IMO reach-suppression operations would also target comments from the Man and Woman on the Street opining away on their devices trying to save the world.
Germane to today’s subject, I can’t help but notice that my stories generate far fewer Reader Comments than they once did. I’ve also noted that articles from fellow “Covid Contrarian” authors with similar subscription numbers generate two or three times as many Reader Comments as my articles do. (I’ve studied this at the newsletters of my buddies Jenna McCarthy, Mark Oshinskie and Simulation Commander).
Furthermore, the most popular comments made at these sites will often get, say, 40 or 50 “likes.” The most popular comments at my site rarely get 8 “likes.” (Update: I just read Jenna's excellent piece on the Fauci hearings. The most popular post has, so far, received 74 "likes." The most popular post on this thread at the moment has six "likes.")
I just looked at yesterday’s article where I summarized the Fauci hearing. This story got some flattering reviews in the Comments Section, but it only generated 59 Reader Comments(and about 15 of those were from me!).
Of course, this could be more “paranoia” on my part and I know this analysis comes across as whining to some readers, but I still think “someone” is somehow screwing with my “reach,” which manifests itself in a study of “likes” and “Reader Comments.”
I will also note that maybe 10 readers have told me they can't hit one of my stories with a "like," can't make a Reader Comment and/or get no "notifications" when I comment on one of their comments.
Also, germane to today's subject, I think many of my "subscribers" aren't really real human beings. If anyone has any theories on what might be happening and how, please comment in today's Reader Comments!
Bill - ever since I’ve posted comments to your stack or replied to one of your comments on another stack. I’ve never once received an email notification that you liked and/or replied.
Thank you for this intelligence, Laura. You are one of the 10 people I referenced in another post. We're both thermo-nuclear content creators because we both are committed to making the embalmers' clots go viral.
just posted, but now my brain can ask this question:
>>>>>> explain how nanoparticles can strip glycocalyx and trigger EndMT in the endothelium please
The interaction between engineered nanoparticles (NPs) and the vascular endothelium involves a complex cascade of events. When nanoparticles disrupt the endothelial glycocalyx (GCX) and subsequently trigger Endothelial-to-Mesenchymal Transition (EndMT), it represents a transition from acute physical/chemical disruption to a deeper chronic cellular reprogramming.
Phase 1: How Nanoparticles Strip the Glycocalyx
The endothelial glycocalyx is a gel-like, negatively charged layer composed of proteoglycans, glycoproteins, and glycosaminoglycans (like heparan sulfate and hyaluronan) that lines the luminal surface of blood vessels. Nanoparticles can strip or degrade this protective layer through several interrelated mechanisms:
Electrostatic Disruption and Competitive Binding: Many types of engineered nanoparticles (e.g., heavily cationic nanoparticles like those functionalized with branched polyethyleneimine) possess high positive surface charges. These particles strongly bind to the natively negative components of the glycocalyx via electrostatic attraction. This intense binding neutralizes and compresses the matrix, collapsing its brush-like structure.
Catalytic and Oxidative Degradation: Certain nanoparticles (such as specific metal or metal-oxide nanoparticles like iron oxide) exhibit intrinsic enzyme-like activities (nanozyme activity), generating localized reactive oxygen species (ROS) such as hydroxyl radicals (⋅OH). These ROS chemically cleave the delicate sugar chains and backbone proteins of the glycocalyx.
Mechanical Friction and Shear Stress Alteration: Nanoparticles alter local fluid dynamics and hemodynamics at the cell surface. High concentrations or poorly designed particle-protein coronas can create focal mechanical stress points, displacing fluid-bound domains of the glycocalyx.
Enzymatic Activation: Nanoparticle interaction can inadvertently stimulate endothelial cells or adherent leukocytes/platelets to release endogenous enzymes (such as heparanase, hyaluronidases, and matrix metalloproteinases [MMPs]), which autodigest the glycocalyx components from the inside out.
Phase 2: From Glycocalyx Stripping to EndMT Triggering
Once the glycocalyx is stripped or compromised, the underlying endothelial cell membrane—previously shielded—is directly exposed to nanoparticles, fluid shear stresses, and blood-borne pro-inflammatory factors. This triggers EndMT, a cellular program where endothelial cells lose their characteristic markers and acquire mesenchymal/fibroblast-like features.
The pathway from GCX loss to EndMT involves several sequential steps:
Loss of Mechanotransduction and Quiescence: An intact glycocalyx is vital for transmitting smooth blood flow-derived shear stress to endothelial nitric oxide synthase (eNOS). When the GCX is stripped, mechanotransduction fails, lowering protective nitric oxide (NO) production and throwing the cell into a pro-inflammatory, stressed state.
Direct Nanoparticle Internalization & Cytotoxicity: Without the GCX gatekeeper (which normally restricts particle penetration based on size and charge), nanoparticles gain unhindered access to the plasma membrane. They bind avidly to exposed cell surface receptors and are internalized in large quantities.
Intracellular Oxidative Stress (ROS Overload): Inside the cell, high nanoparticle loads or catalytic surfaces disrupt mitochondrial respiration and stimulate NADPH oxidases, driving a massive surge in intracellular ROS.
Activation of EndMT Master Transcription Factors: The surge in oxidative stress, combined with unbuffered inflammatory signaling (such as TGF-β signaling pathways that are normally sequestered or modulated by a healthy glycocalyx), activates key transcription factors associated with EndMT, including Snail, Slug, Twist, and Zeb1/2.
Phenotypic Switch:
Downregulation: Endothelial cells lose classic markers such as CD31 (PECAM-1) and VE-cadherin, destroying tight junctions and barrier integrity.
Upregulation: They simultaneously upregulate mesenchymal markers such as α-smooth muscle actin (α-SMA), vimentin, and fibroblast-specific protein (FSP).
Summary Outcome
The stripping of the glycocalyx acts as the priming event that removes the endothelium's primary defense barrier. This exposes the bare cell membrane to direct nanoparticle binding and chemical irritation, setting off intracellular oxidative and inflammatory cascades that reprogram endothelial cells into a mesenchymal, migratory, and fibrogenic phenotype (EndMT).
--
>>>>> where do the fibers come from?
When we talk about the "fibers" generated during Endothelial-to-Mesenchymal Transition (EndMT)—such as α-smooth muscle actin (α-SMA), vimentin, and fibronectin—they do not come from the outside, nor are they leftover fragments of the stripped glycocalyx.
Instead, they are synthesized de novo (built from scratch) from within the endothelial cells themselves as a direct result of cellular reprogramming.
The origin of these fibers breaks down into two distinct categories:
1. Intracellular Cytoskeletal Fibers (α-SMA and Vimentin)
Where they come from: The interior cytoplasm of the transforming endothelial cell.
How they are made: Once master transcription factors like Snail, Slug, and Twist are activated inside the cell, they bind to DNA and switch on genes that are normally silenced in healthy endothelium. This triggers the cell's internal protein-manufacturing machinery (ribosomes and the endoplasmic reticulum) to mass-produce structural and contractile proteins.
Result: These newly translated proteins polymerize and assemble into heavy actin stress fibers and vimentin intermediate filaments, giving the cell a stretched, spindle-like, fibroblast shape capable of physical contraction and movement.
2. Extracellular Matrix (ECM) Fibers (Fibronectin and Collagens)
Where they come from: Secreted outward by the newly transformed, fibroblast-like cells into the surrounding subendothelial space.
How they are made: Just like intracellular fibers, the genetic instructions to build extracellular matrix proteins are unlocked during EndMT. The cells synthesize these proteins and actively export (secrete) them across the cell membrane.
