Purpose: High breast cancer incidence and dense breast prevalence among women in forties are specific to Asian. This study examined the natural history of breast cancer among Korean women. Materials and Methods: We applied a three-state Markov model (i.e., healthy, preclinical, and clinical state) to fit the natural history of breast cancer to data in the Korean National Cancer Screening Program. Breast cancer was ascertained by linkage to the Korean Central Cancer Registry. Disease-progression rates (i.e., transition rates between three states), mean sojourn time (MST) and mammographic sensitivity were estimated across 10-year age groups and levels of breast density determined by the Breast Imaging, Reporting and Data System. Results: Overall prevalence of dense breast was 53.9%. Transition rate from healthy to preclinical state, indicating the preclinical incidence of breast cancer, was higher among women in forties (0.0019; 95% confidence interval [CI], 0.0017 to 0.0021) and fifties (0.0020; 95% CI, 0.0017 to 0.0022), than women in sixties (0.0014; 95% CI, 0.0012 to 0.0017). The MSTs, in which the tumor is asymptomatic but detectable by screening, were also fastest among younger age groups, estimated as 1.98 years (95% CI, 1.67 to 2.33), 2.49 years (95% CI, 1.92 to 3.22), and 3.07 years (95% CI, 2.11 to 4.46) for women in forties, fifties, and sixties, respectively. Having dense breasts increased the likelihood of the preclinical cancer risk (1.96 to 2.35 times) and decreased the duration of MST (1.53 to 2.02 times). Conclusion This study estimated Korean-specific natural history parameters of breast cancer that would be utilized for establishing optimal screening strategies in countries with higher dense breast prevalence.

Despite the availability of direct-acting antivirals (DAAs) for chronic hepatitis C virus (HCV) infection in Korea, need remains for pangenotypic regimens that can be used in the presence of hepatic impairment, comorbidities, or prior treatment failure. We investigated the efficacy and safety of sofosbuvir–velpatasvir and sofosbuvir–velpatasvir–voxilaprevir for 12 weeks in HCV-infected Korean adults. Methods: This Phase 3b, multicenter, open-label study included 2 cohorts. In Cohort 1, participants with HCV genotype 1 or 2 and who were treatment-naive or treatment-experienced with interferon-based treatments, received sofosbuvir–velpatasvir 400/100 mg/day. In Cohort 2, HCV genotype 1 infected individuals who previously received an NS5A inhibitor-containing regimen ≥ 4 weeks received sofosbuvir–velpatasvir–voxilaprevir 400/100/100 mg/day. Decompensated cirrhosis was an exclusion criterion. The primary endpoint was SVR12, defined as HCV RNA < 15 IU/mL 12 weeks following treatment. Results: Of 53 participants receiving sofosbuvir–velpatasvir, 52 (98.1%) achieved SVR12. The single participant who did not achieve SVR12 experienced an asymptomatic Grade 3 ASL/ALT elevation on day 15 and discontinued treatment. The event resolved without intervention. All 33 participants (100%) treated with sofosbuvir–velpatasvir–voxilaprevir achieved SVR 12. Overall, sofosbuvir–velpatasvir and sofosbuvir–velpatasvir–voxilaprevir were safe and well tolerated. Three participants (5.6%) in Cohort 1 and 1 participant (3.0%) in Cohort 2 had serious adverse events, but none were considered treatment-related. No deaths or grade 4 laboratory abnormalities were reported. Conclusions: Treatment with sofosbuvir–velpatasvir or sofosbuvir–velpatasvir–voxilaprevir was safe and resulted in high SVR12 rates in Korean HCV patients.

Objective: The goal of the present study was to identify factors related to the growth and growth patterns of unruptured intracranial aneurysms (UIAs). Methods: Between January 2011 and December 2018, a total of 275 patients were diagnosed with UIAs in our institution. Of them, 91 patients were evaluated using computed tomography angiography, magnetic resonance angiography, or digital subtraction angiography. Aneurysm size, morphology, location, and its changes were investigated. Patient factors, including gender, history of stroke, smoking, hypertension, diabetes mellitus, and excessive alcohol consumption, were studied to identify factors associated with aneurysm growth. Results: A total of 91 patients (121 aneurysms) with a mean follow-up duration of 37.2±23.9 months and a mean age of 64.0±11.4 years were included. The growth of unruptured aneurysms was identified in 23 patients (27 aneurysms, 22.3%). Regarding morphology, the diffuse growth pattern was the most common (12 aneurysms in 10 patients, 44.4%). Univariate analysis showed that patients with multiple aneurysms (p=0.010), history of stroke (p=0.021), and aneurysm location in the posterior circulation (p=0.029) were significantly associated with aneurysm growth. Conclusion The growth of an UIA is associated with the history of stroke, posterior location, and multiplicity. Considering the risk of unruptured aneurysm growth, patients with such risk factors should receive additional attention during follow-up.

