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Thermoluminescence Dosimetry
Published in Arash Darafsheh, Radiation Therapy Dosimetry: A Practical Handbook, 2021
Many more materials exist and the table has been provided more to illustrate certain features than to provide an exhaustive summary of materials. Another important material is Beryllium Oxide (BeO) [41] because of its tissue equivalence and the fact that like Aluminum Oxide it is also useful for OSL dosimetry which extends usability (and scientific interest).
Inorganic Chemical Pollutants
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
The source of beryllium is usually the fluorescent lamp industry. Beryllium was not thought to be a toxic element until it was commercially produced. Then workers engaged in extracting it from its ores began to suffer from a number of ailments such as dermatitis, tracheobronchitis, and pneumonitis. A study807 showed that chronic lung disease developed among workers in fluorescent lamp plants, where fluorescent powder containing finely divided beryllium,808 can cause chemical sensitivity. The particle size of beryllium oxide dust is a critical factor in exposure that leads to lung injury.809 Although the TLV for beryllium is 0.992 mg/m3, it may be too high for the chemically sensitive to tolerate.
Granulomas and Granulomatous Inflammation
Published in Philip T. Cagle, Timothy C. Allen, Mary Beth Beasley, Diagnostic Pulmonary Pathology, 2008
Berylliosis is another allergic epithelioid cell granulomatosis. The granulomas tend to be larger than in EAA or sarcoidosis; however, it might be impossible to differentiate them from those of sarcoidosis on morphologic grounds alone (Fig. 23). The granuloma itself is histologically identical to the granuloma in sarcoidosis (18). As in sarcoidosis, no infectious organisms can be demonstrated in the granulomas. No large series of BAL has been reported for berylliosis so far. However, from experimental data, a predominance of T-helper lymphocytes has been reported, making BAL a potentially useless tool for the differentiation of berylliosis and sarcoidosis (18). For diagnosis, a lymphocyte transformation test is usually recommended, and an exposure anamnesis is necessary to suggest berylliosis (19). By electron microscopy and energy-dispersive X-ray analysis (EDXA), beryllium oxide may be demonstrated in the granulomas. However, it should be remembered that in routinely processed specimens the beryllium oxide might be leached out from the tissue by the solvents used for fixation, dehydration, and embedding. The same is true for a laser-assisted mass spectrophotometric analysis (LAMA) using formalin-fixed tissue.
Epidemiology and Risk Factors of Osteosarcoma
Published in Cancer Investigation, 2020
Leissan R. Sadykova, Atara I. Ntekim, Musalwa Muyangwa-Semenova, Catrin S. Rutland, Jennie N. Jeyapalan, Nataliya Blatt, Albert A Rizvanov
Environmental conditions were also named as risk factors of osteosarcoma. Vu et al. (90) have shown that the risk of osteosarcoma is a linear function of local doses of radiation. Similar data was presented by Arlen et al. (91), who showed that residents of areas with radiation ranging from 1,200 rads/few weeks to 24,000 rads/2 years were more likely to develop osteosarcoma. Additionally, a link between radiation exposure and osteosarcoma was reported among radium dial workers (92). Accordingly, treatment using teriparatide, a parathyroid hormone peptide, was suggested to increase the risk of radiation-induced osteosarcoma (93). Bassin et al. (94) also proposed that exposure to fluoridated water was a potential risk factor for osteosarcoma. Similar observations were published by Gandhi et al. (95), which suggested that fluoride-induced oxidative and inflammatory stress contribute to the pathogenesis of osteosarcoma. Other chemical risk factors include methylcholanthrene and chromium salts (96), beryllium oxide (97), zinc beryllium silicate (98), asbestos, and aniline dyes (99).
Beryllium inhibits apoptosis via mitochondria in beryllium-induced lung disease in the rat
Published in Experimental Lung Research, 2019
Zhihong Liu, Kai Wang, Qing Yan, Hejing Wang, Na Zhang, Aihong Gong, Xiong Guo
We conclude that inhibition of apoptosis by beryllium oxide involves mitochondrial apoptosis pathway in rat model of beryllium oxide-induced pulmonary disease. The treatment of SD rats with beryllium oxide blocks cell death that regulates the mitochondrial membrane permeability and mitochondrial membrane potential by the up-regulation of Bcl-2, down-regulation of Bax and inhibits the cyt c release from mitochondrial into cytosol and the activation of caspase 3.
Advances and challenges in nintedanib drug delivery
Published in Expert Opinion on Drug Delivery, 2021
Varalakshmi Velagacherla, Akhil Suresh, Chetan H Mehta, Usha Y Nayak
Lung cancer is considered as one of the important epidemic diseases in the 20th century, and currently, it is a major health problem. Worldwide, lung cancer stands in the first place in the case of deaths, and one out of four deaths from all cancers is due to lung cancer. The survival rate of lung cancer is 4.5–5.5%. There are two types of lung cancers, namely, small cell lung cancer and N.S.C.L.C [18]. 85% of the lung cancers are of N.S.C.L.C type. N.S.C.L.C is further classified into [19] adenocarcinoma (40%) [20], squamous cell carcinoma (25–30%) [21], and large cell carcinoma (5–10%) [22]. The main risk factor of this cancer is smoking, the risk of developing lung cancer in nonsmokers is 1.14–5.20%, and the chances of developing cancer in smokers are 20–30%. Apart from smoking, other risk factors include exposure to radon, asbestos, uranium, arsenic, beryllium oxide, cadmium, nickel, vinyl chloride, and silica. Pollutants emitted from vehicles like polyacrylic aromatic hydrocarbons also cause lung cancer. Alteration in the TP53 sequence is more likely to develop lung cancer when compared to nonsmokers [23]. Epigenetic changes like D.N.A methylation, which occurred in a network of complex chromatin structures, and D.N.A methylation may occur due to modifications in the structure of histone. There are three important forms of D.N.A methylation, which were involved in the pathology of N.S.C.L.C, and they include hypermethylation of genes that suppresses tumor, global hypomethylation, and methylation of some miR.N.As. Methylation in N.S.C.L.C occurs at earlier stages of cancer. Important genes that were studied in the pathogenesis of N.S.C.L.C are RASSF1A, RARB, TIMP3, CDKN2A, MGMT, CDH1, DAPK, and CDH13 [24]. Often I.P.F leads to N.S.C.L.C, and N.T.B is used in the management of I.P.F; it can be advantageous to use N.T.B along with an anti-cancer agent. Treatment of N.S.C.L.C depends on the type of oncogenic factors that causes the disease. Various drugs and treatments used for treating N.S.C.L.C are given in Table 4 [18]. The pathophysiology of N.S.C.L.C is shown in Figure 3.