Result: Once outside the cell, these secreted proteins polymerize into insoluble fibronectin and collagen fibers, changing the local tissue architecture from a smooth, fluid-lined vascular wall into a dense, scarred, fibrotic matrix.
Really really interesting!!! A human body manufacturing a brand new substance / material. Just think how novel that is. Think about how mice and rats have been injected with , grafted with, and fed unusual foreign materials and produced or grown unusual things. Think about all the behavior studies that have been done on animals. We are all lab rats now.
Bone morphogenetic proteins (BMPs) are a group of multi-functional growth factors and cytokines originally discovered by their ability to induce the formation of bone and cartilage. They are now recognized as critical signaling molecules that orchestrate tissue architecture, cell proliferation, differentiation, and apoptosis throughout the body.
Classification and Biology
Superfamily: BMPs belong to the Transforming Growth Factor-beta (TGF-β) superfamily.
Mechanism of Action: They bind to specific serine/threonine kinase receptors on the cell surface (Type I and Type II receptors), which then trigger intracellular signaling cascades—most notably the SMAD pathway (specifically SMAD1, SMAD5, and SMAD8).
Embryonic Development: Beyond osteogenesis, BMPs play vital roles in early embryonic development, including limb bud formation, heart development, neural differentiation, and vasculogenesis.
Clinical and Therapeutic Applications
Because of their powerful osteoinductive properties, recombinant human BMPs (rhBMPs) are manufactured using recombinant DNA technology and used across multiple medical specialties:
Orthopedics: Used in treatments for severe long-bone nonunions (fractures that fail to heal), acute open tibia fractures, and spinal fusion surgeries as an alternative to autologous bone grafts. rhBMP-2 and rhBMP-7 are the most prominent variants utilized clinically.
Dentistry and Oral Surgery: Applied in alveolar ridge augmentation, sinus lifts, and periodontal defect regeneration to stimulate jawbone growth prior to dental implant placement.
Pathology and Disease Involvement
Dysregulation or mutations in BMP signaling pathways are implicated in several human disorders:
Skeletal Disorders: Mutations in BMP receptors can lead to rare genetic conditions like Fibrodysplasia Ossificans Progressiva (FOP), where connective tissue and muscle gradually turn into bone (heterotopic ossification).
Cancer: BMP signaling exhibits dual roles in oncology. Depending on the tissue context, they can act as tumor suppressors or promote tumor cell migration, invasion, and metastasis in cancers such as breast, prostate, colorectal, and multiple myeloma.
would cationic nanoparticles upregulate or downregulate? propose LNP triggered pathways that would provide a delta of some kinds
Whether cationic nanoparticles (or cationic lipid nanoparticles, LNPs) upregulate or downregulate Bone Morphogenetic Protein (BMP) signaling depends entirely on their payload, surface chemistry, and the specific cellular context. Rather than acting as a simple on/off switch, cationic carriers dynamically modulate the pathway, producing a distinct biochemical "delta" (Δ).
1. Upregulation vs. Downregulation: The Directional Delta
Downregulation (Gene Silencing / Inhibition): If cationic nanoparticles are loaded with interfering RNA (such as siRNA targeting BMP antagonists like Noggin, or targeting pathway inhibitors like SMURF1), they effectively upregulate downstream BMP signaling output by removing inhibitory blocks. Conversely, if they deliver siRNA against BMP receptors (like ALK3 or ALK2), they actively downregulate BMP signaling.
Upregulation (Gene Delivery / Expression): If cationic LNPs encapsulate and deliver mRNA encoding BMP ligands (e.g., BMP-2 or BMP-7) or transcription factors (like RUNX2), they drive the intracellular machinery to overexpress these proteins, directly upregulating the pathway.
When cationic nanoparticles interact with cells, they set off a cascade of biophysical and biochemical events. The primary pathways and their respective Δ shifts include:
A. The Cationic Endosomal/Lysosomal Stress Pathway (Δ in Cytotoxicity & UPR)
Trigger: Cationic lipids possess positive charges that strongly interact with negatively charged cell membranes, facilitating cellular uptake via endocytosis. Inside the endosome, they cause proton sponge effects, swelling, and membrane rupture.
Pathway: This sudden osmotic stress and endosomal leakage trigger the Unfolded Protein Response (UPR) and endoplasmic reticulum (ER) stress.
The Delta: UPR activation alters transcription factors (like ATF4 and CHOP). In osteoprogenitor or endothelial cells, chronic ER stress crosstalks with TGF-β/BMP signaling components, often blunting canonical R-SMAD (SMAD1/5/8) responsiveness while tipping non-canonical pathways (like p38 MAPK or JNK) toward apoptosis or inflammation.
B. The Toll-Like Receptor (TLR) Inflammatory Axis (Δ in Cytokines)
Trigger: Extracellular exposure to cationic surfaces and nucleic acid payloads triggers innate immune recognition.
Pathway: Activation of TLR3, TLR4, or TLR7/8 signaling cascades, relying on downstream adaptors like MyD88.
The Delta: This produces a surge of pro-inflammatory cytokines (e.g., TNF-α, IL-6). Inflammation has a complex, bidirectional feedback loop with BMPs: acute inflammatory signals can induce certain BMP ligands (like BMP-2/4) as part of tissue repair or vascular remodeling, while chronic inflammation often downregulates osteogenic BMP receptors via inhibitory Smads (Smad6/7).
C. The Non-Canonical Kinase Crosstalk (Δ in PI3K/AKT vs. MAPK)
Trigger: LNP membrane fusion alters local fluidity and clusters cell-surface receptors.
Pathway: Activation of non-canonical BMP/TGF-β branching, particularly PI3K/AKT/mTOR or RhoA/ROCK cytoskeletal remodeling pathways.
The Delta: Even without altering core ligand transcription, the nanoparticle-induced membrane perturbation shifts the cell toward survival, migration, or metabolic switching. This alters the phosphorylation status of shared downstream kinases, changing how effectively the cell translates a native BMP signal into gene transcription.
what organs could downregulate BMP? i wonder if stress in the parathyroid or kidneys from nanoparticles would downregulate. any other tissues that would do it if not these?
When cationic nanoparticles or lipid nanoparticles (LNPs) circulate in the body, their biodistribution heavily favors clearance organs and filtering tissues. Cellular stress, oxidative damage, and inflammation in these organs can significantly downregulate BMP signaling pathways, shifting tissue responses away from repair and toward fibrosis or apoptosis.
1. The Kidneys (High Susceptibility)
Why they are targeted: Nanoparticles within specific size ranges (roughly 10 to 100 nm) accumulate heavily in the renal mesangium and proximal tubular epithelial cells via glomerular filtration or peritubular capillary uptake.
The Downregulation Effect: The kidneys rely heavily on endogenous protective pathways—most notably BMP-7, which maintains renal tubular integrity and acts as an anti-fibrotic factor. When cationic nanoparticles induce endoplasmic reticulum (ER) stress or oxidative damage in tubular cells, BMP-7 expression is often suppressed. This downregulation removes a vital protective brake, accelerating the transition from acute kidney injury (AKI) to chronic renal fibrosis.
2. The Parathyroid Glands (Indirect/Systemic Stress)
Why they are targeted: Unlike the kidneys or liver, the parathyroid glands are not primary clearance hubs for nanoparticles, meaning direct accumulation is usually low.
The Downregulation Effect: Parathyroid cells are extremely sensitive to systemic calcium/phosphate balance and metabolic stress. If nanoparticle toxicity heavily impacts kidney function (disrupting mineral homeostasis), the parathyroid glands undergo secondary compensatory stress. While direct downregulation of BMP signaling in parathyroid cells by nanoparticles is less documented, systemic inflammation and uremic toxins secondary to renal nanoparticle stress can alter calcium-sensing and local growth factor regulation.
