Objectives: This study analyzed the relationship between parental body mass index (BMI; BMI_p) and hypertension in their adolescent offspring (HTN_a), focusing on the mediating effect of adolescents’ BMI (BMI_a). Methods: Utilizing data from the Korea National Health and Nutrition Examination Survey, including participants aged 12-18, we conducted a mediation analysis while controlling for confounding factors such as age, sex, physical activity, dietary habits, household income quartile, and parents’ alcohol and smoking habits. Results: The study included a total of 5731 participants, of whom 3381 and 5455 participants had data on fathers’ and mothers’ BMI, respectively. For adolescent systolic blood pressure (SBP_a), the father’s BMI (BMI_f) had a significant total effect (β, 0.23; 95% confidence interval [CI], 0.12 to 0.34) and average controlled mediated effect (ACME) (β, 0.27; 95% CI, 0.23 to 0.32), but the average direct effect (ADE) was not significant. The mother’s BMI (BMI_m) had a significant total effect (β, 0.17; 95% CI, 0.09 to 0.25), ACME (β, 0.25; 95% CI, 0.22 to 0.28) and ADE (β, -0.08; 95% CI, -0.16 to 0.00). For adolescent diastolic blood pressure, both BMI_f and BMI_m had significant ACMEs (β, 0.10; 95% CI, 0.08 to 0.12 and β, 0.09; 95% CI, 0.07 to 0.12, respectively), BMI_m had a significant ADE (β, -0.09; 95% CI, -0.16 to -0.02) but BMI_f had an insignificant ADE and total effect. Conclusions The study found that parental BMI had a significant effect on SBP_a, mediated through BMI_a. Therefore, a high BMI in parents could be a risk factor, mediated through BMI_a, for systolic hypertension in adolescents, necessitating appropriate management.

Background: Tinea capitis in adults has been increasing recently. Nevertheless, studies related to difference in tinea capitis between adults and children in Korea are scarce. Objective: To investigate the clinical and mycological features of tinea capitis in adults and children. Methods: The medical records of 60 adult and 58 pediatric patients with tinea capitis during a 24-year period were retrospectively examined. Results: The proportion of adult patients among all patients with tinea capitis had increased from 32.3% between 1999 and 2010 to 57.5% between 2011 and 2022 (p=0.016). The proportion of postmenopausal women among all adult patients with tinea capitis was 70.0%. Among those aged <50 years, the incidence rate ratio in males to that in females was 2:1. However, among those aged ≥50 years, the incidence rate ratio in males to that in females was 1:4.7, indicating a higher incidence in females (p=0.005). Microsporum canis was the most common etiological agent (48.8%), followed by Trichophyton rubrum (36.6%). M. canis was the most prevalent dermatophyte in adults (48.8%) and children (85.0%). However, the proportion of dermatophytes other than M. canis was higher in adults (51.2%) than in children (15.0%) (p＜0.001). Conclusion Tinea capitis in adults has increased, particularly in postmenopausal women. M. canis was the most prevalent dermatophyte; however, the prevalence of other species, notably T. rubrum, was higher in adults compared with that in children. These findings are expected to offer valuable insights for the early diagnosis and treatment of tinea capitis in adults.

Parkinson’s disease (PD) is the most prevalent neurodegenerative motor disorder. While PD has been attributed to dopaminergic neuronal death in substantia nigra pars compacta (SNpc), accumulating lines of evidence have suggested that reactive astrogliosis is critically involved in PD pathology. These pathological changes are associated with α-synuclein aggregation, which is more prone to be induced by an A53T mutation. Therefore, the overexpression of A53T-mutated α-synuclein (A53T-α-syn) has been utilized as a popular animal model of PD. However, this animal model only shows marginal-to-moderate extents of reactive astrogliosis and astrocytic α-synuclein accumulation, while these phenomena are prominent in human PD brains. Here we show that Adeno-GFAP-GFP virus injection into SNpc causes severe reactive astrogliosis and exacerbates the A53Tα-syn-mediated PD pathology. In particular, we demonstrate that AAV-CMV-A53T-α-syn injection, when combined with Adeno-GFAP-GFP, causes more significant loss of dopaminergic neuronal tyrosine hydroxylase level and gain of astrocytic GFAP and GABA levels. Moreover, the combination of AAV-CMV-A53T-α-syn and Adeno-GFAP-GFP causes an extensive astrocytic α-syn expression, just as in human PD brains. These results are in marked contrast to previous reports that AAV-CMV-A53T-α-syn alone causes α-syn expression mostly in neurons but rarely in astrocytes. Furthermore, the combination causes a severe PD-like motor dysfunction as assessed by rotarod and cylinder tests within three weeks from the virus injection, whereas Adeno-GFAP-GFP alone or AAV-CMV-A53T-α-syn alone does not. Our findings implicate that inducing reactive astrogliosis exacerbates PD-like pathologies and propose the virus combination as an advanced strategy for developing a new animal model of PD.

