Automated GPR Rebar Analysis for Robotic Bridge Deck Evaluation.

Ground penetrating radar (GPR) is used to evaluate deterioration of reinforced concrete bridge decks based on measuring signal attenuation from embedded rebar. The existing methods for obtaining deterioration maps from GPR data often require manual interaction and offsite processing. In this paper, a novel algorithm is presented for automated rebar detection and analysis. We test the process with comprehensive measurements obtained using a novel state-of-the-art robotic bridge inspection system equipped with GPR sensors. The algorithm achieves robust performance by integrating machine learning classification using image-based gradient features and robust curve fitting of the rebar hyperbolic signature. The approach avoids edge detection, thresholding, and template matching that require manual tuning and are known to perform poorly in the presence of noise and outliers. The detected hyperbolic signatures of rebars within the bridge deck are used to generate deterioration maps of the bridge deck. The results of the rebar region detector are compared quantitatively with several methods of image-based classification and a significant performance advantage is demonstrated. High rates of accuracy are reported on real data that includes thousands of individual hyperbolic rebar signatures from three real bridge decks.

The effects of an H3 receptor antagonist (PF-03654746) with fexofenadine on reducing allergic rhinitis symptoms.

BACKGROUND: Nasal H(3) receptors might have a role in mediating the effects of histamine in patients with allergic rhinitis. OBJECTIVE: This study explored the effect of the potent oral H(3) receptor antagonist PF-03654746 in combination with an oral H(1) receptor antagonist on the objective (acoustic rhinometry) and subjective (symptoms) responses to nasal allergen challenge. METHODS: Twenty patients with out-of-season allergic rhinitis displaying a 30% or greater decrease in minimum nasal cross-sectional area (A(min)) after bolus (ragweed) complete nasal allergen challenge at screening were studied by using a randomized, double-blind, single-dose, 4-way crossover design. Treatments included 10 mg of PF-03654746 plus 60 mg of fexofenadine (group 1), 1 mg of PF-03654746 plus 60 mg of fexofenadine (group 2), 60 mg of fexofenadine/120 mg of pseudoephedrine (group 3), and placebo (group 4). After dosing, subjects underwent complete nasal allergen challenge. Nasal symptom scores (no. of sneezes and 0- to 5-point scores for severity of congestion, itching, and rhinorrhea), A(min) (in square centimeters), and nasal volume (in cubic centimeters) were recorded 15, 30, 45, and 60 minutes after allergen. There was a minimum 10-day washout between periods. RESULTS: The following symptom scores were significantly (P ≤ .05) reduced by active treatments versus placebo: group 1, congestion of -0.7 (SE, 0.3), itching of -1.0 (SE, 0.3), rhinorrhea of -1.3 (SE, 0.3), and sneeze of -8.8 (SE, 1.5); group 2, itching of -0.6 (SE, 0.3), rhinorrhea of -0.8 (SE, 0.3), and sneeze of -9.1 (SE, 1.5); and group 3, rhinorrhea of -0.7 (SE, 0.3) and sneeze of -7.0 (SE, 1.5). There was no significant effect of any treatment on mean A(min) proportion or nasal volume proportion after nasal allergen challenge. CONCLUSIONS: In combination with fexofenadine, single doses of PF-03654746 caused a reduction in allergen-induced nasal symptoms. H(3) receptor antagonism might be a novel therapeutic strategy to further explore in patients with allergic rhinitis.

Time-dependent effects of inhaled corticosteroids on lung function, bronchial hyperresponsiveness, and airway inflammation in asthma.

