Database : MEDLINE
Search on : bone and marrow [Words]
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[PMID]: 29524678
[Au] Autor:Ghanmi S; Trigui M; Baya W; Ellouz Z; Elfeki A; Charfi S; Fricain JC; Keskes H
[Ad] Address:Experimental Surgery of the Musculoskeletal System Laboratory, Sfax Faculty of Medicine, Sfax, Tunisia; Tissue Bioengineering Laboratory, U1026, Inserm, University of Bordeaux, France. Electronic address: ghanmisahar@yahoo.fr.
[Ti] Title:The periosteum-like effect of fresh human amniotic membrane on bone regeneration in a rabbit critical-sized defect model.
[So] Source:Bone;, 2018 Mar 07.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: The purpose of this study was to investigate the effect of fresh human amniotic membrane (FHAM) as a substitute of periosteum to enhance bone regeneration in critical-sized defects. METHODS: Tibial diaphyseal bone defects were created in forty New Zealand white rabbits and treated with FHAM or left empty. Treatment groups consisted of: FHAM implanted in the place of removed periosteum (FHAMP group); FHFAM implanted to fill the entire defect (FHAMF group) compared to negative control group; empty defect with removing the periosteum (NC group) and positive control group; and empty defect without removing the periosteum (PC group). Bone regeneration was evaluated by radiographic, micro-computed tomography (µ-CT) and histological analyses at 4 and 8 weeks post-surgery. RESULTS: Radiographic and µ-CT analysis demonstrated clearly enhanced new bone formation in positive control group (PC) and FHAMP group compared to negative control group (NC) and FHAMF group. Histological staining exhibited remaining woven bones and cartilage matrix in the FHAMP group, immature lamellar bone with medellury cavity and marrow bone formation in PC group from 4 weeks post-operatively. For FHAMF group, a little new bone formation was detected only from 8 weeks post-operatively, and an absence of any sign of healing in NC group at both time points. CONCLUSION: The results provide that FHAM increases bone regeneration in critical-sized defects when it is implanted in the place of the removed periosteum, but its additive effect does not have the same effect of the natural periosteum.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 368311 MEDLINE  
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[PMID]: 29524567
[Au] Autor:Hollinger MK; Giudice V; Cummings NA; Rivell G; Zhang H; Kajigaya S; Keyvanfar K; Chen J; Feng X; Young NS
[Ad] Address:Hematology Branch, National Heart, Lung, and Blood Institute (NHLBI), NIH, Bethesda, MD 20892-1202, USA.
[Ti] Title:PD-1 deficiency augments bone marrow failure in a minor-histocompatibility antigen mismatch lymphocyte infusion model.
[So] Source:Exp Hematol;, 2018 Mar 07.
[Is] ISSN:1873-2399
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:While PD-1 blockade has revolutionized cancer immunotherapy, immune-related adverse events (irAEs) present life-threatening complications. Recent reports of aplastic anemia (AA) as irAEs implicate PD-1/PD-L1 as important in preventing immune-mediated destruction of the hematopoietic niche. Infusion of PD-1-deficient (PD-1 KO) lymph node (LN) cells into minor-antigen mismatched mice resulted in early mortality, as well as more severe BM hypoplasia, anemia, and BM microarchitecture disruption in PD-1 KO LN-infused mice relative to mice that received B6 LN cell infusion. Mice that received PD-1 KO LN cells had more CD8 T cell infiltration of the BM and greater expansion of H60-specific CD8 T cells than did their B6 LN-infused counterparts. In the spleen, CD8 T cells were skewed to an effector memory phenotype, suggesting accelerated differentiation of PD-1 KO T cells. Our data suggest that PD-1 dysregulation has a role in murine BM failure, and vigilance in irAE monitoring may be desirable to treat early AA and related cytopenias.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 368311 MEDLINE  
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[PMID]: 29524470
[Au] Autor:Zheng Y; Huang C; Liu F; Lin H; Niu Y; Yang X; Zhang Z
[Ad] Address:Department of Anatomy, Institute of Biomedical Engineering, Second Military Medical University, Shanghai 200433, China.
[Ti] Title:Reactivation of denervated Schwann cells by neurons induced from bone marrow-derived mesenchymal stem cells.
[So] Source:Brain Res Bull;, 2018 Mar 07.
