#Lipopolysaccharides

[evil-jennifer-hamilton-wb]

Considering murder because i'm in google looking for a diagram of a lipopolysaccharide in the gram negative bacterial cell wall.

And google is like "did you mean polysaccharide?" and it only displays polysaccharides in the search results.

And so I go and I make the search term "lipopolysaccharide" in quotations. and it says "did you mean "polysaccharide"?"

And I understand I could search for endotoxin but it's the principle of the thing I want the search engine to search the word I give it! not something approximate! Google should consider the concept that LPSs exist, and putting search terms in quotations should work!

so when the google servers are destroyed tomorrow in an arson attack at 2PM GMT+8, It wasn't me that did it but I really wish it was.

[tony789456123]

Lipopolysaccharides Immunoassay Market

[longhaulerbear]

Abstract

There is a link between high lipopolysaccharide (LPS) levels in the blood and the metabolic syndrome, and metabolic syndrome predisposes patients to severe COVID-19. Here, we define an interaction between SARS-CoV-2 spike (S) protein and LPS, leading to aggravated inflammation in vitro and in vivo. Native gel electrophoresis demonstrated that SARS-CoV-2 S protein binds to LPS. Microscale thermophoresis yielded a KD of ∼47 nM for the interaction. Computational modeling and all-atom molecular dynamics simulations further substantiated the experimental results, identifying a main LPS-binding site in SARS-CoV-2 S protein. S protein, when combined with low levels of LPS, boosted nuclear factor-kappa B (NF-κB) activation in monocytic THP-1 cells and cytokine responses in human blood and peripheral blood mononuclear cells, respectively. The in vitro inflammatory response was further validated by employing NF-κB reporter mice and in vivo bioimaging. Dynamic light scattering, transmission electron microscopy, and LPS-FITC analyses demonstrated that S protein modulated the aggregation state of LPS, providing a molecular explanation for the observed boosting effect. Taken together, our results provide an interesting molecular link between excessive inflammation during infection with SARS-CoV-2 and comorbidities involving increased levels of bacterial endotoxins.

[justkidneying]

Fever

I see a lot of misconceptions about fever floating around the web, so I'm gonna try and set some things straight. We're gonna talk about what fever is, how it is caused, and types of fever. Then I'll give some writing tips. Just a note, with a lot of things, there are exceptions and special cases. I'm going to go over the most common stuff cause this isn't an immunology course.

What is a fever? The normal body temp (the average of a bunch of people) is 98.2°F. Individuals can differ from this within a degree. A fever is usually a temperature greater than 100°F. There's some leeway to this, and it takes a lot of experience to get a feel for what should be a normal temperature. But if someone comes into the office with a 100°F temp, I'm going to say that they have a fever.

So with fever (ignoring the symptoms of whatever caused it), you're generally going to have malaise, chills, paleness, and rigors (muscle contractions). There may also be behavioral symptoms such as seeking warmer environments, altered mental status, and assuming a fetal position to help warm the body. The peripheral vessels will constrict in order to keep blood in the central body. Once the fever has passed, there will be chills and sweating.

What causes fever? Fever is caused by pyrogens. These can be endogenous (from you) or exogenous (from something else). The main endogenous ones are interlueukin-1, interferon gamma, and tumor necrosis factor α. These are made by immune cells and a few other cell types. Exogenous pyrogens are made by other microorganisms. An example of this is lipopolysaccharide, which is made by gram-negative bacteria. Exogenous pyrogens induce the production of endogenous pyrogens, which induce the production of Prostaglandin E2. PGE2 acts on the hypothalamus to set the body's thermostat higher. This induces the effects seen in order to raise the body's temperature. Fever helps to stimulate the immune system and inhibits microorganism growth (too hot for them). So it's a good thing, unless it gets too high and your organs shut down and your brain melts like butter (i'm kidding...but really, it's bad). I'd say over 110°F and you're probably going to die.

What are the patterns of fever? There are three fever patterns, and they are associated with different pathologies. They are sustained, intermittent, and remittent fever. Sustained fevers are exactly what they sound like. They don't fluctuate more than a degree in a day and never touch normal baseline temp. These are typically seen with pneumonia, typhoid, bacterial meningitis, and UTI.

