Ethylene glycol (EG) poisoning is highly lethal and difficult to diagnose. EG is metabolized through enzymatic reactions, producing glycolic acid, leading to high anion gap acidosis. The authors report a case wherein EG poisoning produced a large lactate gap between the two measuring methods. A 33-year-old male presented to the emergency department with an altered level of consciousness. The lactate levels measured using a point-of-care test (POCT) revealed severe lactic acidosis. The POCT lactate level corresponded to the amount of anion gap. Follow-up tests in the intensive care unit revealed a serum lactate level of 1.91 mmol/L, while the arterial POCT test yielded 28.1 mmol/L. Based on the lactate gap observed between the two methods, the possibility of EG poisoning was re-considered. EG poisoning was later confirmed by detecting EG in the patient’s system. Thus, EG poisoning should be considered when there is a severe lactate gap between the measuring methods.

Ethylene glycol (EG) poisoning is highly lethal and difficult to diagnose. EG is metabolized through enzymatic reactions, producing glycolic acid, leading to high anion gap acidosis. The authors report a case wherein EG poisoning produced a large lactate gap between the two measuring methods. A 33-year-old male presented to the emergency department with an altered level of consciousness. The lactate levels measured using a point-of-care test (POCT) revealed severe lactic acidosis. The POCT lactate level corresponded to the amount of anion gap. Follow-up tests in the intensive care unit revealed a serum lactate level of 1.91 mmol/L, while the arterial POCT test yielded 28.1 mmol/L. Based on the lactate gap observed between the two methods, the possibility of EG poisoning was re-considered. EG poisoning was later confirmed by detecting EG in the patient’s system. Thus, EG poisoning should be considered when there is a severe lactate gap between the measuring methods.

Ethylene glycol (EG) poisoning is highly lethal and difficult to diagnose. EG is metabolized through enzymatic reactions, producing glycolic acid, leading to high anion gap acidosis. The authors report a case wherein EG poisoning produced a large lactate gap between the two measuring methods. A 33-year-old male presented to the emergency department with an altered level of consciousness. The lactate levels measured using a point-of-care test (POCT) revealed severe lactic acidosis. The POCT lactate level corresponded to the amount of anion gap. Follow-up tests in the intensive care unit revealed a serum lactate level of 1.91 mmol/L, while the arterial POCT test yielded 28.1 mmol/L. Based on the lactate gap observed between the two methods, the possibility of EG poisoning was re-considered. EG poisoning was later confirmed by detecting EG in the patient’s system. Thus, EG poisoning should be considered when there is a severe lactate gap between the measuring methods.

Ethylene glycol (EG) poisoning is highly lethal and difficult to diagnose. EG is metabolized through enzymatic reactions, producing glycolic acid, leading to high anion gap acidosis. The authors report a case wherein EG poisoning produced a large lactate gap between the two measuring methods. A 33-year-old male presented to the emergency department with an altered level of consciousness. The lactate levels measured using a point-of-care test (POCT) revealed severe lactic acidosis. The POCT lactate level corresponded to the amount of anion gap. Follow-up tests in the intensive care unit revealed a serum lactate level of 1.91 mmol/L, while the arterial POCT test yielded 28.1 mmol/L. Based on the lactate gap observed between the two methods, the possibility of EG poisoning was re-considered. EG poisoning was later confirmed by detecting EG in the patient’s system. Thus, EG poisoning should be considered when there is a severe lactate gap between the measuring methods.

Pulmonary nocardiosis is a rare opportunistic infection that commonly affects immunocompromised hosts, such as patients with organ transplants, acquired immunodeficiency syndrome, or prolonged immunosuppression. Recently, we encountered a case of pulmonary nocardiosis with empyema that progressed to severe sepsis. The patient was treated in the intensive care unit. Thereafter, medical thoracoscopy was performed to improve drainage of the pleural fluid. Nocardia was identified in the culture of the pleural fluid.
Acquired Immunodeficiency Syndrome ; Drainage ; Empyema* ; Humans ; Immunocompromised Host ; Immunosuppression ; Intensive Care Units ; Nocardia Infections ; Nocardia* ; Opportunistic Infections ; Sepsis* ; Thoracoscopy ; Transplants

Absorptiometry, Photon ; Adult ; Bone Density ; Bone Diseases, Metabolic ; Calcium ; Confounding Factors (Epidemiology) ; Cross-Sectional Studies ; Epidemiology ; Female ; Femur ; Femur Neck ; Hip ; Humans ; Logistic Models ; Male ; Methods ; Nutrition Surveys ; Osteoporosis ; Population Surveillance ; Potassium ; Potassium, Dietary ; Prevalence ; Retrospective Studies ; Spine ; Vitamin D

