In this letter we investigate if SARS-CoV-2 RNA is involved in the increased ageing of alveolar cells. Our in silico study is explorative. With the results we are able to outline experiments with AEC2 repair of bleomycin damaged alveolar cells. If AEC2 repair capability is diminished by spike RNA then perhaps this result provides a first step on a route to treat immortal lung cancer cells.

The premise regarding COVID-19 disease is that it is a spectrum which begins with infection with viral SARS-CoV-2 exposure via airborne or oral virus particles. The individual response to it depends on many factors including co-morbid conditions. An important aspect of SARS-CoV-2 virus infection is the cytokine storm that develops after the infection. The immuno-chemical chaos created in this cytokine storm is to the benefit of the virus. In this meta analysis the authors explore ways to let the cytokine storm die down by looking into the role of histamine. Histamine is a metabolic product of the essential aminoacid histidine. Histamine has 4 known receptors: H1, H2, H3 and H4. The immunoglobulines IgE and IgM are indicative for a COVID-19 infection. This immune response is related to inflammation. Inflammation, in turn, runs mainly via histamine after e.g. virus inoculation. The goal of the meta-study is to gather evidence to primarily block the H4 receptor (H4R) in gastrointestinal cells to diminish the cytokine overproduction in the $\approx$ 30\% of the patients suffering from gastrointestinal problems caused by SARS-CoV-2. Our concept is as follows. If we can strike a careful balance between hampering the gastrointestinal spreading of the virus and histamine antagonists to tackle the cytokine storm, then the natural immunity can later on come on line again and attack the virus without being led astray by cytokine chaos. We will concentrate on H4R but also look at H1R and H2R related effects. The proposed substances in our systemic approach can be balanced for an effective early treatment. The nature of our work is by its method and results theoretical. In that respect we also may note the structural chemistry indol skeleton resemblance among a number of different drugs.

If a clear and valid no-go for Einsteinian hidden parameters is real, it must in no way be possible to violate the CHSH with a local hidden variables based computer simulation. In the paper we show that with the use of a modied Glauber-Sudarshan method it is possible to violate the CHSH.The criterion value comes close to the quantum value and is approximately 2.4. The proof (POC) is presented with the use of an R computer program. The important snippets of the code are discussed and the complete code is presented in an appendix.

In the paper it is demonstrated that a valid path to a contradiction in complex number theory exists. In the path use is made of Euler’s identity and simple trigonometry. Each step can be easily verified.

Bell’s correlation formula is based on a classical Kolmogorov probability theory. It is tested in experiment with an estimate correlation. The latter is the raw product moment (rpm) correlation that is classical Kolmogorov based as well. We note that the famous Bell inequalities are derived from Bell’s correlation formula. The problem is that the hypothesis: “is it possible that in experiment Bell’s correlation is equal to quantum”, can only found to be false. This is not because the data generating process does not produce the required data. Or that the inequalities sufficiently show that the data cannot violate the inequalities. It is because the statistics of the Bell experiment is flawed. The rpm correlation in experiment cannot be equal to the quantum value in principle. This is because it requires the classical Kolmogorov rpm correlation to be not Kolmogorov.