Intermittent fever is a fever that is only present for a few times throughout the day, with the temp going up above normal and back down to normal. This is seen with malaria, septicemia (a serious bacterial infection -> think septic shock), pyogenic infections (bacteria that cause pus formation), and TB.

Remittent fever fluctuates more than two degrees throughout the day, but does not ever touch normal baseline temps. These are seen with infectious diseases.

These patterns are okayish, but sometimes people don't always have a disease that matches the fever type. I think typhoid, TB, and tick-borne diseases (they cause a relapsing fever) are the best diseases to use fever patterns for.

Writing Tips

Okay, so first off I think fever is great for writing. So to find out what's going to happen, you need to pick out what the nature of the illness is. The most common one I see is infection from a wound of some kind. So this is going to be bacterial. I would say that you are most likely to have an infection with staph, strep, or pseudomonas. These are naturally found on the body, but are not meant to be inside you. A cut in your skin lets them in. This is bad. So your immune system will notice them and release pyrogens, and then you get PGE2, and then you get fever.

I would probably say you'd get the standard symptoms above, plus pain, swelling, and redness at the site of the infection. It's going to be an intermittent fever probably (could end up as remittent). So you would want to treat the infection itself. If there are no antibiotics or antipyretics (anti fever drugs), then you would have to clean and disinfect the wound, and basically hope that the immune system can do its thing. You can wipe the person down or use a cool compress on them, but this doesn't really reduce fever that much and is more of just a temporary relief.

Anyways, I hope this was helpful and as always, sources are in the comments. You can let me know if you have a specific situation you would want some info on in the comments/askbox/DM.

[tapwater118]

Which lps would book be

which LipoPolySaccharide would book be? its been a bit since ive touched up on my bacterial biology, but i’d probably say the bis-phosphorylated β-1-6 glucosamine disaccharides associated with enterobacteriacea

[darkmaga-returns]

From 1 January 2025, Chris H Boshoff will take over as Pfizer's new chief scientific officer. Previously he led its Cancer Research and Marketing.

GeoffPainPhD

Nov 20, 2024

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Very interesting appointment given Pfizer market strategy to exploit his knowledge of Bird diseases and Respiratory Syncytia.

In 1992 he was funded by the Goverment of South Africa and proved that Endotoxin causes spontaneous fusion between Myeloma cells and Splenocytes from Mice immunized with formalin-inactivated Haemophilus paragallinarum cells.12

See related posts on the hazards of Cell Fusion3 4 caused by Endotoxin.56

Multiple Myeloma is of great interest to Pfizer.7

I will add other relevant publications by Boshoff later, but thought you should know.

1

C H Boshoff, L Coetzee, L Visser, J A Verschoor. 1992. Spontaneous hybridoma formation induced by immunization with Haemophilus paragallinarum: evidence for a lipopolysaccharide fusion inducer. https://www.liebertpub.com/doi/10.1089/hyb.1992.11.257

2

3

Pneumonia caused by Wuhan Covid19 involved Syncytia

[worldbuilding-tomfoolery]

my toxic trait is the lipopolysaccharides embedded in my cell wall

[theolddivorcedzukka]

name a more annoying power couple than peptidoglycans and lipopolysaccharides. peptidoglycans are responsible for disease symptoms and lipopolysaccharides resist the entry of some antibiotics. god forbid anyone mess with its queen

[spacedlexi]

Problem is for people in the bacteria fandom LPS is lipopolysaccharide or endotoxin

how will we ever avoid confusion now??

[netpen-info]

