The human gut microbiome consists of a variety of microorganisms that inhabit the intestinal tract. This flora has recently been shown to play an important role in human disease. The crosstalk between the gut and brain axis has been investigated through hepcidin, derived from both hepatocytes and dendritic cells. Hepcidin could potentially play an anti-inflammatory role in the process of gut dysbiosis through a means of either a localized approach of nutritional immunity, or a systemic approach. Like hepcidin, mBDNF and IL-6 are part of the gut-brain axis: gut microbiota affects their levels of expression, and this relationship is thought to play a role in cognitive function and decline, which could ultimately lead to a number of neurodegenerative diseases such as Alzheimer’s disease. This review will focus on the interplay between gut dysbiosis and the crosstalk between the gut, liver, and brain and how this is mediated by hepcidin through different mechanisms including the vagus nerve and several different biomolecules. This overview will also focus on the gut microbiota-induced dysbiotic state on a systemic level, and how gut dysbiosis can contribute to beginnings and the progression of Alzheimer’s disease and neuroinflammation.

<p><b>Introduction: </b>Despite years of research and scientific work, it has not yet been possible to produce such a valuable medication as blood. The pandemic does not reduce the need for blood, quite the opposite. However, due to the pandemic, the number of blood donors has dropped dramatically across the country. The aim of the study was to find out the opinions and attitudes of the respondents towards blood donation during the pandemic period and to assess their knowledge of the principles related to safe blood donation during this period. <p><b>Material and methods: </b>The study was conducted using a diagnostic survey method and the tool was our own research questionnaire. The study was conducted in February 2021, using Google Forms platform. In total, data were collected from 150 individuals (females: 60.6%, males 39.4%) aged between 16 and 73 years (mean 31.4 ± 12.4 years). Statistical analyses used a significance level of p = 0.05.<p><b> Results: </b>Nearly 39.7% of the respondents were regular blood donors, 12% of the respondents donated blood several times (12.3%). Blood was donated more often by men, people aged over 30 years, urban residents, and people with higher education (p < 0.001). Most people continued to donate blood despite the COVID-19 pandemic (49.7%). Respondents who have donated blood so far still mostly want to donate blood after the pandemic (90%), among those who have not done so 38% want to do so after the pandemic (p < 0.001). The vast majority of respondents believed it was safe to donate blood during the pandemic (93%), and most were aware that symptoms of infection disqualify a blood donor (83.2%). Only 43.2% knew that “Convalescents who donate plasma are entitled to a blood donation deduction”. <p><b>Conclusions: </b>The current pandemic situation is not an obstacle to donating blood. Blood donations should not be withheld unless there are health contraindications. Due to additional procedures, it is still safe to donate blood. Efforts to promote blood donation during the Covid-19 pandemic should be continued.

Acne vulgaris is a chronic inflammatory skin condition caused by the blockage of sebaceous glands and colonization of Propionibacterium acnes. 1 While acne affects hundreds of thousands of individuals physically, it has been shown to increase one's risk of psychological disturbances including depression, anxiety, and low self-esteem. 2 One longitudinal study reported that even after 15 years, the probability of developing major depressive disorder among acne patients was 18.5%. 2 While several treatment options are available including

