Database : MEDLINE
Search on : Bone and Marrow [Words]
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[PMID]: 23577956
[Au] Autor:Defarges A; Abrams-Ogg A; Foster RA; Bienzle D
[Ad] Address:Department of Clinical Studies, University of Guelph, Guelph, ON, Canada.
[Ti] Title:Comparison of sternal, iliac, and humeral bone marrow aspiration in Beagle dogs.
[So] Source:Vet Clin Pathol;42(2):170-6, 2013 Jun.
[Is] ISSN:1939-165X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Sternal bone marrow aspiration in dogs is not commonly performed as it is considered technically challenging in smaller dogs. However, the sternum is readily accessible and associated with less pain from aspiration compared with other sites. OBJECTIVES: The aim of the study was to investigate feasibility, ease, number of attempts, safety, and sample quality of sternal bone marrow aspirates in small dogs. METHODS: Bone marrow aspirates were obtained in a randomized order from 3 sites in 26 clinically healthy Beagles under general anesthesia. Samples were obtained from the sternum using one-inch 20- or 22-gauge hypodermic needles, from the right greater tubercle of the humerus, and the right iliac crest using 18-gauge Illinois needles. The difficulty of each procedure was scored. Two types of bone marrow smears were prepared and reviewed by a pathologist unaware of site of aspiration or dog. The number of particles per slide and overall slide quality were scored. The site of aspiration and the cranial thoracic wall were evaluated at autopsy for evidence of trauma or pneumothorax. RESULTS: The number of attempts and time for bone marrow aspiration were greater for ilium than for sternum or humerus, but the sternum was the easiest to aspirate. Smear quality and particle number were similar for all sites. Neither trauma at the site of aspiration nor pneumothorax were identified. CONCLUSIONS: Aspiration of sternal bone marrow with hypodermic needles is feasible and safe in Beagle dogs. Samples equivalent in quality to those from the humerus or ilium can be obtained from clinically normal dogs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1306
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1111/vcp.12036

  2 / 293040 MEDLINE  
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[PMID]: 23730494
[Au] Autor:Kolibaba KS; Sterchele JA; Joshi AD; Forsyth M; Alwon E; Beygi H; Kennealey GT
[Ad] Address:Compass Oncology, 120 SE 136th Avenue, Vancouver, WA 98684, USA.
[Ti] Title:Demographics, treatment patterns, safety, and real-world effectiveness in patients aged 70 years and over with chronic lymphocytic leukemia receiving bendamustine with or without rituximab: a retrospective study.
[So] Source:Ther Adv Hematol;4(3):157-71, 2013 Jun.
[Is] ISSN:2040-6207
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVES: Bendamustine is a unique cytotoxic agent active against various human malignancies, including chronic lymphocytic leukemia (CLL). In vitro studies suggest that cytotoxic activity of bendamustine on CLL-derived cells is synergized by rituximab. A retrospective chart review was conducted to characterize treatment-naïve outpatients and those with relapsed disease aged 70 years and over with CLL receiving bendamustine (with or without rituximab) and to evaluate real-world patterns of care, safety, and effectiveness. METHODS: Using McKesson Specialty Care/US Oncology Network iKnowMed databases, 91 outpatients with at least two recorded visits and at least two cycles of bendamustine monotherapy or bendamustine-rituximab combination therapy were identified and included. Mean age at diagnosis and start of first therapy was 70.3 and 77.4 years respectively, and 63.7% of patients were men. RESULTS: Observed overall response rate was 56.3% in pooled treatment-naïve patients [n = 9; complete response (CR) 18.8%; partial response (PR) 37.5%; nodular partial response (nPR) 0%] and 58.7% in pooled patients with relapsed disease (n = 44; CR 13.3%; PR 44.0%; nPR 1.3%). Median time to progressive disease has not been reached for the 16 treatment-naïve patients (median follow up 15.1 months), and was 18.4 months for those with relapsed disease (n = 73). No unexpected toxicities were observed. Overall rate of blood/bone marrow toxicities (all grades) was 40.7%; grade 3/4 rates were 18.8% in treatment-naïve patients and 25.3% in those with relapsed disease. Most frequent nonhematologic adverse events were fatigue and rash. CONCLUSION: In this retrospective chart review of 91 outpatients with CLL aged 70 years and over, bendamustine (with or without rituximab) was an effective therapeutic option with manageable toxicity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1306
[St] Status:In-Data-Review
[do] DOI:10.1177/2040620713478629

