2-D path following for fixed wing UAV using global fast terminal sliding mode control.

This paper considers the finite time convergence problem of 2-D path following for fixed wing unmanned air vehicle. Firstly, the UAV path following model is divided into an outer guidance loop and an inner control loop. Then, the guidance loop and control loop controllers of the UAV are derived by global fast terminal sliding mode control technique, which is able to guarantee the system state variables converge to expected values in finite time and eliminate the chattering phenomenon caused by the switching control action. Furthermore, the stability of the two-loops system is proven by Lyapunov stability theory. Finally, the simulation results are shown to verify the performance of the proposed method.

Low-loss channel optical waveguide fabrication in Nd(3+)-doped silicate glasses by femtosecond laser direct writing.

Optical waveguides were fabricated in neodymium-doped silicate glass by using a low-repetition-rate (1 kHz) femtosecond laser inscription. Two different types of waveguide structure are fabricated. In the first, guiding occurs in the focal spot. In the second, guiding occurs in the region between the two filaments. The near-field intensity distribution, propagation loss, index profile reconstruction, and calculation of the modal intensity distribution by the beam propagation method of these waveguides are presented. On the basis of near-field intensity distribution of the light guided through the waveguides and the propagation loss measurement, the optimum writing conditions such as the pulse energy and scan velocity were determined. The waveguide written with 2.2 µJ pulse energy and 50 µm/s scan velocity shows strong guidance at 632.8 nm, with an index contrast of 7 × 10(-4) and a propagation loss of ~0.8 dB/cm.

Pitavastatin attenuates AGEs-induced mitophagy via inhibition of ROS generation in the mitochondria of cardiomyocytes.

This study aimed to investigate whether pitavastatin protected against injury induced by advanced glycation end products products (AGEs) in neonatal rat cardiomyocytes, and to examine the underlying mechanisms. Cardiomyocytes of neonatal rats were incubated for 48 hours with AGEs (100 µg/mL), receptor for advanced glycation end products (RAGE), antibody (1 µg/mL) and pitavastatin (600 ng/mL). The levels of p62 and beclin1 were determined by Western blotting. Mitochondrial membrane potential (ΔΨm) and the generation of reactive oxygen species (ROS) were measured through the JC-1 and DCFH-DA. In the AGEs group, the expression of beclin1 was remarkably increased compared to the control group, while the expression of p62 was significantly decreased. AGEs also markedly decreased ΔΨm and significantly increased ROS compared with the control group. After treatment with RAGE antibody or pitavastatin, the level of beclin1 was markedly decreased compared with the AGEs group, but the level of p62 was remarkably increased. In the AGEs+ RAGE antibody group and AGEs+ pitavastatin group, ΔΨm was significantly increased and ROS was remarkably decreased compared with the AGEs group. In conclusion, AGEs-RAGE may induce autophagy of cardiomyocytes by generation of ROS and pitavastatin could protect against AGEs-induced injury against cardiomyocytes.

[Cyclin E overexpression and centrosome amplification in squamous cell carcinoma of oral cavity].

OBJECTIVE: To study the correlation between cyclin E protein overexpression and centrosome amplification in oral squamous cell carcinoma (OSCC). METHODS: Formalin-fixed, paraffin-embedded tissues from 12 normal oral epithelium cases and 46 cases of OSCC were studied. Their centrosome status was analyzed by indirect immunofluorescence double staining with antibodies to centrosome protein gamma-tubulin and cytokeratin. The expression of cyclin E protein was studied by immunohistochemical methods. The correlation between cyclin E protein expression and centrosome amplification in OSCC was statistically analyzed by SPSS 12.0. RESULTS: Thirty-seven of the 46 OSCC cases (80.4%) studied showed evidence of centrosome amplification, as signified by enlargement and/or increase in number of centrosomes, while normal oral epithelium possessed centromeres of normal size and number. Positive staining for cyclin E protein was observed in 30 of the 46 OSCC cases (65.2%), while all the normal oral epithelium cases were cyclin E protein-negative. The percentage of centrosome amplification in OSCC with positive cyclin E protein staining (90.0%, 27/30) was higher than that in OSCC with negative cyclin E protein staining (62.5%, 10/16) (chi(2) = 5.014, P < 0.05). Centrosome amplification showed positive correlation with cyclin E protein overexpression (r = 0.330, P < 0.05). CONCLUSION: Up-regulation of cyclin E protein may represent one of the possible mechanisms for centrosome amplification in OSCC.