Introduction The human gut microbiome colonizes 70% of total microorganisms in the body and its composition can be impacted by several environmental factors, particularly a high fat and high sugar diet called the Western diet. The Western diet has been extensively studied for its consequential shift towards gut dysbiosis and inflammation in the host and other negative health outcomes including brain disorders such as Alzeihmer’s and Parkinson's disease. This so‐called gut‐brain axis may be mediated by key biomarkers including hepcidin and trimethylamine N‐oxide (TMAO). In the setting of the inflamed gut, hepatocyte‐derived hepcidin levels are increased relative to baseline levels as it could potentially have an anti‐inflammatory effect. Dendritic cell‐derived hepcidin also has an anti‐inflammatory effect, but operates differently than the hepcidin derived by hepatocytes. It could be hypothesized that dendritic cell‐derived hepcidin works through a more localized approach through nutritional immunity versus hepatocyte‐derived hepcidin that functions through a systemic approach. Very few studies have focused on dendritic cell‐derived hepcidin and its effects on gut dysbiosis and neurologic disorder. This literature review aims to offer a thorough analysis of the importance of both dendritic cell and hepatocyte‐derived hepcidin in the fight against gut dysbiosis and neuroinflammation through two separate mechanisms. Methods In order to better understand the role of dendritic cell‐derived hepcidin, a literature review of over 80 papers was conducted using a search for key terms including Western diet, gut dysbiosis, gut microbiome, hepcidin, brain, dendritic cell, hepatocyte, inflammation, vagus nerve, iron, TMAO, and brain disorder. Results Breakthrough studies focused on dendritic‐cell derived hepcidin show evidence of mucosal healing after blunt trauma to the intestines in experimental animal models containing the gene for this specific hepcidin, and signs of persistent weight loss, disruption of epithelial architecture, shorter colon lengths and lower systemic hepatocyte‐derived hepcidin levels in models that lacked the gene. Conclusions This new relationship between dendritic cell hepcidin opens a new conversation regarding the gut‐brain axis. There could be a potential relationship between hepcidin produced by dendritic cells and the repair and maintenance of intestinal mucosa. While hepcidin released from the liver could be sequestering iron systemically, the hepcidin from dendritic cells could potentially be working through a means of nutritional immunity by keeping a tight control on local iron and its availability to pathogenic bacteria to promote intestinal homeostasis by starving them of their food source. Future studies can focus on experimentally determining whether both dendritic cell and hepatocyte‐derived hepcidin upregulation causes downregulation of iron in the brain, or vice versa. It is important for future researchers to account for all of the key players in the complex crosstalk between the gut...

Introduction The human microbiome in relation to the ‘gut‐brain’ bi‐directional axis is becoming increasingly relevant in our study to understand the effects of gastro‐intestinal microbiota on brain development and neurological diseases such as Alzheimer’s disease. One particular protein of interest is called brain‐derived neurotrophic factor (BDNF), which is a protein found in the brain that is important for learning and memory through stabilization of long‐term potentiation (LTP). Through past research, its expression levels have been found to be greatly affected by diet and exercise. Furthermore, in events such as aging, decreased levels of BDNF is associated with cognitive decline and increased susceptibility to neurodegenerative diseases such as Alzheimer’s disease (AD). Our study aims to look at how the human microbiome, particularly that of a Western diet, affects BDNF expression levels and modulation in the ‘gut‐brain’ bi‐directional axis. Methods In order to explore our research topic further, we conducted a literature review of about 80 papers using keywords: Small intestines, brain, liver, hepcidin, TMAO, BDNF, iron, astrocytes, Western Diet, microbiota, gut microbiome, gut dysbiosis, iron, inflammation, oxidative stress, IL‐6, vagus nerve. Results After reviewing papers, it was concluded that a Western diet decreases brain BDNF expression. However, the exact mechanism of how gut microbiota modulates this expression and function in the brain is unclear. Some papers mentioned BDNF in the gut and the periphery, but not much else other than that they existed. Conclusions This study sparked further questions: Does gut microbiota affect brain BDNF directly through the gut‐brain axis? Or is it indirect through an intermediate such as gut BDNF? Is there a relationship between gut BDNF and brain BDNF? It is known that brain BDNF is associated with learning and memory and is important for preserving cognitive abilities, however little is known about how gut microbiota affects it through the gut‐brain axis or even its relation to other peripheral BDNF. Looking forward, we plan on measuring different protein levels, including that of BDNF, in the brains and guts across different cohorts of mice. The cohorts will differ in diet, age, and having the APP gene. From this analysis we hope to find more insight on the unknown mechanism that bridges gut microbiota to BDNF in the brain, which may ultimately help in finding ways to prevent cognitive decline seen in many neurological diseases.