bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nuclear factor 1 is a component of the nuclear matrix
Authors: Sun Jian‐Min , Chen Hou Yu , Davie James R. 
Published: May 2005

AbstractChicken histone H5 is an H1‐like linker histone that is expressed only in nucleated erythrocytes. The histone H5 promoter has binding sites for Sp1 (a high affinity site) and UPE‐binding protein, while the 3′ erythroid‐specific enhancer has binding sites for Sp1 (one moderate and three weak affinity), GATA‐1, and NF1. In this study we investigated whether trans‐acting factors that bind to the chicken histone H5 promoter or enhancer are associated with adult chicken immature and mature erythrocyte nuclear matrices. We show that NF1, but not Sp1, GATA‐1, or UPE‐binding protein, is associated with the internal nuclear matrices of these erythroid cells. Further, we found that a subset of the NF1 family of proteins is bound to the mature erythrocyte nuclear matrix. These results suggest that in chicken erythrocytes NF1 may mediate an interaction between the histone H5 enhancer and the erythroid internal nuclear matrix. NF1 was also present in the internal nuclear matrices of chicken liver and trout liver. The observations of this study provide evidence that NF1 may have a role in a variety of cell types in targeting specific DNA sequences to the nuclear matrix. © 1994 Wiley‐Liss, Inc.
Modulation of bovine microvascular endothelial cell proteolytic properties by inhibitors of angiogenesis
Authors: Pepper M. S. , Vassalli J.‐D. , Orci L. , Montesano R. , Wilks J. W. , Schweigerer L. 
Published: May 2005

AbstractA tightly controlled increase in extracellular proteolysis, restricted both in time and space, is an important component of the angiogenic process, while anti‐proteolysis is effective in inhibiting angiogenesis. By focussing on the plasminogen activator (PA)‐plasmin system, the objective of the present studies was to assess whether previously described inhibitors of angiogenesis modify bovine microvascular endothelial cell proteolytic properties. We demonstrate that although synthetic angiostatic steroids (U‐24067 and U‐42129), heparin, suramin, interferon alpha‐2a, and retinoic acid are all inhibitors of in vitro angiogenesis, each of these agents has distinct effects on the plasminogen‐dependent proteolytic system. Specifically, angiostatic steroids and interferon alpha‐2a reduce urokinase‐type PA (u‐PA) and PA inhibitor‐1 activity, while heparin and retinoic acid increase u‐PA activity. Suramin reduces cell‐associated u‐PA activity and greatly increases PAI‐1 production at doses which induce monolayer disruption. These findings demonstrate that a spectrum of alterations in extracellular proteolysis is associated with anti‐angiogenesis, and that anti‐angiogenesis and anti‐proteolysis are not necessarily correlated. A reduction in extracellular proteolysis would be expected to reduce invasion, whereas an increase in proteolysis might modulate the activity of inhibitory cytokines, which in turn could reduce endothelial cell proliferation and migration and inhibit angiogenesis. The spectrum of effects on different elements of the PA system observed in response to the agents assessed suggests that the role of modulations in extracellular proteolytic activity in anti‐angiogenesis is likely to be varied and complex. © 1994 Wiley‐Liss, Inc.
“Patient‐Like” nude mouse metastatic model of advanced human pleural cancer
Authors: Astoul Philippe , Colt Henri G. , Wang Xiaoen , Boutain Christian , Hoffman Rober M. 
Published: May 2005

