Nonpruritic erythematous plaques.

A 43-year-old man visiting Texas from Hawaii sought care at our dermatology clinic for nonpruritic erythematous plaques on his chest, back, and extremities. The patient reported occasional numbness in his fingers and feet, but denied constitutional symptoms. The patient, who'd had these symptoms for a year, had been previously diagnosed with chronic urticaria and treated with oral antihistamines. He reported that the lesions were never particularly pruritic and he had not responded to previous treatments. An avid outdoorsman, our patient was born and raised in Texas and had been living in Hawaii. His past medical history was significant for severe hand eczema and when asked about medications he was taking, he listed cetirizine, doxepin, and hydroxyzine. On physical examination the patient had multiple pink to red, nonscaly to minimally scaly flat plaques on his forehead, chest, proximal upper extremities, lower back, and distal lower extremities. A 4-mm punch biopsy was taken from a lesion on his lower back and sent for histologic evaluation. The patient's erythrocyte sedimentation rate, rapid plasma reagin, and complete blood count were all within normal limits. What is your diagnosis? How would you treat this patient?

An unusual cause of knee pain 10 years after arthroscopy.

Arthroscopic surgery, although relatively minimally invasive, is associated with specific complications. Cases of instruments retained in the knee joint after arthroscopy have been reported. There have been reports of scalpel blades detaching into the joint during the approach that were immediately retrieved, with or without arthrotomy. We report the case of a scalpel blade retained in the knee joint for 10 years after arthroscopy. This case demonstrates the need for the surgeon and the whole operating room staff to be aware of the instrumentation and to systematically check the instruments at the beginning, middle, and end of the procedure. The significance of reporting this case is to make the orthopaedic community aware of possible complications that can occur even with relatively "low-risk" procedures.

Activation of PI3-kinase is required for AMPA receptor insertion during LTP of mEPSCs in cultured hippocampal neurons.

Hippocampal CA1 homosynaptic long-term potentiation (LTP) is expressed specifically at activated synapses. Increased insertion of postsynaptic alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptors (AMPARs) appears to be crucial for CA1 LTP. However, the mechanism underlying AMPAR insertion during LTP remains largely unknown. We now report that phosphatidylinositol 3-kinase (PI3K) is complexed with AMPARs at synapses and activated by selective stimulation of synaptic N-methyl-D-aspartate (NMDA) receptors. Activation of the AMPAR-associated PI3K is required for the increased cell surface expression of AMPARs and LTP. Thus, our results strongly suggest that the AMPAR-PI3K complex may constitute a critical molecular signal responsible for AMPAR insertion at activated CA1 synapses during LTP, and consequently, this lipid kinase may serve to determine the polarity of NMDA receptor-dependent synaptic plasticity.

Upregulation of Kv 1.4 protein and gene expression after chronic spinal cord injury.

After spinal cord injury (SCI), white matter tracts are characterized by demyelination and increased sensitivity to the K(+) channel blocker 4-aminopyridine (4-AP). These effects appear to contribute to neurological impairment after SCI, although the molecular changes in K(+) channel subunit expression remain poorly understood. We examined changes in gene expression of the 4-AP-sensitive voltage-gated K(+) channel Kv 1.4 after chronic SCI in the rat. Quantitative immunoblotting showed that Kv 1.4 protein was significantly increased at 6 weeks, but not at 1 week, after SCI in spinal cord white matter. Kv 1.4 was localized to astrocytes, oligodendrocytes, and oligodendrocyte progenitor cells but not to axons in both the normal and the injured spinal cord white matter. Because glial cells proliferate after SCI, we used immunogold electron microscopy to quantify Kv 1.4 protein in individual glial cells and found a sixfold increase of Kv 1.4 in cells of the oligodendrocyte lineage after chronic injury. Finally, quantitative in situ hybridization showed that Kv 1.4 mRNA was significantly upregulated in spinal cord white matter, but not gray matter, after SCI. In summary, we show that Kv 1.4 is expressed in glial cells and not in axons in the rat spinal cord white matter and that its expression is markedly increased in cells of the oligodendrocyte lineage after chronic SCI. Given that K(+) channels play a role in glial cell proliferation, cells exhibiting changes in Kv 1.4 expression may represent proliferating oligodendroglia in the chronically injured spinal cord.