  3 / 293040 MEDLINE  
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[PMID]: 23636780
[Au] Autor:Demicheli R
[Ad] Address:Scientific Directorate, Fondazione IRCCS Istituto Nazionale Tumori di Milano, Via Venezian 1, 20133, Milan, Italy, demicheliromano@istitutotumori.mi.it.
[Ti] Title:Tumours and tissues: similar homeostatic systems?
[So] Source:Target Oncol;8(2):97-105, 2013 Jun.
[Is] ISSN:1776-260X
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:The currently prevalent somatic mutation theory of carcinogenesis and metastases explicitly assumes that cancer is a cellular disease, i.e. a disease of the control of cell proliferation and/or cell differentiation. Accordingly, explanations should always be sought for at a gene and/or gene product level, regardless of the level of organization at which the phenomenon is observed. Such a reductionist approach characterized the century-old effort to find cancer cell singularities, absent in normal cells, without apparent success, however. More recently alternative views have been put forward, assuming that cancer is a tissue-based disease involving disturbed interactions within the tissue architecture. In this review, selected reports on normal tissue homeostasis and bone marrow contribution to both tumour cells and tumour stroma are reviewed. Regarding normal tissues, the existence of a complex homeostatic system actually involving the whole organism emerges. Regarding tumours, remarkable similarities with normal tissue activities are apparent, providing some evidence that tumours share many biological features and processes with normal tissues. The review supports the concept that cancer is a tissue-based disease and that its pathological nature may result from unbalanced/untimely activation of otherwise normal physiological processes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1306
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s11523-013-0277-6

  4 / 293040 MEDLINE  
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[PMID]: 23660338
[Au] Autor:Liedtke S; Freytag EM; Bosch J; Houben AP; Radke TF; Deenen R; Köhrer K; Kögler G
[Ad] Address:Institute for Transplantation Diagnostics and Cell Therapeutics, Heinrich-Heine-University Medical Center, Düsseldorf, Germany. Electronic address: liedtke@itz.uni-duesseldorf.de.
[Ti] Title:Neonatal mesenchymal-like cells adapt to surrounding cells.
[So] Source:Stem Cell Res;11(1):634-46, 2013 Jul.
[Is] ISSN:1876-7753
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Hematopoietic cord blood (CB) transplantations are performed to treat patients with life-threatening diseases. Besides endothelial cells, the neonatal multipotent stromal cell subpopulations CDSCs (CB-derived stromal cells) and USSCs (unrestricted somatic stromal cells) are like bone marrow (BM) SCs interesting candidates for clinical applications if detailed knowledge is available. Clonal USSC compared to CDSC and BMSC lines differ in their developmental origin reflected by a distinct HOX expression. About 20 (out of 39) HOX genes are expressed in CDSCs (HOX+), whereas native USSCs reveal no HOX gene expression (HOX-). Moreover, USSCs display a lineage-specific absence of the adipogenic differentiation potential. As the specific HOX code can be ascribed to topographic bodysites it may be important to match the HOX code of transplanted cells to the tissue of interest. Herein co-culture experiments were performed, presenting a novel approach to modulate the differentiation potency of USSCs towards HOX positive stromal cells. After co-culturing native USSCs with CDSCs and BMSCs, USSCs adapt a positive HOX code and gain the adipogenic differentiation capacity. These results present for the first time modulation of a lineage-specific differentiation potential by co-culture. Finally, USSCs can be claimed as potential candidates to substitute unique progenitor cell populations in clinical approaches.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1306
[Js] Journal subset:IM
[St] Status:In-Data-Review

