Serum IgG4 level predicts COVID-19 related mortality
"Specifically, a concentration of serum IgG4 > 700 mg/dl and an IgG4/IgG1 ratio > 0.05 were associated with a significantly increased mortality at 30-days"
That's a bit messy. If IgG4 is a byproduct of chronic inflammatory / autoimmune / fibrotic conditions, then it is just generally a marker for "bad health." So you could have 7 or so high-IgG4 patients that die because of the same comorbidities that led to IgG4, and viola, IgG4 "predicts" mortality. But take those seven outliers out from Fig 1A and the IgG4 levels of diers and survivors would be identical.
And generally at this point I regard studies from Milan as "handle with care," like studies from China. A lot of possible propaganda or op material. Example: Azzolini Long Covid study that wantonly mixed 2020 "unvaccinated" infections with 2021/2 "vaccinated" infections, pure toxic trash https://jamanetwork.com/journals/jama/fullarticle/2794072
The Borg has responded claiming that it's all fake and ghey because she claimed they were not seeing less effective clearance of the virus and IgG1 levels are similar and are great.
I will have to read the paper to see if they measured the levels of IgG1&3 and IgG4 often enough to determine of all the relevant B cells had class switched to producing only IgG4 antibodies because they do not hang around for ever.
I think there are a couple of different possibilities:
1. Only some portion of the relevant B cells have switched to IgG4, but that portion is likely to increase the more #ClotShots they get, and
2. They had all already switched but the measurements were taken while a significant number of IgG1 and IgG3 antibodies were still circulating.
Hmmm, how can you tell the IgG type a B-cell produces?
I thought you could only measure the ratios of IgG1/3 vs IgG4 antibodies present and not determine what type of IgG antibodies any collection of B-cells will produce.
Here the authors put B Cells in a big machine that sorts the spike-binding and non-spike-binding. Then they amplify/sequence the VDJ genes to see what IgG phenotype the B Cells are. It's in the "Single B cell sequencing analysis" section of Methods. This is why there are only four donors and two time-points for this part.
"Frequencies of IgG4 anti- spike memory B cells for individual donors as determined through scRNA seq thereby mirrored serological IgG4 anti-spike levels (Suppl. Table 2). In contrast, IgG4 isotypes were barely detectable among non-binders [ie the donors' other, not-spike-binding B Cells] (Fig. 4C). These results underscore the unusually high frequency of this type of vaccine-induced IgG isotype response."
So, the circulating spike antibodies at the 2 dose followup and post-3rd timepoints are a mirror of the spike memory B Cell pool.
I saw an article (polemical, adversarial, as is necessary) from someone else and thought - hmmm I wonder if... scrolled up 4 emails and there's your email to this post. Yep, as I thought.
I do have H1 and H2 blockers but have never had to use them, nor the horse paste I have.
He also published this:
Immunological Mechanisms Explaining the Role of Vaccines, IgE, Mast Cells, Histamine, Elevating Ferritin, IL-6, D-dimer, VEGF Levels in COVID-19 and Dengue, Potential Treatments Such as Mast Cell Stabilizers, Antihistamines: Predictions and Confirmations
There is a lot of confusion on the pathology front. Evidence that the virus turns lungs and vasculature into soup is more consistent than evidence that “immune overreaction” is the problem.
Chankara Chetty in SA was saying the same thing: that a severe covid-19 case was the result of post-infection hyper immune reaction that then goes systemic. Not so much to the viral replication but to the residue (spike). However, the mechanisms of harm are deeply different between a natural infection which has to progress past the mucosa into the system (and which may or may not trigger an overreaction) to the mRNA transfections which are by their nature systemic to begin with.
https://rumble.com/v1w6kuq-dr.-sucharit-bhakdi-the-path-to-living-hell.html it isn't the Spike (tho it is bad) It is the mRNA technology itself that shuts down the native immune system leading to ADE and thus inability to defend against CANCER CELLS and other infections and which ALSO creates the autoimmune disruption IgG4 etc. And the methodology the thinking is flawed. Yet they will say, are saying the concept of the xperiment (you and your vaxxed cohors) is successful, yayy! Lets go make MORE mRNA tech jabs for Tetnus, for Measles etc etc etc... and mandate them all. Pretty soon, a dead and dying population - and those NOT dying are having brain damage from vascular clotting and become more tractable and biddable... and less intelligent and able to use their higher logic.
