Database : MEDLINE
Search on : Bone and Marrow [Words]
References found : 330924 [refine]
Displaying: 1 .. 10   in format [Detailed]

page 1 of 33093 go to page                         

  1 / 330924 MEDLINE  
              next record last record
select
to print
Photocopy
Full text

[PMID]: 26617290
[Au] Autor:Baccini V; Alessi MC
[Ad] Address:Laboratoire d'hématologie, hôpital Nord, CHU de Marseille, chemin des Bourrelly, 13015 Marseille, France; Centre de référence des pathologies plaquettaires (CRPP), CHU Timone, 264, rue Saint-Pierre, 13385 Marseille cedex 5, France. Electronic address: veronique.baccini@ap-hm.fr.
[Ti] Title:Les thrombopénies constitutionnelles : démarche diagnostique. [Diagnosis of inherited thrombocytopenia].
[So] Source:Rev Med Interne;37(2):117-26, 2016 Feb.
[Is] ISSN:1768-3122
[Cp] Country of publication:France
[La] Language:fre
[Ab] Abstract:Inherited thrombocytopenias are rare, heterogenous and probably under-diagnosed because often classified as autoimmune thrombocytopenia. About 20 genes were described responsible for these thrombocytopenias. Precise diagnosis is necessary because the prognosis is different and some of them can evolve into hemopathies. First of all, it is important to gather a body of evidence to orientate towards an inherited cause: presence of the thrombocytopenia since childhood and of other family cases is a strong argument. Secondly, it is difficult to target the genetic investigations that settle the precise diagnosis. Genetic variants responsible for inherited thrombocytopenias affect different stage during megakaryocytopoiesis and cause thrombocytopenias with distinct characteristics. Presence of extra-hematological features, platelets' size measurement and evaluation of bone marrow megakaryocyte morphology when it is possible allow a primary orientation. We propose a diagnostic approach considering extra-hematological features, mode of inheritance, morphology, molecular and functional platelets' studies and bone marrow megakaryocyte morphology in order to better target genetic study. Nevertheless, despite this approach, some inherited thrombocytopenias remain still unexplained and could benefit from new methods of new generation sequencing in the future.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1601
[Js] Journal subset:IM
[St] Status:In-Data-Review

  2 / 330924 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 26548745
[Au] Autor:Park JY; Kim SG; Kim JS; Jung HC
[Ad] Address:Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea....
[Ti] Title:Bone marrow involvement is rare in superficial gastric mucosa-associated lymphoid tissue lymphoma.
[So] Source:Dig Liver Dis;48(1):81-6, 2016 Jan.
[Is] ISSN:1878-3562
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: The initial staging work-up of gastric mucosa-associated lymphoid tissue (MALT) lymphoma includes bone marrow examination. Since gastric MALT lymphoma is mostly detected in early stages with the national cancer screening programme in Korea, bone marrow is rarely involved. AIMS: To investigate the incidence of bone marrow involvement in gastric MALT lymphomas and the role of bone marrow examination for an initial staging work-up. METHODS: Patients diagnosed with gastric MALT lymphoma at Seoul National University Hospital from January 2005 to July 2014 were enrolled. Clinical databases of the patients were retrospectively reviewed. RESULTS: Out of 105 patients, 91 (86.7%) were classified as stage IE1. Among these patients, 78 patients with Helicobacter pylori infection underwent eradication therapy, and complete remission was achieved in 74 cases (94.9%). Twelve out of 13 patients (92.3%) without H. pylori infection underwent radiotherapy or surgery and all achieved complete remission. Bone marrow involvement was proven in only one patient (1.0%). CONCLUSION: Bone marrow involvement was rare in patients with only superficial gastric MALT lymphoma without extragastric invasion. Further studies are warranted to identify the risk factors of bone marrow involvement in gastric MALT lymphoma.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1601
[Js] Journal subset:IM
[St] Status:In-Data-Review