BACKGROUND: Exhaled nitric oxide (F(ENO)) and exhaled breath condensate (EBC) are noninvasive markers that directly measure airway inflammation and may potentially be useful in assessing asthma control and response to therapy. OBJECTIVE: To examine the time-dependent effects of inhaled corticosteroids on F(ENO) and EBC markers concomitantly with lung function and bronchial hyperresponsiveness. METHODS: Eleven steroid-naive adults with mild-to-moderate persistent asthma were treated with mometasone furoate dry powder inhaler, 400 microg/d, for 8 weeks, followed by a 4-week washout. Forced expiratory volume in 1 second (FEV1), the concentration of methacholine calculated to cause a 20% decline in FEV1 (PC20), F(ENO), EBC pH, and EBC nitrite measurements before, during, and after treatment were analyzed and compared. RESULTS: The mean (SEM) FEV1 increased from 3.01 (0.13) L (82% predicted) to 3.24 (0.18) L (87% predicted) by week 8 (P < .05). The PC20 level increased from 1.28 (0.31) mg/mL to 2.99 (0.51) mg/mL by treatment week 8 (P < .05) and remained relatively stable through washout week 4 (P < .05). The F(ENO) level decreased from 31.1 (4.1) ppb to 20.6 (4.5) ppb by treatment week 1 (P < .01), remained low through treatment week 8 (P < .01), then trended back to the baseline level by washout week 1 (P < .01). The median EBC pH increased from 7.81 (interquartile range, 7.49-8.09) to 8.02 (interquartile range, 7.87-8.12) by treatment week 4, but did not achieve statistical significance. The EBC nitrite level decreased from 17.6 (1.6) microM to 9.3 (0.9) microM by treatment week 8 (P < .01), and remained low throughout washout week 4 (P < .05). There was a negative correlation between F(ENO) and PC20 (Spearman rank correlation coefficient = -0.50, P < .001). CONCLUSION: The F(ENO) level responded the earliest to treatment and withdrawal of inhaled corticosteroids, whereas changes in EBC markers were delayed but more sustained.

Effect of interleukin 13 on bronchial hyperresponsiveness and the bronchoprotective effect of beta-adrenergic bronchodilators and corticosteroids.

BACKGROUND: Fluticasone affects airway bronchial hyperresponsiveness (BHR) and enhances bronchodilation and bronchoprotection induced by beta-adrenergic agonists. Interleukin 13 (IL-13), however, induces BHR. OBJECTIVE: To test the hypotheses that fluticasone inhibits BHR after either allergen sensitization or IL-13 administration and that fluticasone restores the bronchodilation and bronchoprotective effects of beta-agonists. METHODS: The BHR to methacholine induced by IL-13 or ovalbumin was determined in BALB/c mice, and the provocation concentration of methacholine that caused an increase in enhanced pause in expiration of 200% (PC200) was calculated. We compared this response to methacholine in control mice with the response after treatment with IL-13 receptor alpha 2-IgGFc fusion protein (IL-13R alpha 2) (an IL-13 blocker), fluticasone, albuterol, salmeterol, fluticasone-albuterol, and fluticasone-salmeterol. RESULTS: IL-13R alpha 2 (PC200, 17.59) completely blocks the BHR-induced effects of IL-13 (PC200, 7.28; P < .005). After IL-13 therapy (PC200, 5.90; P < .005), 1 mg/mL of albuterol (PC200, 3.38; P = .33), fluticasone (PC200, 4.59; P = .40), or fluticasone plus 50 microg/mL of salmeterol (PC200, 5.59; P = .11) showed no significant bronchoprotection. In nonsensitized mice, fluticasone plus 0.25 microg/mL of salmeterol (PC200, 25.90; P < .005) showed significantly greater bronchoprotection than did salmeterol alone (PC200, 11.08; P = .26). Fluticasone plus 0.3 mg/mL of albuterol and fluticasone plus 1 mg/mL of albuterol were significantly more protective than was fluticasone or albuterol alone in ovalbumin-sensitized mice. CONCLUSIONS: The protective effects of fluticasone, beta-agonists, and fluticasone plus beta-agonists are significantly less in IL-13-treated mice than in nonsensitized or ovalbumin-sensitized mice.

Time-dependent inhibition of histamine-induced cutaneous responses by oral and intramuscular diphenhydramine and oral fexofenadine.

