We describe a system for monitoring and controlling i.v. anaesthesia in rats using burst suppression ratio (BSR) detection in the extradural EEG. After bolus injection, peak BSR values of 95% were achieved with propofol 8 mg kg-1, etomidate 3.5 mg kg-1 and alphaxalone 4.5 mg kg-1. Thiopental 32 mg kg-1 produced a peak BSR of 70% (larger doses were not tolerated). Recovery was fastest with propofol, followed by etomidate and alphaxalone with equal duration, and slowest with thiopental. In further experiments, a closed-loop infusion system maintained BSR accurately at targets of 30%, 50%, 70% or 90% for 60 min with propofol or etomidate. During these experiments the infusion rates were found to decrease with time, more so with etomidate (approximately 40%) than with propofol (approximately 20%). Recovery times were 2-3 times longer with etomidate than with propofol. This model demonstrated differences between i.v. anaesthetics and may be useful in screening new compounds in preclinical development.

The statistical properties of the EEG and the MEG are described mathematically as the result of randomly distributed dipoles. These dipoles represent the interactions of cortical neurons. For certain dipole distributions, the first- and second-order moments of the electric and magnetic fields are derived analytically. If the dipoles are in a spherical volume conductor and have no preference for any direction, the variance of a differentially measured EEG-signal is only a function of the electrode distance. In this paper, the theoretically derived variance function will be compared with EEG- and MEG-measurements. It is shown that a dipole with a fixed position and a randomly fluctuating amplitude is an adequate model for the alpha-rhythm. An expression for the covariance between the magnetic field and a differentially measured EEG-signal is derived. This covariance is considered as a function of the magnetometer position, and is compared with the measurements of Chapman et al. [23]. The theory can be used to obtain a (spatial) covariance matrix of the background noise, which occurs in evoked potential measurements. Such a covariance matrix can be used to obtain a maximum likelihood estimator of the dipole parameters in evoked potential studies, to evaluate the merits of the so-called "Laplacian derivation," and for the interpolation of electromagnetic data.

IntroductionThe immune modulatory role of estrogens in inflammation is complex. Both pro- and anti-inflammatory effects of estrogens have been described. Estrogens bind both estrogen receptor (ER)α and β. The contribution of ERα and ERβ to ER-mediated immune modulation was studied in delayed type hypersensitivity (DTH) and in experimental arthritisMethodsER-mediated suppression of rat adjuvant arthritis (AA) was studied using ethinyl-estradiol (EE) and a selective ERβ agonist (ERB-79). Arthritis was followed for 2 weeks. Next, effects of ER agonists (ethinyl-estradiol, an ERα selective agonist (ERA-63) and a selective ERβ agonist (ERB-79) on the development of a tetanus toxoid (TT)-specific delayed type hypersensitivity response in wild type (WT) and in ERα - or ERβ-deficient mice were investigated. Finally, EE and ERA-63 were tested for their immune modulating potential in established collagen induced arthritis in DBA/1J mice. Arthritis was followed for three weeks. Joint pathology was examined by histology and radiology. Local synovial cytokine production was analyzed using Luminex technology. Sera were assessed for COMP as a biomarker of cartilage destruction.ResultsEE was found to suppress clinical signs and symptoms in rat AA. The selective ERβ agonist ERB-79 had no effect on arthritis symptoms in this model. In the TT-specific DTH model, EE and the selective ERα agonist ERA-63 suppressed the TT-specific swelling response in WT and ERβKO mice but not in ERαKO mice. As seen in the AA model, the selective ERβ agonist ERB-79 did not suppress inflammation. Treatment with EE or ERA-63 suppressed clinical signs in collagen induced arthritis (CIA) in WT mice. This was associated with reduced inflammatory infiltrates and decreased levels of proinflammatory cytokines in CIA joints.ConclusionsERα, but not ERβ, is key in ER-mediated suppression of experimental arthritis. It remains to be investigated how these findings translate to human autoimmune disease.

When multi-channel EP recordings are used for source localization, the electrode positions have to be determined with respect to a common reference frame. In this paper a method is described for determining the electrode positions on the head. Since it is difficult to fix electrodes accurately at a priori chosen positions, it is better to measure these positions afterwards. For this we have developed a practical method. The method also finds the best fitting sphere for the electrode position, which is useful when a multi-sphere volume conductor is used in the inverse algorithm.

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