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https://www.selleckchem.com/products/pepstatin-a.html The sensor with the thickest film exhibits slightly higher sensitivity than the sensor with a thinner film. The sensitivity of the 120-cycle-coated MOF sensor is 13.7 nm/% (R2 = 0.951) with a limit of detection (LoD) of 0.005% in the measurement of acetone, 15.5 nm/% (R2 = 0.996) with an LoD of 0.003% in the measurement of ethanol and 6.7 nm/% (R2 = 0.998) with an LoD of 0.011% in the measurement of methanol. The response and recovery times were calculated as 9.35 and 3.85 min for acetone; 5.35 and 2.12 min for ethanol; and 2.39 and 1.44 min for methanol. The humidity and temperature crosstalk of 120-cycle-coated MOF was measured as 0.5 ± 0.2 nm and 0.5 ± 0.1 nm in the humidity range of 50-75% relative humidity (RH) and temperature range of 20-25 °C, respectively.Gout is a type of inflammatory arthritis caused by the deposition of monosodium uric acid (MSU) crystals in tissues. The etiology of gout is directly linked to the NLRP3 inflammasome, since MSU crystals are NLRP3 inflammasome activators. Therefore, we decided to search for a small-molecule inhibitor of the NLRP3 inflammasome for the prevention of gout inflammation. We found that loganin suppressed MSU crystals-induced caspase-1 (p20) and interleukin (IL)-1β production and apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) specks formation in mouse primary macrophages, showing its ability to inhibit the NLRP3 inflammasome. In an air pouch inflammation model, oral administration of loganin to mice prevented MSU crystals-induced production of mature IL-1β and IL-18 in air pouch exudates, resulting in decreased neutrophil recruitment. Furthermore, oral administration of loganin suppressed MSU crystals-induced gout inflammation in a mouse foot gout model, which was accompanied by the inhibition of the NLRP3 inflammasome. Loganin blocked de novo synthesis of mitochondrial DNA in air pouches and foot tissues injected with MSU

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