Previous studies have shown that testosterone activates the GPRC6A-Duox1 axis, resulting in the production of H 2O 2 which leads to the apoptosis of keratinocytes and ultimately hair loss. Here, we elucidated a molecular mechanism by which the non-genomic action of testosterone regulates cellular redox status in androgenetic alopecia (AGA). Building upon this molecular understanding, we conducted a high-throughput screening assay of Nox inhibitors from a natural compounds library. This screening identified diterpenoid compounds, specifically Tanshinone I, Tanshinone IIA, Tanshinone IIB, and Cryptotanshinone, derived from Salviae Miltiorrhizae Radix. The IC50 values for Nox isozymes were found to be 2.6-12.9 μM for Tanshinone I, 1.9-7.2 μM for Tanshinone IIA, 5.2-11.9 μM for Tanshinone IIB, and 2.1-7.9 μM for Cryptotanshinone. Furthermore, 3D computational docking analysis confirmed the structural basis by which Tanshinone compounds inhibit Nox activity. These compounds were observed to substitute for NADPH at the π-π bond site between NADPH and FAD, leading to the suppression of Nox activity. Notably, Tanshinone I and Tanshinone IIA effectively inhibited Nox activity heightened by testosterone, consequently reducing the production of intracellular H2O2 and preventing cell apoptosis. In an animal study involving the application of testosterone to the back skin of 8-week-old C57BL/6J mice to inhibit hair growth, subsequent treatment with Tanshinone I or Tanshinone IIA alongside testosterone resulted in a substantial increase in hair follicle length compared to testosterone treatment alone. These findings underscore the potential efficacy of Tanshinone I and Tanshinone IIA as therapeutic agents for AGA by inhibiting Nox activity.

Previous studies have shown that testosterone activates the GPRC6A-Duox1 axis, resulting in the production of H 2O 2 which leads to the apoptosis of keratinocytes and ultimately hair loss. Here, we elucidated a molecular mechanism by which the non-genomic action of testosterone regulates cellular redox status in androgenetic alopecia (AGA). Building upon this molecular understanding, we conducted a high-throughput screening assay of Nox inhibitors from a natural compounds library. This screening identified diterpenoid compounds, specifically Tanshinone I, Tanshinone IIA, Tanshinone IIB, and Cryptotanshinone, derived from Salviae Miltiorrhizae Radix. The IC50 values for Nox isozymes were found to be 2.6-12.9 μM for Tanshinone I, 1.9-7.2 μM for Tanshinone IIA, 5.2-11.9 μM for Tanshinone IIB, and 2.1-7.9 μM for Cryptotanshinone. Furthermore, 3D computational docking analysis confirmed the structural basis by which Tanshinone compounds inhibit Nox activity. These compounds were observed to substitute for NADPH at the π-π bond site between NADPH and FAD, leading to the suppression of Nox activity. Notably, Tanshinone I and Tanshinone IIA effectively inhibited Nox activity heightened by testosterone, consequently reducing the production of intracellular H2O2 and preventing cell apoptosis. In an animal study involving the application of testosterone to the back skin of 8-week-old C57BL/6J mice to inhibit hair growth, subsequent treatment with Tanshinone I or Tanshinone IIA alongside testosterone resulted in a substantial increase in hair follicle length compared to testosterone treatment alone. These findings underscore the potential efficacy of Tanshinone I and Tanshinone IIA as therapeutic agents for AGA by inhibiting Nox activity.

Previous studies have shown that testosterone activates the GPRC6A-Duox1 axis, resulting in the production of H 2O 2 which leads to the apoptosis of keratinocytes and ultimately hair loss. Here, we elucidated a molecular mechanism by which the non-genomic action of testosterone regulates cellular redox status in androgenetic alopecia (AGA). Building upon this molecular understanding, we conducted a high-throughput screening assay of Nox inhibitors from a natural compounds library. This screening identified diterpenoid compounds, specifically Tanshinone I, Tanshinone IIA, Tanshinone IIB, and Cryptotanshinone, derived from Salviae Miltiorrhizae Radix. The IC50 values for Nox isozymes were found to be 2.6-12.9 μM for Tanshinone I, 1.9-7.2 μM for Tanshinone IIA, 5.2-11.9 μM for Tanshinone IIB, and 2.1-7.9 μM for Cryptotanshinone. Furthermore, 3D computational docking analysis confirmed the structural basis by which Tanshinone compounds inhibit Nox activity. These compounds were observed to substitute for NADPH at the π-π bond site between NADPH and FAD, leading to the suppression of Nox activity. Notably, Tanshinone I and Tanshinone IIA effectively inhibited Nox activity heightened by testosterone, consequently reducing the production of intracellular H2O2 and preventing cell apoptosis. In an animal study involving the application of testosterone to the back skin of 8-week-old C57BL/6J mice to inhibit hair growth, subsequent treatment with Tanshinone I or Tanshinone IIA alongside testosterone resulted in a substantial increase in hair follicle length compared to testosterone treatment alone. These findings underscore the potential efficacy of Tanshinone I and Tanshinone IIA as therapeutic agents for AGA by inhibiting Nox activity.

