Cryoglobulinernia occurs in about 5% of the cases of multiple myeloma. The most common finding in patient with cryoglobulinemia is ulceraticn that oceurs about ankle, hands, and occasionally the ears, upon prolonged exposue to cold. A 59-year old male had had 5 years of pain in his ears. There were black or dark brown colored ischemic ulcerations on his both helix. He also had mottled purpuric patches on his both ankles. A test for cryoglobulinema was positive. X-ray examination of the skull showed multiple punched but lesions. The bone marrow study revealed myeloma cell infiltration.
Ankle ; Bone Marrow ; Cryoglobulinemia* ; Ear ; Hand ; Humans ; Male ; Middle Aged ; Multiple Myeloma* ; Skull ; Ulcer

Juvenile spring eruption(JSE) of the ears is an unusual type of photodermatosis, which develops on the light exposed areas of the ears of boys and young male adults in the early spring months. JSE has received little attention in the literature, and to our knowledge no cases have been reported in Korea until now. Herein we report a case of JSE occurring in a 17-year-old man who has suffered from a recurrent pruritic erythematous papulovesicular eruption of both helix, followed by crusting and healing without scarring within one to two months early each spring for six years.
Adolescent ; Adult ; Cicatrix ; Ear* ; Humans ; Korea ; Male

OBJECTIVES: Biosignal data include important physiological information. For that reason, many devices and systems have been developed, but there has not been enough consideration of how to collect and integrate raw data from multiple systems. To overcome this limitation, we have developed a system for collecting and integrating biosignal data from two patient monitoring systems. METHODS: We developed an interface to extract biosignal data from Nihon Kohden and Philips monitoring systems. The Nihon Kohden system has a central server for the temporary storage of raw waveform data, which can be requested using the HL7 protocol. However, the Philips system used in our hospital cannot save raw waveform data. Therefore, our system was connected to monitoring devices using the RS232 protocol. After collection, the data were transformed and stored in a unified format. RESULTS: From September 2016 to August 2017, we collected approximately 117 patient-years of waveform data from 1,268 patients in 79 beds of five intensive care units. Because the two systems use the same data storage format, the application software could be run without compatibility issues. CONCLUSIONS: Our system collects biosignal data from different systems in a unified format. The data collected by the system can be used to develop algorithms or applications without the need to consider the source of the data.
Electrocardiography ; Humans ; Information Storage and Retrieval ; Intensive Care Units ; Monitoring, Physiologic* ; Photoplethysmography

Acknowledgements section was missing. The publisher apologises for these errors.

Lung cancer is a leading cause of cancer-related death in the world. Smoking is definitely the most important risk factor for lung cancer. Radon (222Rn) is a natural gas produced from radium (226Ra) in the decay series of uranium (238U). Radon exposure is the second most common cause of lung cancer and the first risk factor for lung cancer in never-smokers. Case–control studies have provided epidemiological evidence of the causative relationship between indoor radon exposure and lung cancer. Twenty-four case–control study papers were found by our search strategy from the PubMed database. Among them, seven studies showed that indoor radon has a statistically significant association with lung cancer. The studies performed in radon-prone areas showed a more positive association between radon and lung cancer. Reviewed papers had inconsistent results on the dose–response relationship between indoor radon and lung cancer risk. Further refined case–control studies will be required to evaluate the relationship between radon and lung cancer. Sufficient study sample size, proper interview methods, valid and precise indoor radon measurement, wide range of indoor radon, and appropriate control of confounders such as smoking status should be considered in further case–control studies.
Lung Neoplasms* ; Lung* ; Natural Gas ; Radium ; Radon* ; Risk Factors* ; Sample Size ; Smoke ; Smoking ; Uranium

BACKGROUND: Apoptosis plays a role in the development of pleural effusion. Caspase-cleaved cytokeratin 18, a marker for epithelial cell apoptosis, was evaluated in pleural effusion. METHODS: A total of 79 patients with pleural effusion were enrolled. The underlying causes were lung cancer (n=24), parapneumonic effusion (n=15), tuberculous effusion (n=28), and transudates (n=12). The levels of M30, an epitope of caspase-cleaved cytokeratin 18, were measured in blood and pleural fluids using enzyme-linked immunosorbent assay along with routine cellular and biochemical parameters. The expression of M30 was evaluated in the pleural tissues using immunohistochemistry for M30. RESULTS: The M30 levels in pleural fluid were significantly higher in patients with tuberculosis (2,632.1+/-1,467.3 U/mL) than in patients with lung cancer (956.5+/-618.5 U/mL), parapneumonic effusion (689.9+/-413.6 U/mL), and transudates (273.6+/-144.5 U/mL; all p<0.01). The serum levels were not significantly different among the disease groups. Based on receiver operating characteristics analysis, the area under the curve of M30 for differentiating tuberculous pleural effusion from all other effusions was 0.93. In the immunohistochemical analysis of M30, all pathologic types of cancer cells showed moderate to high expression, and the epithelioid cells in granulomas showed high expression in tuberculous pleural tissues. CONCLUSION: Caspase-cleaved cytokeratin 18 was most prominently observed in tuberculous pleural effusion and showed utility as a clinical marker. The main source of M30 was found to be the epithelioid cells of granulomas in tuberculous pleural tissues.
Apoptosis ; Biomarkers ; Cytoskeleton ; Enzyme-Linked Immunosorbent Assay ; Epithelial Cells ; Epithelioid Cells ; Exudates and Transudates ; Granuloma ; Humans ; Immunohistochemistry ; Keratin-18* ; Keratins* ; Lung Neoplasms ; Pleural Effusion* ; ROC Curve ; Tuberculosis ; Tuberculosis, Pleural

