13 research outputs found

    Regional distribution in female representation in US otolaryngology faculty

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    Objectives: To quantify the current proportion of women in otolaryngology at different levels of professorship and determine whether these proportions differ by US region. Methods: Academic rank and gender at all ACGME-accredited otolaryngology programs in the United States were determined from departmental websites, Doximity, and LinkedIn from November 2021 to March 2022. Individuals were then further organized using US Census Bureau-designated regions. Results: Among the 2682 faculty positions at 124 ACGME-accredited programs, women held 706 (26.3%) of these positions. Female representation was highest at the assistant professorship level, with women holding 286 (37.2%) positions out of a total 769. At the associate professorship level, women held 141 (27.6%) of the 511 total positions. The largest gender disparity is seen at the full professorship level; only 69 (13.6%) positions out of 508 were held by women. Out of every region and rank, only assistant professorship in the West had no significant difference in percentages of men and women (p = .710). Female representation of professors in the Northeast was significantly lower than that of our reference group (the South; β =β€‰βˆ’10.9, p = .020). Conclusions: Otolaryngology has exhibited great progress in increasing female representation, with assistant professorship in the West reaching gender parity. However, the gender gap at other faculty levels still leaves much to be desired, particularly in senior ranks. The lack of otolaryngologists at senior ranks is detrimental to mentorship of junior faculty, residents, and medical students. Renewed efforts should be made to decrease the gender disparity in the South, Northeast, and particularly at the professorship level.</p

    Intestinal Tissues Induce an SNP Mutation in <em>Pseudomonas aeruginosa</em> That Enhances Its Virulence: Possible Role in Anastomotic Leak

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    <div><p>The most feared complication following intestinal resection is anastomotic leakage. In high risk areas (esophagus/rectum) where neoadjuvant chemoradiation is used, the incidence of anastomotic leaks remains unacceptably high (∼10%) even when performed by specialist surgeons in high volume centers. The aims of this study were to test the hypothesis that anastomotic leakage develops when pathogens colonizing anastomotic sites become <em>in vivo</em> transformed to express a tissue destroying phenotype. We developed a novel model of anastomotic leak in which rats were exposed to pre-operative radiation as in cancer surgery, underwent distal colon resection and then were intestinally inoculated with <em>Pseudomonas aeruginosa,</em> a common colonizer of the radiated intestine. Results demonstrated that intestinal tissues exposed to preoperative radiation developed a significant incidence of anastomotic leak (>60%; p<0.01) when colonized by <em>P. aeruginosa</em> compared to radiated tissues alone (0%). Phenotype analysis comparing the original inoculating strain (MPAO1- termed P1) and the strain retrieved from leaking anastomotic tissues (termed P2) demonstrated that P2 was altered in pyocyanin production and displayed enhanced collagenase activity, high swarming motility, and a destructive phenotype against cultured intestinal epithelial cells (i.e. apoptosis, barrier function, cytolysis). Comparative genotype analysis between P1 and P2 revealed a single nucleotide polymorphism (SNP) mutation in the <em>mexT</em> gene that led to a stop codon resulting in a non-functional truncated protein. Replacement of the mutated <em>mexT</em> gene in P2 with <em>mexT</em> from the original parental strain P1 led to reversion of P2 to the P1 phenotype. No spontaneous transformation was detected during 20 passages in TSB media. Use of a novel virulence suppressing compound PEG/Pi prevented <em>P. aeruginosa</em> transformation to the tissue destructive phenotype and prevented anastomotic leak in rats. This work demonstrates that <em>in vivo</em> transformation of microbial pathogens to a tissue destroying phenotype may have important implications in the pathogenesis of anastomotic leak.</p> </div

    Scanning electron microscopy (SEM) images of anastomosis tissues.

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    <p>Blue arrows indicate healed anastomosis (30x), intact intestinal epithelium (300x), and macrophages on epithelial surface (3,500x) in group II. Orange arrows indicate discontinuity near or at the anastomosis (30x), disrupted intestinal epithelium (300x), and a high degree of bacterial colonization/adherence at the edge of non-healed anastomoses (5,000x). 50 images from each group of 5 mice were obtained, and representative images are displayed.</p

    Wound healing assay.