Sounds like a fabulous plan. Because if a large population people are barely tolerable, surely the solution is to bump that to a large population of mentally unstable, degenerating people.
Easier to control them with the fear, and the 'solution' more shots (not to mention food, jobs etc). That's really what they want. Keep everyone pacified until it is too late and they have managed to plant the poison deep enough to prune/kill the tree of life to their liking (humanity). Extinction level events are occuring, no joke. Except for themselves of course. They believe (strong delusions) they can survive and thrive using the 'tech' they've developed. However, the law of unintended consequences and Murphy's Law are not in their favor.
Having been flooded with IgG4 news the last couple of days, I was looking forward to your take on it. I haven't had time to read it yet but I already appreciate it.
The question that arose was how does the S-protein get into the circulatory system in large enough quantity such that it can produce such large clots?
Then I wondered about the papers I have seen that demonstrate the less-than-perfect copy fidelity of the mRNA-based #ClotShots and thought about the possibility that some people are creating S proteins with defective trans-membrane anchors and they slip right through when they try to anchor in the cell membrane prior to the virion forming.
Do we know enough about the packaging of SARS-CoV-2 or other viruses to understand how packaging occurs. I very much doubt there is some sort of viral shepherd that shepherds all the constituent parts to the cell membrane for those viruses that use our own cell membranes as their own membranes. Perhaps the S protein has some sort of affinity for the cell membrane and naturally inserts itself into the cell membrane and then the remaining components are attracted to the trans-membrane anchor tails and some other signal causes the virion to pinch off the cell membrane and form.
But if those anchors are defective the S protein will slip into the intracellular space and if the cells happen to be circulatory epithelial cells they get into the blood stream and form clots.
Defective anchors are not required. Furin and cathepsin cleavage make it so that the S1 head subunit is always ready to fly off. This is necessary for fusion, but can happen early. And Pretorius et al. demonstrated that S1 alone can produce fibrinolysis-resistant fibrin clots https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8380922/
So infection or transfection, you're at risk of S1 flying around and making microclots and of somehow lingering in NC/I monocytes for months as in Patterson et al (https://www.researchsquare.com/article/rs-1844677/v1).
But we don't have a baseline for how unusual or scary that is in the infection front. Regular human OC43 also has a functional FCS. So it's probably not a big deal for kids, and more of a risk for less immunocompetent adults in terms of this "novel" coronavirus.
The big scam with the vaccines was they used proline-subs to prevent fusion but didn't touch the FCS, so the S1 unit can still fly off from anchored spike. Relevant links for the cleavage sites and proline subs are in my spike aa map https://unglossed.substack.com/i/84331912/resource-upload-spike-structure-map
"But we don't have a baseline for how unusual or scary that is in the infection front. Regular human OC43 also has a functional FCS. So it's probably not a big deal for kids, and more of a risk for less immunocompetent adults in terms of this "novel" coronavirus."
Hmmm, however, OC43 seems to bind to sialic acid so it might not have an affinity for RBCs or such a high affinity for RBCs.
Yes, flu spike protein is one of many type ii fusion glycoproteins in viruses, they are basically as common a biological design as claws in animals. The flu spike usually only has one base (R or K) so it's less easy to cleave; whereas High Pathogenicity Avian Influenzas are those that have more bases dropped in at the site. These might make disease worse but limit how durably the virus can spread from animal to animal, hence [theoretically] why HPAIs don't thrive in nature but do well in farmed chickens. Here is a good paper on HA cleavage https://journals.asm.org/doi/10.1128/JVI.00797-10
This begs the question of whether SARS-CoV-2 is truly replication/transmission-competent or if we are once again in "It has to be continual release from ICs" territory. I'm still mulling over the question.
1. What about this: https://rumble.com/v1w6kuq-dr.-sucharit-bhakdi-the-path-to-living-hell.html Dr. Bkhardi (sp) says it isn't the spike, its the mRNA shutting down the native immune system that will doom people... even though the spike is not a good thing... 2. Protecting yourself from the macrophages not lysing, a little nicotine goes a looong way I hear? 3. IVM blocks attachment ....
There is so much noise being made about the IgG4 paper that the CDC, the FDA and all other organs of Government are going to have to do something, like declare that it is anti-Science and witchcraft.
