#oxidation reduction potential

[electronalytics]

Oxidation-Reduction Potential Sensor Market

[sofiyalabtronus]

Pocket ORP (Oxidation-Reduction Potential) tester

A Pocket ORP (Oxidation-Reduction Potential) tester is a portable device used to measure the ORP of a solution. ORP is a measure of the ability of a solution to act as an oxidizing or reducing agent. In practical terms, it indicates the potential for electron transfer in a chemical reaction.The device has electrode that is immersed in the solution being tested.When the electrode comes into contact with the solution, it generates a voltage that is proportional to the ORP of the solution. The device then converts this voltage into a numerical ORP value. The ORP value is usually displayed on a digital screen.Connector-BNC;ORP measurement range(-999) to 999 mV;ORP accuracy-± 2 mV;ORP calibration points-1 point (only for relative mV mode) for more visit labtron

[whats-in-a-sentence]

The standard reduction potentials in table 12.1 would predict that acids (represented by H+(aq) or H3O+) can oxidise certain metals, such as Fe, Zn, Sn and Mg (see figure 12.17), but not other metals, such as Ag, Cu and Au.

"Chemistry" 2e - Blackman, A., Bottle, S., Schmid, S., Mocerino, M., Wille, U.

[selfcaredoc]

Nikken PiMag Waterfall the Best Water Filtration System?

Stay Calm and Drink Better Water

In this week’s The Impetus, Dr. Gary Lindner explores what is needed in a water filtration system. Find out if the Nikken PiMag Waterfall checks all of the boxes. If you like this video please hit the Like button and Subscribe.

Be Healthy By Choice

[covid-safer-hotties]

Also preserved in our archive (Daily updates!)

Published Sept 3, 2024

By Chuck Dinerstein, MD, MBA

New research reveals that fibrin, a key component of blood clots, may be the secret culprit behind the devastating neurological and inflammatory aftermath of the virus, including long COVID. From dense, stubborn clots to brain fog, the interaction of COVID’s spike protein with fibrin could be the missing link — and a potential target for life-saving therapies.

Coagulopathy, the formation of small blood clots that go on to wreck respiratory and neurologic havoc, has long been a clinical hallmark of COVID, and now it's oft-ignored Long COVID. A new study suggests that fibrin, a key component of blood clots, plays a role.

Fibrin provides structure to a blood clot and is derived from fibrinogen, a soluble blood protein when the coagulation cascade is activated. If you think of a blood clot as nature’s way of plugging a leak, fibrin deposition is frequently found where there is damage to the walls of blood vessels and the vessels making up the blood-brain barrier. Fibrin serves as a plug and a signal for a greater inflammatory and immune response.

Given the unique clinical presentation of clotting in COVID compared to other respiratory viruses, the researchers hypothesized that COVID directly binds to fibrinogen, promoting blood clot formation and altering clot structure and function. They found that the spike protein of the virus binds to fibrinogen and fibrin at specific binding sites, suggesting that the virus might contribute to abnormal clotting by interacting with fibrinogen.

They found that the spike protein altered the structure of clots, making them denser and more resistant to the body’s natural means of removing clots, a process called fibrinolysis. Additionally, the spike protein enhanced the inflammatory signals from fibrin, increasing oxidative forces (reactive oxygen species or ROS) released from macrophages, a first responder of the immune system.

In converting fibrinogen to fibrin, the spike's binding site (epitope) is exposed. Therapeutically, having identified binding regions, the research found that antibodies could disrupt and reduce these pro-inflammatory effects implicated in acute and long COVID. Among the inflammatory effects reduced by blocking the actions of fibrinogen was the deposition of collagen in the lungs, which creates a barrier to oxygen passage and helps to explain the refractory response to supplemental oxygen we have seen in patients.

Fibrin also suppresses natural killer (NK) cells, which are called "natural killers" because they can recognize and kill stressed cells without prior exposure to a particular pathogen, making them critical first responders. The suppression of NK cell activity results in enhancing viral persistence and lung inflammation.

In additional studies in mice, the researchers found that this fibrin-dependent inflammatory response occurs independently of the active virus, suggesting a potential mechanism for persistent symptoms in Long COVID. [1] Therapeutically, in their mouse model, the use of a monoclonal antibody targeting the fibrin epitope, in addition to reducing the lung’s inflammatory response, reduced neuroinflammation (associated with long COVID’s brain fog). There were reductions in fibrin deposition and microglial reactivity “leading to improved neuronal survival and reduced white-matter injury.” Microglia are the primary immune cells of the central nervous system.

To summarize:

Coagulopathy in COVID-19 is a primary driver of thrombo-inflammation and neuropathology rather than a consequence of systemic inflammation. Fibrin plays a causal immunomodulatory role in promoting hyperinflammation, neuropathological alterations, and increased viral load in COVID-19 by modulating NK cells, macrophages, and microglia. Elevated fibrinogen levels and BBB permeability in COVID-19 contribute to neuropathology, and targeting fibrin may offer a dual mechanism of action by inhibiting fibrin-spike interactions and exerting anti-inflammatory effects. A fibrin-targeting antibody effectively blocks many pathological effects of fibrin, providing neuroprotection and reducing thrombo-inflammation. Their findings have limitations, including how they measured changes in brain tissue, the use of mouse models, and the fact that our inflammatory response may have more than one pathway that results in COVID-19’s deleterious effects. For Long COVID, the fibrin-targeted antibody does not interfere with normal clotting, acting solely on fibrin's inflammatory responses, making it a candidate to protect against pulmonary and cognitive impairment; that will, of course, require clinical trials.

And there you have it—the silent saboteur behind the lingering specter of Long COVID. Fibrin is not just a bystander in the aftermath of COVID-19; it's a key player driving the chronic symptoms that continue to baffle patients and clinicians alike. The discovery that the virus’s spike protein meddles with fibrin, transforming it into a resilient, inflammatory force, opens a new frontier in the fight against the pandemic’s long tail. The research, though groundbreaking, is still in its early days, confined to animal models, and the complexities of human biology could introduce new challenges.

