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Acoustic data were recorded on two vertical line arrays (VLAs) deployed in the New England Mud Patch during the Seabed Characterization Experiment 2017 in about 75 m of water. The sound recorded during the passage of merchant ships permits identification of singular points for the waveguide invariant ß for mode pairs (1,n):ß1,n,for n=2,3,4,5, in the 15-80 Hz band. Using prior geophysical information and an acoustic data sample from the merchant ship KALAMATA, a geoacoustic model M of the seabed was developed. Then, using data samples from other merchant ships, a feature-ensemble maximum entropy method is employed to infer the statistical properties of geoacoustic parameter values for the sound speeds in a surface mud layer and a deep sand layer. Technical challenges include a sparsity of observed singular points, the unique identification of mode pairs for an observed singular point, and the deviation of the waveguide from horizontal stratification. A geoacoustic model M is developed that reproduced the observed ß≈-1 for f < 20 Hz and mode cutoff features at about 15 Hz. The statistical low-frequency inference of the singular point structure from multiple ships provides evidence of an angle of intromission at the water sediment interface with an average sound speed ratio of about 0.986 and an average sound speed for the deeper sand layer of about 1775 m/s.

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To calculate the impulse response of a bubble cloud in a compressible medium, a methodology is developed that incorporates multiple scattering effects between bubbles and coherent interactions of their individual scattered fields. This method is based on a perturbation theory, and provides for an approximate solution formulated by adding a perturbation to the mathematical description of a linear problem. The solution is defined as a power series, where the first term of the expansion corresponds to the solution of a linear uncoupled equation. The convergence of the expansion is determined by the parameters of the physical bubbles and the acoustic interactions. The model is successfully applied to describe experimental measurements of a model bubble cloud response in a shallow freshwater environment.

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Acoustic measurements were made on a sand ridge on the New Jersey continental shelf. Data collected on two L arrays separated by 20 km from a single multi-frequency tow suggest small horizontal environmental variability. Values for the sound speed structure of the seabed are extracted by first applying a geo-acoustic inversion method to broadband and narrowband acoustic data from short-range sources. Then, a parabolic equation algorithm is used to properly include the bathymetry and sub-bottom layering. Finally, the frequency dependence of the seabed attenuation is inferred by optimizing the model fit to long-range transmission loss data in the 50-3000 Hz band.

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The estimation of long memory is often restricted by missing data. We examine the effects on the estimation of long memory of three simple gap-filling techniques: interpolation, random, and mean filling. Numerical simulations show that the gap-filling techniques introduce significant deviations from the expected scaling behavior for both persistent and antipersistent time series. For persistent time series the interpolation method provides a reliable estimation of long memory for scales longer than the largest likely gap.

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The aim of this study was to determine which anaesthetic and vasoconstrictor preparations UK Otorhinolaryngologists use for rhinological surgery, with particular reference to cocaine and adrenaline. The incidence and types of adverse reactions to cocaine were also recorded. A postal survey of all BAO-HNS consultant members was performed. Of the 360 consultant surgeons included in the survey, the majority still use peri-operative cocaine on a regular basis, 66 per cent use cocaine and adrenaline together and more than 40 per cent use cocaine in paediatric patients. Sixteen per cent of respondents did not use cocaine. Only 11 per cent of surgeons had experienced cocaine toxicity in their patients, with only one recorded case of mortality. Most surgeons in the UK use cocaine because of the superior operative field it provides and because they consider it to be safe even with adrenaline. The actual incidence of adverse reactions to cocaine is low, with serious complications being less common than the risks from general anaesthesia. Cocaine remains a valuable agent in the armamentarium of the rhinologist.

