These TriNetX studies are usually garbage because they’re entirely dependent on how accurate/up-to-date the medical record is.
These TriNetX studies are usually garbage because they’re entirely dependent on how accurate/up-to-date the medical record is.
Earlier in the paper:
“Our preregistered screening criteria were: … [history of homelessness less than 2 years and] nonsevere levels of substance use (DAST-10), alcohol use (AUDIT),and mental health symptoms Colorado Symptom Index (CSI) based on predefined thresholds. These screening criteria were used to reduce any potential risks of harm (e.g., overdose) from the cash transfer.”
… Are you kidding me? Talk about hypocrisy.
> We recently reported the development of a “universal” phage T4 vaccine design platform by Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) engineering that can rapidly generate multivalent vaccine candidates.
> Intriguingly, the T4-CoV-2 vaccine induced high levels of Spike-specific serum IgA antibodies (endpoint titers up to 62,500) when administered by either the i.m. [intramuscular] or the i.n. [intranasal] route. This is notable because IgA stimulation is not commonly observed in traditional vaccines…
> … significantly elevated percentages of CD4+ T cells producing IFN-γ were detected in the i.n. group (1%) in comparison to the i.m. group (0.55%) of vaccinated mice (P < 0.001 between i.n. and i.m.). These data indicated an enhanced Th1-mediated immunity induced by i.n. administration of the vaccine.
> … high titers of mucosal sIgA antibodies were elicited by i.n. vaccination (endpoint titers up to 12,500), in addition to high levels of systemic immune responses as described above. In contrast, i.m. immunization failed to produce sIgA, which is not unexpected.
We actually learned about this in med school last week, but I never thought it actually happened to people... Licorice contains glycyrrhetinic acid which inhibits the conversion of cortisol to cortisone. If you have too much cortisol floating around because of this, that cortisol starts activating receptors in your kidneys that are normally activated by aldosterone. This in turn increases your sodium resorption and potassium excretion, so you get high blood pressure and low potassium which can cause arrhythmias. It's called the Syndrome of Apparent Mineralocorticoid Excess and is a usually genetic problem with the enzyme that breaks down cortisol.
Also agree that using a PD-L1 mab feels like it’s for show especially considering the cancer model they’re using (Colon-26) was shown to be substantially less responsive to PD-L1 inhibitors…
Not the world’s best paper imo