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  1. Lim PE, Wong TF, Lim DV
    Environ Int, 2001 May;26(5-6):425-31.
    PMID: 11392762
    This study was conducted to: (1) assess the role of wetland vegetation in the removal of oxygen demand and nitrogen under tropical conditions, (2) estimate the uptake of nitrogen and copper by wetland plants and (3) investigate the speciation of Cu in wetland media among four operationally defined host fractions, namely exchangeable, carbonate, reducible and organically bound. Four laboratory-scale wetland units, two free-water-surface (FWS) and two subsurface-flow (SF) with one of each planted with cattails (Typha augustifolia), were fed with primary-treated sewage and operated at nominal retention times of 0.6-7 days. The influent and effluent BOD/COD and nitrogen concentrations were monitored to assess the performance of the wetland units for various mass loading rates. At the end of the study, all cattail plants were harvested and analyzed for total Kjeldahl nitrogen (TKN). Four other wetland units, which were identical to the first four, were fed with domestic wastewater spiked with copper in increasing concentrations. Copper speciation patterns in the sand layer were determined at the end of the study. The results showed that wetland vegetation did not play an important role in oxygen demand removal but were capable of removing about 22% and 26% of the nitrogen input in the FWS and SF wetland units, respectively. Mass balance analysis indicated that less than 1% of copper introduced was taken up by the cattails. Copper speciation patterns in the sand media showed that the exchangeable fraction contributed 30-57% and 63-80% of the nonresidual copper in the planted and unplanted FWS wetlands, respectively. For SF units, the percentages were 52-62% and 59-67%, respectively. This indicates that large amount of copper in the media were potentially remobilizable.
  2. Lim DV, Woo WH, Lim JX, Loh XY, Soh HT, Lim SYA, et al.
    Curr Mol Pharmacol, 2024;17(1):e140923221042.
    PMID: 37711005 DOI: 10.2174/1874467217666230914090621
    BACKGROUND: Mutations in the TP53 gene are the most common among genetic alterations in human cancers, resulting in the formation of mutant p53 protein (mutp53). Mutp53 promotes proliferation, migration, invasion, and metastasis in cancer cells. Not only does the initiation of oncogenesis ensue due to mutp53, but resistance towards chemotherapy and radiotherapy in cancer cells also occurs. This review aims to summarise and discuss the oncogenesis of mutant p53 in cancer cells and introduce the various mutant p53 inhibitors currently being evaluated at the pre-clinical and clinical stages. Compounds that induce the wild-type conformation on the targeted p53 missense mutation, restore or enhance the DNA binding of mutant p53, and inhibit cancer cells' growth are highlighted. In addition, the progression and development of the mutant p53 inhibitors in clinical trials are updated.

    CONCLUSION: The progress of developing a cancer treatment that may successfully and efficiently target mutant p53 is on the verge of development. Mutant p53 proteins not only initiate oncogenesis but also cause resistance in cancer cells to certain chemo or radiotherapies, further endorse cancer cell survival and promote migration as well as metastasis of cancerous cells. With this regard, many mutant p53 inhibitors have been developed, some of which are currently being evaluated at the pre-clinical level and have been identified and discussed. To date, APR-246 is the most prominent one that has progressed to the Phase III clinical trial.

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