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  1. Fathinul F, Nordin AJ, Lau WF
    Cell Biochem Biophys, 2013 May;66(1):37-43.
    PMID: 22790883 DOI: 10.1007/s12013-012-9395-5
    Molecular imaging employing (18)[F]FDG-PET/CT enables in-vivo visualization, characterisation and measurement of biological process in tumour at the molecular and cellular level. In oncology, this approach can be directly applied as translational biomarkers of disease progression. In this article, the improved roles of FDG as an in-vivo glycolytic marker which reflect biological changes across in-vitro cellular environment are discussed. New understanding in how altered metabolism via glycolytic downstream drivers of malignant transformation as reviewed below offers unique promise as to monitor tumour aggressiveness and hence optimize the therapeutic management.
  2. Moad AI, Muhammad TS, Oon CE, Tan ML
    Cell Biochem Biophys, 2013 Jul;66(3):567-87.
    PMID: 23300026 DOI: 10.1007/s12013-012-9504-5
    Autophagy is an evolutionarily conserved lysosomal degradation pathway and plays a critical role in the homeostatic process of recycling proteins and organelles. Functional relationships have been described between apoptosis and autophagy. Perturbations in the apoptotic machinery have been reported to induce autophagic cell deaths. Inhibition of autophagy in cancer cells has resulted in cell deaths that manifested hallmarks of apoptosis. However, the molecular relationships and the circumstances of which molecular pathways dictate the choice between apoptosis and autophagy are currently unknown. This study aims to identify specific gene expression of rapamycin-induced autophagy and the effects of rapamycin when the autophagy process is inhibited. In this study, we have demonstrated that rapamycin is capable of inducing autophagy in T-47D breast carcinoma cells. However, when the autophagy process was inhibited by 3-MA, the effects of rapamycin became apoptotic. The Phlda1 gene was found to be up-regulated in both autophagy and apoptosis and silencing this gene was found to reduce both activities, strongly suggests that Phlda1 mediates and positively regulates both autophagy and apoptosis pathways.
  3. Karkada G, Maiya GA, Arany P, Rao M, Adiga S, Kamath SU
    Cell Biochem Biophys, 2021 Jul 30.
    PMID: 34331219 DOI: 10.1007/s12013-021-01021-9
    BACKGROUND: Prolonged and overlapping phases of wound healing in diabetes are mainly due to the redox imbalance resulting in the chronicity of the wound. Photobiomodulation therapy works on the principle of absorption of photon energy and its transduction into a biological response in the living tissue. It alleviates the cellular responses, thereby improving the mechanism of wound healing in diabetes.

    OBJECTIVE: To find out the effect of photobiomodulation therapy of dosage 4 J/cm2 in the healing dynamics of diabetic neuropathic wounds in Wistar rats and its relation with oxidative stress markers.

    METHODOLOGY: Diabetes was induced using Streptozotocin of 60 mg/kg of body weight to eighteen female Wistar rats. Neuropathy was induced by the sciatic nerve crush injury followed by an excisional wound of 2 cm2 on the back of the animal. Experimental group animals were treated with dosage 4 J/cm2 of wavelength 655 and 808 nm, and control group animals were kept unirradiated. The biomechanical, histopathological, and biochemical changes were analysed in both groups.

    RESULTS: There was a reduction in mean wound healing time and an increased rate of wound contraction in the experimental group animals compared to its control group. The experimental group showed improved redox status, and histopathological findings revealed better proliferative cells, keratinisation, and epithelialization than un-irradiated controls.

    CONCLUSIONS: Photobiomodulation therapy of dosage 4 J/cm2 enhanced the overall wound healing dynamics of the diabetes-induced neuropathic wound and optimised the oxidative status of the wound, thereby facilitating a faster healing process.

  4. Samad MA, Saiman MZ, Abdul Majid N, Karsani SA, Yaacob JS
    Cell Biochem Biophys, 2024 Mar;82(1):153-173.
    PMID: 38198024 DOI: 10.1007/s12013-023-01210-8
    Colorectal cancer (CRC) is the most common cancer in both men and women and is associated with increased telomerase levels and activity. The potential downstream effects of TERT and/or TERC downregulation by berberine (a telomerase inhibitor) or RNA interference (RNAi) on various target RNAs, proteins, relative telomerase activity (RTA), relative telomere length (RTL), hydrogen peroxide concentration [H2O2], percentage of cell cycle distribution, cell size and granularity as well as cellular metabolites were explored in HCT 116 cell line. Knockdown of TERT decreased TERC. The downregulation of TERT and/or TERC caused increment of [H2O2], G0/G1 phase arrest in addition to decreased S and G2/M phases, as well as diminished cell size. RTL was later reduced as a result of TERT, TERT and/or TERC downregulation which decreased RTA. It was discovered that xanthine oxidase (XO) was significantly and positively correlated at FDR-adjusted p value 
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