3. Other Tissues Prone to BMP Downregulation
If you look beyond the kidneys and parathyroid glands, several other organs experience severe nanoparticle-induced stress that results in suppressed or dysregulated BMP signaling:
The Liver (The Primary Clearance Sink):
Mechanism: Kupffer cells (liver macrophages) and hepatocytes rapidly sequester the vast majority of systemic LNPs.
The Shift: High nanoparticle loads trigger massive reactive oxygen species (ROS) production and inflammatory cytokine release (TNF-α, IL-1$\beta$). This inflammatory milieu often downregulates local regenerative BMP networks (such as BMP-9, which is liver-derived), impairing hepatocyte maintenance.
The Bone Marrow (The Osteogenic Niche):
Mechanism: Bone marrow sinusoidal endothelium and resident macrophages take up circulating nanoparticles efficiently.
The Shift: Mesenchymal stem cells (MSCs) residing in the bone marrow are exquisitely sensitive to BMPs for osteogenic differentiation. Nanoparticle-induced oxidative stress or inflammatory signaling can downregulate BMP receptors (like ALK3/6) on MSCs, effectively stalling bone regeneration and favoring adipogenesis or cell death instead.
The Lungs:
Mechanism: Particularly relevant for intravenous administration (first-pass pulmonary capillary bed trapping) or inhalation.
The Shift: Alveolar macrophages and epithelial cells undergo stress that suppresses normal BMP-mediated tissue repair, frequently tipping the microenvironment toward chronic inflammation or pulmonary fibrosis.
of these you just listed, can they trigger phosphorus release from tissues into the bloodstream?
Yes, severe cellular stress, necrosis, or lysis in these tissues can indeed trigger a release of intracellular phosphorus into the bloodstream, leading to hyperphosphatemia.
Because phosphorus is predominantly an intracellular anion (bound in ATP, nucleic acids, phospholipids, and proteins), any event that compromises cell membrane integrity causes these intracellular stores to flood into the extracellular fluid and general circulation.
1. How the Listed Organs Contribute to Phosphorus Release
The Liver (Direct Cellular Lysis):
The liver is the primary clearance sink for systemic nanoparticles. If high concentrations of cationic LNPs induce severe hepatotoxicity, oxidative stress, and widespread hepatocyte necrosis, massive amounts of intracellular ions—including phosphorus—are spilled directly into the hepatic venous outflow and systemic circulation.
The Bone Marrow (Cell Turnover & Mineral Matrix Proximity):
The bone marrow is densely packed with rapidly dividing hematopoietic and stem cells. Nanoparticle-induced apoptosis or cytotoxicity here causes the breakdown of nucleic acids and intracellular phosphorus pools. Furthermore, because the marrow is encased within the bone matrix (which stores roughly 85% of the body's total phosphorus as calcium phosphate), local inflammatory remodeling or matrix degradation can mobilize mineral stores.
The Lungs (Acute Injury & Alveolar Lysis):
Severe pulmonary toxicity or acute lung injury (ALI) resulting from nanoparticle exposure causes the breakdown of vast numbers of endothelial and epithelial cells, contributing to the systemic pool of circulating cellular debris and free phosphate.
2. The Renal Factor: Release vs. Failure to Clear
While the liver and bone marrow can release phosphorus through cell lysis, the kidneys play a different, equally critical role:
Impaired Excretion: The kidneys are the primary organs responsible for filtering and excreting excess dietary and endogenous phosphorus.
The Double-Whammy Effect: When cationic nanoparticles induce acute tubular necrosis or renal dysfunction, the kidneys lose their ability to clear phosphorus. Therefore, even a modest cellular release of phosphorus from the liver or bone marrow can quickly spiral into severe systemic hyperphosphatemia because the damaged kidneys cannot excrete it.
Cutting room floor text (a trademarked staple of my Readers Comment Fortum!)
... For example, Facebook once suspended my account three times because I was making posts that were labeled dangerous disinformation.
Not only could I not make an original post, I couldn’t comment in the Reader Comments of any other Facebook user. (As long as I restricted my posts to content like “what a cute photo of your puppy!” I was safe.)
I should note that Facebook seems to have done away with its more Orwellian posting policies that were in effect in Peak Covid. I say this because, every now and then, you can see a post that is critical of Covid policies and I see plenty of posts that are both pro-Iran War and anti-Iran war, which is good to see.
Still, my peak "reach" on Facebook might be 200 of my 2,000 friends … and when I do share a link to one of my “contrarian” Substack articles, these usually get zero likes and zero Reader Comments, meaning I’m still not sold that Mr. Zuckerberg has found religion on the importance of free speech.
SimCon, I can reply but I can’t like your comment. That happened to me the other day when I was participating in the comment section of your “Let’s watch the Shitweasel together” article!!! Sometimes the like button would work, and sometimes it wouldn’t.
I skimmed it over. Chock full of buzz words and phrases arranged in a way to make it sound reasonable and kind. Reminded me of HR emails from the last few years I was working before I retired. They were full of buzz words that were reasonable and kind, but they could have been replaced with a bulleted list of things that were going away or result in being terminated.
I should note that, just in the past few weeks, al.com has gone back to allowing Reader Comments, but with a new twist. Only paid subscribers can make posts, which are heavily moderated. When the editor announced this change, he/she gave quite the lecture on how these posting priviliges must be used.
It seems to me that almost nobody is making Reader Comments because every story I click on says, "Be the first person to comment on this article."
My take-away from this change is that al.com is bleeding money and realizes they lost a lot of readers or "reader engagement" when they did away with their previous very popuar Reader Comment Section. Also, the site now only runs the first two paragraphs of most of its stories, meaning you have to pay to get the full story - which is a program to generate more revenue (which I certainly understand).
However, the site gave away free stories for so long I don't think many readers are buying the paid content (which - generally speaking, with a few exceptions, is awful IMO.) Of course, at one time, the business model was that these websites would create so much reader traffic, they would make up for the loss in paid subscriptions by a flood of businesses that wanted to place digital ads at the website.
This didn't happen either.
Not long ago, I tried to count all of the journalists who produce "straight news" articles at this website. (This was a challenge as the site doesn't run employee staff boxes anymore.) As best i could determine, this website has approximately 20 full-time staff journalists (not counting a couple of sports writers). Once upon a time, the three newspapers that became al.com would have employed 200 full-time journalists and editors.
All three newspapers would have had more full-time sports reporters than the site has total news reporters today.
We are there already! Screws are being tightened! X has.banned me for supporting RFK Jr goals. Controlling the narrative goes on and on. Coverage of Fauci in mass media did not cover the sociopaths actions that has created great harm and death!
My friend who runs Citizen Free Press has gone silent. He and I were in touch, and he was posting some of my pieces as well. He said to send him links whenever I had something. But he stopped responding to messages maybe two years ago. (I've never met him but we happen to live in the same town and know some of the same people.)
I ended up getting Kane's email. I even pitched a business idea to him - something I think would be a big improvement on the Substack subscription model. He read the proposal, which I appreciate, but passed on it.
I appreciate him running as many of my stories as he did. And I do still check out his site, although I think it has changed and I think his political bent might have changed for some reason..
One thing Kane is proud of is he doesn't run any ads, which he could do. A couple of times a year, he runs donation fund-raisers. He's got millions of loyal weekly visitors to his website and he should be able to monetize that ... big time. Of course, he runs right-wing and politically incorrect stories so, like Zero Hedge**, he'll never get any advertising revenue from the Big Advertisers of the Big Advertising Agencies.
