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ECOSYSTEM DYSBALANCE. "This promotes the increased translocation of pathogenic bacterial components from the intestinal mucosa to the systemic circulation, where they activate innate immunity, characterized by production of proinflammatory cytokines, resulting in systemic inflammation and abnormal gut function. These mechanisms potentially lead to impaired CNS function such as altered neurochemistry, cognition, behavior, stress response, and visceral pain." https://lnkd.in/egTKHRg View in LinkedIn

ECOLOGICAL BALANCE. "A change in the balance of symbionts and pathobionts favoring pathobiont overgrowth results in dysbiosis, which can induce inflammation. During inflammatory responses, macrophages contribute to pathogenesis through inappropriate responses to enteric microbial stimuli, inefficient clearance of microbes from host tissues, and impaired proinflammatory and anti-inflammatory responses, and loss of barrier function." https://lnkd.in/egTKHRg View in LinkedIn

PATHOLOGICAL DYSBIOSIS. "Under pathological stress and/or disease conditions, intestinal dysbiosis can adversely influence gut physiology leading to inappropriate brain–gut axis signaling and associated consequences for CNS functions and disease states." https://lnkd.in/egTKHRg View in LinkedIn

HEALTHY SYMBIOSIS. "Under healthy conditions, the predominance of symbiotic bacteria, an intact intestinal barrier, a healthy innate immunity controlling pathobiont overgrowth inside the intestinal tract and healthy gut function support the symbiotic relationship between CNS function and gut microbiota." https://lnkd.in/egTKHRg View in LinkedIn

MICROBES AND BLOOD-BRAIN BARRIER. "Our indigenous microbes contribute to the mechanism that closes the blood-brain barrier before birth...the transport of molecules across the blood-brain barrier can be modulated by gut microbes -- which therefore play an important role in the protection of the brain." https://lnkd.in/e34HgSe View in LinkedIn

MICROBE-BRAIN RELATIONSHIP. "A body of evidence largely gained from preclinical studies suggests that microbiota can affect brain development, brain signalling systems and affective behaviour in rodents. A role of intestinal microbiota on the development of stress, emotion and pain modulation systems has been identified involving neuroplastic changes in emotion regulation regions and signalling systems." https://lnkd.in/eVmBTKH View in LinkedIn

DYSBIOSIS AND LACK OF REMEDIATION. "The role of the gut serotonin system in mediating microbiota to brain communication is also under investigation. Studies in animal models have demonstrated that CNS neurotransmission can be disturbed by the absence of a normal gut microbiota and the aberrant serotonin profile is resistant to restoration of a normal gut microbiota in later life." https://lnkd.in/eVmBTKH View in LinkedIn

BACTERIA AND MENTAL HEALTH. "Gut bacteria produce hundreds of neurotransmitters, which are used by the body to regulate learning, memory and mood. In addition, gut bacteria are also known to produce up to 95% of the body's supply of serotonin, which is a contributor to feelings of wellbeing and happiness. The evidence suggests that an increased understanding of gut microbiota may produce novel treatments for anxiety and depression." https://lnkd.in/eas2ze6 View in LinkedIn

ROLES IN TIME AND SPACE. "Greater than 95% of human multi-exon genes express multiple splice isoforms. Furthermore, there is evidence for alternatively splicing events that are often differentially regulated across tissues and during development, as well as among individuals and populations, suggesting that individual isoforms may serve specific spatial or temporal roles." http://bitesizebio.com/10148/what-is-alternative-splicing-and-why-is-it-important/ View in LinkedIn

ANCIENT VIRAL BITS AND PIECES. "By far the dominant type of nongenic DNA are transposable elements (TEs), including various well-described retroelements such as Short and Long Interspersed Nuclear Elements (SINEs and LINEs), endogenous retroviruses, and cut-and-paste DNA transposons." http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1004351 View in LinkedIn