  3 / 330924 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 26729810
[Au] Autor:Baum R; Nündel K; Pawaria S; Sharma S; Busto P; Fitzgerald KA; Gravallese EM; Marshak-Rothstein A
[Ad] Address:Division of Rheumatology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605; and....
[Ti] Title:Synergy between Hematopoietic and Radioresistant Stromal Cells Is Required for Autoimmune Manifestations of DNase II-/-IFNaR-/- Mice.
[So] Source:J Immunol;196(3):1348-54, 2016 Feb 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Detection of endogenous nucleic acids by cytosolic receptors, dependent on STING, and endosomal sensors, dependent on Unc93b1, can provoke inflammatory responses that contribute to a variety of autoimmune and autoinflammatory diseases. In DNase II-deficient mice, the excessive accrual of undegraded DNA leads to both a STING-dependent inflammatory arthritis and additional Unc93b1-dependent autoimmune manifestations, including splenomegaly, extramedullary hematopoiesis, and autoantibody production. In this study, we use bone marrow chimeras to show that clinical and histological inflammation in the joint depends upon DNase II deficiency in both donor hematopoietic cells and host radioresistant cells. Additional features of autoimmunity in these mice, known to depend on Unc93b1 and therefore endosomal TLRs, also require DNase II deficiency in both donor and host compartments, but only require functional TLRs in the hematopoietic cells. Collectively, our data demonstrate a major role of both stromal and hematopoietic cells in all aspects of DNA-driven autoimmunity. These findings further point to the importance of cytosolic nucleic acid sensors in creating an inflammatory environment that facilitates the development of Unc93b1-dependent autoimmunity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1601
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1502130

  4 / 330924 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 26615915
[Au] Autor:Babushok DV; Grignon AL; Li Y; Atienza J; Xie HM; Lam HS; Hartung H; Bessler M; Olson TS
[Ad] Address:Comprehensive Bone Marrow Failure Center, Division of Hematology, Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania....
[Ti] Title:Disrupted lymphocyte homeostasis in hepatitis-associated acquired aplastic anemia is associated with short telomeres.
[So] Source:Am J Hematol;91(2):243-7, 2016 Feb.
[Is] ISSN:1096-8652
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Hepatitis-associated aplastic anemia (HAA) is a variant of acquired aplastic anemia (AA) in which immune-mediated bone marrow failure (BMF) develops following an acute episode of seronegative hepatitis. Dyskeratosis congenita (DC) is an inherited BMF syndrome characterized by the presence of short telomeres, mucocutaneous abnormalities, and cancer predisposition. While both conditions may cause BMF and hepatic impairment, therapeutic approaches are distinct, making it imperative to establish the correct diagnosis. In clinical practice, lymphocyte telomere lengths (TL) are used as a first-line screen to rule out inherited telomeropathies before initiating treatment for AA. To evaluate the reliability of TL in the HAA population, we performed a retrospective analysis of TL in 10 consecutively enrolled HAA patients compared to 19 patients with idiopathic AA (IAA). HAA patients had significantly shorter telomeres than IAA patients (P = 0.009), including four patients with TL at or below the 1st percentile for age-matched controls. HAA patients had no clinical features of DC and did not carry disease-causing mutations in known genes associated with inherited telomere disorders. Instead, short TLs were significantly correlated with severe lymphopenia and skewed lymphocyte subsets, features characteristic of HAA. Our results indicate the importance of caution in the interpretation of TL measurements in HAA, because, in this patient population, short telomeres have limited specificity. Am. J. Hematol. 91:243-247, 2016. © 2015 The Authors. American Journal of Hematology Published by Wiley Periodicals, Inc.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1601
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1002/ajh.24256