I think I know what they will do. They will declare all those who died from the #ClotShots as Heroes of Science for helping humanity extend its science to create more perfect vaccines.
I come from a self employed business background where I am always solving new problems. We often use the synergy of different minds in a group setting to solve problems. Different ideas start building on each other and these individual minds become a "mastermind " where ideas and creativity feed off each other and come up with solutions that one individual could never have come up with on their own. I see similarities in Substack contributors on this topic, feeding off each others ideas and leading to understanding a very complex problem.
For example, in the original article last summer Brian states "Only two time points are shown for this group; my best guess is that “post 2nd” means 14 days, due to the high level of IgG1."
Jessica's article states that "post 2nd" was after 210 days.
This 210 days becomes an important part of the puzzle that Igor expands on. IgG4 growth that occurs months after the boost could be the reason for increasing mortality stats appearing months after the booster instead of occurring immediately after the booster. In effect, creating a delay in the deaths as the IgG4 levels have had a chance to build.
I know Brian was being facetious about being first, but it really isn't about credit for being first. The sharing of ideas by different creative minds is creating the insight into a very complex problem.
Ah but yes, the 2nd cohort time-points are now shown in the Science version - ty for that tip. *Edit: So for that group it was 165 days after dose 2 (or 188 after dose 1), vs my previously reported 210/233 post d2/1 for the first cohort. This is listed in the new Table 1 though the line spacing is totally wonky.
*Edit 2: But for the cohort 2 graph in question on my original post, it was actually the "post 2nd" time point, 14 days after the 2nd shot exactly as I guessed.
I don't disagree about the value of collaboration - however, it's not clear if substack is great at fostering a "marketplace of ideas" since the ones that catch on are really just going to be whatever the biggest accounts decide they like. So OAS was totally a big huge well-known fact for a whole year even while I was saying it's a ridiculous fraud and bringing actual evidence to the table. And eventually the big shots just stop mentioning OAS because no evidence on their side ever arrived (except egm still trots around his NY hospitalizations as if they somehow mean something; and eugypius only mentions it in protected posts so he can't be challenged in his comments). Does that resemble collaboration?
Super late response, but who will take over Unglossed now?? I think that random guy I found in the back of an Arby's should do well! I think he used to work at Pfizer (that's how the gag works right?).
I haven't kept with Berenson, but is it common to use a pen name for one's own works? I suppose that's what is being alluded to? Which would be a strange incident if true!
Also, would it be off for me to assume that your post on the RSV surge may be related to cross-reactive antibodies and their class shift to IgG4? 😉
Oh, I see! Well, I guess that's what then big Substack buckaroos can net you I suppose!
You mean that there will be ambiguity?!! Perish the thought, Brian! Your assessment will clearly show that everything has been (and should be) figured out!!
Indeed. It's actually just good customer service on his part. In the not Covid-vaccine space most high-income writers invest in editors, graphics, etc. Berenson should have been outsourcing his pitiful phone screenshots to someone over a year ago.
Meanwhile, you’re getting mentions. https://www.americanthinker.com/articles/2023/01/its_time_to_ask_whether_repeated_mrna_vaccine_shots_weaken_the_immune_response_to_covid19.html
Ah, thanks for the heads-up!
Clearly they haven’t heard about your voluminous and egregious failures.
It's very nice attitude in Science, pro-vaxers are't.
Please continue adventure in Science, with us.
What are your thoughts on this paper?
Serum IgG4 level predicts COVID-19 related mortality
"Specifically, a concentration of serum IgG4 > 700 mg/dl and an IgG4/IgG1 ratio > 0.05 were associated with a significantly increased mortality at 30-days"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8461218/
That's a bit messy. If IgG4 is a byproduct of chronic inflammatory / autoimmune / fibrotic conditions, then it is just generally a marker for "bad health." So you could have 7 or so high-IgG4 patients that die because of the same comorbidities that led to IgG4, and viola, IgG4 "predicts" mortality. But take those seven outliers out from Fig 1A and the IgG4 levels of diers and survivors would be identical.