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The routine use of topical anaesthesia during flexible nasendoscopy has been questioned, and the degree to which topical vasoconstrictors can affect patient discomfort has yet to be elucidated. Patients' experiences with Lignocaineand phenylephrine, Lignocaine alone, xylometazoline and no preparation were compared. One hundred patients were recruited in this double-blind, randomised control trial and put into these four groups. Each patient completed a visual analogue scoring chart to determine the severity of unpleasantness and other undesirable effects (pain, bad taste, burning, choking, numbness and difficulty in swallowing). The results confirmed that vasoconstriction is a major contributing factor towards reducing overall unpleasantness (P = 0.022), topical anaesthesia can produce a bad taste (P = 0.022), and that none of the preparations have any effect on the pain during nasendoscopy. In conclusion, xylometazoline is recommended for nasendoscopy as it is effective and is significantly cheaper than the other preparations. Not using any preparations leads to the experience of severe symptoms.

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The effects of cocaine on endothelial cell macromolecular transport, electrical resistance, and morphology were assessed. In confluent endothelial monolayers grown on microporus filters, cocaine (0.01 to 1 mmol/L) induced a rapid concentration-dependent increase in permeability to peroxidase and low density lipoprotein. Along with increased transport, the cocaine effect was paralleled by a decrease in transendothelial electrical resistance. Alterations in membrane resistance were fully reversible following washout of the drug, providing evidence that cocaine does not cause permanent injury to the integrity of the monolayer. Cocaines major metabolites, benzoylecgonine and ecgonine methyl ester, had minimal effect on electrical resistance properties, whereas monolayer impedance was markedly depressed by the novel cocaine/alcohol metabolite, cocaine ethyl ester (cocaethylene). Morphologic studies of cocaine-treated endothelial cells revealed a marked disruption of F-actin and the formation of intercellular gaps; no evidence of cell lysis and/or detachment was noted. Forskolin, a potent activator of adenylate cyclase known to promote the endothelial cell barrier function, impaired cocaine-induced changes in electrical resistance and morphology. Cocaine, however, had no effect on resting levels of intracellular adenosine 3',5'-cyclic monophosphate (cAMP) in confluent endothelial monolayers. In summary, the results indicate that cocaine directly induces structural defects in the endothelial cell barrier which enhance the transport of macromolecular tracers, the mechanism does not appear to involve intracellular cAMP.

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The aim of this prospective study was to determine the suitability of 'direct listing' of patients for tonsillectomy by their General Practitioner. All General Practitioners were issued guidelines outlining the indications and contraindications for direct listing. One hundred consecutive patients, referred over a 6-month period, were screened by an otolaryngologist. Thirty-three of these patients were referred inappropriately. The high rate of inappropriate referrals would suggest that this is an unacceptable practice.

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Vascular shear stress increases when blood flow or blood viscosity increases or when vessel diameter decreases. In the systemic circulation, shear stress is a potent stimulus for endothelial nitric oxide synthesis. We studied isolated rat lungs to determine whether increasing shear stress increases nitric oxide synthesis in the pulmonary circulation. Lungs were given the vasoconstrictor, U46619 (a thromboxane analogue), and perfused at constant flow rates or at constant pressure, since constant pressure perfusion minimizes changes in shear stress with vasoconstriction. The subsequent effect of the NOS inhibitor, N omega-methyl-L-arginine (LMA), or the soluble guanylyl cyclase inhibitor, 6-anilino-5,8-quinolinodione (LY83583) was assessed. Changes in pulmonary vascular resistance (PVR), pulmonary vascular compliance, and perfusate cyclic GMP concentration were measured as indicators of nitric oxide synthesis. The effect of the cyclic GMP-specific (type V) phosphodiesterase inhibitor, zaprinast, on perfusate cyclic GMP concentrations was also examined. An infusion of U46619 consistently increased PVR and decreased compliance. LMA and LY83583 also increased PVR in U46619-treated lungs perfused at constant flow rates, primarily by increasing precapillary resistance. LMA had no effect in U46619-treated lungs perfused at constant pressure. Perfusate cyclic GMP concentrations increased significantly after U46619 in lungs perfused at constant flow rates, but cyclic GMP levels did not change after U46619 in lungs perfused at constant pressure. Zaprinast also increased perfusate cyclic GMP, demonstrating that increases in intracellular cyclic GMP are reflected in circulating cyclic GMP concentrations. We conclude that vasoconstriction with U46619 increases nitric oxide synthesis in isolated rat lungs. Lungs perfused at constant pressure respond differently to NOS inhibitors compared to those perfused at constant flow, suggesting that shear stress may increase nitric oxide synthesis in the lung. Perfusate concentrations of cyclic GMP reflect activation of soluble guanylyl cyclase in this model.

