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Background Acute transverse myelitis (ATM) has been reported as a potential association between COVID‐19 vaccination. In this study, we aimed to investigate the association between the COVID‐19 vaccination and ATM. Methods A self‐controlled case series study was performed using a large database that combine the COVID‐19 vaccine registry and the national claims database. The COVID‐19 vaccination data included information on individuals aged 18 and above who received COVID‐19 vaccination from February 26, 2021, to August 31, 2022. The claims database covered the entire Korean population for the period between January 1, 2002 to August 31, 2022. Patients who develop ATM within 1–42 days following COVID‐19 vaccination were included. The observation period was 270 days after the first dose of the COVID‐19 vaccine. The incidence rate ratio (IRR) and 95% confidence interval (CI) were estimated using a conditional Poisson regression model. Results A total of 159 ATM patients were included. Among them, 82 (51.6%) were male, and mean age was 55.4 (±17.4) years. The IRR was 2.41 (95% CI: 1.76–3.30) for the ATM risk within 1–42 days after COVID‐19 vaccination. The IRR by vaccine product was 3.31 (95% CI: 1.81–6.05) for ChAdOx1‐S; 1.99 (95% CI: 1.30–3.03) for BNT162b2; 2.57 (95% CI: 1.14–5.97) for mRNA‐1273; and 3.33 (95% CI: 0.30–36.44) for Ad26.COV2.S. Conclusion These findings indicated an increased risk of ATM following COVID‐19 vaccination within 42 days. An association with the risk of ATM was found both for viral vector and mRNA vaccines.

Neuronal inflammation is a systematically organized physiological step often triggered to counteract an invading pathogen or to rid the body of damaged and/or dead cellular debris. At the crux of this inflammatory response is the deployment of nonneuronal cells: microglia, astrocytes, and blood-derived macrophages. Glial cells secrete a host of bioactive molecules, which include proinflammatory factors and nitric oxide (NO). From immunomodulation to neuromodulation, NO is a renowned modulator of vast physiological systems. It essentially mediates these physiological effects by interacting with cyclic GMP (cGMP) leading to the regulation of intracellular calcium ions. NO regulates the release of proinflammatory molecules, interacts with ROS leading to the formation of reactive nitrogen species (RNS), and targets vital organelles such as mitochondria, ultimately causing cellular death, a hallmark of many neurodegenerative diseases. AD is an enervating neurodegenerative disorder with an obscure etiology. Because of accumulating experimental data continually highlighting the role of NO in neuroinflammation and AD progression, we explore the most recent data to highlight in detail newly investigated molecular mechanisms in which NO becomes relevant in neuronal inflammation and oxidative stress-associated neurodegeneration in the CNS as well as lay down up-to-date knowledge regarding therapeutic approaches targeting NO.

The association between Guillain-Barré syndrome (GBS) and certain COVID-19 vaccines is inconclusive. We investigated the risk of GBS after COVID-19 vaccination or SARS-CoV-2 infection. Using a common protocol, we conducted a self-controlled case series study from 1 December 2020 to 9 August 2023 at 20 global sites within the Global Vaccine Data Network™ (GVDN®). Brighton Collaboration case definition criteria were used to determine the level of certainty (LOC) of medical record-reviewed GBS cases at 15 sites. GBS cases following SARS-CoV-2 infection were identified from electronic data sources (EDS) from 11 sites. We estimated the relative incidence (RI) of GBS within 1–42 days following receipt of adenoviral vector, mRNA, or inactivated COVID-19 vaccines or SARS-CoV-2 infection using conditional Poisson regression models, controlling for seasonality. We used random effects meta-analysis to pool the estimates across sites. Of 410 medical record-reviewed post-vaccination GBS cases (out of 2086 EDS-identified cases), 49 were LOC 1 or 2, 187 were LOC 3 or 4, and 174 were LOC 5. These cases received a total of 794 doses of COVID-19 vaccines (160 [20 %] adenoviral vector vaccine doses, 556 [70 %] mRNA vaccine doses, 77 [10 %] inactivated vaccine doses, and 1 [0.1 %] protein-based vaccine dose) during the observation period. We observed an increased risk of confirmed (LOC 1–2) GBS after receiving ChAdOx1-S/nCoV-19 (Vaxzevria/Covishield) (RI = 3.10; 95 % confidence interval [CI], 1.12–8.62). Decreased risks of LOC 1–4 GBS were observed after receiving BNT162b2 (Comirnaty/Tozinameran) (RI = 0.48; 95 %CI, 0.27–0.85) and CoronaVac/Sinovac (RI = 0.04; 95 %CI, 0.00–0.61). For 489 EDS-identified GBS cases after SARS-CoV-2 infection, we found GBS risk to be increased (RI = 3.35; 95 %CI, 1.83–6.11). In this large multinational study, we found increased risks of GBS within 42 days after Vaxzevria/Covishield vaccination or SARS-CoV-2 infection, and decreased risks after receiving Comirnaty/Tozinameran or CoronaVac/Sinovac COVID-19 vaccines.