[ad_1] To summarize: something ending in “-ose”, in addition to “syrups” and “sweeteners” are virtually at all times sugar.Indicators you're consuming an excessive amount of sugarWith all this sneakiness, it may be robust to acknowledge that your sugar consumption is getting out of hand. We put this query to Dr. Lela Ahlemann, a specialist in dermatology, phlebology, proctology, and dietary drugs. Listed here are the doable warning indicators you're consuming an excessive amount of sugar.1. Weight achieve and fixed starvationIt is no secret that sugar has quite a lot of energy. However there may be another excuse why sugar makes us achieve weight so shortly: “Should you eat an excessive amount of sugar, you're continuously hungry,” says Ahlemann. “The explanation for that is that sugar drives up blood glucose ranges within the quick time period, however has no lasting satiating impact because of the lack of fiber. The persistent starvation and the ensuing continued consuming finally result in weight achieve, which we're all conscious of as an indication of an excessive amount of sugar.”2. Zits“After we eat sugar, not solely does the insulin stage rise, but in addition a hormone within the blood known as insulin-like progress issue 1, or IGF-1 for brief,” says Ahlemann. “Along with insulin, this IGF-1 stimulates the sebaceous glands and extreme keratinization within the space of the sebaceous glands, which is why they develop into clogged resulting in pimples and irritation.”3. Cravings and temper swings“The excessive improve in glucose ranges within the blood results in an insulin launch —however that is usually so robust that the blood sugar is just not lowered to the conventional stage, however under the ‘baseline’, so that you've got a relative hypoglycemia, and this results in cravings. In some individuals, it additionally results in temper swings and crankiness,” says Ahlemann.4. Irritation and weak immune system“Usually, sugar is absorbed by the physique through the small gut. Nonetheless, if the quantity of easy sugars akin to glucose and fructose that we eat exceeds the capability of our small gut, this easy sugar results in the big gut,” explains Ahlemann.Based on the diet skilled, it turns into meals for micro organism that belong within the massive gut: “Selective feeding results in a proliferation of those micro organism. The issue is that, sadly, they carry endotoxins on their bacterial floor. These are so-called lipopolysaccharides. These endotoxins can then go away the intestine, enter the bloodstream and result in silent irritation, which accelerates the growing old of the physique, and weakens the immune system.”5. Accelerated growing old“It's scientifically confirmed that the excessive consumption of sugars results in the formation of so-called AGEs or Superior Glycation Finish Merchandise,” Ahlemann explains. She compares the impact to caramelization: “In our collagen, the fibers ought to ideally run in parallel; when the tissue is saccharified, there are cross-links within the collagen connective tissue, which makes it stiff, brittle, simpler to degenerate and—very importantly—the physique can be much less in a position to restore itself. Which means the standard of our collagen deteriorates.” [ad_2]

[cailynnjohnson]

How Complement System Enhances Antibodies to Regulate Immune Responses?

The complement system, or complement cascade, is regarded as a portion of the innate immune system and may appear 6-7 million years earlier than adaptive immunity. Recent studies have shown that the complement system can get involved in the communication of multiple cells and regulating immune responses, working as a bridge between the innate and adaptive immune responses.

Main Tasks of the Complement System

The complement system plays an important role not only in defending infection but also in the development of autoimmune diseases. The core function of the complement system is to lyse cells, bacteria, and viruses, as well as to initiate phagocytosis by opsonization. What’s more, it exerts influence in triggering inflammation by engaging with immune system cells.

To be straightforward, the complement system is expected to take these functions:

Mark the invading pathogens by opsonin that promotes phagocytosis.

Enhance the generation of inflammatory signaling agents (e.g. histamine) and capillary permeability to attract macrophages and neutrophils.

Attack and rupture the wall of pathogens with membrane attack complex (MAC).

How Does the Complement System Work?

The complement system consists of a variety of proteins and protein fragments that are synthesized by the liver and circulate in the blood as inactive precursors (known as zymogens). Zymogens need to cleavage and become active enzymes for cytolytic and bactericidal activity.

The activation of the complement system may be triggered by antigen-antibody complex, lipopolysaccharide, mannosans, peptidoglycan, etc. Stimulated proteases in the system will cleave specific proteins to release cytokines, further inducing an amplifying cascade of cleavages.

There are three different pathways involved in the activation of the complement system.

Classical pathway is initiated by the combination of C1q and the classical pathway activator (antigen-antibody complex). And later sequential classic complement activation will form a membrane attack complex (MAC), making the target cell swell and rupture to death because the osmotic pressure cannot be maintained.

Alternative pathway starts from the component C3b binding to factor B. It’s independent of the immune response and exerts an important anti-infective effect in the early stage of bacterial infection when no specific antibodies are produced.

Lectin complement pathway is activated when mannose-binding lectin (MBL) or ficolin binds to the mannose residues of pathogens based on the pathogen-associated molecular patterns (PAMPs). Similar to the classical pathway, it will later form MAC for opsonization, phagocytosis, and lysis of target microorganisms.