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The association of sensorineural hearing loss and ulcerative colitis is well documented and it is speculated that this is autoimmune in origin. A case in a 12-year-old boy is described, that initially responded to steroid therapy, but four years later resulted in bilateral, profound sensorineural hearing loss in spite of good control of his bowel disease. Immunological tests may provide a clue as to the aetiology of suspected cases of autoimmune inner ear disease. Immediate treatment with steroids with or without immunosuppressive therapy is essential as delay may lead to irreversible hearing loss.

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It has been postulated that the bacteraemia rate following guillotine tonsillectomy is lower than that following dissection tonsillectomy due to intra-operative compression of tonsillar blood vessels by the guillotine. The aim of this study was to evaluate the incidence of bacteraemia following dissection and guillotine tonsillectomy. Sixty-four patients undergoing elective tonsillectomy for recurrent acute tonsillitis were randomly selected, 32 underwent dissection tonsillectomy and 32 guillotine tonsillectomy. Positive intra-operative blood cultures were obtained in 16 patients (25 per cent), nine (28.1 per cent) of the dissection group and seven (21.8 per cent) of the guillotine group. There was no significant difference between the two methods (Chi-squared test, p = 0.77).

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The traditional meatoplasty operations performed for chronic otitis externa, which has entered the 'fibrotic' phase, are often unsatisfactory because the results in terms of canal patency, hearing gain and patient satisfaction are variable. Although the use of laser in chronic ear surgery is well recognized, it has not been previously reported as a meatoplasty technique. Ten KTP laser meatoplasty operations were performed on eight patients with chronic otitis externa. This pilot study shows the technique to be effective, fast and with a high patient satisfaction rate in the short-term (mean follow-up period 9.3 months). The average increase in hearing thresholds was 24 dB HL. Significant patient benefit was obtained in at least six out of eight patients using the Belfast rule of thumb. The technique has many advantages over the traditional meatoplasty operations but the long-term results require evaluation.

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We studied the effects of nitric oxide synthase (NOS) inhibitors and nitric oxide (NO.) donors on ischemia-reperfusion (I/R)-induced microvascular permeability increase in isolated buffer-perfused rat lungs. Microvascular permeability (Kf,c) was significantly increased in lungs subjected to 45 min of ischemia followed by 30 min of reperfusion. Lungs that were pretreated with 300 and 600 microM N omega-nitro-L-arginine methyl ester (L-NAME), 1, 300, and 600 microM NG-monomethyl-L-arginine (L-NMMA), or 600 microM L-N6-(1-iminoethyl) ornithine (L-NIO) still showed significant increases in Kf,c after I/R. Lungs that were pretreated with 5 mM L-NAME or 5 mM N omega-nitro-D-arginine methyl ester showed no increase in Kf,c after I/R. However, both compounds at these concentrations produced significant decreases in perfusate pH. The decreased pH was responsible for the protective effects, since lungs pretreated with 5 mM L-NAME and supplemented with NaHCO3 to prevent the perfusate pH decrease still showed a significant elevation in Kf,c after I/R. In additional experiments, NO.donors were administered to isolated lungs at the onset of reperfusion. Spermine-NO (100 microM) and S-nitroso-N-acetylpenacillamine (300 microM) both prevented the increase in Kf,c associated with I/R. We conclude from these studies that peroxynitrite does not mediate microvascular permeability increase after lung I/R injury in this model, and exogenous NO. does not exacerbate injury; rather, it prevents microvascular damage.