  5 / 293040 MEDLINE  
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[PMID]: 23584083
[Au] Autor:Mirabella T; Gentili C; Daga A; Cancedda R
[Ad] Address:Department of Experimental Medicine (DIMES), University of Genova, 16132 Genova, Italy; IRCCS AOU San Martino - IST National Institute for Cancer Research, 16132 Genova, Italy; Cardiovascular Research Center, Yale Medical School, 06511, New Haven, CT, USA. Electronic address: teodelinda.mirabella@yale.edu.
[Ti] Title:Amniotic fluid stem cells in a bone microenvironment: Driving host angiogenic response.
[So] Source:Stem Cell Res;11(1):540-51, 2013 Jul.
[Is] ISSN:1876-7753
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The repair of skeletal defects remains a substantial economic and biomedical burden. The extra-embryonic fetal stem cells derived from amniotic fluid (AFSCs) have been used for the treatment of large bone defects, but mechanisms of repair are not clear. Here we studied the potential contribution of human AFSCs to the modeling of an ectopic bone. We found that AFSCs are not osteogenic in vivo, and, compared to bone marrow-derived stromal cells, recruit more host CD31 and VEGF-R2 positive cells. Finally, when AFSCs were co-implanted with human-bone forming cells, a normo-osteosynthesis occurred, the engineered ossicle was hyper-vascularized, but AFSCs were not retrieved in the implant within 2weeks. We concluded that AFSCs do not contribute to the deposition of new bone, but act as a powerful proinflammatory/proangiogenic boost, driving a host response, ending in AFSC clearance and vascularization of the bone environment. In our model, a source of osteocommitted cells, capable to engraft and proliferate in vivo, is needed in order to engineer bone. The angio-attractant properties of AFSCs could be exploited in strategies of endogenous cell homing to actively recruit host progenitors into a predefined anatomic location for in situ bone tissue regeneration.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1306
[Js] Journal subset:IM
[St] Status:In-Data-Review

  6 / 293040 MEDLINE  
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[PMID]: 23730368
[Au] Autor:Knoll A; Brockmeyer T; Chevalier R; Zscheppang K; Nielsen H; Dammann C
[Ad] Address:Hannover Medical School, Hannover, Germany ; Division of Newborn Medicine, Floating Hospital for Children at Tufts Medical Center, Boston, MA, USA.
[Ti] Title:Adult Rat Bone Marrow-Derived Stem Cells Promote Late Fetal Type II Cell Differentiation in a Co-Culture Model.
[So] Source:Open Respir Med J;7:46-53, 2013.
[Is] ISSN:1874-3064
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Bronchopulmonary dysplasia develops in preterm infants due to a combination of lung immaturity and lung injury. Cultured pluripotent bone marrow stem cells (BMSC) are known to reduce injury and induce repair in adult and in immature lungs, possibly through paracrine secretion of soluble factors. The paracrine relationship between BMSC and primary fetal lung epithelial type II cells is unknown. We determined the effects of BMSC on type II cell and fibroblast behavior using an in vitro co-culture model. Rat BMSC were isolated and co-cultured with primary fetal E21 rat type II cells or lung fibroblasts in a Transwell(®) system without direct cell contact. Effects of BMSC conditioned media (CM) on type II cell and fibroblast proliferation and on type II cell surfactant phospholipid (DSPC) synthesis and mRNA expression of surfactant proteins B and C (sftpb and sftpc) were studied. We also determined the effect of fibroblast and type II cell CM on BMSC proliferation and surface marker expression. Co-culture with BMSC significantly decreased type II cell and fibroblast proliferation to 72.5% and 83.7% of controls, respectively. Type II cell DSPC synthesis was significantly increased by 21% and sftpb and sftpc mRNA expressions were significantly induced (2.1 fold and 2.4 fold, respectively). BMSC proliferation was significantly reduced during the co-culture. Flow cytometry confirmed that BMSC retained the expression of undifferentiated stem cell markers despite their exposure to fetal lung cell CM. We conclude that BMSC induce fetal type II cell differentiation through paracrine release of soluble factors. These studies provide clues for how BMSC may act in promoting alveolar repair following injury.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1306
[St] Status:In-Data-Review
[do] DOI:10.2174/1874306401307010046

