Transection of the brachial artery after closed posterior elbow dislocation.

Although elbow dislocations are common orthopaedic lesions, vascular complications remain rare. We report the cases of three patients who presented with a rupture of the brachial artery after closed posterior dislocation, which is even more uncommon. Arteriograms were performed in all cases because of the persistent absence of pulses at the wrist after emergency reduction. In each patient, the treatment consisted of the insertion of reversed end-to-end saphenous bridges. None of them presented mid-term vascular complications (mean follow-up, 17 months). Brachial artery disruption can result from closed posterior elbow dislocation and responds well to vascular repair.

Tumor necrosis factor-alpha inhibits hTERT gene expression in human myeloid normal and leukemic cells.

Telomerase catalytic subunit (hTERT) has been shown to play a critical role not only in telomere homeostasis but also in cellular survival, DNA repair, and genetic stability. In a previous study, we described that tumor necrosis factor-xalpha (TNFxalpha) induced in the leukemic KG1 cells a senescence state characterized by decreased hTERT activity followed by prolonged growth arrest, increasedx beta-galactosidase activity, telomere shortening, and major chromosomal instability. Interestingly, granulocyte-macrophage colony-stimulating factor (GM-CSF) abrogated all these events. In the present study, we show for the first time that TNFxalpha acts by inhibiting the hTERT gene in both normal CD34x+ cells and fresh leukemic cells. Using KG1 cells as a representative cellular model, we show that TNFxalpha induced sphingomyelin hydrolysis, ceramide production, and c-Jun N-terminal kinase (JNK) activation, all of which are critical components of TNFxalpha signaling, resulting in hTERT gene inhibition. Moreover, we provide evidence that the protective effect of GM-CSF is related to its capacity to interfere with both ceramide generation and ceramide signaling. Negative regulation of the hTERT gene may represent one mechanism by which TNFxalpha interferes with normal hemopoiesis.