According to the questionnaire that we have conducted, only 11.66 percent of our participants reach the standard sleeping hour level, 8 hours. The two surveys taken during 2017 to 2018 proved a common phenomenon nowadays for juveniles to stay up late, since the percent of the participants who recognize staying up late is astoundingly only 5%. Over half of them choose not to get sleep until at least midnight. Additionally, there are an increasing number of white-collar employees staying till midnight on account of overwhelmed workload.
Worse still, harms brought by staying up late can seriously damage to human’s physical health. Fatigue, irritability, and difficulty concentrating will torment people and influence their career negatively1. Neuroscientists at Harvard Medical School (HMS) have discovered an unexpected causal relationship between insufficient sleep and premature death2. Most of these adverse consequences that are caused by insufficient sleeping, this finding inspires us to investigate this topic.
Staying up late is always accompanied with issues that are related with inadequate sleep. While you are staying till midnight, molecules called Reactive Oxygen Species (ROS) are accumulating in your gut and invading into your body.These highly reactive oxygen-containing molecules can, in large amounts damage DNA and other components within cells, leading to cell death, which is the main factor that leads to shorter life span and cancer. Nowadays, however, there is no any effective clinic method that shows to reduce the harm which those who are keen on staying up late suffer from3.
In this study on sleep-deprived fruit flies, scientists found that if the peroxygen compounds in the intestine of fruit flies are neutralized and eliminated from gut by antioxidant compounds, the flies deprived of sleep can still remain active and escape premature death.. This research will help us development of new approaches to counteracting the adverse effects of lack of sleep in humans. The current papers reveal that ways that can reduce the activity of ROS is by oral administration of vitamin C and vitamin E4. It inspire us that antioxidant enzymes such as superoxide dismutase (SOD) and catalyse(CAT) can scavenge ROS effectively5,6, several studies have investigated the protective effects of exogenously administered SOD or SOD and catalase combinations in experimental animal models7. By contrast, the strategies for oral delivery may not remain the activity of SOD and CAT enzyme because of degradation in the gastrointestinal tract (presence of digestive enzymes and pH-dependent factors)8.
The gut microbiome offers an opportunity to regulate host metabolism either by production of drugs or nutrients and by degradation of toxic products. Applications of bacteria as engineered therapeutics have targeted diseases as disparate as diabetes mellitus9, inflammatory bowel disease10 and phenylketonuria11, which suggests that bacterially delivered SOD and CAT has potential as a therapy for sleep deprivation.
Thus, we decide to process synthetic gut bacterial products which haven’t existed in the markets. We are designated to design a brand-new product, combining many technologies. To demonstrate our biochemical product, we designed and constructed a resolution for delivering SOD and CAT enzyme through engineered gut microbes, which can eliminate the amount of ROS in our intestine and thus allows harm reduction when we stay up late. We believe that this product can save every night owl from the harm of less sleep brought and boost the efficiency of young people with healthier bodies.
1.Alexandra Vaccaro et al. Sleep Loss Can Cause Death through Accumulation of Reactive Oxygen Species in the Gut, CELL (2020). DOI: https://doi.org/10.1016/j.cell.2020.04.049
2.Mycos 2018 Sleep Survey of College Students (麦可思2018年大学生睡眠情况调查)
3.Tencent Education-Mycos 2017 Sleep Survey of College Students (腾讯教育-麦可思2017大学生睡眠情况调查)
4.Cawkwell, P., Lawler, A., Maneta, E. & Coffey, B. J. Staying Up at Night: Overlapping Bipolar and Obsessive-Compulsive Disorder Symptoms in an Adolescent with Autism Spectrum Disorder. J Child Adolesc Psychopharmacol 26, 74-77, doi:10.1089/cap.2016.29100.bjc (2016).
5.Vaccaro, A. et al. Sleep Loss Can Cause Death through Accumulation of Reactive Oxygen Species in the Gut. Cell 181, 1307-1328 e1315, doi:10.1016/j.cell.2020.04.049 (2020).
6.Irwin, M. R., Olmstead, R. & Carroll, J. E. Sleep Disturbance, Sleep Duration, and Inflammation: A Systematic Review and Meta-Analysis of Cohort Studies and Experimental Sleep Deprivation. Biol Psychiatry 80, 40-52, doi:10.1016/j.biopsych.2015.05.014 (2016).
7.Lim, J. Y. et al. Vitamin C induces apoptosis in AGS cells via production of ROS of mitochondria. Oncol Lett 12, 4270-4276, doi:10.3892/ol.2016.5212 (2016).
8.Xu, J., Duan, X., Yang, J., Beeching, J. R. & Zhang, P. Enhanced reactive oxygen species scavenging by overproduction of superoxide dismutase and catalase delays postharvest physiological deterioration of cassava storage roots. Plant Physiol. 161, 1517-1528, doi:10.1104/pp.112.212803 (2013).
9.Melov, S. et al. Extension of life-span with superoxide dismutase/catalase mimetics. Science 289, 1567-1569, doi:10.1126/science.289.5484.1567 (2000).
10.Chan, P. H. Antioxidant-dependent amelioration of brain injury: role of CuZn-superoxide dismutase. J Neurotrauma 9 Suppl 2, S417-423 (1992).
11.Muheem, A. et al. A review on the strategies for oral delivery of proteins and peptides and their clinical perspectives. Saudi Pharm J 24, 413-428, doi:10.1016/j.jsps.2014.06.004 (2016).
12.Takiishi, T. et al. Reversal of Diabetes in NOD Mice by Clinical-Grade Proinsulin and IL-10-Secreting Lactococcus lactis in Combination With Low-Dose Anti-CD3 Depends on the Induction of Foxp3-Positive T Cells. Diabetes 66, 448-459, doi:10.2337/db15-1625 (2017).
13.Braat, H. et al. A phase I trial with transgenic bacteria expressing interleukin-10 in Crohn's disease. Clin Gastroenterol Hepatol 4, 754-759, doi:10.1016/j.cgh.2006.03.028 (2006).
14.Isabella, V. M. et al. Development of a synthetic live bacterial therapeutic for the human metabolic disease phenylketonuria. Nat. Biotechnol. 36, 857-864, doi:10.1038/nbt.4222 (2018).
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