Those aircraft mats look like they'd be handy! I'm guessing they'd be a small fortune nowadays, but probably not too many on the market at this point (70 years of rust, I wonder what's become of them?).
Anyway, looking into more about Protein A's "Binding and Inactivating antibodies" which I /strongly/ suspect underlies arthersclerosis, I was brought to this page.
https://en.wikipedia.org/wiki/Protein_A
And this part of the role in pathogenesis contains the clues.
As a pathogen, Staphylococcus aureus utilizes protein A, along with a host of other proteins and surface factors, to aid its survival and virulence. To this end, protein A plays a multifaceted role:
1.By binding the Fc portion of antibodies, protein A renders them inaccessible to the opsonins, thus impairing phagocytosis of the bacteria via immune cell attack.
2.Protein A facilitates the adherence of S. aureus to human von Willebrand factor (vWF)-coated surfaces, thus increasing the bacteria's infectiousness at the site of skin penetration.
3.Protein A can inflame lung tissue by binding to tumor necrosis factor 1(TNFR-1) receptors. This interaction has been shown to play a key role in the pathogenesis of staphylococcal pneumonia.
4.Protein A has been shown to cripple humoral (antibody-mediated) immunity which in turn means that individuals can be repeatedly infected with S. aureus since they cannot mount a strong antibody response.
5.Protein A has been shown to promote the formation of biofilms both when the protein is covalently linked to the bacterial cell wall as well as in solution.[11]
It appears that #2 and #5 are a bit suspicious. Looking into the von willebrand factor, I get this page.
https://en.wikipedia.org/wiki/Von_Willebrand_factor
And find...
Von Willebrand factor (vWF) (/ˌfʌnˈvɪlᵻbrɑːnt/) is a blood glycoprotein involved in hemostasis. It is deficient or defective in von Willebrand disease and is involved in a large number of other diseases, including thrombotic thrombocytopenic purpura, Heyde's syndrome, and possibly hemolytic-uremic syndrome.[3] Increased plasma levels in a large number of cardiovascular, neoplastic, and connective tissue diseases are presumed to arise from adverse changes to the endothelium, and may contribute to an increased risk of thrombosis.
Already seeing mention of thrombosis... and the word cardiovascular, and connective tissues and "adverse changes to the endothelium"(I.e., vessell walls) and that last part, "increased risk of thrombosis". A.k.a, blood clot... a.k.a., heart attack, stroke and pulmonary embolisms. Seems we've found our guy and the exact mechanism! Wow, all the clues are already on wikipedia if you're know what you're looking for, it's puzzling this isn't already mentioned on the atherosclerosis wikipedia page.
Now, how would this be put if we were playing Clue?
Staph Aureus did it in the endothelium/blood-vessel-walls with Protein A! lol
Now I'm wondering if Protein A, and Staph Aureus, are the only the protein/bacteria capable of these effects. It appears that Staph Aureus is the only one containing Protein A in nature, but it appears scientists have been able to foist the protein onto E. Coli and Brevibacillus.
And, wow, my poop still doesn't stink. Man, this low grain / high fruit+vegetable / high fat diet seems to be working. (Now I can retort "Yes, I sure do" when grammy complains that I don't think my poop doesn't stink, lol.)
It'd be interesting to find out if the animals that aren't suscectible to Protein A and the various common viruses rarely have clots. Like, hamsters. Do hamsters have heart attacks? (The list of animals and their susceptibility is at https://en.wikipedia.org/wiki/Protein_A ). A quick google search indicates that they do, but their achilles heel seems to be Amyloidosis, which is rare in humans. Though, i wonder if more subtle presentations of Amlysoidosis are actually more common than thought...
https://en.wikipedia.org/wiki/Amyloidosis
, AA is more likely to occur from autoimmune inflammatory states.[6] Most common etiologies of AA amylodosis in the west are rheumatoid arthritis, inflammatory bowel disease, psoriasis and familial Mediterranean fever.
Looks like we have immune activity, with the possible associated nemesis Staph Aureus and its weapon of choice, Protein A... but that can't be readily concluded here. Psoriasis... was that mentioned as being caused by Staph Aureus? Let's double check.
