Omni-Directional Scanning Localization Method of a Mobile Robot Based on Ultrasonic Sensors.

Improved ranging accuracy is obtained by the development of a novel ultrasonic sensor ranging algorithm, unlike the conventional ranging algorithm, which considers the divergence angle and the incidence angle of the ultrasonic sensor synchronously. An ultrasonic sensor scanning method is developed based on this algorithm for the recognition of an inclined plate and to obtain the localization of the ultrasonic sensor relative to the inclined plate reference frame. The ultrasonic sensor scanning method is then leveraged for the omni-directional localization of a mobile robot, where the ultrasonic sensors are installed on a mobile robot and follow the spin of the robot, the inclined plate is recognized and the position and posture of the robot are acquired with respect to the coordinate system of the inclined plate, realizing the localization of the robot. Finally, the localization method is implemented into an omni-directional scanning localization experiment with the independently researched and developed mobile robot. Localization accuracies of up to ±3.33 mm for the front, up to ±6.21 for the lateral and up to ±0.20° for the posture are obtained, verifying the correctness and effectiveness of the proposed localization method.

Neuropeptide proenkephalin A is associated with in-hospital mortality in patients with acute intracerebral hemorrhage.

High plasma proenkephalin A (PENK-A) levels are associated with poor clinical outcome after ischemic stroke. However, not much is known regarding the change of its level in acute intracerebral hemorrhage. Thus, we sought to determine PENK-A in plasma of patients with acute spontaneous basal ganglia hemorrhage and evaluate its relation with disease severity and in-hospital mortality. One hundred and two patients and 100 healthy controls were recruited. Plasma samples were obtained on admission for patients and at study entry for controls. Its concentration was measured by chemoluminescence sandwich immunoassay. Plasma PENK-A levels were substantially higher in patients than in healthy controls (235.5±85.4 pmol/L vs. 90.1±31.3 pmol/L; P<0.0001). A forward stepwise logistic regression selected plasma PENK-A as an independent predictor for in-hospital mortality of patients (odds ratio 1.080, 95% confidence interval 1.018-1.147, P<0.001). A multivariate linear regression demonstrated that plasma PENK-A level was positively associated with National Institutes of Health Stroke Scale (NIHSS) score (t=6.189, P<0.001) and hematoma volume (t=5.388, P<0.001). A receiver operating characteristic curve identified a plasma PENK-A level>267.1 pmol/L predicted in-hospital mortality of patients with 80.0% sensitivity and 74.7% specificity (area under curve, 0.836; 95% confidence interval, 0.750-0.902). Its predictive value was similar to NIHSS score's and hematoma volume's (both P>0.05). However, it did not statistically significantly improve the predictive values of NIHSS score and hematoma volume (both P>0.05). Thus, increased plasma PENK-A levels are associated with disease severity and in-hospital mortality after acute intracerebral hemorrhage.

[Changes in expression of gene aba I in biofilm of Acinetobacter baumannii strains isolated from burn patients].

OBJECTIVE: To study the changes in expression of quorum sensing gene aba I in Acinetobacter baumannii (AB) strains isolated from burn patients during biofilm formation process, and its influences on the extracellular matrix of biofilm and drug resistance of AB. METHODS: Six drug-resistant and five drug-sensitive AB strains isolated from wound excretion, blood and venous catheter were collected from burn patients hospitalized in Ruijin hospital of Shanghai Jiao Tong University School of Medicine from January to October 2011. The AB standard strain ATCC 19606 was used as control. (1) Clinical strains and standard strain were normally cultured 10, 24, and 48 h respectively in vitro. The bacteria samples were stained with propidium iodide to measure biofilm thickness with confocal laser scanning microscope. (2) Clinical strains and standard strain were cultured in tubes 10, 24, and 48 h respectively in vitro under shaking condition. The bacteria floating in the medium were regarded as free bacteria, while those adhered to the tube wall as the bacteria within biofilm (biofilm bacteria). Relative expression value of genes aba I and pgaB was detected by real-time fluorescent quantitative PCR with the expression value of the standard strain set at 1. Data were processed with analysis of variance. RESULTS: (1) At post culture hour (PCH) 10, 24, 48, biofilm thickness of clinical strains was thicker than that of standard strain; biofilm thickness of drug-resistant strains [(28.8 ± 0.6), (31.7 ± 1.1), and (38.1 ± 3.1) µm] was respectively thicker than that of drug-sensitive strains [(17.1 ± 0.4), (20.1 ± 1.6), and (25.8 ± 1.7) µm, with F value respectively 1274.38, 206.60, and 61.73, P values all below 0.05]. (2) Biofilm bacteria: at PCH 10, 24, 48, expression values of aba I in drug-resistant strains (6.6 ± 1.7, 25.7 ± 3.5, 9.8 ± 3.6) were much higher than those of drug-sensitive strains (2.7 ± 1.0, 15.0 ± 3.5, 4.7 ± 3.2, with F value respectively 21.82, 25.24, and 6.22, P values all below 0.05); expression values of pgaB in drug-resistant strains (37.4 ± 1.1, 44.5 ± 3.6, 33.1 ± 11.5) were obviously higher than those of drug-sensitive strains (14.6 ± 0.8, 20.0 ± 6.9, 18.7 ± 6.8, with F value respectively 1488.44, 57.26, and 6.01, P values all below 0.05). (3) Free bacteria: at PCH 10, 24, 48, there was no significant statistical difference between drug-resistant strains and drug-sensitive strains in expression value of aba I (with F value respectively 0.24, 2.33, and 0.11, P values all above 0.05); expression values of pgaB in drug-resistant strains (13.8 ± 3.8, 12.5 ± 2.9, 23.7 ± 2.1) were obviously higher than those of drug-sensitive strains (7.0 ± 5.9, 5.0 ± 1.3, 15.6 ± 6.7, with F value respectively 5.44, 28.42, and 7.76, P values all below 0.05). (4) Comparison between biofilm bacteria and free bacteria in resistant strains: expression value of aba I in biofilm bacteria at each time point was respectively higher than that of free bacteria (with F value respectively 43.69, 286.61, and 9.98, P values all below 0.05); expression values of pgaB in biofilm bacteria at PCH 10, 24 were higher than those in free bacteria (with F value respectively 214.26 and 283.20, P values below 0.05). (5) Comparison between biofilm bacteria and free bacteria in sensitive strains: expression value of aba I in BF bacteria at PCH 24 was higher than that of free bacteria (F = 70.28, P < 0.05); expression values of pgaB in biofilm bacteria at PCH 10, 24 were higher than those of free bacteria (with F value respectively 8.03 and 22.62, P values below 0.05). CONCLUSIONS: During biofilm formation process, the increasing expression of quorum sensing gene aba I in drug-resistant AB strains isolated from burn patients may up-regulate the expression of gene pgaB, which leads to high production of extracellular matrix and biofilm formation, and enhances drug resistance of AB.