Crack Propagation in As-Extruded and Heat-Treated Mg-Dy-Nd-Zn-Zr Alloy Explained by the Effect of LPSO Structures and Their Micro- and Nanohardness.

The investigation of the crack propagation in as-extruded and heat-treated Mg-Dy-Nd-Zn-Zr alloy with a focus on the interaction of long-period stacking-ordered (LPSO) structures is the aim of this study. Solution heat treatment on a hot extruded Mg-Dy-Nd-Zn-Zr (RESOLOY®) was done to change the initial fine-grained microstructure, consisting of grain boundary blocky LPSO and lamellar LPSO structures within the matrix, into coarser grains of less lamellar and blocky LPSO phases. C-ring compression tests in Ringer solution were used to cause a fracture. Crack initiation and propagation is influenced by twin boundaries and LPSO lamellae. The blocky LPSO phases also clearly hinder crack growth, by increasing the energy to pass either through the phase or along its interface. The microstructural features were characterized by micro- and nanohardness as well as the amount and location of LPSO phases in dependence on the heat treatment condition. By applying nanoindentation, blocky LPSO phases show a higher hardness than the grains with or without lamellar LPSO phases and their hardness decreases with heat treatment time. On the other hand, the matrix increases in hardness by solid solution strengthening. The microstructure consisting of a good balance of grain size, matrix and blocky LPSO phases and twins shows the highest fracture energy.

An uncommon presentation of orbital apex syndrome.

BACKGROUND: Bilateral total ophthalmoplegia secondary to a malignancy or infection of the cavernous sinus and orbital apex is an unusual presentation. Bilateral ophthalmoplegia as the initial sign of this type of rhinocerebral pathology is also uncommon. CASE REPORT: A 34-year old Haitian woman presented with bilateral vision loss, ptosis, total ophthalmoplegia, and ocular pain. A physical and neurologic examination, laboratory analysis, chest x-rays, and neurologic imaging studies were requested. Cranial and facial computed tomography (CT) scans showed swelling of the soft tissues proximal to the sphenoid extending into the dorsal sella and prepontine cistern, obliteration of the nasopharyngeal reflection, opacification of the ethmoid and sphenoid sinus, bony destruction of the mid-skull base, and bilateral lymphadenopathy of the neck. Magnetic resonance imaging (MRI) showed the presence of a soft tissue mass causing destruction of the skull base. Involvement of the clivus, cavernous sinuses, and sella with nasopharynx extension was observed. Hypodense centers within nasopharyngeal tissues suggested the presence of necrosis. Differential diagnosis included nasopaharyngeal carcinoma, lymphoma, or an infectious process. The patient did not consent to a biopsy and refused treatment. CONCLUSION: This presentation is a medical emergency. A combination of surgical, medical, or radiological intervention may be required to manage rhino-cerebral diseases responsible for orbital apex syndrome. Despite advances in neurologic imaging, histologic examination of tissue obtained from a biopsy may ultimately be necessary to obtain a precise diagnosis.