And generally at this point I regard studies from Milan as "handle with care," like studies from China. A lot of possible propaganda or op material. Example: Azzolini Long Covid study that wantonly mixed 2020 "unvaccinated" infections with 2021/2 "vaccinated" infections, pure toxic trash https://jamanetwork.com/journals/jama/fullarticle/2794072
The Borg has responded claiming that it's all fake and ghey because she claimed they were not seeing less effective clearance of the virus and IgG1 levels are similar and are great.
https://twitter.com/SabiVM/status/1607915944877211651
The Borg. LOL
I will have to read the paper to see if they measured the levels of IgG1&3 and IgG4 often enough to determine of all the relevant B cells had class switched to producing only IgG4 antibodies because they do not hang around for ever.
I think there are a couple of different possibilities:
1. Only some portion of the relevant B cells have switched to IgG4, but that portion is likely to increase the more #ClotShots they get, and
2. They had all already switched but the measurements were taken while a significant number of IgG1 and IgG3 antibodies were still circulating.
The B Cell percentages are similar. It’s 1. As for IgG3 it isn’t supposed to be long term.
Hmmm, how can you tell the IgG type a B-cell produces?
I thought you could only measure the ratios of IgG1/3 vs IgG4 antibodies present and not determine what type of IgG antibodies any collection of B-cells will produce.
Perhaps I am wrong.
Here the authors put B Cells in a big machine that sorts the spike-binding and non-spike-binding. Then they amplify/sequence the VDJ genes to see what IgG phenotype the B Cells are. It's in the "Single B cell sequencing analysis" section of Methods. This is why there are only four donors and two time-points for this part.
"Frequencies of IgG4 anti- spike memory B cells for individual donors as determined through scRNA seq thereby mirrored serological IgG4 anti-spike levels (Suppl. Table 2). In contrast, IgG4 isotypes were barely detectable among non-binders [ie the donors' other, not-spike-binding B Cells] (Fig. 4C). These results underscore the unusually high frequency of this type of vaccine-induced IgG isotype response."
So, the circulating spike antibodies at the 2 dose followup and post-3rd timepoints are a mirror of the spike memory B Cell pool.
I saw an article (polemical, adversarial, as is necessary) from someone else and thought - hmmm I wonder if... scrolled up 4 emails and there's your email to this post. Yep, as I thought.
Lemme guess... nothing burger?
No… this is the one I called as a something burger (months ago).
I wrote before reading, that'll learn me.
This guy is claiming that the deaths are a result of a severe allergic reaction, as far as I can see:
https://vinuarumugham.substack.com/p/covid-19-severity-is-a-result-of
I do have H1 and H2 blockers but have never had to use them, nor the horse paste I have.
He also published this:
Immunological Mechanisms Explaining the Role of Vaccines, IgE, Mast Cells, Histamine, Elevating Ferritin, IL-6, D-dimer, VEGF Levels in COVID-19 and Dengue, Potential Treatments Such as Mast Cell Stabilizers, Antihistamines: Predictions and Confirmations
https://europepmc.org/article/PPR/PPR241819
There is a lot of confusion on the pathology front. Evidence that the virus turns lungs and vasculature into soup is more consistent than evidence that “immune overreaction” is the problem.
Chankara Chetty in SA was saying the same thing: that a severe covid-19 case was the result of post-infection hyper immune reaction that then goes systemic. Not so much to the viral replication but to the residue (spike). However, the mechanisms of harm are deeply different between a natural infection which has to progress past the mucosa into the system (and which may or may not trigger an overreaction) to the mRNA transfections which are by their nature systemic to begin with.
https://rumble.com/v1w6kuq-dr.-sucharit-bhakdi-the-path-to-living-hell.html it isn't the Spike (tho it is bad) It is the mRNA technology itself that shuts down the native immune system leading to ADE and thus inability to defend against CANCER CELLS and other infections and which ALSO creates the autoimmune disruption IgG4 etc. And the methodology the thinking is flawed. Yet they will say, are saying the concept of the xperiment (you and your vaxxed cohors) is successful, yayy! Lets go make MORE mRNA tech jabs for Tetnus, for Measles etc etc etc... and mandate them all. Pretty soon, a dead and dying population - and those NOT dying are having brain damage from vascular clotting and become more tractable and biddable... and less intelligent and able to use their higher logic.
Sounds like a fabulous plan. Because if a large population people are barely tolerable, surely the solution is to bump that to a large population of mentally unstable, degenerating people.
