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Applied Chemistry and Physics
Published in Robert A. Burke, Applied Chemistry and Physics, 2020
Methyl ethyl ketone is a polar industrial solvent, which is also known by the trade name MEK. It is a colorless liquid with an acetone-like odor. MEK is flammable with an explosive limit of 2%–10% in air. It is a narcotic by inhalation with a TLV of 200 ppm in air. Another common industrial solvent of the ketone family is dimethyl ketone, more commonly known by the trade name acetone.
Coating Defects and Inspection
Published in Karan Sotoodeh, Coating Application for Piping, Valves and Actuators in Offshore Oil and Gas Industry, 2023
There are numerous ways to test paint curing, but the most common and traditional way is to use methyl ethyl keton (MEK); this method is known as the MEK rub test (see Figure 4.33). MEK is a highly volatile and flammable liquid solvent. The MEK curing test for inorganic zinc-rich primers is performed according to the ASTM D4752 requirements.
Chemicals from Olefin Hydrocarbons
Published in James G. Speight, Handbook of Petrochemical Processes, 2019
Secondary butyl alcohol is formed on absorption of 1-butylene or 2-butylene by 78%–80% sulfuric acid, followed by dilution and hydrolysis. Secondary butyl alcohol is converted into methyl ethyl ketone (MEK) by catalytic oxidation or dehydrogenation.
Targeting gap junctional intercellular communication by hepatocarcinogenic compounds
Published in Journal of Toxicology and Environmental Health, Part B, 2020
Kaat Leroy, Alanah Pieters, Andrés Tabernilla, Axelle Cooreman, Raf Van Campenhout, Bruno Cogliati, Mathieu Vinken
Polycyclic aromatic hydrocarbons (PAHs) are toxic environmental pollutants that act through the aryl hydrocarbon receptor (AhR) (Kabatkova et al. 2015), a receptor controlling migration, proliferation, cell adhesion and cell-cell communication (Andrysik et al. 2013). PAHs with lower molecular weight, consisting of maximum 4 benzene rings, are less genotoxic compared to PAHs that consist of at least 5 benzene rings. The former, however, inhibit GJIC and disrupt contact inhibition, and are therefore involved in tumor promotion (Kabatkova et al. 2015). In rat epithelial cells, PAHs reduce Cx43 levels and gap junction plaques, possibly through upregulated proteasomal degradation (Andrysik et al. 2013). GJIC is inhibited through phosphatidylcholine-specific phospholipase C (PC-PLC) and MAPK/extracellular signal-regulated kinase (ERK) pathways, but not through mitogen-activated protein kinase kinase (MEK) mechanisms (Sovadinova et al. 2015; Upham et al. 2008).
Instance-based learning of marker proteins of carcinoma cells for cell death/ survival
Published in Computer Methods in Biomechanics and Biomedical Engineering: Imaging & Visualization, 2020
Initially authors have considered Mitogen-activated protein kinase-activated protein kinase 2 (MK2), c-jun N-terminal kinases(JNK), Forkhead transcription factor (FKHR), Mitogen-activated protein kinase and extracellular-regulated kinase (MEK), Extracellular-regulated kinase (ERK), Insulin receptor substrate (IRS), AkT, IKK, Phospho-to-total EGFR (ptEGFR), Phospho-to-total Akt (ptAkt), and pAkT proteins that are due to the combination of three input proteins (Jain et al. 2012). To make data consistent, outlier and erroneous data were removed. The signal values were normalised (1: red; 0.5: black; 0: green) to the maximum. Authors have calculated different statistical parameters like harmonic mean, geometric mean, standard error, median, mode, sum, minimum value, maximum values, and coefficient variance. Figure 5 represents the P-P plot, box plot and Kolmogorov–Smirnov (KS) plot, p-value of a normal distribution of FKHR protein (Jain 2017b). Due to the constraint of space, data of FKHR protein are shown in the Figure. Based on the calculation of different statistical parameters and different plots, it is seen that AkT, EGFR, IRS, MEK, ERK, JNK, and FKHR yields better results which was also validated experimentally as shown in Figure 3. All the selected proteins are used for further analysis except AkT. Author has already done all simulations using AkT in (Jain and Salau 2019).
Core genes in lung adenocarcinoma identified by integrated bioinformatic analysis
Published in International Journal of Environmental Health Research, 2023
Liu Yang, Qi Yu, Yonghang Zhu, Manthar Ali Mallah, Wei Wang, Feifei Feng, Qiao Zhang
The PI3K-AKT pathway is one of the key signaling pathways involved in proliferation, migration and invasion of lung cancer cells (Jiang et al. 2020). It has been noted that aberrant activation of PI3K-AKT pathway is related to cancer tumorigenesis and progression (Mayer and Arteaga 2016). We found that six genes (ANGPT1, TEK, COL1A1, SPP1, THBS2 and VWF) involved in PI3K-AKT pathway (Figure 8). COL1A1, SPP1, THBS2 and VWF in extracellular matrix (ECM) activate focal adhesion kinase (FAK) by binding to integrin (ITGA and ITGB), which activates the PI3K/AKT signaling in turn. As a growth factor, ANGPT1 activates the PI3K/AKT and MEK/ERK signaling pathways by combining with TEK receptor tyrosine kinase. Club cell secretory protein (CC16) is encoded by the SCGB1A1 gene (Almuntashiri et al. 2020). Studies have showed that SPARCL1 (Ma et al. 2018) and CC16 (Zhou et al. 2019) can inhibit the transduction of mitogen‑activated protein kinase kinase (MEK)/extracellular signal‑related kinase (ERK) signaling. Previous studies demonstrated that hepatic stellate cells (HSCs)-derived cartilage oligomeric matrix protein (COMP) collaborated with CD36 and subsequently activate MEK/ERK and PI3K/AKT signaling pathways (Li et al. 2018). Stromal cell-derived factor 1 (SDF-1) could induce PECAM-1 through Src family tyrosine kinases to enhance the chemotactic signaling pathway involving PI3K/AKT/mTORC1 (Umezawa et al. 2017). Core genes could affect cell survival, migration, proliferation and metabolism by activating or inhibiting the PI3K-AKT signaling pathway. Taken together, we speculated that core genes may modulate LUAD through PI3K-AKT pathway.