BACKGROUND/AIMS: Oxidative stress results in protein oxidation and is implicated in carcinogenesis. Sulfiredoxin (Srx) is responsible for the enzymatic reversal of inactivated peroxiredoxin (Prx). Nuclear factor E2-related factor 2 (Nrf2) binds to antioxidant responsive elements and upregulates the expression of Srx and Prx during oxidative stress. We aimed to elucidate the biological functions and potential roles of Srx in lung cancer. METHODS: To study the roles of Srx and Prx III in lung cancer, we compared the protein levels of Nrf2, Prxs, thioredoxin, and Srx in 40 surgically resected human lung cancer tissues using immunoblot and immunohistochemical analyses. Transforming growth factor-beta1, tumor necrosis factor-alpha, and camptothecin treatment were used to examine Prx III inactivation in Mv1Lu mink lung epithelial cells and A549 lung cancer cells. RESULTS: Prx I and Prx III proteins were markedly overexpressed in lung cancer tissues. A significant increase in the oxidized form of a cysteine sulfhydryl at the catalytic site of Prxs was found in carcinogenic lung tissue compared to normal lung tissue. Densitometric analyses of immunoblot data revealed significant Srx expression, which was higher in squamous cell carcinoma tissue (60%, 12/20) than in adenocarcinoma (20%, 4/20). Also, Nrf2 was present in the nuclear compartment of cancer cells. CONCLUSIONS: Srx and Prx III proteins were markedly overexpressed in human squamous cell carcinoma, suggesting that these proteins may play a protective role against oxidative injury and compensate for the high rate of mitochondrial metabolism in lung cancer.
Adenocarcinoma/*enzymology/genetics/mortality/pathology ; Animals ; Antineoplastic Agents, Phytogenic/pharmacology ; Blotting, Western ; Camptothecin/pharmacology ; Carcinoma, Squamous Cell/*enzymology/genetics/mortality/pathology ; Cell Line, Tumor ; Humans ; Immunohistochemistry ; Lung Neoplasms/*enzymology/genetics/mortality/pathology ; Mink ; NF-E2-Related Factor 2/*metabolism ; Oxidoreductases Acting on Sulfur Group Donors/genetics/*metabolism ; Peroxiredoxin III/*metabolism ; Peroxiredoxins/metabolism ; Prognosis ; RNA Interference ; Reactive Oxygen Species/metabolism ; Transfection ; Transforming Growth Factor beta1/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Up-Regulation

BACKGROUND/AIMS: Peroxiredoxin (Prx) belongs to a ubiquitous family of antioxidant enzymes that regulates many cellular processes through intracellular oxidative signal transduction pathways. Silica-induced lung damage involves reactive oxygen species (ROS) that trigger subsequent toxic effects and inflammatory responses in alveolar epithelial cells resulting in fibrosis. Therefore, we investigated the role of Prx in the development of lung oxidant injury caused by silicosis, and determined the implication of ROS in that process. METHODS: Lung epithelial cell lines A549 and WI26 were treated with 1% silica for 0, 24, or 48 hours, following pretreatment of the A549 cells with N-acetyl-L-cysteine and diphenylene iodonium and no pretreatment of the WI26 cells. We transfected an HA-ubiquitin construct into the A549 cell line and then analyzed the cells via Western blotting and co-immunoprecipitation. RESULTS: Silica treatment induced cell death in the A549 lung epithelial cell line and selectively degraded Prx I without impairing protein synthesis in the A549 cells, even when the ROS effect was blocked chemically by N-acetyl-L-cysteine. A co-immunoprecipitation study revealed that Prx I did not undergo ubiquitination. CONCLUSIONS: Silica treatment induces a decrease of Prx I expression in lung epithelial cell lines regardless of the presence of ROS. The silica-induced degradation of Prx does not involve the ubiquitin-proteasomal pathway.
Cell Line ; Epithelial Cells/drug effects/metabolism ; Humans ; Lung/chemistry/*drug effects/metabolism ; Peroxiredoxins/analysis/*physiology ; Protein Isoforms ; Reactive Oxygen Species/metabolism ; Silicon Dioxide/*toxicity ; Ubiquitin/metabolism

No abstract available.
Bronchial Arteries* ; Hemoptysis* ; Risk Factors*

No abstract available.
Bronchial Arteries* ; Hemoptysis* ; Risk Factors*