Database : MEDLINE
Search on : Bone and Marrow [Words]
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[PMID]: 26136429
[Au] Autor:Mongini PK; Gupta R; Boyle E; Nieto J; Lee H; Stein J; Bandovic J; Stankovic T; Barrientos J; Kolitz JE; Allen SL; Rai K; Chu CC; Chiorazzi N
[Ad] Address:The Feinstein Institute for Medical Research, North Shore-Long Island Jewish Health System, Manhasset, NY 11030; Department of Molecular Medicine, Hofstra North Shore-LIJ School of Medicine, Hempstead, NY 11549; pmongini@nshs.edu....
[Ti] Title:TLR-9 and IL-15 Synergy Promotes the In Vitro Clonal Expansion of Chronic Lymphocytic Leukemia B Cells.
[So] Source:J Immunol;195(3):901-23, 2015 Aug 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Clinical progression of B cell chronic lymphocytic leukemia (B-CLL) reflects the clone's Ag receptor (BCR) and involves stroma-dependent B-CLL growth within lymphoid tissue. Uniformly elevated expression of TLR-9, occasional MYD88 mutations, and BCR specificity for DNA or Ags physically linked to DNA together suggest that TLR-9 signaling is important in driving B-CLL growth in patients. Nevertheless, reports of apoptosis after B-CLL exposure to CpG oligodeoxynucleotide (ODN) raised questions about a central role for TLR-9. Because normal memory B cells proliferate vigorously to ODN+IL-15, a cytokine found in stromal cells of bone marrow, lymph nodes, and spleen, we examined whether this was true for B-CLL cells. Through a CFSE-based assay for quantitatively monitoring in vitro clonal proliferation/survival, we show that IL-15 precludes TLR-9-induced apoptosis and permits significant B-CLL clonal expansion regardless of the clone's BCR mutation status. A robust response to ODN+IL-15 was positively linked to presence of chromosomal anomalies (trisomy-12 or ataxia telangiectasia mutated anomaly + del13q14) and negatively linked to a very high proportion of CD38(+) cells within the blood-derived B-CLL population. Furthermore, a clone's intrinsic potential for in vitro growth correlated directly with doubling time in blood, in the case of B-CLL with Ig H chain V region-unmutated BCR and <30% CD38(+) cells in blood. Finally, in vitro high-proliferator status was statistically linked to diminished patient survival. These findings, together with immunohistochemical evidence of apoptotic cells and IL-15-producing cells proximal to B-CLL pseudofollicles in patient spleens, suggest that collaborative ODN and IL-15 signaling may promote in vivo B-CLL growth.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1403189

  2 / 323399 MEDLINE  
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[PMID]: 26109647
[Au] Autor:Vaeth M; Zee I; Concepcion AR; Maus M; Shaw P; Portal-Celhay C; Zahra A; Kozhaya L; Weidinger C; Philips J; Unutmaz D; Feske S
[Ad] Address:Department of Pathology, New York University School of Medicine, New York, NY 10016; and....
[Ti] Title:Ca2+ Signaling but Not Store-Operated Ca2+ Entry Is Required for the Function of Macrophages and Dendritic Cells.
[So] Source:J Immunol;195(3):1202-17, 2015 Aug 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Store-operated Ca(2+) entry (SOCE) through Ca(2+) release-activated Ca(2+) (CRAC) channels is essential for immunity to infection. CRAC channels are formed by ORAI1 proteins in the plasma membrane and activated by stromal interaction molecule (STIM)1 and STIM2 in the endoplasmic reticulum. Mutations in ORAI1 and STIM1 genes that abolish SOCE cause severe immunodeficiency with recurrent infections due to impaired T cell function. SOCE has also been observed in cells of the innate immune system such as macrophages and dendritic cells (DCs) and may provide Ca(2+) signals required for their function. The specific role of SOCE in macrophage and DC function, as well as its contribution to innate immunity, however, is not well defined. We found that nonselective inhibition of Ca(2+) signaling strongly impairs many effector functions of bone marrow-derived macrophages and bone marrow-derived DCs, including phagocytosis, inflammasome activation, and priming of T cells. Surprisingly, however, macrophages and DCs from mice with conditional deletion of Stim1 and Stim2 genes, and therefore complete inhibition of SOCE, showed no major functional defects. Their differentiation, FcR-dependent and -independent phagocytosis, phagolysosome fusion, cytokine production, NLRP3 inflammasome activation, and their ability to present Ags to activate T cells were preserved. Our findings demonstrate that STIM1, STIM2, and SOCE are dispensable for many critical effector functions of macrophages and DCs, which has important implications for CRAC channel inhibition as a therapeutic strategy to suppress pathogenic T cells while not interfering with myeloid cell functions required for innate immunity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1403013