But if the science holds, targeting fibrin could offer a two-for-one punch against the clotting and inflammation that underpin much of the damage COVID-19 leaves in its wake. For the millions grappling with the enduring effects of Long COVID, this could be a glimmer of hope—a chance to reclaim their lives.

[1] The inquisitive with a conspiratorial bent might link these inflammatory responses in the absence of infection to deaths felt to be due to the COVID vaccines, which employ the spike as antigenic stimulus. The researchers note that most hematologic changes are triggered by the vaccine vector (an adenovirus) and that “COVID-19 RNA vaccines lead to small amounts of spike protein accumulating locally and within draining lymph nodes where the immune response is initiated, and the protein is eliminated.”

Source: Fibrin drives thrombo-inflammation and neuropathology in COVID-19 Nature DOI: 10.1038/s41586-024-07873-4 www.nature.com/articles/s41586-024-07873-4

[quietus-system]

Vanadyl(IV) sulfate describes a collection of inorganic compounds of vanadium with the formula, VOSO4(H2O)x where 0 ≤ x ≤ 6. The pentahydrate is common. This hygroscopic blue solid is one of the most common sources of vanadium in the laboratory, reflecting its high stability. It features the vanadyl ion, VO2+, which has been called the "most stable diatomic ion".[1]

Vanadyl sulfate is an intermediate in the extraction of vanadium from petroleum residues, one commercial source of vanadium.[2] Synthesis, structure, and reactions

Vanadyl sulfate is most commonly obtained by reduction of vanadium pentoxide with sulfur dioxide:V2O5 + 7 H2O + SO2 + H2SO4 → 2 [V(O)(H2O)4]SO4

From aqueous solution, the salt crystallizes as the pentahydrate, the fifth water is not bound to the metal in the solid. Viewed as a coordination complex, the ion is octahedral, with oxo, four equatorial water ligands, and a monodentate sulfate.[1][3] The trihydrate has also been examined by crystallography.[4] A hexahydrate exists below 13.6 °C (286.8 K).[5] Two polymorphs of anhydrous VOSO4 are known.[6]

The V=O bond distance is 160 pm, about 50 pm shorter than the V–OH2 bonds. In solution, the sulfate ion dissociates rapidly.

Being widely available, vanadyl sulfate is a common precursor to other vanadyl derivatives, such as vanadyl acetylacetonate:[7][V(O)(H2O)4]SO4 + 2 C5H8O2 + Na2CO3 → [V(O)(C5H7O2)2] + Na2SO4 + 5 H2O + CO2

In acidic solution, oxidation of vanadyl sulfate gives yellow-coloured vanadyl(V) derivatives. Reduction, e.g. by zinc, gives vanadium(III) and vanadium(II) derivatives, which are characteristically green and violet, respectively. Occurrence in nature

Like most water-soluble sulfates, vanadyl sulfate is only rarely found in nature. Anhydrous form is pauflerite,[8] a mineral of fumarolic origin. Hydrated forms, also rare, include hexahydrate (stanleyite), pentahydrates (minasragrite, orthominasragrite,[9] and anorthominasragrite) and trihydrate - bobjonesite.[10] Medical research

Vanadyl sulfate is a component of food supplements and experimental drugs. Vanadyl sulfate exhibits insulin-like effects.[11]

Vanadyl sulfate has been extensively studied in the field of diabetes research as a potential means of increasing insulin sensitivity. No evidence indicates that oral vanadium supplementation improves glycaemic control.[12][13] Treatment with vanadium often results in gastrointestinal side-effects, primarily diarrhea.

Vanadyl sulfate is also marketed as a health supplement, often for bodybuilding. Deficiencies in vanadium result in reduced growth in rats.[14] Its effectiveness for bodybuilding has not been proven; some evidence suggests that athletes who take it are merely experiencing a placebo effect.[15]

Are you telling me these ions have a dissociative disorder

[materialsscienceandengineering]

Adding nitrogen to concrete could significantly reduce global levels of potentially harmful nitrogen oxides (NOx) created by the construction industry in developing towns and cities, a new study reveals. Researchers believe that concrete nitrogenation could contribute to a reduction in NOx emissions by 3.4-6.9 megatonnes (Mt) -- representing 6-13% of industry-related emissions in 2021. By 2050 the process could reduce NOx by a total of 131-384 Mt. It could represent the equivalent to 75-260 years potentially lost to premature death and reduced quality of life, estimated in terms of disability-adjusted life years (DALY). NOx are highly reactive toxic air pollutants which can contribute to acid rain, ozone layer depletion and pose significant health threats -- particularly in relation to respiratory disease -- contributing to air pollution-related mortality.

Read more.

[aressida]

Wrote a long one cos the in law family wanted him to take the flu shot, I said no.

"Dear Family, Friends, and Medical Professionals,

I am writing to share some thoughts and questions about vaccines, particularly in light of recent developments.

Do we believe that vaccines are the ultimate solution in medicine?

It is commonly known that influenza vaccines are reformulated each season due to the virus’s constant mutation, making it challenging to predict and protect against new strains accurately.

Is it true that these vaccines bypass the liver’s natural filtration system, potentially causing a shock to our bodies?

How should we classify these ingredients—as toxic or benign?

Here are just some vaccine ingredients, and these are being injected into your body and into your children’s bodies if you choose to vaccinate:

– Formaldehyde/Formalin – Highly toxic systemic poison and carcinogen.

– Betapropiolactone – Toxic chemical and carcinogen. May cause death or permanent injury after very short exposure to small quantities. Corrosive chemical.

– Hexadecyltrimethylammonium bromide – May cause damage to the liver, cardiovascular system, and central nervous system. May cause reproductive effects and birth defects.

– Aluminum hydroxide, aluminum phosphate, and aluminum salts – Neurotoxin. Carries risk for long-term brain inflammation/swelling, neurological disorders, autoimmune disease, Alzheimer’s, dementia, and autism. It penetrates the brain where it persists indefinitely.

– Thimerosal (mercury) – Neurotoxin. Induces cellular damage, reduces oxidation-reduction activity, cellular degeneration, and cell death. Linked to neurological disorders, Alzheimer’s, dementia, and autism.

– Polysorbate 80 & 20 – Trespasses the blood-brain barrier and carries with it aluminum, thimerosal, and viruses; allowing them to enter the brain.

