4%), arm paresthesia (50.4%), hyporeflexia/areflexia (48%), and ataxia (22.7%). 38.6% (n = 17) were found to have facial paralysis. Among 37 patients in whom nerve-conduction studies and electromyography were performed, of which 14 patients (31.8%) were consistent with the acute inflammatory demyelinating polyneuropathy (AIDP) subtype of the GBS. S-888711 The present retrospective analysis support the role of the SARS-CoV-2 infection in the development of the GBS, may trigger GBS as para-infectious disease, and lead to SARS-CoV-2-associated GBS.The standard genetic code (SGC) has been extensively analyzed for the biological ramifications of its nonrandom structure. For instance, mismatch errors due to point mutation or mistranslation have an overall smaller effect on the amino acid polar requirement under the SGC than under random genetic codes (RGCs). A similar observation was recently made for frameshift errors, prompting the assertion that the SGC has been shaped by natural selection for frameshift-robustness-conservation of certain amino acid properties upon a frameshift mutation or translational frameshift. However, frameshift-robustness confers no benefit because frameshifts usually create premature stop codons that cause nonsense-mediated mRNA decay or production of nonfunctional truncated proteins. We here propose that the frameshift-robustness of the SGC is a byproduct of its mismatch-robustness. Of 564 amino acid properties considered, the SGC exhibits mismatch-robustness in 93-133 properties depending on the mismatch pattern and frameshift-robustness in 55 properties, respectively, and that the latter is largely a subset of the former. For each of the 564 real and 564 randomly constructed fake properties of amino acids, there is a positive correlation between mismatch-robustness and frameshift-robustness across one million RGCs; this correlation arises because most amino acid changes resulting from a frameshift are also achievable by a mismatch error. Importantly, the SGC does not show significantly higher frameshift-robustness in any of the 55 properties than RGCs of comparable mismatch-robustness. These findings support that the frameshift-robustness of the SGC need not originate through direct selection and can instead be a site effect of its mismatch-robustness. Autoimmune/inflammatory syndrome induced by adjuvants (ASIA syndrome) can be seen as a post-vaccination phenomenon that occurs after exposure to adjuvants in vaccines that increase the immune responses. There is very limited data regarding ASIA syndrome following SARS-CoV-2 vaccines. This work aims to report cases of subacute thyroiditis related to the SARS-CoV-2 vaccine. We describe the clinical, laboratory, and imaging features of three cases of subacute thyroiditis after inactivated SARS-CoV-2 vaccine (CoronaVac®). Three female healthcare workers have applied to our clinic with anterior neck pain and fatigue four to seven days after SARS-CoV-2 vaccination. Two of them were in the breastfeeding period. They were negative for thyroid antibodies, and there was no previous history of thyroid disease or upper respiratory tract infection, or COVID-19. Laboratory test results and imaging findings were consistent with subacute thyroiditis. SARS-CoV-2 vaccination can lead to subacute thyroiditis as a phenomenon of ASIA syndrome. Subacute thyroiditis may develop within a few days after the SARS-CoV-2 vaccination. Being in the postpartum period may be a facilitating factor for the development of ASIA syndrome after the SARS-CoV-2 vaccination. This is the first report of subacute thyroiditis as a phenomenon of ASIA syndrome after inactivated COVID-19 vaccination. Clinicians should be aware that subacute thyroiditis may develop as a manifestation of ASIA syndrome after the inactive SARS-CoV-2 vaccine.This is the first report of subacute thyroiditis as a phenomenon of ASIA syndrome after inactivated COVID-19 vaccination. Clinicians should be aware that subacute thyroiditis may develop as a manifestation of ASIA syndrome after the inactive SARS-CoV-2 vaccine. Hearing loss is prevalent and associated with adverse functional outcomes in older adults. Prevention thus has far-reaching implications, yet few modifiable risk factors have been identified. Hypertension may contribute to age-related hearing loss, but epidemiologic evidence is mixed. We studied a prospective cohort of 3,343 individuals from the Atherosclerosis Risk in Communities study, aged 44-65 years at baseline with up to 30 years of follow-up. Hearing was assessed in late-life (2016-17) using a better-ear audiometric pure tone average (PTA, 0.5, 1, 2, 4kHz) and the Quick Speech-in-Noise (QuickSIN) test. Hypertension was defined as systolic blood pressure ≥140 mmHg, diastolic blood pressure ≥90 mmHg or antihypertensive medication use. Mid-life hypertension was defined by hypertension at two consecutive visits between 1987-89 and 1996-98. Late-life hypertension was defined in 2016-17. Late-life low blood pressure was defined as systolic blood pressure <90 mmHg or diastolic blood pressure <60 mmHg, irrespective of antihypertensive medication use. Associations between blood pressure patterns from mid-to-late-life and hearing outcomes were assessed using multivariable-adjusted linear regression. Compared to persistent normotension, persistent hypertension from mid-to-late-life was associated with worse central auditory processing (difference in QuickSIN score = -0.66 points, 95% CI -1.14, -0.17) but not with audiometric hearing. Participants with persistent hypertension had poorer late-life central auditory processing. These findings suggest that hypertension may be more strongly related to hearing-related changes in the brain than in the cochlea.Participants with persistent hypertension had poorer late-life central auditory processing. These findings suggest that hypertension may be more strongly related to hearing-related changes in the brain than in the cochlea.Reactive oxygen species (ROS) are unstable reactive molecules that are toxic to cells. Regulation of ROS homeostasis is crucial to protect cells from dysfunction, senescence and death. In plant leaves, ROS are mainly generated from chloroplasts and are tightly temporally restricted by the circadian clock. However, little is known about how ROS homeostasis is regulated in non-photosynthetic organs, such as petals. Here, we showed that H2O2 levels exhibit typical circadian rhythmicity in rose (Rosa hybrida) petals, consistent with the measured respiratory rate. RNA-seq and functional screening identified a B-box gene, RhBBX28, whose expression was associated with H2O2 rhythms. Silencing RhBBX28 accelerated flower senescence and promoted H2O2 accumulation at night in petals, while overexpression of RhBBX28 had the opposite effects. RhBBX28 influenced the expression of various genes related to respiratory metabolism, including the TCA cycle and glycolysis, and directly repressed the expression of SUCCINATE DEHYDROGENASE 1, which plays a central role in mitochondrial ROS homeostasis.