S. aureus can cause a range of illnesses, from minor skin infections, such as pimples,[8] impetigo, boils, cellulitis, folliculitis, carbuncles, scalded skin syndrome, and abscesses, to life-threatening diseases such as pneumonia, meningitis, osteomyelitis, endocarditis, toxic shock syndrome, bacteremia, and sepsis
See no mention of psoriasis here, but there seems to be some overlap with the various skin disorders listed. Looking at the various skin disorder listed, it appears to be a localized affect (Appearing in small spots/bumps/etc.), where as the google images of psoriasis at https://www.google.com/search?site=&tbm=isch&source=hp&biw=1440&bih=832&q=impetigo&oq=impetigo&gs_l=img.3..0l10.16710.17724.0.17948.9.7.0.0.0.0.423.674.2-1j0j1.2.0....0...1ac.1.64.img..7.2.670.0..35i39k1.yfKVW4bH1_I#tbm=isch&q=psoriasis&imgrc=h-H-QIDZm1djLM%3A appears to also come in a localized appearance with "spots", although a bit larger. Seems somewhat similar to impetigo in appearance. So the association of Staph Aureus with AA in humans is suspected, and by extension, animals susceptible to it like Hamsters.
Found an article on Staph's ability to evade antibodies.
http://www.popsci.com/why-staph-infections-are-so-hard-to-control
This clue pointed the finger at one particular Staph molecule: Extracellular Fibrinogen-Binding Protein. Back in 2008, this molecule was shown to inhibit the ability of CR2 to function properly. Based on all the evidence from the previous experiments, this one molecular appeared to be the reason for effective evasion.
This discovery reveals how Staph is quite likely one of the most proficient pathogens. The results also offer up the opportunity to find a means to block the evasion mechanism through treatment. While at the moment no such medicine exists, the door is now open to finding potential candidates. This in turn may help to reduce the chances of injury and death in those unfortunate enough to suffer the wrath of this rather common yet at times vicious bacterium.
As to effective treatment, ooo, ooo, I know! Antiobiotics like Coconuts, Cocoa, Coffee, Limes/Lemons, Garlic, Red wine, Vinegar, etc.
"At times", oh man, they act like this thing only occurs during serious life-threatening infections. Little do they know is that it's /very active/ in 90+% of the western population in causing arthersclerosis with their high sugar and typically high-refined-carb diets (Bread is the prototypical refined carb. That includes whole wheat bread, too, just the fact the wheat has been pulverized and turn into a powder known as flour makes it refined.). I already show signs of arthersclerosis with my persistent widened pulse pressures (120/60, 110/70 is optimal - typical of native coconut-and-fish-eating tropical islanders).
Anyway, this HEB brand pink salmon is both better tasting and cheaper than the honeyboy's pink salmon. It tastes like the honeyboy's pink salmon was left out a little while before packaging, whereas HEB's pink salmon was packaged (or preserved by ice, whatever) right away, so it has that "soft fresh salmon" taste to it. It's rather nice. Higher quality and cheaper, can't beat that! [Alaskan pink salmon is ridiculously cheap in Texas compared to Washington. It almost seems like Washington puts a 100% tax on these things or something; a $6.50 can there goes for $3.29 here, and that's assuming you can find someone that carries it! My lord, Washington acts as if wild alaskan salmon is a rarity, whereas Texas has it in abundance.]
Also, while at the grocery store, saw this asian women struggling to find fresh organic 1 lb. bag of carrots. I saw that they sold out of the 5 lb bags (The kind I buy, since I go through them in like 3-4 days), so I gave up on organic and just bough some pesticide laden ones. I figure these aren't the worst culprits when it comes to pesticides since they're underground and I'm assuming the top/leaves get most of the pesticide exposure. I figure I need to be at HEB whenever they get shipments in and that's likely thursday, so I think thursday will be the required grocery shopping day. Meaning, from now on, I'm only going thursday, regardless if I haven't ran out yet or if I ran out 2 days ago. Thursdays.
Anyway, will report that the reversed tape worked wonderfully on the existing trailer jack for preventing insects from climbing up it and into my RV.This one cricket looking creature was stuck for like 2-3 days, but now I noticed today his body is missing and his leg is still attached to the tape. Oh no! What happened? I'd imagine he's dead (They'd die within a few days of no water and food, right?), and I didn't see his body anywhere, so I'm guessing a bird picked him off or something. Poor cricket.
Anyway, as to how long I'm staying here in the NF... I don't know yet. I arrived the night of Jan 14, so the earliest the NF could have spotted me would've been Jan 15, so I guess Jan 29 would be the safest last day to stay (Leave morning of Jan 30), but I'm just betting that they didn't notice me until Jan 16, so I have until the morning of Jan 31st to leave. I'm going to be proceeding with the work with full persistence, and I'm hoping it should be done by the 31st, if not by the 30th (I'd imagine a full day of digging and wheelbarrowing should get most of it done.). Looks kind of tight, but probably doable.
