Delayed hydrocephalus after excision of a colloid cyst: a case report.

Background: In this case report we describe an unusual case of a patient who underwent resection of a colloid cyst and then presented 6 weeks postoperatively with obstructive hydrocephalus. There appear to be no prior reports of such a delayed complication after colloid cyst resection.

Case Presentation: A 50-year-old Caucasian woman underwent resection of a colloid cyst with an uncomplicated perioperative course.

Specific inhibition of the plasmodial surface anion channel by dantrolene.

The plasmodial surface anion channel (PSAC), induced on human erythrocytes by the malaria parasite Plasmodium falciparum, is an important target for antimalarial drug development because it may contribute to parasite nutrient acquisition. However, known antagonists of this channel are quite nonspecific, inhibiting many other channels and carriers. This lack of specificity not only complicates drug development but also raises doubts about the exact role of PSAC in the well-known parasite-induced permeability changes.

Malaria parasites are rapidly killed by dantrolene derivatives specific for the plasmodial surface anion channel.

Dantrolene was recently identified as a novel inhibitor of the plasmodial surface anion channel (PSAC), an unusual ion channel on Plasmodium falciparum-infected human red blood cells. Because dantrolene is used clinically, has a high therapeutic index, and has desirable chemical synthetic properties, it may be a lead compound for antimalarial development. However, dantrolene derivatives would need to preferentially interact with PSAC over the sarcoplasmic reticulum (SR) Ca2+ release channel to avoid unwanted side effects from antimalarial therapy.

Plasmodial surface anion channel-independent phloridzin resistance in Plasmodium falciparum.

The plasmodial surface anion channel (PSAC) is an unusual ion channel induced on the human red blood cell membrane after infection with the malaria parasite, Plasmodium falciparum. Because PSAC is permeant to small metabolic precursors essential for parasite growth and is present on red blood cells infected with geographically divergent parasite isolates, it may be an ideal target for future antimalarial development. Here, we used chemically induced mutagenesis and known PSAC antagonists that inhibit in vitro parasite growth to examine whether resistance mutations in PSAC can be readily induced.