HIGHLIGHTS: • Intrabeam x-ray source and spherical applicators were simulated and skin dose was calculated. • Skin dose for constant skin to applicator distance strongly depends on applicator size. • Use of larger applicators generally results in higher skin dose. • The recommended 0.5-1 cm skin to applicator distance does not guarantee skin safety.
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: Seventy patients (20-76 aged) with MRI imaging (pre- and post-RT (6 months-1 year)) and complete cognitive assessments were recruited. Hippocampus, temporal lobes (TLs), and cerebellum were delineated and dosimetry parameters were extracted. Assessments were given post-RT via telephone (Telephone Interview Cognitive Status (TICS), Telephone Montreal Cognitive Assessment (T-MoCA), Telephone Mini Addenbrooke's Cognitive Examination (Tele-MACE), and QLQ-H&N 43). Regression and deep neural network (DNN) models were used to predict post-RT cognition using anatomical and treatment dose features.
RESULTS: Remote cognitive assessments were inter-correlated (r > 0.9). TLs showed significance in pre- and post-RT volume differences and cognitive deficits, that are correlated with RT-associated volume atrophy and dose distribution. Good classification accuracy based on DNN area under receiver operating curve (AUROC) for cognitive prediction (T-MoCA AUROC = 0.878, TICS AUROC = 0.89, Tele-MACE AUROC = 0.919).
CONCLUSION: DL-based prediction models assessed using remote assessments can assist in predicting cognitive deficit following NPC RT. Comparable results of remote assessments in assessing cognition suggest its possibility in replacing standard assessments.
IMPLICATIONS FOR CANCER SURVIVORS: Application of prediction models in individual patient enables tailored interventions to be provided in managing cognitive changes following NPC RT.
METHOD: In this study, we investigated the effects of methanol neurotoxicity on memory function and pathological outcomes in the hippocampus of adolescent rats and examined the efficacy of Light- Emitting Diode (LED) therapy. Methanol induced neurotoxic rats showed a significant decrease in the latency period, in comparison to controls, which was significantly improved in LED treated rats at 7, 14 and 28 days, indicating recovery of memory function. In addition, methanol neurotoxicity in hippocampus caused a significant increase in cell death (caspase3+ cells) and cell edema at 7 and 28 days, which were significantly decreased by LED therapy. Furthermore, the number of glial fibrillary acid protein astrocytes was significantly lower in methanol rats, compared to controls, whereas LED treatment caused their significant increase. Finally, methanol neurotoxicity caused a significant decrease in the number of brain-derived neurotrophic factor (BDNF+) cells, but also circulating serum BDNF, at 7 and 28 days, compared to controls, which were significantly increased by LED therapy. Importantly, LED significantly increased the number of Ki-67+ cells and BDNF levels in the serum and hypothalamus in control-LED rats, compared to controls without LED therapy.
CONCLUSION: In conclusion, chronic methanol administration caused severe memory impairments and several pathological outcomes in the hippocampus of adolescent rats which were improved by LED therapy.