Going back to Linoleic acid, what's the relationship between that and Staph Aureus? (Common in North American tree nuts, seeds and vegetable oils)
https://www.ncbi.nlm.nih.gov/pubmed/93615
Linoleic acid probably inhibits growth by increasing the permeability of the bacterial membrane as a result of its surfactant action, and the presence of the PC plasmid increases these effects.
Here's another supporting paper, which generalizes to "unsaturated long chain free fatty acids". (I.e., NA nuts and seeds)
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0004344
Seems like nut consumption would then correspond to decreased CVD risk which the food/CVD table paper above tells us. -.6 correlation between nut consumption and CVD (.6 = somewhat strong association.).
So, then the relationship between linoleic acid and CVD should be preventative. Is that what papers are telling us?
http://circ.ahajournals.org/content/early/2014/08/26/CIRCULATIONAHA.114.010236
In prospective observational studies, dietary LA intake is inversely associated with CHD risk in a dose-response manner. These data provide support for current recommendations to replace saturated fat with polyunsaturated fat for primary prevention of CHD.
Indeed, it is. So this girl's hearty stance against linoleic fatty acid is unfounded in my opinion. She's probably looking at the wrong scapegoat, which is likely refined carb, especially refined wheat, consumption since that's what most commercially used oils are used in as a cheap butter substitute. [The problem with eating vegetable oil doused wheat products is that the gliadin protein in the wheat acts on the Zonulin signal molecule, which relaxes the cell junction tightness in the gut lining, which essentially widens the holes for bacteria to enter the bloodstream. So, even though the vegetable oil might inhibit Staph growth, it doesn't seem to kill it off, and other foods consumed in conjunction or "in the near future or recent past" could increase staph colony sizes, like sugary drinks. I'd imagine that gliadin protein might persist in the digestive tract for a little while... I'm not sure how long...]
I'm wondering... absent wheat and gliadin containing grains(Barley/rye)... if staph aureus can 'fit' through the holes in the gut lining. And, how much does gliadin actually expand the holes? This would be an interesting question if staph couldn't ordinary fit through the holes, but gliadin expands the holes making it possible, and that might be why wheat free societies tend to have very low CVD incidences. I wouldn't think so, but it's a hypothesis worth knowing/investigating. I would think it ordinarily can fit, just a lot less get in.
Well, here's some hard numbers.
https://en.wikipedia.org/wiki/Intestinal_epithelium
Gap junctions[edit]
Gap junctions bring the adjacent cells within 2 nanometers of each other. They are formed by several homologous proteins encoded by the connexin gene family coming together to form a multiprotein complex. The molecular structure of this complex is in the form of a hexamer. The complex, which is embedded in the cell walls of the two joined cells, forms a gap or channel in the middle of the six proteins. This channel allows various molecules, ions and electrical impulses to pass between the two cells.[13]
Desmosomes[edit]
These complexes, consisting of transmembrane adhesion proteins of the cadherin family, link adjacent cells together through their cytoskeletons.[14] Desmosomes leave a gap of 30 nanometers between cells.[13]
So, we have 2 nm and 35 nm. Staph aureus is normally .5 um or 500 nm. It would seem that staph aureus couldn't /ordinarily/ penetrate the intestinal eptithelium/lining. I wonder if there are special conditions under which they could? Like, maybe gliadin... or... maybe if there's a lot of pressure due to high food consumption... I wonder...
I wonder if, and how, potassium/sodium/magnesium affect the cell junction tightness...
Can't seem to find hard numbers on how much gliadin expands the gap junctions/desmomemes... other than it's thought to "increase intestinal permeability". Hmm... I wonder if this is hard to measure in practice. It only makes too much sense that the cell junctions wouldn't /ordinarily/ allow bacteria through (Seems like that'd lead to selecting those bad genes out of the gene pool, lol.)... so it seems fairly plausible that gliadin is enabling the staph aureus to penetrate.
Oh well, this is interesting to know. Bacteria affects the junction gaps.
http://jn.nutrition.org/content/141/5/769.full
Studies have shown that the intestinal bacteria target various intracellular pathways, change the expression and distribution of TJ proteins, and thereby regulate intestinal barrier function. The presence of some commensal and probiotic strains leads to an increase in TJ proteins at the cell boundaries and in some cases prevents or reverses the adverse effects of pathogens. Various dietary components are also known to regulate epithelial permeability by modifying expression and localization of TJ proteins.
I'm going to take a wild guess and say that staph aureus tries to expand it!
This paper has more information on gliadin, though it doesn't quantify the increase in the junction gap size, sadly.
