A case report of refractory warm autoimmune hemolytic anemia treated with plasmapheresis and rituximab.

A 30-year-old male presented with severe, warm autoimmune hemolysis 17 months subsequent to a matched, unrelated peripheral hematopoietic stem cell transplant. The patient responded poorly to conventional therapy with steroids and immunoglobulin, prompting the initiation of rituximab. On account of persistent, severe hemolysis, therapeutic plasma exchange was employed as a bridge until the rituximab therapy became effective.

Critical molecular determinants of voltage-gated sodium channel sensitivity to mu-conotoxins GIIIA/B.

GIIIA/B mu-conotoxins block the rat skeletal muscle sodium channel (rNa(v)1.4) with high affinity by binding to specific residues in the pore. However, human Na(v)1.