Taste buds relay taste sensory information to the primary taste neurons but depend on those same neurons for essential components to maintain function. While denervation-induced taste bud degeneration and subsequent regeneration were discovered decades ago, the mechanisms underlying these phenomena (e.g., heterogenous cellular responses to nerve injury and the signaling pathways involved) remain poorly understood. Here, using mouse genetics, nerve injury models, pharmacologic manipulation, and taste bud organoid models, we identify a specific subpopulation of taste cells, predominantly c-Kit-expressing sweet cells, that exhibit superior resistance to nerve injury. We found the c-Kit inhibitor imatinib selectively reduced the number of residual c-Kit-expressing sweet cells at post-operation week 2, subsequently attenuating the re-emergence of other type II cells by post-operation week 4. In taste bud organoids, c-Kit-expressing cells were resistant to R-spondin withdrawal but susceptible to imatinib, while other taste cell types showed the opposite behavior. We also observed a distinct population of residual taste cells that acquired stem-like properties, generating clonal descendent cells among suprabasal keratinocytes independent of c-Kit signaling. Together, our findings reveal that c-Kit signaling confers resilience on c-Kit-expressing sweet cells and supports the broader reconstruction of taste buds during the later regenerative stage following nerve injury.
Animals ; Taste Buds/metabolism* ; Proto-Oncogene Proteins c-kit/metabolism* ; Mice ; Signal Transduction ; Imatinib Mesylate/pharmacology* ; Mice, Inbred C57BL

Background: Anemia is a common complication of chronic kidney disease (CKD). In patients with CKD-related anemia, an inverse relationship between vitamin D and hepcidin levels has been observed. Hepcidin is a key regulator of iron homeostasis, mediated via binding to ferroportin. The aim of this study was to investigate the effects of cholecalciferol and omega-3 fatty acids (FA) on hepcidin levels using 5/6 nephrectomized (Nx) rats. Methods: Male Sprague-Dawley rats were divided into five groups: sham control, 5/6 Nx, 5/6 Nx treated with cholecalciferol, 5/6 Nx treated with omega-3 FA, and 5/6 Nx treated with both cholecalciferol and omega-3 FA. We measured the hepcidin and ferroportin levels in the kidney and liver by enzyme-linked immunosorbent assays and Western blots. We evaluated hepcidin expression in the kidney by immunohistochemical staining. Results: Among the five groups, 5/6 Nx rats exhibited the worst kidney function. Compared with the sham controls, 5/6 Nx rats showed significantly increased serum hepcidin levels and decreased vitamin D levels. Supplementation with either omega-3 FA or cholecalciferol decreased hepcidin and increased vitamin D levels, with a concurrent improvement of anemia. Furthermore, 5/6 Nx rats treated with omega-3 FA/cholecalciferol showed decreased ferroportin and ferritin levels, while iron and total iron-binding capacity levels increased. Conclusions Treatment with a combination of cholecalciferol and omega-3 FA may improve anemia in a CKD rat model by decreasing hepcidin levels.

Objective: The increasing concern over adolescent suicide necessitates suicide prevention training for school teachers, as students spend a significant portion of their time at school. This study’s objective is to develop a suicide prevention program tailored for teachers. Methods: The program was developed by a multidisciplinary research team, drawing on a review of both domestic and international suicide prevention programs, related scholarly articles, and Korean psychological autopsy interviews of adolescents. This was complemented by a survey of teachers to assess the program’s practicality and usability. Results: The developed program comprises three parts, consistent with other versions: Careful Observation, Active Listening, and Risk Evaluation and Expert Referral. Careful Observation focuses on training teachers to recognize verbal, behavioral, and situational warning signs of suicidal ideation in students; Active Listening involves strategies for encouraging students to express their suicidal thoughts and techniques for being an empathetic and attentive listener; Risk Evaluation and Expert Referral provides instruction on how to assess suicide risk and assist students safely. Conclusion It is anticipated that this program will equip teachers with valuable knowledge and skills, contributing to a reduction in adolescents suicide rates.

Purpose: Benign prostate hyperplasia (BPH) is a common age-related chronic condition. Its pathogenesis involves androgen imbalance, inflammation, oxidative stress, and endoplasmic reticulum (ER) stress. This study aims to assess the protective effect of finasteride, a 5α-reductase inhibitor, against testosterone propionate (TP)-induced BPH in rats and explore its potential mechanism of action. Materials and Methods: TP-induced BPH rats received either saline or finasteride (1 mg/kg) orally once a day for 7 weeks. Prior to sacrificing the animals, blood samples were collected. After sacrifice, prostate and tissue around the prostate were dissected from seminal vesical for further analysis. Body weight, prostate weight, dihydrotestosterone (DHT), 5α-reductase type 2 (5-AR2), and prostate-specific antigen (PSA) levels were measured. In addition, HIF-1α, VEGF, MMP-2 expressions in prostate, oxidative stress, inflammation, and ER stress responses were analyzed to understand the mechanism of action of finasteride. Results: Finasteride administration inhibited prostate enlargement, DHT, 5-AR2, and PSA levels in BPH rats. Additionally, finasteride inhibited angiogenesis markers such as HIF-1α, VEGF, and MMP-2. Moreover, components of oxidative stress, inflammation, and ER stress responses were significantly regulated by finasteride treatment. Conclusions This study suggests that finasteride prevents BPH-associated symptoms by regulating angiogenesis, reactive oxygen species, ER stress responses, and inflammation, another mechanism to explain the effect of the 5α-reductase against BPH.

Objective: Research on fetal mortality due to congenital anomalies is insufficient, particularly that utilizing data specific to South Korea. Thus, we aimed to investigate the characteristics and risk factors for fetal death due to congenital anomalies in Korea. Methods: Fetal deaths registered from 2009-2020 with Statistics Korea were assessed. Fetal charac teristics included gestational age, body weight, sex, and multiple fetuses, while maternal characteri stics included age, educational level, nationality, and place of residence. Risk factors for fetal death were analyzed using simple comparison and logistic regression. Changes in fetal mortality by year were examined using Poisson regression analysis. Results: A total of 37,928 fetal deaths occurred, among which 3,758 were classified as congenital anomaly, 710 as non-congenital anomaly, and 33,460 as unknown cause. Fetal mortality for gesta tional weeks 20 to 27 and ≥28 were 75.3% and 24.7%, respectively. The proportion of congenital anomalies among fetal deaths during these gestational age periods is 11.3% and 5.8%. Multiple fetuses, maternal age of <20 years or ≥40 years were identified as risk factors for fetal death due to congenital anomalies. Among the top 30 causes, covering 97.5% of all deaths, unspecified causes were 88.2%, congenital malformations 8.2%, and other causes 2.0%, respectively. Fetal mortality and deaths from congenital anomalies exhibited downward trends. Conclusion Fetal deaths due to congenital anomalies showed a decreasing trend, but the risks, such as multiple fetuses and advanced maternal age are increasing in Korea. Therefore, careful monitoring of fetal deaths due to congenital anomalies are essential.