Endovascular surgery in the French role 3 medical treatment facility: Is there a need? A 10-year retrospective analysis.

Objective: Vascular surgery for war-related traumatic injuries represents 3 to 17.6 % of all emergency surgical procedures, and around 5 % in French Medical Treatment Facilities (MTFs). Most of these lesions are treated by open surgery, but the role of endovascular surgery in French MTFs has not been assessed yet.

Arteriovenous fistulae for access to hemodialysis in Chad : feasibility study of a medical civic action program by a French army surgical unit.

Introduction: Use of chronic intermittent hemodialysis is recent in Chad, where it remains underdeveloped. Vascular access is most commonly by catheter. The objective of our study was to demonstrate the feasibility of arteriovenous fistula (AVF) surgery for hemodialysis during deployments as part of the medical civic action program (MEDCAP).

Management specificities for abdominal, pelvic and vascular penetrating trauma.

Management of patients with penetrating trauma of the abdomen, pelvis and their surrounding compartments as well as vascular injuries depends on the patient's hemodynamic status. Multiple associated lesions are the rule. Their severity is directly correlated with initial bleeding, the risk of secondary sepsis, and lastly to sequelae.

Specific elements of thoracic wound management.

Damage control for thoracic trauma combines definitive and temporary surgical gestures specifically adapted to the lesions present. A systematic assessment of all injuries to prioritize the specific lesions and their treatments constitutes the first operative stage. Packing and temporary closure have a place in the care of chest injuries.

Management of war-related vascular wounds in French role 3 hospital during the Afghan campaign.

Objectives: To describe the management of war-related vascular injuries in the Kabul French military hospital.

Methods: From January 2009 to April 2013, in the Kabul French military hospital, we prospectively included all patients presenting with war-related vascular injuries. We collected the following data: site, type, and mechanism of vascular injury, associated trauma, type of vascular repair, amputation rate and complications.

Challenges in war-related thoracic injury faced by French military surgeons in Afghanistan (2009-2013).

Background: This study reports the challenges faced by French military surgeons in the management of thoracic injury during the latest Afghanistan war.

Methods: From January 2009 to April 2013, all of the civilian, French and Coalition casualties admitted to French NATO Combat Support Hospital situated on Kabul were prospectively recorded in the French Military Health Service Registry (OPEX(®)). Only penetrating and blunt thoracic trauma patients were retrospectively included.

[Catamenial pneumothorax: easy to see, difficult to manage].

Introduction: Catamenial pneumothorax (PNO) is a real clinical occurrence. Several cases are reported in the literature as a spontaneous PNO occurring during the catamenial period among women in their thirties. There is no consensus about management and the recurrence rate is very high whatever the initial treatment.

Trehalose impairs aggregation of PrPSc molecules and protects prion-infected cells against oxidative damage.

Neurodegenerative disorders such as Alzheimer's, Huntington's, and prion diseases are characterized by abnormal protein deposits in the brain of affected patients. In prion diseases, a key event in the pathogenesis is the conversion of the normal prion protein (PrP(c)) into abnormal protease resistant PrP(Sc) deposits, a phenomenon associated with a higher sensitivity to oxidative stress in vitro. In cellular models of Alzheimer and Huntington diseases, the disaccharide trehalose has been shown to be effective in inhibiting huntingtin and Abeta peptide aggregates and reducing their associated toxicity.

Cellular pathogenesis in prion diseases.

Prion diseases are characterised by neuronal loss, vacuolation (spongiosis), reactive astrocytosis, microgliosis and in most cases by the accumulation in the central nervous system of the abnormal prion protein, named PrP(Sc). In this review on the "cellular pathogenesis in prion diseases", we have chosen to highlight the main mechanisms underlying the impact of PrP(C)/PrP(Sc) on neurons: the neuronal dysfunction, the neuronal cell death and its relation with PrP(Sc) accumulation, as well as the role of PrP(Sc) in the microglial and astrocytic reaction.

The truncated 23-230 form of the prion protein localizes to the nuclei of inducible cell lines independently of its nuclear localization signals and is not cytotoxic.

The mechanisms of prion-induced neurological dysfunction observed in prion diseases are poorly understood. Transgenic mice expressing a truncated form of the prion protein (23-230 PrP) acquire cerebellar degeneration (Ma and Lindquist, Science, 2002). To decipher the mechanisms of neurodegeneration induced by 23-230 PrP, we established inducible cell lines expressing this truncated form of PrP.

Cationic phosphorus-containing dendrimers reduce prion replication both in cell culture and in mice infected with scrapie.

Over the last 30 years, many drugs have been tested both in cell culture and in vivo for their ability to prevent the generation of prions and the development of transmissible spongiform encephalopathies. Among the compounds tested, dendrimers are defined by their branched and repeating molecular structure. The anti-prion activity of new cationic phosphorus-containing dendrimers (P-dendrimers) with tertiary amine end-groups was tested.

