Improving Early Sepsis Recognition: Resocializing Intensive Care Unit Nurses in a Large Hospital on the Inpatient Sepsis Bundle Checklist

Problem: Sepsis is a life threatening disease that has caused over a million deaths annually in the nation. Early recognition of sepsis is highly crucial for health care professionals to know to prevent an increase of mortality and morbidity rates. This quality improvement project aimed to increase sepsis bundle checklist awareness to the staff and compliance in the Intensive Care Unit to improve the sepsis cases. Context: Clinical Nurse Leader students completed a microsystem assessment of the Intensive Care Unit at Hospital X in San Mateo County. This unit cares for patients with sepsis, septic shock, severe sepsis, organ failure, and stroke. Interventions: The implemented intervention of sepsis bundle resocialization was ineffective. Measures: After completing an assessment of the microsystem, the students collected data to evaluate if the nurses were aware of the sepsis bundle checklist. The post-survey was to measure if the intervention of resocializing the sepsis bundle checklist was effective. Results: Analysis from the initial survey showed that 42% nurses were aware of the sepsis bundle checklist. From the post survey it showed that 0% nurses were aware of the sepsis bundle checklist. Conclusions: In collaboration, with my CNL colleague student, sepsis champion, registered nurses, assistant nurse managers, and quality improvement consultant, a need for sepsis bundle adherence and awareness was identified at Hospital X in the ICU. This study has the potential to expand on the project of reducing sepsis cases of staffing being aware and adhering to the sepsis bundle checklist. Keywords: sepsis, sepsis bundle, sepsis ICU, sepsis bundle checklist, and sepsis awarenes

Energy Prediction Based Intrusion Detection In Wireless Sensor Networks

A challenge in designing wireless sensor networks is to maximize the lifetime of the network with respect to limited resources and energy. These limitations make the network particularly vulnerable to attacks from adversaries. Denial of Service (DOS) is considered a severely damaging attack in monitoring applications when intruders attack the network and force it to lose its power and die early. There are intrusion detection approaches, but they require communications and calculations which waste the network’s limited resources. In this paper, we propose a new intrusion detection model that is suitable for defending against DOS attacks. We use the idea of energy prediction to anticipate the energy consumption of the network in order to detect intruders based on the each individual node’s excessive usage of power. Our approach does not require a lot of communications or calculations between the nodes and the cluster head. It is energy efficient and accurate in detecting intruders. Simulations show that our energy aware intrusion detection approach can effectively detect intruders based on energy consumption rate

Energy Prediction Based Intrusion Detection In Wireless Sensor Networks

A challenge in designing wireless sensor networks is to maximize the lifetime of the network with respect to limited resources and energy. These limitations make the network particularly vulnerable to attacks from adversaries. Denial of Service (DOS) is considered a severely damaging attack in monitoring applications when intruders attack the network and force it to lose its power and die early. There are intrusion detection approaches, but they require communications and calculations which waste the network’s limited resources. In this paper, we propose a new intrusion detection model that is suitable for defending against DOS attacks. We use the idea of energy prediction to anticipate the energy consumption of the network in order to detect intruders based on the each individual node’s excessive usage of power. Our approach does not require a lot of communications or calculations between the nodes and the cluster head. It is energy efficient and accurate in detecting intruders. Simulations show that our energy aware intrusion detection approach can effectively detect intruders based on energy consumption rate

Protein Tyrosine Phosphatase-1B (PTP1B) Helps Regulate EGF-induced Stimulation of S-phase Entry in Human Corneal Endothelial Cells

Purpose: Human corneal endothelial cells (HCEC), particularly from older donors, only proliferate weakly in response to EGF. The protein tyrosine phosphatase, PTP1B, is known to negatively regulate EGF-induced signaling in several cell types by dephosphorylating the epidermal growth factor receptor (EGFR). The current studies were conducted to determine whether PTP1B plays a role in regulating cell cycle entry in HCEC in response to EGF stimulation. Methods: Donor corneas were obtained from the National Disease Research Interchange and accepted for study based on established exclusion criteria. PTP1B was localized in the endothelium of ex vivo corneas and in cultured cells by immunocytochemistry. Western blot analysis verified PTP1B protein expression in HCEC and then compared the relative expression of EGFR and PTP1B in HCEC from young (60 years old). The effect of inhibiting the activity of PTP1B on S-phase entry was tested by comparing time-dependent BrdU incorporation in subconfluent HCEC incubated in the presence or absence of the PTP1B inhibitor, CinnGEL 2Me, before EGF stimulation. Results: PTP1B was localized in a punctate pattern mainly within the cytoplasm of HCEC in ex vivo corneas and cultured cells. Western blots revealed the presence of three PTP1B-positive bands in HCEC and the control. Further western blot analysis showed no significant age-related difference in expression of EGFR (p=0.444>0.05); however, PTP1B expression was significantly higher in HCEC from older donors (p=0.024<0.05). Pre-incubation of HCEC with the PTP1B inhibitor significantly increased (p=0.019<0.05) the number of BrdU positive cells by 48 h after EGF stimulation. Conclusions: Both immunolocalization and western blot studies confirmed that PTP1B is expressed in HCEC. Staining patterns strongly suggest that at least a subset of PTP1B is localized to the cytoplasm and most likely to the endoplasmic reticulum, the known site of EGFR/PTP1B interaction following EGF stimulation. PTP1B expression, but not EGFR expression, was elevated in HCEC from older donors, suggesting that the reduced proliferative activity of these cells in response to EGF is due, at least in part, to increased PTP1B activity. The fact that inhibition of PTP1B increased the relative number of cells entering S-phase strongly suggests that PTP1B helps negatively regulate EGF-stimulated cell cycle entry in HCEC. These results also suggest that it may be possible to increase the proliferative activity of HCEC, particularly in cells from older donors, by inhibiting the activity of this important protein tyrosine phosphatase