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  1. Romano N, Ashikin M, Teh JC, Syukri F, Karami A
    Environ Pollut, 2018 Jun;237:1106-1111.
    PMID: 29157968 DOI: 10.1016/j.envpol.2017.11.040
    Silver barb Barbodes gonionotus fry were exposed to polyvinyl chloride (PVC) fragments at increasing concentrations of 0.2, 0.5 and 1.0 mg/L for 96 h, following which whole body histological evaluation and analysis of the digestive enzymes trypsin and chymotrypsin were performed. Whole body trypsin and chymotrypsin activities increased significantly in fish exposed to 0.5 and 1.0 mg/L PVC as compared those exposed to zero or 0.2 mg/L PVC. In fish exposed to all tested concentrations, PVCs were observed in both the proximal and distal intestine, and fish exposed to 0.5-1.0 and 1.0 mg/L PVC, respectively, and these particles were associated with localized thickening of the mucosal epithelium. No tissue damage was evident in any other internal organs or gills. This lack of damage may be attributed to the absence of contaminants associated with the PVC fragments and their relatively smooth surface. The increased whole body trypsin and chymotrypsin activities may indicate an attempt to enhance digestion to compensate for epithelial thickening of the intestine and/or to digest the plastics.
  2. Dauda AB, Teh JC, Amin SMN, Kamarudin MS, Romano N
    J Pestic Sci, 2016 Aug 20;41(3):83-86.
    PMID: 30363129 DOI: 10.1584/jpestics.D16-055
    Trypsin-modulating oostatic factor (TMOF) is an effective mosquito larvicide, but information on its potential toxicity to non-target organisms is limited. To investigate this, triplicate groups of 10 Macrobrachium rosenbergii were exposed to 0, 10, 50 or 100 mg/L nominal TMOF concentrations for 12 days. Tail moisture, crude protein, and hepatopancreatic glycogen/histopathology were unaffected, but increasing TMOF linearly decreased survival and growth. TMOF at the lowest concentration employed significantly decreased trypsin and chymotrypsin activities.
  3. Khairun Waheeda AI, Teh JC, Arshad A, Wong NLWS
    Mar Pollut Bull, 2023 Jul;192:115111.
    PMID: 37295254 DOI: 10.1016/j.marpolbul.2023.115111
    This study investigated the impacts of the removal of sand bund on the macrobenthos community structure, seagrass cover, and sediment particle size in Merambong Shoal, Malaysia. The reclamation project deposited sand bund in the middle of Merambong seagrass shoal, resulting in its division into northern (NS) and southern (SS) halves. Ecosystem changes were monitored over a 31-month period using the transect lines method. Bi-monthly samples were collected for assessment. The results revealed a substantial decline in macrobenthos densities compared to previous studies. However, after the removal of the sand bund, there was a significant increase in macrobenthos density, specifically Polychaeta and Malacostraca, at NS. Seagrass cover at NS was initially lower than SS but showed an increase after the complete removal of the sand blockage. Sediment particle analysis reported a higher silt percentage at NS, indicating greater sedimentation at NS, which was partially sheltered from wave actions.
  4. Gee HY, Sadowski CE, Aggarwal PK, Porath JD, Yakulov TA, Schueler M, et al.
    Nat Commun, 2016 Feb 24;7:10822.
    PMID: 26905694 DOI: 10.1038/ncomms10822
    Steroid-resistant nephrotic syndrome (SRNS) causes 15% of chronic kidney disease (CKD). Here we show that recessive mutations in FAT1 cause a distinct renal disease entity in four families with a combination of SRNS, tubular ectasia, haematuria and facultative neurological involvement. Loss of FAT1 results in decreased cell adhesion and migration in fibroblasts and podocytes and the decreased migration is partially reversed by a RAC1/CDC42 activator. Podocyte-specific deletion of Fat1 in mice induces abnormal glomerular filtration barrier development, leading to podocyte foot process effacement. Knockdown of Fat1 in renal tubular cells reduces migration, decreases active RAC1 and CDC42, and induces defects in lumen formation. Knockdown of fat1 in zebrafish causes pronephric cysts, which is partially rescued by RAC1/CDC42 activators, confirming a role of the two small GTPases in the pathogenesis. These findings provide new insights into the pathogenesis of SRNS and tubulopathy, linking FAT1 and RAC1/CDC42 to podocyte and tubular cell function.
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