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IMPORTANCE Large and complex nasal septal perforations may cause considerable patient discomfort and are challenging to repair. Posterior septal resection (PSR) is a simple procedure and can be incorporated into the surgical management algorithm for this patient population. OBJECTIVE To evaluate PSR for the treatment of symptomatic complex and large nasal septal perforations. DESIGN, SETTING, AND PARTICIPANTS Retrospective medical chart review from 1995 through 2007 of patients who underwent PSR. Medical charts were reviewed, and a follow-up telephone questionnaire was performed. INTERVENTIONS Posterior septal resection. MAIN OUTCOMES AND MEASURES Improvement of selected symptoms after PSR. RESULTS Twenty-one patients were identified, 16 patients had thorough documentation of perioperative information contained in their medical charts, and 12 patients were available for follow-up survey. All patients tolerated the procedure well without long-term sequelae from surgery. Overall nasal discomfort was significantly improved in 12 of 12 patients (P < .001). All nasal symptom scores of obstruction, pain, whistling, drainage, crusting, and epistaxis showed statistically significant (P < .05) improvement from preoperative values. Nasal obstruction and crusting were symptoms that improved with high statistical significance (P < .001). Patients reported on average a 79% improvement (range, 45%-100% improvement) in nasal airway, with only 1 patient reporting no improvement. All patients were satisfied with their surgery and would undergo the procedure again and recommend it to others. CONCLUSIONS AND RELEVANCE Posterior septal resection provides overall patient satisfaction and improvement in subjective nasal symptom scores when used for large and complex septal perforations. This simple procedure may be included in the treatment algorithm of large and complex symptomatic septal perforations.

Natural killer (NK) cells are an early source of immunoregulatory cytokines during the innate immune response to viruses, bacteria, and parasites. NK cells provide requisite IFN-γ to monocytes for the elimination of obligate intracellular pathogens. IL-1β is a pro-inflammatory cytokine produced by monocytes (i.e. a monokine) during the early immune response to infection, but its role in promoting human NK cell IFN-γ production is unknown. The current study examines the ability of the monokine IL-1β, plus IL-12, to costimulate IFN-γ production by resting CD56^bright and CD56^dim human NK cell subsets. CD56^bright NK cells stimulated with IL-1β plus IL-12 produced abundant IFN-γ protein, while little IFN-γ was produced in identical cultures of CD56^dim cells. In addition, upon activation with IL-1β, CD56^bright NK cells exhibited considerably greater phosphorylation of extracellular signal-regulated kinases p42/44 as compared to CD56^dim NK cells. Quantitative PCR analysis showed brisk induction of IFN-γ gene expression following costimulation with IL-1β plus IL-12 in CD56^bright NK cells, but intracellular flow cytometry revealed that only a fraction (42±2.3%) of CD56^bright NK cells account for this high IFN-γ production. These data suggest that the monokine IL-1β is a potent costimulus of IFN-γ production by a subset of NK cells following infectious insult.

Inflammation likely has a role in the early genesis of certain malignancies. Interleukin (IL)-15, a proinflammatory cytokine and growth factor, is required for lymphocyte homeostasis. Intriguingly, the expression of IL-15 protein is tightly controlled by multiple posttranscriptional mechanisms. Here, we engineered a transgenic mouse to overexpress IL-15 by eliminating these posttranscriptional checkpoints. IL-15 transgenic mice have early expansions in natural killer (NK) and CD8+ T lymphocytes. Later, these mice develop fatal lymphocytic leukemia with a T-NK phenotype. These data provide novel evidence that leukemia, like certain other cancers, can arise as the result of chronic stimulation by a proinflammatory cytokine.