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Background: Antiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by arterial and venous thrombosis or pregnancy morbidity in patients with persistent antiphospholipid antibodies. However, nationwide population-based epidemiology studies regarding APS are still unavailable. Methods: We analyzed claims data extracted from the Korean Health Insurance and Review Agency (HIRA) covering more than 52 million Koreans, between January 1, 2008, and December 31, 2017. Patients diagnosed with APS, as determined by the Korean Classification of Disease, 7th edition (D68.6), and a rare intractable disease program (V253), were identified in HIRA. Results: A total of 3,088 newly diagnosed incident cases of 1,215 men and 1,873 women were identified during 2009-2016. The mean age was 44.6 ± 16.6 (men, 47.4 ± 16.3; women, 42.8 ± 16.6) years. The incidence was 0.75 per 10 5 person-year (95% confidence interval, 0.73-0.78). The prevalence in 2016 was 6.19 per 10 5 people. For incident cases, women showed incidence peak at ages of 30-39 years and 70-79 years, whereas for men, it was highest at ages of 70-79 years only. Of all patients, 1,766 (57%, 810 men and 956 women) had primary APS, 1,322 (43%, 405 men and 917 women) had secondary APS, and 845 (27%, 216 men and 629 women) were associated with systemic lupus erythematosus (SLE). Conclusion:The incidence of APS differs according to age groups and gender. The incidence of primary APS was higher than that of secondary APS in both gender. Furthermore, as already reported, secondary APS is highly associated with SLE; however, we observed that rheumatoid arthritis is also highly related.

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Lung injury is characterized by diffuse lung inflammation, alveolar-capillary destruction, and alveolar flooding, resulting in respiratory failure. Polydexyribonucleotide (PDRN) has an anti-inflammatory effect, decreasing inflammatory cytokines, and suppressing apoptosis. Thus, we investigated its efficacy in the treatment of lung injury, which was induced in rats using lipopolysaccharide (LPS). Rats were randomly divided into three groups according to sacrifice time, and each group split into control, lung injury-induced, and lung injury-induced + PDRN-treated groups. Rats were sacrificed 24 h and 72 h after PDRN administration, according to each group. Lung injury was induced by intratracheal instillation of LPS (5 mg/kg) in 0.2 mL saline. Rats in PDRN-treated groups received a single intraperitoneal injection of 0.3 mL distilled water including PDRN (8 mg/kg), 1 h after lung injury induction. Percentages of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive, cleaved caspase-3-, -8-, and -9-positive cells, the ratio of Bcl-2-associated X protein (Bax) to B-cell lymphoma 2 (Bcl-2), and expressions of inflammatory cytokines (tumor necrosis factor-α, interleukin-6) were decreased by PDRN treatment in the LPS-induced lung injury rats. Therefore, treatment with PDRN reduced lung injury score. This anti-apoptotic effect of PDRN can be ascribed to the enhancing effect of PDRN on adenosine A2A receptor expression. Based on these results, PDRN might be considered as a new therapeutic agent for the treatment of lung injury.

This study demonstrated that COPD could affect the axonal integrity in multiple brain regions, and change in DTI might be related with the severity of the COPD.

