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BackgroundThe prevalence of hypoglycemia is increasing due to the growing incidence of diabetes and the latest strict guidelines for glycated hemoglobin (HbA1c) levels under 7%. This study examined the clinical characteristics, causal factors, and medical costs of severely hypoglycemic patients in an emergency room (ER) of Uijeongbu St. Mary's Hospital.MethodsThe study consisted of a retrospective analysis of the characteristics, risk factors, and medical costs of 320 severely hypoglycemic patients with diabetes who presented to an ER of Uijeongbu St. Mary's Hospital from January 1, 2006 to December 31, 2009.ResultsMost hypoglycemic patients (87.5%, 280/320) were over 60 years old with a mean age of 69.5±10.9 years and a mean HbA1c level of 6.95±1.46%. Mean serum glucose as noted in the ER was 37.9±34.5 mg/dL. Renal function was decreased, serum creatinine was 2.0±2.1 mg/dL and estimated glomerular filtration rate (eGFR) was 48.0±33.6 mL/min/1.73 m2. In addition, hypoglycemic patients typically were taking sulfonylureas or insulin and a variety of other medications, and had a long history of diabetes.ConclusionSevere hypoglycemia is frequent in older diabetic patients, subjects with low HbA1c levels, and nephropathic patients. Therefore, personalized attention is warranted, especially in long-term diabetics with multiple comorbidities who may not have been properly educated or may need re-education for hypoglycemia.

Aquatic toxicities of six benzimidazole-based anthelmintics-namely, albendazole, thiabendazole, flubendazole, febantel, fenbendazole, and oxfendazole-were evaluated with a marine bacterium, Vibrio fischeri, and a freshwater invertebrate, Daphnia magna. Delayed and chronic toxicity tests using D. magna also were conducted for benzimidazoles with high acute toxicity. Vibrio fischeri was greater than 10-fold less sensitive to most of the benzimidazoles tested compared to daphnids. For D. magna, the most acutely toxic anthelmintic compound tested was fenbendazole (48-h median effective concentration [EC50s], 16.5 microg/L), followed by flubendazole (48-h EC50, 66.5 micro/L), albendazole (48-h EC50, 67.9 microg/L), febantel (48-h EC50, 216.5 microg/L), thiabendazole (48-h EC50, 843.6 microg/L), and oxfendazole (48-h EC50, 1,168.4 microg/L). The lipophilicity parameter, log Kow, explained the observed acute D. magna toxicity of the individual benzimidazoles (r = -0.91, p < 0.01). Delayed expression of toxicity observed for 21 d after 96-h exposure to fenbendazole and flubendazole was not notable, which might result from the relatively high elimination constants for the chemicals. With chronic exposure to fenbendazole, D. magna survival, reproduction, and growth were significantly impacted at 1.25 to 4.1 microg/L (p < 0.05). Hazard quotients estimated for fenbendazole, albendazole, flubendazole, and febantel were 2,770, 9.7, 4, and 1.2, respectively, suggesting a need for further investigation and a potential for environmental concerns, particularly with fenbendazole.

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Based on the central dogma of protein synthesis, traditional methods for protein engineering require that altering protein structure and function must be accompanied by changing the nucleotide sequence of the genes encoding the protein. However, the preparation of a template gene for each individual protein requires a great deal of time and effort, thereby limiting the throughput and scope of studying engineered proteins. In this study, we describe translation-level engineering of proteins using cell-free protein synthesis. Taking advantage of the promiscuity of aminoacyl tRNA synthetases in accepting structurally similar amino acid analogues, unnatural amino acids were introduced into elastin-like polypeptides in place of the corresponding cognate amino acids. Through the incorporation of various analogues and starting from the same gene, the phase transition temperatures of elastin-like polypeptides became tunable. Our results demonstrate the usefulness of cell-free protein synthesis for protein engineering using unnatural amino acids without the need for cloning.