Otogenic intracranial complications can be fatal if not managed appropriately. Broad-spectrum intravenous antibiotics for 6 weeks is usually sufficient treatment. Management of the intracranial disease takes precedence, but direct drainage of the abscess may not be necessary if a patient's symptoms, neurologic status, and radiographic findings progress favorably. A high index of suspicion should be maintained on all patients presenting with symptoms not typically seen with routine otitis media.

Telomerase is a reverse transcriptase that maintains chromosome integrity through synthesis of repetitive telomeric sequences on the ends of eukaryotic chromosomes. In the yeast Saccharomyces cerevisiae, telomere length homeostasis is achieved through negative regulation of telomerase access to the chromosome terminus by telomere-bound Rap1 protein and its binding partners, Rif1p and Rif2p, and positive regulation by factors such as Ku70/80, Tel1p, and Cdc13p. Here we report the identification of mutations within an N-terminal region (region I) of the yeast telomerase catalytic subunit (Est2p) that cause telomere lengthening without altering measurable catalytic properties of the enzyme in vitro. These telomerase mutations affect telomere length through a Ku-independent mechanism and do not alter chromosome end structure. While Tel1p is required for expression of the telomere-lengthening phenotype, Rif1p and Rif2p are not, suggesting that telomere overextension is independent of Rap1p. Taken together, these data suggest that specific amino acids within region I of the catalytic subunit of yeast telomerase play a previously unanticipated role in the response to Tel1p regulation at the telomere.Telomeres are nucleoprotein structures that cap the ends of linear eukaryotic chromosomes. In most species, these termini are composed of tandem, short G-rich repeats and associated protein complexes (reviewed in reference 56). Telomeres play an essential role in genome stability by preventing recognition of the normal chromosome terminus as a DNA double-strand break. However, the inability of the conventional DNA polymerase machinery to fully replicate terminal sequences results in gradual erosion of telomeric repeats, leading to checkpoint activation and cellular senescence. In cells that maintain proliferative potential, this end replication problem is counteracted by telomerase, a reverse transcriptase capable of synthesizing telomeric repeats onto chromosome ends using an intrinsic RNA template (18,19). In budding yeast, TLC1 and EST2 encode the template RNA and reverse transcriptase subunit, respectively, of the catalytic core of the telomerase holoenzyme (27,31,50). As predicted, strains lacking these genes undergo progressive telomere shortening and senescence (referred to as the EST [ever shorter telomere] phenotype). Mutations of three additional genes (EST1, EST3, and EST4 [CDC13]) result in the same phenotype (27,34,41). However, unlike strains lacking EST2 or TLC1, strains bearing these mutations retain telomerase catalytic activity, suggesting that these proteins are essential regulators of telomere replication in vivo (30,41).Est2p belongs to a family of proteins (TERT; telomerase reverse transcriptase) that contains a domain characteristic of reverse transcriptases in its C-terminal half (31). Sequence alignment among numerous TERT proteins as well as functional analysis in ciliate, yeast, and human TERT (1,12,13,36,38,39,59) TERT region I contributes several functions to the telomerase holoenzyme, many of ...

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AlloDerm reacts similarly when comparing the postparotidectomy bed to the dorsum. DermaMatrix induces a more marked inflammatory reaction in the postparotidectomy bed when compared with the dorsum.

This telerobotic system proved to be capable of being rapidly deployed to the upper airways while exerting minimal forces to the surrounding structures and successfully simulated injection medialization laryngoplasty.