OBJECTIVES: To describe the characteristics of a mumps epidemic in Cheju-do, 1998 and to identify the risk factors associated with mumps infection. METHODS: To estimate attack rate, previously collected data from the Nationally Notifiable Communicable Disease Reporting System and School Health Reporting System, temporarily administered by Division of Education, as well as additional surveillance data were used. In order to identify the clinical characteristics and risk factors associated with mumps, we conducted a questionnaire survey in 17 schools (9 elementary, 4 middle, and 4 high schools) among a population that included healthy students. RESULTS: From March 3 to August 31, 2,195 cases of mumps were identified, and patients under 20 years of age accounted for 2,162 cases (attack rate 13.2, 95% CI 12.6-13.7/1,000). The attack rate for the population under 20 years of age was the highest in Nam county (44.7/1,000), and in the 7-12 years old sub-group(>20.0/1,000). There was no sexual difference. 80.9% and 59.7% of patients presented periauricular and submandibular swelling respectively. Aseptic meningitis was a complication in 2.9% of cases, orchitis in 1.3%, epididymitis in 0.9% and oophoritis in 0.6% respectively. The overall MMR vaccination rate was 59.1% and it decreased in accordance with increasing age. In students aged 10 years old or below, household contact and MMR vaccination status was significantly associated with infection, and only among students with household contact, the risk of one dose MMR(OR=10.22, 95% CI 2.92-35.78) and non-vaccination (OR=11.62, 95% CI 1.96-68.96) was significantly greater when compared with that of two dose vaccination. Among students aged 11 years old or above, household contact history was significantly associated and MMR vaccination status was not associated. CONCLUSIONS: Low vaccination rate and vaccine failure were thought to predispose the population for this large outbreak. To prevent sustained mumps outbreaks, a second MMR vaccination should be encouraged and catch up vaccinations should be given to elderly children who remain susceptible.
Aged ; Child ; Communicable Diseases ; Disease Outbreaks ; Education ; Epididymitis ; Family Characteristics ; Female ; Humans ; Jeju-do* ; Male ; Meningitis, Aseptic ; Mumps* ; Oophoritis ; Orchitis ; Questionnaires ; Risk Factors ; School Health Services ; Vaccination

AMP-activated protein kinase (AMPK) activators have garnered significant attention for their potential to prevent the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) into liver fibrosis and to fundamentally improve liver function. The broad spectrum of pathways regulated by AMPK activators makes them promising alternatives to conventional liver replacement therapies and the limited pharmacological treatments currently available. In this study, we aim to illustrate the newly detailed multiple mechanisms of MASLD progression based on the multiple-hit hypothesis. This model posits that impaired lipid metabolism, combined with insulin resistance and metabolic imbalance, initiates inflammatory cascades, gut dysbiosis, and the accumulation of toxic metabolites, ultimately promoting fibrosis and accelerating MASLD progression to irreversible hepatocellular carcinoma (HCC). AMPK plays a multifaceted protective role against these pathological conditions by regulating several key downstream signaling pathways. It regulates biological effectors critical to metabolic and inflammatory responses, such as SIRT1, Nrf2, mTOR, and TGF-β, through complex and interrelated mechanisms. Due to these intricate connections, AMPK’s role is pivotal in managing metabolic and inflammatory disorders. In this review, we demonstrate the specific roles of AMPK and its related pathways. Several agents directly activate AMPK by binding as agonists, while some others indirectly activate AMPK by modulating upstream molecules, including adiponectin, LKB1, and the AMP: ATP ratio. As AMPK activators can target each stage of MASLD progression, the development of AMPK activators offers immense potential to expand therapeutic strategies for liver diseases such as MASH, MASLD, and liver fibrosis.

AMP-activated protein kinase (AMPK) activators have garnered significant attention for their potential to prevent the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) into liver fibrosis and to fundamentally improve liver function. The broad spectrum of pathways regulated by AMPK activators makes them promising alternatives to conventional liver replacement therapies and the limited pharmacological treatments currently available. In this study, we aim to illustrate the newly detailed multiple mechanisms of MASLD progression based on the multiple-hit hypothesis. This model posits that impaired lipid metabolism, combined with insulin resistance and metabolic imbalance, initiates inflammatory cascades, gut dysbiosis, and the accumulation of toxic metabolites, ultimately promoting fibrosis and accelerating MASLD progression to irreversible hepatocellular carcinoma (HCC). AMPK plays a multifaceted protective role against these pathological conditions by regulating several key downstream signaling pathways. It regulates biological effectors critical to metabolic and inflammatory responses, such as SIRT1, Nrf2, mTOR, and TGF-β, through complex and interrelated mechanisms. Due to these intricate connections, AMPK’s role is pivotal in managing metabolic and inflammatory disorders. In this review, we demonstrate the specific roles of AMPK and its related pathways. Several agents directly activate AMPK by binding as agonists, while some others indirectly activate AMPK by modulating upstream molecules, including adiponectin, LKB1, and the AMP: ATP ratio. As AMPK activators can target each stage of MASLD progression, the development of AMPK activators offers immense potential to expand therapeutic strategies for liver diseases such as MASH, MASLD, and liver fibrosis.

AMP-activated protein kinase (AMPK) activators have garnered significant attention for their potential to prevent the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) into liver fibrosis and to fundamentally improve liver function. The broad spectrum of pathways regulated by AMPK activators makes them promising alternatives to conventional liver replacement therapies and the limited pharmacological treatments currently available. In this study, we aim to illustrate the newly detailed multiple mechanisms of MASLD progression based on the multiple-hit hypothesis. This model posits that impaired lipid metabolism, combined with insulin resistance and metabolic imbalance, initiates inflammatory cascades, gut dysbiosis, and the accumulation of toxic metabolites, ultimately promoting fibrosis and accelerating MASLD progression to irreversible hepatocellular carcinoma (HCC). AMPK plays a multifaceted protective role against these pathological conditions by regulating several key downstream signaling pathways. It regulates biological effectors critical to metabolic and inflammatory responses, such as SIRT1, Nrf2, mTOR, and TGF-β, through complex and interrelated mechanisms. Due to these intricate connections, AMPK’s role is pivotal in managing metabolic and inflammatory disorders. In this review, we demonstrate the specific roles of AMPK and its related pathways. Several agents directly activate AMPK by binding as agonists, while some others indirectly activate AMPK by modulating upstream molecules, including adiponectin, LKB1, and the AMP: ATP ratio. As AMPK activators can target each stage of MASLD progression, the development of AMPK activators offers immense potential to expand therapeutic strategies for liver diseases such as MASH, MASLD, and liver fibrosis.