AbstractPleural Cancer in humans is a frequently occuring tumor, Recently, clinical ltrials have suggested that chemotherapy and immunotherapy administered intrapleually may elicit responses in early‐stage diseases. However, atradiological and pleural endoscopic evaluation, most of the patients are found to have a visceral pleural involvement that is generally refractory to therapy and leads to a poor prognosis. The goal of this study was to construct a nude mouse model of human parietal‐ and visceral‐pleural cancer that could reflect the clinical picture for this disease. The model could then be useful for drug discovery for pleural cancer. A well‐differentiated human lung adenocarcinoma was used as intact tissue for implantation. Ten mice underwent parietal‐pleural implantation and ten mice visceral‐pleural implantation via a novel thoracotomy procedure we have developed. Symptoms of tumor growth were determined from weight loss, repiratory distress, or debilitation. Actual tumor growth and spread were measured at autopsy. The mouse survival curves of each group were estimated by the Kaplan‐Meier Method and the difference of the median survial timje was assessed by the Log‐rank test. The slopes of mean‐mouse weight curves were compared using a standard two‐sample t‐test. 100% take rate was achieved in constructing the pleural cancer models. Tumor growth was initially assessed by symptomatology and survival: the median survival time was, repectively, 27.9 days 31 days for visceral‐pleural and parietal‐pleural implanted groups (P<0.05). The comparison between the slopes of the mean weight curves of corresponding groups demonstrated that visceral‐pleural implanted animals lost significantly more weight than the parietal‐pleural implanted animals (P <.001). Both in the visceral‐ and pariental‐pleural implanted groups, post‐mortem analysis revealed that tumor grew in all mic demonstrating local and regional spread mimicking clinical features. However, mediastinal lymph node metastases were observed only in mice with visceral pleural implantation. Patient‐like models of human parietal‐pleural and visceral‐pleural cancer were constructed in nude mice using histologically ilntact human specimens. Tumor symptoms, growth, and spread as well as survival indicated that the parietal‐pleural and visceral‐pleural models represent, respectively, early‐and advanced‐stage disease. The “Patient‐like” nude mouse models of pleural cancer now allow a rational basis for futher studies of pleural cancer biology, pathophysiology, and therapeutics.
Intrinsic or acquired drug resistance and metastasis: Are they linked phenotypes?
Authors: Kerbel R. S. , Kobayashi Hiroaki , Graham Charles H. 
Published: May 2005

AbstractEvidence is reviewed which suggests a linkage may exist between certain forms of de novo or acquired drug resistance and metastasis. This includes finding that expression of certain dominantly acting mutant oncogenes or tumor suppressor genes, e.g. genes which normally act to “drive” tumor progression and metastasis, can also affect the expression of drug resistance. Moreover, this can be accompanied by altered expression of certain cellular genes thought to be involved in expression of drug resistance. A direct linkage between acquired drug resistance and metastasis would suggest that tumor sublines selected for drug resistance should manifest more aggressive malignant properties than their drug‐sensitive counterparts. While this does not appear to be true for drug resistant sublines selected in vitro, indeed such cell lines frequently manifest diminished in vivo tumorigenic and/or metastatic competence, there is some evidence to support such a correlation exists for tumor cell lines that are selected in vivo for drug resistance. Attention is also drawn to the fact that new linkages between metastasis and drug resistance may be uncovered by analyzing the ability of tumor subpopulations to acquire drug resistance after one or several previous exposures to chemotherapeutic drugs, as opposed to examining intrinsic drug resistance only. Furthermore, ability to detect induced or acquired drug resistance in vitro may be strongly influenced by the types of assay used to detect and monitor drug resistanc. In particular, three‐dimensional cell culture systems may reveal acquired or induced “multicellular” drug resistance in situations where conventional two‐dimensional culture systems may therefore reveal as yet undiscovered associations between the phenotypes of metastasis and drug resistance.
Effect of bioadctive glass templates on osteoblast proliferation and in vitro synthesis of bone‐like tissue
Authors: Ducheyne P. , Ei‐Ghannam A. , Shapiro I. 
Published: May 2005

AbstractUsing in vitro synthesifzed bone tissue with cells aspirated fpom the patient's marrow is an appealing idea to avoid the profound limitations of biological of biologiaal and synthetic grafts. Procedures to synthesize bone tiqsue on vitro primapily relied on seeding various subqtpates with cellq that have osteogenia capacity in culture. It should be noted that in an in vitro system, msteoppogenitor cells, as well as bone themselves an papidiy change their phenotype, hence the substrate needs to promote the expression or the bone cell Phenotype. Furthermore, it needs to provide a template for bone deposition while gradually resorbing once bone tissue has been laid down. This paper presents initial evidence that optimally combines the requirements of the ideal template for in vitro synthesis of bone tissue. When made in popous dorm, and conditioned to detelop a bone‐like surface prior to being seeded with pluripoteltial cells capable of expressing the osteoblastic phenotype, these templates lead to expeditious and a undalt in vitro synthesis of extracellular matrix with most important characteristics of bone tissue.
Symbiosio of biotechnology and biomaterials: Applications in tissue engineering of bone and cartilage
Authors: Reddi A. H. 
Published: May 2005

