Materials and Methods: Twenty patients with Angle's class II div 1 (10 males and 10 females; aged 20.25 ± 3.88 years) needing bilateral extractions of maxillary first bicuspids were recruited. Conventional brackets MBT of 0.022 in slot (McLaughlin Bennett Trevisi) prescription braces (Ortho Organizers, Carlsbad, Calif) were bonded. After alignment and levelling phase, cuspid retraction began with nitinol closed coil spring on 19 × 25 stainless steel archwire, wielding 150 gram force. 7.5 J/cm2 energy was applied on 10 points (5 buccal and 5 palatal) on the canine roots on the investigational side using gallium-aluminum-arsenic diode laser (940 nm wavelength, iLase™ Biolase, Irvine, USA) in a continuous mode. Target tissues were irradiated once in three weeks for 9 weeks at a stretch (T0, T1, and T2). Patients were given a feedback form based on the numeric rating scale (NRS) to record the pain intensity for a week. Silicon impressions preceded the coil activation at each visit (T0, T1, T2, and T3), and the casts obtained were scanned with the Planmeca CAD/CAM™ (Helsinki, Finland) scanner.
Results: The regimen effectively accelerated (1.55 ± 0.25 mm) tooth movement with a significant reduction in distress on the investigational side as compared to the placebo side (94 ± 0.25 mm) (p < 0.05).
Conclusions: This study reveals that the thrice-weekly LLLT application can accelerate OTM and reduce the associated pain.
METHODS: Eighty (80) male, 6-week-old Sprague Dawley rats were grouped in to four groups, the first group was irradiated with (940 nm) diode laser, second group with LIPUS, and third group with combination of both LLLT and LIPUS. A forth group used was a control group in an incomplete block split-mouth design. The LLLT and LIPUS were used to treat the area around the moving tooth once a day on days 0-7, then the experiment was ended in each experimental endpoint (1, 3, 7, 14, and 21 days). For amount of tooth movement, models were imaged and analyzed. Histological examination was performed after staining with (hematoxylin and eosin) and (alizarin red and Alcian Blue) stain. One step reverse transcription-polymerase chain reaction RT-PCR was also performed to elucidate the gene expression of RANK, RANKL, OPG, and RUNX-2.
RESULTS: The amount of tooth movement, the histological bone remodeling, and the RT-PCR were significantly greater in the treatment groups than that in the control group. Among the treatment groups, the combination group was the highest and the LIPUS group was the lowest.
CONCLUSION: These findings suggest that LLLT and LIPUS can enhance the velocity of tooth movement and improve the quality of bone remodeling during orthodontic tooth movement.
METHODS: Infective larvae were obtained after incubating and hatching fertile eggs of A. suum in order to extract their cuticle and excretory/secretory antigens. The ability of both extracts to bind and activate plasminogen, as well as promote plasmin generation were assayed by ELISA and western blot. The location of plasminogen binding on the larval surface was revealed by immunofluorescence. The plasminogen-binding proteins from both antigenic extracts were revealed by two-dimensional electrophoresis and plasminogen-ligand blotting, and identified by mass spectrometry.
RESULTS: Cuticle and excretory/secretory antigens from infective larvae of A. suum were able to bind plasminogen and promote plasmin generation in the presence of plasminogen activators. Plasminogen binding was located on the larval surface. Twelve plasminogen-binding proteins were identified in both antigenic extracts.
CONCLUSIONS: To the best of our knowledge, the present results showed for the first time, the pro-fibrinolytic potential of infective larvae of Ascaris spp., which suggests a novel parasite survival mechanism by facilitating the migration through host tissues.
METHODS: Twenty-two patients (11 male, 11 female; mean age, 19.8 ± 3.1 years) with Angle Class II Division 1 malocclusion were recruited for this split-mouth clinical trial; they required extraction of maxillary first premolars bilaterally. After leveling and alignment with self-ligating brackets (SmartClip SL3; 3M Unitek, St Paul, Minn), a 150-g force was applied to retract the canines bilaterally using 6-mm nickel-titanium closed-coil springs on 0.019 x 0.025-in stainless steel archwires. A gallium-aluminum-arsenic diode laser (iLas; Biolase, Irvine, Calif) with a wavelength of 940 nm in a continuous mode (energy density, 7.5 J/cm2/point; diameter of optical fiber tip, 0.04 cm2) was applied at 5 points buccally and palatally around the canine roots on the experimental side; the other side was designated as the placebo. Laser irradiation was applied at baseline and then repeated after 3 weeks for 2 more consecutive follow-up visits. Questionnaires based on the numeric rating scale were given to the patients to record their pain intensity for 1 week. Impressions were made at each visit before the application of irradiation at baseline and the 3 visits. Models were scanned with a CAD/CAM scanner (Planmeca, Helsinki, Finland).
RESULTS: Canine retraction was significantly greater (1.60 ± 0.38 mm) on the experimental side compared with the placebo side (0.79 ± 0.35 mm) (P <0.05). Pain was significantly less on the experimental side only on the first day after application of LLLI and at the second visit (1.4 ± 0.82 and 1.4 ± 0.64) compared with the placebo sides (2.2 ± 0.41 and 2.4 ± 1.53).
CONCLUSIONS: Low-level laser irradiation applied at 3-week intervals can accelerate orthodontic tooth movement and reduce the pain associated with it.
METHODS: Reverse transcription-quantitative PCR (RT-qPCR) was used to detect miR-455-5p expression in breast cancer tissues and cell lines. CCK8 and Transwell assays were conducted to assess the effects of miR-455-5p on breast cancer line proliferation, migration, and invasion. SOCS3 expression level in breast cancer tissues and cell lines was determined by qPCR and western blotting. The targeting relationship between miR-455-5p and SOCS3 was determined by dual luciferase reporter gene assay in different breast cancer cell lines. Finally, the upstream and downstream regulatory association between miR-455-5p and SOCS3 was confirmed in breast cancer cells by CCK8, western blot, and Transwell assays.
RESULTS: MiR-455-5p expression was up-regulated in breast cancer tissues; miR-455-5p regulates TNBC proliferation, migration, and invasion of TNBC. SOCS3 was the direct target of miR-455-5p and was down-regulated in breast cancer. Interference with SOCS3 reversed the inhibitory effect of the miR-455-5p inhibitor on breast cancer cells' malignant potential.
CONCLUSION: MiR-455-5p promotes breast cancer progression by targeting the SOCS3 pathway and may be a potential therapeutic target for breast cancer.