China
Africa
Explore chapters and articles related to this topic
Cancer Biology and Genetics for Non-Biologists
Published in Trevor F. Cox, Medical Statistics for Cancer Studies, 2022
Chemotherapy has its roots in World Wars I and II, when mustard gas was used as a weapon. It was noticed that those not killed had immune cells destroyed by the gas. That lead to a nitrogen mustard as the first chemotherapy agent that could kill tumour cells. Since then more and more chemotherapy drugs have been discovered, and now over 100 are in current use. The drugs kill cancer cells that are dividing, but at the same time, they also kill normal cells. However, as cancer cells divide much more often than normal cells, more cancer cells than normal cells are destroyed. It is a balance between too little of the drug, and the cancer is not treated enough, or too much of the drug that will kill the cancer completely, but also the patient.
Designer Poisons
Published in Alan Perkins, Life and Death Rays, 2021
Change, fear and mistrust led to a number of accusations and reorganisations. In 1938 Boris Zbarsky, a narcotics expert and professor at the Department of Biochemistry and Analytical Chemistry at the First Moscow Medical Institute, was appointed head of the facility. Several scientists from the Biochemistry Institute collaborated on the research projects. In 1939 the Special Laboratory was split into two special departments for the development of chemical and bacteriological agents. Grigory Moisevich Mairanovsky was appointed head of the chemical facility which was known as Laboratory No 1. Mairanovsky headed several secret laboratories in the Bach Institute of Biochemistry in Moscow between 1928 and 1935. He completed his PhD titled ‘Biological activity of the products of interaction of mustard gas with skin tissues’ in 1940. This was kept as a ‘classified’ document. Mustard gas (sulphur mustard) was developed in Europe during the 1800s and became the first chemical weapon of war when it was used by the German Army against British and Canadian soldiers near Ypres in Belgium in 1915. Under Mairanovsky the laboratory became known as the Kamera, which translates in English to cell or chamber, as in Kamera pytok or torture chamber. Mairanovsky gained a reputation as a sadistic butcher, equalling the depravity and acts of Joseph Mengelev, the SS doctor at Auschwitz, who took pleasure in selecting subjects for experimentation and supervised the administration of Zyklon B, the cyanide-based pesticide used for the mass killings in the Auschwitz-Birkenau gas chambers.
The development of pharmaceutical hegemony
Published in Kevin Dew, Public Health, Personal Health and Pills, 2018
The synthetic dye industry of the nineteenth century played a major role in the industrialisation of pharmaceutical production; the chemical skills developed there were applied to the development of new drugs (Weatherall 2006). Developments in physiology led to other advances, like the discovery that myxoedema, a condition caused by an underactive thyroid, could be treated by extracts of thyroid from sheep, and synthetic versions of this hormone were developed. Penicillin and other antibiotics appeared in the 1940s. War efforts too played a role in the development of industrial pharmaceuticals; technological changes allowing for the development of mass produced capsules and tablets occurred in the mid-nineteenth century, with the compression of tablets being modelled on the technology used to make bullets for firearms (Martin 2006a). Work to develop chemical warfare agents during the Second World War had positive therapeutic spinoffs with substances related to mustard gas found to be useful in the treatment of some cancers (Weatherall 2006).
