Faculty Bibliography

Plexiform fibrohistiocytic tumor (PFT) is a low-grade, superficial, soft tissue neoplasm with a limited but significant ability to metastasize. This type of tumor only rarely presents in the skin of the head and neck. Clinicians first encountering young patients with facial neoplasia, such as a PFT, might be unaware of its exact oncologic potential and instead be primarily concerned with the cosmetic outcome. We treated a 17-year-old boy with a PFT on his cheek who was initially treated only by shave biopsy. The tumor subsequently recurred and metastasized to the cervical lymph nodes 3 years after the initial biopsy. Therefore, appropriate initial therapy for PFT requires complete excision with negative resection margins

Escherichia coli grows over a wide range of pHs (pH 4.4 to 9.2), and its own metabolism shifts the external pH toward either extreme, depending on available nutrients and electron acceptors. Responses to pH values across the growth range were examined through two-dimensional electrophoresis (2-D gels) of the proteome and through lac gene fusions. Strain W3110 was grown to early log phase in complex broth buffered at pH 4.9, 6.0, 8.0, or 9.1. 2-D gel analysis revealed the pH dependence of 19 proteins not previously known to be pH dependent. At low pH, several acetate-induced proteins were elevated (LuxS, Tpx, and YfiD), whereas acetate-repressed proteins were lowered (Pta, TnaA, DksA, AroK, and MalE). These responses could be mediated by the reuptake of acetate driven by changes in pH. The amplified proton gradient could also be responsible for the acid induction of the tricarboxylic acid (TCA) enzymes SucB and SucC. In addition to the autoinducer LuxS, low pH induced another potential autoinducer component, the LuxH homolog RibB. pH modulated the expression of several periplasmic and outer membrane proteins: acid induced YcdO and YdiY; base induced OmpA, MalE, and YceI; and either acid or base induced OmpX relative to pH 7. Two pH-dependent periplasmic proteins were redox modulators: Tpx (acid-induced) and DsbA (base-induced). The locus alx, induced in extreme base, was identified as ygjT, whose product is a putative membrane-bound redox modulator. The cytoplasmic superoxide stress protein SodB was induced by acid, possibly in response to increased iron solubility. High pH induced amino acid metabolic enzymes (TnaA and CysK) as well as lac fusions to the genes encoding AstD and GabT. These enzymes participate in arginine and glutamate catabolic pathways that channel carbon into acids instead of producing alkaline amines. Overall, these data are consistent with a model in which E. coli modulates multiple transporters and pathways of amino acid consumption so as to minimize the shift of its external pH toward either acidic or alkaline extreme.

IL-13 potently stimulates eosinophilic and lymphocytic inflammation and alveolar remodeling in the lung, effects that depend on the induction of various matrix metalloproteinases (MMPs). Here, we compared the remodeling and inflammatory effects of an IL-13 transgene in lungs of wild-type, MMP-9-deficient, or MMP-12-deficient mice. IL-13-induced alveolar enlargement, lung enlargement, compliance alterations, and respiratory failure and death were markedly decreased in the absence of MMP-9 or MMP-12. Moreover, IL-13 potently induced MMPs-2, -12, -13, and -14 in the absence of MMP-9, while induction of MMPs-2, -9, -13, and -14 by IL-13 was diminished in the absence of MMP-12. A deficiency in MMP-9 did not alter eosinophil, macrophage, or lymphocyte recovery, but increased the recovery of total leukocytes and neutrophils in bronchoalveolar lavage (BAL) fluids from IL-13 transgenic mice. In contrast, a deficiency in MMP-12 decreased the recovery of leukocytes, eosinophils, and macrophages, but not lymphocytes or neutrophils. These studies demonstrate that IL-13 acts via MMPs-9 and -12 to induce alveolar remodeling, respiratory failure, and death and that IL-13 induction of MMPs-2, -9, -13, and -14 is mediated at least partially by an MMP-12-dependent pathway. The also demonstrate that MMPs-9 and -12 play different roles in the generation of IL-13-induced inflammation, with MMP-9 inhibiting neutrophil accumulation and MMP-12 contributing to the accumulation of eosinophils and macrophages.

The patterns of cellular organization and intercellular communication in excitable tissues are extraordinarily complex. This article reviews a new set of tools for the imaging and statistical analysis of multicellular circuits in real time, and describes the findings from analysis of neuronal networks from slices of rodent neocortex loaded with fluorescent calcium indicators. Spontaneous activation of multineuronal networks was found to be generated by both synaptic and intrinsic mechanisms, and these cortical microcircuits have a precise spatial organization. In general, these techniques and methods of analysis, which can detect patterns of activity with single-cell and millisecond resolution, are applicable to the study of calcium and electrical signaling in cell populations of excitable tissues such as the heart, skeletal muscle, and the nervous system

Approximately 2,000 patients a year are diagnosed with oral cancer in New York State. In an effort to control this deadly disease, Governor George Pataki has taken a leadership role in the United States by mandating and funding training for dentists in the prevention and early detection of oral cancer. The purpose of this article is to highlight the epidemiology of oral cancer, to show how the dental profession can contribute to the health of the citizens of New York State, and to provide practical guidelines for both tobacco cessation intervention and utilization of existing technology for the early detection of oral cancer and precancerous conditions in the general dental practice setting

