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Cells Fake 15 ((EXCLUSIVE))

This article summarizes those research activities in the area of artificial cells which are related to medicine and biotechnology. This includes the applications of artificial cells in: (1) chronic renal failure, (2) drug poisoning, (3) aluminium and iron removal, (4) fulminant hepatic failure, (5) immunosorbent for direct blood perfusion, (6) enzyme therapy and metabolic function replacement, (7) immobilized cell cultures for Bioartificial Organs, (8) blood substitutes, (9) microencapsulation, (10) biotechnology and other areas.

cells fake 15

No mechanism by which ELF-EMFs or radiofrequency radiation could cause cancer has been identified. Unlike high-energy (ionizing) radiation, EMFs in the non-ionizing part of the electromagnetic spectrum cannot damage DNA or cells directly. Some scientists have speculated that ELF-EMFs could cause cancer through other mechanisms, such as by reducing levels of the hormone melatonin. There is some evidence that melatonin may suppress the development of certain tumors.

In recent years, artificial sweeteners have become popular as a non-caloric additive to sweeten foods and drinks. Artificial sweeteners, such as sucralose and aspartame, provide the sweet taste in low-calorie foods, which have increased their popularity worldwide [16]. As these sweeteners are cheap, easily available, and result in enhanced food flavour, they have been incorporated into many food products and beverages, as well as pharmaceutical products. Epidemiological studies have evidenced the beneficial role of sweeteners in weight loss and for people suffering from glucose intolerance and type 2 diabetes mellitus [16,17,18]; there are, however, studies which indicate opposing results. Using animal and human studies, artificial sweetener consumption has been linked with conditions leading to metabolic disease development [15]. Indeed, sweeteners were reported to induce glucose intolerance by altering the composition and function of the gut microbiota. In mice, sweetener-intake was linked with dysbiosis leading the host to be prone to symptoms related to metabolic disease. These symptoms were abrogated by treatment with the antibiotics, ciprofloxacin, metronidazole, and vancomycin, which affected the commensal microbiota and ameliorated the metabolic disease symptoms [14]. Further studies have confirmed that aspartame exposure, over 8 weeks, increases fasting glucose levels and insulin intolerance in rats [18]. These studies show that perturbed gut microbiota occurred, in response to sweetener treatment, with an increase in abundance of Enterobacteriaceae and Clostridium leptum. In a human study on 4-day food intake, the relationship between aspartame and acesulfame potassium intake and microbiota was demonstrated; no differences in the abundance and genetic composition of bacteria were noted between the artificial sweetener consumers and non-consumers, however, a significant difference in microbial diversity was observed [19]. Bian et al. demonstrated that numerous pro-inflammatory mediators were potentially produced by gut bacteria following the consumption of sweeteners in the diet, which is associated with other metabolic disease conditions like diabetes and obesity [20,21]. Interestingly, in gut epithelial cells, our recent studies demonstrate that exposure to artificial sweeteners increases apoptosis and permeability across the intestinal epithelium associated with inflammatory gut leak [22]. Despite controversy in the field, there is strong evidence that without changing the bacterial composition, artificial sweeteners in the diet cause changes in bacterial diversity, and potentially pathogenicity, which is likely to exert a negative impact to the host. However, how artificial sweeteners affect symbiotic bacteria and contribute to pathogenicity remained veiled yet.

Intact E. coli or E. faecalis, which were pre-exposed to artificial sweeteners, were incubated with Caco-2 cells to establish adhesion ability of the model gut bacteria. All three artificial sweeteners studied, saccharin, sucralose, and aspartame, significantly increased adhesion of both E. coli and E. faecalis to intestinal epithelial cells (Figure 3a,d). Interestingly, a more dramatic fold-increase in bacterial adhesion to Caco-2 cells was observed with E. faecalis compared to E. coli for saccharin (E. coli 2.3 0.4 versus E. faecalis 5.2 2.1), sucralose (E. coli 2.0 0.3 versus E. faecalis 5.4 1.8), and aspartame (E. coli 2.9 0.7 versus E. faecalis 6.6 1.9).