In addition to bacteria, TJ are also regulated by dietary components. In celiac disease, pathogenesis is induced by gliadin, a glycoprotein present in wheat. When IEC6 and Caco-2 cells are exposed to gliadin in vitro, interaction between occludin and ZO-1 is compromised and the cytoskeleton is rearranged, leading to increased monolayer permeability (73). The mechanism for this has been linked to zonulin, the human homolog of the zonnular occludens toxin from Vibrio cholera that is known to modulate TJ (74). Gliadin induces zonulin release, leading to PKC-mediated cytoskeletal reorganization (75). Ex vivo human intestinal samples from celiac patients in remission also showed zonulin release when exposed to gliadin, causing cytoskeletal rearrangement and ZO-1 reorganization, leading to increased permeability (73). Gliadin causes zonulin release by binding to the CXCR3 receptor in intestinal cells (76).
EDIT: What the hell?! It looks like a ladybug just jumped on my hand while I was eating and bit me and now it scratches. What? I didn't know ladybugs eat people, lol.
Well, apparently it's a look alike that's actually an "asian beetle".
http://austin.blog.statesman.com/2016/12/15/those-arent-ladybugs-central-texas-sees-influx-of-bitinwww.scienceforums.net/topic/49133-size-of-lymphocytes/
g-asian-lady-beetles/
And, looks like I arrived just in time, lol. (Article dated Dec 16, 2016)
Those aren’t ladybugs — Central Texas sees influx of biting Asian Lady Beetles
What’s cuter than an invasion of ladybugs? Arguably nothing. What’s less cute? An invasion of Asian Lady Beetles. Although Central Texans might be seeing a lot of what look like ladybugs this winter, Texas Parks and Wildlife clarified on Facebook earlier this week that they may in fact be a nonnative species of ladybugs, Asian Lady Beetles.
Ok, so no mercy for this species, lol.
OK, going back to the further up research on gliadin. I looked more into this CXCR3 receptor, because I wondered what exactly its purpose would be if it just increased permeability and it apparently ordinarily facilitates the trafficking of T-cells (Say, if the immune system needs access to the intestinal epithelium, I'm assuming it triggers the CXCR3 receptor to let the T-cells through). How large are T-cells? According to http://www.scienceforums.net/topic/49133-size-of-lymphocytes/
, a T-cell is ordinarily 7-8 uM = 700-800 nm. Staph Aureus at 500nm then could probably get through the intestinal epithelium if Glidian bonded to this receptor.
So, I looked up the wikipedia page on this receptor and found....
https://en.wikipedia.org/wiki/CXCR3#Clinical_significance
CXCR3 has been implicated in the following diseases, atherosclerosis,[10] multiple sclerosis,[11] pulmonary fibrosis,[12] type 1 diabetes,[13] autoimmune myasthenia gravis, nephrotoxic nephritis,[14] acute cardiac allograft rejection[15] and possibly Celiac Disease.[16] Development of agents to block CXCR3-ligand interactions may provide new ways to treat these diseases.
Cardiovascular implications[edit]
Evidence from pre-clinical and clinical investigations has revealed the involvement of CXCR3 and its ligands in several cardiovascular diseases (CVDs) of diverse etiologies including atherosclerosis, hypertension, Kawasaki disease, myocarditis, dilated cardiomyopathies, Chagas, cardiac hypertrophy and heart failure, as well as in heart transplant rejection and transplant coronary artery disease (CAD).[3][17] CXCL9-10-11 have been recognized to be valid biomarkers for the development of heart failure and left ventricular dysfunction in two pilot studies, suggesting an underlining correlation between levels of the interferon (IFN)-γ-inducible chemokines and the development of adverse cardiac remodeling.[18] [19]
WOW! Wheat with the Protein gliadin, and its accomplice Staph Aureus with Protein A, seems to be responsible for a lot more than just heart disease! [On the secondhand, gliadin might not be the only trigger for CXCR3 activation. If the immune system triggers it, and if certain states cause immune system overactivity (Say, anxiety), then the immune system might also contribute to some of these diseases. That is, there might be multiple complementary triggers for the CXCR3 receptor, though I suspect Staph Aureus with protein A is the sole cause regardless of the trigger.]
So, it literally /is/ a matter of the gliadin in wheat opening the gates to the castle for the invading hordes. Not some 'ordinarily a little comes in, wheat just makes more come in'. Ordinarily, nothing comes in.
Wheat causes MS, that's a surprise. Not super obvious how staph A would cause dymyelination of the nerve sheath, but I'm assuming it does somehow.
Now, I'm just really curious how long does gliadin ordinarily bond to the CXCR3 receptor. That is, how 'persistent' are the effects of wheat consumption.
la-41454795529&wl5=9027916&wl6=&wl7=&wl8=&wl9=pla&wl10=8175035&wl11=online&wl12=10741110&wl13=&veh=sem