  3 / 323399 MEDLINE  
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[PMID]: 26101326
[Au] Autor:Wynn JL; Scumpia PO; Stocks BT; Romano-Keeler J; Alrifai MW; Liu JH; Kim AS; Alford CE; Matta P; Weitkamp JH; Moore DJ
[Ad] Address:Division of Neonatology, Department of Pediatrics, Vanderbilt University, Nashville, TN 37232; james.wynn@peds.ufl.edu....
[Ti] Title:Neonatal CD71+ Erythroid Cells Do Not Modify Murine Sepsis Mortality.
[So] Source:J Immunol;195(3):1064-70, 2015 Aug 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Sepsis is a major cause of neonatal mortality and morbidity worldwide. A recent report suggested that murine neonatal host defense against infection could be compromised by immunosuppressive CD71(+) erythroid splenocytes. We examined the impact of CD71(+) erythroid splenocytes on murine neonatal mortality to endotoxin challenge or polymicrobial sepsis and characterized circulating CD71(+) erythroid (CD235a(+)) cells in human neonates. Adoptive transfer or an Ab-mediated reduction in neonatal CD71(+) erythroid splenocytes did not alter murine neonatal survival to endotoxin challenge or polymicrobial sepsis challenge. Ex vivo immunosuppression of stimulated adult CD11b(+) cells was not limited to neonatal splenocytes; it also occurred with adult and neonatal bone marrow. Animals treated with anti-CD71 Ab showed reduced splenic bacterial load following bacterial challenge compared with isotype-treated mice. However, adoptive transfer of enriched CD71(+) erythroid splenocytes to CD71(+)-reduced animals did not reduce bacterial clearance. Human CD71(+)CD235a(+) cells were common among cord blood mononuclear cells and were shown to be reticulocytes. In summary, a lack of effect on murine survival to polymicrobial sepsis following adoptive transfer or diminution of CD71(+) erythroid splenocytes under these experimental conditions suggests that the impact of these cells on neonatal infection risk and progression may be limited. An unanticipated immune priming effect of anti-CD71 Ab treatment, rather than a reduction in immunosuppressive CD71(+) erythroid splenocytes, was likely responsible for the reported enhanced bacterial clearance. In humans, the well-described rapid decrease in circulating reticulocytes after birth suggests that they may have a limited role in reducing inflammation secondary to microbial colonization.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1500771

  4 / 323399 MEDLINE  
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[PMID]: 26091720
[Au] Autor:Sa Q; Ochiai E; Tiwari A; Perkins S; Mullins J; Gehman M; Huckle W; Eyestone WH; Saunders TL; Shelton BJ; Suzuki Y
[Ad] Address:Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky College of Medicine, Lexington, KY 40536;...
[Ti] Title:Cutting Edge: IFN-γ Produced by Brain-Resident Cells Is Crucial To Control Cerebral Infection with Toxoplasma gondii.
[So] Source:J Immunol;195(3):796-800, 2015 Aug 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:In vitro studies demonstrated that microglia and astrocytes produce IFN-γ in response to various stimulations, including LPS. However, the physiological role of IFN-γ production by brain-resident cells, including glial cells, in resistance against cerebral infections remains unknown. We analyzed the role of IFN-γ production by brain-resident cells in resistance to reactivation of cerebral infection with Toxoplasma gondii using a murine model. Our study using bone marrow chimeric mice revealed that IFN-γ production by brain-resident cells is essential for upregulating IFN-γ-mediated protective innate immune responses to restrict cerebral T. gondii growth. Studies using a transgenic strain that expresses IFN-γ only in CD11b(+) cells suggested that IFN-γ production by microglia, which is the only CD11b(+) cell population among brain-resident cells, is able to suppress the parasite growth. Furthermore, IFN-γ produced by brain-resident cells is pivotal for recruiting T cells into the brain to control the infection. These results indicate that IFN-γ produced by brain-resident cells is crucial for facilitating both the protective innate and T cell-mediated immune responses to control cerebral infection with T. gondii.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1500814