  5 / 330924 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 26794716
[Au] Autor:Annamalai RT; Mertz DR; Daley EL; Stegemann JP
[Ad] Address:Department of Biomedical Engineering, University of Michigan, Ann Arbor, Michigan, USA....
[Ti] Title:Collagen Type II enhances chondrogenic differentiation in agarose-based modular microtissues.
[So] Source:Cytotherapy;18(2):263-77, 2016 Feb.
[Is] ISSN:1477-2566
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND AIMS: Cell-based therapies have made an impact on the treatment of osteoarthritis; however, the repair and regeneration of thick cartilage defects is an important and growing clinical problem. Next-generation therapies that combine cells with biomaterials may provide improved outcomes. We have developed modular microenvironments that mimic the composition of articular cartilage as a delivery system for consistently differentiated cells. METHODS: Human bone marrow-derived mesenchymal stem cells (MSC) were embedded in modular microbeads consisting of agarose (AG) supplemented with 0%, 10% and 20% collagen Type II (COL-II) using a water-in-oil emulsion technique. AG and AG/COL-II microbeads were characterized in terms of their structural integrity, size distribution and protein content. The viability of embedded MSC and their ability to differentiate into osteogenic, adipogenic and chondrogenic lineages over 3 weeks in culture were also assessed. RESULTS: Microbeads made with <20% COL-II were robust, generally spheroidal in shape and 80 ± 10 µm in diameter. MSC viability in microbeads was consistently high over a week in culture, whereas viability in corresponding bulk hydrogels decreased with increasing COL-II content. Osteogenic differentiation of MSC was modestly supported in both AG and AG/COL-II microbeads, whereas adipogenic differentiation was strongly inhibited in COL-II containing microbeads. Chondrogenic differentiation of MSC was clearly promoted in microbeads containing COL-II, compared with pure AG matrices. CONCLUSIONS: Inclusion of collagen Type II in agarose matrices in microbead format can potentiate chondrogenic differentiation of human MSC. Such compositionally tailored microtissues may find utility for cell delivery in next-generation cartilage repair therapies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1601
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[St] Status:In-Data-Review

  6 / 330924 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 26348890
[Au] Autor:Cowan AJ; Stevenson PA; Cassaday RD; Graf SA; Fromm JR; Wu D; Holmberg LA; Till BG; Chauncey TR; Smith SD; Philip M; Orozco JJ; Shustov AR; Green DJ; Libby EN; Bensinger WI; Shadman M; Maloney DG; Press OW; Gopal AK
[Ad] Address:Clinical Research Division, Fred Hutchinson Cancer Research Center, University of Washington, Seattle, Washington....
[Ti] Title:Pretransplantation Minimal Residual Disease Predicts Survival in Patients with Mantle Cell Lymphoma Undergoing Autologous Stem Cell Transplantation in Complete Remission.
[So] Source:Biol Blood Marrow Transplant;22(2):380-5, 2016 Feb.
[Is] ISSN:1523-6536
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Autologous stem cell transplantation (ASCT) is standard therapy for mantle cell lymphoma (MCL) in remission after induction chemotherapy, with the best results for patients in complete remission (CR). We hypothesized that evaluation of minimal residual disease (MRD) before ASCT could further stratify outcomes for these patients. Patients with MCL who underwent ASCT in clinical CR between 1996 and 2011 with pretransplantation MRD testing were eligible. Presence of a clonal IgH rearrangement, t(11; 14) by PCR or positive flow cytometry from blood or bone marrow, was considered positive. An adjusted proportional hazards model for associations with progression-free (PFS) and overall survival (OS) was performed. Of 75 MCL patients in CR, 8 (11%) were MRD positive. MRD positivity was associated with shorter OS and PFS. The median OS for MRD-negative patients was not reached, with 82% survival at 5 years, whereas for the MRD-positive patients, median OS was 3.01 years (hazard ratio [HR], 4.04; P = .009), with a median follow-up of 5.1 years. The median PFS for MRD-negative patients was not reached with 75% PFS at 5 years, whereas for MRD-positive patients, it was 2.38 years (HR, 3.69; P = .002). MRD positivity is independently associated with poor outcomes after ASCT for MCL patients in CR.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1601
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[St] Status:In-Data-Review

  7 / 330924 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
PubMed Central Full text
Full text

