Pegylated-Catalase Is Protective in Lung Ischemic Injury and Oxidative Stress.

BACKGROUND: Lung transplant ischemia-reperfusion injury is typified by toxic metabolites and oxygen free radicals leading to worse graft function. Catalase is an enzyme involved in oxidative-stress detoxification. We hypothesize that direct delivery of highly concentrated polyethylene glycol-catalase (PEG-CAT) during normothermic ex vivo lung perfusion (EVLP) significantly reduces ischemia-reperfusion injury. METHODS: To demonstrate protection, primary culture porcine endothelial cells were treated with PEG-CAT (0 to 1250 U/mL) in a model of oxidative stress (400 µM H2o2). In vivo, rat lungs were subjected to 0 hours or 1 hour of warm ischemic injury and 2 hours of EVLP with or without PEG-CAT. Perfusate was collected throughout the perfusion duration and tissue was collected at the end. Tissue and perfusate underwent analysis for markers of apoptosis and a biometric signature of lung health. RESULTS: Uptake of PEG-CAT into primary endothelial cells was demonstrated with Alexa Fluor 488-labeled PEG-CAT. Oxidatively stressed cells pretreated with PEG-CAT had significantly decreased cytotoxicity and caspase 3/7 activity and increased cell viability and cell membrane integrity. In a rat model of warm ischemia with EVLP, PEG-CAT improved allograft viability as measured by indications of cell membrane integrity (lactate dehydrogenase and hyaluronic acid), presence of vasoconstrictive peptides (endothelin-1 and big endothelin-1) released from endothelial cells, and reduced apoptosis (terminal deoxynucleotidyl transferase dUTP nick-end labeling). CONCLUSIONS: In vitro and ex vivo, PEG-CAT protects against oxidative stress-induced cytotoxicity, maintains cellular metabolism, and mitigates lung ischemia-reperfusion in an experimental model. Together, these data suggest that PEG-CAT is a potential therapeutic target for donor organs at risk for ischemia-reperfusion injury.

Smartphone-based mobile health monitoring.

We developed a health monitoring system based on the smartphone. A compact and low-power-consuming biosignal monitoring unit (BMU) measured electrocardiogram (ECG), photoplethysmogram (PPG), temperature, oxygen saturation, energy expenditure, and location information. The 2.4 GHz Bluetooth(®) (Bluetooth SIG) network in the BMU communicated with a smartphone. Health information was sent to a remote healthcare server through a built-in 3G or Wi-Fi network in the smartphone. The remote server monitored multiple users in real-time. Normally data of vital signs were being transmitted to the server. In an emergency or for a special care case, additional information such as the waveform of the ECG and PPG were displayed at the server. For increased transmission efficiency, data compression and a simple error correction algorithm were implemented. Using a widespread smartphone, an efficient personal health monitoring system was developed and tested successfully for multiple users.

Inhibitory effects of fermented nutraceuticals on NO production and T cell proliferation in juvenile atopic dermatitis.

As the most common inflammatory skin disease in children, atopic dermatitis begins in infancy or early childhood, with about 90% of cases appearing under age of 5. The prevalence of atopic dermatitis has rapidly increased among children in recent years. Physiological and psychological abnormalities and social impact are also well known in children with atopic dermatitis and in their families. Atopic dermatitis not only seriously affects the quality of life of the children and their families but also is leading chronic disease in children with hard-to-cure.Recently, we found that the fermented extract of several plants had considerable potential to treat juvenile atopic dermatitis. This extract therefore is now under investigation to find the underlying immunopathological mechanism by determining its inhibitory effects on nitric oxide (NO) release and T cell proliferation. The fermented extract dose dependently blocked NO production. In particular, the inhibitory effect of the extract was maximized up until 80-fold dilution of the original extract. This extract did not induce cytotoxic effects up to 80-fold dilution. Interestingly, doses between 320- and 80-fold dilution significantly protected cell death mediated by LPS-induced NO production. The fermented extract also significantly suppressed CD3 induced T cell proliferation in a dose dependent manner.