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Information storage in synthetic DNA oligomers is attractive due to the inherent physical density, stability, and energy efficiency of nucleic acids. Information retention –during writing, storage, and retrieval processes– requires development of efficient encoding/decoding systems. Additionally, potential intrusion of artificial or organic malevolent biologically active molecular machines could potentially cause catastrophic biosecurity concerns. Here we present an improved information storage method that focuses on efficiency and biosecurity. Herein this paper, we have developed and experimentally tested an algorithm to write data in pool of DNA strands by applying a fountain code (rateless erasure code), a Reed Solomon code, and an oligomer mapping code that ensures Bio-Security. We validated our method through wet-lab experiments and wrote, stored, and fully retrieved 105,360 bits of information. We validated the biosecurity aspects of our method through in-silico experimentation using a BLAST-run to compare our generated oligomers to existing genes documented in the public databases, a Plasmidhawk software analysis to determine our oligomers could not be artificially traced to have originated from another lab, and utilized an open-source software to determine whether our oligomers could have expressed any sequences that potentially originate or empower biologically meaningful functions. 

Aims: Clinical and experimental evidence has shown that females in humans and other mammals have higher glutathione (GSH) levels than males, which are caused by higher levels of estradiol. Understanding how hepatic GSH level and synthesis velocity depend on the sex hormones is an extremely important question since oxidative stress contributes to the risk for heart disease and cancer, and oxidative stress is reduced by GSH. Our aim is to develop a systems approach to understanding GSH metabolism and use this to explain the causes of GSH differences in males and females, how GSH changes during the menstrual cycle, and why women may be less susceptible to acetaminophen toxicity. Methods: We use mathematical models for hepatic glutathione metabolism, including one-carbon metabolism and acetaminophen detoxification, to investigate how the activation of certain enzymes by estradiol leads to dramatic changes in reaction velocities and metabolite concentrations. Results: The models explain why women of childbearing age have higher glutathione than men, and that this is caused by the balance of activation of glutamyl cysteine synthetase (GCL) and glutathione peroxidase (GPX) by estradiol. The steady-state concentration of glutathione in women depends on the strength of the activation of GCL and GPX and is quite homeostatic over a wide range of activations. Conclusions: During the menstrual cycle, the GSH concentration changes daily but over a relatively narrow range. We explain how this dynamic homeostasis depends on the biochemical network that produces GSH. The model is also consistent with published results that show that female mice are less susceptible than males to hepatotoxicity due to acetaminophen overdose and suggests that this might also be true for humans, though the human epidemiological data are contradictory.