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Posted by Nick Maggiulli

On Financial Relativity and Overcoming YourBiases

Imagine you are sitting on an asteroid in deep space and you have a friend who has a spaceship that can travel at 99% the speed of light. Yes, this is physically impossible for a host of reasons, but bear with me for now. Out of boredom you decide to challenge your friend to a race — their spaceship vs. a beam of light. Your friend agrees, but you have to give them a small head start.

Shortly after the race begins, your friend is moving away from your asteroid at 99% of the speed of light when you send out the beam of light to race alongside them. From your perspective on the asteroid, you will see the beam of light pass your friend’s spaceship like a faster car passing a slower car on a freeway. After all, 100% the speed of light is faster than 99% the speed of light. However, what will your friend experience on their spaceship?

You might think that your friend will also see the light beam pass them like a slightly faster car on a freeway, but this is incorrect. Your friend will see the light beam pass them at the speed of light . Why? Physicists discovered that the speed of light is constant for all observers. Given this is true, how is it possible that you and your friend can see the same event, but it will take you more time to view it?

Physicists discovered that the speed of light is constant for all observers.

The answer is: as your friend’s velocity approaches the speed of light, their time slows down . You can calculate how much time slows as you approach light speed using the Lorentz factor . For example, in the thought experiment above (i.e. 99% the speed of light), 7 seconds of your time would only take 1 second of your friend’s time. This idea, which is one of the most amazing and unintuitive in all of physics, is known as time dilation and comes from Einstein’s theory of special relativity .

as your friend’s velocity approaches the speed of light, their time slows down

I tell you about time dilation and special relativity because they illustrate an important truth about the universe and investor experience… it’s all relative . In the thought experiment above you and your friend experience the same event very differently without noticing it. You both will experience 1 second of time the same way, but what happens in that second is very different. This is just as true in investing where you and I will experience the same market event very differently because of our biases, our personal investment history, and other ideas that have shaped our worldview.

it’s all relative This is just as true in investing where you and I will experience the same market event very differently because of our biases, our personal investment history, and other ideas that have shaped our worldview.

In 2008, Milner and colleagues [ 87 ] demonstrated that T cells in subjects with AD-HIES failed to produce interleukin (IL)-17 (but not interferon gamma) after mitogenic stimulation with staphylococcal enterotoxin B or after antigenic stimulation with Candida albicans or streptokinase. Purified naïve T cells were unable to differentiate into IL-17 producing the T helper (Th17) cells in vitro and had a lower expression of the retinoid-related orphan receptor (ROR)-γt, which is consistent with the crucial role of STAT3 signaling in the generation of Th17 cells. These Th17 cells have emerged as an important subset of helper T cells being critical in the clearance of fungal and extracellular bacterial infections. The Th17 cytokines, IL-17 (IL-17A) and IL-17F form biologically active homo- or heterodimers. Il-17 initiates nuclear factor kappa B (NF-κB) activation, leading to the transcription of multiple target genes involved in innate immunity. These include chemokines, such as CXCL8 (IL-8) and CCL20, the cytokines IL-6, tumor necrosis factor alpha (TNF-α), granulocyte- and granulocyte-macrophage colony-stimulating factor (G-CSF and GM-CSF, respectively), acute phase proteins such as C-reactive protein, antimicrobial peptides and mucins [ 88 ]. Thus, IL-17 plays an important role in antimicrobial defenses by recruiting and expanding the neutrophil lineage and producing antimicrobial peptides. The proinflammatory cytokines produced by Th17 cells include TNFα, IL-22 and IL-26, which are involved in innate immunity, and IL-6 which directs CD4+T cells differentiation towards the Th17 lineage. IL-22 has been associated with the generation of defensins, acute phase proteins and inflammatory cytokines [ 89 ]. This multidirectional, fundamental role of Th17 cells, including cells with specificities against candidal antigens explains the pattern of infection susceptibility characteristic of mutated HIES patients. In the recent report by Conti et al [ 90 ] a decrease of salivary antimicrobial peptides, such as β-defensin 2 and Histatins has been demonstrated in AD-HIES patients, providing a mechanism for the severe susceptibility to oropharyngeal candidiasis. This finding supports this hypothesis of the crucial role of the Th17-dependent responses in immunity to .

Immune assessments of mutated AR-HIES patients reveal T cell lymphopenia with low counts of both CD4+ and CD8+ T cells, as well as impaired T cell expansion from activated peripheral blood mononuclear cells in vitro. In autosomal recessive HIES eosinophilia and the elevated serum IgE may be more pronounced than in AD-HIES []. In contrast to the latter syndrome, DOCK8 deficiency is associated with low IgM concentrations and impaired generation of a durable secondary antibody response to specific antigens, which accounts for the functional antibody abnormalities []. In a single patient with AR-HIES due to mutation, a normal number of lymphocytes was observed.

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