Scrapie-like prion protein is translocated to the nuclei of infected cells independently of proteasome inhibition and interacts with chromatin.

Prion diseases are fatal transmissible neurodegenerative disorders characterized by the accumulation of an abnormally folded isoform of the cellular prion protein (PrP(C)) denoted PrP(Sc). Recently, wild-type and pathogenic PrP mutants have been shown to be degraded by the endoplasmic reticulum-associated degradation proteasome pathway after translocation into the cytosol. We show here that a protease resistant form of PrP accumulated in the nuclei of prion-infected cells independently of proteasome activity, and that this nuclear translocation required an intact microtubule network.

Alpha- and beta- cleavages of the amino-terminus of the cellular prion protein.

It is commonly assumed that the physiological isoform of prion protein, PrP(C), is cleaved during its normal processing between residues 111/112, whereas the pathogenic isoform, PrP(Sc), is cleaved at an alternate site in the octapeptide repeat region around position 90. Here we demonstrated both in cultured cells and in vivo, that PrP(C) is subject to a complex set of post-translational processing with the molecule being cleaved upstream of position 111/112, in the octapeptide repeat region or at position 96. PrP has therefore two main cleavage sites that we decided to name alpha and beta.

Stimulation of PrP(C) retrograde transport toward the endoplasmic reticulum increases accumulation of PrP(Sc) in prion-infected cells.

Prion diseases are fatal and transmissible neurodegenerative disorders characterized by the accumulation of an abnormally folded isoform of the cellular prion protein (PrP(C)) denoted PrP(Sc). To identify intracellular organelles involved in PrP(Sc) formation, we studied the role of the Ras-related GTP-binding proteins Rab4 and Rab6a in intracellular trafficking of the prion protein and production of PrP(Sc). When a dominant-negative Rab4 mutant or a constitutively active GTP-bound Rab6a protein was overexpressed in prion-infected neuroblastoma N2a cells, there was a marked increase of PrP(Sc) formation.

A novel Rho GTPase-activating-protein interacts with Gem, a member of the Ras superfamily of GTPases.

Gem is a Ras-related protein whose expression is induced in several cell types upon activation by extracellular stimuli. With the aim of isolating the cellular partners of Gem that mediate its biological activity we performed a yeast two-hybrid screen and identified a novel protein of 970 amino acids, Gmip, that interacts with Gem through its N-terminal half, and presents a cysteine-rich domain followed by a Rho GTPase-activating protein (RhoGAP) domain in its C-terminal half. The RhoGAP domain of Gmip stimulates in vitro the GTPase activity of RhoA, but is inactive towards other Rho family proteins such as Rac1 and Cdc42; it is also specific for RhoA in vivo.

[Cell culture models of transmissible spongiform encephalopathies].

Cell cultures represent versatile and useful experimental models of transmissible spongiform encephalopathies. These models include chronically prion infected cell lines, as well as cultures expressing variable amounts of wild-type, mutated or chimeric prion proteins. These cultures have been widely used to investigate the biology of both the normal and the pathological isoform of the prion protein.

Cell culture models of transmissible spongiform encephalopathies.

In this review, we describe the generation and use of cell culture models of transmissible spongiform encephalopathies, also known as prion diseases. These models include chronically prion-infected cell lines, as well as cultures expressing variable amounts of wild-type, mutated, or chimeric prion proteins. These cell lines have been widely used to investigate the biology of both the normal and the pathological isoform of the prion protein.

An extracellular activator of the Drosophila JAK/STAT pathway is a sex-determination signal element.

Metazoans use diverse and rapidly evolving mechanisms to determine sex. In Drosophila melanogaster an X-chromosome-counting mechanism determines the sex of an individual by regulating the master switch gene, Sex-lethal (Sxl). The X-chromosome dose is communicated to Sxl by a set of X-linked signal elements (XSEs), which activate transcription of Sxl through its 'establishment' promoter, SxlPe.

Muscle differentiation is antagonized by SOX15, a new member of the SOX protein family.

SOX proteins belong to a multigenic family characterized by a unique DNA binding domain, known as the high mobility group box, that is related to that of the testis determining gene SRY. cDNA sequences for more than 30 SOX genes have been identified, and some are known to have diverse roles in vertebrate differentiation and development. Here, we report the isolation and characterization of mouse Sox15 that was uncovered during a screen for high mobility group box containing transcription factors that are expressed at different levels during skeletal muscle differentiation.

Getting more from the two-hybrid system: N-terminal fusions to LexA are efficient and sensitive baits for two-hybrid studies.

Two-hybrid methods detect interactions between two proteins fused at the C-termini of, respectively, a DNA-binding domain and the activation domain of a transcriptional activator. Thus the N-terminus of none of these proteins is available for interaction. We have tested whether a bait protein with a reverted polarity (i.