– Glutaraldehyde – Toxic chemical used as a disinfectant for heat-sensitive medical equipment.

– Fetal Bovine Serum – Harvested from bovine (cow) fetuses taken from pregnant cows before slaughter.

– Human Diploid Fibroblast Cells – Aborted fetal cells. Foreign DNA has the ability to interact with our own.

– African Green Monkey Kidney Cells – Can carry the SV-40 cancer-causing virus that has already tainted about 30 million Americans.

– Acetone – Can cause kidney, liver, and nerve damage.

– E. Coli – Yes, you read that right.

– DNA from porcine (pig) Circovirus type-1

– Human embryonic lung cell cultures (from aborted fetuses)

You can view all of these ingredients on the CDC’s website. I encourage everyone to do their own research. Look up the MSDS on these chemicals. Read the thousands of peer-reviewed studies that have evaluated the biological consequences these chemicals can have on the body, especially when being injected.

Injecting foreign substances directly into the bloodstream—viruses, toxins, and proteins—has been linked to various diseases and disorders. These include conditions like atypical measles, cancer, leukemia, multiple sclerosis, and even SIDS (Sudden Infant Death Syndrome).

Conditions like Addison’s disease, anaphylactic shock, arthritis, asthma, asymptomatic COVID-19, Crohn’s disease, epilepsy, facial paralysis, fibromyalgia, fetal distress syndrome, foreign body embolism, genital herpes, hepatitis, hyperthyroidism, inflammatory bowel disease, jugular vein embolism, lung abscess, lupus, meningitis, MERS-CoV test positive, migraine-triggered seizures, multiple organ dysfunction syndrome, multiple sclerosis, multisystem inflammatory syndrome in children, pneumonia, stiff leg syndrome, stiff person syndrome, stillbirth, sudden heart attack, sudden respiratory failure, type 1 diabetes, uterine rupture, viral bronchitis—and much more.

This does not mean everyone will experience these reactions, but a significant number of test subjects have experienced one or more.

It is more than enough evidence to show that vaccine mandates are completely anti-scientific.

How can you make an informed decision if you do not have all the information?

We have also seen a shift where flu vaccines are now mRNA-based. But does a "vaccine" really prevent a virus or its recurrence as we expect it to?

The annual flu shot is, at best, a partial defense, aimed at last year’s strain. Does it truly help against the ever-mutating new flu, or is it just a temporary fix?

My concern is that this mindset—that a vaccine is a quick fix for everything—is flawed. The immune system may struggle to handle these types of agents, leading to breakthrough infections and potentially higher mortality rates.

For those who are vaccinated, I respect your choice. I simply ask for the same respect in return for my decision not to vaccinate. My reasons are personal and grounded in a belief that the government should not dictate my health choices and my family's.

Have you heard about Pfizer’s side effects?

Have you read the Pfizer documentation? Ask yourself if a drug with 32 pages of side effects is right for you.

The list of potential vaccine side effects released by Pfizer is alarming, ranging from autoimmune disorders to serious conditions like multiple organ dysfunction and sudden respiratory failure. Yet, this information was kept under wraps and only recently made public. Shouldn’t we be informed of the risks?

Do we even know the medium- or long-term effects of these vaccines?

Are they still in clinical trials? Is there a control group? What about Antibody-Dependent Enhancement (ADE) – has it been adequately tested? And why are ingredients like formaldehyde and mercury, known toxins, included in these vaccines?

Do you truly think this vaccine is 100% safe?

Transparency is crucial.

How can we make informed decisions if we are not given all the information?

We must ask ourselves, do we trust the pharmaceutical companies and their relationships with organizations like the CDC and FDA?

The FDA requested 75 years to release data on the Pfizer vaccine—why? Why did it take only 108 days to approve this vaccine, yet it supposedly requires decades to fully understand its effects?

Do you believe that SARS-CoV-2 has been isolated?

How well-informed are you about the CDC, FDA, pharmaceutical companies, and their donors? Do you think their qualifications are reliable?

These are important questions that deserve honest discussions. And, I believe it is crucial to acknowledge the existence of these alternative perspectives and engage in open discussions to gain a more comprehensive understanding.

Our health and freedom are at stake, and I urge everyone to think critically and seek out all the information before making decisions.

Thank you for taking the time to consider these points."

[rjzimmerman]

As a native of Gary, Indiana, and a former "summer employee" at U.S. Steel (to pay for my college education), I'm obviously invested in what happens to the Gary Works of U.S. Steel. This story answers several of my questions, and puts me on the "no" side of this proposal. Excerpt from this story from Grist:

U.S. Steel, once the world’s largest company of any kind, can take substantial credit for the growth of American industrial power in the 20th century. But in recent decades, it’s been shuttering mills and shedding workers. Now, the iconic Pittsburgh-based manufacturer is set to be acquired by a Japanese steelmaker, Nippon Steel — if the federal government allows the deal to proceed.

Earlier this month, reports emerged that the Biden administration is preparing to block the nearly $15 billion merger on the grounds that it presents a threat to America’s national security interests. The United Steelworkers union opposes it, fearing future layoffs and weaker labor protections under new ownership. So do both major candidates for president, who are vying for votes in the Rust Belt. Supporters of the deal, like the Washington Post editorial board and the nonpartisan think tank The Atlantic Council, have cast the politicians’ opposition as election-season pandering, and argued that the national security rationale on which Biden may block it is flimsy. But one area, in which the question of whether the merger goes through could be particularly consequential, has gone largely unremarked upon in the conversation: what it means for the climate.

Some environmentalists say the deal could slow the crucial progress that the steel industry must make in order to decarbonize. Their argument stems from the fact that both U.S. Steel and Nippon Steel have been slow, compared to industry peers, to adopt the most impactful decarbonization technologies, even with federal funding available in the U.S. to do so.

The most common process by which primary steel is produced is massively carbon-intensive. The reasons for this lie in chemistry. Steel is made from iron, but the form in which iron ore occurs in the Earth’s crust is mostly iron oxide (similar to rust). In order to get usable iron from it, one needs to remove the oxygen. For centuries, iron-makers have accomplished this by using coke, a fuel made from coal, which is heated alongside iron ore in a blast furnace at such high temperatures that the iron melts into a liquid while the oxygen bonds with the carbon in the coke and produces carbon dioxide.

