Cystatin-C has interested me for some time. It is used as a marker of Kidney function and in theory is a better marker than Creatinine. Creatinine has its problems, but it appears so does Cystatin-C. What I found interesting about Cystatin-C is that it is also a signalling molecule whilst Creatinine is a metabolic by product. Creatinine is produced mainly inside skeletal muscle by the spontaneous, non-enzymatic breakdown of creatine and phosphocreatine. Creatinine is also produced in blood samples between the sample being taken and then tested. As it is excreted by the kidneys a low value is an indicator of good kidney function or low muscle mass. High values can result from exercise and high muscle mass as well as bad kidney function. I have tasked three LLMs to produce some summaries of research and I attach those below. However, there is only one relatively straighforward conclusion I can come to at this point which is that Cystatin-C is a complex molecule and although the...
There has been some press attention to Endometriosis recently. To me it looks like a splicing/acetylation type of disease (which requires that sort of intervention to resolve). I have put some prompts into an AI (chatGPT) to produce a more detailed argument with citations and here is the response: Could Endometriosis Result from Aberrant Splicing Caused by Reduced Nuclear Acetylation? Summary: Endometriosis is usually described as an inflammatory, hormonal and fibrotic disease in which endometrial-like tissue grows outside the uterus. However, a growing body of evidence suggests another layer of explanation: endometriosis may involve abnormal RNA splicing, and that abnormal splicing may in some cases arise from reduced acetylation of nuclear proteins. This article sets out the argument for that hypothesis. The evidence does not yet prove that reduced nuclear acetylation is the root cause of endometriosis, but it does make the hypothesis biologically plausible an...