CONCLUSION

Chemical exposure within the Mohs laboratory can

present a significant occupational hazard. Acutely toxic and potentially carcinogenic formaldehyde was found at high levels in a relatively standard laboratory configuration. A laboratory can be designed with a combination of physical environment and operational protocols that minimizes hazards and creates a safe working environment.

The authors have indicated no significant interest with commercial supporters.”
“Study Design. A prospective study in 19 patients after cervical laminoplasty, using magnetic resonance imaging.

Objective. To evaluate the value of spinal cord shift at 24 hours after cervical laminoplasty.

Summary of Background Data. Postoperative C5 palsy is a noticeable complication within 1 week after cervical laminoplasty. The root tethering CCI-779 cost due to the posterior shift

of the spinal cord after laminoplasty was reported as one of the causes of C5 palsy. However, the spinal cord shift after surgery within 1 week is unknown.

Methods. The posterior shift of the spinal cord was measured in 19 consecutive patients on magnetic resonance images at 24 hours and 2 weeks after cervical laminoplasty.

Results. PR-171 The mean posterior shift of the spinal cord at 24 hours was 2.8 mm, with the maximum at the C5 level, decreasing to 1.9 mm at 2 weeks. The posterior shift of the spinal cord at C5 was correlated with the amount of the dura mater at C4, C5, and C6 levels. In a patient with right C5 palsy, posterior shift at C5 level HSP990 was 5.5 mm, decreasing to 3.0 mm at 2 weeks after surgery. The posterior shift of the spinal cord was not correlated with the sagittal alignment.

Conclusion. The posterior shift of the spinal cord at 24 hours had a tendency to shift more posteriorly

than that observed at 2 weeks after cervical laminoplasty. C5 palsy may be prevented if the expansion of dura mater, which is strongly correlated with the posterior shift, can be controlled.”
“Purpose of review

An increased expression of type I interferon (IFN) regulated genes (an IFN signature) has been reported in blood and tissue cells from patients with SLE and other autoimmune diseases. We review the possible mechanisms behind the IFN signature as well as clinical and therapeutic consequences of this observation.

Recent findings

Autoantigens from dying cells trigger plasmacytoid dendritic cells to a continuous synthesis of type I IFN, which is promoted by natural killer (NK) cells and B cells. A growing number of genes connected to type I IFN production and response associates with an increased susceptibility to autoimmunity. Besides type I IFN, type III IFN (IFN-lambda) may contribute to the IFN signature.