Blast furnaces are responsible for the lion’s share of carbon emissions from steelmaking, and the inextricability of carbon emissions from the ironmaking process is a large part of the reason why, overall, steelmaking is responsible for 7 percent of global carbon emissions, and a quarter of industrial carbon emissions. These percentages will likely grow as other sectors of the economy are decarbonized. In the U.S., demand for steel is also expected to grow dramatically over the next decade to provide the raw material of the industrial growth sparked by the Inflation Reduction Act and the planned buildout of clean energy infrastructure and transmission lines. For these reasons, the task of decarbonizing steel is as urgent as it is difficult and expensive.

Fortunately, there is a solution on offer that has recently become viable due to new technological advances — and one that the Biden administration has sought to heavily subsidize: replacing blast furnaces with a process called direct reduction, and using hydrogen as a reducing agent in place of carbon, ultimately discharging water rather than carbon dioxide. “The chemistry is sound, it’s being built, it’s been piloted and demonstrated,” said Yong Kwon, a senior advisor with the Sierra Club’s Industrial Transformation Campaign. “The question is now: Will industries adopt it?”

There are eight operating steel mills in the United States that make “primary” steel (newly created steel, rather than the generally lower-quality “secondary” steel produced from scrap metal). Three are owned by U.S. Steel. Cleveland-Cliffs, the owner of the other five, has also made an offer to buy U.S. Steel and has been much more proactive in making the shift to greener production. “The Department of Energy has made available a great deal of money to do partnerships with industry to demonstrate the value of decarbonized projects,” said Todd Tucker, director of the industrial policy and trade program at the Roosevelt Institute. Both Cleveland-Cliffs and U.S. Steel have availed themselves of such funding to embark on decarbonization programs. U.S. Steel has partnered with the Department of Energy on carbon capture projects at several of their steel mills, and funded research and development of hydrogen-based ironmaking technology. The company also plans to install a carbon capture program at a blast furnace at its steel mill in Gary, Indiana, which it says will turn up to 50,000 metric tons of carbon dioxide annually into limestone — a tiny fraction of that facility’s overall emissions. But critics note that U.S. Steel has yet to take a step as ambitious as its rival by actually replacing one of its blast furnaces with direct reduction of iron.

The stakes of the potential U.S. Steel-Nippon Steel merger are perhaps best illustrated in the city of Gary, Indiana, which was built in 1906 by U.S. Steel to house workers at its Gary Works steel mill. That mill is home to the country’s largest and most carbon-emitting blast furnace — and it’s nearing the end of its lifespan. This situation hypothetically presents the furnace’s owner with an ideal opportunity to switch to a cleaner technology, with federal funding on the table to do so. But in August, Nippon Steel announced its prospective plans for Gary Works, which include a $300 million investment in relining the furnace to extend its lifespan for another 20 years. With this announcement, Kwon said, “Not only have they back in Japan not pursued solutions that we feel are responsible; they’ve now explicitly come out and said that they’re not going to pursue the solution that is on the table for reducing the climate change and public health harms that are currently produced by the iron-making process.”

[tomasorban]

Berries and cognitive function are closely related

and research has shown that consuming berries can have a positive impact on cognitive function, particularly in older adults. Here are some ways in which berries may benefit cognitive function:

Antioxidant properties: Berries are rich in antioxidants, which help protect the brain from oxidative stress and inflammation. This can lead to improved cognitive function and a reduced risk of age-related cognitive decline.

Neuroprotection: Berries contain various polyphenolic compounds, such as anthocyanins, flavonoids, and phenolic acids, which have been shown to have neuroprotective effects. These compounds may help protect against age-related neurodegenerative diseases, such as Alzheimer's and Parkinson's.

Inflammation reduction: Berries have anti-inflammatory properties, which can help reduce inflammation in the brain and potentially reduce the risk of cognitive decline.

Cognitive improvement: Studies have shown that consuming berries can improve cognitive function, including attention, memory, and processing speed. For example, a study published in the Journal of Agricultural and Food Chemistry found that consuming blueberry juice improved memory and cognitive function in older adults.

Neuroplasticity: Berries may also help promote neuroplasticity, which is the brain's ability to adapt and change in response to new experiences. This can lead to improved cognitive function and a reduced risk of age-related cognitive decline.

Some specific berries that may have a positive impact on cognitive function include:

Blueberries: Blueberries are one of the most well-studied berries when it comes to cognitive function. They are rich in anthocyanins, which have been shown to have neuroprotective effects.

Strawberries: Strawberries are another berry that has been shown to have a positive impact on cognitive function. They contain a variety of polyphenolic compounds, including ellagic acid, which has been shown to have anti-inflammatory effects.

Raspberries: Raspberries are a good source of antioxidants and may help protect against oxidative stress and inflammation in the brain.

Cranberries: Cranberries are a good source of flavonoids, which have been shown to have anti-inflammatory effects and may help protect against age-related cognitive decline.

Incorporating berries into your diet is a simple and delicious way to support cognitive function and overall health. Enjoy them as a snack, add them to your oatmeal or yogurt, or blend them into a smoothie.

more: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4192974/

[helen0086]

Progress in the Study of the Protective Effect and Mechanism of C-phycocyanin on Liver Injury

Abstract: C-phycocyanin (C-phycocyanin) is a pigment-containing protein from marine algae that has shown promising results in the treatment of many inflammatory diseases and tumors. C-alpha-cyanobilin is a pigment-containing protein from marine algae that has been shown to be effective in the treatment of various inflammatory diseases and tumors. C-alpha-cyanobilin has a protective effect on various liver diseases, such as drug-induced or toxic substance-induced liver damage, non-alcoholic fatty liver disease, hepatic fibrosis, and hepatic ischemia-reperfusion injury. The protective effect of C-alginin on liver injury is mainly realized through the regulation of signaling pathways such as nuclear factor (NF)-κB, phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) and AMP-dependent protein kinase (AMPK), and the inhibition of oxidative stress, etc., and is not toxic to normal cells. Therefore, C-alginin has a broad application prospect as a potential natural hepatoprotective marine active substance. In recent years, the research progress of the protective effect of C-alginin on liver injury and its mechanism is summarized.