  5 / 323399 MEDLINE  
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[PMID]: 26085685
[Au] Autor:Harker JA; Wong KA; Dolgoter A; Zuniga EI
[Ad] Address:Section of Molecular Biology, Division of Biological Sciences, University of California San Diego, La Jolla, CA 92093 j.harker@imperial.ac.uk eizuniga@ucsd.edu....
[Ti] Title:Cell-Intrinsic gp130 Signaling on CD4+ T Cells Shapes Long-Lasting Antiviral Immunity.
[So] Source:J Immunol;195(3):1071-81, 2015 Aug 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The IL-6 cytokine family utilizes the common signal transduction molecule gp130, which can mediate a diverse range of outcomes. To clarify the role of gp130 signaling in vivo during acute viral infection, we infected Cd4-cre Il6st(fl/fl) mice, in which gp130 is conditionally ablated in T cells, with acute lymphocytic choriomeningitis virus. We found that by day 12, but not at day 8, after infection the number of virus-specific CD4(+) T cells was reduced in the absence of gp130, and this was sustained for up to 2 mo postinfection. Additionally, gp130-deficient T follicular helper cells had lower expression of Maf, IL-21, and ICOS, and this was accompanied by a reduction in the proportion of germinal center B cells and plasmablasts. Remarkably, at 2 mo postinfection the proportion of IgG2a/c(+) memory B cells and the systemic levels of lymphocytic choriomeningitis virus-specific IgG2 Abs were dramatically decreased, whereas there was a corresponding increase in IgG1(+) memory B cells and virus-specific IgG1 Abs. In the same animals gp130-deficient virus-specific CD8(+) T cells showed a reduced proportion of memory cells, which expressed lower levels of Tcf7, and displayed diminished recall responses on secondary infection. Mixed bone marrow chimeras revealed that the aforementioned gp130 effects on CD4(+) T cells were cell intrinsic. Overall, our data show that gp130 signaling in T cells influences the quantity and quality of long-lasting CD4(+) T cell responses as well as CD8(+) T cell- and Ab-mediated immunity after acute viral infection.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1402402

  6 / 323399 MEDLINE  
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[PMID]: 26052898
[Au] Autor:Styner M; Pagnotti GM; Galior K; Wu X; Thompson WR; Uzer G; Sen B; Xie Z; Horowitz MC; Styner MA; Rubin C; Rubin J
[Ad] Address:Department of Medicine (M.S., K.G., X.W., G.U., B.S., Z.X., J.R.), University of North Carolina, Chapel Hill, North Carolina; Department of Physical Therapy (W.R.T.), Indiana University, Indianapolis, Indiana; Department of Computer Science (M.A.S.), University of North Carolina, Chapel Hill, North ...
[Ti] Title:Exercise Regulation of Marrow Fat in the Setting of PPARγ Agonist Treatment in Female C57BL/6 Mice.
[So] Source:Endocrinology;156(8):2753-61, 2015 Aug.
[Is] ISSN:1945-7170
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The contribution of marrow adipose tissue (MAT) to skeletal fragility is poorly understood. Peroxisome proliferator-activated receptor (PPAR)γ agonists, associated with increased fractures in diabetic patients, increase MAT. Here, we asked whether exercise could limit the MAT accrual and increase bone formation in the setting of PPARγ agonist treatment. Eight-week-old female C57BL/6 mice were treated with 20-mg/kgd rosiglitazone (Rosi) and compared with control (CTL) animals. Exercise groups ran 12 km/d when provided access to running wheels (CTL exercise [CTL-E], Rosi-E). After 6 weeks, femoral MAT (volume of lipid binder osmium) and tibial bone morphology were assessed by microcomputer tomography. Rosi was associated with 40% higher femur MAT volume compared with CTL (P < .0001). Exercise suppressed MAT volume by half in CTL-E mice compared with CTL (P < .01) and 19% in Rosi-E compared with Rosi (P < .0001). Rosi treatment increased fat markers perilipin and fatty acid synthase mRNA by 4-fold (P < .01). Exercise was associated with increased uncoupling protein 1 mRNA expression in both CTL-E and Rosi-E groups (P < .05), suggestive of increased brown fat. Rosi increased cortical porosity (P < .0001) but did not significantly impact trabecular or cortical bone quantity. Importantly, exercise induction of trabecular bone volume was not prevented by Rosi (CTL-E 21% > CTL, P < .05; Rosi-E 26% > Rosi, P < .01). In summary, despite the Rosi induction of MAT extending well into the femoral diaphysis, exercise was able to significantly suppress MAT volume and induce bone formation. Our results suggest that the impact of PPARγ agonists on bone and marrow health can be partially mitigated by exercise.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.1210/en.2015-1213

