes into circulation via interacting with ferroportin1 (FP1). Based on the putative function of Heph, and the similarity between the process of iron transport in the enterocytes and that in the blood‐brain barrier (BBB) cells, it has also been proposed that Heph plays a similar role in exporting iron from the BBB cells and other brain cells as it works in the enterocytes via interacting with FP1. The existence of FP1 in the brain has been demonstrated. In this study, we investigated Heph expression and effects of development and iron in the cortex, hippocampus, striatum, and substantia nigra. The data demonstrated that all the four regions we examined have the ability to express Heph mRNA and protein. The findings also showed that both the development and iron status have a significant effect on Heph expression and the effects of iron status are regionally specific. It was also suggested that Heph expression is probably regulated at the transcriptional level by the development and iron in these brain regions. These findings, together with other published data, support a putative role of Heph in the iron metabolism in the brain. J. Cell. Biochem. 102: 1225–1233, 2007. © 2007 Wiley‐Liss, Inc.
Cilostazol attenuates MCP‐1 and MMP‐9 expression in vivo in LPS‐administrated balloon‐injured rabbit aorta and in vitro in LPS‐treated monocytic THP‐1 cells
Authors: Tsai Chien‐Sung , Lin Feng‐Yen , Chen Yung‐Hsiang , Yang Tung‐Lin , Wang Hsiao‐Jung , Huang Guo‐Shine , Lin Chih‐Yuan , Tsai Yi‐Tin , Lin Shing‐Jong , Li Chi‐Yuan 
Published: May 2007

AbstractMonocyte chemoattractant protein‐1 (MCP‐1) and matrix metalloproteinase‐9 (MMP‐9) are involved in vascular inflammation. We tested the hypothesis, and explored the underlining mechanisms that cilostazol, a phosphodiesterase 3 inhibitor with antiplatelet and antithrombotic properties, inhibits lipopolysaccharide (LPS)‐induced MCP‐1 and MMP‐9 expression. In a rabbit aorta balloon‐injury model, administration of LPS increased macrophage infiltration and MCP‐1 and MMP‐9 expression; cilostazol supplementation prevented this phenomenon and reduced intimal hyperplasia. In contrast, the reverse zymography showed that cilostazol did not affect TIMP‐1 expression in serum. In monocytic THP‐1 cells, cilostazol and N6,O2′‐dibutyryl‐cAMP (dioctanoyl‐cAMP, a cAMP analog) dose‐dependently inhibited LPS‐induced MCP‐1 protein expression and MMP‐9 activation, but did not affect the tissue inhibitor of metalloproteinase‐1. Quantitative real‐time polymerase chain reaction (PCR) showed that cilostazol inhibited MCP‐1 and MMP‐9 mRNA expression. Cilostazol significantly inhibited LPS‐induced activation of p38, JNK, and nuclear factor‐κB, and the respective inhibitors of p38 and JNK greatly reduced the level of LPS‐induced MCP‐1 and MMP‐9, suggesting the involvement of the p38 and JNK pathways. In conclusion, cilostazol administered with LPS in vivo reduced neointimal hyperplasia and macrophage infiltration in the balloon‐injured rabbit aorta; in vitro, cilostazol inhibits LPS‐induced MCP‐1 and MMP‐9 expression. These data suggest that cilostazol may play an important role in preventing endotoxin‐ and injured‐mediated vascular inflammation. J. Cell. Biochem. 103: 54–66, 2008. © 2007 Wiley‐Liss, Inc.
Dexamethasone promotes osteoclastogenesis by inhibiting osteoprotegerin through multiple levels
Authors: Kondo Takeshi , Kitazawa Riko , Yamaguchi Akira , Kitazawa Sohei 
Published: May 2007