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It is generally accepted that microvascular permeability is controlled by intercellular endothelial cell gap size. This process is controlled in endothelial cell monolayers and peripheral blood vessels by calmodulin (CaM)-dependent myosin light-chain kinase (MLCK), which phosphorylates MLC20 with subsequent actin-myosin interaction. In the present study both CaM and MLCK blockers were studied during ischemia-reperfusion (I/R)-induced injury in isolated buffer-perfused rat lungs. The effects of a calcium ionophore (CaI) were tested in isolated intact rat lungs to compare the effects of increasing intracellular Ca2+ to I/R-induced damage. Because protein kinase C (PKC) could also be a mediator of I/R injury, a PKC inhibitor was studied in lungs subjected to either I/R or CaI. In lungs subjected to I/R alone, a fivefold increase in microvascular permeability occurred after 30 min of reperfusion (P < 0.001), and a tenfold increase was present after an additional 60 min of reperfusion (P < 0.01). Pretreatment of the I/R lungs with a CaM inhibitor (trifluoperazine, 100 microM) or with a MLCK inhibitor (ML-7,500 nM) blocked the microvascular damage at both 30 and 90 min of reperfusion. When the CaM inhibitor was introduced into the venous reservoir after 46 min of reperfusion, after the microvascular damage was present, no further increase in microvascular permeability occurred. Pretreatment of the lungs with a PKC inhibitor (staurosporine, 100 nM) did not alter the magnitude of the increased microvascular permeability produced by I/R or the time course of the damage. The calcium ionophore A23187 (7.5 microM) caused increases in Kfc values similar to those produced by I/R. Pretreatment of A23187-treated lungs with a CaM inhibitor produced no protective effect on the microvascular injury at 30 min after administration. Pretreatment of the CaI-challenged lungs with staurosporine significantly increased the microvascular barrier injury at 30 min compared with that occurring with I/R. When a beta-adrenergic receptor agonist (isoproterenol, 10 microM) was introduced to the lung after CaI-induced damage had occurred, no further increase in microvascular permeability was observed, and a trend toward reversal of injury occurred. We conclude from these studies that CaM/MLCK/MLC20 system is involved in our model of I/R-induced rat lung injury but is not involved in lung injury associated with Ca2+ entering the cell.

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The pulmonary vascular responses to changes in perfusate viscosity were studied in isolated rat lungs treated with the nitric oxide synthase (NOS) inhibitors, N omega-nitro-L-arginine methyl ester (L-NAME) and N omega- monomethyl-L-arginine (L-NMMA). Lungs were isolated according to standard protocols and perfused with varying concentrations of albumin in physiological salt solution (PSS) and with low, intermediate, and normal hematocrits using washed erythrocytes. Pressure-flow curves were generated by increasing pulmonary arterial pressure (PPA) while keeping pulmonary venous pressure (PPV) constant and measuring flow at each pressure interval. Neither perfusate flow nor pulmonary vascular resistance changed after L-NAME or L-NMMA (300 microM) at any pressure interval in lungs perfused with 4 and 10% albumin/PSS. In lungs perfused with 20% albumin/PSS, L-NMMA decreased flow at all PPA tested except 10 cm H2O (P < 0.05). L-NAME decreased flow in lungs perfused with normal (39.2 +/- 2.1%) hematocrits at all PPA tested. Conversely, L-NAME decreased flow in lungs perfused with low and intermediate hematocrits only at the highest pressure intervals. L-Arginine, when given after NOS inhibitors, failed to restore flow to baseline values in any group of lungs. N omega-nitro-D-arginine methyl ester (300 microM) did not change flow at any pressure interval in lungs perfused with normal (43 +/- 1.5%) hematocrit, washed erythrocytes. We conclude that lungs perfused with intermediate and normal hematocrit, washed erythrocytes, as well as with high-viscosity albumin/PSS solutions, show increased pulmonary vascular responses to NOS inhibitors.

