Gastrointestinal, Liver, Pancreas, Oral and Psychological Long-term Symptoms of COVID-19 After Recovery: A Review.

Due to the importance of control and prevention of COVID-19-correlated long-term symptoms, the present review article has summarized what has been currently known regarding the molecular and cellular mechanisms linking COVID-19 to important long-term complications including psychological complications, liver and gastrointestinal manifestations, oral signs as well as even diabetes. COVID-19 can directly affect the body cells through their Angiotensin-converting enzyme 2 (ACE-2) to induce inflammatory responses and cytokine storm. The cytokines cause the release of reactive oxygen species (ROS) and subsequently initiate and promote cell injuries. Another way, COVID-19-associated dysbiosis may be involved in GI pathogenesis. In addition, SARS-CoV-2 reduces butyrate-secreting bacteria and leads to the induction of hyperinflammation. Moreover, SARS-CoV-2-mediated endoplasmic reticulum stress induces de novo lipogenesis in hepatocytes, which leads to hepatic steatosis and inhibits autophagy via increasing mTOR. In pancreas tissue, the virus damages beta-cells and impairs insulin secretion. SARS-COV-2 may change the ACE2 activity by modifying ANGII levels in taste buds which leads to gustatory dysfunction. SARS-CoV-2 infection and its resulting stress can lead to severe inflammation that can subsequently alter neurotransmitter signals. This, in turn, negatively affects the structure of neurons and leads to mood and anxiety disorders. In conclusion, all the pathways mentioned earlier can play a crucial role in the disease's pathogenesis and related comorbidities. However, more studies are needed to clarify the underlying mechanism of the pathogenesis of the new coming virus.

The Influence of Psychological Stress on the Initiation and Progression of Diabetes and Cancer.

CONTEXT: Psychological stress can be considered a risk factor for the initiation and progression of many pathological conditions, including type 1 and 2 diabetes mellitus and cancer. OBJECTIVES: The aim of this review article was to evaluate the molecular and cellular mechanisms linking psychological stress to the onset and progression of diabetes and cancer. EVIDENCE ACQUISITION: The current review was conducted to survey and analyze studies related to the effects of psychological stress on diabetes and cancer. RESULTS: Psychological stress may make individuals prone to the development of diabetes through the impairment of the hypothalamic-pituitary-adrenal (HPA) axis function, sympathetic nerves system (SNS), lipid profile, cytokines balance, renin-angiotensin system (RAS), and insulin signaling pathway. Additionally, psychological stress can contribute to the development of cancer through the perturbation in the HPA axis, SNS function, and cytokines balance. Psychological stress is also capable of decreasing the levels of oxytocin and dopamine, leading to an increased risk of cancer in susceptible individuals. CONCLUSIONS: It seems that psychological stress plays a significant role in the onset and progression of diabetes and cancer. The identification of the pathways triggered by psychological stress would open up a new avenue for the understanding of molecular mechanisms by which diabetes and cancer could be managed or even prevented.

Relationship between Personality and Biological Reactivity to Stress: A Review.

Objective Personality traits can be the basis for individual differences in the biological response of stress. To date, many psychobiological studies have been conducted to clarify the relationship between personality and biological reactivity to stress. This review summarizes the most important findings in this area of research. Results Key findings related to the relationship between personality factors and stress-sensitive biological systems in four research models have been summarized; model of psychosocial characteristics, model based on Rumination and Emotional Inhibition, Eysenck's biopsychological model, and Five-Factor Approach of Personality. Conclusion According to the results of this review, it can be concluded that personality typology of individuals influenced their biological reactivity to stressful events. Understanding the biological basis of personality can help to better understand vulnerability to stress. Future research can be continuing based on framework of the four models.

Salivary Testosterone Levels Under Psychological Stress and Its Relationship with Rumination and Five Personality Traits in Medical Students.

OBJECTIVE: The purpose of this study was to evaluate the salivary testosterone levels under psychological stress and its relationship with rumination and five personality traits in medical students. METHODS: A total of 58 medical students, who wanted to participate in the final exam, were selected by simple random sampling. Two months before the exam, in the basal conditions, the NEO Inventory short form, and the Emotional Control Questionnaire (ECQ) were completed. Saliva samples were taken from students in both the basal conditions and under exam stress. Salivary testosterone was measured by ELISA. Data was analyzed using multivariate analysis of variance with repeated measures, paired samples t-test, Pearson correlation and stepwise regression analysis. RESULTS: Salivary testosterone level of men showed a significant increase under exam stress (p<0.05). However, a non-significant although substantial reduction observed in women. A significant correlation was found between extroversion (r=-0.33) and openness to experience (r=0.30) with salivary testosterone (p<0.05). Extraversion, aggression control and emotional inhibition predicted 28% of variance of salivary testosterone under stress. CONCLUSION: Salivary testosterone reactivity to stress can be determined by sexual differences, personality traits, and emotional control variables which may decrease or increase stress effects on biological responses, especially the salivary testosterone.