Biomedical subjects

Pilar Martin

Publications and source records attributed to Pilar Martin.

4 recordsLinked to original sources

PubMed2003

Regulation of mature T lymphocyte proliferation and differentiation by Par-4.

The genetic inactivation of the atypical protein kinase C (aPKC) inhibitor, Par-4, gives rise to increased NF-kappaB activation and decreased stimulation of JNK in embryo fibroblasts. Here we have characterized the immunological phenotype of the Par-4(-/-) mice and found that the loss of this gene leads to an increased proliferative response of peripheral T cells when challenged through the TCR. This is accompanied by a higher increase in cell cycle entry and inhibition of apoptosis, with enhanced IL-2 secretion but normal CD25 synthesis. Interestingly, the TCR-triggered activation of NF-kappaB was augmented and that of JNK was severely abrogated. Consistent with previous data from knock outs of different JNKs, NFATc1 activation and IL-4 secretion were augmented in the Par-4-deficient CD4+ T cells, suggesting that the loss of Par-4 drives T-cell differentiation towards a Th2 response. This is compelling evidence that Par-4 is a novel modulator of the immune response through its ability to impact aPKC activity, which translates into lower JNK signaling.

Animals↗

PubMed2002

Role of zeta PKC in B-cell signaling and function.

The atypical protein kinase C isoform, zeta PKC, has been implicated in the control of extracellular signal-regulated kinase (ERK) and nuclear factor (NF)-kappa B pathways. Recent evidence from zeta PKC knock-out mice demonstrates that this kinase is important for NF-kappa B transcriptional activity but not for ERK activation in embryonic fibroblasts. The lack of zeta PKC produces in mice a number of alterations in the development of secondary lymphoid tissues that could be accounted for, at least in part, by defects in B-cell function. Here, we present evidence that the loss of zeta PKC selectively impairs signaling through the B-cell receptor, resulting in inhibition of cell proliferation and survival, as well as defects in the activation of ERK and the transcription of NF-kappa B-dependent genes. Furthermore, zeta PKC-/- mice are unable to mount an optimal T-cell-dependent immune response. Collectively, these results genetically establish a critical role for zeta PKC in B-cell function in vitro and in vivo.

Animals↗

PubMed2002

Percutaneous renal artery embolisation of non-functioning renal allografts with clinical intolerance.

The aim of the study was to evaluate the efficacy and safety of percutaneous renal artery embolisation of non-functioning renal allografts in patients with graft intolerance syndrome (GIS). Transcatheter artery embolisation was performed in 30 kidney transplant recipients with GIS. The duration of graft function had been 60+/-45 months. Infectious disease was ruled out in all patients. Embolisation consisted of the injection of polyvinyl alcohol microspheres followed by the insertion of a stainless steel coil in the renal artery branches. Symptoms of GIS included: fever-graft pain (44%, n=13), fever-hematuria-pain (20%, n=6), fever-hematuria (13%, n=4) and fever alone (23%, n=7). Latency time between graft failure and embolisation was 184+/-227 (17-1181) days. Embolisation was clinically successful with the prolonged disappearance of GIS in 24 patients (80%). Six patients showed initial clinical improvement, but GIS reappeared at 40+/-18 days, and graft nephrectomy was required. There were no major complications associated with embolisation and no deaths. Perirenal collateral supply was a risk factor for the reappearance of GIS. Renal vascular embolisation is a simple, safe and effective technique for treating renal allograft intolerance syndrome and could be a feasible alternative for the first-line treatment.

Embolization, Therapeutic↗

PubMed2002

Spanish language mapping using MEG: a validation study.

The purpose of the present study was to compare magnetoencephalography (MEG) data with the results of the intracarotid amytal procedure (IAP). Twenty-one native Spanish-speaking patients with intractable epilepsy underwent MEG language mapping. A subset of 8 patients also underwent an IAP. With the exception of 2 patients who showed right hemisphere dominance, all other patients showed left hemisphere dominance for language on the MEG recording. The IAP findings were consistent with MEG results in 7 patients. The eighth patient who, according to the MEG data, had probable right hemisphere dominance for language did not show clear hemispheric specialization for language on the IAP and suffered a transient global aphasia following a right temporal lobotomy. These results suggests that MEG-based language mapping can play an important role in presurgical clinical evaluation.

Adult↗