Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Objectives: Healthcare facilities are high-risk sites for infection. This study analyzed the epidemiological characteristics of a coronavirus disease 2019 (COVID-19) outbreak in a tertiary hospital after COVID-19 vaccination had been introduced in Republic of Korea. Vaccine effectiveness (VE) and shared anti-infection strategies are also assessed. Methods: The risk levels for 4,074 contacts were evaluated. The epidemiological characteristics of confirmed cases were evaluated using the chi-square test. The “1 minus relative risk” method was used to determine VE in preventing infection, progression to severe disease, and death. In the largest affected area (the 8th floor), a separate relative risk analysis was conducted. A multivariate logistic regression analysis (with 95% confidence interval [CIs]) was used to identify transmission risk factors with a significance level <10% via the backward elimination method. Results: In total, 181 cases of COVID-19 were confirmed, with an attack rate of 4.4%. Of those cases, 12.7% progressed to severe disease, and 8.3% died. In the cohort isolation area on the 8th floor, where 79.0% of the confirmed cases occurred, the adjusted odds ratio was 6.55 (95% CI, 2.99–14.33) and 2.19 (95% CI, 1.24–3.88) for caregivers and the unvaccinated group, respectively. VE analysis revealed that 85.8% of the cases that progressed to severe disease and 78.6% of the deaths could be prevented by administering a second vaccine. Conclusion Caregiver training for infection prevention and control is necessary to reduce infection risk. Vaccination is an important intervention to reduce the risk of progression to severe disease and death.

Purpose: This study investigated correlations between the actual sleep time 24 hours prior to an examination and the time to achieve chloral hydrate sedation in pediatric patients. Methods: With parental consent, 84 children who were placed under moderate or deep sedation with chloral hydrate for examinations from November 19, 2020 to July 9, 2022 were recruited. Results: Patients' average age was 19.9 months. Pediatric neurology patients and those who underwent electroencephalography took significantly longer to achieve sedation with chloral hydrate. There was a negative correlation between the time to achieve sedation and actual sleep time within 24 hours prior to the examination. Positive correlations were found between the actual sleep time 24 hours prior to the examination and the second dose per weight, as well as between the sedation recovery time and awake hours before the examination. Conclusion Sleep restriction is not an effective adjuvant therapy for chloral hydrate sedation in children, and sedation effects vary according to pediatric patients' characteristics. Therefore, it would be possible to reduce the unnecessary efforts of caregivers who restrict children's sleep for examinations. It is more important to educate parents about safe sedation than about sleep restriction.

Purpose: The isocitrate dehydrogenase (IDH) family plays an essential role in metabolism and energy production. The relative expression levels of IDH isoforms (IDH1, IDH2, and IDH3) have prognostic significance in several malignancies, including breast carcinoma. However, the IDH isozyme expression levels in different cancer stages and types have not been determined in breast carcinoma tissues. Methods: We analyzed the messenger RNA (mRNA) and protein levels of IDH (IDH1, IDH2, and IDH3A) and α-ketoglutarate (α-KG) in 59 breast carcinoma tissues. Results: The mRNA level of IDH2 was significantly increased at stages 2 and 3 in triple-negative and (ER-/PR-/HER+) breast cancers. However, the elevated α-KG level was only observed in stages 2 and 3, with no differences in the various breast carcinoma types. Western blotting analysis showed that IDH2 protein expression increased in the patient tissues and cell lines. An in vitro study showed IDH2 downregulation in the triple-negative breast cancer cell line MDA-MB-231 that inhibited cell proliferation and migration and induced cell cycle arrest in the G0/G1 phase. Conclusion These findings suggest that different from IDH1 and IDH3, IDH2 is more highly expressed in stages 2 and 3 breast cancer tissues, especially in triple-negative breast cancer. IDH2 potentially serves as a target to detect unknown mechanisms in breast cancer.

Purpose: The purpose of this study was to identify the influence of health literacy and insight on medication adherence in mental illness.
Methods: A cross-sectional, descriptive correlational study design was used. Participants were 135 adults diagnosed with mental disorders and living in D city. Collected data were analyzed using descriptive statistics, t-test, ANOVA, Pearson’s correlation, and hierarchical multiple regression with SPSS 26.0.
Results: On multiple regression analysis, clinical insight (β=.32, p<.001) and reading response (β=.23, p=008) were statistically significant factors for medication adherence and showed a total explanatory power of 20%.
Conclusion In order to enhance medication adherence, strategies and programs are needed to improve the insight and health literacy among patients with severe mental illness.

We constructed an age-to-age infection matrix to characterize the household transmission pattern of coronavirus disease 2019 (COVID-19) in Korea. Among 4,048 household clusters, within-age group infection dominated the overall household transmissions. Transmission of severe acute respiratory syndrome coronavirus 2 was more common from adults to children than from children to adults.