[PMID]: 26681308
[Au] Autor:Ameziane N; May P; Haitjema A; van de Vrugt HJ; van Rossum-Fikkert SE; Ristic D; Williams GJ; Balk J; Rockx D; Li H; Rooimans MA; Oostra AB; Velleuer E; Dietrich R; Bleijerveld OB; Maarten Altelaar AF; Meijers-Heijboer H; Joenje H; Glusman G; Roach J; Hood L; Galas D; Wyman C; Balling R; den Dunnen J; de Winter JP; Kanaar R; Gelinas R; Dorsman JC
[Ad] Address:Department of Clinical Genetics, VU University Medical Center, Van der Boechorststraat 7, Amsterdam 1081 BT, The Netherlands....
[Ti] Title:A novel Fanconi anaemia subtype associated with a dominant-negative mutation in RAD51.
[So] Source:Nat Commun;6:8829, 2015.
[Is] ISSN:2041-1723
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Fanconi anaemia (FA) is a hereditary disease featuring hypersensitivity to DNA cross-linker-induced chromosomal instability in association with developmental abnormalities, bone marrow failure and a strong predisposition to cancer. A total of 17 FA disease genes have been reported, all of which act in a recessive mode of inheritance. Here we report on a de novo g.41022153G>A; p.Ala293Thr (NM_002875) missense mutation in one allele of the homologous recombination DNA repair gene RAD51 in an FA-like patient. This heterozygous mutation causes a novel FA subtype, 'FA-R', which appears to be the first subtype of FA caused by a dominant-negative mutation. The patient, who features microcephaly and mental retardation, has reached adulthood without the typical bone marrow failure and paediatric cancers. Together with the recent reports on RAD51-associated congenital mirror movement disorders, our results point to an important role for RAD51-mediated homologous recombination in neurodevelopment, in addition to DNA repair and cancer susceptibility.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1512
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/ncomms9829

  8 / 330924 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 26627716
[Au] Autor:Yu Q; Zhao B; Gui J; Katlinski KV; Brice A; Gao Y; Li C; Kushner JA; Koumenis C; Diehl JA; Fuchs SY
[Ad] Address:Department of Animal Biology, School of Veterinary Medicine, Philadelphia, PA 19104;...
[Ti] Title:Type I interferons mediate pancreatic toxicities of PERK inhibition.
[So] Source:Proc Natl Acad Sci U S A;112(50):15420-5, 2015 Dec 15.
[Is] ISSN:1091-6490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The great preclinical promise of the pancreatic endoplasmic reticulum kinase (PERK) inhibitors in neurodegenerative disorders and cancers is marred by pancreatic injury and diabetic syndrome observed in PERK knockout mice and humans lacking PERK function and suffering from Wolcott-Rallison syndrome. PERK mediates many of the unfolded protein response (UPR)-induced events, including degradation of the type 1 interferon (IFN) receptor IFNAR1 in vitro. Here we report that whole-body or pancreas-specific Perk ablation in mice leads to an increase in IFNAR1 protein levels and signaling in pancreatic tissues. Concurrent IFNAR1 deletion attenuated the loss of PERK-deficient exocrine and endocrine pancreatic tissues and prevented the development of diabetes. Experiments using pancreas-specific Perk knockouts, bone marrow transplantation, and cultured pancreatic islets demonstrated that stabilization of IFNAR1 and the ensuing increased IFN signaling in pancreatic tissues represents a major driver of injury triggered by Perk loss. Neutralization of IFNAR1 prevented pancreatic toxicity of PERK inhibitor, indicating that blocking the IFN pathway can mitigate human genetic disorders associated with PERK deficiency and help the clinical use of PERK inhibitors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1512
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1073/pnas.1516362112