BACKGROUND: Diphenhydramine is often the treatment of choice for acute urticarial or allergic reactions despite its adverse effects of sedation and impairment. Second- and third-generation histamine1-antihistamines are generally devoid of these adverse effects but are typically not used because of a perceived slower onset of action. OBJECTIVE: To examine the time-dependent effects of oral fexofenadine and oral and intramuscular diphenhydramine to reduce histamine-induced wheal-and-flare responses. METHODS: Eighteen healthy patients were included in a double-blind, placebo-controlled, 3-way, randomized, crossover study with oral fexofenadine (180 mg) and oral and intramuscular diphenhydramine (50 mg). Histamine-induced skin tests were performed before and more than 6 hours subsequent to dosing. The primary end point was time to induce a 50% reduction in histamine-induced flare. Secondary end points included change from baseline at each time point in wheal-and-flare responses and area under the curve at more than 6 hours for flare. RESULTS: No significant differences were found in the 50% inhibitory responses of histamine-induced flares among the 3 groups (P = .09). No significant differences were found among the 3 groups in change from baseline at each time point except for 30 minutes during which fexofenadine had no inhibitory effect. Area under the curve analyses for wheal-and-flare responses revealed no differences among treatments at more than 6 hours. CONCLUSION: Diphenhydramine tended to work more rapidly than fexofenadine, but the differences were not statistically significant. Given the adverse effect profile of diphenhydramine, but only marginal onset of action advantage, the risk-to-benefit ratio may be more favorable for oral fexofenadine when treating an acute urticarial or allergic reaction.

Intranasal noninhaled carbon dioxide for the symptomatic treatment of seasonal allergic rhinitis.

BACKGROUND: Noninhaled intranasal carbon dioxide (CO2) has been shown to be effective in the abortive treatment of migraine headache. Migraine headache is associated with trigeminal neuronal activation and release of calcitonin gene-related peptide, events also implicated in allergic rhinitis. Intranasal CO2 might inhibit trigeminal neuronal activation and suppress the release of calcitonin gene-related peptide. OBJECTIVE: We studied whether noninhaled intranasal CO2 would be effective in the treatment of seasonal allergic rhinitis. METHODS: We conducted a single-center, randomized, double-blind, placebo-controlled, parallel-group study. Treatment consisted of either CO2 (verum) or air (placebo) at a 2:1 ratio administered in each nostril for 60 seconds per nostril at a flow rate of 10 mL/s. The primary efficacy end point was the change from baseline in total nasal symptom score (TNSS), the sum of congestion, rhinorrhea, itching, and sneezing scored on a 0- to 5-point scale, at 30 minutes. RESULTS: Eighty-nine subjects received treatment, 60 with CO2 and 29 with placebo, and all subjects completed the study. CO2 resulted in a statistically significant improvement in TNSS at 30 minutes over placebo (absolute changes of 5.0 for CO2 and 2.2 for placebo, P = .00019). Improvement from baseline in TNSS (CO2 vs placebo) was statistically significant at 10 minutes and remained so for 24 hours. CONCLUSION: Two 60-second intranasal CO2 treatments resulted in rapid (10 minutes) and sustained (24 hours) relief of seasonal allergic rhinitis symptoms.

Safety of the intranasal toll-like receptor 4 agonist CRX-675 in allergic rhinitis.

BACKGROUND: CRX-675 is an aqueous formulation of a toll-like receptor 4 agonist and an inducer of TH1 responses. Studies in allergic dogs showed that pretreatment with CRX-675 reduced nasal congestion induced by allergen challenge. OBJECTIVE: To study the safety of intranasal CRX-675 treatment in patients with seasonal allergic rhinitis. METHODS: We conducted a single-center, randomized, double-blind, placebo-controlled, dose-escalating safety trial of single doses of CRX-675 given intranasally before intranasal ragweed challenges. Patients with ragweed-induced seasonal allergic rhinitis received increasing concentrations of ragweed to determine the dose that would result in a 30% reduction in nasal volume (PD30) during screening. Two weeks later, each patient was rechallenged with their assigned PD30 ragweed dose. Fourteen days later, patients were treated with either placebo (n = 16) or CRX-675 (2, 20, 100, or 200 microg intranasally, n = 12 per arm) 24 hours before a subsequent PD30 ragweed challenge. Patients were rechallenged with ragweed 14 days thereafter. RESULTS: No serious or severe adverse events were reported. Most adverse events were mild (grade 1) and either were considered unrelated to CRX-675 or resolved without intervention. The adverse event profile of CRX-675-treated patients was similar to that of placebo-treated patients, and no dose-related toxic effects were observed. There was no clear trend in the ability of CRX-675 to inhibit nasal allergen challenge responses, but improvement in nasal symptom scores was observed at 100 microg. CONCLUSIONS: This preliminary trial suggests that intranasally applied CRX-675 is safe at the doses tested. Appropriate dosing and timing will ultimately define its potential therapeutic role for allergies.