Parkinson’s disease (PD) is the most prevalent neurodegenerative motor disorder. While PD has been attributed to dopaminergic neuronal death in substantia nigra pars compacta (SNpc), accumulating lines of evidence have suggested that reactive astrogliosis is critically involved in PD pathology. These pathological changes are associated with α-synuclein aggregation, which is more prone to be induced by an A53T mutation. Therefore, the overexpression of A53T-mutated α-synuclein (A53T-α-syn) has been utilized as a popular animal model of PD. However, this animal model only shows marginal-to-moderate extents of reactive astrogliosis and astrocytic α-synuclein accumulation, while these phenomena are prominent in human PD brains. Here we show that Adeno-GFAP-GFP virus injection into SNpc causes severe reactive astrogliosis and exacerbates the A53Tα-syn-mediated PD pathology. In particular, we demonstrate that AAV-CMV-A53T-α-syn injection, when combined with Adeno-GFAP-GFP, causes more significant loss of dopaminergic neuronal tyrosine hydroxylase level and gain of astrocytic GFAP and GABA levels. Moreover, the combination of AAV-CMV-A53T-α-syn and Adeno-GFAP-GFP causes an extensive astrocytic α-syn expression, just as in human PD brains. These results are in marked contrast to previous reports that AAV-CMV-A53T-α-syn alone causes α-syn expression mostly in neurons but rarely in astrocytes. Furthermore, the combination causes a severe PD-like motor dysfunction as assessed by rotarod and cylinder tests within three weeks from the virus injection, whereas Adeno-GFAP-GFP alone or AAV-CMV-A53T-α-syn alone does not. Our findings implicate that inducing reactive astrogliosis exacerbates PD-like pathologies and propose the virus combination as an advanced strategy for developing a new animal model of PD.

OBJECTIVE: To evaluate the short-term changes in masticatory muscle activity and mandibular movement patterns after orthognathic surgery in skeletal Class III patients with facial asymmetry. METHODS: Twenty-seven skeletal Class III adult patients were divided into two groups based on the degree of facial asymmetry: the experimental group (n = 17 [11 male and 6 female]; menton deviation ≥ 4 mm) and control group (n = 10 [4 male and 6 female]; menton deviation < 1.6 mm). Cephalography, electromyography (EMG) for the anterior temporalis (TA) and masseter muscles (MM), and mandibular movement (range of motion [ROM] and average chewing pattern [ACP]) were evaluated before (T0) and 7 to 8 months (T1) after the surgery. RESULTS: There were no significant postoperative changes in the EMG potentials of the TA and MM in both groups, except in the anterior cotton roll biting test, in which the masticatory muscle activity had changed into an MM-dominant pattern postoperatively in both groups. In the experimental group, the amount of maximum opening, protrusion, and lateral excursion to the non-deviated side were significantly decreased. The turning point tended to be shorter and significantly moved medially during chewing in the non-deviated side in the experimental group. CONCLUSIONS In skeletal Class III patients with facial asymmetry, the EMG activity characteristics recovered to presurgical levels within 7 to 8 months after the surgery. Correction of the asymmetry caused limitation in jaw movement in terms of both ROM and ACP on the non-deviated side.

Alveolar Bone Loss ; Alveolar Process ; Alveolar Ridge Augmentation ; Bone Regeneration ; Dentistry ; Female ; Humans ; Inlays ; Mandible ; Osteoblasts ; Osteogenesis ; Osteogenesis, Distraction ; Polytetrafluoroethylene ; Titanium ; Transplants

Digital therapeutics based on software, such as artificial intelligence, virtual reality, games, and smartphone applications, are in the spotlight as new therapeutic alternatives in child and adolescent psychiatry. It draws attention to overcoming conventional therapeutics’ limitations, such as toxicity, cost, and accessibility, and encourages patients to participate in the treatment attractively. The growth potential of the digital therapeutics market for psychiatric disorders in children and adolescents in Korea and abroad has been highlighted. Clinical studies and Food and Drug Administration approvals for digital therapeutics have increased, and cases approved by the Ministry of Food and Drug Safety have emerged in Korea. As seen above, digital transformation in child and adolescent psychiatry will change treatment paradigms significantly. Therefore, as this new field has just begun to emerge, it is necessary to verify the effectiveness and scope of the application of digital therapeutics and consider preparing a compensation system and institutional arrangements. Accordingly, this study analyzed the development trends and application status of digital therapeutics in children and adolescents and presented limitations and development directions from the perspective of application in healthcare. Further, the study is expected to identify the utility and limitations of digital therapeutics for children and adolescents and establish effective application measures.

Interleukin-1 receptor-associated kinase 4 (IRAK4) is a pivotal enzyme in the Toll-like receptor (TLR)/MYD88 dependent signaling pathway, which is highly activated in rheumatoid arthritis tissues and activated B cell-like diffuse large B-cell lymphoma (ABC-DLBCL). Inflammatory responses followed by IRAK4 activation promote B-cell proliferation and aggressiveness of lymphoma. Moreover, proviral integration site for Moloney murine leukemia virus 1 (PIM1) functions as an anti-apoptotic kinase in propagation of ABC-DLBCL with ibrutinib resistance. We developed a dual IRAK4/PIM1 inhibitor KIC-0101 that potently suppresses the NF-κB pathway and proinflammatory cytokine induction in vitro and in vivo. In rheumatoid arthritis mouse models, treatment with KIC-0101 significantly ameliorated cartilage damage and inflammation. KIC-0101 inhibited the nuclear translocation of NF-κB and activation of JAK/STAT pathway in ABC-DLBCLs. In addition, KIC-0101 exhibited an anti-tumor effect on ibrutinib-resistant cells by synergistic dual suppression of TLR/MYD88-mediated NF-κB pathway and PIM1 kinase. Our results suggest that KIC-0101 is a promising drug candidate for autoimmune diseases and ibrutinib-resistant B-cell lymphomas.