Tucker Carlson never did and he had the No. 1 talk show in the world.
**P.S. I can't remember the company, but the other day I saw a display ad at Zero Hedge for a mainstream company. I have never seen this before. So I wonder if these changes at this site might result in an end to the advertising discrimination?
I also think Substack will be sold one day and one of the captured usual suspects will take it over. That's why Notes (a knock off of X) is so important and that's probably why the content on Substack is now as liberal as the MSM. The new owner could sell advertising around Notes. As long as the site played ball and pushed the right narratives, the cabal of big advertisers would support the site.
IMO, even media companies which lose tons of money (like most do) are very important to the Powers that Be because of all the stories they do run and, more importantly, all the stories the could run that would bring down the system if they did.
The Washington Post is losing massive amounts of money, but Bezos IMO uses it as "leverage" and a "loss leader.". The thinking probably goes a little like this: "You pay my other companies a lot of money, or give us this contract, or leave us alone ... and I won't come after you with the Washington Post."
Kane has ads now. I remember he posted something about needing to do that to keep operating. It pops up at the bottom of the screen. Nothing that gets annoying. I also have noticed a change with him that I can't quite put my finger on.
He could sell the business for a lot of money, I would think. someone would buy it just to stop all this content just like someone must have bought Drudge. He is not as bold or independent as he used to be. He “discovered” me and now I’m radioactive. It’s odd.
It is odd. I may see if I can find him through our mutual friends. It's worrisome to learn from you today that like me, you also lost contact with Kane and that he seems to have changed. Esp. given that Matt Drudge disappeared. There have been no sightings of him that I know of. Strangely, I lived on Miami Beach when Matt lived there, though I never saw him. The last place he lived was the agricultural area in south Miami-Dade County called The Redlands. He sold the house a few years ago and no one has seen him since. I find this pretty disturbing. Maybe he is in Latin America or something. My understanding is that every few years, around the election, he would get quite nervous as he was receiving some threats and had reason to believe his life was being threatened. I don't believe he was paranoid. I think there probably were quite a few people who wanted him dead, and maybe some who were willing to act.
I quit reading CFP regularly (my thrice daily checks were usually rewarded with insights and news not found elsewhere). Things changed. I check headlines at CFP 2X per week now.
CitKane positioned the site for sale (my theory) as he constantly battled other news feeds for eyes-on supremacy, quit generating separate page posts (thus ending news-specific-posting-comments pages).
Linking directly to stories eliminated curator-responsible comments, and the liability associated with them. Imho, a business decision based on liability not free speech suppression.
Chasing page views for these publishers is like ambulance-chasing lawyers seeking high dollar injury clients.
Here is my view - local business is better and it is more than obvious - I mean Kropotkin spoke of it more than a century ago but his ideas got stifled - did they not?
Thanks for this report, Bill. I appreciate your keeping your eye on these things. I would add to your list that, as you mention later in your article, it seems bots have been peppering up the comments sections of some blogs. I've seen that sort of thing here in your substack, but in particular I note that Steve Kirsch's has been getting a lot of bot-shills-for-"the narrative" comments— or simply nonsensical comments, probably from bots. I take that as a sign that he's slam over the target.
The bots sometimes gang up and attack from out out no where. They also steal your identity and make 300 nonsensical posts under your name. There's numerous reach-suppression and Narrative Control ops being used in the Reader Comments.
I just saw that Jenna McCarthy's story on the Fauci hearing got about 240 likes and 200 reader comments. It's a great story and deserves those accolades. I'd just note I posted my Fauci story 12 hours before she did and got about 1/5 of the likes and Reader Comments as her article. Jenna does have more subscribers than I do, but not a whole lot more.
Strange. Doesn't make sense ... unless there is some reach-suppression op that's being used against my newsletter.
They all are compromised - tis a conspiracy against us no doubt.
But as a faithful member of North Carolina constituency as well as Virginia no doubt, I send out a peace message to Alabama - can you feel it Bill...Geoff and I wonder if you realize the value of the patent info passed onto you Bill.
Troy Alabama knows the power of NC, VA, TN, KY, and WV.
I must admit I haven't done a deep dive yet on the patent info, but I've read enough (from you and others) to know it's probably very significant.
Say what you want about me, but I'm the most famous Substack author from Troy, Alabama. (As far as I know Troy has two Substack authors and the other one, a friend of mine, has only 63 subscribers. I actually think I have more Substack subcribers and followers than any other person in Sweet Home Alabama.
I would like to add 1) Dr. Malone does not allow comments unless you pay for his thoughts, and 2) It figures that Dan Blather would pull a stunt like that, but at 94 you'd think he would have either learned something or had accrued some humility.
I couldn't agree more. The comments sections are and have been the best bridge to additional information on any given subject. Before YouTube started censoring, their comments section was outstanding. Information about 911, and other historical subjects that were re-written to fit a narrative, was easy to find and verify. Of course there were trolls and bots trying to muddy the water, but they became easily identifiable over time.
Zionists seem to own or control a disturbing amount of our media and big tech, not to mention hollywood, publishing, etc. If anyone has the power and motive to censor, I think it's them. They are the enemy of the entire planet.
ZH is not what it used to be. The news stories include planted Goldman Sachs narrative crap and the comments section is rife with (paid by Israel?) trolls. It has degraded since Tyler sold out.
Recently, I check it out for their "Iran War" updates. I usually go straight to the Reader Comments. While many posters are "out there," sophomoric and specialize in juvenile insults, many posters are also pretty sharp and several are quite astute IMO. Several regular posters also provide excellent links from the alternative media that help me get a fuller picture of what might be happening.
I have noted when I make a post, in two seconds I immediately have two or three down votes. That has to be bots.
..."The “Powers that Be”...and exactly who are these bums? If they be censoring anyone it is because they are afraid of the truth. That can be the only reason. I expect that 99% of the people on the planet have no or few opinions about much of anything. Or if they do, they keep them hidden from the public and the snoopy big tech swine.
Even if the silly powers that be erased all written opinions, you can still have opinions. They can be shared with others in real time, face to face. Eventually, substack will go the way of "My Space" especially if it goes public (as in a stock IPO) as this is the only reason for its existence. So the owners can become instant billionaires.
I don't do social media or news feeds or TV news or much of the MSM. If I get any news it's in passing through the articles I might read on substack and sometimes that is more than I care about. I imagine the powers that be are psychos run amok and if the pitchforks come out, for sure it is because they deserve a good thrashing. My "fork" will be the one with the golden tines.
Bonus Content:
Germane to today’s subject, I can’t help but notice that my stories generate far fewer Reader Comments than they once did. I’ve also noted that articles from fellow “Covid Contrarian” authors with similar subscription numbers generate two or three times as many Reader Comments as my articles do. (I’ve studied this at the newsletters of my buddies Jenna McCarthy, Mark Oshinskie and Simulation Commander).
Furthermore, the most popular comments made at these sites will often get, say, 40 or 50 “likes.” The most popular comments at my site rarely get 8 “likes.” (Update: I just read Jenna's excellent piece on the Fauci hearings. The most popular post has, so far, received 74 "likes." The most popular post on this thread at the moment has six "likes.")
I just looked at yesterday’s article where I summarized the Fauci hearing. This story got some flattering reviews in the Comments Section, but it only generated 59 Reader Comments(and about 15 of those were from me!).
Of course, this could be more “paranoia” on my part and I know this analysis comes across as whining to some readers, but I still think “someone” is somehow screwing with my “reach,” which manifests itself in a study of “likes” and “Reader Comments.”