Objectives: Several factors associated with the prognosis of patients with NSCLC have been reported in the literature; however, most of these factors cannot be examined preoperatively. In this study, the clinical utility of platelet parameters in patients with NSCLC who underwent curative resection was evaluated. Materials and Methods: A retrospective study on patients with NSCLC who underwent curative resection from July 2006 to September 2016 was conducted. The Cox proportional hazard regression model was applied to evaluate the variables that demonstrated effects on disease-free and overall survival (DFS and OS). Results: A total of 116 patients with NSCLC were analyzed. There were 15 patients with plateletcrit greater than 0.2755%, and 101 patients whose plateletcrit was 0.2755% or lower. Multivariate analysis identified plateletcrit higher than 0.2755% (hazard ratio [HR] = 4.18, 95% confidence interval [CI] = 1.54-11.34, P =0.004), patient age of 65 years or more (HR = 4.02, 95% CI = 1.67−9.66, P = 0.001), and stage II or IIIA disease (HR = 2.95, 95% CI = 1.26−6.87, P = 0.012) as independent factors for OS that predicted a poor prognosis. Multivariate analysis identified plateletcrit higher than 0.2755% (HR = 4.07, 95% CI = 1.52−10.94, P = 0.005), stage II or IIIA disease (HR = 5.38, 95% CI = 2.71−10.66, P < 0.001) and non-adenocarcinoma (HR = 1.92, 95% CI = 1.02-3.59, P = 0.040) as independent prognostic factors for DFS that predicted a poor prognosis. Conclusion: Our results suggest a potential role of preoperative plateletcrit as an independent prognostic marker for patients with resectable NSCLC.

Bacillus Calmette-Guérin (BCG) vaccine has a good safety profile in immune competent children and considerable risks such as disseminated BCG disease in individuals with immune deficiencies. However, some complications including local subcutaneous infection, regional suppurative lymphadenitis may occur after BCG vaccination in immune competent children. A 17-month-old female child was admitted with a painless protruding mass on the anterior chest wall. There was no evidence of previous tuberculous infection and contact with a tuberculosis patient. Chest-computed tomography revealed an oval shaped low attenuated 1.8 x 1.0 cm mass at subcutaneous and muscle layers just below sternum, but the pulmonary parenchyma seemed to be normal. We excised the mass and the histopathologic examination revealed granulomatous lesions that suggestive of mycobacterial disease process. We considered that the chest wall abscess was a complication of BCG vaccination occurred by hematogenous dissemination of the inoculated mycobacteria. She recovered without any complications and was treated with isoniazid (150 mg/day) and rifampin (150 mg/day) for 6 months as an outpatient, not directly observed therapy but monthly follow-up.

Particulate matter (PM) of 10‐μm‐sized fine dust in the air penetrates the respiratory tract and contributes to the increasing incidence of various lung diseases, but its definite mechanism is not known. Recently, polydeoxyribonucleotide (PDRN) has been shown to have anti‐inflammatory and regenerative effects in various tissues. However, the bronchial‐related mechanism is not well‐understood. Hence, this experiment is intended to demonstrate the beneficial effect of PDRN administration on PM10‐induced injury in human bronchial‐derived NCI‐H358 cells. To confirm the protective effect of PDRN, PM10 was applied after PDRN pretreatment to confirm changes in NCI‐H358 cells. Experiments were conducted to measure cell survival, cytotoxicity, inflammation, and apoptotic factor changes. WST‐8 assay was used to confirm cell viability, and lactate dehydrogenase assay was used to obtain cytotoxicity. In addition, changes in inflammatory cytokines and apoptotic factors were confirmed by enzyme‐linked immunosorbent assay and Western blot. Decreased cell viability and increased cytotoxicity, inflammatory cytokines, and apoptotic factors were observed after exposure to PM10. However, pretreatment with PDRN enhanced cell viability and reduced cytotoxicity. In addition, the expression of inflammatory cytokines such as tumor necrosis factor‐α, interleukin‐6 (IL‐6), and IL‐1β, and cell death factors such as Apaf‐1, cyt c, caspase‐3, caspase‐9, Bid, and Bax/Bcl‐2 ratio were decreased by PDRN administration in PM10‐exposed NCI‐H358 cells. PDRN, an A2AR agonist, affects cAMP activation and regulation of phosphorylation of PKA and CREB. In addition, treatment with A2AR antagonist 3,7‐dimethyl‐1‐propargylxanthine significantly blocked PDRN's effect. These anti‐cytotoxicity, anti‐inflammation, and anti‐apoptosis effects of PDRN can be attributed to the adenosine A2AR enhancing effect on PM10‐exposed bronchial cells.