 C-phycocyanin (C-phycocyanin) is a complex protein of cyanobacteria and a natural food protein pigment with pharmacological effects such as antioxidant, anti-inflammatory and anti-tumor effects, as well as fast-acting and low-toxicity, it can be used as a functional food [1-2]. C-Alginin can also enhance immunity and is safe, without causing acute and subacute toxic reactions [3]. Selenium-enriched PC has been shown to have stronger pharmacological effects [4]. Therefore, C-alginate has important research value both as a drug and a functional food, and has become a hot spot in the field of pharmaceutical research [5]. In this paper, we summarize the progress of research on the application and mechanism of C-alginin in liver diseases.

1 Ameliorative effect of C-phycocyanin on liver injury caused by drugs and toxic substances

The liver is the metabolic center of drugs and exogenous toxic substances, and metabolites are prone to liver injury. C-PC can inhibit the synthesis and release of inflammatory factors such as tumor necrosis factor (TNF)-α and interferon-γ, and increase the activities of catalase and superoxide dismutase (SOD), which can inhibit hepatic inflammation and alleviate hepatic injury [3]. It has been found that C-PC can significantly prevent thioacetamide-induced liver injury, significantly reduce the levels of alanine aminotransferase (ALT) and aliquot aminotransferase (AST), shorten the prothrombin time and reduce the hepatic histopathological damage, and improve the survival rate of rats with fulminant hepatic failure [6]. C-alginin also has a good effect on thioacetamide-induced hepatic encephalopathy, which can be seen in the reduction of tryptophan and lipid peroxidation indexes in different regions of the brain, and the enhancement of catalase and glutathione peroxidase activities in rats with fulminant hepatic failure [6].

Another study found that C-alginin not only attenuates the oxidative stress induced by 2-acetylaminofluorene and reduces the generation of reactive oxygen species (ROS) radicals, but also inhibits the phosphorylation of protein kinase B (Akt) and the nuclear translocation of nuclear factor (NF)-κB induced by 2-acetylaminofluorene, thus inhibiting the expression of multidrug resistance genes [7]. Osman et al. [8] also showed that C-alginin could normalize the levels of ALT, AST, catalase, urea, creatinine, SOD and glutathione-s-transferase in the livers of rats poisoned with carbon tetrachloride (CCl4). This result was also verified in human liver cell line (L02) [9]. C-phycocyanin can effectively scavenge ROS and inhibit CCl4-induced lipid peroxidation in rat liver [10], and C-PC can improve the antioxidant defense system and restore the structure of hepatocytes and hepatic enzymes in the liver of gibberellic acid-poisoned albino rats [11]. As a PC chromophore, phycocyanin can also significantly inhibit ROS generation and improve liver injury induced by a variety of drugs and toxic substances [10]. Liu et al. [12] found that phycocyanin showed strong anti-inflammatory effects in a CCl4-induced hepatic injury model in mice, which could significantly reduce the levels of ALT, AST, the expression of TNF-α and cytochrome C, increase the levels of albumin and SOD, and proliferate cytosolic nuclei. It can significantly reduce ALT and AST levels and the expression of TNF-α and cytochrome C, increase albumin levels and the expression of SOD and proliferating cell nuclear antigen, promote hepatocyte regeneration and improve the survival rate of mice with acute liver failure.

Gammoudi et al [13] used response surface method to optimize the extraction process of C-phycocyanin, and obtained high extraction recovery. C-phycocyanin extracted by the optimized method has the ability of scavenging hydroxyl, superoxide anion and nitric oxide radicals as well as the ability of metal chelating, and it has stronger antioxidant effect; C-PC significantly increased the activity of SOD and inhibited the increase of ALT, AST, and bilirubin in cadmium-poisoned rats. C-PC significantly increased the activity of SOD and inhibited the increase of ALT, AST and bilirubin in rats with cadmium poisoning. The above studies show that C-phycocyanin can effectively protect liver injury caused by drugs and toxic substances, and has the efficacy as the basis for drug development.

2 Preventive effect of C-alginin on hepatic fibrosis

Liver fibrosis is an inevitable process in the development of various chronic liver diseases and may be reversed with early and timely treatment. The key to liver fibrosis is the activation of hepatic stellate cells. Previous studies have found that low-dose C-alginin combined with soy isoflavones can inhibit hepatic stellate cell activation by inhibiting the activity of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase［14］, but it is not clear whether C-alginin alone can inhibit the activity of NADPH oxidase. Therefore, the combination of C-algin and soy isoflavones at appropriate doses may have a preventive effect on liver fibrosis in high-risk groups. C-alginin may inhibit the progression of NADPH by suppressing oxidative damage, thereby inhibiting the development of hepatic fibrosis [15].

Epithelial mesenchymal transition (EMT) is one of the key mechanisms contributing to the development of fibrotic diseases. C-alginin inhibits transforming growth factor β1 (TGF-β1)-induced human EMT [16]. Although the effect of C-alginin on EMT in hepatic fibrosis has not been reported, it has been found that C-alginin can reduce pulmonary fibrosis by inhibiting epithelial mesenchymal transition [17]. Another study found that C-alginin could reduce the expression of α-smooth muscle actin (α-SMA) and connective tissue growth factor (CTGF) mRNA in human dermal fibroblasts and alleviate fibrous contracture [18]. The results of these studies also have significance for the inhibition of hepatic fibrosis, and provide a theoretical basis for the further study of C-PC as a potential antifibrotic drug.

