Une cause exceptionnelle des péritonites: une perforation iléale par un corps étranger lors de la réduction d’une hernie inguinale

La péritonite secondaire est fréquemment rapportée dans la littérature. Les causes sont multiples. Nous rapportons un cas d'une perforation iléale par une cause exceptionnelle. Il s'agit d'une perforation iléale par un corps étranger lors de la réduction d'une hernie inguinale, responsable d'une péritonite grave avec tableau de défaillance multiviscérale

Shear Bond Strength of Three Composite Resins to Fluorosed and Sound Dentine: In Vitro Study

Introduction. This in vitro study compared the shear strength of three composite resin systems to fluorosed and normal dentin. Methods. Silorane FiltekTM P90, FiltekTMZ250 XT in combination with the adhesive system AdperTM Single bond 2, and Amelogen® Plus in association with Peak Universal Bond® were tested. Fifteen normal and 15 fluorosed dentine disks were prepared per material. The shear bond strength test was performed using a universal machine. Results. One-way ANOVA revealed significant differences in bond strength between the tested composite resins. All tested materials had significantly different adhesion at the fluorosed and the nonfluorosed interface. FiltekTM Z250 XT and Silorane had lower adhesion values to fluorosed than to normal dentin. In contrast, Amelogen® Plus presented a better average resistance at the fluorosed interface. Conclusion. Amelogen® Plus presented a better average shear bond strength on the fluorosed dentine. FiltekTMZ250 XT showed the best adhesion forces and shear bond strength with sound dentine. Further studies are needed to better understand the sealing of these systems

Bidirectional crosstalk between endoplasmic reticulum stress and mTOR signaling

Many cellular processes including apoptosis, autophagy, translation, energy metabolism, and inflammation are controlled by the mammalian target of rapamycin (mTOR) kinase and the endoplasmic reticulum (ER) stress pathway, also known as the unfolded protein response (UPR). Although both of these signaling nodes have attracted wide attention in fundamental cell biology and drug discovery, crosstalk between the two pathways has emerged only very recently. mTOR complex 1 (mTORC1) operates both upstream and downstream of ER stress signals, which can either enhance or antagonize the anabolic output of mTORC1. Upon prolonged ER stress, mTORC1 contributes to apoptotic signaling by suppressing the survival kinase Akt through feedback inhibition. Likewise, chronic ER stress obstructs activation of Akt by mTOR complex 2. This review surveys our knowledge of mTOR-ER stress intersections and highlights potential therapeutic implications