I will also note that maybe 10 readers have told me they can't hit one of my stories with a "like," can't make a Reader Comment and/or get no "notifications" when I comment on one of their comments.
Also, germane to today's subject, I think many of my "subscribers" aren't really real human beings. If anyone has any theories on what might be happening and how, please comment in today's Reader Comments!
Update: I just added a new last sentence for this essay:
Also, if you are being censored, this means you are doing something good and right.
Bill - ever since I’ve posted comments to your stack or replied to one of your comments on another stack. I’ve never once received an email notification that you liked and/or replied.
Thank you for this intelligence, Laura. You are one of the 10 people I referenced in another post. We're both thermo-nuclear content creators because we both are committed to making the embalmers' clots go viral.
Indeed we are my friend. 💪🙏🏻
Building an arch requires all the bricks.
https://badprotein.substack.com/p/baby-blood
just posted, but now my brain can ask this question:
>>>>>> explain how nanoparticles can strip glycocalyx and trigger EndMT in the endothelium please
The interaction between engineered nanoparticles (NPs) and the vascular endothelium involves a complex cascade of events. When nanoparticles disrupt the endothelial glycocalyx (GCX) and subsequently trigger Endothelial-to-Mesenchymal Transition (EndMT), it represents a transition from acute physical/chemical disruption to a deeper chronic cellular reprogramming.
Phase 1: How Nanoparticles Strip the Glycocalyx
The endothelial glycocalyx is a gel-like, negatively charged layer composed of proteoglycans, glycoproteins, and glycosaminoglycans (like heparan sulfate and hyaluronan) that lines the luminal surface of blood vessels. Nanoparticles can strip or degrade this protective layer through several interrelated mechanisms:
Electrostatic Disruption and Competitive Binding: Many types of engineered nanoparticles (e.g., heavily cationic nanoparticles like those functionalized with branched polyethyleneimine) possess high positive surface charges. These particles strongly bind to the natively negative components of the glycocalyx via electrostatic attraction. This intense binding neutralizes and compresses the matrix, collapsing its brush-like structure.
Catalytic and Oxidative Degradation: Certain nanoparticles (such as specific metal or metal-oxide nanoparticles like iron oxide) exhibit intrinsic enzyme-like activities (nanozyme activity), generating localized reactive oxygen species (ROS) such as hydroxyl radicals (⋅OH). These ROS chemically cleave the delicate sugar chains and backbone proteins of the glycocalyx.
Mechanical Friction and Shear Stress Alteration: Nanoparticles alter local fluid dynamics and hemodynamics at the cell surface. High concentrations or poorly designed particle-protein coronas can create focal mechanical stress points, displacing fluid-bound domains of the glycocalyx.
Enzymatic Activation: Nanoparticle interaction can inadvertently stimulate endothelial cells or adherent leukocytes/platelets to release endogenous enzymes (such as heparanase, hyaluronidases, and matrix metalloproteinases [MMPs]), which autodigest the glycocalyx components from the inside out.
Phase 2: From Glycocalyx Stripping to EndMT Triggering
Once the glycocalyx is stripped or compromised, the underlying endothelial cell membrane—previously shielded—is directly exposed to nanoparticles, fluid shear stresses, and blood-borne pro-inflammatory factors. This triggers EndMT, a cellular program where endothelial cells lose their characteristic markers and acquire mesenchymal/fibroblast-like features.
The pathway from GCX loss to EndMT involves several sequential steps:
Loss of Mechanotransduction and Quiescence: An intact glycocalyx is vital for transmitting smooth blood flow-derived shear stress to endothelial nitric oxide synthase (eNOS). When the GCX is stripped, mechanotransduction fails, lowering protective nitric oxide (NO) production and throwing the cell into a pro-inflammatory, stressed state.
Direct Nanoparticle Internalization & Cytotoxicity: Without the GCX gatekeeper (which normally restricts particle penetration based on size and charge), nanoparticles gain unhindered access to the plasma membrane. They bind avidly to exposed cell surface receptors and are internalized in large quantities.
Intracellular Oxidative Stress (ROS Overload): Inside the cell, high nanoparticle loads or catalytic surfaces disrupt mitochondrial respiration and stimulate NADPH oxidases, driving a massive surge in intracellular ROS.
Activation of EndMT Master Transcription Factors: The surge in oxidative stress, combined with unbuffered inflammatory signaling (such as TGF-β signaling pathways that are normally sequestered or modulated by a healthy glycocalyx), activates key transcription factors associated with EndMT, including Snail, Slug, Twist, and Zeb1/2.
Phenotypic Switch:
Downregulation: Endothelial cells lose classic markers such as CD31 (PECAM-1) and VE-cadherin, destroying tight junctions and barrier integrity.
Upregulation: They simultaneously upregulate mesenchymal markers such as α-smooth muscle actin (α-SMA), vimentin, and fibroblast-specific protein (FSP).
Summary Outcome
The stripping of the glycocalyx acts as the priming event that removes the endothelium's primary defense barrier. This exposes the bare cell membrane to direct nanoparticle binding and chemical irritation, setting off intracellular oxidative and inflammatory cascades that reprogram endothelial cells into a mesenchymal, migratory, and fibrogenic phenotype (EndMT).
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>>>>> where do the fibers come from?
When we talk about the "fibers" generated during Endothelial-to-Mesenchymal Transition (EndMT)—such as α-smooth muscle actin (α-SMA), vimentin, and fibronectin—they do not come from the outside, nor are they leftover fragments of the stripped glycocalyx.
Instead, they are synthesized de novo (built from scratch) from within the endothelial cells themselves as a direct result of cellular reprogramming.
The origin of these fibers breaks down into two distinct categories:
1. Intracellular Cytoskeletal Fibers (α-SMA and Vimentin)
Where they come from: The interior cytoplasm of the transforming endothelial cell.
How they are made: Once master transcription factors like Snail, Slug, and Twist are activated inside the cell, they bind to DNA and switch on genes that are normally silenced in healthy endothelium. This triggers the cell's internal protein-manufacturing machinery (ribosomes and the endoplasmic reticulum) to mass-produce structural and contractile proteins.
Result: These newly translated proteins polymerize and assemble into heavy actin stress fibers and vimentin intermediate filaments, giving the cell a stretched, spindle-like, fibroblast shape capable of physical contraction and movement.
2. Extracellular Matrix (ECM) Fibers (Fibronectin and Collagens)
Where they come from: Secreted outward by the newly transformed, fibroblast-like cells into the surrounding subendothelial space.
How they are made: Just like intracellular fibers, the genetic instructions to build extracellular matrix proteins are unlocked during EndMT. The cells synthesize these proteins and actively export (secrete) them across the cell membrane.
Result: Once outside the cell, these secreted proteins polymerize into insoluble fibronectin and collagen fibers, changing the local tissue architecture from a smooth, fluid-lined vascular wall into a dense, scarred, fibrotic matrix.
https://badprotein.substack.com/p/baby-blood
- and i could be wrong !! - the post asks for a debunk - in the comments..
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Really really interesting!!! A human body manufacturing a brand new substance / material. Just think how novel that is. Think about how mice and rats have been injected with , grafted with, and fed unusual foreign materials and produced or grown unusual things. Think about all the behavior studies that have been done on animals. We are all lab rats now.
bone morphogenetic proteins (BMPs)
Bone morphogenetic proteins (BMPs) are a group of multi-functional growth factors and cytokines originally discovered by their ability to induce the formation of bone and cartilage. They are now recognized as critical signaling molecules that orchestrate tissue architecture, cell proliferation, differentiation, and apoptosis throughout the body.
