"Exercise Changes Our Gut Microbes, But How Isn’t Yet Clear?" Ashley Yeager

Sara Campbell, an assistant professorship in exercise science, at Rutgers University wondered if exercise could influence the microbes in the gut. Everyone knows all the benefits that come along with exercising, including keeping down inflammation and the enhancement of antioxidant defenses. Campbell realized the symbiosis and mutualism that goes on between the host and the microbes, which led to the beginning of the research process. After creating a research team, Campbell designed an experiment to analyze fecal samples of male mice that were fed a normal or high-fat diet for 12 weeks, while some mice were allowed to exercise and others were not(Yeager 2019). The mice that participated in physical activity generated a "unique microbiome in the guts" and also hosted, "Faecalibacterium, Clostridium, and Allobaculum"(Yeager 2019). In contrast, the mice on the high-fat diet, without any exercise, had inflammation in the gut. Exercising does boost the levels of gut microbes, which also produces butyrate. Which means, "exercise alone, without any dietary changes, is enough to change the composition of gut bacteria"(Sandoiu 2018). Overall, exercise has a larger impact on the human body than ever expected.

Moving more in depth into the research, looking at obese individuals who began to exercise had changes in their gut microbes. Although, lean individuals had different changes, "developed higher levels of Clostridiales, Lachnospira, Roseburia, and Faecalibacterium in their guts, but those microbes returned to baseline levels when the individuals stopped exercising"(Yeager 2019).the difference in changes between lean and obese individuals is still unknown, bur regardless of diet or body composition, change in the gut microbiota is still apparent. Researchers are still unsure of how exercise exactly changes the gut microbes, or if the changes are beneficial to the health, but are determined to find answers.

https://www.the-scientist.com/news-opinion/exercise-changes-our-gut-microbes--but-how-isnt-yet-clear-66281

https://www.medicalnewstoday.com/articles/323351.php

Why we sleep?

Of all the articles I have posted, this by far is the most interesting to me, because it is a topic in which I have high interest in? I came across an article which covers some hypothesis that seems credible and logical to me, on why we sleep. For years numerous of hypothesis were proposed on why we sleep but it isn't until now, scientist have propose an hypothesis that compliments common sense. The article reveals that we sleep to forget things--as the memory bank can only store a certain amount thus, when we sleep we forget something in order to make space to learn new things. https://www.nytimes.com/2017/02/02/science/sleep-memory-brain-forgetting.html?rref=collection%2Fsectioncollection%2Fscience&action=click&contentCollection=science&region=rank&module=package&version=highlights&contentPlacement=9&pgtype=sectionfront

http://www.sleepreviewmag.com/2017/02/purpose-sleep-forget-scientists-say/

Virus

how virus high jack cels
 

http://dx.doi.org/10.1126/science.aal2130

The article gives an indepth explanation of the process when a cell becomes compromise by a virus. The article refers to the most common disease, HIV,  that highjack the cells most often violently. The article explains the process of the cell becomes overpowered by such disease.

"Identification of the Antineoplastic Agent 6-Mercaptopurine as an Activator of the Orphan Nuclear Hormone Receptor Nurr1"

In a 2003 publication by Peter Ordentlich, Yingzhuo Yan, Sihong Zhou, and Richard A. Heyman, the role of Agent 6- Mercaptopurine, commonly known as the drug 6-MP, was studied in relation to the protein Nurr1. Nurr1 is encoded by the NR4A2 Gene. 6-MP is used for many diseases, including Crohn's Disease, in an attempt to reduce inflammation. It was demonstrated that the regulation of the transcriptional activity of Nurr1 by 6-Mercaptopurine can be inhibited by certain factors in the purine biosynthesis pathway. This lends to the possibility of Nurr1 interfering with the antiproliferative effects of 6- MP. One of the ways that the specific effects of 6- MP on Nurr1 was tested was by using other nuclear hormone receptors for comparison, specifically LXR, FXR, RXR, ER, and ROR, which did not show activation for up to 50 microM. 

Understanding the receptor function of Nurr1 is critical due to the fact that Nurr1 may lead to the expression of inflammatory hormones. It was also found that the 6-MP effect was not dependent on the ligand-binding domain. 6-MP seemed to be specific to Nurr1 in that other compounds with a similar mechanism do not activate Nurr1. Additionally, it was discovered that the level of adenine, adenosine, or guanosine molecules affect Nurr1. The reduction of adenosine molecules resulted in less of ATP, suggesting that there is an ATP-dependent pathway. When this pathway is blocked, the transcriptional activation occurs. By modifying the mechanism of 6-MP, new findings can be generated on the methods used to regulate Nurr1. 

It is interesting but not surprising that a protein could involve so much complexity in the way of treating diseases such as Crohn's Disease, which can infect the entire gastrointestinal tract in a human body. It is important to try and modify drugs to target certain proteins and therefore possibly result in the expression of particular genes. Crohn's Disease can result in bleeding, pain, and weight loss. 

Links: 

http://www.jbc.org/content/278/27/24791.full.pdf+html?sid=dcdef3a7-3fcc-43e3-8808-fcc7d1719254

http://www.genecards.org/cgi-bin/carddisp.pl?gene=NR4A2

http://www.ccfa.org/resources/maintenance-therapy.html?referrer=https://www.google.com/