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Practice Paper 1: Answers
Published in Anthony B. Starr, Hiruni Jayasena, David Capewell, Saran Shantikumar, Get ahead! Medicine, 2016
Anthony B. Starr, Hiruni Jayasena, David Capewell
Cystic fibrosis (CF) is the commonest autosomal recessive condition in white populations in the UK, affecting 1 in 3000 live births. CF is caused by an abnormal gene coding for the cystic fibrosis transmembrane regulator protein (CFTR), located on chromosome 7. CFTR is a cAMP-dependent chloride channel blocker. The most common mutation in CF is the ΔF508 mutation. The poor transport of chloride ions and water across epithelial cells of the respiratory and pancreatic exocrine glands in CF results in an increased viscosity of secretions. The range of presentations is varied, including recurrent chest infections, failure to thrive due to malabsorption and liver disease. In the neonatal period, infants may present with prolonged neonatal jaundice, bowel obstruction (meconium ileus) or rectal prolapse.
Protective effects and mechanism of action of ruscogenin in a mouse model of ovalbumin-induced asthma
Published in Journal of Asthma, 2022
Shanshan Zhan, Wei Wang, Lingfei Kong
HBE cells were treated with 50 µmol/L 4,4’-diisothiocyanate octadecene-2,2’-disodium disulfonate salt solution (DIDS) for 1 h, which is a chloride-channel blocker that affects the activity of various transporters, including Ca2+-activated chloride channels. DIDS has been shown to directly form a planar lipid bilayer with VDAC1 to inhibit its oligomerization. After DIDS treatment, the cells were treated with 10 µmol/L ruscogenin for 2 h, followed by treatment with 400 µmol/L H2O2 for 1 h.
Short-term exposure of Balb/c mice to buprofezin insecticide induces biochemical, enzymatic, histopathologic and genotoxic damage in liver and kidney tissues
Published in Toxicology Mechanisms and Methods, 2019
The present study on mice following 24 h exposure to buprofezin demonstrated dose-dependent toxicity. AST and ALT are transaminase enzymes that indicate hepatocellular damage (Nnodim et al. 2010; Tousson et al. 2011; Alm-Eldeen et al. 2015). Since ALT is found mainly in the liver, cellular damage to this tissue causes a substantial increase in the serum concentration of this enzyme, a fact rendering it an excellent marker of cellular necrosis. Presently observed elevation of serum ALT and AST upon exposure to buprofezin is an effect very similar to subacute toxicity caused by Chlorpyriphos and Cypermetherin in male mice (Khan 2006). Fipronil, a GABA gated chloride channel blocker causes similar increases in the activities of AST, ALT, ALP and LDH in rats after 45 days exposure to 1 and 10 mg/L doses (Mossa et al. 2015). Studies also indicate that serum ALT activity is though frequently associated with hepatotoxic effect; it is not always correlated with the histological findings (Ozer et al. 2010). However, in our case increase in AST and ALT was well correlated with histopathologic findings. Liver histology of mice exposed to buprofezin revealed tissue disruption. Importantly, the activities of these enzymes are roughly proportional to the extent of tissue damage (Ekam and Ebong 2007; Ogbonnia et al. 2008; Nwaehujor et al. 2011; El-Naggar et al. 2015). Since we found significant increases in the levels of liver enzymes in the serum and parallel tissue damage, buprofezin appears to be highly hepatotoxic. Presently observed increase in serum urea and creatinine not only indicated liver and kidney damage but also corroborates with the decrease in total tissue protein. Histopathology of kidneys confirmed radical kidney damage that left the kidneys of buprofezin treated animals to near failure. Very similar to our study on buprofezin, exposure of rats to 1.0 and 10.0 mg/L of fipronil in drinking water for 45 days has been shown to cause significant increases in serum creatinine and urea concentrations (Mossa et al. 2015).