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Environmental Protection
Published in Lawrence S. Chan, William C. Tang, Engineering-Medicine, 2019
For patients suffered from acute arsenic toxicity, defined as arsenic level 1–3 mg/kg detected on hair sample, usually manifested the followings (Ratnaike 2003): Death: lethal dose is around 100 mg to 300 mg (about 0.6 mg/kg/day).Gastrointestinal: nausea, vomiting, abdominal pain, severe diarrhea, excessive salivation, esophagitis, gastritis, hepatic steatosis.Neurological: encephalopathy, peripheral neuropathy, seizure, acute psychosis.Cardiovascular: cardiomyopathy, blood volume loss from diarrhea, circulatory collapse from blood volume loss.Hematological: hematuria, intravascular coagulation, bone marrow depression, pancytopenia.Renal: failure.Pulmonary: edema, respiratory failure.Cutaneous: rash.
Biotechnological Application of Scanning Electrochemical Microscopy
Published in Allen J. Bard, Michael V. Mirkin, Scanning Electrochemical Microscopy, 2022
Benjamin R. Horrocks, Gunther Wittstock
Immunoassays have also been developed for carcinoembryonic Ag (CEA) [23], human chorionic gonadotropin (HCG) [49] and human placental lactogen (HPL) [49]. CEA is a tumor marker with a molecular weight (MW) of 180,000–200,000; HCG (MW = 38,000) and HPL (MW = 22,000) are peptide hormones that are pregnancy indicators. Yasukawa et al. [130] reported a sandwich immunoassay for pepsinogens (PG) 1 and 2, which are important in the diagnosis of atrophic gastritis and gastric cancer. Anti-PG1 and anti-PG2 Abs were spotted on glass or poly(dimethyl-siloxane) substrates at distinct locations. After capturing the respective Ags, the substrates were exposed to HRP-labeled antibodies forming the sandwich structure. The tip was positioned by recording the hindered diffusion of ferrocene methanol FcCH2OH oxidation at ET = 0.5 V. All assays were performed in the GC mode using an HRP enzyme label after addition of 0.5-mM H2O2 to the working solution and switching the working potential of the tip microelectrode to 0.05 V. At this value FcCH2OH+ formed by HRP can be reduced. Thus, the activity and location of the enzyme label HRP bound in the Ab:Ag:Ab-HRP complex could be detected (Figure 10.24). If the analyte solution contained PG1 or PG2, HRP activity was found only above the active region with the corresponding Ab. When both analytes were present, corresponding levels of activity could be detected over both sensing areas. The assays benefit from structuring the substrates for easy relocation of the spots [49] or using more advanced microfabricated cavities on the substrate to obtain sharper images [130].
Gastrointestinal system
Published in David A Lisle, Imaging for Students, 2012
Upper GIT bleeding is defined as bleeding from the oesophagus to the ligament of Treitz. Acute upper GIT bleeding usually presents with haematemesis and/or malaena. It can usually be distinguished clinically from acute lower GIT bleeding, which presents with red blood loss per rectum. Causes of acute upper GIT bleeding include peptic ulcer disease, erosive gastritis, varices, Mallory–Weiss tear and carcinoma. An upper GIT source for GIT bleeding is diagnosed by emergency upper GIT endoscopy in the majority of cases. Endoscopic haemostatic therapies include injection of sclerosants, injection of vasoconstrictors, thermal coagulation and mechanical methods.
Blood lead level and Helicobacter pylori infection in a healthy population: A cross-sectional study
Published in Archives of Environmental & Occupational Health, 2020
Won-Ju Park, Soo-Hyeon Kim, WonYang Kang, Ji-Sung Ahn, Seunghyeon Cho, Dae-Young Lim, Suwhan Kim, Jai-Dong Moon
The subjects were healthy people over 20 years of age who visited a university hospital for general health examination from January 1, 2014, to December 31, 2016. All subjects underwent upper gastrointestinal endoscopy, and BLL was measured along with the blood test values during the basic medical examination. The endoscopy and blood tests were performed after 12 h of fasting. During the endoscopy, subjects underwent histologic examination for abnormal lesions including gastritis. The presence or absence of H. pylori infection was detected in all those who underwent histologic examination using Giemsa staining. Those without any special suspicious lesion did not undergo a biopsy and were excluded from this study. Endoscopy was performed by a gastroenterologist, and respective histologic examination was evaluated by two pathologists. Those who were treated with past or present malignant diseases were excluded. Additional exclusion criteria are as follows: those who ate meat only or were on a vegetarian diet in terms of dietary habit. Four subjects who had BLLs greater than the adult reference value of 10 μg/dL as defined by the Adult Blood Lead Epidemiology and Surveillance from the National Institutes of Occupational Safety and Health (NIOSH) were excluded from this study.12 Elevated BLLs of ≥10 μg/dL were caused by the use of lead-contaminated traditional herbal medicine. A total of 1,752 men and 873 women were finally selected for this study (Figure 1).
Overview of biological mechanisms of human carcinogens
Published in Journal of Toxicology and Environmental Health, Part B, 2019
Nicholas Birkett, Mustafa Al-Zoughool, Michael Bird, Robert A. Baan, Jan Zielinski, Daniel Krewski
Non-cardia gastric carcinoma normally arises in areas of chronic inflammation. H. pylori is the primary cause of gastritis. An especially intense inflammatory response to H. pylori is postulated to induce more serious damage in gastric epithelial cells, more rapid cell turnover, and eventual emergence of epithelial cells carrying cancer-prone mutations. H. pylori is not directly genotoxic in vitro although there is limited evidence in vivo for an increased frequency of DNA strand-breaks, micronuclei, and DNA adducts. Several reports showed that H. pylori alters the expression of specific oncogenes and tumor suppressor genes implicated in gastric carcinogenesis. Hyper-methylation of E-cadherin and p14 was reported likely as a consequence of the inflammatory process induced by H. pylori. Infection with H. pylori promotes the nuclear translocation of β-catenin, thereby activating downstream β-catenin-responsive genes including cyclin D. H. pylori upregulates the p53 homologue p73 in gastric cells, which leads to promotion of apoptosis, and decreases expression of the cell-cycle inhibitory protein p27, which is known to be lost in aggressive gastric cancers.
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
Endoscopic biopsy (gastroscopy) is considered the clinical diagnostic gold standard test for H. pylori in patients with gastritis, with very high sensitivity (Patel et al. 2014). However, the invasive nature and high costs (largely related to performing the endoscopic procedure) make endoscopic biopsy a poor choice for a test-and-treat programme (Ansari and Yamaoka 2018). Less invasive tests for H. pylori are commonly used in clinical practice (Best et al. 2018) and also have sensitivity and specificity sufficient for population-based prevention programmes, although each has advantages and disadvantages. These less invasive tests are each discussed below.