3 Protective effect of C-alginin on hepatic ischemia-reperfusion injury

Liver ischemia/reperfusion injury is an important clinicopathophysiological phenomenon. It was found that the addition of two different doses (0.1 g/L and 0.2 g/L) of C-alginin to the Krebs Henseleit preservation solution significantly decreased hepatic ALT, AST and alkaline phosphatase activities, and reduced the rate of lipid peroxidation and malondialdehyde content in an isolated perfused rat liver model, and increased the activities of hepatic glutathione-s-transferase and glutathione peroxidase, as well as sulfhydryl groups in hepatic tissue. On the other hand, it can increase the activities of hepatic glutathione-s-transferase and glutathione peroxidase and the content of sulfhydryl groups in liver tissues, therefore, C-alginin can significantly reduce hepatic ischemia/reperfusion injury as an antioxidant [19]. In isolated perfused mouse livers, it was found that C-alginin significantly reduced the phagocytosis and respiratory burst activity of hepatic macrophages (Kupffer cells), attenuated cytotoxicity and inflammation induced by highly active Kupffer cells, and dose-dependently inhibited carbon phagocytosis and carbon-induced oxygen uptake by perfused livers, and then inhibited the increase of hepatic nitric oxide synthase activity induced by gonadotropins [20]. and thus inhibit the thyroid hormone-induced elevation of hepatic nitric oxide synthase activity [20].

However, C-alginin has a very short half-life in vivo, which limits its application in vivo. It was found that the use of polyethylene glycol-b-(polyglutamic acid-g-polyethyleneimine), a macromolecular material with good drug-carrying capacity and slow-release properties, as a nanocarrier of C-alginin could solve this problem, and the release of C-alginin could be delayed by subcutaneous injection into the abdominal region of rats, which could attenuate islet damage caused by hepatic ischemia/reperfusion and enhance the function of the islets [21]. This study broadens the scope of application of C-alginin in vivo and improves the therapeutic effect of C-alginin.

4 Inhibitory effect of C-alginin on hepatocellular carcinoma

It was found that C-alginin significantly reduced the expression of matrix metalloproteinase (MMP)-2 and MMP-9 and the expression of tissue inhibitor of metalloproteinase 2 (TIMP2) mRNA in human hepatocellular carcinoma cells (HepG2 cells) [22]. C-alginin is a natural photosensitizer, and photodynamic therapy (PDT) mediated by alginin microcystin induced a large accumulation of ROS in HepG2 cells, which promoted mitochondrial damage and cytochrome C release, and led to apoptosis of hepatocellular carcinoma cells [23].

Liu et al. [24] used nanoscale C-alginate particles prepared by lactobionic acid grafting and adriamycin loading to enhance the growth inhibition of HepG2 cells when combined with chemo-PDT, and the C-alginate particles could effectively accumulate and diffuse in tumor multicellular spheres. In vitro and in vivo studies on the effects of selenium-enriched PCs on PDT in hepatocellular carcinoma showed that selenium-enriched PCs could migrate from lysosomes to mitochondria in a time-dependent manner, and that selenium-enriched PCs could induce the death of tumor cells through the generation of free radicals in vivo, increase the activities of antioxidant enzymes in vivo, induce mitochondria-mediated apoptosis, and inhibit autophagy, thus offering a relatively safe pathway to tumor treatment and showing new development perspectives [4]. It can provide a relatively safe way to treat tumors and shows a new development prospect [4].

Lin et al. [25] combined C-phycocyanin with single-walled carbon nanohorns and prepared phycocyanin-functionalized single-walled carbon nanohorn hybrids, which enhanced the photostability of C-phycocyanin and protected the single-walled carbon nanohorns from adsorption of plasma proteins, and synergistically used with PDT and photothermal therapy (PTT) to treat tumors. C-phycocyanin covalently coupled with biosilica and PDT or non-covalently coupled with indocyanine green and PTT on tumor-associated macrophages can also increase the apoptosis rate of tumor cells [26-27]. The development of PDT and PTT synergistic methods for the treatment of cancer has broadened the application of C-PC and enhanced its value in the treatment of hepatocellular carcinoma.

In addition, C-phycocyanin can inhibit the expression of multidrug-resistant genes in HepG2 cells through NF-κB and activated protein-1 (AP-1)-mediated pathways, and C-phycocyanin increases the accumulation of adriamycin in HepG2 cells in a dose-dependent manner, which results in a 5-fold increase in the susceptibility of cells to adriamycin [28]. Even in adriamycin-resistant HepG2 cells, C-PC induced the activation of apoptotic pathways such as cytochrome C and caspase-3 [29], and the results of Prabakaran et al. [30] also confirmed the inhibitory effect of C-PC on the proliferation of HepG2 cells, mediated by the inactivation of BCR-ABL signaling and the downstream PI3K/Akt pathway. mediated by BCR-ABL signaling and inactivation of downstream PI3K/Akt pathway. In addition, C-phycocyanin modifies the mitochondrial membrane potential and promotes apoptosis in cancer cells [30]. Currently, C-phycocyanin is a synergistic molecule with other drugs that have been widely used in the treatment of cancer [31]. The above studies demonstrate that C-phycocyanin has good therapeutic potential in the field of hepatocellular carcinoma.

5 Amelioration of metabolic syndrome and non-alcoholic fatty liver disease by C-phycocyanin

It has been found that C-alginin can reduce ALT and AST levels, decrease ROS production and NF-κB activation, and attenuate hepatic fibrosis in rats induced by high-fat choline-deficient diets, and thus C-alginin has a protective effect on NAFLD rats through anti-inflammatory and antioxidant mechanisms [15].

Another study on the effects of aqueous extract of Spirulina (mainly C-alginin) on NAFLD induced by a high-calorie/high-fat Western diet in C57Bl/6J mice showed that aqueous extract of Spirulina significantly improved glucose tolerance, lowered plasma cholesterol, and increased ursodeoxycholic acid in bile in mice [32]. Kaspi-Chadli et al. Kasbi-Chadli et al. [33] showed that aqueous extract of Spirulina could reduce cholesterol and sphingolipid levels in the liver and aortic cholesterol levels in hamsters fed a high-fat diet by significantly decreasing the expression of hydroxy-3-methylglutaryl-coenzyme A reductase (HMG CoA) gene, a limiting enzyme for cholesterol synthesis, and TGF-β1 gene, and that ursodeoxycholic acid levels in the feces of hamsters fed high-fat diets were increased in the high Spirulina aqueous extract treatment group.