Classification and Biology
Superfamily: BMPs belong to the Transforming Growth Factor-beta (TGF-β) superfamily.
Mechanism of Action: They bind to specific serine/threonine kinase receptors on the cell surface (Type I and Type II receptors), which then trigger intracellular signaling cascades—most notably the SMAD pathway (specifically SMAD1, SMAD5, and SMAD8).
Embryonic Development: Beyond osteogenesis, BMPs play vital roles in early embryonic development, including limb bud formation, heart development, neural differentiation, and vasculogenesis.
Clinical and Therapeutic Applications
Because of their powerful osteoinductive properties, recombinant human BMPs (rhBMPs) are manufactured using recombinant DNA technology and used across multiple medical specialties:
Orthopedics: Used in treatments for severe long-bone nonunions (fractures that fail to heal), acute open tibia fractures, and spinal fusion surgeries as an alternative to autologous bone grafts. rhBMP-2 and rhBMP-7 are the most prominent variants utilized clinically.
Dentistry and Oral Surgery: Applied in alveolar ridge augmentation, sinus lifts, and periodontal defect regeneration to stimulate jawbone growth prior to dental implant placement.
Pathology and Disease Involvement
Dysregulation or mutations in BMP signaling pathways are implicated in several human disorders:
Skeletal Disorders: Mutations in BMP receptors can lead to rare genetic conditions like Fibrodysplasia Ossificans Progressiva (FOP), where connective tissue and muscle gradually turn into bone (heterotopic ossification).
Cancer: BMP signaling exhibits dual roles in oncology. Depending on the tissue context, they can act as tumor suppressors or promote tumor cell migration, invasion, and metastasis in cancers such as breast, prostate, colorectal, and multiple myeloma.
would cationic nanoparticles upregulate or downregulate? propose LNP triggered pathways that would provide a delta of some kinds
Whether cationic nanoparticles (or cationic lipid nanoparticles, LNPs) upregulate or downregulate Bone Morphogenetic Protein (BMP) signaling depends entirely on their payload, surface chemistry, and the specific cellular context. Rather than acting as a simple on/off switch, cationic carriers dynamically modulate the pathway, producing a distinct biochemical "delta" (Δ).
1. Upregulation vs. Downregulation: The Directional Delta
Downregulation (Gene Silencing / Inhibition): If cationic nanoparticles are loaded with interfering RNA (such as siRNA targeting BMP antagonists like Noggin, or targeting pathway inhibitors like SMURF1), they effectively upregulate downstream BMP signaling output by removing inhibitory blocks. Conversely, if they deliver siRNA against BMP receptors (like ALK3 or ALK2), they actively downregulate BMP signaling.
Upregulation (Gene Delivery / Expression): If cationic LNPs encapsulate and deliver mRNA encoding BMP ligands (e.g., BMP-2 or BMP-7) or transcription factors (like RUNX2), they drive the intracellular machinery to overexpress these proteins, directly upregulating the pathway.
2. Proposed LNP-Triggered Pathways & Biochemical Deltas
When cationic nanoparticles interact with cells, they set off a cascade of biophysical and biochemical events. The primary pathways and their respective Δ shifts include:
A. The Cationic Endosomal/Lysosomal Stress Pathway (Δ in Cytotoxicity & UPR)
Trigger: Cationic lipids possess positive charges that strongly interact with negatively charged cell membranes, facilitating cellular uptake via endocytosis. Inside the endosome, they cause proton sponge effects, swelling, and membrane rupture.
Pathway: This sudden osmotic stress and endosomal leakage trigger the Unfolded Protein Response (UPR) and endoplasmic reticulum (ER) stress.
The Delta: UPR activation alters transcription factors (like ATF4 and CHOP). In osteoprogenitor or endothelial cells, chronic ER stress crosstalks with TGF-β/BMP signaling components, often blunting canonical R-SMAD (SMAD1/5/8) responsiveness while tipping non-canonical pathways (like p38 MAPK or JNK) toward apoptosis or inflammation.
B. The Toll-Like Receptor (TLR) Inflammatory Axis (Δ in Cytokines)
Trigger: Extracellular exposure to cationic surfaces and nucleic acid payloads triggers innate immune recognition.
Pathway: Activation of TLR3, TLR4, or TLR7/8 signaling cascades, relying on downstream adaptors like MyD88.
The Delta: This produces a surge of pro-inflammatory cytokines (e.g., TNF-α, IL-6). Inflammation has a complex, bidirectional feedback loop with BMPs: acute inflammatory signals can induce certain BMP ligands (like BMP-2/4) as part of tissue repair or vascular remodeling, while chronic inflammation often downregulates osteogenic BMP receptors via inhibitory Smads (Smad6/7).
C. The Non-Canonical Kinase Crosstalk (Δ in PI3K/AKT vs. MAPK)
Trigger: LNP membrane fusion alters local fluidity and clusters cell-surface receptors.
Pathway: Activation of non-canonical BMP/TGF-β branching, particularly PI3K/AKT/mTOR or RhoA/ROCK cytoskeletal remodeling pathways.
The Delta: Even without altering core ligand transcription, the nanoparticle-induced membrane perturbation shifts the cell toward survival, migration, or metabolic switching. This alters the phosphorylation status of shared downstream kinases, changing how effectively the cell translates a native BMP signal into gene transcription.
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what organs could downregulate BMP? i wonder if stress in the parathyroid or kidneys from nanoparticles would downregulate. any other tissues that would do it if not these?
When cationic nanoparticles or lipid nanoparticles (LNPs) circulate in the body, their biodistribution heavily favors clearance organs and filtering tissues. Cellular stress, oxidative damage, and inflammation in these organs can significantly downregulate BMP signaling pathways, shifting tissue responses away from repair and toward fibrosis or apoptosis.
1. The Kidneys (High Susceptibility)
Why they are targeted: Nanoparticles within specific size ranges (roughly 10 to 100 nm) accumulate heavily in the renal mesangium and proximal tubular epithelial cells via glomerular filtration or peritubular capillary uptake.
The Downregulation Effect: The kidneys rely heavily on endogenous protective pathways—most notably BMP-7, which maintains renal tubular integrity and acts as an anti-fibrotic factor. When cationic nanoparticles induce endoplasmic reticulum (ER) stress or oxidative damage in tubular cells, BMP-7 expression is often suppressed. This downregulation removes a vital protective brake, accelerating the transition from acute kidney injury (AKI) to chronic renal fibrosis.
2. The Parathyroid Glands (Indirect/Systemic Stress)
Why they are targeted: Unlike the kidneys or liver, the parathyroid glands are not primary clearance hubs for nanoparticles, meaning direct accumulation is usually low.
The Downregulation Effect: Parathyroid cells are extremely sensitive to systemic calcium/phosphate balance and metabolic stress. If nanoparticle toxicity heavily impacts kidney function (disrupting mineral homeostasis), the parathyroid glands undergo secondary compensatory stress. While direct downregulation of BMP signaling in parathyroid cells by nanoparticles is less documented, systemic inflammation and uremic toxins secondary to renal nanoparticle stress can alter calcium-sensing and local growth factor regulation.
3. Other Tissues Prone to BMP Downregulation
If you look beyond the kidneys and parathyroid glands, several other organs experience severe nanoparticle-induced stress that results in suppressed or dysregulated BMP signaling:
The Liver (The Primary Clearance Sink):
Mechanism: Kupffer cells (liver macrophages) and hepatocytes rapidly sequester the vast majority of systemic LNPs.
