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O-Acetylated pectins are abundant in the primary cell wall of plants and growing evidence suggests they have important roles in plant cell growth and interaction with the environment. Despite their importance, genes required for O-acetylation of pectins are still largely unknown. In this study, we showed that TRICHOME BIREFRINGENCE LIKE 10 (AT3G06080) is involved in O-acetylation of pectins in Arabidopsis (Arabidopsis thaliana). The activity of the TBL10 promoter was strong in tissues where pectins are highly abundant (e.g. leaves). Two homozygous knock-out mutants of Arabidopsis, tbl10-1 and tbl10-2, were isolated and shown to exhibit reduced levels of wall-bound acetyl esters, equivalent of ~50% of the wild-type level in pectin-enriched fractions derived from leaves. Further fractionation revealed that the degree of acetylation of the pectin rhamnogalacturonan-I (RG-I) was reduced in the tbl10 mutant compared to the wild type, whereas the pectin homogalacturonan (HG) was unaffected. The degrees of acetylation in hemicelluloses (i.e. xyloglucan, xylan and mannan) were indistinguishable between the tbl10 mutants and the wild type. The mutant plants contained normal trichomes in leaves and exhibited a similar level of susceptibility to the phytopathogenic microorganisms Pseudomonas syringae pv. tomato DC3000 and Botrytis cinerea; while they displayed enhanced tolerance to drought. These results indicate that TBL10 is required for O-acetylation of RG-I, possibly as an acetyltransferase, and suggest that O-acetylated RG-I plays a role in abiotic stress responses in Arabidopsis.

Background and Objectives: Tooth whitening is a relatively conservative and effective option to treat discolored teeth. However, questions remain whether in-office or at-home tooth whitening products with short treatment durations are as effective and stable as products with longer treatment durations. Materials and Methods: Forty human third molars with intact enamel surfaces were divided into four groups of ten each, subjected to discoloration challenges with coffee for 60 h, and they were treated with four professional tooth whitening systems: two for take-home use—6% hydrogen peroxide for 30 min/d for a total of 7 h in 14 days (HP6), 10% carbamide peroxide for 10 h/d for 140 h in 14 days (CP10), as well as two for in-office use—35% HP for 10 min × 3 (HP35) for a total of 30 min and 40% HP for 20 min × 3 (HP40) for a total of 60 min. Teeth colors were assessed in the CIE L*a*b* color space with a spectrophotometer immediately and six months after whitening treatments. Surface roughness (Sa) for the treated and untreated enamel surfaces of the teeth in all groups were evaluated with a three-dimensional laser scanning microscope after six months. Results: No significant differences were found between HP6 and CP10 groups immediately after whitening (∆E 10.6 ± 1.6 vs. 11.4 ± 1.7, p > 0.05) and at six months after treatments (∆E 9.0 ± 1.9 vs. 9.2 ± 2.5, p > 0.05), or between HP35 and HP40 groups immediately after whitening (∆E 5.9 ± 1.2 vs. 5.3 ± 1.7, p > 0.05) and at six months after treatments (∆E 7.2 ± 1.6 vs. 7.7 ± 1.3, p > 0.05). The two at-home whitening systems achieved significantly better whitening outcomes than the two in-office products immediately after whitening (p < 0.05). However, at six months after treatments, the differences between at-home and in-office treatments had narrowed significantly (p > 0.05). There were no statistically significant differences with respect to the Sa values between the treated and untreated surfaces (p > 0.05). Conclusions: Tooth whitening products in the same product category have similar whitening efficacies, despite significant differences in treatment durations (7 vs. 140 h, and 30 min vs. 60 min, respectively). Take-home products achieved better whitening outcomes than in-office products, but they needed 14 to 280 times longer treatment durations. [ABSTRACT FROM AUTHOR]

Background: Exercise is a known trigger of the inhibitory pain modulation system and its analgesic effect is termed exercise‐induced hypoalgesia (EIH). Previous studies have demonstrated that rats with deficient analgesic response following exercise develop more significant hypersensitivity following nerve injury compared to rats with substantial analgesic response following exercise. Objectives: A rat model of EIH as an indicator of the pain inhibitory system's efficiency was used to explore the association between EIH profiles and the effect of pharmacotherapy on rat's neuropathic pain. Methods: EIH profiles were assessed by evaluating paw responses to mechanical stimuli before and after exercise on a rotating rod. Rats with a reduction of ≤33% in responses were classified as low EIH and those with ≥67% as high EIH. Low and high EIH rats underwent sciatic nerve chronic constriction injury (CCI). Paw responses to mechanical stimuli were measured at baseline, following CCI, and after treatment with diclofenac, duloxetine or pregabalin. In a different group of low and high EIH rats, EIH was measured before and following treatment with the same medications. Results: Low EIH rats developed more significant hypersensitivity following CCI. Duloxetine and pregabalin successfully reduced hypersensitivity, although significantly more so in low EIH rats. Diclofenac had limited effects, and only on low EIH rats. Four days of duloxetine administration transformed low EIH rats' profiles to high EIH. Conclusions: The findings of this study suggest that EIH profiles in rats can not only predict the development of hypersensitivity following injury but may also support targeted pharmacological treatment. Significance: Exercise is a known trigger of the inhibitory pain modulation. Rats with deficient analgesic response following exercise develop more significant hypersensitivity following nerve injury. Pain modulation profiles in rats can also support targeted pharmacological treatment; rats with deficient analgesic response following exercise benefit more from treatment with duloxetine and gabapentin. Treatment with duloxetine can improve pain modulation profile. [ABSTRACT FROM AUTHOR]