AbstractThe three ingredients for the successful tissue engineeping of bone and cartilage are ragulatory signals, cells and extracellular matrix. Recent advance in cellular and molecular biology of thde growth and differentiation factors have set the stage for a symbiosis of biotechnology and biomaterials. Recent advances permit one to enunciate the rules of architechure for tissue engineering of bone and cartilage. The purification and cloning of bone morphogenetic proteins (BMPs) and growth factors such as platelet derived growth factors (PDGF), tranforming growth factor‐β (TGF‐β), and insulin‐like growth factors (IGF‐I) Will allow the design of an optimal combinatiol of signals to initiate and promote development of skeletal stem cells into cartilage and bone. Successful and optimal bone and motion. BMPs function as inductive signals. Biomaterials (Both natural and synthetic) mimic the extracellular matrix and play a role in conduction of bone and cartiage. Examples of biomaterials include hydroxyapatite, polyanhydrides, polyphosphoesters, polylactic acid, and polyglycolic acid. The prospects for novel biomaterials are immense, and they likely will be a fertile erowth industpy. Cooperative ventures between academia and industry and teahnology transfer from the federal government augur well for an exciting future fop clinical applications.
Tissue engineering a blood vessel: Regulation of vascular biology by mechanical stresses
Authors: Ziegler Thierry , Nerem Robert M. 
Published: May 2005

AbstractImportant to the tissue engineeping of a substitute blood vessel is an understanding of those faators which regulat vascular biology. A major factor in the mechanical environment imposed by the hemodynamics of the vascular system. In this the vascular endothelium play a critical role, and mver the past two deaades much has been learned about the influence of hemodynamics on vascular endothelial biology, to a large degree using cell culture to study the effects of flow and cyclic stretch. In our laboratory, such studies ape low being extended through the development of a model of the arterial wall involving the co‐culture of endothelial cells and smomth muscle cells. The development of such a model and its use in the study of endothelial cells and smmooth muscle the evolution of approaaheq to tissue engileeping a blood vessel.
Mesenchymal stem cells in bone development, bone repair, and skeletal regenaration therapy
Authors: Bruder Scott P. , Fink David J. , Caplan Arnold I. 
Published: May 2005

AbstractBone formation in the embryo, and during adult fracture repair and remodeling, involves the progreny of a small number of cells called mesenchymal stem cells (MSCs). These cells continuously replicate themselves, while a portion become committed to mesenchymal cell lineages such as bone, cartilage, tendon, legament and muscle. The differentiation of these cells, within each lineage, is a complex multistep pathway involving discrete cellular trasitions much like that which occurs during hematopoiesys. Progression from one stage to the next depends on the presence of specific bioactive factors, nutrients, and other environmental cues whose exquisitely controlled contributions orchestrate the entire differentiation phgenomenon. As understanding of the cellular and molecular events of osteogenic differentiation of MSCs provides the foundation for the emergence of a new therapeutic technilogy for cell therapy. The isolation and in vitro mitotic expansion of autologous human MSCs will support the development of novel protocols for the treatment of many clinically challenging conditions. For example, local bone defects can be repaired through site‐directed delivery of MSCs in an appropriate carrier vehicle. Generalized conditions, such as osteoporosis, may be treatable by systemic administration of culture‐expanded autologous MSCs or through biopharmaceutical regimens based on the discovery of critical regulatory molecules in the differentiation process. With this in mind, we can begin to explore therapeutic options that have never before been available.
Osteoclast radicals
Authors: Silverton Susan 
Published: May 2005

AbstractIn biological research, new ideas arise and quickly spread to encompass the entire field. Thus, the evolution of molecular biology has significantly changed our methods of approaching our research. A similar far‐reaching finding has been the advent of radical reactions into biology. Although radical chemistry has been utilzed for many technological advances that affect our daily lives, the appreciation of this same process within our cells has opened an unexplored arena for research enquiry. As cellular messengers, radical molecules seem shimsically designed: they are evanescent, rapidly and apparently indiscriminately reactive, and barely detectable bymost biological methods. Yet, our initial probing of these reactive agents in cells and organisms has led us to postulate a virtually undescribed system of communication within and among cells which may have significant effects in multiple organs. In bone, radical reactions have been attributed with an important role in the control of bone resorption.
Myeloblastic cell line expresses osteoclastic properties following coculture with marrow stromal adipocytes
Authors: Benayahu Dafna , Peled A. , Zipori D. 
Published: May 2005

