Meniscal Root Tears: An Update Focused on Preoperative and Postoperative MRI Findings.

Meniscal root tears represent radial tears or avulsions of the meniscal cartilage at the tibial attachment site that profoundly affect meniscal biomechanics and kinematics. Meniscal root tears have the functional effect of a total meniscectomy and can lead to rapid degenerative change with development of early knee osteoarthritis (OA). A growing range of arthroscopic surgical techniques have been developed to repair meniscal root tears with the aim of restoring joint kinematics and contact pressures and delaying the development of OA. With increased understanding of the anatomy and biomechanics of the meniscal root, meniscal root injury repair has become the treatment of choice in knees with nonadvanced OA. This article reviews the anatomy and biomechanics of the meniscal roots, clinical and imaging diagnostic criteria of meniscal root tears, correlation between arthroscopy and MRI in the diagnosis and classification of meniscal root tears, and expected and abnormal MRI findings after meniscal root repair. Familiarity with MRI signs and classifications of meniscal root tears, as well as with root repair surgical techniques, can aid radiologists in correctly reporting preoperative and postoperative MRI findings.

The Cratylia mollis seed lectin induces membrane permeability transition in isolated rat liver mitochondria and a cyclosporine a-insensitive permeability transition in Trypanosoma cruzi mitochondria.

Previous results provided evidence that Cratylia mollis seed lectin (Cramoll 1,4) promotes Trypanosoma cruzi epimastigotes death by necrosis via a mechanism involving plasma membrane permeabilization to Ca(2+) and mitochondrial dysfunction due to matrix Ca(2+) overload. In order to investigate the mechanism of Ca(2+) -induced mitochondrial impairment, experiments were performed analyzing the effects of this lectin on T. cruzi mitochondrial fraction and in isolated rat liver mitochondria (RLM), as a control. Confocal microscopy of T. cruzi whole cell revealed that Cramoll 1,4 binding to the plasma membrane glycoconjugates is followed by its internalization and binding to the mitochondrion. Electrical membrane potential (∆Ψm ) of T. cruzi mitochondrial fraction suspended in a reaction medium containing 10 µM Ca(2+) was significantly decreased by 50 µg/ml Cramoll 1,4 via a mechanism insensitive to cyclosporine A (CsA, membrane permeability transition (MPT) inhibitor), but sensitive to catalase or 125 mM glucose. In RLM suspended in a medium containing 10 µM Ca(2+) this lectin, at 50 µg/ml, induced increase in the rate of hydrogen peroxide release, mitochondrial swelling, and ∆Ψm disruption. All these mitochondrial alterations were sensitive to CsA, catalase, and EGTA. These results indicate that Cramoll 1, 4 leads to inner mitochondrial membrane permeabilization through Ca(2+) dependent mechanisms in both mitochondria. The sensitivity to CsA in RLM characterizes this lectin as a MPT inducer and the lack of CsA effect identifies a CsA-insensitive MPT in T. cruzi mitochondria.

Ferromagnetic levan composite: an affinity matrix to purify lectin.

A simple and inexpensive procedure used magnetite and levan to synthesize a composite recovered by a magnetic field. Lectins from Canavalia ensiformis (Con A) and Cratylia mollis (Cramoll 1 and Cramoll 1, 4) did bind specifically to composite. The magnetic property of derivative favored washing out contaminating proteins and recovery of pure lectins with glucose elution. Cramoll 1 was purified by this affinity binding procedure in two steps instead of a previous three-step protocol with ammonium sulfate fractionation, affinity chromatography on Sephadex G-75, and ion exchange chromatography through a CM-cellulose column.