Plasma cells release membrane microparticles in a mouse model of multiple myeloma.

Microparticles (MPs) released from the plasma membrane play a role in tumor progression. Involvement of MPs in myeloma (MM) has been poorly investigated. Because of the strong interaction of MM cells with bone microenvironment, we hypothesized an implication of MPs in MM using a murine model. Forty-four mice were injected with 5THL-MM cells and compared with 14 non-injected mice. Blood was collected at the early and end stages of MM development (EMM and LMM) to characterize the circulating MPs. At LMM, MPs were isolated from bone marrow (BM) of long bones of 22 mice, after centrifugation. Electron microscopy immunohistochemistry and Western blotting using CD138 were performed on BM-derived MPs. At EMM, MPs circulating level was significantly lower versus controls. In LMM, a significant increase of the total MP number from plasma was observed versus controls. Characterization of circulating MPs showed an increase of leukocyte- and erythrocyte-derived MPs. In LMM, serum M-protein was correlated with circulating MP number. BM-derived MPs increased in LMM and expressed CD138. Anti-CD138 coupled with nanobeads localized at the MP surface. There is evidence of an association between increase of MPs and MM development; the results underscore the participation of plasma cell-derived MPs originating from BM

Impact strength of composites with nano-enhanced resin after fire exposure

Composite materials have been widely used in several engineering applications. However, there are very few studies about the effects of nanoclays on the impact strength of laminates after exposure to the fire. Therefore, this paper intends to study this subject and the impact performance was analysed by low velocity impact tests carried out at different incident impact energy levels. For better dispersion and interface adhesion matrix/clay, nanoclays were previously subjected to a silane treatment appropriate to the epoxy resin. The exposure to the fire decreases the maximum load and increases the displacement in comparison with the respective values obtained at room temperature. Mathematical relationships are proposed to estimate the maximum impact force and displacement, based on the total impact energy and flexural stiffness. Finally, a decrease of the elastic recuperation can be found, independently of the benefits introduced by the nanoclays

Topological quantization of boundary forces and the integrated density of states

For quantum systems described by Schr\"odinger operators on the half-space \RR^{d-1}\times\RR^{leq 0} the boundary force per unit area and unit energy is topologically quantised provided the Fermi energy lies in a gap of the bulk spectrum. Under this condition it is also equal to the integrated density of states at the Fermi energy.Comment: 7 page

8-Bromo-1,3-diphenyl-2,3-dihydro-1H-naphtho­[1,2-e][1,3]oxazine

The title compound, C24H18BrNO, consists of an envelope-configured oxazine ring with a fused 8-bromo-1,3-diphenyl group and two bonded phenyl rings. The dihedral angles between the mean planes of the 8-bromo-1,3-diphenyl and the phenyl rings are 54.5 (6) and 87.4 (8)°, respectively. The oxazine is essentially coplanar with the 8-bromo-1,3-diphenyl [dihedral angle = 9.4 (1)°]. Weak C—H⋯π inter­actions contribute to the crystal packing

Microparticle-mediated transfer of the viral receptors CAR and CD46, and the CFTR channel in a CHO cell model confers new functions to target cells

Cell microparticles (MPs) released in the extracellular milieu can embark plasma membrane and intracellular components which are specific of their cellular origin, and transfer them to target cells. The MP-mediated, cell-to-cell transfer of three human membrane glycoproteins of different degrees of complexity was investigated in the present study, using a CHO cell model system. We first tested the delivery of CAR and CD46, two monospanins which act as adenovirus receptors, to target CHO cells. CHO cells lack CAR and CD46, high affinity receptors for human adenovirus serotype 5 (HAdV5), and serotype 35 (HAdV35), respectively. We found that MPs derived from CHO cells (MP-donor cells) constitutively expressing CAR (MP-CAR) or CD46 (MP-CD46) were able to transfer CAR and CD46 to target CHO cells, and conferred selective permissiveness to HAdV5 and HAdV35. In addition, target CHO cells incubated with MP-CD46 acquired the CD46-associated function in complement regulation. We also explored the MP-mediated delivery of a dodecaspanin membrane glycoprotein, the CFTR to target CHO cells. CFTR functions as a chloride channel in human cells and is implicated in the genetic disease cystic fibrosis. Target CHO cells incubated with MPs produced by CHO cells constitutively expressing GFP-tagged CFTR (MP-GFP-CFTR) were found to gain a new cellular function, the chloride channel activity associated to CFTR. Time-course analysis of the appearance of GFP-CFTR in target cells suggested that MPs could achieve the delivery of CFTR to target cells via two mechanisms: the transfer of mature, membrane-inserted CFTR glycoprotein, and the transfer of CFTR-encoding mRNA. These results confirmed that cell-derived MPs represent a new class of promising therapeutic vehicles for the delivery of bioactive macromolecules, proteins or mRNAs, the latter exerting the desired therapeutic effect in target cells via de novo synthesis of their encoded proteins

PV cohomology of pinwheel tilings, their integer group of coinvariants and gap-labelling

In this paper, we first remind how we can see the "hull" of the pinwheel tiling as an inverse limit of simplicial complexes (Anderson and Putnam) and we then adapt the PV cohomology introduced in a paper of Bellissard and Savinien to define it for pinwheel tilings. We then prove that this cohomology is isomorphic to the integer \v{C}ech cohomology of the quotient of the hull by $S^1$ which let us prove that the top integer \v{C}ech cohomology of the hull is in fact the integer group of coinvariants on some transversal of the hull. The gap-labelling for pinwheel tilings is then proved and we end this article by an explicit computation of this gap-labelling, showing that \mu^t \big(C(\Xi,\ZZ) \big) = \dfrac{1}{264} \ZZ [\dfrac{1}{5}].Comment: Problems of compilation by arxiv for figures on p.6 and p.7. I have only changed these figure