Exhaled nitric oxide in children with asthma receiving Xolair (omalizumab), a monoclonal anti-immunoglobulin E antibody.

OBJECTIVE: To evaluate the effect of a humanized monoclonal antibody to immunoglobulin E, omalizumab (Xolair, Novartis Pharmaceuticals, East Hanover, NJ; Genentech Inc, South San Francisco, CA), on airway inflammation in asthma, as indicated by the fractional concentration of exhaled nitric oxide (FE(NO)), a noninvasive marker of airway inflammation. Xolair was approved recently by the US Food and Drug Administration for moderate-to-severe allergic asthma in adolescents and adults. STUDY DESIGN: As an addendum at 2 sites to a randomized, multicenter double-blind, placebo-controlled trial, FE(NO) was assessed in children with allergic asthma over 1 year. There were 3 consecutive study periods: 1) stable dosing of inhaled beclomethasone dipropionate (BDP) when the dose was optimized (period of 16 weeks); 2) inhaled steroid-reduction phase (period of 12 weeks), during which BDP was tapered if subjects remained stable; and 3) open-label extension phase, during which subjects receiving placebo were switched to active omalizumab (period of 24 weeks). The primary outcome was area under the FE(NO) versus time curve (AUC) for adjusted FE(NO), defined as the ratio of FE(NO) at each time point compared with the value at baseline. RESULTS: Twenty-nine subjects participated and were randomized to omalizumab (n = 18) and placebo (n = 11) treatment groups in a 2:1 ratio dictated by the main study. There was a significant difference for age, resulting in a difference in absolute forced expiratory volume in 1 second but no difference in asthma severity based on the forced expiratory volume in 1 second percentage predicted. Baseline BDP dose was comparable between groups, as were baseline values of mean FE(NO) (active: 38.6 +/- 25.6 ppb; placebo: 52.7 +/- 52.9 ppb). The degree of BDP dose reduction during the steroid-reduction and open-label phases was equivalent between the omalizumab and placebo-treated groups; subjects in the omalizumab- and placebo-treated groups had reduced their BDP dose by an average of 51% and 60%, respectively, at the end of the steroid-reduction phase and by 68% and 94%, respectively, by the end of the open-label period. In the active and placebo groups, 44% and 27% and 75% and 73% of subjects had stopped use of inhaled corticosteroids at the end of the steroid-reduction and open-label phases, respectively. There was no significant difference between the active and placebo groups during the steroid-stable phase for AUC of adjusted nitric oxide (1.31 +/- 1.511 vs 1.45 +/- 0.736). However, during the steroid-reduction phase, the variability of adjusted FE(NO) in the placebo-treated group was greater than that of the omalizumab-treated group at most visits, with a significant difference between groups for AUC of adjusted nitric oxide (0.88 +/- 0.69 vs 1.65 +/- 1.06). FE(NO) fell from 82.1 +/- 55.6 ppm at the end of the steroid-reduction phase to 33.3 +/- 21.6 ppb at the end of the open-label period in the placebo group who were placed on active omalizumab. This decrease occurred while the mean dose of BDP remained very low. Analysis of FE(NO) over 52 weeks of omalizumab treatment in the active group demonstrated that there was a significant reduction from baseline to the end of the open-label period (41.9 +/- 29.0 to 18.0 +/- 21.8 ppb) despite a high degree of steroid reduction. CONCLUSION: In this preliminary study based on FE(NO), a noninvasive marker of airway inflammation, treatment with omalizumab may inhibit airway inflammation during steroid reduction in children with allergic asthma. The degree of inhibition of FE(NO) was similar to that seen for inhaled corticosteroids alone, suggesting an antiinflammatory action for this novel therapeutic agent in asthma. This is in keeping with recent evidence that omalizumab inhibits eosinophilic inflammation in induced sputum and endobronchial tissue.