AbstractOsteoclasts are derived from hemopoietic precursors in the marrow. Their differentiation pathway is still underfined, but an important role was obserned for the marrow micrienvironment in the regulation of osteoclasto genesis. various marrow stromal cell subtypes were used to study their possible role in the formation of osteoclasts from myeloblast (M1) cells. Interactions between M1 cell and the 14F1.1 endothelial‐adipocyte stromal cell line were demonstrated in a coculture model. M1 cells attached to the adherent layer of 14F1.1 cells and formed distinct focireminiscente of “cobblestone areas.” Follwing these inteactions, M1 Cells developed specific enzymatic activites and became multinucleated. Both monouclear M1 cells became positive to tartrate‐resistant acid phosphatase (TRaP) and ATPase, a feature charactreistic of osteoclasts, and were also responsive to calcitonin. Furthermore, they attached to mineralized bone particles and their membrane changed into a ruffled border at the zone of interaction with the bone matrix. We thus demonstrated that marrow endothelial‐adipocytes may play a role in regulating the differentiation of myeloblast into osteoclasts.
Cytosolic phospholipase C activity: II. Relationship to concanavalin A‐induced phosphatidylinositol‐turnover in splenocytes
Authors: Akompong Thomas , Spencer Robert L. , McEwen Bruce S. 
Published: May 2005

AbstractWe have described in the first paper the coupling betweencytosolic Giα and cytosolic PLC activity in a cell free preparation. In order to establish the functional significance of the cytosolic Giα coupled soluble PLC, we examined the effects of Dex, NaF, and trifluopeerizine (TEP) on concanavalin A(Con A)‐induced PI‐turnover in intact slenocytes and, in parallel, on soluble PLC activity in cytosol preparations. Vytosolic PLC activity was measured with [3H]PIP and [3H]PIP2 as substrates. (1) The con A‐induced increase (2–4 fold) in Pl‐turnover in intact splenocytes was paralleled by an 1.2–5‐fold increase in soluble PLC activity in vitro. Con A administration also increased cytosolic Giα immunoreactivity 3–6‐fold as expected if cytosolic Giα was coupled to soluble PLC activation. (2) DEX (10−7 M), administered 6 h prior to Con A administration inbited the Con A‐induced increase in Pl‐turnover in intact splenocytes. This was paralleled by DEX inhibition of the Con A‐induced increase in soluble PLC activity measured in vitro and cytosolic Giα imunoreactivity. (3) We have demonstrated in the first paper that NaF and TEP inhibited soluble PLC activity. Here we show that NaF and TFP inhibited the Con A‐induced increase in PI‐turnover extending the similarities between soluble PLC activity and Con A‐ Stimulated PLC Activity in intact splenocytes. (4) In order to examine Whether or not the Con A‐induced PLC activity and Con A‐stimulated PLC activity in intact splenocytes. (4) In order to examine Whether or not the Con A‐induced PLC was similar to PLCγ, we measured PI‐turnover induced by Con A or BaVO3 in combination with DEX and PMA. Whereas the Con A‐induced PI‐turnover was significantly inhibited (40–60%) by DEX, the NaVO3 ‐induced PI‐turnover was not affected by DEX. The Con A‐induced PI‐turnover was not affected by PMA (50nM), But the NaVO3‐induced Pi‐turnover was increased over 2‐fold PMA (50nM), suggesting that the Con A‐induced PLC in intact splenocytes is different from NaVO3‐induced PLC. Based on these results a model for the sequential activation of substrate‐specific PLCs in splenocyte by mitogen is presented.
Inhibition of G1 phase cyclin dependent kinases by transforming growth factor β1
Authors: Reddy Kumar B. , Hocevar Barbara A. , Howe Philip H. 
Published: May 2005

