Aurora borealis are easier to spot because places like Scandinavia, Iceland, and Alaska are above 60°N and they’re relatively easy to visit. It is very rare to see auroras outside these polar latitudes.

New Zealand and Patagonia, the southernmost inhabited places, only reach about 50° and 56°S respectively. These regions are extremely remote and difficult to travel to, and conditions are always less than ideal. The only place you can reliably see aurora australis is Antarctica, which is pretty much inaccessible.

If you want to experience the most loving solar embrace visit the Altiplano in December and play a football match at 3500m! The sun is exactly directly overhead, and the UV index is over 20 every day. The crazy thing is, it’s the craddle of South American civilisation.

Thank you for the detailed answer. I had a question regarding mirtazapine, an atypical antidepressant which is useful to treat insomnia because of its extremely high affinity to H1 receptors (Ki = 0.14nM). Essentially at lower doses mirtazapine binds exclusively to H1 instead of adrenergic and serotonin receptors. Would mirtazapine treatment upregulate/sensitise H1 over time, reducing its effectiveness as a sedative and potentially increasing the risk of allergies?

I’m also curious about the molecular mechanisms by which tolerance to antihistamines develops. IIRC antagonists and inverse agonists inhibit the receptor, except the latter bind at the agonist site and induce an opposite response instead of blocking it. Would inverse H1 agonists hence be more likely to sensitise H1 as the body tries to return to baseline? How does the neuron achieve this? By increasing the amount of H1 or by decoupling G proteins from the receptor?

‘There is no significant difference in employability between these languages’

Thank you for such useful information…

Look at some of the proteins upregulated in the chart: YAP1, ITGB1, VASP, EZR, EGFR, RHOQ, NFKB, CDK2… All of these proteins are associated with increased tension in the cellular microenvironment as a result of abnormal matrix deposition, inflammation, oxidative stress.