[Place of preperitoneal pelvic packing in severe pelvic traumatisms: 20 cases in a French level 1 trauma center]. / Place du packing pré-péritonéal pelvien dans les traumatismes graves du bassin : étude à partir de 20 cas réalisés dans un trauma center de niveau 1 français.

BACKGROUND: The overall mortality of hemodynamically unstable patients with pelvic trauma is high. Their management is controversial concerning places of arterioembolization and pelvic packing associated with pelvic stabilization. The aim of this study was to collect the pre-peritoneal pelvic packing (PPP) performed in our institution over 10years in order to propose a management algorithm. METHOD: From January 2010 to December 2020, all patients with a hemodynamically unstable pelvic fracture who had PPP combined with pelvic stabilization were included. Data were collected prospectively and analyzed retrospectively. The main judgement criteria were early hemorrhage-induced mortality (<24h) and overall mortality (<30d). RESULTS: Twenty patients had PPP out of 287 polytrauma patients with pelvic fracture. The first-line PPP proposed in our algorithm significantly reduced the number of red blood cells (RBCs) (P=0.0231) and improved systolic blood pressure (SBP) (P<0.001) within 24hours of first-line PPP (compared with preoperative). Six patients (30%) were embolized postoperatively for active bleeding not necessarily pelvic. The overall mortality at 30days was 50% (10/20). CONCLUSION: PPP is a fast, easy, effective and safe procedure for venous, bone and sometimes arterial bleeding. PPP is part of damage control surgery and we propose it as a first-line procedure. AE remains complementary in a second step.

Preperitoneal pelvic packing.

Severe pelvic traumatisms are associated with elevated mortality because of the high risk of exsanguination from multiple sources of bleeding. Treatment should encompass resuscitation, bone stabilization and hemorrhage control by arterio-embolization or surgery. Pre-peritoneal packing has been described in hemodynamically unstable patients who need damage control. The surgical technique of this simple and effective procedure is fully described by the authors with some complementary useful technical advices.

Cyclin E drives human keratinocyte growth into differentiation.

Human epidermis is continuously exposed to environmental mutagenic hazard and is the most frequent target of human cancer. How the epidermis coordinates proliferation with differentiation to maintain homeostasis, even in hyperproliferative conditions, is unclear. For instance, overactivation of the proto-oncogene MYC in keratinocytes stimulates differentiation. Here we explore the cell cycle regulation as proliferating human keratinocytes commit to terminal differentiation upon loss of anchorage or overactivation of MYC. The S-phase of the cell cycle is deregulated as mitotic regulators are inhibited in the onset of differentiation. Experimental inhibition of mitotic kinase cdk1 or kinases of the mitosis spindle checkpoint Aurora B or Polo-like Kinase, triggered keratinocyte terminal differentiation. Furthermore, hyperactivation of the cell cycle by overexpressing the DNA replication regulator Cyclin E induced mitosis failure and differentiation. Inhibition of Cyclin E by shRNAs attenuated the induction of differentiation by MYC. In addition, we present evidence that Cyclin E induces DNA damage and the p53 pathway. The results provide novel clues for the mechanisms committing proliferative keratinocytes to differentiate, with implications for tissue homeostasis maintenance, HPV amplification and tumorigenesis.

Etoposide and adriamycin but not genistein can activate the checkpoint kinase Chk2 independently of ATM/ATR.

We have investigated the effects of three unrelated topoisomerase 2 inhibitors, genistein, adriamycin, and etoposide, on phosphorylation/activation of the checkpoint kinase Chk2 in normal or ATM-deficient (ATM-) human fibroblasts and in cells overexpressing a catalytically inactive ATR kinase. We demonstrate that genistein activates Chk2 in a strictly ATM-dependent manner, whereas etoposide and adriamycin can trigger Chk2 activation in long-term cultures of ATM- cells. Moreover, these two latter genotoxic compounds were found to activate Chk2 in fibroblasts expressing the dominant negative form of ATR. We also report a significant decrease in the accumulation in G2-phase of ATM- cells when genistein did not activate Chk2. In conclusion, our results strongly support that activation of Chk2 could be dependent on the type and/or extent of DNA damage and under the control of either an ATM-dependent or an ATM and, maybe, an ATR-independent pathway.

[Bilateral traumatic dislocation of the hip. Report on three cases (author's transl)]. / Luxations traumatiques bilatérales de hanche. A propos de 3 cas.

Three patients with simultaneous bilateral traumatic dislocation of the hip have been treated, one case developing double intra-articular incarceration after orthopedic reduction. This type of lesion is reputed to be extremely rare, but a review of the published literature demonstrated that more than 100 cases have probably been described.