The Shift: High nanoparticle loads trigger massive reactive oxygen species (ROS) production and inflammatory cytokine release (TNF-α, IL-1$\beta$). This inflammatory milieu often downregulates local regenerative BMP networks (such as BMP-9, which is liver-derived), impairing hepatocyte maintenance.
The Bone Marrow (The Osteogenic Niche):
Mechanism: Bone marrow sinusoidal endothelium and resident macrophages take up circulating nanoparticles efficiently.
The Shift: Mesenchymal stem cells (MSCs) residing in the bone marrow are exquisitely sensitive to BMPs for osteogenic differentiation. Nanoparticle-induced oxidative stress or inflammatory signaling can downregulate BMP receptors (like ALK3/6) on MSCs, effectively stalling bone regeneration and favoring adipogenesis or cell death instead.
The Lungs:
Mechanism: Particularly relevant for intravenous administration (first-pass pulmonary capillary bed trapping) or inhalation.
The Shift: Alveolar macrophages and epithelial cells undergo stress that suppresses normal BMP-mediated tissue repair, frequently tipping the microenvironment toward chronic inflammation or pulmonary fibrosis.
of these you just listed, can they trigger phosphorus release from tissues into the bloodstream?
Yes, severe cellular stress, necrosis, or lysis in these tissues can indeed trigger a release of intracellular phosphorus into the bloodstream, leading to hyperphosphatemia.
Because phosphorus is predominantly an intracellular anion (bound in ATP, nucleic acids, phospholipids, and proteins), any event that compromises cell membrane integrity causes these intracellular stores to flood into the extracellular fluid and general circulation.
1. How the Listed Organs Contribute to Phosphorus Release
The Liver (Direct Cellular Lysis):
The liver is the primary clearance sink for systemic nanoparticles. If high concentrations of cationic LNPs induce severe hepatotoxicity, oxidative stress, and widespread hepatocyte necrosis, massive amounts of intracellular ions—including phosphorus—are spilled directly into the hepatic venous outflow and systemic circulation.
The Bone Marrow (Cell Turnover & Mineral Matrix Proximity):
The bone marrow is densely packed with rapidly dividing hematopoietic and stem cells. Nanoparticle-induced apoptosis or cytotoxicity here causes the breakdown of nucleic acids and intracellular phosphorus pools. Furthermore, because the marrow is encased within the bone matrix (which stores roughly 85% of the body's total phosphorus as calcium phosphate), local inflammatory remodeling or matrix degradation can mobilize mineral stores.
The Lungs (Acute Injury & Alveolar Lysis):
Severe pulmonary toxicity or acute lung injury (ALI) resulting from nanoparticle exposure causes the breakdown of vast numbers of endothelial and epithelial cells, contributing to the systemic pool of circulating cellular debris and free phosphate.
2. The Renal Factor: Release vs. Failure to Clear
While the liver and bone marrow can release phosphorus through cell lysis, the kidneys play a different, equally critical role:
Impaired Excretion: The kidneys are the primary organs responsible for filtering and excreting excess dietary and endogenous phosphorus.
The Double-Whammy Effect: When cationic nanoparticles induce acute tubular necrosis or renal dysfunction, the kidneys lose their ability to clear phosphorus. Therefore, even a modest cellular release of phosphorus from the liver or bone marrow can quickly spiral into severe systemic hyperphosphatemia because the damaged kidneys cannot excrete it.
I agree. From everything I've read, you are being censored.
I am a meat Popsicle!
So do you only last if frozen?
Cutting room floor text (a trademarked staple of my Readers Comment Fortum!)
... For example, Facebook once suspended my account three times because I was making posts that were labeled dangerous disinformation.
Not only could I not make an original post, I couldn’t comment in the Reader Comments of any other Facebook user. (As long as I restricted my posts to content like “what a cute photo of your puppy!” I was safe.)
I should note that Facebook seems to have done away with its more Orwellian posting policies that were in effect in Peak Covid. I say this because, every now and then, you can see a post that is critical of Covid policies and I see plenty of posts that are both pro-Iran War and anti-Iran war, which is good to see.
Still, my peak "reach" on Facebook might be 200 of my 2,000 friends … and when I do share a link to one of my “contrarian” Substack articles, these usually get zero likes and zero Reader Comments, meaning I’m still not sold that Mr. Zuckerberg has found religion on the importance of free speech.
Zucky and religion...what an oxymoron that is.
Relevant document you may be interested in:
https://unesdoc.unesco.org/ark:/48223/pf0000387339
Guidelines for the Governance of Digital Platforms
Safeguarding freedom of expression and access to information through a multistakeholder approach
This is literally the playbook for the censorship we've been seeing around the world. Brought to you by our "friends" at UNESCO.
Thank you, SC, a Great American.
SimCon, I can reply but I can’t like your comment. That happened to me the other day when I was participating in the comment section of your “Let’s watch the Shitweasel together” article!!! Sometimes the like button would work, and sometimes it wouldn’t.
Same with me, KIng. I've tried to "like" your comments and couldn't do it ... but other places and other times, I can.
I skimmed it over. Chock full of buzz words and phrases arranged in a way to make it sound reasonable and kind. Reminded me of HR emails from the last few years I was working before I retired. They were full of buzz words that were reasonable and kind, but they could have been replaced with a bulleted list of things that were going away or result in being terminated.
Yep. I call it "government-speak," though UNESCO isn't technically government, it just wants to control them.
I should note that, just in the past few weeks, al.com has gone back to allowing Reader Comments, but with a new twist. Only paid subscribers can make posts, which are heavily moderated. When the editor announced this change, he/she gave quite the lecture on how these posting priviliges must be used.
It seems to me that almost nobody is making Reader Comments because every story I click on says, "Be the first person to comment on this article."
My take-away from this change is that al.com is bleeding money and realizes they lost a lot of readers or "reader engagement" when they did away with their previous very popuar Reader Comment Section. Also, the site now only runs the first two paragraphs of most of its stories, meaning you have to pay to get the full story - which is a program to generate more revenue (which I certainly understand).
However, the site gave away free stories for so long I don't think many readers are buying the paid content (which - generally speaking, with a few exceptions, is awful IMO.) Of course, at one time, the business model was that these websites would create so much reader traffic, they would make up for the loss in paid subscriptions by a flood of businesses that wanted to place digital ads at the website.
This didn't happen either.
Not long ago, I tried to count all of the journalists who produce "straight news" articles at this website. (This was a challenge as the site doesn't run employee staff boxes anymore.) As best i could determine, this website has approximately 20 full-time staff journalists (not counting a couple of sports writers). Once upon a time, the three newspapers that became al.com would have employed 200 full-time journalists and editors.
All three newspapers would have had more full-time sports reporters than the site has total news reporters today.
What the heck good it that? Nothing questioning the "news" will ever see the light of day.
We are there already! Screws are being tightened! X has.banned me for supporting RFK Jr goals. Controlling the narrative goes on and on. Coverage of Fauci in mass media did not cover the sociopaths actions that has created great harm and death!
Experts Suck!
Never trust the experts!
My friend who runs Citizen Free Press has gone silent. He and I were in touch, and he was posting some of my pieces as well. He said to send him links whenever I had something. But he stopped responding to messages maybe two years ago. (I've never met him but we happen to live in the same town and know some of the same people.)
I ended up getting Kane's email. I even pitched a business idea to him - something I think would be a big improvement on the Substack subscription model. He read the proposal, which I appreciate, but passed on it.
I appreciate him running as many of my stories as he did. And I do still check out his site, although I think it has changed and I think his political bent might have changed for some reason..