Easier to control them with the fear, and the 'solution' more shots (not to mention food, jobs etc). That's really what they want. Keep everyone pacified until it is too late and they have managed to plant the poison deep enough to prune/kill the tree of life to their liking (humanity). Extinction level events are occuring, no joke. Except for themselves of course. They believe (strong delusions) they can survive and thrive using the 'tech' they've developed. However, the law of unintended consequences and Murphy's Law are not in their favor.
Having been flooded with IgG4 news the last couple of days, I was looking forward to your take on it. I haven't had time to read it yet but I already appreciate it.
Rampant Speculation Time. I was thinking about the claims that IVM can help prevent and even break up S-protein reported in this twitter thread: https://twitter.com/GabinJean3/status/1606984534767042560
The question that arose was how does the S-protein get into the circulatory system in large enough quantity such that it can produce such large clots?
Then I wondered about the papers I have seen that demonstrate the less-than-perfect copy fidelity of the mRNA-based #ClotShots and thought about the possibility that some people are creating S proteins with defective trans-membrane anchors and they slip right through when they try to anchor in the cell membrane prior to the virion forming.
Do we know enough about the packaging of SARS-CoV-2 or other viruses to understand how packaging occurs. I very much doubt there is some sort of viral shepherd that shepherds all the constituent parts to the cell membrane for those viruses that use our own cell membranes as their own membranes. Perhaps the S protein has some sort of affinity for the cell membrane and naturally inserts itself into the cell membrane and then the remaining components are attracted to the trans-membrane anchor tails and some other signal causes the virion to pinch off the cell membrane and form.
But if those anchors are defective the S protein will slip into the intracellular space and if the cells happen to be circulatory epithelial cells they get into the blood stream and form clots.
As I said, rampant speculation.
Defective anchors are not required. Furin and cathepsin cleavage make it so that the S1 head subunit is always ready to fly off. This is necessary for fusion, but can happen early. And Pretorius et al. demonstrated that S1 alone can produce fibrinolysis-resistant fibrin clots https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8380922/
So infection or transfection, you're at risk of S1 flying around and making microclots and of somehow lingering in NC/I monocytes for months as in Patterson et al (https://www.researchsquare.com/article/rs-1844677/v1).
But we don't have a baseline for how unusual or scary that is in the infection front. Regular human OC43 also has a functional FCS. So it's probably not a big deal for kids, and more of a risk for less immunocompetent adults in terms of this "novel" coronavirus.
The big scam with the vaccines was they used proline-subs to prevent fusion but didn't touch the FCS, so the S1 unit can still fly off from anchored spike. Relevant links for the cleavage sites and proline subs are in my spike aa map https://unglossed.substack.com/i/84331912/resource-upload-spike-structure-map
"But we don't have a baseline for how unusual or scary that is in the infection front. Regular human OC43 also has a functional FCS. So it's probably not a big deal for kids, and more of a risk for less immunocompetent adults in terms of this "novel" coronavirus."
Hmmm, however, OC43 seems to bind to sialic acid so it might not have an affinity for RBCs or such a high affinity for RBCs.
Coming back for some more punishment.
Is HA similarly able to be cleaved from Influenza?
Would you create a bioweapon with these properties by accident (the incompetent bioweapon creator hypothesis) or would you do so deliberately?
Yes, flu spike protein is one of many type ii fusion glycoproteins in viruses, they are basically as common a biological design as claws in animals. The flu spike usually only has one base (R or K) so it's less easy to cleave; whereas High Pathogenicity Avian Influenzas are those that have more bases dropped in at the site. These might make disease worse but limit how durably the virus can spread from animal to animal, hence [theoretically] why HPAIs don't thrive in nature but do well in farmed chickens. Here is a good paper on HA cleavage https://journals.asm.org/doi/10.1128/JVI.00797-10
This begs the question of whether SARS-CoV-2 is truly replication/transmission-competent or if we are once again in "It has to be continual release from ICs" territory. I'm still mulling over the question.
1. What about this: https://rumble.com/v1w6kuq-dr.-sucharit-bhakdi-the-path-to-living-hell.html Dr. Bkhardi (sp) says it isn't the spike, its the mRNA shutting down the native immune system that will doom people... even though the spike is not a good thing... 2. Protecting yourself from the macrophages not lysing, a little nicotine goes a looong way I hear? 3. IVM blocks attachment ....
Quite a reversal from the original alarm-raiser on spike. But plausible.
Damn it Brian. Every time I come up with some whacky idea you show me the shallowness of my thinking.
