OBJECTIVEHospital hyperglycemia, in individuals with and without diabetes, has been identified as a marker of poor clinical outcome in cardiac surgery patients. However, the impact of perioperative hyperglycemia on clinical outcome in general and noncardiac surgery patients is not known.RESEARCH DESIGN AND METHODSThis was an observational study with the aim of determining the relationship between pre- and postsurgery blood glucose levels and hospital length of stay (LOS), complications, and mortality in 3,184 noncardiac surgery patients consecutively admitted to Emory University Hospital (Atlanta, GA) between 1 January 2007 and 30 June 2007.RESULTSThe overall 30-day mortality was 2.3%, with nonsurvivors having significantly higher blood glucose levels before and after surgery (both P < 0.01) than survivors. Perioperative hyperglycemia was associated with increased hospital and intensive care unit LOS (P < 0.001) as well as higher numbers of postoperative cases of pneumonia (P < 0.001), systemic blood infection (P < 0.001), urinary tract infection (P < 0.001), acute renal failure (P = 0.005), and acute myocardial infarction (P = 0.005). In multivariate analysis (adjusted for age, sex, race, and surgery severity), the risk of death increased in proportion to perioperative glucose levels; however, this association was significant only for patients without a history of diabetes (P = 0.008) compared with patients with known diabetes (P = 0.748).CONCLUSIONSPerioperative hyperglycemia is associated with increased LOS, hospital complications, and mortality after noncardiac general surgery. Randomized controlled trials are needed to determine whether perioperative diabetes management improves clinical outcome in noncardiac surgery patients.

OBJECTIVETo determine the effect of total parenteral nutrition (TPN)-induced hyperglycemia on hospital outcome.RESEARCH DESIGN AND METHODSThe study determined whether blood glucose values before, within 24 h, and during days 2–10 of TPN are predictive of hospital complications and mortality.RESULTSSubjects included a total of 276 patients receiving TPN for a mean duration of 15 ± 24 days (±SD). In multiple regression models adjusted for age, sex, and diabetes status, mortality was independently predicted by pre-TPN blood glucose of 121–150 mg/dl (odds ratio [OR] 2.2, 95% CI 1.1–4.4, P = 0.030), 151–180 mg/dl (3.41, 1.3–8.7, P = 0.01), and >180 mg/dl (2.2, 0.9–5.2, P = 0.077) and by blood glucose within 24 h of >180 mg/dl (2.8, 1.2–6.8, P = 0.020). A blood glucose within 24 h of >180 mg/dl was associated with increased risk of pneumonia (OR 3.1, 95% CI 1.4–7.1) and acute renal failure (2.3, 1.1–5.0).CONCLUSIONSHyperglycemia is associated with increased hospital complications and mortality in patients receiving TPN.

Pulmonary mucormycosis is an opportunistic angioinvasive fungal infection. Physicians must have a high level of suspicion in immunocompromised patients with fever and respiratory symptoms refractory to antibiotics. A low threshold should be had for performing an invasive procedure to gain reliable diagnosis, as early, aggressive medical and surgical interventions are needed for successful treatment.

Kir4.1, a glial-specific K+ channel, is critical for normal CNS development. Studies utilizing both global and glial-specific knockout of Kir4.1 reveal abnormal CNS development with the loss of the channel. Specifically, Kir4.1 knockout animals are characterized by ataxia, severe hypomyelination, and early postnatal death. Additionally, Kir4.1 has emerged as a key player in several CNS diseases. Notably, decreased Kir4.1 protein expression occurs in several human CNS pathologies including CNS ischemic injury, spinal cord injury, epilepsy, ALS, and Alzheimer’s disease. Despite the emerging significance of Kir4.1 in normal and pathological conditions, its mechanisms of regulation are unknown. Here we report the first epigenetic regulation of a K+ channel in the CNS. Robust developmental upregulation of Kir4.1 expression in rats is coincident with reductions in DNA methylation of the Kir4.1 gene, KCNJ10. Chromatin immunoprecipitation reveals a dynamic interaction between KCNJ10 and DNA methyltransferase 1 during development. Finally, demethylation of the KCNJ10 promoter is necessary for transcription. These findings indicate DNA methylation is a key regulator of Kir4.1 transcription. Given the essential role of Kir4.1 in normal CNS development, understanding the regulation of this K+ channel is critical to understanding normal glial biology.