Wouldn’t Gas Chromatograph or Mass Spectroscopy be the cheapest way to test? And therefore the most desirable? Or is GC/MS slower than the other options?

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Reading your post, thank you Aldebaran, something came as a flash to me: are they somehow assuming what they are supposed to “prove”? They assume that somatic degradation is non zero and then they prove that somatic degradation is non zero! I must have it wrong as it looks too simple and I must have it wrong when making somatic degradation equivalent to multicellular aging.

To further assess whether HIF-1α affects the transcription of miR-322, we transfected A7r5 cells with an adenoviral vector expressing modified oxygen dependent degradation domains (ODDD-wt) that express a HIF-1α ODDD domain from amino acids 531 to 575. This domain competes with endogenous HIF-1α/-2α for pVHL recognition and degradation22. Another adenoviral vector expressing mutant ODDD (ODDD-mut), with a mutation of proline 564 to alanine, was constructed which can be recognized by the VHL complex for HIF-2α but not HIF-1α22. This was used as a negative control for HIF-1α stabilization. Luciferase assays showed that HIF-1α stabilization specifically activated miR-322 promoter activity but not that of the mutant (Fig. 3d). As shown in Fig. 3e,f, qRT–PCR and western blotting revealed that the endogenous expression levels of miR-322 also dramatically increased with HIF-1α accumulation.

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        We enrolled a total of 29 patients across three cohorts in the Phase 2 clinical program in PNH. The first cohort enrolled ten patients who had not previously been treated with eculizumab. We refer to these patients as eculizumab naïve patients. The second cohort enrolled 16 patients, who, prior to the trial, were treated with an eculizumab regimen and, in connection with the trial, were switched over to treatment with zilucoplan. We refer to these patients as eculizumab switch patients. The third cohort enrolled three patients. These patients are U.S. based and were inadequate responders to eculizumab and who were also switched over to zilucoplan. We refer to these patients as eculizumab inadequate responders.

Rats’ carotid aortas were isolated, fixed in formalin (10%), processed for paraffin sectioning (3 mm thick) and stained with hematoxylin-eosin (H&E). The lumen of blood vessels, vascular walls and vascular endothelial cells of the carotid aortas were observed with microscope.