You are forgiven. Take your shoes off and set a spell.
Dr Michael Burry: Leukemia - Look for it in the wake of the vaccine
There is so much noise being made about the IgG4 paper that the CDC, the FDA and all other organs of Government are going to have to do something, like declare that it is anti-Science and witchcraft.
I wish they would - let's just get to the part where science is a Vaccine Church already, my posts from summer 2021 will look a lot more prescient.
I think I know what they will do. They will declare all those who died from the #ClotShots as Heroes of Science for helping humanity extend its science to create more perfect vaccines.
I come from a self employed business background where I am always solving new problems. We often use the synergy of different minds in a group setting to solve problems. Different ideas start building on each other and these individual minds become a "mastermind " where ideas and creativity feed off each other and come up with solutions that one individual could never have come up with on their own. I see similarities in Substack contributors on this topic, feeding off each others ideas and leading to understanding a very complex problem.
For example, in the original article last summer Brian states "Only two time points are shown for this group; my best guess is that “post 2nd” means 14 days, due to the high level of IgG1."
Jessica's article states that "post 2nd" was after 210 days.
https://jessicar.substack.com/p/the-immunological-mechanism-of-action
This 210 days becomes an important part of the puzzle that Igor expands on. IgG4 growth that occurs months after the boost could be the reason for increasing mortality stats appearing months after the booster instead of occurring immediately after the booster. In effect, creating a delay in the deaths as the IgG4 levels have had a chance to build.
https://igorchudov.substack.com/p/booster-caused-immune-tolerance-explains
I know Brian was being facetious about being first, but it really isn't about credit for being first. The sharing of ideas by different creative minds is creating the insight into a very complex problem.
Ah but yes, the 2nd cohort time-points are now shown in the Science version - ty for that tip. *Edit: So for that group it was 165 days after dose 2 (or 188 after dose 1), vs my previously reported 210/233 post d2/1 for the first cohort. This is listed in the new Table 1 though the line spacing is totally wonky.
*Edit 2: But for the cohort 2 graph in question on my original post, it was actually the "post 2nd" time point, 14 days after the 2nd shot exactly as I guessed.
I think Igor's theory might be right and have listed it in my sudden deaths theory list https://unglossed.substack.com/i/80639846/ii-non-recovery-means-sudden-deaths-are-not-arrhythmia - I think the big driver of the "delay" in this case is that for tolerance to kill, the virus has to launch an infection, which for a lot of people didn't happen until this summer.
I don't disagree about the value of collaboration - however, it's not clear if substack is great at fostering a "marketplace of ideas" since the ones that catch on are really just going to be whatever the biggest accounts decide they like. So OAS was totally a big huge well-known fact for a whole year even while I was saying it's a ridiculous fraud and bringing actual evidence to the table. And eventually the big shots just stop mentioning OAS because no evidence on their side ever arrived (except egm still trots around his NY hospitalizations as if they somehow mean something; and eugypius only mentions it in protected posts so he can't be challenged in his comments). Does that resemble collaboration?
😂😂😂 you and John Paul.
Better late than never. Good to read it again actually. I was trying to explain it to quad-jabbed just a couple days ago. Good refresher.
Super late response, but who will take over Unglossed now?? I think that random guy I found in the back of an Arby's should do well! I think he used to work at Pfizer (that's how the gag works right?).
Whoever *clearly* ghost-wrote today's Berenson post, ha.
I haven't kept with Berenson, but is it common to use a pen name for one's own works? I suppose that's what is being alluded to? Which would be a strange incident if true!
Also, would it be off for me to assume that your post on the RSV surge may be related to cross-reactive antibodies and their class shift to IgG4? 😉
I am alluding to the fact that his IgG4 post just switches to having clearly been written by someone familiar with the subject after the introduction.
No, my RSV post is just going to try to parse case rates. As with the subhead to Pt 1, little will be made clear
Oh, I see! Well, I guess that's what then big Substack buckaroos can net you I suppose!
You mean that there will be ambiguity?!! Perish the thought, Brian! Your assessment will clearly show that everything has been (and should be) figured out!!
Indeed. It's actually just good customer service on his part. In the not Covid-vaccine space most high-income writers invest in editors, graphics, etc. Berenson should have been outsourcing his pitiful phone screenshots to someone over a year ago.