The Role of Inflammatory Cytokines in Neovascularization of Chemical Ocular Injury
Published in Ocular Immunology and Inflammation, 2022
Alireza Shahriary, Milad Sabzevari, Khosrow Jadidi, Farshad Yazdani, Hossein Aghamollaei
Sulfur mustard is a vesicant agent that severely affects living tissues such as eyes, skin, and lung. The eyes due to humid surface environment are susceptible tissue to mustard gas damages a few hours after exposure.23 More than 100,000 Iranians were wounded by the use of SM during the Iran-Iraq war (1980–1988). Sadly, there are currently around 35,000 victims suffering from chronic symptoms of SM. 75% to 90% of exposed people are suffering from acute ocular injury, and some cases will burden the chronic phase.24 The early ocular complications of mustard gas include photophobia, burning pain, swelling of the eyelids and excessive lacrimation; however, limbal ischemia, visual impairments, and corneal neovascularization are the most characteristics of patients in chronic phase.25 Mustard gas, which is in the form of a small oily aerosol, has a toxicity ability to disrupt cell functions. Mustard is able to alkylate nitrogenous bases in the DNA and protein molecules. In consistent with abruption in DNA and protein synthesis, the cell cycle in the G2-M phase is arrested leading to a reduction in repairing and healing systems.26 Furthermore, the mustard dramatically depletes the compound of intracellular glutathione (GSH) using ROS production and H2O2 in particular. The accumulation of ROS in cells causes a massive oxidative stress in the anterior segment of the eyes. It increases inflammation of the corneal surface as the pathophysiologic basis of dry eye as well as the presence of CNV.27,28
Ebselen oxide attenuates mechlorethamine dermatotoxicity in the mouse ear vesicant model
Published in Drug and Chemical Toxicology, 2020
Hemanta C. Rao Tumu, Benedette J. Cuffari, Maria A. Pino, Jerzy Palus, Magdalena Piętka-Ottlik, Blase Billack
There are no specific antidotes currently available for mustard gas exposure. Modified Dakins solution (0.025% sodium hypochlorite) has been used as an irrigating and antiseptic agent during World War I and the Iran–Iraq War (Anderson 2012) but more effective countermeasures are needed. To this end, numerous in vivo studies have evaluated various classes of compounds such as non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, chelators, povidone-iodine, zinc oxide, capsaicin, and anti-TNFα antibodies for treating vesicant-induced inflammatory responses (Casillas et al. 2000, Dachir et al. 2002, Kenar et al. 2005, Wormser et al. 2005), but each of these have had limitations. More recently, a novel formulation of doxycycline has shown promise in healing dermal wounds caused by NM (Anumolu et al. 2011) and a novel bifunctional anti-inflammatory prodrug (NDH 4338) has been found to reduce vesicant-induced edema and markers of epidermal proliferation (Chang et al.2014, Composto et al.2016). None of these compounds, however, have completely reduced vesication. Therefore, there is an urgent need to identify antidotes to the blistering effects of mustard gas.
Defining the timing of 25(OH)D rescue following nitrogen mustard exposure
Published in Cutaneous and Ocular Toxicology, 2018
Lopa M. Das, Amy M. Binko, Zachary P. Traylor, Lori Duesler, Kurt Q. Lu
Mustard gas exposure affects various organs including lungs, bone marrow and skin leading to early and late manifestations of morbidity2,5,12,13. If left untreated, mustard induced skin injury is characterized by erythema and edema that progresses to vesication of the skin resulting in epidermal separation, vacuolization and epidermal necrosis14. In the interest of practical application of treating victims of mass exposure to chemical injury it is essential to determine the maximum length of time post-exposure that can lapse where treatment is still possible. In this study, we use a mouse model of NM-induced skin wound to evaluate the window of time within which 25(OH)D must be administered to accelerate wound healing and recovery from systemic toxicity. Furthermore, we assessed whether a higher dose of drug is more efficacious at a later time point when low dose therapy is no longer able to rescue mice from exacerbated inflammation and toxic effects of NM. Topical application of NM on an 8 mm area of the dorsum of mouse induced a wound as early as 1 day post-exposure. Without treatment, the lesion deepened and progressively worsened by day 10 post-exposure. The systemic toxic effects of NM reaches beyond local injury to cause cytopenia in blood, loss of intestinal barrier function, dilation of capillaries in the kidney, and bone marrow suppression9,15. Thus, the model is consistent with work previously reported by us and others that NM and SM induced skin vesication progressively deteriorates into a full thickness wound if continued inflammation is not suppressed by intervention with an anti-inflammatory drug9,16.