14 Matching Annotations
  1. Oct 2021
    1. Wenzel, J., Lampe, J., Müller-Fielitz, H., Schuster, R., Zille, M., Müller, K., Krohn, M., Körbelin, J., Zhang, L., Özorhan, Ü., Neve, V., Wagner, J. U. G., Bojkova, D., Shumliakivska, M., Jiang, Y., Fähnrich, A., Ott, F., Sencio, V., Robil, C., … Schwaninger, M. (2021). The SARS-CoV-2 main protease Mpro causes microvascular brain pathology by cleaving NEMO in brain endothelial cells. Nature Neuroscience, 1–12. https://doi.org/10.1038/s41593-021-00926-1

  2. Sep 2021
    1. I think Marshall McLuhan knew it all. I really do. Not exactly what it would look like, but his view and Postman’s view that we are creating a digital global nervous system is a way they put it, it was exactly right. A nervous system, it was such the exact right metaphor. And he didn’t — it’s not that they saw it exactly, but I really love those mid-century media critics because they saw something happening clearer than we see it now. And it is a nervous system. I’m a huge Marshall McLuhan stan.

      We are creating physical infrastructure to scale, enhance, and amplify human capabilities to extend our reach beyond the constraints of time and space.

  3. Jun 2021
    1. The PDMs of this model show promise in revealing the important dynamic characteristics of the underlying physiological mechanisms and allow the formulation of specific quantitative hypotheses about the role of the sympathetic and parasympathetic activity (corresponding to specific PDMs) in cerebral perfusion and autoregulation. Consistent with the widely held view regarding the temporal characteristics of autonomic control of the cardiovascular system, it is posited that the HR PDMs with a resonant spectral peak around 0.2 Hz may be associated with parasympathetic activity, whereas the PDMs with a resonant spectral peak around 0.12 Hz may be associated with sympathetic activity
  4. Feb 2021
  5. Jan 2021
  6. Jul 2020
  7. Aug 2018
    1. CONCLUSIONS: These findings suggest that higher standing BP is a biomarker that helps identify persons with combat PTSD who are likely to benefit from prazosin. These results also are consistent with α1AR activation contributing to PTSD pathophysiology in a subgroup of patients.

      This is precisely the results I would expect. However, I completely disagree with their interpretation.

      People with high blood pressure (BP) can tolerate a reduction in BP without instigating compensatory mechanisms. People with normal or low BP would invoke compensation by the sympathetic nervous system in response to alpha blockade. This would counteract the depressant effects of adrenergic antagonism. Indeed, adrenaline and noradrenaline elevate in response to standing, which I find to be an obvious prediction. Thus, the lack of benefit from prazosin in these subjects may be mediated by an increase in adrenergic receptor activation other than the apha1-adrenoreceptor; in particular, the beta-adrenergic receptors are likely at fault. Propranolol, a beta-blocker, is used for PTSD, so this mechanism seems well substantiated.

      The study apparently found benefit for patients with BP over 110 (with more benefit for higher BP). Thus, I would conclude that systolic pressure below 110 induce compensation.

  8. Oct 2016