AbstractIncreased bone fragility attributed to osteopenia is a serious side effect of glucocorticoid treatment. Glucocorticoid‐induced bone loss is caused primarily by hypofunction and apoptosis of osteoblasts, and secondarily by accelerated bone resorption. To explore the mechanism whereby dexamethasone (Dex) stimulates osteoclastogenesis in the coculture system, we analyzed the effect of Dex on the expression of both mouse osteoprotegerin (OPG) and receptor activator of NF‐κB ligand (RANKL). Dex reduced OPG transcripts and OPG protein secretion by the ST2 osteoblastic cells. Since mainly the c‐Jun homodimer maintains the steady‐state transcription of the OPG gene, we examined the effect of Dex on c‐Jun signaling in ST2 cells. Western blotting disclosed that Dex decreased the amount of phospho‐c‐Jun protein (p‐c‐Jun) and, correspondingly, the amount of the phosphorylated p46 isoform of Jun N‐terminal kinase (JNK). The amount of phospho‐SEK1 also decreased after Dex treatment, while the amounts of phospho‐ERK and p38 remained constant. Among mitogen‐activated protein (MAP) kinase inhibitors, the JNK inhibitor mimicked the inhibitory effect of Dex on OPG promoter activity. On the other hand, Dex treatment per se showed a nominal increase of RANKL gene expression. A part of Dex‐mediated OPG gene suppression was achieved by the suppression of β‐catenin signaling. We speculate therefore that the bone resorptive action of Dex is mediated mainly by the inhibition of OPG by transrepressing the OPG gene through the AP‐1 site, with a reduction (mediated mainly by the decrease in the p46 isoform of JNK) in the proportion of p‐c‐Jun in a JNK‐dependent manner. J. Cell. Biochem. 103: 335–345, 2008. © 2007 Wiley‐Liss, Inc.
On the extendability of steiner t‐designs
Authors: Baartmans Alphonse H. , Blake Ian F. , Tonchev Vladimir D. 
Published: May 2007

AbstractNecessary and sufficient conditions for the extendability of residual designs of Steiner systems S(t,t + 1,v) are studied. In particular, it is shown that a residual design with respect to a single point is uniquely extendable, and the extendability of a residual design with respect to a pair of points is equivalent to a bipartition of the block graph of a related design. © 1993 John Wiley & Sons, Inc.
Incomplete perfect mendelsohn designs with block size 4 and one hole of size 7
Authors: Bennett F. E. , Shen H. , Yin J. 
Published: May 2007

AbstractLet v,k, and n be positive integers. An incomplete perfect Mendelsohn design, denoted by k‐IPMD(v,n), is a triple (X, Y, 𝔹) where X is a v‐set (of points), Y is an n‐subset of X, and 𝔹 is a collection of cyclically ordered k‐subsets of X (called blocks) such that every ordered pair (a, b) ∈ (X × X)∖(Y × Y) appears t‐apart in exactly one block of 𝔹 and no ordered pair (a,b) ∈ Y × Y appears in any block of 𝔹 for any t, where 1 ≤ t ≤ k − 1. In this article, we obtain conclusive results regarding the existence of 4‐IPMD(v,7) where the necessary conditions are v = 2 or 3(mod 4) and v ≥ 22. We also provide an application to the problem relating to coverings of PMDs with block size 4. © 1993 John Wiley & Sons, Inc.
Sprouty2 downregulation plays a pivotal role in mediating crosstalk between TGF‐β1 signaling and EGF as well as FGF receptor tyrosine kinase‐ERK pathways in mesenchymal cells
Authors: Ding Wei , Shi Wei , Bellusci Saverio , Groffen John , Heisterkamp Nora , Minoo Parviz , Warburton David 
Published: May 2007

AbstractMammalian Sprouty2 (Spry2) is a key regulator of the receptor tyrosine kinase/ERK signaling pathway and is involved in many biological processes, including cell growth, differentiation, migration, and embryonic lung branching morphogenesis. Previous studies have shown that Spry2 expression is upregulated by many mitogens, particularly epidermal growth factor (EGF) and fibroblast growth factors (FGFs). In contrast, we report that transforming growth factor‐β1 (TGF‐β1), which stimulates the growth of quiescent Swiss 3T3 cells, induced a dose dependent decrease of mouse Spry2 protein level within 24‐h of treatment, and this effect was mediated by a MAP kinase‐independent pathway. A concomitant reduction of the level of Spry2 mRNA indicates the involvement of a transcriptional mechanism, which requires histone deacetylase (HDAC) activity and de novo protein synthesis. On the other hand, the turnover rate of Spry2 protein was increased by TGF‐β1 treatment, suggesting enhanced Spry2 degradation. Treatment with lysosomal inhibitors, but not proteasome inhibitors, prevented the degradation of Spry2, thus, indicating that the degradation of Spry2 is mediated through the lysosomal pathway in Swiss 3T3 cells. Furthermore, we demonstrate that TGF‐β1 signaling can modulate EGF and FGF‐induced ERK‐MAP kinase activation by controlling Spry2 expression and function. Moreover, rescue of the TGF‐β1‐induced downregulation of Spry2 by gene over‐expression led to inhibition of the mitogenic effect of TGF‐β1 in Swiss 3T3 cells. Together, the combined operation of transcriptional and post‐translational mechanisms suggests that regulation of Spry2 is a crucial event and emphasizes the important role that Spry2 plays in controlling cell behaviors. J. Cell. Physiol. 212:796–806, 2007. © 2007 Wiley‐Liss, Inc.
Mitochondrial association of myocilin, product of a glaucoma gene, in human trabecular meshwork cells
Authors: Sakai Hiroshi , Shen Xiang , Koga Takahisa , Park Bum‐Chan , Noskina Yelina , Tibudan Martin , Yue Beatrice Y.J.T. 
Published: May 2007