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Although the cardiovascular benefits of the hormone estrogen are at least, in part, mediated by its antiproliferative effect on vascular smooth muscle, its action on the migration of these cells is unknown. To explore this relationship, female rat aortic smooth muscle cells were grown in hormone-free medium, and the effect of various concentrations of beta-estradiol on directed cellular migration was measured in vitro using a microwell Boyden chamber apparatus. Migration of smooth muscle cells to the known chemoattractants platelet-derived growth factor, insulin-like growth factor-1, and fibronectin (all at peak doses for migratory activity) was attenuated by beta-estradiol (0.5 to 10 ng/ml) in a concentration-dependent manner relative to control cells treated with vehicle (0.01% ethanol). This response was insensitive to pretreatment with indomethacin and was stereospecific (17 alpha-estradiol lacked response). Like beta-estradiol, the synthetic estrogen diethylstilbestrol attenuated directed smooth muscle cell migration whereas the male hormone testosterone was ineffective. Additional studies showed that beta-estradiol-mediated suppression of migration was inhibited by the anti-estrogen ICI 164,384 and the gene transcription inhibitor actinomycin D. These are the first results demonstrating a reduction in directed smooth muscle cell migration by beta-estradiol. The mechanism of this estrogen-mediated response appears to involve conventional estrogen receptors.

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The present study investigated the ability of atropine and different muscarinic receptor subtypes to affect acetylcholine (ACh)-induced bronchoconstriction and vasodilation in the isolated rat lung model. ACh (10(-7) M) given after U-46619 decreased total (RT), precapillary, and postcapillary vascular resistances and increased peak airway pressure. Atropine (20 microM) decreased RT and precapillary and postcapillary vascular resistances and blocked ACh-induced increases in peak airway pressure. The M1-selective agonist McN-A-343 (1.3 x 10(-5) M) decreased RT from 40.27 +/- 2.98 to 29.20 +/- 2.81 cmH2O.l-1.min-100 g lung wt (P = 0.01), and ACh caused no further dilation. The M1-selective antagonist pirenzepine (1.6 x 10(-6) M) blocked ACh-induced vasodilation. The M2-selective antagonist gallamine (7.5 x 10(-7) M) decreased RT from 45.50 +/- 3.19 to 34.86 +/- 1.25 cmH2O.l-1.min.100 g lung wt (P < 0.05), and after gallamine, ACh further decreased RT to 28.59 +/- 1.75 cmH2O.l-1.min.100 g lung wt (P < 0.01). Neither the selective muscarinic agonists nor antagonists affected peak airway pressures. We conclude that ACh-induced vasodilation in isolated rat lungs preconstricted with U-46619 is mediated by M1 receptors. Atropine-induced vasodilation in this model is mediated through the inhibition of the M2 receptor. We postulate that this represents either a blockade of postganglionic receptors, permitting release of vasodilator substances from local nerve terminals, or a direct vasodilatory effect on the vascular smooth muscle.

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To evaluate the adenosine systems ability to reverse the endothelial damage produced by ischemia and reperfusion (I/R), we studied several different selective adenosine-receptor agonists and antagonists, a protein kinase A inhibitor, and a beta-adrenoreceptor antagonist in isolated buffer-perfused rat lungs. I/R (45 min/105 min) produced a sixfold increase in endothelial permeability as measured by the capillary filtration coefficient. Both a selective A2-receptor agonist (CGS-21680, 300 nM) and a beta-receptor agonist (isoproterenol, 10 microM) reversed the increased microvascular permeability. A nonselective adenosine-receptor antagonist (SPT, 20 microM) and a selective A1-receptor antagonist (DPCPX, 10 nM) had no effect on increased microvascular permeability. Also, isoproterenol and CGS-21680 reversed the damage being introduced after a selective A1-receptor agonist (CCPA, 100 nM). The nonspecific adenosine A1- and A2-receptor agonist NECA (12 nM) appeared to desensitize the A2 receptors and a protein kinase A inhibitor, adenosine-3',5'-cyclic monophosphothioate (Rp-cAMPS, 100 microM), blocked the reversal of endothelial damage by isoproterenol or A2-receptor agonist. Propranolol (100 microM) blocked the effect of isoproterenol but not the effect of CGS-21680. From this study we conclude that A2-receptor activation reverses endothelial damage associated with I/R by a mechanism independent of beta-receptors or Gi protein. However, a protein kinase A-3',5',-cyclic adenosine monophosphate pathway is activated by both the adenosine systems and beta-receptor activation.

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