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  1. Lim JX, Vadivelu VM
    J Environ Manage, 2014 Dec 15;146:217-225.
    PMID: 25173730 DOI: 10.1016/j.jenvman.2014.07.023
    A sequencing batch reactor (SBR) with a working volume of 8 L and an exchange ratio of 25% was used to enrich biomass for the treatment of the anaerobically treated low pH palm oil mill effluent (POME). The influent concentration was stepwise increased from 5000 ± 500 mg COD/L to 11,500 ± 500 mg COD/L. The performance of the reactor was monitored at different organic loading rates (OLRs). It was found that approximately 90% of the COD content of the POME wastewater was successfully removed regardless of the OLR applied to the SBR. Cycle studies of the SBR show that the oxygen uptake by the biomass while there is no COD reduction may be due to the oxidation of the storage product by the biomass. Further, the growth kinetic parameters of the biomass were determined in batch experiments using respirometer. The maximum specific growth rate (μmax) was estimated to be 1.143 day(-1) while the half saturation constant (Ks) with respect to COD was determined to be 0.429 g COD/L. The decay coefficient (bD) and biomass yield (Y) were found to be 0.131 day(-1) and 0.272 mg biomass/mg COD consumed, respectively.
  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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