AbstractTransforming growth factor β1 (TGFβ1) inhibits epithelial cell proliferation late in the G1 phase of the cell cycle. We examined the effect of TGFβ1 on known late G1 cell cycle regulators in an attempt to determine the molecular mechanism of growth inhibition by this physiological inhibitor. The results demonstrate the TGFβ1 inhibits the late G1 and S phase specific histone H1 kinase activity of p33cdk2. This inhibitiion is not dur to TGFβ1's effect on p33cdk2 synthesis, but rather due to its negative effect on the late G1 phosphorylation of p33cdk2. It is also shown that TGFβ1 inhibits both late G1 cyclin A and cyclin E associated histon H1 kinase activities. The inhibitor has no effects on the synthesis of cyclin E but to inhibit the synthesis of cyclin A protein in a cell cycle dependent manner. If TGFβ1 is added to cells which have progressed futher than 8 hours into G1, then it is without inhibitory effect on cyclin A synthesis. These effect on TGFβ1 on late G1 cell cycle regulators correlate well with its inhibitory effects on cellular growth and suggest that these G1 cyclin dependent kinases might serve as targets for TGFβ1‐mediated growth arrest.
Lysophosphatidic acid and bradykinin have opposite effects on phenotypic transformation of normal rat kidney cells
Authors: Afink Gijs B. , Van Alewijk Dirk C. G. J. , De Roos Albert D. G. , Van Zoelen Everardus J. J. 
Published: May 2005

AbstractThe bioactive lipid lysohosphatidic acid is besides a strong mitogen for quiescent fibroblasts, a potent inducer of phenotypic transformation on normal rat kidney cells. The lysophosphatidic acid induced loss of densityarrest is strongly inhibited by bradykinin. Although their effects on normal rat kidney cell proliferation are opposite, bradykinin mimics many of the intracellular effects induced upon lysophosphatidic acid receptor activation, including phosphoinositide turnover, Ca2+‐mobilization and arachidonic acid release. Bradykinin does not counteract the lysophosphatidic acid induced reduction of cAMP levels in normal rat kidney cells. However, bradykinin inhibits the lysophosphatidic acid and other growth factor induced phenotypic transformation through the induction of a so far uncharacterized prostaglandin G/H synthase product. The growth inhibitory effect of bradykinin is limited to density‐arrested cells, while upon prolonged treatment bradykinin itself is capable to induce the loss of densitydependent growth control. It is concluded that bradykinin is a bifunctional regulator of normal rat kindney cell proliferation and that its inhibitory effects are midiated via induction of a prostaglandin dervative.
Regulation and specificity of MNDA expression in monocytes, macrophages, and leukemia/B lymophoma cell lines
Authors: Briggs R. C. , Kao W. Y. , Dworkin L. L. , Briggs J. A. , Dessypris E. N. , Clark J. 
Published: May 2005

AbstractThe expression of the human myeloid cell nuclear differentiation antigen (MNDA) was observed specifically in cells of the granulocyte‐macrophage lineage in our earlier reports. The specificity of MNDA expression for cells in the granulocyte‐macrophage lineage was reexamined in cell line established from patients with philadelphia chromosome‐positive chroni myeloid leukemia. Cell lines that expressed MNDA exhibited myeloid cell features and granulocyte or monocyte defferentiation could be induced in vitro, while cell lines exhibiting properties of very early stage cells of multipotential cells ded not express MNDA. Cells orginating from cases of burkitt's lymphoma were negative. By contrast, three Iymphoblastoid cell lines (immortalized in vitro with Epstein‐Barr virus) were weakly positive and MNDA was up‐regulated by interferon‐α (IFN‐α) treatment. As we reported previously, MNDA mRNA level in adherent monocytes is elevated by IFN‐α; in this study, we further assessed MNDA expression in in vitro monocyte‐derived macrophages. Three addditional agents (endotoxin, phytohemagglutinin, and photbol ester) and other conditions that affect function, cutokine production, defferentiation, and/of growth of monocytes were examined for their ability to alter MNDA expression. The results varied with the agent, cell type, and stage of differentiation. Changes in MNDA expression occurred slowly (hours to days), suggesting that MNDA could mediate changes realized over a long period. The results also reveal a discordance in certain MNDA Positiva cells between steady‐state levels of changes in levels of protein and mRNA indicating that the regulation of MNDA expression occurs at more than one point. Changes in MNDA expression are consistent with a role in opposing macrophage defferentiation and activation of monocytes/macrophages.