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Limitations of epidemiologic exposure studies on the health effects of asbestos
Published in Dorsett D. Smith, The Health Effects of Asbestos, 2015
The important issue in all cancer epidemiologic studies is confounding. It is difficult to control for confounders such as Helicobacter pylori infection, atrophic gastritis, and diet in gastric cancer, or esophageal reflux in esophageal and laryngeal cancer. Some subtypes of cancer, such as lung cancer, may have different confounders, such as the role of HPV in the causation of squamous cell cancer of the lung, oropharynx, and rectum. Radon exposure is the second leading cause of lung cancer in the United States, but is seldom mentioned in epidemiologic studies. Race, ethnicity, sex, age at the time of first exposure, genetic susceptibility, tobacco exposure, and socio-economic factors are important. Many important confounders have not been identified. Exposure information such as heavy prolonged or intermittent heavy exposure are often confused. Information on fiber type, fiber length, and fiber diameter is usually not reported. Many authors report “asbestos exposure” as if any and all asbestos exposure has equal carcinogenicity! For instance, exposure to occasional brake or clutch dust is often included as a significant asbestos exposure in various epidemiologic studies, in spite of the fact that this is not supported in the scientific medical literature. Other authors assume that any asbestos exposure is a significant exposure. The difficulty in distinguishing between gastrointestinal neoplasms and epithelial peritoneal mesotheliomas is not mentioned in many published papers. The reader needs to be aware of papers in which potential or incomplete lists of confounders are missing or ignored. This creates a bias, which is a type of lack of information about confounder bias due to an absence or lack of inclusion of potential confounders. Confounding is particularly important when there are only small differences between those exposed versus nonexposed populations to asbestos, such as in carcinoma of the larynx. There are at least15 different causes of carcinoma of the larynx (Chapter 11), which makes data interpretation of epidemiologic studies very difficult when there is no correction for confounding.
Bacteria-targeting chitosan/carbon dots nanocomposite with membrane disruptive properties improve eradication rate of Helicobacter pylori
Published in Journal of Biomaterials Science, Polymer Edition, 2021
Muhammad Arif, Mohamed Sharaf, Quanjiang Dong, Lili Wang, Zhe Chi, Chen-Guang Liu
Helicobacter pylori (H. pylori) has been attributed to gastric cancer, chronic atrophic gastritis, and gastro-oesophagal reflux disease [1]. H. pylori increase mucus permeability, penetrates the mucus membrane, and colonizes the gastric epithelium's deepest layer. H. pylori persist in harsh gastric environments by hydrolyzing urea into NH3 and carbamate, which neutralize the gastric pH [2]. H. Pylori is currently treated with standard triple therapy, which consists of a proton pump inhibitor (PPI), clarithromycin, and amoxicillin [3]. However, due to an increase in antibiotic-resistant H. pylori in recent years, the efficacy of standard triple therapy has been severely reduced. Furthermore, unfavorable side effects and poor patient compliance are significant impediments to eradicating H. pylori using standard triple therapy. As a result, novel treatment strategies to improve eradication rates are desperately needed. Micro- or nano-scaled mucoadhesive particles, such as liposome, polymeric, and metallic nanoparticles that may diffuse through the stomach mucosa and reach H. pylori, have recently emerged as promising delivery mechanisms to improve bacterial eradication efficacy [4–7]. Despite the promise of these mucoadhesive particles, only a few studies have shown complete bacterial eradication, and explicitly targeting H. pylori has also proven problematic [8].
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.