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    Validation of impaired Transient Receptor Potential Melastatin 3 ion channel activity in natural killer cells from CFS/ME, 2019, Cabanas et al

    Thank you so much for your reply Neli. I think that I understand your writing perfectly, you should be proud of your English, not apologising! So what I am taking from this is that NK cell "activation" (memory maybe? I am not great with the immune system!) is calcium signalling dependent, and...
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    Validation of impaired Transient Receptor Potential Melastatin 3 ion channel activity in natural killer cells from CFS/ME, 2019, Cabanas et al

    How is an isolated calcium mobilisation defect proof of autoimmunity?
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    Evidence of Clinical Pathology Abnormalities in People with ME/CFS from an Analytic Cross-Section (2019) Nacul et al.

    CK levels are thought to decrease with inactivity due to not being released from muscle fibres. (https://www.ncbi.nlm.nih.gov/pubmed/9443588).
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    Insights into myalgic encephalomyelitis/chronic fatigue syndrome phenotypes through comprehensive metabolomics, 2018, Lipkin et al

    Running trend in these kind of studies, seems to me, to be disturbances to lipid utilisation and maybe the TCA cycle?
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    ME/CFS International Research Symposium, March 2019, Australia

    There are more but some are differentially expressed between tissues. I wonder if multiple could be at play?
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    ME Association: ME/CFS researcher Cara Tomas explains the results from a new study on energy production and mitochondria

    Nuclear genes encode for mitochondrial proteins. mtDNA also codes for mitochondrial proteins. Some complexes, for example, possess subunits encoded by both. It is definitely appropriate to consider both together in terms of using DNA centric methods to infer downstream consequences.
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