Optical planar waveguide fabricated in Nd:LuVO4 crystal by MeV oxygen implantation.

We report the first time optical planar waveguide fabricated in vanadate laser crystal Nd:LuVO4 by 3.0 MeV oxygen ion implantation with the dose of 6x1014 ions/cm2 at room temperature. After the implantation, an enhanced ordinary refractive index region was formed with a width of about 2.1 microm beneath the sample surface to act as a waveguide structure. The modes were observed at 633 nm, while only one mode was observed at 1539 nm after annealing at 300 degrees C for 60 min in air. The changes of ordinary refractive index in the guiding region were about 4.42% and 4.07% before and after annealing.

Monomode optical waveguide excited at 1540 nm in LiNbO(3) formed by MeV carbon ion implantation at low doses.

The monomode enhanced-index LiNbO(3) waveguide excited at 1540 nm is reported. X-cut LiNbO(3) crystals were implanted at room temperature by 6.0 MeV C(3+) ions with a dose of 2.0x10(15) ions/cm(2). Low loss planar optical waveguides were obtained and characterized by the prism coupling technique. Four dark modes were observed for extraordinary light at 633 nm, while only one enhanced-index mode was observed at 1540 nm. The propagation loss of the waveguide is 1.01 dB/cm measured with the moving fiber method. Reflectivity calculation method (RCM) was applied to simulate the refractive index profiles in waveguide. The width of waveguide structure induced by carbon ion implantation is ~3.6 microm.

Low propagation loss of the waveguides in fused quartz by oxygen ion implantation.

The planar waveguides have been fabricated in fused quartz by 3.0 MeV oxygen ion implantation at dose of 1x10;15 ions/cm2. The guiding modes were observed at wavelengths of both 633 nm and 1539 nm before and after annealing at 320 masculineC, 450 masculineC and 500 masculineC in 60 min characterized by the prism-coupling method. The width of the waveguide structure induced by oxygen ion implantation is about 3 microns. After suitable annealing, the minimum propagation loss of the waveguide in fused quartz can be reduced to -0.14 dB/cm.

Low propagation loss of the waveguides in fused quartz by oxygen ion implantation: errata.

The calculated data of propagation loss of the waveguide were incorrect. Corrected data show the actual results in the measurements.

[Centrosome amplification and chromosome instability in oral squamous cell carcinomas].

OBJECTIVE: To investigate the relationship between centrosome abnormalities and aneuploidy in oral squamous cell carcinoma (OSCC) and elucidate the possible underlying mechanisms of chromosome instability (CIN) in OSCC. METHODS: Formalin-fixed, paraffin-embedded tissues of 8 cases of normal oral epithelium and 32 cases of OSCC were examined for centrosome status by using indirect immunofluorescence staining, and chromosome instability (aneuploidy) in some tissues were detected by flow cytometry. The correlation between centrosome abnormalities and aneuploidy in OSCC was statistically analyzed by SPSS12.0. RESULTS: Normal oral epithelium showed normal size and number of centrosomes in epithelium cells, while 25 out of 32 cases of OSCC showed the evident centrosome amplification characterized by huge size and/or supernumerary centrosomes in a fraction of tumor cells, and 21 out of 32 cases were aneuploidy. The percentage of cases with abnormal centrosomes in aneuploid OSCC (19/21) was significantly higher than that in diploid OSCC(6/11) (P =0.032). Centrosome abnormality was significantly correlated with aneuploidy (Spearman r = 0.413, P = 0.047), and a positive correlation was found between the degree of centrosome amplification and the degree of DNA ploidy abnormality (Pearson r = 0.364, P = 0.041). CONCLUSIONS: Centrosome abnormality may be a contributing factor for chromosome instability in OSCC.