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Biology Questions
Question 1
Exposure to methyl isocyanate occurs through inhalation, skin contact, eyes, or ingestion. The most typical outcomes of this exposure include irritation in the skin, eyes, and respiratory tract. Acute exposure to high concentrations of methyl isocyanate may lead to severe pulmonary edema and alveolar damage. Additionally, methyl cyanate toxin severe corneal damage and carries the risk of death. People who survive from toxin exposure develop long-term effects such as respiratory and ocular difficulties. A pregnant woman exposed to methyl isocyanate may have miscarriages, fetal death, or spontaneous abortions. These effects can persist for years especially, the reproductive and ocular effects (Limaye).
The mechanisms of isocyanate reactivity are poorly understood. However, it is postulated that when someone is exposed, the toxin supplements the production of the mitochondrial reactive oxygen species (ROS), hastens the depletion of enzymes that antagonize ROS, and causes an increase in the actions of pro-inflammatory cytokines. The imbalance between ROS and antioxidants leads to the damaging of endothelial cells. Therefore, when inhaled, the toxin induces apoptosis of endothelial cells by jeopardizing the balance of the mitochondrial-nuclear cross talk (Panwar et al.). On the other hand, isocyanate methyl can damage the DNA strands by hyper-phosphorylating various proteins such as the phosphoinositide 3-kinase. DNA damage is characterized by the initiation of numerous signaling cascades that result in cell cycle arrests and jeopardize various regulations in cell cycle checkpoints (Panwar et al.).
Methyl isocyanate causes pulmonary edema, electrolyte imbalance, and bronchospasm (Limaye). Other adverse effects include skin irritation, ocular damages, gastrointestinal effects including nausea, vomiting, abdominal soreness, and irritation of the respiratory tract, causing compromises in the lung tissue. Also, the damaged lung tissue can easily be infected by bacteria, resulting in pneumonia. Skin irritations may be manifested as chemical burns when one is exposed to high concentrations of the gas.
Question 2
The extracellular matrix (ECM) comprises elements such as collagen, hyaluronan, laminin, syndecan, and elastin. ECM can either exist as the basement membrane or as an interstitial matrix. The ECM offers physical support to the cell and enhances signaling regulations. Moreover, the EMC provides a fibril-like environment to the cells or a sheet-like membrane of the epithelial cells’ basement and supports developing tissues by enhancing cell adhesion, movement, shape, and cell differentiation. Also, the ECM provides anchorage to the cell via the cell adhesion molecules such as the integrin.
The ECM is essential during embryonic developmental stages, especially during the separation of embryonic layers. Cells are sensitive to the mechanical triggers generated from the ECM, hence their response to the stimuli generated by the ECM microenvironment. Such stimuli include changes in the ECM topography, toughness, and structure. These signals are transformed into cellular responses through a process known as mechanotransduction.
Regarding neoplasia, the ECM acts as the microenvironment for cancer cells. The matrix is significantly heterogeneous and comprises cellular and non-cellular components. The cellular components are made of fibroblasts, endothelial cells, and adipocytes. The non-cellular component comprises proteins, glycosaminoglycans, and proteoglycans. Tumor progression relies on tumor cells’ capability to pass through the EMC barrier, enter the bloodstream, and form distal metastases. Signaling between cancer cells and the ECM is crucial for tumor growth. Tumor cells can readily alter their physiological traits to enable them to thrive in unfavorable environments. Researchers believe that the ECM can induce cancer cell plasticity. Besides, high deposition of ECM components such as collagen facilitates tumor cells’ stiffness because, in cancer microenvironments, collagen fibers increasingly form crosslinks. The collagen fibers aid the growth of cancer cells as well as migration and formation of metastasis. Hyaluronan and POSTN, ECM components, are essential in the metastatic niche. POSTN also facilitates the maintenance of cancer stem cells by augmenting the WNT signaling pathway. Hyaluronan receptor supports disseminated cancer tumor cells during metastasis. Studies show that cancer cells produce significant amounts of ECM to aid in disease progression (Holle et al.).
Drugs could be designed that target the interaction between the cancer cells and the extracellular matrix. However, there have not been many drug discoveries that target the signaling between tumor cells and the extracellular matrix. Drugs targeting the integrin or collagen could be useful in inhibiting metastasis. Designing drugs that target particular integrin interactions focus on inhibiting protective downstream signaling influences convened by the specific receptors. ATN-161 is a drug developed to target fibronectin. It non-competitively inhibits fibronectin PHSRN sequence. The drug is exceptional; it does not inhibit integrin-dependent adhesion; instead, it inhibits downstream signaling through alpha5beta1 and alphavbeta3 integrin. The drug has anti-angiogenic and ant-pro-survival properties, which are important in inhibiting cancer cells’ proliferation (Holle et al.).
Question 3
Cyclins and cyclin-dependent kinases are the two positive regulator molecules that ensure the cell cycle’s progression through various checkpoints. The levels of cyclin molecules are affected by internal and external triggers. Their concentrations vary in different phases of the cell cycle. To be effective, cyclins bind to Cdks, and the complex undergoes phosphorylation. Phosphorylation is important in activating the complex—the phosphorylated complex the advances the cell cycle.
Works cited
Holle, Andrew W., Jennifer L. Young, and Joachim P. Spatz. “In vitro cancer cell–ECM interactions inform in vivo cancer treatment.” Advanced drug delivery reviews 97 (2016): 270-279. https://doi.org/10.1016/j.addr.2015.10.007
Limaye, P. “Methyl Isocyanate.” (2014): 306-309. https://www.sciencedirect.com/topics/chemistry/methyl-isocyanate
Panwar, Hariom, et al. “Imbalance of mitochondrial-nuclear cross talk in isocyanate mediated pulmonary endothelial cell dysfunction.” Redox biology 1.1 (2013): 163-171. https://doi.org/10.1016/j.redox.2013.01.009