Coronavirus disease (CoVID-19), caused by recently identified severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2), is characterized by inconsistent clinical presentations. While many infected individuals remain asymptomatic or show mild respiratory symptoms, others develop severe pneumonia or even respiratory distress syndrome. SARS-CoV-2 is reported to be able to infect the lungs, the intestines, blood vessels, the bile ducts, the conjunctiva, macrophages, T lymphocytes, the heart, liver, kidneys, and brain. More than a third of cases displayed neurological involvement, and many severely ill patients developed multiple organ infection and injury. However, less than 1% of patients had a detectable level of SARS-CoV-2 in the blood, raising a question of how the virus spreads throughout the body. We propose that nerve terminals in the orofacial mucosa, eyes, and olfactory neuroepithelium act as entry points for the brain invasion, allowing SARS-CoV-2 to infect the brainstem. By exploiting the subcellular membrane compartments of infected cells, a feature common to all coronaviruses, SARS-CoV-2 is capable to disseminate from the brain to periphery via vesicular axonal transport and passive diffusion through axonal endoplasmic reticula, causing multiple organ injury independently of an underlying respiratory infection. The proposed model clarifies a wide range of clinically observed phenomena in CoVID-19 patients, such as neurological symptoms unassociated with lung pathology, protracted presence of the virus in samples obtained from recovered patients, exaggerated immune response, and multiple organ failure in severe cases with variable course and dynamics of the disease. We believe that this model can provide novel insights into CoVID-19 and its long-term sequelae, and establish a framework for further research.

We hypothesize that threat of dehydration provided selection pressure for the evolutionary emergence and persistence of the anterior communicating artery (ACoA – the inter‐arterial connection that completes the Circle of Willis) in early amniotes. The ACoA is a hemodynamically insignificant artery, but, as we argue in this paper, its privileged position outside the blood‐brain barrier gives it a crucial sensing function for the osmolarity of the blood against the background of the rest of the brain, which efficiently protects itself from dehydration. Till now, the questions of why the ACoA evolved, and what its physiological function is, have remained unsatisfactorily answered. The traditional view—that the ACoA serves as a collateral source of vascularization in case of arterial stenosis—is anthropocentric, and not in accordance with principles of natural selection that apply more generally. Diseases underlying arterial stenosis are associated with aging and the human lifestyle, so this cannot explain why the ACoA formed hundreds of millions of years ago and persisted in amniotes to this day. The peculiar hemodynamic properties of the ACoA could be selected traits that allowed for more efficient forebrain detection of dehydration and complex behavioral responses to water loss, a major advantage in the survival of early amniotes. This hypothesis also explains insufficient hydration often seen in elderly humans.

Together with our previously published data, our results lead to the conclusion that alteration of postnatal diet can lead to TNF-α and adipocyte morphology changes.

The effect of nicotine is complex and most of the research of the heart rate variability is done with tobacco in participants trying to cease smoking. Such studies are limited with desensitization of nicotinic receptors, emergence of abstinence symptoms, and the overall modified activation of the autonomic nervous system. The aim of this study is to show the effect of nicotine on young smokers and nonsmokers using descriptive and spectral analytical methods of the heart rate variability. The research was conducted on 50 participants (m=23, f=27), average age of 21.8±1.49 years, who were divided into nonsmokers (n=26, m=11, f=15) and smokers (n=24, m=12, f=12). Smokers were smoking 14.8±6 cigarettes on average for 4.77±2.19 years. A baseline ECG lasting 100s was recorded, followed by chewing a gum containing 4 mg of nicotine, after which an ECG lasting 100 s was re-recorded. The ECG analysis was followed by the analysis of the heart rate variability using time domain and frequency domain methods. In order to show the effects of nicotine more precisely, the resulting changes (Δn) were calculated as the difference between the final and initial values of variables, after which the changes (Δn = T2-T1) were statistically compared between smokers and nonsmokers. After the application of nicotine, a significant difference was observed in the changes of the average length of the RR intervals (p=0.01) and the heart rate (p<0.01) between smokers and nonsmokers. Within the spectral analysis, a significant difference was observed in the changes of the absolute value of the spectrum of low frequencies (LF, p<0.05), the standardized values of high and low frequency spectra (LF (n.u.), HF (n.u.), p<0.05) and the LF and HF ratio (LF/HF, p<0.05). The heart rate variability analysis proved to be a valuable indirect method for analyzing the autonomic nervous system. The obtained results confirm that the effect of nicotine significantly affects nonsmokers, reducing their heart rate variability and the parasympathetic tone, while increasing the heart rate and the sympathetic tone.