Conservative management of infections in cochlear implant recipients.

OBJECTIVE: The goal of this study was to evaluate a conservative management strategy of postoperative infection after cochlear implantation. METHODS: A retrospective review of the medical records of 108 cochlear implant patients operated on at the University of California, San Francisco between 1991 and 2000 and 133 cochlear implant patients from the University of Iowa between 1997 and 2000 showed 4 patients with evidence of postoperative infections. The clinical presentation, intervention, laboratory results, and outcome are analyzed in each case. RESULTS: Minimal surgical intervention with limited incision and drainage with prolonged postoperative antibiotics was effective in treating postoperative cochlear implant infections without the need for device removal. Implant function remained unaffected after surgery. CONCLUSION: Postoperative cochlear implant infections can be effectively controlled with limited surgical and prolonged medical management. Chronic implant infections may be explained by a primary immunodeficiency. With appropriate treatment leading to infection control, a conservative management strategy is advocated before consideration of device explantation.

Trophic support of cultured spiral ganglion neurons by depolarization exceeds and is additive with that by neurotrophins or cAMP and requires elevation of [Ca2+]i within a set range.

Spiral ganglion neurons (SGNs) require both pre- and postsynaptic contacts to maintain viability. BDNF, NT-3, chlorphenylthio-cAMP, and depolarization (veratridine or elevated [K+]o) all promote survival of SGNs in vitro, depolarization being the most effective. Combining different trophic stimuli increases survival in an additive manner. Neurotrophins and depolarization maintain comparable soma size and neurite extension, but SGNs are shrunken in cAMP. Elevated [K+]o has a biphasic effect on SGN survival; survival improves as [K+]o is raised to 30 mM (30K) and falls as [K+]o is further increased; SGN survival in 80 mM [K+]o (80K) is poor relative to survival in 30K. These responses to elevated [K+]o are potentiated by an L-type channel agonist, whereas L-type Ca2+ channel blockers antagonize the trophic effect of depolarization. Four hours after depolarization, steady-state [Ca2+]i is elevated in SGNs in 30K and further elevated in SGNs in 80K. At 22 hr after depolarization, by which time death of neurons in 80K has begun, elevated [Ca2+]i levels in surviving neurons in 80K are not higher than those in neurons in 30K ( approximately 150-450 nM), suggesting that neurons with high [Ca2+]i are preferentially lost. Veratridine causes oscillatory increases in [Ca2+]i to 250-350 nM. Thus, [Ca2+]i is predictive of cell survival; [Ca2+]i elevated to 100-500 nM in a sustained or oscillatory manner permits SGN survival independent of exogenous neurotrophic factors. Higher [Ca2+]i is associated with cell death.

A timetable of events during programmed cell death induced by trophic factor withdrawal from neuronal PC12 cells.

We describe a timetable of events during programmed cell death (PCD) in neuronal PC12 cells, specifically, Ras signaling, immediate-early gene (IEG) expression, DNA fragmentation and commitment to PCD. Commitment occurs over a period from 10-20 hr after NGF withdrawal. Ras signaling declines rapidly after NGF removal, reaching minimal levels within 2-4 hr, well before the onset of commitment. DNA fragmentation, detected by TUNEL reaction, begins about 24 hr after NGF withdrawal, well after all cells are committed, but coincident with the onset of cell dissolution previously determined by trypan blue exclusion (Mesner et al., 1992). Among the IEGs studied here, c-jun and TIS21 are expressed within 6 hr after NGF withdrawal. Expression of c-fos, egr-1, and TIS11 does not begin until 20 hr after NGF withdrawal. IEG expression generally ends by 24 hr after NGF withdrawal. The IEGs TIS7 and nur77 are not expressed during PCD, yielding a pattern distinct from that following other stimuli. An identical pattern of IEG expression occurs in non-neuronal PC12 cells deprived of serum, although expression begins at 10-14 hr after serum withdrawal. A similar IEG expression pattern was observed in Rat-1 fibroblasts, with various genes expressed 6-18 hr after serum withdrawal. In none of these cell types did expression of the stress-related gene Hsp70 change following trophic factor withdrawal. The distinctive pattern of IEG expression described here should facilitate identification of intracellular regulatory signals active during PCD.

Amyloidoma of the nasopharynx: CT and MR findings.

A case of nasopharyngeal amyloidoma with extensive skull base erosion is presented. CT revealed a large, relatively homogeneous, enhancing lesion; MR revealed a signal intensity iso- or slightly hyperintense compared to muscle on T1- and T2-weighted images, with a moderate degree of contrast enhancement. When an erosive mass is encountered at the skull base in a submucosal location in the nasopharynx, and MR demonstrates short T2 relaxation with signal iso- or slightly hyperintense relative to muscle, amyloidoma should be included in the differential diagnosis.

Dibutyryl cAMP activates bumetanide-sensitive electrolyte transport in Malpighian tubules.

The effects of dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP) and bumetanide (both 10(-4) M) on transepithelial Na+, K+, Cl-, and fluid secretion and on tubule electrophysiology were studied in isolated Malpighian tubules of the yellow fever mosquito Aedes aegypti. Peritubular DBcAMP significantly increased Na+, Cl-, and fluid secretion but decreased K+ secretion. In DBcAMP-stimulated tubules, bumetanide caused Na+, Cl-, and fluid secretion to return to pre-cAMP control rates and K+ secretion to decrease further. Peritubular bumetanide significantly increased Na+ secretion and decreased K+ secretion so that Cl- and fluid secretion did not change. In bumetanide-treated tubules, the secretagogue effects of DBcAMP are blocked. In isolated Malpighian tubules perfused with symmetrical Ringer solution, DBcAMP significantly hyperpolarized the transepithelial voltage (VT) and depolarized the basolateral membrane voltage (Vbl) with no effect on apical membrane voltage (Va). Total transepithelial resistance (RT) and the fractional resistance of the basolateral membrane (fRbl) significantly decreased. Bumetanide also hyperpolarized VT and depolarized Vbl, however without significantly affecting RT and fRbl. Together these results suggest that, in addition to stimulating electroconductive transport, DBcAMP also activates a nonconductive bumetanide-sensitive transport system in Aedes Malpighian tubules.