  7 / 293040 MEDLINE  
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[PMID]: 23730212
[Au] Autor:Rodero MP; Auvynet C; Poupel L; Combadière B; Combadière C
[Ad] Address:Institut National de la Santé et de la Recherche Médicale, (INSERM) UMR-S 945-IUC and Université Pierre et Marie Curie (Paris 6), Laboratory of Immunity and Infection, Institut Universitaire du Cancer, Paris, France.
[Ti] Title:Control of Both Myeloid Cell Infiltration and Angiogenesis by CCR1 Promotes Liver Cancer Metastasis Development in Mice.
[So] Source:Neoplasia;15(6):641-8, 2013 Jun.
[Is] ISSN:1476-5586
[Cp] Country of publication:Canada
[La] Language:eng
[Ab] Abstract:Expression of the CC chemokine receptor 1 (CCR1) by tumor cells has been associated with protumoral activity; however, its role in nontumoral cells during tumor development remains elusive. Here, we investigated the role of CCR1 deletion on stromal and hematopoietic cells in a liver metastasis tumor model. Metastasis development was strongly impaired in CCR1-deficient mice compared to control mice and was associated with reduced liver monocyte infiltration. To decipher the role of myeloid cells, sublethally irradiated mice were reconstituted with CCR1-deficient bone marrow (BM) and showed better survival rates than the control reconstituted mice. These results point toward the involvement of CCR1 myeloid cell infiltration in the promotion of tumor burden. In addition, survival rates were extended in CCR1-deficient mice receiving either control or CCR1-deficient BM, indicating that host CCR1 expression on nonhematopoietic cells also supports tumor growth. Finally, we found defective tumor-induced neoangiogenesis (in vitro and in vivo) in CCR1-deficient mice. Overall, our results indicate that CCR1 expression by both hematopoietic and nonhematopoietic cells favors tumor aggressiveness. We propose CCR1 as a potential therapeutical target for liver metastasis therapy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1306
[Js] Journal subset:IM
[St] Status:In-Data-Review

  8 / 293040 MEDLINE  
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[PMID]: 23199365
[Au] Autor:Reeves KJ; Hou J; Higham SE; Sun Z; Trzeciakowski JP; Meininger GA; Brown NJ
[Ad] Address:Microcirculation Research Group, Department of Oncology, School of Medicine, University of Sheffield, S10 2RX, UK.
[Ti] Title:Selective measurement and manipulation of adhesion forces between cancer cells and bone marrow endothelial cells using atomic force microscopy.
[So] Source:Nanomedicine (Lond);8(6):921-34, 2013 Jun.
[Is] ISSN:1748-6963
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Aims: The lack of understanding of the biology of bone cancer metastasis has limited the development of effective treatment strategies. The aim of this study was to characterize tumor cell adhesion molecules and determine active tumor cell interactions with human bone marrow endothelial (BME) cells using atomic force microscopy. Materials & methods: A single prostate (PC3) cancer cell was coupled (concanavalin A) to the atomic force microscopy cantilever then placed in contact with BME cells for cell force spectroscopy measurements. Results & discussion: Strong adhesive interactions between PC3 and BME cells were significantly (p < 0.05) reduced by anti-ICAM-1, anti-ß1 and anti-P-selectin, but not anti-VCAM-1. The combined blocking antibodies or the therapeutic agent zoledronic acid significantly (p < 0.005) reduced the adhesive interactions by 65 and 63%, respectively, which was confirmed using a functional in vitro assay. Conclusion: Atomic force microscopy provides a highly sensitive screening assay to determine and quantify nanoscale adhesion events between different cell types important in the metastatic cascade. Original submitted 21 February 2012; Revised submitted 30 July 2012; Published online 2 December 2012.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1306
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.2217/nnm.12.139