  7 / 323399 MEDLINE  
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[PMID]: 24523831
[Au] Autor:Sato A; Sano F; Ishii T; Adachi K; Negishi R; Matsumoto N; Okuse C
[Ad] Address:Division of Gastroenterology, Department of Internal Medicine, St. Marianna University School of Medicine Yokohama City Seibu Hospital, 1197-1 Yasashicho Asahi-ku, Yokohama, 241-0811 Japan....
[Ti] Title:Pure red cell aplasia associated with autoimmune hepatitis successfully treated with cyclosporine A.
[So] Source:Clin J Gastroenterol;7:74-8, 2014.
[Is] ISSN:1865-7265
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:A 47-year-old female with a 17-year history of autoimmune hepatitis had been treated with prednisolone, azathioprine, and ursodeoxycholic acid. Although her alanine aminotransferase level occasionally showed mild abnormality, the prednisolone dose could not be increased because she had developed cataract during the course of her illness. In May 2012, she developed severe normochromic normocytic anemia without hemorrhage, and azathioprine was discontinued because it was suspected of being the cause. However, anemia recurred frequently even after discontinuation, necessitating repeated blood transfusions. Bone marrow analysis revealed selective erythroblastopenia, thus leading to a diagnosis of pure red cell aplasia. Cyclosporine A was administered, which led to a dramatic recovery from anemia, and stabilized her alanine aminotransferase levels. Furthermore, the prednisolone dose could be gradually tapered. Pure red cell aplasia associated with autoimmune hepatitis is extremely rare. The present case shows that patients with autoimmune hepatitis refractory to the standard treatment regimen and those with concomitant pure red cell aplasia may be treated with cyclosporine A.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s12328-013-0448-0

  8 / 323399 MEDLINE  
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[PMID]: 26053123
[Au] Autor:Blaho VA; Galvani S; Engelbrecht E; Liu C; Swendeman SL; Kono M; Proia RL; Steinman L; Han MH; Hla T
[Ad] Address:1] Center for Vascular Biology, Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, New York 10065, USA [2] Brain and Mind Research Institute, Weill Medical College of Cornell University, New York, New York 10065, USA....
[Ti] Title:HDL-bound sphingosine-1-phosphate restrains lymphopoiesis and neuroinflammation.
[So] Source:Nature;523(7560):342-6, 2015 Jul 16.
[Is] ISSN:1476-4687
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Lipid mediators influence immunity in myriad ways. For example, circulating sphingosine-1-phosphate (S1P) is a key regulator of lymphocyte egress. Although the majority of plasma S1P is bound to apolipoprotein M (ApoM) in the high-density lipoprotein (HDL) particle, the immunological functions of the ApoM-S1P complex are unknown. Here we show that ApoM-S1P is dispensable for lymphocyte trafficking yet restrains lymphopoiesis by activating the S1P1 receptor on bone marrow lymphocyte progenitors. Mice that lacked ApoM (Apom(-/-)) had increased proliferation of Lin(-) Sca-1(+) cKit(+) haematopoietic progenitor cells (LSKs) and common lymphoid progenitors (CLPs) in bone marrow. Pharmacological activation or genetic overexpression of S1P1 suppressed LSK and CLP cell proliferation in vivo. ApoM was stably associated with bone marrow CLPs, which showed active S1P1 signalling in vivo. Moreover, ApoM-bound S1P, but not albumin-bound S1P, inhibited lymphopoiesis in vitro. Upon immune stimulation, Apom(-/-) mice developed more severe experimental autoimmune encephalomyelitis, characterized by increased lymphocytes in the central nervous system and breakdown of the blood-brain barrier. Thus, the ApoM-S1P-S1P1 signalling axis restrains the lymphocyte compartment and, subsequently, adaptive immune responses. Unique biological functions imparted by specific S1P chaperones could be exploited for novel therapeutic opportunities.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, N.I.H., INTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/nature14462

