Background: The management of critically ill hyperglycemic patients in the intensive care unit (ICU) has been fraught with recent controversy. Only one randomized trial has demonstrated a mortality benefit to intensive glycemic control, with all subsequent studies failing to confirm this benefit and revealing a markedly increased risk of severe hypoglycemia (SH) in intensively treated patients. In most of these trials, adherence to the protocols were neither tracked nor reported. Methods: A retrospective analysis of all patients admitted to an ICU who were treated with an insulin infusion directed by the GlucoCareÔ IGC System, an FDA-cleared insulin-dosing calculator (Yale 100-140 mg/dL protocol). Mean blood glucose (BG) levels, time to target range and incidence of SH ( < 40 mg/dL) and moderate hypoglycemia (MH) (40-69 mg/dL) were determined, and potential causes of hypoglycemic episodes were assessed. Results: Mean post-target BG was approximately 123 mg/dL. Of > 55,000 readings in 1,657 patients, overall incidence of SH was 0.01% of readings and 0.3% of patients. MH occurred in 1.1% of readings and 17.6% of patients. The top potential causes of MH were: (1) Protocol-directed recommendations including continuation of insulin with BG < 100 mg/dL and decreases in the frequency of BG checks (63.7%), and (2) Staff non-adherence to protocol directives (15.3%). Conclusions:The results of the GlucoCare-directed Yale 100-140 mg/dL protocol experience revealed an extremely low incidence of SH and an incidence of MH of 1.1%. The incidence of SH in this study was lower than the control group of the NICE-SUGAR study and are supportive of the new Society of Critical Care guidelines to target BG levels of 100-150 mg/dL in critically ill patients. Further refinements to the original protocol and emphasis on staff adherence to protocol directives could potentially further reduce these very low hypoglycemia rates.

We investigated the effects of genistein, an inhibitor of tyrosine protein phosphorylation, on mouse 1-cell embryos, since in response to mitogenic stimuli tyrosine protein phosphorylation in somatic cells is implicated in initiation of DNA synthesis. Genistein inhibits cleavage of 1-cell embryos in a concentration-dependent and reversible manner; biochanin A, which is a less potent inhibitor of tyrosine protein phosphorylation, is a less potent inhibitor of cell cleavage. Genistein does not inhibit [35S]methionine incorporation, but does inhibit [3H]thymidine incorporation. Consistent with genistein's ability to inhibit cleavage by inhibiting DNA synthesis is that the loss of genistein's ability to inhibit cleavage corresponds with exit of the 1-cell embryos from S phase. Genistein is likely to inhibit tyrosine protein phosphorylation in situ, since it reduces by 80% the relative amount of [32P]phosphotyrosine present in 1-cell embryos; genistein does not inhibit either [32P]orthophosphate uptake or incorporation. As anticipated, genistein has little effect on inhibiting changes in the pattern of phosphoprotein synthesis during the first cell cycle, since tyrosine protein phosphorylation constitutes a small percentage of total protein phosphorylation. Alkalai treatment of [32P]radiolabeled phosphoproteins transferred to Immobilon reveals a base-resistant set of phosphoproteins of Mr = 32,000 that displays cell-cycle changes in phosphorylation. Although these properties suggest that these phosphoproteins may be related to the p34cdc2 protein kinase, phosphoamino acid analysis of [32P]radiolabeled phosphoproteins reveals that they are not enriched for phosphotyrosine; the inactive for p34cdc2 protein kinase contains a high level of phosphotyrosine. Results of these experiments suggest that tyrosine protein phosphorylation in response to the fertilizing sperm may be involved in initiating DNA synthesis in the 1-cell embryo, as well as converting a meiotic cell cycle to a mitotic one.

