Effect of a Er, Cr:YSGG laser and a Er:YAG laser treatment on oral biofilm-contaminated titanium

Implant surface decontamination is a challenging procedure for therapy of peri-implant disease. Objective: This study aimed to compare the effectiveness of decontamination on oral biofilm-contaminated titanium surfaces in Er:YAG laser, Er, Cr:YSGG laser, and plastic curette. Methodology: For oral biofilms formation, six participants wore an acrylic splint with eight titanium discs in the maxillary arch for 72 hours. A total of 48 contaminated discs were distributed among four groups: untreated control; decontamination with plastic curettes; Er, Cr:YSGG laser; and Er:YAG laser irradiation. Complete plaque removal was estimated using naked-eye and the time taken was recorded; the residual plaque area was measured and the morphological alteration of the specimen surface was observed by scanning electron microscopy. The total bacterial load and the viability of adherent bacteria were quantified by live or dead cell labeling with fluorescence microscopy. Results: The mean treatment time significantly decreased based on the treatment used in the following order: Er:YAG, Er, Cr:YSGG laser, and plastic curettes (234.9±25.4 sec, 156.1±12.7 sec, and 126.4±18.6 sec, P=0.000). The mean RPA in the Er, Cr:YSGG laser group (7.0±2.5%) was lower than Er:YAG and plastic curettes groups (10.3±2.4%, 12.3±3.6%, p=0.023). The viable bacteria on the titanium surface after Er, Cr:YSGG laser irradiation was significantly lower compared to the decontamination with plastic curette (P=0.05) but it was not significantly different from the Er:YAG laser irradiation. Conclusion: We found that Er:YAG laser and Er, Cr:YSGG laser irradiation were effective methods for decontaminations without surface alterations

A Planetary lensing feature in caustic-crossing high-magnification microlensing events

Current microlensing follow-up observations focus on high-magnification events because of the high efficiency of planet detection. However, central perturbations of high-magnification events caused by a planet can also be produced by a very close or a very wide binary companion, and the two kinds of central perturbations are not generally distinguished without time consuming detailed modeling (a planet-binary degeneracy). Hence, it is important to resolve the planet-binary degeneracy that occurs in high-magnification events. In this paper, we investigate caustic-crossing high-magnification events caused by a planet and a wide binary companion. From this study, we find that because of the different magnification excess patterns inside the central caustics induced by the planet and the binary companion, the light curves of the caustic-crossing planetary-lensing events exhibit a feature that is discriminated from those of the caustic-crossing binary-lensing events, and the feature can be used to immediately distinguish between the planetary and binary companions. The planetary-lensing feature appears in the interpeak region between the two peaks of the caustic-crossings. The structure of the interpeak region for the planetary-lensing events is smooth and convex or boxy, whereas the structure for the binary-lensing events is smooth and concave. We also investigate the effect of a finite background source star on the planetary-lensing feature in the caustic-crossing high-magnification events. From this, we find that the convex-shaped interpeak structure appears in a certain range that changes with the mass ratio of the planet to the planet-hosting star.Comment: 14 pages, 4 figures. Accepted for publication in Ap

Liquid Crystal Display with Different Twisting Directions of Liquid Crystal Molecules

A liquid crystal display includes a first alignment film having a first alignment direction, a second alignment film having a second alignment direction, and a liquid crystal layer having liquid crystal molecules between the first and second alignment films. The liquid crystal layer is doped with a chiral material that tends to induce a first twist in directors of the liquid crystal molecules when an electric field is applied to the liquid crystal layer. The first and second alignment films have orientations that tends to induce a second twist in the directors when an electric field is applied to the liquid crystal layer, in which the direction of the first twist is different from the direction of the second twist

Limits of Binaries That Can Be Characterized by Gravitational Microlensing

Due to the high efficiency of planet detections, current microlensing planet searches focus on high-magnification events. High-magnification events are sensitive to remote binary companions as well and thus a sample of wide-separation binaries are expected to be collected as a byproduct. In this paper, we show that characterizing binaries for a portion of this sample will be difficult due to the degeneracy of the binary-lensing parameters. This degeneracy arises because the perturbation induced by the binary companion is well approximated by the Chang-Refsdal lensing for binaries with separations greater than a certain limit. For binaries composed of equal mass lenses, we find that the lens binarity can be noticed up to the separations of $\sim 60$ times of the Einstein radius corresponding to the mass of each lens. Among these binaries, however, we find that the lensing parameters can be determined only for a portion of binaries with separations less than $\sim 20$ times of the Einstein radius.Comment: 5 pages, 3 figures, 1 tabl

Human AP endonuclease suppresses DNA mismatch repair activity leading to microsatellite instability

The multifunctional mammalian apurinic/apyrimidinic (AP) endonuclease (APE) participates in the repair of AP sites in the cellular DNA as well as participating in the redox regulation of the transcription factor function. The function of APE is considered as the rate-limiting step in DNA base excision repair. Paradoxically, an unbalanced increase in APE protein leads to genetic instability. Therefore, we investigated the mechanisms of genetic instability that are induced by APE. Here, we report that the overexpression of APE protein disrupts the repair of DNA mismatches, which results in microsatellite instability (MSI). We found that expression of APE protein led to the suppression of the repair of DNA mismatches in the normal human fibroblast cells. Western blot analysis revealed that hMSH6 protein was markedly reduced in the APE-expressing cells. Moreover, the addition of purified Mutα (MSH2 and MSH6 complex) to the extracts from the APE-expressing cells led to the restoration of mismatch repair (MMR) activity. By performing MMR activity assay and MSI analysis, we found that the co-expression of hMSH6 and APE exhibited the microsatellite stability, whereas the expression of APE alone generated the MSI-high phenotype. The APE-mediated decrease in MMR activity described here demonstrates the presence of a new and highly effective APE-mediated mechanism for MSI

