2,821 research outputs found
Causes and prevention of lymphoma
No full textNon-Hodgkin lymphoma (NHL) represents a heterogeneous group of lymphocytic disorders ranging in aggressiveness from indolent cellular proliferation to highly aggressive and rapidly proliferative processes. As discussed in detail elsewhere in this volume, the incidence of NHL has risen steadily worldwide during the past two decades.1 The causes of this upward trend are largely unknown, and in general the current understanding of the etiology of NHL is incomplete. More than 300 000 new cases of NHL are estimated to occur annually worldwide.2. © 2010 by Taylor & Francis Group, LLC
megakaryocytes and the HEL cell line
No full textWe investigated whether cells belonging to the megakaryocytic lineage could be infected in vitro with human immunodeficiency virus type-1 (HIV-1). Primary GPIIb/IIIa+ bone marrow (BM) cells and HEL continuous cell line were first phenotypically characterized for the presence of megakaryocytic markers and CD4 antigen, then challenged in vitro with the laboratory strain IIIB of HIV-1. Both GPIIb/IIIa+ BM and HEL cells expressed significant levels of CD4 receptor (> 50%) and were efficiently infected with HIV-1, as judged by the presence of proviral DNA after polymerase chain reaction analysis and by quantitative evaluation of gag p24 antigen in the culture supernatants. Of note, infection with HIV-1 in both primary BM megakaryocytes and HEL cells was specifically blocked by soluble recombinant CD4. To ascertain whether the CD4 receptor was essential for infection of megakaryocytic cells, HEL were subcloned into CD4+ and CD4- cells. Although unfractionated and CD4+ HEL cells were productively infected with HIV-1, CD4- HEL cells could not be infected. Infection of HEL cells did not induce gross cytotoxic effects or a significant increase of apoptosis. On the other hand, treatment of unfractionated or CD4+ HEL cells with cross-linked recombinant env gp120 or Leu3a anti-CD4 monoclonal antibody markedly (P < 0.01) increased the degree of apoptosis with respect to HEL cells infected with HIV-1 or treated with cross-linked gag p24 or anti-GPIIb/IIIa antibody. Taken together, these data indicate that the CD4 receptor represents the main route of infection in cells belonging to the megakaryocytic lineage. Moreover, an inappropriate engagement of CD4 by either free env gp120 or anti-CD4 monoclonal antibody could be more relevant than a direct infection with HIV-1 in the induction of the frequent BM megakaryocyte abnormalities found in HIV-1 seropositive thrombocytopenic patients
Interface statistics of OBody HEL-binding compared to other known HEL-binding proteins, calculated by PDBePISA.
No full text<p>Interface statistics of OBody HEL-binding compared to other known HEL-binding proteins, calculated by PDBePISA.</p
Anatomy of the AM3L09-HEL interface.
No full text<p>(a) AM3L09 is coloured blue with interface residues shown as stick models. HEL residues calculated to make a hydrogen bond with AM3L09 are shown as green stick models. Potential hydrogen bonds are indicated by a dashed yellow line. (b) HEL electrostatic surface. The highly electronegative HEL active site (AS) is filled by R35 from AM3L09. (c) AM3L09 electrostatic surface, shown in the same orientation as panel a. The negatively charged patch containing D91 associates with a complementary positively charged patch on the HEL interface. (d) Comparative binding positions of AM3L09 (blue, thick Cα trace) and NL8 (red, narrow Cα trace) to HEL (green surface). (e) The AM3L09-HEL interface, shown in wall-eye stereo. Bridging water molecules between AM3L09 (blue) and HEL (green) are shown as red spheres. Potential hydrogen bonds are indicated by a dashed yellow line labelled with the length in angstroms.</p
Informations sur la HEL
No full textInformations sur la HEL. In: Histoire Épistémologie Langage, tome 24, fascicule 2, 2002. Politiques linguistiques (1/2) p. 1
Differential scanning calorimetry thermal denaturation and HEL inhibition assay for HEL-binding and control OBodies.
No full text<p>(a) Thermal denaturation by differential scanning fluorimetry of HEL-binding OBodies and a control non-HEL-binding OBody U81. Calculated T<sub>m</sub> values are shown alongside the number of amino acid mutations as compared to the wild-type AspRS OB-fold domain from <i>P. aerophilum</i>. (b) HEL activity assay showing inhibition by OBodies AM3L09, AM3L15 and AM2EP06 and negative control U81. Lines show the nonlinear fit of a variable-slope dose-response model. Error bars show the 95% confidence interval derived from triplicate data points. The data shown are representative of that obtained from multiple independent repeats of the same assay.</p
Informations sur la HEL
No full textInformations sur la HEL. In: Histoire Épistémologie Langage, tome 24, fascicule 2, 2002. Politiques linguistiques (1/2) p. 1
Th17 population induces higher titres of anti-HEL antibodies.
No full text<p>Serum was taken from the animals and was assessed for the presence of HEL-specific IgM<sup>a</sup> antibodies at day 3(A), 7(B) and 10(C). *: Th1/HEL-OVA vs. Th17/HEL-OVA. Data represent mean ±SEM. *p<0.05, **p<0.01, ***p<0.001 (n = 3). Similar results were obtained in one additional experiment.</p
The alignment of SsDFV3 Hel-2.
No full text(A) The 5 most similar viruses with the Hel-2 of SsDFV3 in Protein Data Bank (PDB). (B) Sequence alignment of the Hel-2 domain from SsDFV3 and Chrysanthemum virus B. (TIF)</p
HEL<sup>+</sup> and HEL<sup>−</sup> B cells are both infected by MuHV-4 in vitro.
No full text<p>In vitro infection by co-culture assay was performed as described in the material and methods. Briefly, freshly isolated SW<sub>HEL</sub> splenocytes were exposed to free viruses or co-culture with BHK-21 or RAW-264 cells previously infected with EF1α-eGFP<sup>+</sup> or EF1α-eGFP<sup>+</sup>-gp150<sup>−</sup> MuHV-4. GFP expression in HEL<sup>+</sup> and HEL<sup>−</sup> B cells was monitored by FACS after 48 h of co-culture. Representative FACS plots are shown on top, compiled data representing average percentage and standard deviation are shown below. Splenocytes were identified based on FSC SSC parameters, excluding BHK-21 and RAW-264. Cells were then gated on CD19<sup>+</sup> CD11b<sup>−</sup> and GFP expression was monitored in HEL<sup>+</sup> and HEL<sup>−</sup> B cell. Data were obtained from two independent experiments with two splenocytes suspensions in each.</p
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