The hygiene hypothesis, first proposed in 1989, suggested that reduced exposure to infections in early life leads to allergic diseases by the defects in the establishment of immune tolerance. Although many studies provided evidence that some exposure conditions, including family size, antibiotics, probiotics, and viral or bacterial infections, are strongly related to the prevalence of allergic diseases, thereby supporting the hygiene hypothesis, some evidence does not provide acceptable results for the hygiene hypothesis. Further, most studies have focused on patients with asthma or atopic dermatitis, not allergic rhinitis. In this review, we summarize the recent studies for and against the ‘hygiene hypothesis’ and identify causal association with the prevalence of allergic rhinitis.

Allergic rhinitis (AR) is a type of rhinitis accompanied by sensitization to allergens. One of the most clinically important allergens is pollen. Recently, due to climate change and CO 2 air pollution, the flowering period starts earlier and persists longer. In addition, antigenicity due to environmental pollution is also being strengthened. As a result, the sensitization rate to pollen antigens is on the rise. It is known that the prevalence of AR especially caused by pollen is rapidly escalating. Although the causal relationship between pollen exposure and the severity of rhinitis is not precisely established, an association of rhinitis symptoms with the time of pollen scattering exists. In addition, the mixed effect of environmental pollution and pollen may play a role in the development of rhinitis symptoms. Therefore, in order to avoid pollen, it is necessary to constantly improve pollen forecast and minimize the contact with pollen indoors and outdoors. Treatment of AR should be performed according to guidelines. Also, continuous efforts to solve the environmental problems affecting the ecology of pollen are needed.

Among allergic diseases of the Korean pediatric population, allergic rhinitis shows the most rapidly increasing prevalence. Its economic burden is substantial in many Asian countries including South Korea. This investigation of its risk factors aims to reduce the socioeconomic burden by blocking exposure of susceptible individuals to identified causes. However, the risk factors of allergic rhinitis varied considerably depending on the seasons, geographical locations, and populations involved. This review article primarily deals with studies on the risk factors for allergic rhinitis in Korean children that were published during the last 10 years and additionally investigates associated large scale international studies. Our investigation identified several single-nucleotide polymorphisms, inhalant allergens, pollution, tobacco smoke, chemicals, and family affluence as risk factors for allergic rhinitis. In contrast, breastfeeding, older sibling, and microbial diversity were protective factors against allergic rhinitis. This suggests that various genetic and environmental factors might affect the manifestation and presentation of allergic rhinitis complexly. These findings are beneficial as they can provide insights into modifiable risk factors that may hinder the development of allergic rhinitis.

The prevalence of allergic rhinitis in children and adolescents is constantly increasing. However, few studies exist on the relationship between smoking and allergic rhinitis. In addition to conventional cigarettes, electronic and heated cigarettes have recently been introduced, which have several harmful effects. It is hypothesized that smoking and rhinitis are correlated; however, this relationship is complex. Previous studies reported that exposure to smoking during pregnancy is associated with allergic rhinitis development.Unlike the varied results reported in adults, studies on children and adolescents have often correlated direct/indirect smoke with allergic rhinitis, with prolonged exposure being associated with a higher risk of allergic rhinitis, particularly when exposed at an early age. Nonallergic inflammatory reactions and immunoglobulin E-mediated allergic sensitization are assumed to be the underlying mechanisms for the association between allergic rhinitis and smoking. Measures to reduce smoking are warranted to lower the incidence of allergic rhinitis in children and adolescents and to improve their health.

The global worsening of air pollution has decreased the quality of life. Air pollutants can induce oxidative stress, epigenetic changes, and alterations to microRNA expression in the airway and skin, leading to immune dysregulation. Previous epidemiological studies suggest a strong association between outdoor environmental pollution and childhood allergic disease, especially allergic rhinitis (AR). Moreover, traffic-related air pollution has increased the severity and incidence of AR, and heavy traffic has been associated with an increased prevalence of AR. Thus, this review aimed to define outdoor environmental pollution and clarify the mechanisms by which air pollutants aggravate AR. In addition, we performed a systematic review and meta-analysis to summarize the findings of several domestic and international epidemiological and clinical studies about the effects of air pollution on AR in children.

Allergic rhinitis (AR) is one of the most common allergic diseases characterized by stuffy nose, rhinorrhea, sneezing, and itching. Researchers have indicated an increase in the prevalence of AR and younger-age onset during the last few decades. The increasing burden of AR has caused many researchers to investigate time trends of the prevalence of AR and to identify its risk factors. The most commonly used epidemiological studies are cross-sectional ones such as the International Study of Asthma and Allergies in Childhood study and big data from National Health Insurance Service or National Health and Nutrition Examination Survey. However, these studies have many limitations including recall bias, selection bias, and deficit of objective evaluation. Furthermore, crosssectional studies cannot reflect new risk factors associated with the development of AR. New epidemiological studies will be needed to cover genetic factors, environmental changes, microbiomes, and lifestyles that are known to be risk factors for AR. Further studies will be needed to determine the prevalence, natural history, and risk factors of AR in order to advance our understanding of the pathophysiology, prevention, and management of comorbidities of AR.

The radiographic findings of an osteolytic lesion in the knee may indicate numerous possible impressions. Furthermore, osteolysis is a possible cause if there is a surgical history of total knee arthroplasty (TKA). The authors diagnosed osteolysis of the fibular head after aseptic loosening of the tibial component of a cemented TKA in an 83-year-old female patient who visited with right knee pain and report their treatment with revision TKA along with a literature review.