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S Quadri

Publications and source records attributed to S Quadri.

7 recordsLinked to original sources
PubMed2001

The role of NF-kappaB as a survival factor in environmental chemical-induced pre-B cell apoptosis.

Polycyclic aromatic hydrocarbons (PAH) are ubiquitous environmental chemicals that suppress the immune system at multiple levels, including at the level of B cell development in the bone marrow microenvironment. Specifically, PAH induce preB cell apoptosis in primary bone marrow cultures and in cocultures of an early preB cell line (BU-11) and a bone marrow stromal cell line (BMS2). Previous studies focused on the molecular mechanisms through which PAH induce stromal cells to deliver an apoptosis signal to adjacent preB cells. Apoptosis signaling within the preB cell itself was not investigated. Here, the role of NF-kappaB, a lymphocyte survival factor, in PAH-induced preB cell apoptosis was assessed. Analysis of DNA-binding proteins extracted from the nuclei of untreated BU-11 cells indicated DNA-binding complexes comprising NF-kappaB subunits p50, c-Rel, and/or Rel A. NF-kappaB down-regulation with previously described inhibitors induced BU-11 cell apoptosis, demonstrating that the default apoptosis pathway blocked by NF-kappaB is functional at this early stage in B cell development. Similarly, exposure of BU-11/BMS2 cocultures to 7,12-dimethylbenz[a]anthracene (DMBA), a prototypic PAH, down-regulated nuclear Rel A and c-Rel before overt apoptosis. Finally, ectopic expression of Rel A or c-Rel rescued BU-11 cells from DMBA-induced apoptosis. These results extend previous observations by demonstrating that 1) NF-kappaB is a survival factor at an earlier stage of B cell development than previously appreciated and 2) NF-kappaB down-regulation is likely to be part of the molecular mechanism resulting in PAH-induced preB cell apoptosis. These results suggest nonclonally restricted, PAH-mediated suppression of B lymphopoiesis.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2001

Dual signaling by the alpha(v)beta(3)-integrin activates cytosolic PLA(2) in bovine pulmonary artery endothelial cells.

Vitronectin, which ligates the alpha(v)beta(3)-integrin, increases both lung capillary permeability and lung endothelial Ca(2+). In stable monolayers of bovine pulmonary artery endothelial cells (BPAECs) viewed with confocal microscopy, multimeric vitronectin aggregated the apically located alpha(v)beta(3)-integrin. This caused arachidonate release that was inhibited by pretreating the monolayers with the anti-alpha(v)beta(3) monoclonal antibody (MAb) LM609. No inhibition occurred in the presence of the isotypic MAb PIF6, which recognizes the integrin alpha(v)beta(5). Vitronectin also caused membrane translocation and phosphorylation of cytosolic phospholipase A(2) (cPLA(2)) as well as tyrosine phosphorylation of the mitogen-activated protein kinase (MAPK) extracellular signal-regulated kinase (ERK) 2. The cPLA(2) inhibitor arachidonyl trifluoromethylketone, the tyrosine kinase inhibitor genistein, and the MAPK kinase inhibitor PD-98059 all blocked the induced arachidonate release. PD-98059 did not inhibit the increase of cytosolic Ca(2+) or cPLA(2) translocation, although it blocked tyrosine phosphorylation of ERK2. Moreover, although the intracellular Ca(2+) chelator MAPTAM also inhibited arachidonate release, it did not inhibit tyrosine phosphorylation of ERK2. These findings indicate that ligation of apical alpha(v)beta(3) in BPAECs caused ERK2 activation and an increase of intracellular Ca(2+), both conjointly required for cPLA(2) activation and arachidonate release. This is the first instance of a tyrosine phosphorylation-initiated "two-hit" signaling pathway that regulates an integrin-induced proinflammatory response.

Animals↗
PubMed1996

Carpal tunnel syndrome: which electrodiagnostic path should we follow? A prospective study of 100 consecutive patients.

We prospectively studied 100 consecutive patients (200 hands) sent to our Neurophysiopathology Service for a suspected Carpal Tunnel Syndrome (C.T.S.). We performed 6 different motor and sensitive electrodiagnostic tests on both hands of each patients and on 25 healthy subjects. We calculated the sensibility and the specificity of each test by comparing each parameter with all the other ones, and then, again, using the clinical evaluation as a "gold standard". The routinely performed tests proved to have a high sensibility in detecting C.T.S., nevertheless, sometimes they do not give a definite response. In these cases we suggest to carry out the neurophysiological examination by performing some of the newly proposed tests. We end our study by drawing a "flow-chart", which considers reliability, sensibility, difficulty in performing and/or evaluating, and discomfort for patients, of each test; by this we would give a guide and a practical aid in determining the electrophysiological path for C.T.S. diagnosis.

Action Potentials↗
PubMed1978

The interaction of short-chain aralkyl alcohols and amines with the erythrocyte membrane.

Erythrocytes in isotonic saline are hemolyzed by benzyl alcohol and by 2-phenylethanol, but not by the corresponding amines nor by the ring-or side-chain-hydroxylated analogs. All these compounds could however interact with the erythrocyte membrane since: a) they facilitated the hemolytic effect of benzyl alcohol and/or of phenylelytic effect of benzyl alcohol and/or of phenylethanol; b) they exerted a protective effect against controlled hypotonic hemolysis.

Alcohols↗