Polyglutamine (polyQ) aggregation plays a pivotal role in the pathological process of Huntington's disease and other polyQ disorders. Therefore, strategies aiming at restoring dysfunction and reducing stresses mediated by polyQ toxicity are of therapeutic interest for proteotoxicity diseases. Salidroside, a glycoside from Rhodiola rosea, has been shown to have a variety of bioactivities, including antioxidant activity. Using transgenic Caenorhabditis elegans models, we show here that salidroside is able to reduce neuronal death and behavioral dysfunction mediated by polyQ expressed in ASH neurons, but the neuroprotective effect is not associated with prevention of polyQ aggregation per se. Further experiments reveal that the neuroprotective effect of salidroside in C. elegans models involves its antioxidant capabilities, including decrease of ROS levels and paraquat-induced mortality, increase of antioxidant enzyme activities and reduction of

By using cobalt nitrate and bismuth nitrate as precursor salts and NaOH as a precipitation agent, Co 3 O 4 -Bi 2 O 3 nanocomposite oxides (CBO) were prepared as a heterogeneous catalyst for the activation of peroxymonosulfate (PMS) by a conventional reverse co-precipitation method and post-calcination. The characterization with transmission electron microscopy, X-ray diffractometry, X-ray photoelectron spectroscopy and Raman spectroscopy demonstrated that there was a strong interaction between Bi and Co components in CBO. The presence of Bi increased the content of surface hydroxyl oxygen, which favored the formation of Co(II)-OH complexes that were vital for heterogeneous activation of PMS. CBO showed strong catalytic activity in the heterogeneous activation of PMS for degradation of organic pollutants such as methylene blue (MB), rhodamine B, phenol and 2,4-dichlorophenol. With the addition of 0.5 mmol L À1 PMS, CBO produced fast and full degradation of MB (20 mmol L À1 ) with the apparent rate constant of 0.36 min À1 , being 8.6 fold of that (0.042 min À1 ) over nano-Co 3 O 4 . It decreased the cobalt leaching to 43 mg L À1 , being much less than that (158 mg L À1 ) from Co 3 O 4 under the same conditions. The effects of CBO loading, PMS concentration and calcination temperature on the degradation of MB and cobalt leaching were also investigated.

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This observational retrospective study was conducted on patients with epilepsy (PWE) in China who had at least one dose of COVID-19 vaccine and it investigated the safety of vaccination by analyzing changes in epileptic seizures and their influencing factors. Consecutive PWE who were followed up in the epilepsy clinic between June 2021 and May 2022 were enrolled. Data on vaccine type, demographic information, clinical characteristics of epilepsy, and treatment were collected through a questionnaire survey and retrospectively analyzed. PWE were divided into a stable seizure group and a worsening seizure group based on seizure episodes at least 90 days after the first vaccine dose. A total of 79 PWE were included. After vaccination, 14 patients (17.7%) had worsening seizures, 92.9% of whom had an increased seizure frequency. Compared with patients in the stable seizure group, patients in the worsening seizure group had significant differences in baseline monthly seizure frequency (P = .012), improper antiseizure medication (ASM) administration (P = .003) and a disrupted sleep routine (P = .016). Multivariate logistic regression analysis showed that improper ASM administration (OR 6.186, 95% confidence interval [CI] 1.312–29.170; p = .021) and a disrupted sleep routine (OR 6.326, 95% CI 1.326–30.174; p = .021) were significantly associated with seizure worsening. In short, COVID-19 vaccination is safe for PWE, and only those with poor seizure control have the possibility of seizure exacerbation after COVID-19 vaccination. The vaccination per se does not represent a major influencing factor, but the improper use of ASMs and a disrupted sleep routine may be correlated with seizure aggravation after vaccination.

Direct evidence was first demonstrated for the oxidative degradation of decabromodiphenyl ether (BDE209) in aqueous TiO(2) dispersions under UV irradiation (λ > 340 nm). BDE209 was hardly debrominated over TiO(2) in UV-irradiated acetonitrile dispersions, but the addition of water into the dispersions greatly enhanced its photocatalytic oxidative debromination. The debromination efficiency of BDE209 as high as 95.6% was achieved in aqueous TiO(2) dispersions after 12 h of UV irradiation. The photocatalytic oxidation of BDE209 resulted in generation of aromatic ring-opening intermediates such as brominated dienoic acids, which were further degraded by prolonging UV irradiation time. The photocatalytic oxidative debromination of BDE209 was further confirmed by the observation that the BDE209 degradation in water-acetonitrile mixtures with different water contents was positively correlated with the formation of •OH radicals, but not photogenerated electrons. The use of water not only avoided the scavenging of reactive radicals by organic solvent but also enhanced the adsorption of BDE209 on the surface of TiO(2), both of which favor the contact of BDE209 with photogenerated holes and •OH species. The confirmation of efficient oxidative degradation and debromination of BDE209 is very important for finding new ways to remove polybrominated diphenyl ethers from the environment.