Both cancer patients and the elderly are at high risk of developing flu complications, so influenza vaccination is recommended. We aimed to evaluate potential adverse events (AEs) following influenza vaccination in elderly cancer patients using the self-controlled tree-temporal scan statistic method. From a large linked database of Korea Disease Control and Prevention Agency vaccination data and the National Health Insurance Service claims data, we identified cancer patients aged over 65 who received flu vaccines during the 2016/2017 and 2017/2018 seasons. We included all the outcomes occurring on 1–84 days post-vaccination and evaluated all temporal risk windows, which started 1–28 days and ended 2–42 days. Patients who were diagnosed with the same disease during a year prior to vaccination were excluded. We used the hierarchy of ICD-10 to identify statistically significant clustering. This study included 431,276 doses of flu vaccine. We detected signals for 1 set: other dorsopathies on 1–15 days (attributable risk 16.5 per 100,000, P = 0.017). Dorsopathy is a known AE of influenza vaccine. No statistically significant clusters were found when analyzed by flu season. Therefore, influenza vaccination is more recommended for elderly patients with cancer and weakened immune systems.

•There is a lingering concern regarding the safety of the concomitant vaccinations.•We evaluated the safety of concomitant administration of PPSV-23 and the influenza vaccine.•A cohort study was conducted among individuals aged 65 and older.•Concomitant administration is a safe and effective approach to protect the elderly from pneumonia. The current recommendation for the elderly is to receive both a single dose 23-valent pneumococcal polysaccharide vaccine (PPSV-23) and an annual inactivated influenza vaccine. There is a lack of post-marketing safety studies on concomitant vaccination using real-world data. We aimed to evaluate the safety of administering PPSV-23 and influenza vaccine concomitantly versus sequentially. We performed a retrospective cohort study using a linked database that combines vaccination registry from the Korea Disease Control and Prevention Agency and claims data from the National Health Insurance Service. The study population included all those aged over 65 who received PPSV-23 at least once from Jan 1, 2016, to Dec 31, 2020. This study evaluated the 16 prespecified events of interest. Concomitant vaccination was defined as receiving both PPSV-23 and influenza vaccine on the same day. For sequential vaccination, we defined it as receiving influenza vaccination during the period from 30 to 365 days prior to the date of PPSV-23 injection. We performed 1:4 propensity score matching and estimated adjusted incidence rate ratio (aIRR) with a 95 % confidence interval (CI) using conditional Poisson regression. Of the 2,885,144 elderly patients who received PPSV-23 vaccination at least once from Jan 1, 2016, to Dec 31, 2020, a total 87,899 were included in the concomitant vaccination group and 1,200,091 were included in the sequential vaccination group. After adjusting for confounders, the concomitant group exhibited a significantly lower risk of allergic reactions (aIRR: 0.71, 95 % CI: 0.58–0.87), neuritis (aIRR: 0.72, 95 % CI: 0.57–0.91), and pneumonia (aIRR: 0.85, 95 % CI: 0.80–0.90), while demonstrating significantly higher risks of paralysis (aIRR: 1.63, 95 % CI: 1.05–2.52) compared to the sequential group. Concomitant administration of PPSV-23 and influenza vaccine in the elderly was not associated with a higher risk of most prespecified adverse events (AEs) compared to sequential vaccination. This study supports the safety of concomitant administration of PPSV-23 and influenza vaccine.

Hydrogen sulfide (H2S), a toxic gaseous molecule, plays a physiological role in regulating homeostasis and cell signaling. H2S is produced from cysteine by enzymes, such as cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE), cysteine aminotransferase (CAT), and 3-mercaptopyruvate sulfurtransferase (3MST). These enzymes regulate the overall production of H2S in the body. H2S has a cell-signaling function in the CNS and plays important roles in combating oxidative species such as reactive oxygen species (ROS) and reactive nitrogen species (RNS) in the body. H2S is crucial for maintaining balanced amounts of antioxidants to protect the body from oxidative stress, and appropriate amounts of H2S are required to protect the CNS in particular. The body regulates CBS, 3MST, and CSE levels in the CNS, and higher or lower levels of these enzymes cause various neurodegenerative diseases. This review discusses how H2S protects the CNS by acting as an antioxidant that reduces excessive amounts of ROS and RNS. Additionally, H2S regulates cell signaling to combat neuroinflammation and protect against central neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS).

