The Implications of Hyperoxia, Type 1 Diabetes, and Sex on Cardiovascular Physiology in Mice

BackgroundOxygen supplementation, although a cornerstone of emergency and cardiovascular medicine, often results in hyperoxia, a condition characterized by excessive tissue oxygen which results in adverse cardiac remodeling and subsequent injurious effects to physiological function. Cardiac remodeling is further influenced by various risk factors, including pre-existing conditions and sex. Thus, the purpose of this experiment was to investigate cardiac remodeling in Type I Diabetic (Akita) mice subjected to hyperoxic treatment. MethodsMale and female Akita and wild-type (WT) mice were divided into four groups based on gender and treatment, and were then subjected to either FiO2 > 90% (hyperoxia) for 72 h in an airtight chamber or normal air (normoxia). Physical, functional, and electrophysiological parameters were then evaluated. Finally, we employed correlational analysis and Multi-Way Analysis of Variance (ANOVA) which determined hyperoxia to have the greatest statistical influence on cardiac pathophysiology, followed by sex, and finally genotype.ResultsOverall, we demonstrated that Akita mice experience distinct challenges from wild type (WT) mice. Specifically, Akita males at both normoxia and hyperoxia showed significant decreases in body and heart weights, prolonged PR, QRS, and QTc intervals, and reduced %EF and %FS at normoxia compared to WT controls. Moreover, we found Akita males largely resemble female mice (both WT and Akita) with regards to the parameters studied. ConclusionsTaken together, our data suggest that Type I diabetic patients may have distinct cardiac pathophysiology under hyperoxia compared to uncomplicated patients, with males being at high risk. These findings can be used to enhance the provision of care in ICU patients with Type I diabetes as a comorbid condition.

Disinfection of N95 Respirators with Ozone

The coronavirus disease 2019 crisis is creating a shortage of personal protective equipment (PPE), most critically, N95 respirators for healthcare personnel. Our group was interested in the feasibility of ozone disinfection of N95 respirators as an alternative for healthcare professionals and organizations that might not have access to other disinfection devices. We tested the effectiveness of ozone on killing Pseudomonas aeruginosa (PsA) on three different N95 respirators: 3M 1860, 3M 1870, and 3M 8000. We used an ozone chamber that consisted of: an airtight chamber, an ozone generator, an ozone destruct unit, and an ozone UV analyzer. The chamber was capable of concentrating ozone up to 500 parts per million (ppm) from ambient air, creating an airtight seal, and precisely measuring ozone levels within the chamber. Exposure to ozone at 400 ppm with 80% humidity for two hours effectively killed bacteria on N95 respirators, types 1860, 1870, and 8000. There were no significant changes in filtration efficiency of the 1860 and 1870 type respirators for up to ten cycles of ozone exposure at similar conditions. There was no change in fit observed in the 1870 type respirator after ozone exposure. There was no significant change in the strap integrity of the 1870 type respirator after ozone exposure. Tests for filtration efficiency were not performed on the 8000 type respirator. Tests for fit or strap integrity were not performed on the 8000 or 1860 type respirators. This study demonstrates that an ozone application achieves a high level of disinfection against PsA, a vegetative bacteria that the CDC identifies as more difficult to kill than medium sized viruses such as SARS-CoV-2 (Covid-19). Furthermore, conditions shown to kill these bacteria did not damage or degrade respirator filtration. This is the first report of successful disinfection of N95 PPE with ozone of which the authors are aware. It is also the first report, to the authors' knowledge, to identify necessary conditions for ozone to kill organisms on N95 masks without degrading the function of N95 filters.

Stepped spillway with pre-aeration by a deflector: flow characteristics

ABSTRACT Stepped spillways aim to dissipate part of the upstream energy during the flow passage by the chute. However, the use of these structures is limited to a restrict range of specific discharges due to the risk of cavitation damage. As the air entrainment into the flow assists the concrete protection against the aforementioned damages, a possible solution by aerators installed along the chute, already disseminated to smooth chutes, is being studied to be used also in stepped spillways. The purpose of the present paper is to characterize a flow over a stepped chute with induced aeration by deflector and air supply by an airtight chamber trough tests conducted on a reduced scale physical model. The main regions observed during the tests are presented and were developed four equations that allow to approximately predict the location of the main regions for a given spillway.

269 Attempts to improve equine athletic performance via hypoxia-inducing techniques

Hypoxic conditions encountered at high altitudes result in potential adaptations such as increased hematocrit, hemoglobin, and muscle mitochondrial function. However, living at high altitudes is not practical for many equine athletes. Unfortunately, many trainers have resorted to administering erythropoietin to stimulate red cell production or a large dose of cobalt which reportedly has a hypoxic-inducing effect. Both practices can result in serious health complications (including death) and are typically banned, with a testing threshold of 25 ppb for serum cobalt. Results from Spartan Equine Research confirmed that oral supplementation with 60X the 2007 NRC recommendation of cobalt resulted in serum concentration of 4.7 ppb – far below the testing threshold. These results suggest injectable cobalt, not dietary, is the source of concern. A means of inducing hypoxic effects in humans without living at altitude involves a “tent” covering a bed in which low oxygen concentrations are maintained while sleeping. Similar low-oxygen stalls have been designed for horses. Recent Spartan Equine Research failed to detect any improvement in racing performance in Thoroughbreds housed in such stalls. Challenges not experienced with human athletes were encountered relating to humidity and gases associated with urination and defecation within the airtight chamber – rendering such stalls of limited practicality and safety.

The effects of cysplatin on human adipose tissue derived mesenchymal stromal cells under different oxygen levels

Objective: To evaluate the damaging effects of cisplatin on MMSCs from adipose tissue in a phase of active proliferation and the state of the monolayer, which was exposed at standard (20%) and reduced to 1% and 5% level of oxygen.Methods: The incubation MMSC with cisplatin was performed on cultures of 2 passage in a state in monolayer and cultures in the active growth phase. Profile surface markers of MMSC determined by flow cytometry. MMSCs viability after incubation with cisplatin was detected by the number of apoptotic and necrotic cells using ANNEXIN V-FITC - PI Kit (Immunotech, France). Standard culture conditions (~ 20% O2) created in a CO2 incubator (Sanyo, Japan), 5% O2 created using multigas incubator (Sanyo, Japan), 1% O2 - using an airtight chamber (Stemcell Technologies, USA).Results: Incubation of monolayer MMSC with cisplatin at a concentration of 10 ug/ml for 72 hours leads to death of half of the cells in culture under 20% O2, 5% O2 and 1% O2. Cisplatin increased the fracture of PI+-cell, and PI+/Ann+-cells under all culture conditions. The short-term exposure with cisplatin (24 and 48 hours) did not cause the damaging effect. Effects of cisplatin on the MMSC in the growth phase for 48 hours led to accumulation of Ann+-cells and PI+/Ann +-cells under all culture conditions. However least damaging effect of cisplatin was observed in culture under hypoxic conditions (1% O2).Conclusion: These data suggest that monolayer MMSCs are dying primarily through necrosis, whereas MMSC in the growth phase in response to cisplatin treatment are dying by apoptosis, regardless the oxygen tension.