AbstractThe trabecular meshwork (TM), an ocular tissue next to the cornea, is a major site for regulation of the aqueous humor outflow. Malfunctioning of this tissue is believed to be responsible for development of glaucoma, a major blinding disease. Myocilin is a gene directly linked to the most common form of glaucoma. Its protein product has been localized to both intra‐ and extra‐cellular sites in TM cells. This study was to investigate the association of myocilin with mitochondria in TM cells. In vitro mitochondrial import assays showed that myocilin was imported to the TM mitochondria, targeting to mitochondrial membranes and/or the intermembrane space. The targeting was mediated mostly via the amino‐terminal region of myocilin. When myocilin expression was induced either by treatment with dexamethasone or transfection with a myocilin construct, the mitochondrial membrane potential in TM cells, as assessed by JC‐1 staining, was lowered. Subcellular fractionation and Western blot analyses confirmed that a portion of myocilin sedimented with the mitochondrial fractions. Upon anti‐Fas treatment to provoke apoptosis, an increase of myocilin distribution in cytosolic fraction was observed, suggesting that myocilin was partially released from mitochondrial compartments. These results confirmed the association of myocilin with TM cell mitochondria and indicated that myocilin may have a proapoptotic role in TM cells. J. Cell. Physiol. 213:775–784. © 2007 Wiley‐Liss, Inc.
Adenosine A1 and A2A receptor effects on G‐protein cycling in β‐adrenergic stimulated ventricular membranes
Authors: Fenton Richard A. , Dobson James G. 
Published: May 2007

AbstractIn the heart β1‐adrenergic (β1R) and adenosine A1 (A1R) and A2A (A2AR) receptors modulate contractile and metabolic function. The interaction between these receptors was investigated at the level of G‐protein cycling by determining the effect of receptor agonists on the binding of GTP to G‐proteins and displacement of Gα‐subunit‐bound GDP by GTP. Crude membranes from rat heart or brain were stimulated by agonists for β1R (isoproterenol; ISO), A1R (chlorocyclopentyladenosine, CCPA) and A2AR (CGS‐21680; CGS). GTP binding to membranes was increased by ISO (17%), CCPA (6%) and CGS (12%). Binding values observed with incubation using ISO and CCPA together were significantly less than values obtained by the incubation of individual agents alone. With ISO, GTP binding to Gαs subunits as determined by immunoprecipitation was increased 79% in heart and 87% in brain. These increases were attenuated by CCPA, an effect that was inhibited by CGS. GDP release by membranes was increased 6.9% and 4.6% by ISO and CCPA, respectively. After co‐incubation of these agonists, release was increased less than determined by the addition of the individual agent responses. CGS inhibited the reduced release caused by of CCPA. Adenylyl cyclase activity stimulated by ISO was attenuated 33% by CCPA, an effect inhibited by CGS. Together, these results indicate that A1R exert an antiadrenergic action at the level of β1R stimulated Gs‐protein cycling and that A2AR reduce this action. J. Cell. Physiol. 213:785–792. © 2007 Wiley‐Liss, Inc.
Patch‐clamp ‘mapping’ of ion channel activity in human sperm reveals regionalisation and co‐localisation into mixed clusters
Authors: Jiménez‐González M.C. , Gu Y. , Kirkman‐Brown J. , Barratt C.L.R. , Publicover S. 
Published: May 2007

AbstractIon channels are pivotal to many aspects of sperm physiology and function. We have used the patch clamp technique to investigate the distribution of ion channels in the plasma membrane of the head of human spermatozoa. We report that three types of activity are common in the equatorial and acrosomal regions of the sperm head. Two of these (a chloride‐permeable anion channel showing long stable openings and a second channel which flickered between open and closed states and was dependent upon cyoplasmic factors for activity) were localised primarily to the equatorial segment. A third type, closely resembling the flickering actvivity but with different voltage sensitivity of Popen, was more widely distributed but was not detectable over the anterior acrosome. In the anterior acrosomal area channels were present but showed very low levels of spontaneous activity. A unique feature of channel activity in the sperm equatorial region was co‐localisation into mixed clusters, most patches were devoid of activity but ‘active’ patches typically contained two or more types of activity (in a single 200–300 nM diameter patch). We conclude that ion channels in the sperm membrane show regionalisation of type and activity and that the channels are clustered into functional groups, possibly interacting through local effects on membrane potential. J. Cell. Physiol. 213:801–808. © 2007 Wiley‐Liss, Inc.