[Is] ISSN:1873-2747
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The use of neurons induced from stem cells has been introduced as an effective strategy for promoting peripheral nerve regeneration (PNR). The evolution and role of native denervated Schwann cells (SCs) were often ignored when exploring the mechanisms underlying neural transplantation therapy for PNR. The aim of this study was to understand if following injury, native denervated SCs could be reactivated by transplanting of neurons induced from bone marrow-derived mesenchymal stem cells (NI-BMSCs) to promote PNR. We co-cultured denervated SCs with NI-BMSCs in vitro, tested the proliferation of denervated SCs, and measured the expression and secretion of neurotrophic factors and neural adhesion molecules of the denervated SCs. Concurrently, 48 adult male Sprague-Dawley rats were randomly divided into 4 even groups of 12 rats each: normal group, phosphate-buffered saline (PBS) injection group, BMSCs transplantation group and NI-BMSCs transplantation group. PBS injection and cells transplantation were performed 4 weeks post-injury. After 4 weeks of NI-BMSCs transplantation, the survival of seeded NI-BMSCs was examined, proliferation and ultrastructure of native denervated SCs were detected, and myelination, axonal regeneration and the sciatic functional index measurements were also determinated. Our results demonstrated that NI-BMSCs reactivated denervated SCs both in vitro and in vivo and promoted sciatic nerve regeneration.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 368311 MEDLINE  
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[PMID]: 29524406
[Au] Autor:Zhou Z; Shi G; Zheng X; Jiang S; Jiang L
[Ad] Address:Department of Orthopedic Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China.
[Ti] Title:Autophagy activation facilitates mechanical stimulation-promoted osteoblast differentiation and ameliorates hindlimb unloading-induced bone loss.
[So] Source:Biochem Biophys Res Commun;, 2018 Mar 07.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Autophagy has been indicated to be involved in regulating bone metabolism. However, little is known about the role of autophagy in mechanical stimulation-influenced osteoblast differentiation and bone formation. In the present study, we first demonstrated that autophagy activation was essential for cyclic mechanical stretching-promoted osteoblast differentiation of bone marrow mesenchymal stem cells. To explore the in vivo role of autophagy in osteoblast differentiation, the hindlimb unloading-induced disuse osteoporosis model was used. Compared to the normal controls, hindlimb unloading led to abundant bone loss as well as lessened autophagy activation of osteoblasts. However, the activation of autophagy by ULK1 overexpression or in the presence of rapamycin significantly increased osteoblast differentiation activity and restored the bone volume. The findings implicate autophagy as a novel mechanosensitive pathway that regulates osteoblast differentiation. The pharmacological activation of autophagy may be an interesting approach for the prevention and treatment of disuse osteoporosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 368311 MEDLINE  
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[PMID]: 29524405
[Au] Autor:Nan Z; Fan H; Tang Q; Zhang M; Xu M; Chen Q; Liu Y; Dong Y; Wu H; Deng S
[Ad] Address:Department of Integrated Traditional Chinese and Western Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
[Ti] Title:Dual expression of CXCR4 and IL-35 enhances the therapeutic effects of BMSCs on TNBS-induced colitis rats through expansion of Tregs and suppression of Th17 cells.
[So] Source:Biochem Biophys Res Commun;, 2018 Mar 07.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Bone marrow-derived mesenchymal stem cells (BMSCs) hold great promise for the treatment of inflammatory bowel disease (IBD) owing to the immunosuppressive property and tissue healing potential. The balance of Treg/Th17 plays a crucial part in BMSC-mediated immunosuppression. Interleukin (IL)-35 is a newly identified anti-inflammatory cytokine required for the expansion of regulatory T cells (Tregs) and suppression of Th17 cells differentiation. It could amplify the immunosuppressive property of BMSCs by transfecting into BMSCs. However, the reparative capability of BMSCs in vivo is limited partly due to barren efficiency of BMSCs homing to inflamed colons. Up-regulation of CXC chemokine receptor 4 (CXCR4) expression on BMSCs is supposed to affect the directional homing of implanted BMSCs via stromal-derived factor-1 (SDF-1). In this study, by introducing lentivirus-mediated CXCR4 and IL-35 genes to modify rat BMSCs, we observed promoted migration ability and strengthened immunomodulatory activity of the genetically engineering BMSCs. These results suggest that the modification of BMSCs by dual expression of CXCR4 and IL-35 may provide an effective therapeutic strategy of BMSCs for IBD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 368311 MEDLINE  
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[PMID]: 29515101
[Au] Autor:Kim BH; Jung HW; Seo SH; Shin H; Kwon J; Suh JM
[Ad] Address:Graduate School of Medical Science and Engineering, KAIST, Daejeon, Republic of Korea.