Significance Early detection of cancer positively impacts diagnosis and treatment, ultimately improving patient survival. Using fluorescence imaging offers the promise of safe, noninvasive detection with excellent resolution and guides surgical removal of tumors to improve patient outcomes. However, the success of current optical probes is limited due to high background from tissue autofluorescence, poor penetration depth, and inherently low signal stability. Here, we engineered M13 bacteriophage to stabilize single-walled carbon nanotubes for selective, targeted imaging of ovarian tumors. These nanoprobes fluoresce at longer near-infrared wavelengths than current probes, thereby improving noninvasive detection of small, deep tumors and guidance for surgical removal of submillimeter tumors. This material-based approach may be attractive to guide surgical interventions where deep tissue molecular imaging is informative. Highly sensitive detection of small, deep tumors for early diagnosis and surgical interventions remains a challenge for conventional imaging modalities. Second-window near-infrared light (NIR2, 950–1,400 nm) is promising for in vivo fluorescence imaging due to deep tissue penetration and low tissue autofluorescence. With their intrinsic fluorescence in the NIR2 regime and lack of photobleaching, single-walled carbon nanotubes (SWNTs) are potentially attractive contrast agents to detect tumors. Here, targeted M13 virus-stabilized SWNTs are used to visualize deep, disseminated tumors in vivo. This targeted nanoprobe, which uses M13 to stably display both tumor-targeting peptides and an SWNT imaging probe, demonstrates excellent tumor-to-background uptake and exhibits higher signal-to-noise performance compared with visible and near-infrared (NIR1) dyes for delineating tumor nodules. Detection and excision of tumors by a gynecological surgeon improved with SWNT image guidance and led to the identification of submillimeter tumors. Collectively, these findings demonstrate the promise of targeted SWNT nanoprobes for noninvasive disease monitoring and guided surgery.

Hydrogen sulfide (H2S) is a gasotransmitter that acts as an antioxidant and exhibits a wide variety of cytoprotective and physiological functions in age-associated diseases. One of the major causes of age-related diseases is oxidative stress. In recent years, the importance of H2S has become clear, although its antioxidant function has not yet been fully explored. The enzymes cystathionine β-synthase, cystathionine γ-lya-se, and 3-mercaptopyruvate sulfurtransferase are involved in the enzymatic production of H2S. Previously, H2S was considered a neuromodulator, given its role in long-term hippocampal potentiation, but it is now also recognized as an antioxidant in age-related neurodegeneration. Due to aerobic metabolism, the central nervous system is vulnerable to oxidative stress in brain aging, resulting in age-associated degenerative diseases. H2S exerts its antioxidant effect by limiting free radical reactions through the activation of antioxidant enzymes, including superoxide dismutase, catalase, and glutathione peroxidase, which protect against the effects of aging by regulating apoptosis-related genes, including p53, Bax, and Bcl-2. This review explores the implications and mechanisms of H2S as an antioxidant in age-associated neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, Huntington's disease, and Down syndrome.

To assess the association between COVID-19 vaccination and the risk of the abnormal uterine bleeding (AUB) specifically focusing on vaginal or uterine bleeding that requires hospital care in women. We used a nationwide database in the Republic of Korea that combined COVID-19 registry data, which contains information on COVID-19 vaccination, with the claims database of the National Health Insurance Service. We included women aged 16–64 who received their first vaccine dose and were newly diagnosed with AUB in inpatient or outpatient settings within 180 days after receiving the first dose. A population-based self-controlled case series analysis was used to estimate the incidence rate ratio (IRR) during the risk periods, including 1–14, 1–21, and 1–28 days after each vaccine dose, compared to the baseline period. The baseline period was defined as the period of 1–180 days following the first vaccine dose, excluding the periods that corresponds to the risk periods. To address the SCCS assumption violation from recurrent nature, only the first event during the observation period was considered. Among 83,422 eligible patients, the risk of AUB requiring hospital care within 14 days following COVID-19 vaccination was slightly elevated compared to the baseline period (IRR 1.04, 95 % CI 1.02–1.06). The risk was notably higher after the first dose, regardless of the risk interval (14-day risk period: IRR 1.12, 95 % CI 1.09–1.15; 21-day risk period: IRR 1.08, 95 % CI 1.06–1.10; 28-day risk period: IRR 1.07, 95 % CI 1.05–1.09). No significant increase was observed after the second and third doses. This study found a modest increase in healthcare utilization for AUB after the first dose of COVID-19 vaccination. However, this trend diminished with subsequent doses, showing no significantly increased risk. These findings should be interpreted while considering factors that influence healthcare-seeking behavior for unexpected vaginal or uterine bleeding. •Evaluated the risk of hospital care for abnormal uterine bleeding post-COVID-19 vaccination.•Slightly elevated risk of bleeding was observed within 14 days after vaccination.•Risk was higher after the first dose but not significant after the second or third doses.•Findings should be interpreted considering factors influencing healthcare-seeking behavior.

Mitophagy is activated by a number of stimuli, including hypoxia, energy stress, and increased oxidative phosphorylation activity. Mitophagy is associated with oxidative stress conditions and central neurodegenerative diseases. Proper regulation of mitophagy is crucial for maintaining homeostasis; conversely, inadequate removal of mitochondria through mitophagy leads to the generation of oxidative species, including reactive oxygen species and reactive nitrogen species, resulting in various neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. These diseases are most prevalent in older adults whose bodies fail to maintain proper mitophagic functions to combat oxidative species. As mitophagy is essential for normal body function, by targeting mitophagic pathways we can improve these disease conditions. The search for effective remedies to treat these disease conditions is an ongoing process, which is why more studies are needed. Additionally, more relevant studies could help establish therapeutic conditions, which are currently in high demand. In this review, we discuss how mitophagy plays a significant role in homeostasis and how its dysregulation causes neurodegeneration. We also discuss how combating oxidative species and targeting mitophagy can help treat these neurodegenerative diseases.