Sarcopenia leads to loss of skeletal muscle mass, quality, and strength due to aging; it was recently given a disease code (International Classification of Diseases, Tenth Revision, Clinical Modification, M62.84). As a result, in recent years, sarcopenia-related research has increased. In addition, various studies seeking to prevent and treat sarcopenia by identifying the various mechanisms related to the reduction of skeletal muscle properties have been conducted. Previous studies have identified muscle synthesis and breakdown; investigating them has generated evidence for preventing and treating sarcopenia. Mouse models are still the most useful ones for determining mechanisms underlying sarcopenia through correlations and interventions involving specific genes and their phenotypes. Mouse models used to study sarcopenia often induce muscle atrophy by hindlimb unloading, denervation, or immobilization. Though it is less frequently used, the senescence-accelerated mouse can also be useful for sarcopenia research. Herein, we discuss cases where senescence-accelerated and genetically engineered mouse models were used in sarcopenia research and different perspectives to use them.

Sarcopenia leads to loss of skeletal muscle mass, quality, and strength due to aging; it was recently given a disease code (International Classification of Diseases, Tenth Revision, Clinical Modification, M62.84). As a result, in recent years, sarcopenia-related research has increased. In addition, various studies seeking to prevent and treat sarcopenia by identifying the various mechanisms related to the reduction of skeletal muscle properties have been conducted. Previous studies have identified muscle synthesis and breakdown; investigating them has generated evidence for preventing and treating sarcopenia. Mouse models are still the most useful ones for determining mechanisms underlying sarcopenia through correlations and interventions involving specific genes and their phenotypes. Mouse models used to study sarcopenia often induce muscle atrophy by hindlimb unloading, denervation, or immobilization. Though it is less frequently used, the senescence-accelerated mouse can also be useful for sarcopenia research. Herein, we discuss cases where senescence-accelerated and genetically engineered mouse models were used in sarcopenia research and different perspectives to use them.

The hallmark symptom of sarcopenia is the loss of muscle mass and strength without the loss of overall body weight. Sarcopenia patients are likely to have worse clinical outcomes and higher mortality than do healthy individuals. The sarcopenia population shows an annual increase of ~0.8% in the population after age 50, and the prevalence rate is rapidly increasing with the recent worldwide aging trend. Based on International Classification of Diseases, Tenth Revision, a global classification of disease published by the World Health Organization, issued the disease code (M62.84) given to sarcopenia in 2016. Therefore, it is expected that the study of sarcopenia will be further activated based on the classification of disease codes in the aging society. Several epidemiological studies and meta-analyses have looked at the correlation between the prevalence of sarcopenia and several environmental factors. In addition, studies using cell lines and rodents have been done to understand the biological mechanism of sarcopenia. Laboratory rodent models are widely applicable in sarcopenia studies because of the advantages of time savings, cost saving, and various analytical applications that could not be used for human subjects. The rodent models that can be applied to the sarcopenia research are diverse, but a simple and fast method that can cause atrophy or aging is preferred. Therefore, we will introduce various methods of inducing muscular atrophy in rodent models to be applied to the study of sarcopenia.

BACKGROUND/AIMS: Bicarbonate-containing alginate formulations are reported to be effective for controlling reflux symptoms. However, the efficacy of Lamina G alginate without gas production has not been reported. The aim is to evaluate the efficacy of a non-bicarbonate alginate in individuals with reflux symptoms without reflux esophagitis. METHODS: Participants who had experienced heartburn or regurgitation for 7 consecutive days were randomized to one of the following treatment groups: proton pump inhibitors (PPI) plus alginate (combination) or PPI plus placebo (PPI only). In addition, as a reference group, patients received placebo plus alginate (alginate only). The primary endpoint compared the percentage of patients with complete resolution of symptoms for the final 7 days of the treatment. Secondary endpoints compared changes in symptom score, symptom-free days during the treatment period, the Reflux Disease Questionnaire, Patient Assessment of Upper Gastrointestinal Disorders (PAGI)-Quality of Life and PAGI-Symptoms Severity Index scores, the investigator's assessment of symptoms, and incidence of adverse events. RESULTS: Complete resolution of heartburn or regurgitation was not significantly different between the combination and PPI only groups (58.7% vs 57.5%, p=0.903). The secondary endpoints were not significantly different between the two groups. Complete resolution of heartburn or regurgitation, did not differ between the alginate only reference group and the PPI only group (75.0% vs 57.5%, p=0.146). CONCLUSIONS: The addition of non-bicarbonate alginate to PPI was no more effective than PPI alone in controlling reflux symptoms.
Alginates ; Clinical Study ; Esophagitis, Peptic ; Gastroesophageal Reflux ; Heartburn ; Humans ; Incidence ; Proton Pump Inhibitors ; Treatment Outcome