One thing Kane is proud of is he doesn't run any ads, which he could do. A couple of times a year, he runs donation fund-raisers. He's got millions of loyal weekly visitors to his website and he should be able to monetize that ... big time. Of course, he runs right-wing and politically incorrect stories so, like Zero Hedge**, he'll never get any advertising revenue from the Big Advertisers of the Big Advertising Agencies.
Tucker Carlson never did and he had the No. 1 talk show in the world.
**P.S. I can't remember the company, but the other day I saw a display ad at Zero Hedge for a mainstream company. I have never seen this before. So I wonder if these changes at this site might result in an end to the advertising discrimination?
I also think Substack will be sold one day and one of the captured usual suspects will take it over. That's why Notes (a knock off of X) is so important and that's probably why the content on Substack is now as liberal as the MSM. The new owner could sell advertising around Notes. As long as the site played ball and pushed the right narratives, the cabal of big advertisers would support the site.
IMO, even media companies which lose tons of money (like most do) are very important to the Powers that Be because of all the stories they do run and, more importantly, all the stories the could run that would bring down the system if they did.
The Washington Post is losing massive amounts of money, but Bezos IMO uses it as "leverage" and a "loss leader.". The thinking probably goes a little like this: "You pay my other companies a lot of money, or give us this contract, or leave us alone ... and I won't come after you with the Washington Post."
Kane has ads now. I remember he posted something about needing to do that to keep operating. It pops up at the bottom of the screen. Nothing that gets annoying. I also have noticed a change with him that I can't quite put my finger on.
He could sell the business for a lot of money, I would think. someone would buy it just to stop all this content just like someone must have bought Drudge. He is not as bold or independent as he used to be. He “discovered” me and now I’m radioactive. It’s odd.
It is odd. I may see if I can find him through our mutual friends. It's worrisome to learn from you today that like me, you also lost contact with Kane and that he seems to have changed. Esp. given that Matt Drudge disappeared. There have been no sightings of him that I know of. Strangely, I lived on Miami Beach when Matt lived there, though I never saw him. The last place he lived was the agricultural area in south Miami-Dade County called The Redlands. He sold the house a few years ago and no one has seen him since. I find this pretty disturbing. Maybe he is in Latin America or something. My understanding is that every few years, around the election, he would get quite nervous as he was receiving some threats and had reason to believe his life was being threatened. I don't believe he was paranoid. I think there probably were quite a few people who wanted him dead, and maybe some who were willing to act.
I check out ZeroHedge regularly.
That said, I noticed (©2020) flagrant anti-Semitic reader comments so vile as to pollute the platform and disabuse me of any good opinions of those posting.
I quit reading CFP regularly (my thrice daily checks were usually rewarded with insights and news not found elsewhere). Things changed. I check headlines at CFP 2X per week now.
CitKane positioned the site for sale (my theory) as he constantly battled other news feeds for eyes-on supremacy, quit generating separate page posts (thus ending news-specific-posting-comments pages).
Linking directly to stories eliminated curator-responsible comments, and the liability associated with them. Imho, a business decision based on liability not free speech suppression.
Chasing page views for these publishers is like ambulance-chasing lawyers seeking high dollar injury clients.
I just can't stand their progress.
Here is my view - local business is better and it is more than obvious - I mean Kropotkin spoke of it more than a century ago but his ideas got stifled - did they not?
I mean for goodness sake you read Mutual Aid haven't ya?
Thanks for this report, Bill. I appreciate your keeping your eye on these things. I would add to your list that, as you mention later in your article, it seems bots have been peppering up the comments sections of some blogs. I've seen that sort of thing here in your substack, but in particular I note that Steve Kirsch's has been getting a lot of bot-shills-for-"the narrative" comments— or simply nonsensical comments, probably from bots. I take that as a sign that he's slam over the target.
The bots sometimes gang up and attack from out out no where. They also steal your identity and make 300 nonsensical posts under your name. There's numerous reach-suppression and Narrative Control ops being used in the Reader Comments.
I just saw that Jenna McCarthy's story on the Fauci hearing got about 240 likes and 200 reader comments. It's a great story and deserves those accolades. I'd just note I posted my Fauci story 12 hours before she did and got about 1/5 of the likes and Reader Comments as her article. Jenna does have more subscribers than I do, but not a whole lot more.
Strange. Doesn't make sense ... unless there is some reach-suppression op that's being used against my newsletter.
1984
It is true Bill - as you have already expressed.
They all are compromised - tis a conspiracy against us no doubt.
But as a faithful member of North Carolina constituency as well as Virginia no doubt, I send out a peace message to Alabama - can you feel it Bill...Geoff and I wonder if you realize the value of the patent info passed onto you Bill.
Troy Alabama knows the power of NC, VA, TN, KY, and WV.
Correct?
I must admit I haven't done a deep dive yet on the patent info, but I've read enough (from you and others) to know it's probably very significant.
Say what you want about me, but I'm the most famous Substack author from Troy, Alabama. (As far as I know Troy has two Substack authors and the other one, a friend of mine, has only 63 subscribers. I actually think I have more Substack subcribers and followers than any other person in Sweet Home Alabama.
Maybe so Bill. II respect you -that is why I'll continue to pay to find out what is going on in Troy, AL.
Warm Regards,
Ken
I would like to add 1) Dr. Malone does not allow comments unless you pay for his thoughts, and 2) It figures that Dan Blather would pull a stunt like that, but at 94 you'd think he would have either learned something or had accrued some humility.
Dave, you might win the prize for my most consistent poster. Thank you very much! Also, Thomas, posting below!
cause I don’t have the sense to keep my keyboard still…
I couldn't agree more. The comments sections are and have been the best bridge to additional information on any given subject. Before YouTube started censoring, their comments section was outstanding. Information about 911, and other historical subjects that were re-written to fit a narrative, was easy to find and verify. Of course there were trolls and bots trying to muddy the water, but they became easily identifiable over time.
Zionists seem to own or control a disturbing amount of our media and big tech, not to mention hollywood, publishing, etc. If anyone has the power and motive to censor, I think it's them. They are the enemy of the entire planet.
ZH is not what it used to be. The news stories include planted Goldman Sachs narrative crap and the comments section is rife with (paid by Israel?) trolls. It has degraded since Tyler sold out.
Recently, I check it out for their "Iran War" updates. I usually go straight to the Reader Comments. While many posters are "out there," sophomoric and specialize in juvenile insults, many posters are also pretty sharp and several are quite astute IMO. Several regular posters also provide excellent links from the alternative media that help me get a fuller picture of what might be happening.
I have noted when I make a post, in two seconds I immediately have two or three down votes. That has to be bots.
..."The “Powers that Be”...and exactly who are these bums? If they be censoring anyone it is because they are afraid of the truth. That can be the only reason. I expect that 99% of the people on the planet have no or few opinions about much of anything. Or if they do, they keep them hidden from the public and the snoopy big tech swine.
Even if the silly powers that be erased all written opinions, you can still have opinions. They can be shared with others in real time, face to face. Eventually, substack will go the way of "My Space" especially if it goes public (as in a stock IPO) as this is the only reason for its existence. So the owners can become instant billionaires.
I don't do social media or news feeds or TV news or much of the MSM. If I get any news it's in passing through the articles I might read on substack and sometimes that is more than I care about. I imagine the powers that be are psychos run amok and if the pitchforks come out, for sure it is because they deserve a good thrashing. My "fork" will be the one with the golden tines.
Hear! Hear!
Hasbara and chat bots abound as ever. I used to be prolific on Daily Mail articles but got blocked.
Et tu, Daily Mail?