Background: The management of hyperglycemia in the intensive care unit has been a controversial topic for more than a decade, with target ranges varying from 80–110 mg/dL to <200 mg/dL. Multiple insulin infusion protocols exist, including several computerized protocols, which have attempted to achieve these targets. Importantly, compliance with these protocols has not been a focus of clinical studies.Methods: GlucoCare™, a Food and Drug Administration (FDA)-cleared insulin-dosing calculator, was originally designed based on the Yale Insulin Infusion Protocol to target 100–140 mg/dL and has undergone several modifications to reduce hypoglycemia. The original Yale protocol was modified from 100–140 mg/dL to a range of 120–140 mg/dL (GlucoCare 120–140) and then to 140 mg/dL (GlucoCare 140, not a range but a single blood glucose [BG] level target) in an iterative and evidence-based manner to eliminate hypoglycemia <70 mg/dL. The final modification [GlucoCare 140(B)] includes the addition of bolus insulin “midprotocol” during an insulin infusion to reduce peak insulin rates for insulin-resistant patients. This study examined the results of these protocol modifications and evaluated the role of compliance with the protocol in the incidence of hypoglycemia <70 mg/dL.Results: Protocol modifications resulted in mean BG levels of 133.4, 136.4, 143.8, and 146.4 mg/dL and hypoglycemic BG readings <70 mg/dL of 0.998%, 0.367%, 0.256%, and 0.04% for the 100–140, 120–140, 140, and 140(B) protocols, respectively (P < 0.001). Adherence to the glucose check interval significantly reduced the incidence of hypoglycemia (P < 0.001). Protocol modifications led to a reduction in peak insulin infusion rates (P < 0.001) and the need for dextrose-containing boluses (P < 0.001).Conclusion: This study demonstrates that refinements in protocol design can improve glucose control in critically ill patients and that the use of GlucoCare 140(B) can eliminate all significant hypoglycemia while achieving mean glucose levels between 140 and 150 mg/dL. In addition, attention to the timely performance of glucose levels can also reduce hypoglycemic events.

Physicians were significantly more likely than nurses to have positive responses on their rating of Teamwork Climate (73.0% vs. 36.7%, p=0.004). Conclusions: Physicians and nurses rank Job Satisfaction highly. They give the lowest scores to Perceptions of Management and Working Conditions. For all six domains physicians give higher rankings for safety attitudes, indicating a systematic difference in perception. Nurses and physicians differ most markedly in their opinion of Teamwork Climate with physicians believing that teamwork is better than nurses do. These results could be used to improve working conditions, patient safety, and quality.Learning Objectives: Tracheostomy ties and post-procedural sutures are the standard of care in securing a newly created tracheostomy, as airway loss is life threatening. Sutures may prevent therapies for pressure sore reduction and may contribute to the reported 8% incidence of tracheostomy-related pressure ulcers. No study has evaluated the absence of sutures reducing tracheostomy-related pressure sores. The purpose of this study was to evaluate whether refraining from post-procedural percutaneous tracheostomy (PT) sutures reduced the incidence of pressure sores. In October, 2012 we changed our standard practice, eliminating routine post-procedural sutures in PT, and hypothesized that this would reduce the incidence of tracheostomy related pressure sores. Methods: This retrospective study was conducted in an urban Level 2 Trauma Center. All PT were performed by a dedicated tracheostomy team. All PTs performed in our MICU, SICU and CICU between January, 2010 and June, 2014 were included. Patient characteristics, preprocedural metrics, and outcomes were collected. Patients prior October 2012 had PT sutures placed (sutured group: SG). Sutures remained in place for 4 days and were removed by the team. After October, 2012, patients had no sutures (no sutures: NS). Device-related pressure sore detection was performed by ICU teams and confirmed by the hospital's wound team. Results:141 patients were included: 71 were sutured and 70 were not sutured. There was no significant difference in characteristics (mean age in years: SG 62, NS 61.3 (p=0.82), male gender: SG 42, NS 49 (p=0.46), BMI in kg/m2: SG 30.35, NS 29.53 (p=0.87)). Albumin at time of PT was significantly lower in the SG 2.43 g/dl, NS 2.64 g/dl (p<0.039). Patients without sutures had a statistically different incidence of device-related pressure ulcer related to tracheostomy (SG 6, NS 0 ulcers, p<0.001). Neither group experienced tube dislodgement during their hospital course. Conclusions: Refraining from placement of post-procedural sutures in PT appears to be safe and significantly reduced the incidence of PT related pressure sores in our series.

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