PPARα Is Essential for Microparticle-Induced Differentiation of Mouse Bone Marrow-Derived Endothelial Progenitor Cells and Angiogenesis

BACKGROUND: Bone marrow-derived endothelial progenitor cells (EPCs) are critical for neovascularization. We hypothesized that microparticles (MPs), small fragments generated from the plasma membrane, can activate angiogenic programming of EPCs. METHODOLOGY/PRINCIPAL FINDINGS: We studied the effects of MPs obtained from wild type (MPs(PPARalpha+/+)) and knock-out (MPs(PPARalpha-/-)) mice on EPC differentiation and angiogenesis. Bone marrow-derived cells were isolated from WT or KO mice and were cultured in the presence of MPs(PPARalpha+/+) or MPs(PPARalpha-/-) obtained from blood of mice. Only MPs(PPARalpha+/+) harboring PPAR(alpha) significantly increased EPC, but not monocytic, differentiation. Bone marrow-derived cells treated with MPs(PPARalpha+/+) displayed increased expression of pro-angiogenic genes and increased in vivo angiogenesis. MPs(PPARalpha+/+) increased capillary-like tube formation of endothelial cells that was associated with enhanced expressions of endothelial cell-specific markers. Finally, the effects of MPs(PPARalpha+/+) were mediated by NF-kappaB-dependent mechanisms. CONCLUSIONS/SIGNIFICANCE: Our results underscore the obligatory role of PPARalpha carried by MPs for EPC differentiation and angiogenesis. PPARalpha-NF-kappaB-Akt pathways may play a pivotal stimulatory role for neovascularization, which may, at least in part, be mediated by bone marrow-derived EPCs. Improvement of EPC differentiation may represent a useful strategy during reparative neovascularization

Direct Identification of Monolayer Rhenium Diselenide by an Individual Diffraction Pattern

In the current extensive studies of transition metal dichalcogenides (TMDCs), compared to hexagonal layered materials, like graphene, hBN and MoS2, low symmetry layered two‐dimensional (2D) crystals have shown great potential for applications in anisotropic devices. Rhenium diselenide (ReSe2) has the bulk space group P1ത and belongs to triclinic crystal system with a deformed cadmium iodide type structure. Here we propose an electron diffraction based method to distinguish monolayer ReSe2 membrane from multilayer ReSe2, and its two different vertical orientations, our method could also be applicable to other low symmetry crystal systems, including both triclinic and monoclinic lattices, as long as their third unit‐cell basis vectors are not perpendicular to their basal planes. Our experimental results are well explained by kinematical electron diffraction theory and corresponding simulations. The generalization of our method to other 2D materials, like graphene, is also discussed

Migration towards SDF-1 selects angiogenin-expressing bone marrow monocytes endowed with cardiac reparative activity in patients with previous myocardial infarction

INTRODUCTION: Chemokine-directed migration is crucial for homing of regenerative cells to the infarcted heart and correlates with outcomes of cell therapy trials. Hence, transplantation of chemokine-responsive bone marrow cells may be ideal for treatment of myocardial ischemia. To verify the therapeutic activity of bone marrow mononuclear cells (BM-MNCs) selected by in vitro migration towards the chemokine stromal cell-derived factor-1 (SDF-1) in a mouse model of myocardial infarction (MI), we used BM-MNCs from patients with previous large MI recruited in the TransACT-1&2 cell therapy trials. METHODS: Unfractioned BM-MNCs, SDF-1-responsive, and SDF-1-nonresponsive BM-MNCs isolated by patients recruited in the TransACT-1&2 cell therapy trials were tested in Matrigel assay to evaluate angiogenic potential. Secretome and antigenic profile were characterized by flow cytometry. Angiogenin expression was measured by RT-PCR. Cells groups were also intramyocardially injected in an in vivo model of MI (8-week-old immune deficient CD1-FOXN1(nu/nu) mice). Echocardiography and hemodynamic measurements were performed before and at 14 days post-MI. Arterioles and capillaries density, infiltration of inflammatory cells, interstitial fibrosis, and cardiomyocyte proliferation and apoptosis were assessed by immunohistochemistry. RESULTS: In vitro migration enriched for monocytes, while CD34(+) and CD133(+) cells and T lymphocytes remained mainly confined in the non-migrated fraction. Unfractioned total BM-MNCs promoted angiogenesis on Matrigel more efficiently than migrated or non-migrated cells. In mice with induced MI, intramyocardial injection of unfractionated or migrated BM-MNCs was more effective in preserving cardiac contractility and pressure indexes than vehicle or non-migrated BM-MNCs. Moreover, unfractioned BM-MNCs enhanced neovascularization, whereas the migrated fraction was unique in reducing the infarct size and interstitial fibrosis. In vitro studies on isolated cardiomyocytes suggest participation of angiogenin, a secreted ribonuclease that inhibits protein translation under stress conditions, in promotion of cardiomyocyte survival by migrated BM-MNCs. CONCLUSIONS: Transplantation of bone marrow cells helps post-MI healing through distinct actions on vascular cells and cardiomyocytes. In addition, the SDF-1-responsive fraction is enriched with angiogenin-expressing monocytes, which may improve cardiac recovery through activation of cardiomyocyte response to stress. Identification of factors linking migratory and therapeutic outcomes could help refine regenerative approaches. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13287-015-0028-y) contains supplementary material, which is available to authorized users