  9 / 323399 MEDLINE  
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[PMID]: 25884949
[Au] Autor:Cesano A; Willman CL; Kopecky KJ; Gayko U; Putta S; Louie B; Westfall M; Purvis N; Spellmeyer DC; Marimpietri C; Cohen AC; Hackett J; Shi J; Walker MG; Sun Z; Paietta E; Tallman MS; Cripe LD; Atwater S; Appelbaum FR; Radich JP
[Ad] Address:Nodality, Inc., South San Francisco, California, United States of America....
[Ti] Title:Cell signaling-based classifier predicts response to induction therapy in elderly patients with acute myeloid leukemia.
[So] Source:PLoS One;10(4):e0118485, 2015.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Single-cell network profiling (SCNP) data generated from multi-parametric flow cytometry analysis of bone marrow (BM) and peripheral blood (PB) samples collected from patients >55 years old with non-M3 AML were used to train and validate a diagnostic classifier (DXSCNP) for predicting response to standard induction chemotherapy (complete response [CR] or CR with incomplete hematologic recovery [CRi] versus resistant disease [RD]). SCNP-evaluable patients from four SWOG AML trials were randomized between Training (N = 74 patients with CR, CRi or RD; BM set = 43; PB set = 57) and Validation Analysis Sets (N = 71; BM set = 42, PB set = 53). Cell survival, differentiation, and apoptosis pathway signaling were used as potential inputs for DXSCNP. Five DXSCNP classifiers were developed on the SWOG Training set and tested for prediction accuracy in an independent BM verification sample set (N = 24) from ECOG AML trials to select the final classifier, which was a significant predictor of CR/CRi (area under the receiver operating characteristic curve AUROC = 0.76, p = 0.01). The selected classifier was then validated in the SWOG BM Validation Set (AUROC = 0.72, p = 0.02). Importantly, a classifier developed using only clinical and molecular inputs from the same sample set (DXCLINICAL2) lacked prediction accuracy: AUROC = 0.61 (p = 0.18) in the BM Verification Set and 0.53 (p = 0.38) in the BM Validation Set. Notably, the DXSCNP classifier was still significant in predicting response in the BM Validation Analysis Set after controlling for DXCLINICAL2 (p = 0.03), showing that DXSCNP provides information that is independent from that provided by currently used prognostic markers. Taken together, these data show that the proteomic classifier may provide prognostic information relevant to treatment planning beyond genetic mutations and traditional prognostic factors in elderly AML.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1504
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1371/journal.pone.0118485

  10 / 323399 MEDLINE  
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[PMID]: 26120058
[Au] Autor:Khorshed RA; Hawkins ED; Duarte D; Scott MK; Akinduro OA; Rashidi NM; Spitaler M; Lo Celso C
[Ad] Address:Department of Life Sciences, Imperial College London, London SW7 2AZ, UK. Electronic address: r.khorshed@imperial.ac.uk....
[Ti] Title:Automated Identification and Localization of Hematopoietic Stem Cells in 3D Intravital Microscopy Data.
[So] Source:Stem Cell Reports;5(1):139-53, 2015 Jul 14.
[Is] ISSN:2213-6711
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Measuring three-dimensional (3D) localization of hematopoietic stem cells (HSCs) within the bone marrow microenvironment using intravital microscopy is a rapidly expanding research theme. This approach holds the key to understanding the detail of HSC-niche interactions, which are critical for appropriate stem cell function. Due to the complex tissue architecture of the bone marrow and to the progressive introduction of scattering and signal loss at increasing imaging depths, there is no ready-made software to handle efficient segmentation and unbiased analysis of the data. To address this, we developed an automated image analysis tool that simplifies and standardizes the biological interpretation of 3D HSC microenvironment images. The algorithm identifies HSCs and measures their localization relative to surrounding osteoblast cells and bone collagen. We demonstrate here the effectiveness, consistency, and accuracy of the proposed approach compared to current manual analysis and its wider applicability to analyze other 3D bone marrow components.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Js] Journal subset:IM
[St] Status:In-Data-Review


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