Absent anterior cruciate ligament

This case report presents the MRI findings of aplasia of the anterior cruciate ligament with associated hypoplasia of the posterior cruciate ligament (Manner type 2). Radiographically the presence of a shallow femoral notch and hypoplastic tibial spines (the so-called "dromedar" sign) can aid in the diagnosis. Operative treatment is often not indicated since the congenital absence of the ACL implies long-standing altered biomechanics to which the knee has well adapted in the majority of cases

Formation of energy gap in higher dimensional spin-orbital liquids

A Schwinger boson mean field theory is developed for spin liquids in a symmetric spin-orbital model in higher dimensions. Spin, orbital and coupled spin-orbital operators are treated equally. We evaluate the dynamic correlation functions and collective excitations spectra. As the collective excitations have a finite energy gap, we conclude that the ground state is a spin-orbital liquid with a two-fold degeneracy, which breaks the discrete spin-orbital symmetry. Possible relevence of this spin liquid state to several realistic systems, such as CaV$_4$V$_9$ and Na$_2$Sb$_2$Ti$_2$O, are discussed.Comment: 4 pages with 1 figur

N\'eel and Spin-Peierls ground states of two-dimensional SU(N) quantum antiferromagnets

The two-dimensional SU(N) quantum antiferromagnet, a generalization of the quantum Heisenberg model, is investigated by quantum Monte Carlo simulations. The ground state for $N\le 4$ is found to be of the N\'eel type with broken SU(N) symmetry, whereas it is of the Spin-Peierls type for $N\ge 5$ with broken lattice translational invariance. No intermediate spin-liquid phase was observed in contrast to previous numerical simulations on smaller lattices [Santoro et al., Phys. Rev. Lett. {\bf 83} 3065 (1999)].Comment: 4 pages, 4 figure

E-cadherin expression in macrophages dampens their inflammatory responsiveness in vitro, but does not modulate M2-regulated pathologies in vivo

IL-4/IL-13-induced alternatively activated macrophages (M(IL-4/IL-13), AAMs or M2) are known to express E-cadherin, enabling them to engage in heterotypic cellular interactions and IL-4-driven macrophage fusion in vitro. Here we show that E-cadherin overexpression in Raw 264.7 macrophages inhibits their inflammatory response to LPS stimulation, as demonstrated by a reduced secretion of inflammatory mediators like interleukin (IL)-6, tumor necrosis factor (TNF) and nitric oxide (NO). To study the function of E-cadherin in M(IL-4/IL-13) macrophages in vivo, we generated macrophage-specific E-cadherin-deficient C57BL/6 mice. Using this new tool, we analyzed immunological parameters during two typical AAM-associated Th2-driven diseases and assessed Th2-associated granuloma formation. Although E-cadherin is strongly induced in AAMs during Taenia crassiceps helminth infections and allergic airway inflammation, its deletion in macrophages does not affect the course of both Th2 cytokine-driven diseases. Moreover, macrophage E-cadherin expression is largely redundant for granuloma formation around Schistosoma mansoni ova. Overall, we conclude that E-cadherin is a valuable AAM marker which suppresses the inflammatory response when overexpressed. Yet E-cadherin deletion in macrophages does not affect M(LPS+IFN gamma) and M(IL-4) polarization in vitro, nor in vivo macrophage function, at least in the conditions tested