[Ti] Title:Synergistic actions of FGF2 and bone marrow transplantation mitigate radiation-induced intestinal injury.
[So] Source:Cell Death Dis;9(3):383, 2018 Mar 07.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Unwanted radiological or nuclear exposure remains a public health risk for which effective therapeutic countermeasures are lacking. Here, we evaluated the efficacy of fibroblast growth factor-2 (FGF2) in treating radiation-induced gastrointestinal syndrome (RIGS) incurred by lethal whole-body irradiation (WBI) when administered in conjunction with bone marrow transplantation (BMT). In vitro experiments indicated FGF2 treatment increased proliferation, reduced apoptosis, and upregulated AKT-GSK3ß/ß-catenin signaling in irradiated IEC-6 cells. We next established and analyzed mice cohorts consisting of sham irradiation (Group Sh); 12 Gy WBI (Group A); WBI with BMT (Group B); WBI with FGF2 treatment (Group F); and WBI with BMT and FGF2 treatment (Group BF). At 2 weeks post-irradiation, Group BF showed a dramatic increase in survival over all other groups. Intestinal epithelium of Group BF, but not Group B or F, showed augmented proliferation, decreased apoptosis, and preserved crypt numbers and morphology. Furthermore, Group BF maintained intestinal barrier function with minimal inflammatory disturbances in a manner comparable to Group Sh. In accordance, transcriptomic analyses showed significant upregulation of intestinal barrier and stem cell markers in Group BF relative to Groups A and B. Taken together, parenteral FGF2 synergizes with BMT to confer potent mitigation against RIGS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1038/s41419-018-0421-4

  7 / 368311 MEDLINE  
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[PMID]: 29507108
[Au] Autor:Sun C; Chen SY
[Ad] Address:Department of Physiology and Pharmacology, University of Georgia, Athens, GA 30602.
[Ti] Title:RGC32 Promotes Bleomycin-Induced Systemic Sclerosis in a Murine Disease Model by Modulating Classically Activated Macrophage Function.
[So] Source:J Immunol;, 2018 Mar 05.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Systemic sclerosis (SSc) is a multisystem autoimmune disorder that is characterized by inflammation and fibrosis in the skin and internal organs. Previous studies indicate that inflammatory cells and cytokines play essential roles in the pathogenesis of SSc; however, the mechanisms that underlie the inflammation-driven development of SSc are not fully understood. In this study, we show that response gene to complement 32 (RGC32) is abundantly expressed in mouse macrophages in the early stage of bleomycin-induced SSc. Importantly, RGC32 is required to induce the inflammatory response during the onset of SSc, because RGC32 deficiency in mice significantly ameliorates skin and lung sclerosis and inhibits the expression of inflammatory mediators inducible NO synthase (iNOS) and IL-1ß in macrophages. RGC32 appears to be a novel regulator for the differentiation of classically activated macrophages (M1 macrophages). IFN-γ and LPS stimulation induces RGC32 expression in primary peritoneal macrophages and bone marrow-derived macrophages. RGC32 deficiency impairs the polarization of M1 macrophages and attenuates iNOS and IL-1ß production. Mechanistically, RGC32 interacts with NF-κB proteins and promotes iNOS and IL-1ß expression by binding to their promoters. Collectively, our data reveal that RGC32 promotes the onset of SSc by regulating the inflammatory response of M1 macrophages, and it may serve as a promising therapeutic target for treating SSc.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher

  8 / 368311 MEDLINE  
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[PMID]: 29506574
[Au] Autor:Dalugama C; Gawarammana IB
[Ad] Address:Department of Medicine, University of Peradeniya, Peradeniya, Sri Lanka. chamaradalugama@yahoo.com.
[Ti] Title:Fever with pancytopenia: unusual presentation of extrapulmonary tuberculosis: a case report.
[So] Source:J Med Case Rep;12(1):58, 2018 Mar 06.