A daily dose of C-alginin-enriched Spirulina can reduce the harmful effects of oxidative stress induced by a diet rich in lipid peroxides [34]. Ma et al. [35] found that C-alginin promoted the phosphorylation of hepatocyte AMP-dependent protein kinase (AMPK) in vivo and ex vivo, and increased the phosphorylation of acetyl coenzyme A carboxylase. In the treatment of NAFLD in mice, C-alginin can improve liver inflammation by up-regulating the expression of phosphorylated AMPK and AMPK-regulated transcription factor peroxisome proliferator-activated receptor α (PPAR-α) and its target gene, CPT1, and by down-regulating the expression of pro-inflammatory factors such as TNF-α and CD36 [35]. This suggests that C-phycocyanin can also improve lipid deposition in the liver through the AMPK pathway.

Endothelial dysfunction is associated with hypertension, atherosclerosis and metabolic syndrome. Studies in animal models of spontaneous hypertension have shown that long-term administration of C-alginin may improve systemic blood pressure in rats by increasing aortic endothelial nitric oxide synthase levels, with a dose-dependent decrease in blood pressure, and thus C-alginin may be useful in preventing endothelial dysfunction-related diseases in the metabolic syndrome [36]. In the offspring of ApoE-deficient mice fed C-alginate during gestation and lactation, male littermates had an elevated hepatic reduced/oxidized glutathione ratio and significantly lower hepatic SOD and glutathione peroxidase gene expression.

C-PC is effective in preventing atherosclerosis in adult hereditary hypercholesterolemic mice [37]. In vitro, C-phycocyanin also improved glucose production and expression of phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G-6-Pase) in high-glucose-induced insulin-resistant HepG2 cells [38]. C-alginin also increases glucose uptake in high glucose-induced insulin-resistant HepG2 cells through the insulin receptor substrate (IRS)/PI3K/Akt and Sirtuin-1 (SIRT1)/liver kinase B1 (LKB1)/AMPK signaling pathways, activates glycogen synthase, and increases the amount of glycogen [38]. C-phycocyanin can improve blood glucose and fasting serum insulin levels in tetracycline-induced diabetic mice [39]. Therefore, C-phycocyanin can maintain cellular glucose homeostasis by improving insulin resistance in hepatocytes.

6 Hepatoprotective role of C-phycocyanin in other liver diseases

Studies have shown that C-alginin can inhibit total serum cholesterol, triacylglycerol, LDL, ALT, AST, and malondialdehyde levels in mice modeled with alcoholic liver injury, significantly increase SOD levels in the liver, and promote the activation and proliferation of CD4+ T cells, which can have an ameliorative effect on alcoholic liver injury [40]. In addition, C-phycocyanin may enhance the intestinal barrier function, regulate the intestinal flora, reduce the translocation of bacteria and metabolites to the liver, and inhibit the activity of the Toll-like receptor 4 (TLR4)/NF-κB pathway, which may reduce the inflammation of the liver and prevent the occurrence of hepatic fibrosis in mice [41]. In mice with X-ray radiation-induced liver injury, C-phycocyanin can reduce radiation-induced DNA damage and oxidative stress injury by up-regulating the expression of nuclear factor (NF)-E2-related factor 2 (Nrf2) and downstream genes, such as HO-1, and play a hepatoprotective role by enhancing the activities of SOD and glutathione peroxidase [42].

7 Outlook

Liver fibrosis is the common final process of chronic liver diseases, and there is no effective therapeutic drug at present. Although some research progress has been made in the field of traditional Chinese medicine (TCM) on the reversal of liver fibrosis [43], its toxicological effects have not yet been clarified. Although the incidence of viral hepatitis has gradually decreased with the development and popularization of vaccines and antiviral drugs, the incidence of drug-induced liver injury (DILI) and liver diseases such as NAFLD has been increasing year by year with the improvement of people's living conditions [44]. Therefore, there is an urgent need to find drugs or nutrients that can help maintain normal hepatocyte function and effectively inhibit liver inflammation and fibrosis. C-alginin, with its anti-inflammatory, antioxidant, and antitumor effects, as well as good food coloring, has a wide range of applications in both the pharmaceutical and food industries.

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#phycocyanin #cphycocyanin #phycocyaninspirulina

[ppkamy]

Ashwagandha, an adaptogenic herb, has been used in Ayurvedic medicine for centuries. Vegan ashwagandha capsules offer a convenient and cruelty-free way to harness its potential benefits. Here are some of the advantages:

Stress and Anxiety Reduction:

* Ashwagandha helps reduce cortisol levels, the stress hormone, promoting relaxation and reducing anxiety.

* It can improve mood and overall mental well-being.

Enhanced Cognitive Function:

* Ashwagandha may improve memory, focus, and concentration.

* It can protect brain cells from oxidative stress.

Improved Sleep Quality:

* Ashwagandha can help regulate sleep patterns, leading to better sleep quality and reduced insomnia.

Boosted Immunity:

* Ashwagandha has immune-boosting properties, helping to strengthen the body's defense against infections.

Increased Energy Levels:

* By reducing stress and improving sleep, ashwagandha can indirectly boost energy levels.

Support for Hormonal Balance:

* Ashwagandha may help regulate hormones, particularly in women, and support thyroid function.

Anti-inflammatory Effects:

* Ashwagandha has anti-inflammatory properties that can help reduce inflammation in the body.

Potential Benefits for Athletes:

* Ashwagandha may improve athletic performance by reducing muscle damage and increasing strength.

Important Considerations:

* While ashwagandha is generally safe, it's essential to consult with a healthcare professional before starting any new supplement, especially if you have underlying health conditions or are taking medications.

* It's crucial to choose high-quality, vegan ashwagandha capsules from reputable brands to ensure purity and potency.

* While research on ashwagandha is promising, more studies are needed to fully understand its long-term effects and interactions with other medications.

By incorporating vegan ashwagandha capsules into your routine, you may experience a range of benefits, including reduced stress, improved cognitive function, and enhanced overall well-being.

[whats-in-a-sentence]

Table 12.1 lists values obtained for some typical half-reactions. (...) Table 12.1 shows that:

Substances located to the left of the double arrows are oxidising agents, because they become reduced when the reactions proceed in the forward direction.

