China 
Africa 
Explore chapters and articles related to this topic
Adaptive and Robust Methods for Thermoacoustic and Photoacoustic Tomography
Published in Lihong V. Wang, Photoacoustic Imaging and Spectroscopy, 2017
The TAT data was acquired from mastectomy specimens using a TAT system. Microwave sources were used to heat the specimens transiently. In the experiment, the breast specimen was formed into a cylindrical shape inside a plastic bowl. The bowl was immersed in ultrasound coupling medium in a container. The acoustic signals were recorded at 240 equally spaced scanning stops on a circular track of radius 12.9 cm. The thickness of this specimen was about 4 cm in a round plastic bowl of 17 cm in diameter. This lesion was diagnosed as an invasive metaplastic carcinoma with chondroid and squamous metaplasia. The size of the tumor was measured to be 35 mm in diameter by TAT, and 36 mm in diameter by radiography (see Ref. [8] for details).
Carcinogenicity Studies
Published in Leon Golberg, Hazard Assessment of Ethylene Oxide, 2017
Squamous metaplasia of the nasal respiratory epithelium may be caused by repeated exposure to high concentrations of an irritant, and it is reversible up to some critical point in time. When the irritant is removed before that time, the change reverses within a few months. Therefore, nasal metaplasia itself does not necessarily commit an experimental animal to development of nasal malignancy. In addition, where severe rhinitis of infectious or allergic origin is present, squamous metaplasia is a concomitant pathological change, both in man and animals.
Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD)
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Priya Upadhyay, Ching-Wen Wu, Alexa Pham, Amir A. Zeki, Christopher M. Royer, Urmila P. Kodavanti, Minoru Takeuchi, Hasan Bayram, Kent E. Pinkerton
SHRs afford us the opportunity to investigate mechanisms underlying COPD pathogenesis and enable testing of novel drug therapies (Davis et al. 2013). Previously investigators s demonstrated that SHRs manifest neutrophilic airway inflammation and nuclear factor-kappa B (NF-κB) and mitogen activated protein kinase-/activator protein-1 (MAPK/AP-1) activation which likely play a role in TS-induced pathogenesis (Zhong et al. 2005; Zhong, Zhou, and Pinkerton 2008). NF-κB and AP-1 regulate the expression of the inflammatory genes, IL-17, IL-8, and TNF-α, which are produced in COPD (Schuliga 2015). These TS-induced pro-inflammatory cytokines upregulate airway epithelial hyperplasia and squamous metaplasia through NF-κB and MAPK/AP-1 signaling [Figure 1; (Zhong et al. 2005)]. In addition, TS inhibits NF-κB activity and downregulates NF-κB-dependent anti-apoptotic proteins (BCL-2 and c-IAPs), leading to activation of caspases 3, 8, and 9, to induce programmed cell death by apoptosis as illustrated in Figure 3 (Zhong, Zhou, and Pinkerton 2008)]. Similarly, TS produces pulmonary toxicity via MAPK signaling and AP-1 transactivation (Mossman, Lounsbury, and Reddy 2006). SHRs also demonstrate increased expression of TGFβ in epithelial and inflammatory cells, and leukocyte recruitment in response to TS seems to occur mainly through bronchial circulation (Davis et al. 2012; Hoang et al. 2016). Overall, these studies demonstrate that SHRs provide new and unique insights into the molecular mechanisms underlying TS-associated lung diseases that cannot be attained with other COPD models.
Endogenous doesn’t always mean innocuous: a scoping review of iron toxicity by inhalation
Published in Journal of Toxicology and Environmental Health, Part B, 2020
Jody Morgan, Robin Bell, Alison L. Jones
Electric-arc furnaces, which are one method used to recycle Fe into steel, produce between 10 and 25 kg of dust per ton of steel (Bakkar 2014). This dust contains high quantities of Fe, but is contaminated with other metals including lead, chromium, cadmium, and zinc (Bakkar 2014). There was a significant increase in malignant tumors of larynx, trachea, bronchi, and lungs for electric-arc furnace workers with the highest rates attributed to those exposed for 1–5 years (Cappelletti et al. 2016). Squamous metaplasia (benign changes to cells) and cytological atypia (atypical cells which may develop into cancerous tissue) were both significantly higher in Fe industry workers than controls (Ahmed, Mahmoud, and Ginawi 2013). Morbidity analysis also demonstrated a significant rise in relative risk for diabetes, rheumatoid arthritis, non-complicated hypertension, and complicated hypertension among electric-arc furnace workers (Cappelletti et al. 2016).
Risk assessment of benzalkonium chloride in cosmetic products
Published in Journal of Toxicology and Environmental Health, Part B, 2018
Seul Min Choi, Tae Hyun Roh, Duck Soo Lim, Sam Kacew, Hyung Sik Kim, Byung-Mu Lee
BAC is the most commonly used preservative in ophthalmic preparations (Baudouin et al. 2010), owing to its ability to enhance penetration of other compounds and increase drug bioavailability (Rathore and Majumdar 2006; Romanowski et al. 2008). This compound is generally used at 0.01% concentration, although the effective amounts occur in the range from 0.004% to 0.02% (Pisella et al. 2000). Although it has been used for many years without marked safety issues, numerous experimental and clinical studies showed that long-term use of topical drugs that contain BAC might induce ocular toxicities including ocular surface changes, cellular dysfunction of the corneal epithelium, ocular discomfort, tear film instability, loss of goblet cells, inflammation, conjunctival squamous metaplasia, epithelial apoptosis, and subconjunctival fibrosis (Baudouin et al. 2010; Clouzeau et al. 2012; Liang et al. 2012; Wu et al. 2011). Although the molecular mechanisms underlying cytotoxicity are not fully understood, it has been reported that BAC-induced cytotoxicity is associated with activation of the caspase-independent and Wnt pathways (Buron et al. 2006; Zhou et al. 2011). Chang et al. (2015) noted that BAC decreased viability of human trabecular meshwork cells through upregulation of Cx43 expression.