CORRIGENDUM: Phase transition in the two-dimensional frustrated x-y model: scaling equations
The author establishes scaling equations for the two-dimensional x-y model with weak frustration using the electrostatic analogy of Kosterlitz and Thouless. In the limit of small disorder he finds a shift in the critical temperature Tc(x)-Tc(0)=-(Jx/kB)(2 pi 2- pi /2 ln 2x) and the exponents are unchanged from the pure values.
Frequency-Dependent Conductivity in K0.30MoO3
Although conductivity from moving charge density waves (CDWs) was first envisioned in the 1950s [1, 2], it has only been in the last ten years that materials with a conductivity mechanism similar to the sliding ‘Frohlich-mode’ have been investigated. Thus far, about ten compounds show nonlinear conductivity from a moving CDW, and four compounds, K0.30MoO3, NbSe3, TaS3, and (TaSe4)2I have been extensively studied [3–6]. The physical properties of materials with moving charge-density waves (CDWs), while similar to predictions based on the original Peierls—Frohlich ideas, are in reality considerably more rich than would be predicted from the original model. In many anisotropic metals the ground state is periodic distortion of the host structure consisting of two parts, a periodic modulation of the electron density and a periodic lattice distortion [7]. The CDW, which can be thought of as a charged lattice, can couple to an applied electric field and, in the absence of pinning, it can move and carry current. In the original Peierls—Frohlich model, the lattice is neglected and unattenuated conductivity arises because of the uniform translation of a rigid, one-dimensional chargedensity wave that has translational invariance. Non-attenuated conductivity, however, no longer occurs if one includes the pinning effects of a commensurate lattice or impurities. Lee, Rice and Anderson [8] showed that such pinning effects shift the oscillator strength of the CDW sliding mode from zero to finite frequency. This finite frequency mode is referred to as the pinned phase mode, and in models which do not allow for deformations, it is the only mode expected at frequencies less than the single particle gap.
Direct orbital manometry in patients with thyroid-associated orbitopathy.
PURPOSE
To determine orbital tissue tension and orbital compartment compliance in patients with and without thyroid-associated orbitopathy (TAO).


DESIGN
Prospective case series.


PARTICIPANTS
Orbits of patients with TAO (18 orbits) and control patients without TAO (35 orbits) were studied.


METHODS
An orbital manometer was designed to directly measure orbital tissue tension in patients undergoing ocular or orbital surgery.


MAIN OUTCOME MEASURES
Tissue tension was recorded before, during, and for 5 minutes after a 5-ml retrobulbar injection of anesthetic. Orbital compliance was calculated as change in volume divided by change in tissue tension.


RESULTS
Resting orbital tissue tension was 4.4 +/- 2.2 mmHg (mean +/- SD) in normal orbits and 9.7 +/- 4.8 mmHg in orbits of TAO patients (P = 0.0005) Following retrobulbar injection, orbital tissue tension rose to 12.0 +/- 3.6 mmHg (P = 0.0000000000000006 compared with baseline) in the control group and to 36.3 +/- 15.2 mmHg in the TAO group (P = 0.0000007 compared with baseline, and P = 0.000008 TAO group versus control group). Orbital compartment compliance was 0.80 +/- 0.50 ml/mmHg in the control group and 0.27 +/- 0.21 ml/mmHg in the TAO group (P = 0.00001). Resting orbital tissue tension in 8 TAO orbits with compressive optic neuropathy was 12.4 +/- 4.9 mmHg, and was 7.8 +/- 3.5 mmHg in 10 orbits of TAO patients without compressive optic neuropathy (P < 0.05). No adverse events occurred.


CONCLUSIONS
Retrobulbar injection causes consistent measurable changes in orbital tissue tension. Orbital manometry safely demonstrated higher orbital tissue tension and lower orbital compartment compliance in the orbits of TAO patients versus those of normal subjects. Resting orbital tissue tension was higher in the orbits of TAO patients with compressive optic neuropathy than in those orbits without. Compressive optic neuropathy may partially result from an orbital compartment syndrome in some patients with TAO. Directly assessing orbital dynamics in vivo may prove useful as an adjunct in the clinical evaluation of patients with TAO and other orbital disorders.