[Is] ISSN:1752-1947
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Tuberculosis is a major health problem in the developing world. Diagnosis of extrapulmonary tuberculosis is delayed because the presentation is nonspecific. Extrapulmonary tuberculosis can present with various hematological manifestations, including pancytopenia. Pancytopenia could be due to hypersplenism, maturation arrest, hemophagocytic lymphohistiocytosis, or infiltration of the bone marrow by caseating or noncaseating granulomas causing reversible or irreversible fibrosis. CASE PRESENTATION: We report a case of a 56-year-old Sri Lankan Sinhalese man who presented with pyrexia of known origin with significant loss of weight and loss of appetite. He had mild pallor with mild hepatosplenomegaly. He had high inflammatory markers with pancytopenia in a peripheral blood smear. His chest radiograph was unremarkable, and he had a negative Mantoux test result. A diagnosis of disseminated tuberculosis was made on the basis of caseating tuberculous granulomas in the bone marrow. CONCLUSIONS: Disseminated tuberculosis remains a diagnostic challenge because the presentation is vague and nonspecific. In case of pyrexia of unknown origin with peripheral cytopenia, the possibility of disseminated tuberculosis should be considered, particularly in endemic areas. Simultaneous culture and histopathological examination of the bone marrow is important in such instances, because results of common tests such as chest radiography or Mantoux tests can be negative.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1186/s13256-018-1596-0

  9 / 368311 MEDLINE  
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[PMID]: 29505034
[Au] Autor:Zhang B; Nguyen LXT; Li L; Zhao D; Kumar B; Wu H; Lin A; Pellicano F; Hopcroft L; Su YL; Copland M; Holyoake TL; Kuo CJ; Bhatia R; Snyder DS; Ali H; Stein AS; Brewer C; Wang H; McDonald T; Swiderski P; Troadec E; Chen CC; Dorrance A; Pullarkat V; Yuan YC; Perrotti D; Carlesso N; Forman SJ; Kortylewski M; Kuo YH; Marcucci G
[Ad] Address:Gehr Family Center for Leukemia Research, Hematology Malignancies and Stem Cell Transplantation Institute, City of Hope Medical Center, Duarte, California, USA.
[Ti] Title:Bone marrow niche trafficking of miR-126 controls the self-renewal of leukemia stem cells in chronic myelogenous leukemia.
[So] Source:Nat Med;, 2018 Mar 05.
[Is] ISSN:1546-170X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Leukemia stem cells (LSCs) in individuals with chronic myelogenous leukemia (CML) (hereafter referred to as CML LSCs) are responsible for initiating and maintaining clonal hematopoiesis. These cells persist in the bone marrow (BM) despite effective inhibition of BCR-ABL kinase activity by tyrosine kinase inhibitors (TKIs). Here we show that although the microRNA (miRNA) miR-126 supported the quiescence, self-renewal and engraftment capacity of CML LSCs, miR-126 levels were lower in CML LSCs than in long-term hematopoietic stem cells (LT-HSCs) from healthy individuals. Downregulation of miR-126 levels in CML LSCs was due to phosphorylation of Sprouty-related EVH1-domain-containing 1 (SPRED1) by BCR-ABL, which led to inhibition of the RAN-exportin-5-RCC1 complex that mediates miRNA maturation. Endothelial cells (ECs) in the BM supply miR-126 to CML LSCs to support quiescence and leukemia growth, as shown using mouse models of CML in which Mir126a (encoding miR-126) was conditionally knocked out in ECs and/or LSCs. Inhibition of BCR-ABL by TKI treatment caused an undesired increase in endogenous miR-126 levels, which enhanced LSC quiescence and persistence. Mir126a knockout in LSCs and/or ECs, or treatment with a miR-126 inhibitor that targets miR-126 expression in both LSCs and ECs, enhanced the in vivo anti-leukemic effects of TKI treatment and strongly diminished LSC leukemia-initiating capacity, providing a new strategy for the elimination of LSCs in individuals with CML.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1038/nm.4499

  10 / 368311 MEDLINE  
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[PMID]: 29500307
[Au] Autor:Maryanovich M; Takeishi S; Frenette PS
[Ad] Address:Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Albert Einstein College of Medicine, Bronx, New York 10461.
[Ti] Title:Neural Regulation of Bone and Bone Marrow.
[So] Source:Cold Spring Harb Perspect Med;, 2018 Mar 02.
[Is] ISSN:2157-1422
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Bones provide both skeletal scaffolding and space for hematopoiesis in its marrow. Previous work has shown that these functions were tightly regulated by the nervous system. The central and peripheral nervous systems tightly regulate compact bone remodeling, its metabolism, and hematopoietic homeostasis in the bone marrow (BM). Accumulating evidence indicates that the nervous system, which fine-tunes inflammatory responses and alterations in neural functions, may regulate autoimmune diseases. Neural signals also influence the progression of hematological malignancies such as acute and chronic myeloid leukemias. Here, we review the interplay of the nervous system with bone, BM, and immunity, and discuss future challenges to target hematological diseases through modulation of activity of the nervous system.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher


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