Watch for News About "Climate Change Anxiety"
After 24-hr blasting about the end of the world due to climate change, you're going to be told that new neuroses are due to your concern over climate change
I bet there are some pharmaceuticals for that.
I’d rather experience “Corporate Toxic Chemicals Everywhere” anxiety, which I why I teach “Environmental Toxicology: Ecosystem and Health”.
Click on the poor lady who is listening to Sanjay Gupta make up a new psychological syndrome on his podcast to enroll for the fall @ IPAK-EDU. Live chat w/teachers and students - community - can help us stay focused on the real problems we are facing, and solutions.
With "climate change" there is a reason to "change" the ownership of your property - this is WHY this is called "CLIMATE CHANGE"
It is like "SAFE AND EFFECTIVE" "vaccine - it is safe for "THEM" and "effective in what THEY want to achieve
or like "CORONA" "virus"
- https://link.springer.com/chapter/10.1007/978-3-030-58861-8_2 https://ieeexplore.ieee.org/document/9298084 DCCORONA
https://projects.ics.forth.gr/_publications/CORONA2015.pdf
https://www.frontiersin.org/articles/10.3389/fimmu.2017.00673/full
Corona virus...
Intravenously injected nanomaterials can adsorb a wide range of proteins in the blood (39). The bio-corona of blood proteins is rapidly formed, and it has been shown to affect hemolysis and thrombocyte activation (40). Furthermore, complement activation on the surface of nanomaterials is of particular concern when it comes to clinical applications. In fact, complement proteins have been consistently identified in or on nanoparticle coronas (28, 30, 40, 41). The complement system is a critical component of the innate immunity in the blood; it is a proteolytic cascade typically triggered via three distinct pathways (classical, lectin, and alternative) that converge to generate the same set of effector molecules at the third component of complement (C3) (42). Complement proteins opsonize pathogens and cells for engulfment via complement receptors and could conceivably promote nanomaterial uptake as well. However, certain complement factors may instead confer “stealth” properties to nanomaterials by preventing further complement activation, as shown in a recent study on GO (43). Complement activation also liberates two potent effector molecules (C3a and C5a) that play important roles in the recruitment and activation of inflammatory cells as well as anaphylaxis, a serious allergic reaction that is rapid in onset and may cause death (44). Several reports have documented pathway-specific complement activation by various types of nanomaterials including carbon-based nanomaterials such as CNTs (45, 46) and GO (47, 48). The question is: could particle surfaces be engineered to avoid protein adsorption and/or unscheduled complement activation? The attachment of polymers such as poly(ethylene glycol) (PEG) on particle surfaces is a common approach in nanomedicine, and the traditional view has held that PEGylation completely prevents protein adsorption, thereby preventing the clearance of particles by the reticuloendothelial system. However, if this were true, then how does one explain complement activation on PEGylated particles? In recent years, the view has emerged that PEGylation of nanomaterials only partially blocks protein adsorption and may even promote the formation of a bio-corona that is distinct in comparison to the corona formed on pristine nanomaterials (49, 50). Indeed, in a recent study using macrophage-like RAW264.7 cells, the adsorption of specific proteins was shown to be required to prevent uptake of PEG- or poly(ethyl ethylene phosphate) (PEEP)-coated polystyrene particles (51).
The choice of polymer coating matters. Luo et al. (52) reported that PEG-coating prevented uptake of GO by murine peritoneal macrophages while coating with cationic poly(ether imide) (PEI) favored uptake at low doses, but compromised cell viability at high doses. In another recent study, the authors provided evidence that PEGylated GO of approximately 200 nm in lateral size induced immune responses (cytokine release) in murine peritoneal macrophages; interestingly, comparable levels of activation were also observed following PEGylation of the non-carbon-based 2D material, molybdenum-disulfide (MoS2) (53). The authors speculated that integrin signaling could account for the enhanced cytokine responses in cells exposed to PEG-GO. Overall, the study suggested that PEGylation does not serve to passivate the surfaces of 2D materials. Xu et al. (54) prepared a series of GO derivatives including aminated GO (GO-NH2), poly(acrylamide)-functionalized GO (GO-PAM), poly(acrylic acid)-functionalized GO (GO-PAA), and PEG-functionalized GO (GO-PEG), and compared their toxicity with pristine GO. The GO materials all displayed lateral dimensions in the range of 100–500 nm and the ζ-potential was negative for all the materials in cell culture medium due to protein adsorption. Among these GO derivatives, GO-PEG and GO-PAA induced less toxicity toward murine J774A.1 macrophage-like cells than pristine GO, and GO-PAA proved to be the most biocompatible one, both in vitro and in mice (54). The differences in biocompatibility were suggested to be due to differences in the compositions of the bio-corona, especially whether or not immunoglobulin G (IgG) was present; GO-PAA and GO-PEG had less IgG content in their protein coronas (30−40%) than GO, GO-NH2, and GO-PAM (50−70%). IgG is a well-known opsonin that plays a key role in the clearance of pathogens. This study points toward strategies for safe design of GO for biomedical applications and underscores the importance of the bio-corona (54).
What a relief. I though the next big thang was going to be that anxiety about climate change causes blood clots, myocarditis and menstrual irregularities.