Genetic Pollution Puns

Zhi Li, Hao Yan, Xiao Zhang, Shefali Shah, Guang Yang, Qiang Chen, Shizhong Han, Dai Zhang, Daniel R. Weinberger, Weihua Yue, Hao YangTan; Proceedings of the National Academy of Sciences Nov 2021, 118 (46) e2109310118;

DOI:10.1073/pnas.2109310118

URL: https://www.pnas.org/content/118/46/e2109310118

Rev Environ Health. 2021 Sep 16.

https://pubmed.ncbi.nlm.nih.gov/34529912/

doi: 10.1515/reveh-2021-0043. Online ahead of print.

Neurological susceptibility to environmental exposures: pathophysiological mechanisms in neurodegeneration and multiple chemical sensitivity

John Molot  1 , Margaret Sears  2 , Lynn Margaret Marshall  3 , Riina I Bray  3

Affiliations

1    Family Medicine, University of Ottawa Faculty of Medicine, North York, ON, Canada.

2    Ottawa Hospital Research Institute, Ottawa, ON, Canada.

3    Family and Community Medicine, University of Toronto, Toronto, ON, Canada.

PMID: 34529912 DOI: 10.1515/reveh-2021-0043

Abstract

The World Health Organization lists air pollution as one of the top five risks for developing chronic non-communicable disease, joining tobacco use, harmful use of alcohol, unhealthy diets and physical inactivity. This review focuses on how host defense mechanisms against adverse airborne exposures relate to the probable interacting and overlapping pathophysiological features of neurodegeneration and multiple chemical sensitivity.

Significant long-term airborne exposures can contribute to oxidative stress, systemic inflammation, transient receptor subfamily vanilloid 1 (TRPV1) and subfamily ankyrin 1 (TRPA1) upregulation and sensitization, with impacts on olfactory and trigeminal nerve function, and eventual loss of brain mass.

The potential for neurologic dysfunction, including decreased cognition, chronic pain and central sensitization related to airborne contaminants, can be magnified by genetic polymorphisms that result in less effective detoxification.

Onset of MCS may be gradual following long-term low dose airborne exposures, or acute following a recognizable exposure. Upregulation of chemosensitive TRPV1 and TRPA1 polymodal receptors has been observed in patients with neurodegeneration, and chemically sensitive individuals with asthma, migraine and MCS.

In people with chemical sensitivity, these receptors are also sensitized, which is defined as a reduction in the threshold and an increase in the magnitude of a response to noxious stimulation. There is likely damage to the olfactory system in neurodegeneration and trigeminal nerve hypersensitivity in MCS, with different effects on olfactory processing.

Table 2 presents a summary of neurodegeneration and MCS, comparing 16 distinctive genetic, pathophysiological and clinical fea

Pokemon breeding used to work largely like animal breeding. Pokemon babies would be a hybrid of both its parents, but pokemon would largely stick within their species, and mutations and natural selection would differentiate species over time.

Mew is a mutant pokemon. Like many mutants, it's sterile (I like to think that all legendary pokemon are extremely successful mutants), but it had an ability like no other; it could transform into other pokemon. This earned it a reputation in antiquity as the most powerful pokemon; whoever could get their hands on Mew would have the world at their mercy. Somewhere along the way however, the fact that its transforming made it powerful was lost; the misconception that it had superior psychic powers instead began to dominate (even though it was actually less powerful than many known pokemon on its own).

Scientists, many years later, discovered DNA and a sample of Mew's. In an effort to harness the power of a legendary pokemon, team rocket (or a historical progenitor) stole the sample and attempted to clone it (using very crude methods). The cloning was done at an industrial scale, but the experiments were all laughable failures of pokemon, most of which wouldn't survive outside the incubator, to the point where they would just automatically discarding pokemon that didn't resemble what "mew" was meant to look like.

Some of these discards however, were successful in their own way. Indeed, it was quite common for the experiments to generate a certain type of pokemon; one that had Mew's transforming ability, but was also fertile when it transformed. They all were born looking like failed versions of Mew, but they all adapted a "natural" form that was most suitable for survival (small and malleable). These would become known as ditto.

This overwhelmed the pokemon world very quickly. Pokemon would find ideal mating partners in ditto, and no other pokemon could compete with the "perfect matches" ditto would transform into as far as breeding partners went, and Pokemon that previously weren't breeding were finding partners. It could even breed with some sterile pokemon and some inanimate objects (for example, Voltorb is the successful offspring of a pokeball).

While largely unnoticed (due to most Ditto remaining hidden), over the course of only a few generations, pokemon that hadn't bred with Ditto had entirely died out, with the exception of legendaries. When pokemon's DNA were sequenced (there was a long time between the

Doctor's are either shaking their head (the general practitioners) or asking me to pay through the nose for the grace of a visit (a significant fraction of my monthly income.) Reddit, help me! (Or, failing that, at least tell me that the process is inevitable (as long as i continue to live here)).

*the pollution in my crappy little city.