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White spot lesions (WSL) and incipient caries on enamel surfaces are the earliest clinical outcomes for demineralization and caries. If left untreated, the caries can progress and may cause complex restorative procedures or even tooth extraction which destroys soft and hard tissue architecture as a consequence of connective tissue and bone loss. Current clinical practices are insufficient in treating dental caries. A long-standing practical challenge associated with demineralization related to dental diseases is incorporating a functional mineral microlayer which is fully integrated into the molecular structure of the tooth in repairing damaged enamel. This study demonstrates that small peptide domains derived from native protein amelogenin can be utilized to construct a mineral layer on damaged human enamel in vitro. Six groups were prepared to carry out remineralization on artificially created lesions on enamel: (1) no treatment, (2) Ca2+ and PO4 3– only, (3) 1100 ppm fluoride (F), (4) 20 000 ppm F, (5) 1100 ppm F and peptide, and (6) peptide alone. While the 1100 ppm F sample (indicative of common F content of toothpaste for homecare) did not deliver F to the thinly deposited mineral layer, high F test sample (indicative of clinical varnish treatment) formed mainly CaF2 nanoparticles on the surface. Fluoride, however, was deposited in the presence of the peptide, which also formed a thin mineral layer which was partially crystallized as fluorapatite. Among the test groups, only the peptide-alone sample resulted in remineralization of fairly thick (10 μm) dense mineralized layer containing HAp mineral, resembling the structure of the healthy enamel. The newly formed mineralized layer exhibited integration with the underlying enamel as evident by cross-sectional imaging. The peptide-guided remineralization approach sets the foundation for future development of biomimetic products and treatments for dental health care.

Background. Anatomic variations, the presence of the pyramidal lobe (PL), may impact completeness of thyroidectomy and effect of surgical treatment. Method. This study included 166 patients who underwent total thyroidectomy. The anterior cervical region between the thyroid isthmus and the hyoid bone was dissected during thyroid surgery. The incidence, size, and anatomical features of the PL were established in these patients. Results. The incidence of PL was 65.7%. No gender difference was found for PL incidence. The base of the PL was located at the isthmus in 52.3%, the left lobe in 29.4%, and the right lobe in 18.3% of patients. The mean length of the PL was 22.7 (range, 5–59) mm. The PL was longer than 30 mm in 23% of patients. One-third of the patients with short PL were men whereas women accounted for 80% of patients with long PL. Conclusions. The high incidence indicates that the PL is a common part of the thyroid. The PL generally originates from the isthmus near midline and is of variable length, extending from the isthmus up to the hyoid bone. Considering that the PL is a common structure, the prelaryngeal region should be dissected to achieve the completeness of thyroidectomy.

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Obesity is associated with eye diseases, but the underlying structural changes and pathogenic mechanisms have not been examined in detail. Here, we assessed the effects of morbid obesity on the morphometric indices of eye disease. Methods: Morbidly obese volunteers (n=101, body mass index [BMI] ≥40) and healthy individuals (n=95, BMI: 18.50-24.99) were examined by Goldman applanation tonometry, pachymetry, and spectral domain optical coherence tomography. Intraocular pressure, anterior chamber depth, axial length, central corneal thickness, retinal nerve fiber layer thickness, central foveal thickness, and choroidal thickness were compared between groups. Results: Uncorrected intraocular pressure was significantly greater in the morbidly obese group than in the healthy control group (15.5 ± 2.5 vs. 14.5 ± 2.6 mmHg, p=0.009), whereas axial length, anterior chamber depth, and central corneal thickness did not differ between the groups. The mean retinal nerve fiber layer thickness at the temporal quadrant was reduced in the morbidly obese group (72.7 ± 13.6 vs. 85.05 ± 52.6 μm, p=0.024). Similarly, the mean retinal thicknesses at nasal and temporal 1500-μm locations were lower in the morbidly obese group (346.6 ± 18.2 vs. 353.7 ± 18.8 μm, p=0.008; 323.1 ± 20.3 vs. 330.0 ± 18.9 μm, p=0.001). The mean choroidal thickness was also reduced in almost all measurement locations (fovea, temporal 500 and 1000 μm, and nasal 500, 1000, and 1500 μm) of the obese group (p<0.05). Weight and BMI were negatively correlated with subfoveal choroidal thickness (r=-0.186, p=0.009; r=-0.173, p=0.015). Conclusion: Morbid obesity is associated with elevated uncorrected intraocular pressure and signs of neuropathy and retinopathy. Obesity may thus increase the risks of glaucoma and glaucomatous optic neuropathy.

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Amorphous peroxotitantes (APT) are insoluble titanium-based particles that bind a variety of metal compounds with high affinity; these particles could be sequestered locally in a solid phase to deliver metal-based drugs. Previous studies have confirmed the 'biodelivery' of metals from metal-APT complexes to fibroblasts, but not monocytes. Our goal in the current study was to use monocytic cytokine secretion to assess delivery of gold or platinum-based compounds from APT to human THP1 monocytes. Cytokine secretion was not triggered by APT alone or metal-APT complexes. In monocytes activated by lipopolysaccharide (LPS), APT alone enhanced or suppressed IL1beta or IL6 secretion, yet TNFalpha secretion was unaffected. Complexes of APT and Au(III) or cis-platin altered LPS-activated IL6 or IL1beta secretion most, TNFalpha least. Our results suggest that the APT deliver metals to monocytes.