With atomic-layer-deposition grown zinc oxide as the electron selective layer, we developed plastic substrate compatible processing for organic photovoltaic devices and demonstrated flexible inverted organic solar cells on poly(ethylene naphthalate) with a power conversion efficiency of 4.18%.

Stress-induced hyperglycemia (SIH) has been independently associated with an increased risk of mortality in critically ill patients without diabetes. However, it is also necessary to consider preexisting hyperglycemia when investigating the relationship between SIH and mortality in patients with diabetes. We therefore assessed whether the gap between admission glucose and A1C-derived average glucose (ADAG) levels could be a predictor of mortality in critically ill patients with diabetes.We retrospectively reviewed the Acute Physiology and Chronic Health Evaluation II (APACHE-II) scores and clinical outcomes of patients with diabetes admitted to our medical intensive care unit (ICU) between 2011 and 2014. The glycosylated hemoglobin (HbA1c) levels were converted to the ADAG by the equation, ADAG = [(28.7 × HbA1c) − 46.7]. We also used receiver operating characteristic (ROC) curves to determine the optimal cut-off value for the glycemic gap when predicting ICU mortality and used the net reclassification improvement (NRI) to measure the improvement in prediction performance gained by adding the glycemic gap to the APACHE-II score.We enrolled 518 patients, of which 87 (17.0%) died during their ICU stay. Nonsurvivors had significantly higher APACHE-II scores and glycemic gaps than survivors (P < 0.001). Critically ill patients with diabetes and a glycemic gap ≥80 mg/dL had significantly higher ICU mortality and adverse outcomes than those with a glycemic gap <80 mg/dL (P < 0.001). Incorporation of the glycemic gap into the APACHE-II score increased the discriminative performance for predicting ICU mortality by increasing the area under the ROC curve from 0.755 to 0.794 (NRI = 13.6%, P = 0.0013).The glycemic gap can be used to assess the severity and prognosis of critically ill patients with diabetes. The addition of the glycemic gap to the APACHE-II score significantly improved its ability to predict ICU mortality.

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Acute hyperglycemia is a frequent finding in patients presenting to the emergency department (ED) with acute myocardial infarction (AMI). The prognostic role of hyperglycemia in diabetic patients with AMI remains controversial. We retrospectively reviewed patients’ medical records to obtain demographic data, clinical presentation, major adverse cardiac events (MACEs), several clinical scores and laboratory data, including the plasma glucose level at initial presentation and HbA1c levels. The glycemic gap, which represents changes in serum glucose levels during the index event, was calculated from the glucose level upon ED admission minus the HbA1c-derived average glucose (ADAG). We enrolled 331 patients after the review of medical records. An elevated glycemic gap between admission serum glucose levels and ADAG were associated with an increased risk of mortality in patients. The glycemic gap showed superior discriminative power regarding the development of MACEs when compared with the admission glucose level. The calculation of the glycemic gap may increase the discriminative powers of established clinical scoring systems in diabetic patients presenting to the ED with AMI. In conclusion, the glycemic gap could be used as an adjunct parameter to assess the severity and prognosis of diabetic patients presenting with AMI. However, the usefulness of the glycemic gap should be further explored in prospective longitudinal studies.

Background Recent studies have indicated that several critical illnesses are associated with an increased risk of cardiovascular diseases (CVDs). Nonetheless, studies of the association between heat-related illnesses (HRIs) and subsequent CVDs are still limited. We sought to evaluate whether heat stroke (HS) was associated with an increased CVD incidence. Methods The data from the nationwide, population-based, retrospective, cohort study described herein were obtained from the National Health Insurance Research Database in Taiwan. The outcome evaluated in this study was the cumulative incidence of CVDs, which was compared between patients with HS, patients with other HRIs and a control group during a 14-year follow-up period. Results Our analyses included 150 HS cases, 150 patients with other HRIs and 150 patients without HRIs. The HS patients had a significantly higher incidence of developing CVDs than the other HRI and control patients (32.67% vs. 23.33% vs. 16.67%, p = 0.005). Patients with HS had an increased incidence of acute myocardial infarction (AMI) compared with that of the controls (6% vs. 2.67%, p = 0.042) and an increased incidence of acute ischemic stroke (AIS) compared with those of the other HRI and control patients (12% vs. 6% vs. 4.67%, p = 0.038). An increased risk of chronic kidney disease (CKD) was also found in the patients with HS and other HRIs compared to that in the controls (17.33% vs. 14.67% vs. 6.67%, p = 0.016). Conclusion Prior HS was associated with an increased incidence of CVDs, particularly AMI and AIS, and an increased incidence of CKD.

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Acute mountain sickness (AMS) occurs in up to 25% of unacclimatized persons who ascend to 3000 m and can result in high‐altitude pulmonary edema (HAPE). MicroRNAs (miRs) can regulate gene expression at the post‐transcriptional level. Hypoxia selectively disrupts endothelial tight junction complexes through a hypoxia‐inducible factor‐1α (HIF‐1α)‐dependent mechanism. Though increased HIF‐1α expression is associated with adaptation and protection from AMS development in the early stage of hypoxia, a downstream effector of HIF‐1a, VEGF, can induce overzealous endothelial barrier dysfunction, increase vascular permeability, and ultimately result in HAPE and high‐altitude cerebral edema. We hypothesized that the fine‐tuning of downstream effectors by miRs is paramount for the preservation of endothelial barrier integrity and the prevention of vascular leakage. We found that several miRs were up‐regulated in healthy volunteers who were subjected to a 3100‐m height. By reviewing the literature and using online bioinformatics prediction software, we specifically selected miR‐424 for further investigation because it can modulate both HIF‐1α and VEGF. Hypoxia‐induced miR‐424 overexpression is HIF‐1α dependent, and miR‐424 stabilized HIF‐1α, decreased VEGF expression, and promoted vascular endothelial cadherin phosphorylation. In addition, hypoxia resulted in endothelial barrier dysfunction with increased permeability; miR‐424 thus attenuated hypoxia‐induced endothelial cell senescence and apoptosis. miR‐322 knockout mice were susceptible to hypoxia‐induced pulmonary vascular leakage. miR‐322 mimics improved hypoxia‐induced pulmonary vascular leakage in vivo. We conclude that several miRs were up‐regulated in healthy adult volunteers subjected to hypobaric hypoxemia. miR‐424/322 could modulate the HIF‐1α‐VEGF axis and prevent hypoxia‐induced pulmonary vascular leakage under hypoxic conditions.—Tsai, S.‐H., Huang P.‐H., Tsai, H.‐Y., Hsu, Y.‐J., Chen, Y.‐W., Wang, J.‐C., Chen, Y.‐H., Lin, S.‐J. Roles of the hypoximir microRNA‐424/322 in acute hypoxia and hypoxia‐induced pulmonary vascular leakage. FASEB J. 33, 12565–12575 (2019). http://www.fasebj.org