Simultaneous occurrence of lymphoepithelial cysts, cytomegalovirus and mycobacterial infections in the intraparotid lymph nodes of a patient with AIDS.

We report the unusual simultaneous occurrence of lymphoepithelial cysts, cytomegalovirus (CMV) and mycobacterial infections in the intraparotid lymph nodes of a 52-year-old AIDS patient who died of disseminated mycobacteriosis. Although cytomegalovirosis is a common finding in the salivary glands of HIV patients, the association of CMV inclusions with lymphoepithelial cyst (LC) has not been previously reported. Parotid mycobacterial infection is an uncommon finding, despite its usual disseminated presentation in HIV patients. These data emphasize that in immunosuppressed patients, simultaneous diseases of the parotid gland may occur and should be considered for diagnosis and treatment.

Total reconstruction of the alar cartilages with a partially split septal cartilage graft.

The alar cartilage is a unique structure that supports the tip of the nose, keeps the external valve open, and plays an important role in tip aesthetics. Very often the plastic surgeon needs to reconstruct this cartilage, as in secondary rhinoplasties when the lower lateral cartilage is overresected. Many authors have described cartilage grafts taken from the ear and septum, mounted and stitched in various manners, with some very good results. In patients with thin skin, though, any irregularity or distortion in the grafts becomes visible after a short time postoperatively. The authors present an alternative to reconstructing alar cartilage symmetrically using one graft. This graft is obtained by shaping septal cartilage in an "L" form, with a 135-deg angle (instead of a 90-deg angle) between its legs, and then splitting the smaller leg, obtaining a strut from the longer leg and two "lateral crura" from the shorter leg.

Inositol 1,4,5-trisphosphate induced Ca2+ release from chloroquine-sensitive and -insensitive intracellular stores in the intraerythrocytic stage of the malaria parasite P. chabaudi.

Isolated P. chabaudi parasites were permeabilized with digitonin and the function of intracellular Ca2+ stores was studied using the Ca2+ indicators arsenazo III or Fluo 3-acid in the medium. Addition of the second messenger InsP3 (5 microM) to permeabilized parasites leads to Ca2+ release into the medium, with the mean extent of release being 40 nmol Ca2+/10(8) cells. This Ca2+ release was completely abolished in the presence of heparin, an InsP3 receptor antagonist. The amount of Ca2+ released was approximately 50% reduced when InsP3 was added subsequent to the discharge of the endoplasmic reticulum (ER) Ca2+ pool with the SERCA (sarcoplasmic ER Ca2+ ATPase) inhibitors thapsigargin and tBHQ (2,5-di(ter-butyl)-1,4 benzohydroquinone). The thapsigargin- and tBHQ-sensitive pool account for 20 nmol of Ca2+/10(8) cells. If InsP3 was added after the discharge of the residual Ca2+ by addition of either the K+/H+ uncoupler nigericin or the antimalarial drug chloroquine, no further Ca2+ release was observed. This is the first report of InsP3-induced Ca2+ release in a parasite protozoa. In addition our finding that chloroquine depletes an InsP3-sensitive Ca2+ compartment, raises the possibility that the InsP3-dependent Ca2+ release from this store might be important for the regulation of growth and differentiation of the parasite.

Characterization of Ca2+ transport activity associated with a non-mitochondrial calcium pool in the rodent malaria parasite P. chabaudi.

Non-mitochondrial calcium deposits were investigated in the intraerythrocytic malaria parasite Plasmodium chabaudi at the trophozoite stage by means of arsenazo III in the presence of ATP and the mitochondrial poisons, antimycin and oligomycin. Addition of vanadate and 2,5-di-(t-butyl)-1,4-hydroquinone (BHQ), both known to interact with SERCA pump, induced calcium release by permeabilized parasites when the medium free calcium concentration was kept at 3.5 microM. The tumor promoter thapsigargin also caused elevation of the free calcium concentration in permeabilized parasites. Our results support the view that P. chabaudi sequesters calcium in an exchangeable form and maintains its calcium homeostasis by way of an endoplasmic reticulum Ca2+ pump.