Acute gastroenteritis is common infectious disease in community in adults. This work represents an update of ‘Clinical guideline for the diagnosis and treatment of gastrointestinal infections’ that was developed domestically in 2010. The recommendation of this guideline was developed regarding the following; epidemiological factors, test for diagnosis, the indications of empirical antibiotics, and modification of antibiotics after confirming pathogen. Ultimately, it is expected to decrease antibiotic misuse and prevent antibiotic resistance.

BACKGROUND: Acute infectious diarrhea (AID) is a commonly observed condition globally. Several studies recommend against the use of empiric antibiotic therapy for AID, except in some cases of travelers' diarrhea. However, many physicians prescribe antimicrobial agents for AID. We aimed to determine the rate of antibiotic use and the associated prescription patterns among adults with AID. MATERIALS AND METHODS: This population-based, retrospective epidemiological study was performed using Korean National Health Insurance claims data from 2016 to 2017. The study population comprised adults (age ≥18 years) who had visited clinics with AID-related complaints. Exclusion criteria were the presence of Crohn's disease, ulcerative colitis, irritable bowel syndrome, and other non-infectious forms of colitis. Patients who underwent surgery during admission were also excluded. RESULTS: The study population comprised 1,613,057 adult patients with AID (767,606 [47.6%] men). Young patients (age 18 – 39 years) accounted for 870,239 (54.0%) of the study population. Overall, 752,536 (46.7%) cases received antibiotic prescriptions. The rate of antibiotic administration tended to be higher among elderly patients (age ≥65 years) than among younger patients (49.5% vs. 46.4%, P <0.001). The antibiotics most frequently prescribed in both monotherapy and combination regimens were fluoroquinolones (29.8%), rifaximin (26.8%), second-generation cephalosporins (9.2%), third-generation cephalosporins (7.3%), trimethoprim/sulfamethoxazole (5.5%), and β-lactam/β-lactamase inhibitors (5.3%). Patients who visited tertiary care hospitals had lower rates of antibiotic therapy (n = 14,131, 41.8%) than did those visiting private clinics (n = 532,951, 47.1%). In total, 56,275 (62.3%) admitted patients received antibiotic therapy, whereas outpatients had lower rates of antibiotic prescription (n = 694,204, 46.0%). CONCLUSION This study revealed differences between the antibiotics used to treat AID in Korea and those recommended by the guidelines for AID treatment. Multifaceted efforts are necessary to strengthen physicians' adherence to published guidelines.

The enhanced differentiation and activation of osteoclasts (OCs) in the inflammatory arthritis such as rheumatoid arthritis (RA) and gout causes not only local bone erosion, but also systemic osteoporosis, leading to functional disabilities and morbidity. The induction and amplification of NFATc1, a master regulator of OC differentiation, is mainly regulated by receptor activator of NF-κB (RANK) ligand-RANK and calcium signaling which are amplified in the inflammatory milieu, as well as by inflammatory cytokines such as TNFα, IL-1β and IL-6. Moreover, the predominance of CD4+ T cell subsets, which varies depending on the condition of inflammatory diseases, can determine the fate of OC differentiation. Anti-citrullinated peptide antibodies which are critical in the pathogenesis of RA can bind to the citrullinated vimentin on the surface of OC precursors, and in turn promote OC differentiation and function via IL-8. In addition to adaptive immunity, the activation of innate immune system including the nucleotide oligomerization domain leucine rich repeat with a pyrin domain 3 inflammasome and TLRs can regulate OC maturation. The emerging perspectives about the diverse and close interactions between the immune cells and OCs in inflammatory milieu can have a significant impact on the future direction of drug development.
Adaptive Immunity ; Antibodies ; Arthritis ; Arthritis, Rheumatoid ; Calcium Signaling ; Cytokines ; Gout ; Immune System ; Inflammasomes ; Interleukin-6 ; Interleukin-8 ; Leucine ; Osteoclasts ; Osteolysis ; Osteoporosis ; T-Lymphocyte Subsets ; Vimentin