Effect of 5-aminolevulinic acid-based photodynamic therapy via reactive oxygen species in human cholangiocarcinoma cells

Cancer cells have been reported to exhibit an enhanced capacity for protoporphyrin IX (PpIX) synthesis facilitated by the administration of 5-aminolevulinic acid (ALA). We investigated the effect of ALA-based photodynamic therapy (PDT) on human cholangiocarcinoma cells (HuCC-T1). Since protoporphyrin IX (PpIX), a metabolite of ALA, can produce reactive oxygen species (ROS) under irradiation and then induce phototoxicity, ALA-based PDT is a promising candidate for the treatment of cholangiocarcinoma. When various concentrations of ALA (0.05–2 mM) were used to treat HuCC-T1 cells for 6 or 24 hours, the intracellular PpIX level increased according to the ALA concentration and treatment time. Furthermore, an increased amount of PpIX in HuCC-T1 cells induced increased production of ROS by irradiation, resulting in increased phototoxicity

Differential Expression of Glut1 in Pulmonary Neuroendocrine Tumors: Correlation with Histological Grade

Background : Increased glucose uptake, a process that is mediated by glucose transporter (Glut1) proteins, is an important metabolic feature in a variety of cancer cells. The overexpression of Glut1 in human cancers is known to be related to a variety of histopathological parameters, including histological grade, proliferation rate, and lymphatic invasion. The principal objective of this study was to evaluate Glut1 expression in the spectrum of pulmonary neuroendocrine (NE) tumors including typical carcinoid tumor (TC), atypical carcinoid tumor (AC), large cell neuroendocrine carcinoma (LCNEC), and small cell carcinoma (SCC), and to characterize the relationship between Glut1 expression and the histologic grade of NE tumors. Methods : 19 TC, 7 AC, 13 LCNEC, and 6 SCC patients were included in this study. The percentages of Glut1-positive tumor cells in these patients were determined. For statistical analysis, Glut1 expression was subdivided into a Glut1-low expression group (0-30%) and a Glut1-high expression group (31-90%). Results : In our subgroup analyses, the histological grade of pulmonary neuroendocrine (NE) tumors was significantly correlated with Glut1 expression; TC (n=19, 3.6 +/- 4.2%), AC (n=7, 20.0 +/- 4.9%), LCNEC (n=13, 60.0 +/- 21.1%), and SCC (n= 6, 74.2 +/- 16.9%). Glut1-high expression was significantly associated with high-grade NE tumors such as LCNEC and SCC (n=19, 62.6 +/- 21.0%) (p=0.000). Conclusions: The results of this study appear to indicate that Glut1 overexpression is a consistent feature of high-grade NE lung tumors.This work was supported by grant no 02-2008-029 from the SNUBH Research Fund and partly supported by the Korean Science & Engineering Foundation (KOSEF) through the Tumor Immunity Medical Research Center at Seoul National University College of Medicine.Song YS, 2008, LUNG CANCER, V61, P54, DOI 10.1016/j.lungcan.2007.11.012Nguyen XC, 2007, EUR J RADIOL, V62, P214, DOI 10.1016/j.ejrad.2006.12.008Khandani AH, 2007, NUCL MED COMMUN, V28, P173Chung JH, 2004, J NUCL MED, V45, P999TRAVIS WD, 2004, WHO INT HISTOLOGICALKalir T, 2002, CANCER, V94, P1078, DOI 10.1002/cncr.10280Wong CYO, 2001, EUR J NUCL MED, V28, P1702Wang BY, 2000, CANCER, V88, P2774Brown RS, 1999, J NUCL MED, V40, P556Ito T, 1998, MODERN PATHOL, V11, P437Travis WD, 1998, HUM PATHOL, V29, P272Baer SC, 1997, J AM ACAD DERMATOL, V37, P575Younes M, 1997, CANCER, V80, P1046Voldstedlund M, 1997, APMIS, V105, P537Haber RS, 1997, THYROID, V7, P363Younes M, 1997, CANCER EPIDEM BIOMAR, V6, P303Younes M, 1996, CLIN CANCER RES, V2, P1151Younes M, 1996, CANCER RES, V56, P1164Younes M, 1995, ANTICANCER RES, V15, P2895NAGASE Y, 1995, J UROLOGY, V153, P798MELLANEN P, 1994, INT J CANCER, V56, P622BROWN RS, 1993, CANCER, V72, P2979TAKATA K, 1992, CELL TISSUE RES, V267, P407PESSIN JE, 1992, ANNU REV PHYSIOL, V54, P911PARDRIDGE WM, 1990, J BIOL CHEM, V265, P18035ISSELBAC.KJ, 1972, NEW ENGL J MED, V286, P929