  9 / 293040 MEDLINE  
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[PMID]: 23734079
[Au] Autor:Li H; Wang YS
[Ad] Address:Department of Ophthalmology, Eye Institute of Chinese PLA, Xijing Hospital, Fourth Military Medical University, Xi'an, PR China ; Department of ophthalmology, General Hospital of Lanzhou military command, Lan'zhou, PR China.
[Ti] Title:An angiotensin-converting enzyme inhibitor modulates stromal-derived factor-1 through CD26/dipeptidyl peptidase IV to inhibit laser-induced choroidal neovascularization.
[So] Source:Mol Vis;19:1107-21, 2013.
[Is] ISSN:1090-0535
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE: Stromal-derived factor (SDF)-1 is a chemokine that recruits bone marrow-derived endothelial precursor cells (EPCs) for choroidal neovascularization (CNV) development. Angiotensin-converting enzyme (ACE) inhibitors mediate the compensatory effects of ACE and CD26/dipeptidyl peptidase IV (DPP IV), which results in the degradation and inactivation of SDF-1 in vivo. ACE inhibitors, such as imidapril, exhibit potential antiangiogenic effects on laser-induced CNV in mice. The role that this imidapril-mediated effect plays in modulating SDF-1 signals has not been defined. The present study assessed the effect of the CD26/SDF-1 signaling pathway on the inhibitory effect of imidapril in CNV development. METHODS: CNV was induced in C57BL/6J mice by focally rupturing Bruch's membrane using a 532-nm diode laser. The animals were pretreated with PBS, imidapril, diprotin-A (a DPP IV antagonist), or imidapril plus diprotin-A for 5 days before photocoagulation. Treatments were continued daily for 14 days following the laser induction. The normal control group did not undergo laser rupture or receive treatment. CD26 activity was measured using a substrate conversion assay and flow cytometry. SDF-1 levels in both the blood and the bone marrow were measured using an enzyme-linked immunosorbent assay, and the number of circulating endothelial progenitor cells (EPCs) and leukocytes was quantified. Functional analyses of circulating SDF-1 were performed using actin polymerization blood biomarker assays, and the CNV-related responses were evaluated using fluorescein angiography and isolectin-B4-labeled flatmounts. RESULTS: Imidapril directly amplified CD26 activity and had a minor effect on the number of CD26(+) cells in the bone marrow. However, decreased CD26 activity in the plasma was secondary to a decrease in the number of circulating CD26(+) cells and blood leukocytes. Furthermore, imidapril increased SDF-1 concentrations in the peripheral circulation via CD26-induced degradation of SDF-1 in the bone marrow, an effect that coincided with elevated numbers of circulating EPCs. CD26-mediated SDF-1 inactivation was demonstrated by a decrease in SDF-1-induced actin polymerization in the whole blood of imidapril-treated mice. Imidapril markedly decreased angiographic leakage and CNV size. CD26 inhibition completely blocked the CD26/SDF-1 signaling pathway in vivo and reduced the antiangiogenic effect of imidapril. CONCLUSIONS: These results strongly suggest that the antiangiogenic effects of imidapril on laser-induced CNV partially involve the modulation of the CD26/SDF-1 signaling pathway.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1306
[Js] Journal subset:IM
[St] Status:In-Data-Review

  10 / 293040 MEDLINE  
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[PMID]: 23703108
[Au] Autor:Zhang JC; Lü G
[Ad] Address:Department of Orthopedics, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
[Ti] Title:Effect of 17ß­estradiol in rat bone marrow­derived endothelial progenitor cells.
[So] Source:Mol Med Rep;8(1):178-82, 2013 Jul.
[Is] ISSN:1791-3004
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:The aim of the present study was to investigate the bionomics of rat bone marrow endothelial progenitor cells (EPCs) following 17ß­estradiol treatment at various concentrations. Total mononuclear cells were extracted from rat bone marrow by density gradient centrifugation. Following cultivation for 7 days, attached cells were incubated with various concentrations of 17ß­estradiol (0, 10 and 100 nmol/l). The proliferation and migration activities of EPCs were measured by MTT and transwell chamber assays. In vitro vasculogenic activities were measured using type I collagen. Flow cytometry was performed to analyze differentiation into endothelial cells. The results indicated that at 7 days following culture, CD133 and CD34 cell markers were 69.44 and 81.05%, respectively. MTT assay demonstrated that the optical density (OD) value of the 10 nmol/l group was markedly higher than that of the 0 and 100 nmol/l groups. The OD value of the 0 nmol/l group was higher than the 100 nmol/l group (P<0.05). EPC migration, in vitro vascularization and differentiation were higher in the 100 and 10 nmol/l groups compared with the 0 nmol/l group. These parameters were higher in the 100 nmol/l than the 10 nmol/l group (P<0.05). In conclusion, the results of the present study demonstrated that migration, in vitro vasculogenesis and differentiation into endothelial cells is regulated by 17ß­estradiol and enhanced in a concentration-dependent manner. Proliferation levels were contrary to these observations, with levels decreasing as the concentration of 17ß­estradiol increased.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1306
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.3892/mmr.2013.1486


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