BACKGROUND: Numerous reports suggest the role of oxygen in melanogenesis. However, little has been reported on the effect of a hypoxic environment on cellular melanogenesis. OBJECTIVE: The effect of low oxygen tension on cellular melanogenesis was investigated in B16 murine melanoma cells. METHODS: Using cells cultured under an ambient (21% O2) or hypoxic (5% O2) condition, melanin content and tyrosinase activity were measured spectrophotometrically. The expression of tyrosinase, tyrosinase-related protein (TRP)- 1, and TRP-2 were analyzed by RT-PCR and Western blot. RESULTS: Culture of cells under hypoxic conditions caused significant inhibition of isobutylmethylxanthine (IBMX)- induced increase of melanin content. No cytotoxicity was observed during the hypoxic culture periods. Decreased melanin content occurred through the decrease of tyrosinase protein and activity (p<0.01). The mRNA levels of tyrosinase and TRP-2 were also decreased by hypoxia, while that of TRP-1 was unchanged. Similar inhibitions of melanin content and tyrosinase activity were observed in the cells stimulated with dibutyryl-cAMP. CONCLUSION: IBMX-induced melanogenesis in B16 cells was significantly inhibited under hypoxic culture conditions, suggesting the important role of oxygen tension in cellular melanogenesis.
Anoxia* ; Blotting, Western ; Melanins ; Melanoma ; Melanoma, Experimental* ; Monophenol Monooxygenase ; Oxygen ; RNA, Messenger

Smoking is the major risk factor for lung squamous cell carcinoma (SCC), although a small number of lung SCCs occurs in never-smokers. The purpose of this study was to compare 50 hotspot mutations of lung SCCs between never-smokers and smokers. We retrospectively reviewed the medical records of patients newly diagnosed with lung SCC between January 1, 2011 and December 31, 2013 in the Seoul National University Hospital. Formalin-fixed, paraffin-embedded tumor samples were used for analysis of hotspot mutations. Fifty cancer-related genes in never-smokers were compared to those in ever-smokers. Of 379 lung SCC patients, 19 (5.0%) were never-smokers. The median age of these 19 patients was 67 years (interquartile range 57–73 years), and 10 of these patients were women (52.5%). The incidence rates of stage I, II, III, and IV disease in this group were 26.4%, 5.3%, 31.6%, and 36.8%, respectively, and sequencing was performed successfully in 14 cases. In the 26 lung SCC tumor samples (12 from never-smokers and 14 from ever-smokers) sequenced using personal genome machine, the most common mutations were in TP53 (75.0%), RAS (66.7%), and STK11 (33.3%), but mutations were also found in EGFR, KIT, and PTEN. The distribution of hotspot mutations in never-smokers was similar to that in ever-smokers. There was no significant difference in overall survival between the 2 groups. The 50 hotspot mutations of lung SCC in never-smokers were similar to those of ever-smokers.
Carcinoma, Squamous Cell* ; Epithelial Cells* ; Female ; Genome ; Humans ; Incidence ; Lung Neoplasms ; Lung* ; Medical Records ; Retrospective Studies ; Risk Factors ; Seoul ; Smoke ; Smoking

Xanthohumol (XH), the principal prenylflavonoid of the hop plant (Humulus lupulus L.), dose-dependently inhibited isobutylmethylxanthine (IBMX)-induced melanogenesis in B16 melanoma cells, with little cytotoxicity at the effective concentrations. Decreased melanin content was accompanied by reduced tyrosinase enzyme activity, protein and mRNA expression. The levels of tyrosinase-related protein 1 and 2 mRNAs were decreased by XH. XH also inhibited alpha-melanocyte stimulating hormone- or forskolin-induced increases in melanogenesis, suggesting an action on the cAMP-dependent melanogenic pathway. XH downregulated the protein and mRNA expression of microphthalmia-associated transcription factor (MITF), a master transcriptional regulator of key melanogenic enzymes. These results suggest that XH might act as a hypo-pigmenting agent through the downregulation of MITF in the cAMP-dependent melanogenic pathway.
1-Methyl-3-isobutylxanthine/pharmacology ; Animals ; Cell Line ; Cell Survival/drug effects ; Dose-Response Relationship, Drug ; Down-Regulation ; Drug Antagonism ; Forskolin/pharmacology ; *Humulus ; Intramolecular Oxidoreductases/antagonists & inhibitors/biosynthesis ; Melanins/antagonists & inhibitors/*biosynthesis ; Melanocytes/*drug effects/*metabolism ; Melanoma, Experimental ; Membrane Glycoproteins/antagonists & inhibitors/biosynthesis ; Mice ; Microphthalmia-Associated Transcription Factor/antagonists & inhibitors ; Monophenol Monooxygenase/antagonists & inhibitors/biosynthesis/genetics ; Oxidoreductases/antagonists & inhibitors/biosynthesis ; Propiophenones/*pharmacology ; Signal Transduction/drug effects ; alpha-MSH/metabolism