There are a range of virulence factors which bacteria can utilise to become pathogenic to a host, such as prevention of complement activation and escape from phagosomes. Some pathogenic E. coli have been shown to display a range of virulence factors, such as bundle-forming pilus (BFP), type 1 pili and cytolysin A (ClyA), to cause adherence and invasion of host cells, and the production of cytotoxins which kill host cells [33,34,35]. Similarly, pathogenic E. faecalis shows adhesion and invasion of intestinal epithelial cells, via pili and aggregation substances, such as AsaI and glycolipids, and cytotoxicity via secreted factors, such as cytolysin [36,37,38,39]. Other mechanisms of pathogenicity have also been identified. E. coli can exert pathogenic effects, such as biofilm formation, through yafK and Fis gene expression, and α- or β-haemolysis, potentially through a ClyA-mediated pathway [40,41]. Similarly, biofilm formation and haemolysis activity have been shown in pathogenic E. faecalis by the xdh or Esp genes and β-haemolysin, respectively [42,43,44]. Whilst artificial sweeteners have been shown to affect dysbiosis in the gut microbiota, there are limited mechanistic studies which show pathogenic responses of individual bacteria to sweeteners. In the present study, we demonstrate that the artificial sweeteners saccharin, sucralose, and aspartame, at physiological concentrations, impact on all these pathogenic mechanisms except β-haemolysis. The model bacteria, E. coli and E. faecalis, are α- and γ-haemolytic, respectively, in normal conditions, however, they can turn into β-haemolytic when pathogenic [44,45]. It is possible that we noted no change in haemolysis because of the in vitro nature of the study or the use of laboratory strains of each bacteria. Indeed, clinical isolates of E. coli or E. faecalis have been shown to display haemolytic genes, such as hly and ClyA [46,47], which are likely to be lacking from the bacteria we studied. It is also worth noting that model gut bacteria were exposed to artificial sweeteners for 24 h, so only the long-lasting response to the additive was recorded. However, given that artificial sweeteners are consistently present in the diet, in a range of sources from food, drink, and cosmetics, it is likely that the microbiome would be continuously exposed and long-lasting responses are most accurate to study. Further study on the genetic changes of each bacteria, following exposure to saccharin, sucralose, and aspartame, may provide a deeper molecular understanding of the mechanisms regulating their pathogenicity.

Bacteria such as E. faecalis have been shown to translocate across the intestinal wall, disseminate into the blood stream, and cause septicaemia along with congregation in the mesenteric lymph nodes, liver, and spleen [57,58,59]. In our present study, we demonstrate that saccharin, sucralose, and aspartame increased the ability of model gut bacteria to adhere to and invade intestinal epithelial cells, with the exception of saccharin which has no significant effect on E. coli invasion. Furthermore, we and others have previously demonstrated the negative effect of artificial sweeteners, saccharin, sucralose, and aspartame, on intestinal epithelial cell apoptosis and permeability [22,60], thus further increasing the opportunity for bacteria to traverse the gut epithelium and cause septicaemia. However, to date, no studies have been performed to study the link between consumption of artificial sweeteners correlates with incidence of septicaemia.

A colorized scanning-electron-microscope image shows SARS-CoV-2 (the round blue objects) emerging from cells cultured in the lab. SARS-CoV-2 is the coronavirus that causes the disease COVID-19. NIAID-RML/Science Source hide caption

The data suggests omicron may be able to infect people at a lower dose than delta or the original variant, Garcia-Beltran says. "That's a very far-out interpretation," he cautions. "But we think it will probably pan out that way, given that we're looking at a variant with more efficient entry into human cells."

The Food and Drug Administration has taken a first step towards allowing the sale of cultivated "no kill" meat in the U.S, giving a safety nod to Upside Foods, a San Francisco based start-up. The company produces meat grown from animal cells, without slaughtering the animal.

Upside Foods was co-founded by Uma Valeti, a cardiologist who dreamt of producing meat in a different way. Instead of raising livestock on farms and killing them in slaughterhouses, Valeti wanted to find a way to "grow" meat in a production facility, by culturing animal cells.

The concept for what's now called "cultivated" meat came to Valeti when he was working with heart attack patients at the Mayo Clinic more than 15 years ago, growing human heart cells in a lab. It should be possible to grow meat with similar science, he realized.

Scientists could extract cells from an animal via a needle biopsy, place them in tanks, feed them the nutrients they need to proliferate, including fats, sugar, amino acids and vitamins, and end up with meat.

After his aha moment in the cardiology lab, Valeti became convinced he could develop a viable technique for cultivating meat from animal cells. "Once I got that idea into my head it was nearly impossible to get out," Valeti recalls.

It took Valeti and his team years to develop the technology behind these tasty bites. A key challenge was creating the feed for the cells. Cells need a mix of proteins, carbohydrates and fats (just as animals do) but, designing the exact formulation was part alchemy, and a lot of trial and error.


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