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    <p>The P2 strain recovered from anastomotic tissues (<i>in vivo</i>) and the P2 strain recovered after co-incubation of MPAO1 with anastomotic tissues (<i>ex vivo</i>) similarly destroy wounded epithelial IEC-18 monolayers.</p

    SNP mutation in <i>MexT</i> is responsible for P2 phenotype.

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    <p>(A) Genome DNA sequence comparative map of <i>P. aeruginosa</i> MPAO1-P1 and MPAO1-P2 at the DSM-1707 backbone annotated with the MexT locus. Grey and teal bands: annotated coding regions; red tick: location of MexT locus; green ticks: tRNAs; black ticks: rRNAs; inner circle GC content. (B–D) swarming motility in (B) MPAO1-P1 (P1), (C) MPAO1-P2 (P2), and (D) MPAO1-P2 in which <i>mexT</i> was replaced by <i>mexT</i> gene amplified from MPAO1-P1 (P2/<i>mexT</i><sub>P1</sub>). (E) Growth curves at 100 Β΅g/ml chloramphenicol demonstrating acquisition of chloramphenicol resistance in P2/<i>mexT</i><sub>P1.</sub> (F) Collagenase activity measured by fluorescence of fluorescent labeled gelatin as a substrate. nβ€Š=β€Š6, *p<0.01. Results are representative of 3 independent experiments.</p

    Anastomotic leak in rats exposed to pre-operative radiation and intestinal <i>P. aeruginosa</i>.

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    <p>(A) Sketch of anastomosis model and treatment groups. Treatment groups: I, anastomosis only; II, anastomosis + cecal injection of <i>P. aeruginosa</i> MPAO1, 10<sup>7</sup> CFU; III, radiation + anastomosis; IV, radiation +anastomosis + cecal injection of <i>P. aeruginosa</i> MPAO1 (10<sup>7</sup> CFU). Black arrows indicate the anastomotic site. (B) Excised and exposed suture lines of anastomotic sites. All suture lines are grossly intact except for group IV where ulceration/dehiscence is noted by the black arrow. (C) H&E staining of anastomotic tissues. Arrows and brackets indicate width of tissue apposition at suture line. (D, D’, E) Methylene blue assessment of anastomotic integrity demonstrating rare to no leaks in groups I–III (D) and gross extravasation in group IV (D’). Arrows indicate the site of anastomosis. (E) Incidence of anastomotic leak between groups. nβ€Š=β€Š12 (group I), nβ€Š=β€Š16 (group II), nβ€Š=β€Š9 (group III), nβ€Š=β€Š18 (group IV), *p<0.01.</p

    P1 and P2 phenotypes of <i>P. aeruginosa</i> MPAO1.

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    <p>(A) Pyocyanin production seen as green color pigmentation on solid PIA and liquid TSB media. (B) Kaplan-Meyer survival curves of <i>C. elegans</i> N2 feeding on P1 and P2. Cumulative survival is represented of 2 experiments, nβ€Š=β€Š7/dish, 5 dishes/experiment, p<0.01. (C) Swarming motility. (D) Wound healing assay. Wound width was calibrated and measured using the MicroSuite software for imaging applications (Olympus SZX16). Wound healing of βˆ’100% indicates a 2 fold increase in the wound width compared to the baseline width. nβ€Š=β€Š12, *p<0.01. (E,F) Collagenase activity of P1 and P2 measured by degradation of fluorescent labeled collagen I (E) and collagen IV (F) as substrates. nβ€Š=β€Š6, *p<0.01. Fluorescence values were normalized to cell density measured by absorbance at 600 nm. Results are representative of 3 independent experiments. (G) RAPD fingerprint analysis demonstrating a similar genetic background of the P1 and P2 phenotype strains.</p
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