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  1. High sensitivity C-reactive protein (hsCRP): Its relationship with metabolic syndrome and Framingham Risk Score
    Zahari Sham SY, Hanif E, Thambiah SC, Samsudin IN, Mohd Noor S, Osman M, et al.
    Malays J Pathol, 2021 04;43(1):33-40.
    PMID: 33903303
    INTRODUCTION: Cardiovascular disease (CVD) remains the leading cause of death in Malaysia. Identification of asymptomatic at-risk individuals is often achieved by means of a risk prediction algorithm. Traditional CVD risk factors and their associated algorithms are, however, limited by residual CVD risk. High sensitivity C-reactive protein (hsCRP) has emerged as a novel CVD risk factor. This study aimed to evaluate hsCRP as an adjunct CVD risk marker among the adult Malaysian population by determining its correlation with the Framingham Risk Score (FRS). Comparison analyses were done according to sociodemographic, clinical and laboratory factors and between subjects with and without Metabolic Syndrome (MetS).

    METHOD: This cross-sectional study involved eighty-three (n=83) adults attending a health screening program at Universiti Putra Malaysia (UPM). Demographic data, anthropometric measurements and blood samples for fasting blood glucose (FBG), fasting lipid profile (FSL), glycated haemoglobin (HbA1c) and hsCRP were taken. Respondents were grouped according to FRS and the Joint Interim Statement into 10-year CVD risk categories (low, intermediate and high) and MetS, respectively.

    RESULTS: hsCRP was significantly increased in patients with high body mass index (BMI) (p=0.001), at-risk waist circumference (WC) (p=0.001) and MetS (p=0.009). Spearman's correlation coefficient showed a significant positive correlation between hsCRP level and total FRS score (r=0.26, p<0.05) and HDL-C score (r=0.22, p<0.05).

    CONCLUSION: The significant difference of hsCRP levels across obesity levels and MetS with its modest correlation with FRS scores supported the adjunctive role of hsCRP in CVD risk prediction, most likely capturing the inflammatory pathological aspect and thus partly accounting for the residual CVD risk.

  2. Plasmodium falciparum protein kinase as a potential therapeutic target for antimalarial drugs development
    Mahmud F, Lee PC, Abdul Wahab H, Mustaffa KMF, Leow CH, Azhar R, et al.
    Trop Biomed, 2020 Sep 01;37(3):822-841.
    PMID: 33612795 DOI: 10.47665/tb.37.3.822
    Malaria is one of the most dangerous infectious diseases due to its high infection and mortality rates, especially in the tropical belt. Plasmodium falciparum (P. falciparum), the most virulent malaria parasite in humans, was recently reported to develop resistance against the final efficient antimalarial drug, artemisinin. Little is known about the resistance mechanisms, which further complicates the problem as a proper counteraction is unable to be taken. Hence, the understanding of drug mode of action and its molecular target is valuable knowledge that needs to be considered to develop the next generation of antimalarial drugs. P. falciparum protein kinase (Pf PK) is an attractive target for antimalarial chemotherapy due to its vital roles in all P. falciparum life stages. Moreover, overall structural differences and the presence of unique Pf PKs that are absent in human kinome, suggesting specific inhibition of Pf PK without affecting human cells is achievable. To date, at least 86 eukaryotic protein kinases have been identified in P. falciparum kinome, by which less than 40 were validated as potential targets at the erythrocytes stage. In this review, recent progress of the furthest validated Pf PKs; Pf Nek-1, Pf CDPK1, Pf CDPK4, Pf PKG, and Pf CLK-3 will be briefly discussed.
  3. Fulltext Square wave voltammetry based electrochemical determination of affinity of cholesterol triethylene glycol modified DNA-aptamers for protoporphyrin IX
    Aliyu AW, Mohd Nazri MN, Mohd Zaidi NF, Mohd Fadzli Mustaffa K
    Heliyon, 2023 Aug;9(8):e18861.
    PMID: 37609428 DOI: 10.1016/j.heliyon.2023.e18861
    Recent advancement in molecular medicine has seen applications of advanced biotechnology tools such as aptamer technology in therapeutics and diagnostics. Aptamer technology has witnessed various approaches including "Click-Chemistry" towards modifying aptamer structure to improve its potentials, but limited studies have reported the influence of such alteration on aptamer's specificity and affinity for their targets. Here, we utilized square wave voltammetry (SWV) electrochemical sensing based on heme to show the effects of cholesterol-triethylene-glycol (COL-TEG) modification of protoporphyrin-IX DNA-aptamers (OKA_24 and OKA_26) on their affinity for heme. Binding was evaluated by immobilizing 5 μM of heme onto cysteamine-glutaraldehyde-coated gold-electrode to construct electrochemical biosensor. Sensing of native/modified-aptamer was achieved by incubating their varying concentrations (9.76 nM - 10 μM) with heme-coated gold-electrode in HKSCM buffer pH 5, for 15 min. Chloroquine (2.5 μM) and non-binding HPIX-aptamer (2.5 μM) served as controls. Ferrocene was the redox solution used for SWV analysis. Protoporphyrin-IX DNA-aptamers specificity for heme was not tarnish by lipid conjugation. Selective binding of 2.5 μM of COL-TEG-OKA_24 and COL-TEG-OKA_26 to heme induced peak-current reduction by 30.68% and 24% respectively. Incubation of OKA_24 and OKA_26 aptamers produced resistance to current flow through the heme-coated gold-electrode by 23.21% and 14.4 8% respectively. Affinity SWV reveals that cholesterol conjugation decreases the affinity of COL-TEG-OKA_24 (KD = 4 7.13 ± 3.767 nM) and COL-TEG-OKA_24 (KD = 84.6 ± 8.7 nM) by 3- fold. There is a need to check the impact of such alteration on inhibition of heme to hemozoin polymerization, a process mediated by Plasmodium falciparum.
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