4 research outputs found
Guillain-Barre syndrome after lung lobectomy: is there any relationship?
Guillain-Barré syndrome (GBS) is an acute inflammatory polyradiculopathy frequently triggered by infection. It has also been reported in some cases after surgical procedures. We describe the first case of GBS occurring 9 days after lung lobectomy for localized lung cancer and efficiently treated with intravenous immunoglobulins. The exact physiopathology of GBS after surgical procedures is unknown. An immune-mediated process and perioperative infection are the most accepted etiologic hypotheses
p53 activation during ribosome biogenesis regulates normal erythroid differentiation
International audienceThe role of ribosome biogenesis in erythroid development is supported by the recognition of erythroid defects in ribosomopathies in both Diamond-Blackfan anemia and 5q- syndrome. Whether ribosome biogenesis exerts a regulatory function on normal erythroid development is still unknown. In the present study, a detailed characterization of ribosome biogenesis dynamics during human and murine erythropoiesis shows that ribosome biogenesis is abruptly interrupted by the drop of rDNA transcription and the collapse of ribosomal protein neo-synthesis. Its premature arrest by RNA polI inhibitor, CX-5461 targets the proliferation of immature erythroblasts. We also show that p53 is activated spontaneously or in response to CX-5461 concomitantly to ribosome biogenesis arrest, and drives a transcriptional program in which genes involved in cell cycle arrest, negative regulation of apoptosis and DNA damage response were upregulated. RNA polI transcriptional stress results in nucleolar disruption and activation of ATR-CHK1-p53 pathway. Our results imply that the timing of ribosome biogenesis extinction and p53 activation are crucial for erythroid development. In ribosomopathies in which ribosome availability is altered by unbalanced production of ribosomal proteins, the threshold of ribosome biogenesis down-regulation could be prematurely reached and together with pathological p53 activation prevents a normal expansion of erythroid progenitors