  9 / 330924 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 25966666
[Au] Autor:Hossain A; Gumin J; Gao F; Figueroa J; Shinojima N; Takezaki T; Priebe W; Villarreal D; Kang SG; Joyce C; Sulman E; Wang Q; Marini FC; Andreeff M; Colman H; Lang FF
[Ad] Address:Department of Neurosurgery....
[Ti] Title:Mesenchymal Stem Cells Isolated From Human Gliomas Increase Proliferation and Maintain Stemness of Glioma Stem Cells Through the IL-6/gp130/STAT3 Pathway.
[So] Source:Stem Cells;33(8):2400-15, 2015 Aug.
[Is] ISSN:1549-4918
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Although mesenchymal stem cells (MSCs) have been implicated as stromal components of several cancers, their ultimate contribution to tumorigenesis and their potential to drive cancer stem cells, particularly in the unique microenvironment of human brain tumors, remain largely undefined. Consequently, using established criteria, we isolated glioma-associated-human MSCs (GA-hMSCs) from fresh human glioma surgical specimens for the first time. We show that these GA-hMSCs are nontumorigenic stromal cells that are phenotypically similar to prototypical bone marrow-MSCs. Low-passage genomic sequencing analyses comparing GA-hMSCs with matched tumor-initiating glioma stem cells (GSCs) suggest that most GA-hMSCs (60%) are normal cells recruited to the tumor (group 1 GA-hMSCs), although, rarely (10%), GA-hMSCs may differentiate directly from GSCs (group 2 GA-hMSCs) or display genetic patterns intermediate between these groups (group 3 GA-hMSCs). Importantly, GA-hMSCs increase proliferation and self-renewal of GSCs in vitro and enhance GSC tumorigenicity and mesenchymal features in vivo, confirming their functional significance within the GSC niche. These effects are mediated by GA-hMSC-secreted interleukin-6, which activates STAT3 in GSCs. Our results establish GA-hMSCs as a potentially new stromal component of gliomas that drives the aggressiveness of GSCs, and point to GA-hMSCs as a novel therapeutic target within gliomas.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1507
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1002/stem.2053

  10 / 330924 MEDLINE  
              first record previous record
select
to print
Photocopy
PubMed Central Full text

[PMID]: 25738355
[Au] Autor:Armaiz-Pena GN; Gonzalez-Villasana V; Nagaraja AS; Rodriguez-Aguayo C; Sadaoui NC; Stone RL; Matsuo K; Dalton HJ; Previs RA; Jennings NB; Dorniak P; Hansen JM; Arevalo JM; Cole SW; Lutgendorf SK; Sood AK; Lopez-Berestein G
[Ad] Address:Department of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA....
[Ti] Title:Adrenergic regulation of monocyte chemotactic protein 1 leads to enhanced macrophage recruitment and ovarian carcinoma growth.
[So] Source:Oncotarget;6(6):4266-73, 2015 Feb 28.
[Is] ISSN:1949-2553
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Increased adrenergic signaling facilitates tumor progression, but the underlying mechanisms remain poorly understood. We examined factors responsible for stress-mediated effects on monocyte/macrophage recruitment into the tumor microenvironment, and the resultant effects on tumor growth. In vitro, MCP1 was significantly increased after catecholamine exposure, which was mediated by cAMP and PKA. Tumor samples from mice subjected to daily restraint stress had elevated MCP1 gene and protein levels, increased CD14+ cells, and increased infiltration of CD68+ cells. hMCP1 siRNA-DOPC nanoparticles significantly abrogated daily restraint stress-induced tumor growth and inhibited infiltration of CD68+ and F4/80+ cells. In ovarian cancer patients, elevated peripheral blood monocytes and tumoral macrophages were associated with worse overall survival. Collectively, we demonstrate that increased adrenergic signaling is associated with macrophage infiltration and mediated by tumor cell-derived MCP1 production.
[Mh] MeSH terms primary: Carcinoma/pathology
Chemokine CCL2/metabolism
Macrophages/metabolism
Ovarian Neoplasms/pathology
Stress, Psychological/metabolism
[Mh] MeSH terms secundary: Animals
Carcinoma/metabolism
Carcinoma/mortality
Chemotaxis, Leukocyte/physiology
Enzyme-Linked Immunosorbent Assay
Epinephrine/metabolism
Female
Humans
Kaplan-Meier Estimate
Mice
Mice, Nude
Norepinephrine/metabolism
Ovarian Neoplasms/metabolism
Ovarian Neoplasms/mortality
Real-Time Polymerase Chain Reaction
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Name of substance:0 (CCL2 protein, human); 0 (Chemokine CCL2); X4W3ENH1CV (Norepinephrine); YKH834O4BH (Epinephrine)
[Em] Entry month:1512
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[Da] Date of entry for processing:150318
[St] Status:MEDLINE


page 1 of 33093 go to page                         
   


Refine the search
  Database : MEDLINE Advanced form   

    Search in field  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/PAHO/WHO - Latin American and Caribbean Center on Health Sciences Information