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  1. Prikvačeni tweet
    10. ruj 2017.
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  2. 3. velj
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  3. 1. velj

    Hey and you are incredible candidates for this award! Check it out 👊

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  4. proslijedio/la je Tweet
    1. velj
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  5. proslijedio/la je Tweet
    30. sij

    ME/CFS in the Era of the Human Microbiome. Join Solve ME and our presenter, Amy Proal, Ph.D., for a fantastic discussion on persistent pathogens that drive chronic symptoms.

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    29. sij
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    27. sij

    The flag is at half mast today to honor the life of Robert Moir, PhD, an HMS/Mass General Alzheimer's researcher. Dr. Moir died last month at 58 from glilbastoma. We're proud to join them in recognizing his memory.

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  8. 26. sij

    Welp this article (very sadly) sure hits home. 😔 Please read if you want more background on some of the Lyme-related tweets I’ve been writing lately

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  9. proslijedio/la je Tweet
    25. sij

    Article from our fantastic collaborators & describing a fascinating and promising diagnostic technique that measures neutrophil movement in fresh, live blood. In this case it was used to accurately diagnose sepsis.

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  10. proslijedio/la je Tweet
    25. sij

    This half-hour podcast by is a ‘must-listen’ for all pharmacists. It’s a fantastic summary of a lot of what I learnt during my Nutritional Medicine MSc. It explains why we need to look after our human microbiome and why that’s so important.

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  11. proslijedio/la je Tweet
    22. sij

    Today, we roll our eyes at some of last decade's assumptions (autism is caused by cold mothering!). In 50 years, people will be astounded by today's passive, unthinking assumption of sterility in 'autoimmune' and chronic illness.

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  12. 22. sij

    It drives me crazy when is connected to a symptom/condition and the immediate response is to “blame” the human response alone...when there are 100,000+ pathobionts in human tissue/blood/gut capable of driving a very broad range of inflammatory processes

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  13. proslijedio/la je Tweet
    22. sij

    In , a -led team uncovered a broad diversity of large and giant that belong to the NCLDV supergroup: . From and many others! (Art: Zosia Rostomian/)

    Art illustration capturing giant virus genomic diversity. (Zosia Rostomian/Berkeley Lab)
    , , i još njih 6
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  14. 22. sij

    3/ Or since LPS induced lipid formation in the study, cld bacterial infection be involved? () 👉 Especially w/ more teams reporting bacteria inside astrocytes/glia in the brain? () Any thoughts ?

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  15. 21. sij

    2/ Worth noting that persistent target signaling, synthesis + metabolism to remodel host cells like microglia into an environment optimal for their replication 👉 Indeed viral infection of LDAM cells cld explain ROS + proinflammatory state:

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  16. 21. sij

    Study finds a “striking buildup of lipid droplets in microglia w/ aging in mouse/human .” The cells, called ‘lipid-droplet-accumulating (LDAM), are defective in phagocytosis, produce high levels of ROS + secrete proinflammatory cytokines:

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  17. 20. sij

    Yet another reason why studying the /virome + persistent should, IMO, be the top priority of the /CFS research community 👇

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  18. proslijedio/la je Tweet
    20. sij

    Did you know that viruses produce proteins that mimic and act like human hormones? Dr. Altindis is an assistant professor at Boston College who studies viral hormones and how it works. He is looking for postdocs to join his lab. Please spread the word 👇🏽

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  19. 19. sij

    9/Also we must pay more attention to pathogens - or dysbiotic communities of organisms - capable of persisting in the womb and being vertically transmitted from mother to child. Otherwise we run the risk of over assuming chronic symptoms might be communicable via other mechanisms

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  20. 19. sij

    8/ That’s why I push the scientific community to challenge immunosuppression as the current standard of care for conditions increasingly tied to microbiome driven dysfunction (including those tied to an outdated model of “classical autoimmuity”) More here:

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  21. 19. sij

    7/ After reading 100s of papers on the topic a trend that repeatedly stands out is that immunocompromised people seem more susceptible to the possibility of shared organisms. In other words, a healthy immune response seems to at least mitigate organism transfer tied to disease

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