The power function exponent for loudness is traditionally determined by means of a process of magnitude estimation. It is demonstrated in this paper that the exponent can also be obtained by using the procedure of absolute identification of sound intensity. It has been shown that subjects' responses to tones of a given intensity are distributed in a normal distribution whose variance depends on the range, R, over which the tones are distributed. By means of a standard statistical transformation, the normal density in log space is converted to the corresponding probability density in linear space. The power function exponent can then be obtained directly from the linear probability density. We also suggest that there is a direct relationship between the information calculated from experiments on absolute identification of sound intensity and the neurophysiological, poststimulus histogram measured in a nerve fiber in the auditory nerve

OBJECTIVE: To determine the role of genetic mechanisms in the development of pediatric obstructive sleep apnea syndrome (OSAS). DESIGN: Genetic-epidemiologic survey of families of index children with laboratory-confirmed OSAS. SETTING: Tertiary care academic medical center. PARTICIPANTS: Six-hundred nap polysomnograms performed in our institution's pediatric sleep laboratory over a 6-year period (1994-2000) were reviewed, and the 497 children who tested positive for OSAS were selected. A caretaker of 200 of these index patients was contacted, and 115 were enrolled in the study. INTERVENTION AND MAIN OUTCOME MEASURE: Questionnaire-type telephone interviews were conducted with the current caretakers of the index patients to assess the distribution of sleep-disordered breathing in the first-degree relatives. RESULTS: Data were collected for 445 first-degree relatives (256 adults and 189 children) of the 115 index patients. Habitual snoring was found in 194 (43.6%) of the family members, while symptoms highly suggestive of OSAS (nighttime 'gasping for air' or 'cessation of breathing') were found in 91(20.4%). Sixty-eight (26.6%) of the adult first-degree relatives and 23 (12.2%) of the pediatric first-degree relatives had symptoms highly suggestive of OSAS. Of the 115 index children, 50 (43.5%) had at least 1 relative with symptoms highly suggestive of OSAS; 6 (1.3%) of the first-degree relatives had sleep study results positive for OSAS, 4 (0.9%) were using nasal continuous positive airway pressure, and 21 (4.7%) had prior surgery for the treatment of OSAS. CONCLUSION: Considering the established prevalence of OSAS in the general population (2%-4%), the results of this study support a familial basis for this disorder

OBJECTIVE: To determine the relationship between child behavior and quality of life before and after tonsillectomy and adenoidectomy by means of a standardized assessment of child behavior, the Child Behavior Checklist (CBCL), and a validated quality-of-life survey of pediatric obstructive sleep apnea, the OSA-18. DESIGN: Before-after study. SETTING: Hospital-based pediatric otolaryngology practice in a metropolitan area. PARTICIPANTS: Sixty-four children (mean [SD] age, 5.8 [3.1] years; 36 boys, 28 girls) who underwent tonsillectomy and adenoidectomy for treatment of sleep-disordered breathing or recurrent tonsillitis. INTERVENTION: Parents or caretakers completed the OSA-18 and the CBCL for ages 2 to 3 years or 4 to 18 years before surgery and 3 months postoperatively. MAIN OUTCOME MEASURES: The OSA-18 mean survey scores and change scores, and the CBCL total problem T scores and change in total problem T scores. RESULTS: The mean (SD) preoperative OSA-18 score was 3.9 (1.5) and change score was 2.3 (95% confidence interval, 1.9-2.7). The mean total problem score was 7.3 points lower after surgery (95% confidence interval, 4.9-9.7), indicating a significant decrease (P<.001, matched t test). The preoperative CBCL total problem score was consistent with abnormal behavior for 16 children (25%), but only 5 children (8%) scored in the abnormal range postoperatively (P =.03, log-likelihood ratio test). The OSA-18 preoperative mean survey score had fair to good correlation with the preoperative CBCL total problem T score (r = 0.50, P<.001, Pearson correlation), and the OSA-18 change score had fair to good correlation with the change in CBCL total problem T score (r = 0.54, P<.001, Pearson correlation). CONCLUSIONS: Behavioral and emotional difficulties are found in children with sleep-disordered breathing before treatment and improve after intervention. Scores on a standardized measure of assessment of behavior demonstrate significant correlation with scores on a validated quality-of-life instrument

OBJECTIVE: To determine the reliability of the assessment of laryngoscopic findings potentially associated with laryngopharyngeal reflux disease (LPRD). STUDY DESIGN: Prospective randomized blinded study. METHODS: One hundred twenty video segments of rigid fiberoptic laryngeal examinations were prospectively analyzed by five otolaryngologists blinded to patient information and were scored according to several variables potentially associated with LPRD. Separate assessments of the degree of erythema and degree of edema were scored on a five-point scale for the anterior commissure, membranous vocal fold, and interarytenoid region. Similarly, interarytenoid pachydermia, likelihood of LPRD involvement, and severity of LPRD findings were assessed. For each of these scored physical findings, inter-rater and intrarater reliabilities were determined. RESULTS: The inter-rater reliabilities of the laryngoscopic findings associated with LPRD were poor. Intraclass correlation coefficients were 0.161 and 0.461 for edema of the arytenoids and membranous vocal folds, respectively (P <.001). Intraclass correlation coefficients were 0.181 and 0.369 for erythema of the arytenoids and membranous vocal folds, respectively (P <.001). Raters demonstrated poor agreement as to the severity of LPRD findings (intraclass correlation coefficient, 0.265) and the likelihood of an LPRD component for dysphonia (intraclass correlation coefficient, 0.248). Similarly, intrarater reliability was extremely variable for the various physical findings, with Kendall correlation coefficients ranging from -0.121 to 0.837. CONCLUSIONS: Accurate clinical assessment of laryngeal involvement with LPRD is likely to be difficult because laryngeal physical findings cannot be reliably determined from clinician to clinician. Such variability makes the precise laryngoscopic diagnosis of LPRD highly subjective