The strongest oxidising agents are those most easily reduced, and they are located at the top left of the table (e.g. F2).

Substances located to the right of the double arrows are reducing agents; they become oxidised when the reactions proceed from right to left.

The strongest reducing agents are those found at the bottom right of the table (e.g. Li).

We can use the data in table 12.1 to show that we obtain the same spontaneous reaction regardless of how the cell diagram is written. (...) One of the goals of chemistry is to predict reactions. This can be done for redox reactions – whether they occur in a galvanic cell or just in a container with all the chemicals combined in one reaction mixture – using the half-reactions and standard reduction potentials in table 12.1. (...) The reactants and products of spontaneous redox reactions are easy to spot when reduction potentials are listed in order of most positive to least positive (most negative), as in table 12.1. (...) If you look at the location of lithium in the table of reduction potentials (table 12.1), you will see that it has the most negative reduction potential of any metal.

"Chemistry" 2e - Blackman, A., Bottle, S., Schmid, S., Mocerino, M., Wille, U.

[greenpeople]

Nature‘s OZEMPIC

Berberine exerts its effects through various mechanisms within the body, making it a versatile and powerful natural compound. Here’s a closer look at how berberine works:

Mechanism of Action at a Cellular Level

Berberine impacts several cellular processes, including:

AMPK Activation: Berberine activates AMP-activated protein kinase (AMPK), a key enzyme involved in regulating cellular energy metabolism. AMPK activation helps enhance glucose uptake, improve insulin sensitivity, and promote energy production.

Gene Expression Regulation: Berberine can influence gene expression, particularly those related to lipid metabolism and inflammation. This regulation plays a role in its therapeutic effects on metabolic disorders and inflammatory conditions.

Key Biochemical Pathways Affected by Berberine

Berberine interacts with several biochemical pathways, including:

Insulin Signaling: By enhancing insulin sensitivity and reducing insulin resistance, berberine helps regulate blood sugar levels, which is beneficial for individuals with diabetes or metabolic syndrome.

Lipid Metabolism: Berberine can lower lipid levels, including cholesterol and triglycerides, by inhibiting enzymes involved in cholesterol synthesis and promoting bile acid excretion.

Scientific Research Supporting Its Efficacy

Numerous studies have demonstrated berberine's effectiveness in:

Managing Blood Sugar Levels: Berberine has shown comparable efficacy to conventional diabetes medications in controlling blood glucose levels.

Improving Lipid Profiles: It can reduce total cholesterol, LDL cholesterol (often referred to as "bad" cholesterol), and triglycerides, contributing to cardiovascular health.

Benefits of Berberine

Berberine offers a wide range of health benefits, supported by scientific research. Here are some of the key benefits:

Metabolic Support

Blood Sugar Regulation: Berberine helps regulate glucose metabolism by enhancing insulin sensitivity and reducing insulin resistance, making it beneficial for managing diabetes and prediabetes.

Weight Management: It may aid in weight loss by influencing metabolic pathways and promoting fat breakdown.

2. Cardiovascular Health

Cholesterol Reduction: Berberine can lower total cholesterol, LDL cholesterol (the "bad" cholesterol), and triglyceride levels, which are important factors in reducing cardiovascular risk.

Blood Pressure Regulation: Studies suggest berberine may help lower blood pressure, supporting heart health.

3. Anti-inflammatory and Antioxidant Effects

Berberine exhibits anti-inflammatory properties, which can help reduce inflammation in the body and support joint health.

It also acts as an antioxidant, scavenging free radicals and protecting cells from oxidative stress.

4. Gastrointestinal Support

Berberine has been used traditionally to support digestive health, including relief from diarrhea and other gastrointestinal issues.

Its antimicrobial properties may help combat harmful bacteria in the gut.

5. Cognitive Support

Emerging research indicates that berberine may have neuroprotective effects, potentially benefiting cognitive function and brain health.

[covid-safer-hotties]

Cannabis Use Linked To Improved COVID-19 Outcomes, New Study Suggests - Published Sept 9, 2024

by Patricio Liddle

Recent research from Northwell Health, published in late August in the journal Cannabis and Cannabinoid Research, indicates that marijuana users may face better outcomes when battling COVID-19, including lower rates of severe infections and reduced likelihood of intubation or death. This promising development points to the potential immunomodulatory effects of cannabis, which could lessen dangerous inflammation during infection.

Cannabis Users Show Lower COVID-19 Mortality The study analyzed data from the National Inpatient Sample Database, comparing hospital admissions for COVID-19 among cannabis users and non-users. Adjusting for various factors like age, gender, and comorbidities, the findings, as reported by Forbes, revealed a significant reduction in mortality and severe complications such as lung failure among cannabis users. Specifically, the mortality rate among non-users was 5.1%, nearly double the 2.8% observed in cannabis users. Additionally, cannabis users tended to have shorter hospital stays, averaging 6.4 days compared to 7.0 days for non-users.

Cautions Noted Despite Positive Findings However, despite these encouraging results, experts urge caution. Dr. Benjamin Caplan, a cannabis expert and author consulted by Forbes, highlighted potential limitations in the study, such as challenges in adequately matching study subjects and absence of crucial data, including patient inflammation levels and the specific cannabis products used.

Mixed Research Findings On Cannabis And COVID-19 The study's preliminary results as well as previous research also support the potential association between cannabis and reduced COVID-19 severity. For instance, a 2022 study by researchers from Oregon State University showed that certain cannabinoid acids in cannabis could prevent the SARS-CoV-2 virus from entering human cells in vitro by binding to its spike protein, suggesting a possible preventive role against the virus.

Earlier research cited in the Forbes article presents a mixed view: Canadian studies suggest cannabinoids might reduce COVID-19 severity by hindering viral entry and easing oxidative stress. Conversely, a University of Washington study linked marijuana use with increased severe COVID-19 risks, underscoring that no evidence supports smoking cannabis as a preventive or curative measure for the virus.

As cannabis research progresses, more studies are vital to fully understand its potential health benefits and risks, particularly given the long history of prohibition that has stifled scientific exploration in this emerging field.

Study Link: www.liebertpub.com/doi/10.1089/can.2024.0048 (PAYWALLED)