The agreement between magnetic resonance imaging and arthroscopic findings in temporomandibular joint disorders.

The aim of this retrospective observational study was to assess the potential agreement between independent magnetic resonance imaging (MRI) and arthroscopic findings and their respective contributions to a final diagnosis in patients with refractory temporomandibular joint disorders. Two dentomaxillofacial radiologists and two oral and maxillofacial surgeons scored 50 joints. All observers, who were blinded to additional clinical information, used a specific scoring form and selected one or more diagnostic labels. Agreement between MRI and arthroscopy and their contributions to the final diagnosis were assessed as primary outcomes using Fleiss' kappa. Intra-modality agreement and the correlation between signal intensity ratio (SIR) measurements on MRI and synovitis grading on arthroscopy were assessed as secondary outcomes. Agreement between MRI and arthroscopy was poor. A fair level of agreement was only reached for reduction capacity of the disc and disc perforation. Arthroscopic diagnostic labels matched better with the final diagnosis, suggesting a bigger contribution to that diagnosis. Higher SIR measurements correlated with higher synovitis grading scores for the retrodiscal tissue and the posterior band of the disc. Intra-modality agreement was better in arthroscopy. When blinded to clinical information, arthroscopy and MRI observations can lead to different conclusions. The diagnostic outcomes of both examinations should be considered and integrated into a final diagnosis.

Size dependence of microscopic Hall sensor detection limits.

In this paper the magnetic field detection limits of microscopic Hall sensors are investigated as a function of their lateral size. Hall sensors fabricated from GaAs/AlGaAs heterostructures and silicon are experimentally investigated at different temperatures using Hall effect and noise spectrum measurements. At room temperature a clear size dependence of the detection limit is observed, whereas at low temperatures this dependence is found to disappear. The results are explained using the theory of noise in semiconductors.

Kv7/KCNQ/M-channels in rat glutamatergic hippocampal axons and their role in regulation of excitability and transmitter release.

M-current (I(M)) plays a key role in regulating neuronal excitability. Mutations in Kv7/KCNQ subunits, the molecular correlates of I(M), are associated with a familial human epilepsy syndrome. Kv7/KCNQ subunits are widely expressed, and I(M) has been recorded in somata of several types of neurons, but the subcellular distribution of M-channels remains elusive. By combining field-potential, whole-cell and intracellular recordings from area CA1 in rat hippocampal slices, and computational modelling, we provide evidence for functional M-channels in unmyelinated axons in the brain. Our data indicate that presynaptic M-channels can regulate axonal excitability and synaptic transmission, provided the axons are depolarized into the I(M) activation range (beyond approximately -65 mV). Here, such depolarization was achieved by increasing the extracellular K(+) concentration ([K(+)](o)). Extracellular recordings in the presence of moderately elevated [K(+)](o) (7-11 mm), showed that the specific M-channel blocker XE991 reduced the amplitude of the presynaptic fibre volley and the field EPSP in a [K(+)](o)-dependent manner, both in stratum radiatum and in stratum lacknosum moleculare. The M-channel opener, retigabine, had opposite effects. The higher the [K(+)](o), the greater the effects of XE991 and retigabine. Similar pharmacological modulation of EPSPs recorded intracellularly from CA1 pyramidal neurons, while blocking postsynaptic K(+) channels with intracellular Cs(+), confirmed that active M-channels are located presynaptically. Computational analysis with an axon model showed that presynaptic I(M) can control Na(+) channel inactivation and thereby affect the presynaptic action potential amplitude and Ca(2+) influx, provided the axonal membrane potential is sufficiently depolarized. Finally, we compared the effects of blocking I(M) on the spike after-depolarization and bursting in CA3 pyramidal neuron somata versus their axons. In standard [K(+)](o) (2.5 mm), XE991 increased the ADP and promoted burst firing at the soma, but not in the axons. However, I(M) contributed to the refractory period in the axons when spikes were broadened by a low dose 4-aminopyridine (200 microm). Our results indicate that functional Kv7/KCNQ/M-channels are present in unmyelinated axons in the brain, and that these channels may have contrasting effects on excitability depending on their subcellular localization.