Complement System Research and Development

Studies show that though the complement system takes a key part in defense against pathogens and host homeostasis, the possible unfavorable results cannot be overlooked. When the complement system is regulating immune responses with specific signals, excessive or insufficient activation of the system may cause damages to healthy host cells or tissues.

As for the double-edged functions of the complement system, more and more complement therapeutics are developed, including serine protease inhibitors, soluble complement regulators, therapeutic antibodies, complement component inhibitors, and anaphylatoxin receptor antagonists.

Meanwhile, many life science solution providers get into complement antibody development, serine protease inhibitors development, complement-directed drug discovery, commercial complement product manufacturing, etc. in response to complement research.

Up to now, the complement therapeutic research has been undergoing a highly successful and inspiring period, and numerous complement-based drugs are discovered to treat diseases such as autoimmune disease, nephropathy, osteology, genetic disease, infection, neurology, inflammatory disease, ophthalmology, and cardiovascular disease.

[rnomics]

Foods, Vol. 13, Pages 2592: Association between Gut Microbiota Profiles, Dietary Intake, and Inflammatory Markers in Overweight and Obese Women

Being overweight and obesity are significant global public health challenges due to their association with adipose tissue dysfunction, pro-inflammatory marker production, and alterations in gut microbiota composition. To explore the relationship between gut microbiota, dietary factors, and inflammatory markers in overweight or obese women, we conducted a cross-sectional study involving a healthy group (n = 20) and an overweight or obese group (n = 75). We collected data, including clinical, anthropometric, and dietary assessments, and carried out a blood biochemical analysis, the measurement of inflammatory biomarkers (hs-CRP, IL-6, and TNF-α), and the 16S #rRNA gene sequencing of fecal samples. The gut microbiota analysis revealed notable differences in alpha and beta diversity between the two groups. Moreover, the abundance of gut microbiota in the overweight or obese group correlated positively with adiposity markers, blood pressure, lipid profiles, and inflammatory markers. These findings highlight significant changes in gut microbiota associated with obesity, potentially implicating pathways such as lipopolysaccharide biosynthesis. Understanding the role of the gut microbiome in obesity could reveal specific avenues for intervention. https://www.mdpi.com/2304-8158/13/16/2592?utm_source=dlvr.it&utm_medium=tumblr

[moleculardepot]

Hsp90 Polyclonal Antibody

Hsp90 Polyclonal Antibody Catalog number: B2017227 Lot number: Batch Dependent Expiration Date: Batch dependent Amount: 500 µl Molecular Weight or Concentration: N/A Supplied as: Solution Applications: a molecular tool for various biochemical applications Storage: -20°C Keywords: Heat Shock 84 kDa, Hsp84, Hsp86, Heat Shock Protein 90, LAP-2, Lipopolysaccharide-associated Protein 2, LPS-associated…

[darkmaga-returns]

Mostly called Lipopolysaccharide Binding Protein, it is increased in the blood of Astronauts, people infected with Covid19 or on the wrong diet.

GeoffPainPhD

Oct 15, 2024

I have mentioned Lipopolysaccharide Binding Protein (LPB) in various articles but think we should change its name to align with the Therapeutic Goods Administration and all jab regulatory bodies around the world who report that they have conducted Endotoxin tests on all released batches or accepted certificates from other countries accredited testing labs. But for now, let’s look at some exciting recent discoveries.

Astronauts suffer from elevated LBP

I was interested to find an article1 where US Space Shuttle and the International Space Station Astronauts were followed after their space voyage with a focus on their circulating LBP.

The abstract states:

This study investigated the ability of the shuttle crew members’ monocytes to respond to gram-negative endotoxin that they could encounter during infections. Blood specimens were collected from 20 crew members and 15 control subjects 10 days before launch, 3 to 4 h after landing, and 15 days after landing and from crew members during their annual medical examination at 6 to 12 months after landing.

An earlier US study of 27 Astronauts found Cytokine disruption.2

Similar studes of Russian Space Station crew and those in a simulator also found disruption of Cytokines.34

Here is what Mouse LPB looks like when its crystal structure is determined and called a conserved two-domain “boomerang” structure,.5