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Fucoidan
Published in Se-Kwon Kim, Marine Biochemistry, 2023
Ellya Sinurat, Dina Fransiska, Nurhayati, Hari Eko Irianto
According to the hepatology data, blood clots generated against providing aspirin without fucoidan (Figure 12.2B), showing that the ulcer existed in the stomach tissue. There are no blood clots in the different performances (Figure 12.2A without aspirin and Figure 12.2C with aspirin and fucoidan). It indicates that because fucoidan does not affect the stomach tissue lining, it can prevent gastric ulcers by building a barrier in the mucosa. A thick mucus coating is particularly common on the mucous membrane, synthesized by high cylindrical epithelial cells. The gastric mucosa is a polypeptide with two purposes: it lubricates food masses to facilitate transportation within the stomach and acts as a protective coating on the lining epithelium of the stomach cavity. This protective barrier protects the stomach from being digested by its protein-lysine enzymes. It can migrate from the underlying mucosa into the surface layer according to bicarbonate secretion. The acidity of the mucous layer, or hydrogen ion concentration, is balanced in the vicinity of the epithelium and becomes acidic toward the luminal layer. While gastrointestinal mucus is excluded from the surface epithelium, little pits termed foveolae gastrique can be observed with a magnifying glass (Sinurat & Rosmawaty, 2015).
paniculata (C.B. Clarke) Munir Leaves on Various Gastric Aggressive Factors
Published in Parimelazhagan Thangaraj, Phytomedicine, 2020
P. S. Sreeja, K. Arunachalam, Parimelazhagan Thangaraj
The continuous blood flow that bathes the gastric mucosa provides a great supply of oxygen and nutrients to the cells of the gastric mucosa and neutralizes the acid secreted by the parietal cells (Tarnawski 2005). This blood flow also removes and dilutes the ions that can backscatter from the gastric lumen. Describing this another way, the gastric microcirculation is responsible in providing nutrients and bicarbonate to the gastric mucosa. Besides, it is worth emphasizing that blood flow is increased in response to the inflammatory processes, thus contributing to the healing process of gastric mucosa due to lesions (Wallace 2008).
Nanostructures for Improving the Oral Bioavailability of Herbal Medicines
Published in Bhaskar Mazumder, Subhabrata Ray, Paulami Pal, Yashwant Pathak, Nanotechnology, 2019
Following oral administration, the stomach is the first digestive and absorption site the drug product encounters in the alimentary canal. Apart from acting as a temporary storage organ, reduction of the ingested solids and mixing to slurry takes place at the stomach with the help of acid and enzyme secretions which are controlled by complex neural, muscular, and hormonal processes. The pH of the stomach is about 1.3 (pH 1.1–1.6) during fasting state, which may be increased to about 4.9 (pH 3.9–5.5) in the presence of food (Russell et al., 1993). Hydrochloric acid is secreted by the gastric secretory cells, known as the parietal cells, along the surface of the gastric epithelial layers, due to which basic drugs are solubilized rapidly in the stomach. The surface of the gastric mucosa is lined by an epithelial layer of column cells that secrete mucous, which is required to protect the epithelial surface of the stomach from acid, enzymes, and pathogens. A thick layer of about 1.0–1.5 mm of mucous covers this epithelial cell surface. These epithelial cells of the gastric mucosa are one of the most rapidly proliferating epithelial tissues, as they are shed by the normal stomach at a rate of about a half-million cells per minute and the surface of the epithelial layer is therefore renewed every one to three days (Mayersohn, 2002). The absorption of drugs in the stomach is very little and is limited due to the small absorptive surface area and short residence time for the dosage form in the stomach.
A preliminary study on the feasible design of bionic blanket concept
Published in Engineering Applications of Computational Fluid Mechanics, 2021
Lisha Xu, Akio Sagara, Jiming Chen, Junichi Miyazawa, Ming Liu, Ran Wei, Xing Liu, Lei Wang, Min Xu, Takuya Nagasaka, Takeo Muroga, Pengfei Zheng
There is a natural contradiction that inorganic compounds must be used as insulation coating, although they may undergo a strong corrosive effect in liquid lithium. As a result, determining how to deal with the contradiction requires careful consideration. Surprisingly, the answer to this contradiction can be found by studying the structure of an animal’s stomach. For example, the stomachs of humans and animals can digest a variety of foods within a short time, even including the stomachs of prey, but these stomachs are not self-digested by the acids. Although the gastric juice is acidic enough to corrode the stomach wall, the gastric mucosa can secrete bicarbonate and form a mucus-bicarbonate barrier that protects the gastric wall from gastric acid erosion(Evtikhin et al., 1992; Jensen, 1976). This principle provides a bionic model for the application of insulation coating in liquid metal breeder.
Helicobacter pylori, stomach cancer and its prevention in New Zealand
Published in Journal of the Royal Society of New Zealand, 2020
Virginia Signal, Jason Gurney, Stephen Inns, Melissa McLeod, Dianne Sika-Paotonu, Sam Sowerbutts, Andrea Teng, Diana Sarfati
H. pylori is classed as a group one carcinogen by IARC, with the lifetime risk of stomach cancer amongst those infected with H. pylori estimated at 1%–3% (International Agency for Research on Cancer 1994). Infection of the gastric mucosa with H. pylori most commonly occurs in childhood, and can result in chronic long-lasting inflammation or gastritis. Chronic inflammation can promote gastric carcinogenesis, typically via the Correa cascade of atrophic gastritis, intestinal metaplasia, and dysplasia (Figure 2) (Correa 1996; Moss 2017). H. pylori expresses an array of proteins that interact with receptors in stomach epithelial cells, and signal cellular pathways that change the expression of genes involved in inflammation, cellular proliferation, invasion and metastasis (International Agency for Research on Cancer and World Health Organization 2014). Decades of H. pylori-related inflammation can lead to gene methylation (epigenetic changes), and chronic exposure to reactive oxygen and nitrogen species that cause DNA damage and gene mutations leading to the development of cancer (International Agency for Research on Cancer and World Health Organization 2014). H. pylori virulence factors such as cytotoxin-associated gene A (CagA), vacuolating cytotoxin (VacA), or lipopolysaccharide (LPS) also play a role in carcinogenesis by modulating cellular signalling pathways (International Agency for Research on Cancer and World Health Organization 2014). For example, it is known that CagA positive H. pylori increases the risk of stomach cancer more than the Cag-A negative H. pylori strain (Huang et al. 2003). Additionally, different CagA subtypes carry differing risks of cancer. The Eastern strains prevalent in Asia, and in Māori (Fraser 2004) are more pathogenic than Western strains (Yuan et al. 2017). Ethnic differences in the virulence strains of H. pylori may contribute to the Māori/non-Māori stomach cancer incidence gap, although the current pattern of virulence factors in New Zealand is unknown.