Muons, mutations, and planetary shielding

Abstract

Life on earth is protected from astrophysical cosmic rays by the heliospheric magnetic and slowly varying geomagnetic fields, and by collisions with oxygen and nitrogen molecules in the atmosphere. The collisions generate showers of particles of lesser energy; only muons, a charged particle with a mass between that of an electron and a proton, can reach earth’s surface in substantial quantities. Muons are easily detected, used to image interior spaces of pyramids, and known to limit the stability of qubits in quantum computing; yet, despite their charge, average energy of 4 GeV and ionizing properties, muons are not considered to affect chemical reactions or biology. In this Perspective the potential damaging effects of muons on DNA, and hence the repercussions for evolution and disease, are examined. It is argued here that the effect of muons on life through DNA mutations should be considered when investigating the protection provided by the magnetic environment and atmosphere from cosmic rays on earth and exoplanets.

A new, all‐encompassing aetiology of type 1 diabetes

“…These included the event distribution (i.e., the number of neoplasia per person, T1D and the number of other autoimmune diseases per person), a single, critical, somatic mutation (i.e., to explain the tapering, exponential distribution for polyps and autoimmune diseases), the central role of the HLA allele (i.e., the greatest significance on GWAS for T1D), and the presence of mutation‐prone DNA (i.e., to explain population variation and the frequent rate of events in at‐risk persons for colorectal neoplasia and autoimmune diseases) [11, 20, 25]. The clinical observation of the tapering, exponential event distribution forms the basis for all other GWEA steps; an average and median PCC = 0.998 and 0.999 of observed verses modelled distribution for 23 autoimmune studies including lupus, Sjogren's syndrome, rheumatoid arthritis, systemic sclerosis, primary biliary cholangitis ( N = 8), autoimmune hepatitis, stiff person syndrome, psoriasis, aplastic anaemia, celiac disease ( N = 3), multiple sclerosis, autoimmune thyroid disease ( N = 2), and T1D confirms the general applicability of GWEA [12]. Moreover, at least two variable onset primary immunodeficiency diseases, common variable immune deficiency and idiopathic CD40 lymphocytopenia, also show a near perfectly tapering, exponential distribution of AAIDs (PCC = 0.994 and estimated at 0.998, respectively) suggesting that components of the immune system itself may be the target of autoimmunity [61, 62].…”

“…Assuming 20 amino acids as possible replacements in each of these seven locations, the theoretical number of different P4 binding pockets due to one or more somatic mutations is 1.3 billion. Some persons will have somatic P4 mutations during their lifetime, and nearly all these mutations either do not result in a functional HLA protein or will not result in autoimmune disease [12]. Only persons with a pre‐existing DRB1 allele, that after one mutation results in a functional HLA protein able to form a high affinity HLA‐peptide‐TCR complex are at a risk level for autoimmune disease that may actually manifest itself during their lifetime.…”

“…The predictable, tapering, exponential distribution and variation of other autoimmune diseases present in persons with T1D supports a regular rate of a single event in a single at‐risk gene initiating several autoimmune diseases depending on the post‐mutation state of the epitope‐binding groove [11, 12, 59, 60]. The regular rate of disease events in at‐risk persons which varies among populations suggests that the distribution of inherited and somatic mutations along DNA sequence is not totally random; instead, mutations occur more frequently in mutation‐prone DNA such as GC‐rich sequence and SHM hotspots and are facilitated by cellular activation‐induced cytidine deaminase activity [15, 20, 67, 68].…”

“…When the number of individual AAIDs and the total number of AAIDs listed per person did not match (i.e., errors in the published article), the cumulative number of AAIDs and persons was used to estimate the number of AAIDs per person. The omnipresent neoplasia equations (ONE) derived from colonoscopy polyp studies as previously described were used to model the observed data [12]. The versions of the ONE relevant to GWEA are: CE( p ) = X p the chance that an event occurs p times is the event chance X to the power p f ( p ) = X p /(Ʃ p =0→∞ X p ) the fraction in the population with autoimmune diseases for a specific value of p …”

“…Moreover, colorectal cancer is considered the result of a 'field defect': the same risk factors apply to all mucosal cells in the colon. Assuming random distribution of critical, infrequent but constant, somatic mutations, some persons with a lowrisk APC variant may never experience development of colorectal cancer, whereas others develop one or more [10][11][12]. In other words, like T1D development of colorectal cancer in persons with a low-risk APC variant is defined by autosomal dominant inheritance with incomplete penetrance.…”