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Fulltext Awareness on breast cancer screening in Malaysia: a cross sectional study

Lee MS, 'Azmiyaty Amar Ma' Ruf C, Nadhirah Izhar DP, Nafisah Ishak S, Wan Jamaluddin WS, Ya'acob SNM, et al.

Biomedicine (Taipei), 2019 Sep;9(3):18.
PMID: 31453799 DOI: 10.1051/bmdcn/2019090318

INTRODUCTION: The increasing rate of breast cancer (BC) incidence in Malaysia hints a lack of awareness among Malaysians. One (1) woman out of nineteen (19) is at risk with BC and almost up to fifty percent (50%) of women diagnosed with BC were reported to be under the age of fifty (50). Our main concern is to study the level of awareness among the women on risk factors, clinical manifestations, diagnosis, preventions and treatments.
METHOD: A cross-sectional study was conducted exclusively among women in the public with total sample of three hundred and forty six (346), questionnaires were distributed using a simple random technique. Data was collected and analyzed by student T test in SPPS version 20.
RESULTS: Our study reveals insufficient awareness on BC. Overall, awareness on risk factors is inadequate, but good knowledge on the importance of family history and diet as risk factors are discovered. Awareness on the cause and clinical manifestations of BC is required for improvement. As for treatment, alternatives especially surgery and chemotherapy are unclear to public, public is remotely unwitting on cessation of smoking to prevent BC at the early stage.
CONCLUSION: Malaysian has spaces for improvement on awareness of BC in terms of risk factors, clinical manifestations, diagnosis, treatment and prevention. Early detection can be achieved with good awareness because it leads to better prognosis and lower mortality.
Fulltext Preliminary Study of Structural Changes of Glucose-6-Phosphate Dehydrogenase Deficiency Variants

Louis NE, Hamza MA, Baharuddin PNEB, Chandran S, Latif NA, Alonazi MA, et al.

Biomedicine (Taipei), 2022;12(3):12-19.
PMID: 36381187 DOI: 10.37796/2211-8039.1355

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzyme deficiency disorder affecting over 400 million individuals worldwide. G6PD protects red blood cells (RBC) from the harmful effects of oxidative substances. There are more than 400 G6PD mutations, of which 186 variants have shown to be linked to G6PD deficiency by decreasing the activity or stability of the enzyme. Different variants manifest different clinical phenotypes which complicate comprehending the mechanism of the disease. In order to carry out computational approaches to elucidate the structural changes of different G6PD variants that are common to the Asian population, a complete G6PD monomer-ligand complex was constructed using AutoDock 4.2, and the molecular dynamics simulation package GROMACS 4.6.7 was used to study the protein dynamics. The G410D and V291M variants were chosen to represent classes I and II respectively and were created by in silico site-directed mutagenesis. Results from the Root mean square deviation (RMSD), Root mean square fluctuation (RMSF) and Radius of gyration (Rg) analyses provided insights on the structure - function relationship for the variants. G410D indicated impaired dimerization and structural NADP binding while the impaired catalytic activity for V291M was indicated by a conformational change at its mutation site.
Fulltext LEP G2548A polymorphism is associated with increased serum leptin and insulin resistance among T2DM Malaysian patients

Ali LA, Jemon K, Latif NA, Bakar SA, Alwi SSS

Biomedicine (Taipei), 2022;12(3):1-11.
PMID: 36381191 DOI: 10.37796/2211-8039.1326

Background: Type 2 diabetes mellitus (T2DM) is a chronic metabolic syndrome that is rapidly increasing across the world, especially in Malaysia. Leptin plays a vital role in the regulation of metabolism through its effect on peripheral tissues. G2548A polymorphism in the LEP gene promoter has been associated with insulin resistance, leptin, and type 2 diabetes mellitus across different population, but has not been inclusively reported within the Malaysian population.
Objective: Thus, our study aimed to investigate the impact of G2548A polymorphism on serum leptin levels and insulin resistance among Malaysian T2DM patients.
Methods: This case-control study involved 150 T2DM patients and 150 non-diabetic volunteers from ethnic Malays, Chinese and Indians. Genotyping of G2548A polymorphism was carried out using PCR-RFLP. Serum leptin and insulin levels were determined via ELISA. ANOVA and Chi-square tests were used to determine the distribution of genotypes and allelic frequencies based on serum leptin and insulin levels.
Results: Frequency of AA genotype and A allele of G2548A variant were significantly (P < 0.05) higher in T2DM patients of Malay and Indian ethnicities (4%, 35%, and 36%, 57%, respectively) as compared to the control groups (0%, 22%, and 18%, 35%, respectively). Fasting serum leptin levels were significantly (P < 0.001) higher in T2DM patients compared to non-diabetic subjects (166.78 pg/ml, 101.94 pg/ml, respectively). Additionally, elevated serum leptin, insulin levels, and BMI in diabetic patients were found to be associated with the AA genotype of this variant, compared to GG, and GA genotypes (P < 0.05).
Conclusion: Our findings suggest a significant association between G2548A polymorphism among Malaysian T2DM subjects, particularly among Malay and Indian ethnic groups. Moreover, the A allele frequency of the G2548A variant significantly increased the risk of T2DM and is significantly associated with increased serum leptin, insulin levels, and elevated BMI.
Fulltext Crosstalk between fatty acid metabolism and tumour-associated macrophages in cancer progression

Zaidi NE, Shazali NAH, Leow TC, Osman MA, Ibrahim K, Rahman NMANA

Biomedicine (Taipei), 2022;12(4):9-19.
PMID: 36816174 DOI: 10.37796/2211-8039.1381

Over the last few decades, cancer has been regarded as an independent and self sustaining progression. The earliest hallmarks of cancer comprise of sustaining proliferative signalling, avoiding growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Nonetheless, two emerging hallmarks are being described: aberrant metabolic pathways and evasion of immune destruction. Changes in tumour cell metabolism are not restricted to tumour cells alone; the products of the altered metabolism have a direct impact on the activity of immune cells inside the tumour microenvironment, particularly tumour-associated macrophages (TAMs). The complicated process of cancer growth is orchestrated by metabolic changes dictating the tight mutual connection between these cells. Here, we discuss approaches to exploit the interaction of cancer cells' abnormal metabolic activity and TAMs. We also describe ways to exploit it by reprogramming fatty acid metabolism via TAMs.
Fulltext Computational analysis of dimer G6PD structure to elucidate pathogenicity of G6PD variants

Chandran S, Louis NE, Amran SI, Ab Latif N, Hamza MA, Alonazi M

Biomedicine (Taipei), 2024;14(1):47-59.
PMID: 38533298 DOI: 10.37796/2211-8039.1431

An inherent genetic enzyme disorder in humans, known as glucose-6-phosphate dehydrogenase (G6PD) deficiency, arises due to specific mutations. While the prevailing approach for investigating G6PD variants involves biochemical analysis, the intricate structural details remain limited, impeding a comprehensive understanding of how different G6PD variants of varying classes impact their functionality. This study 22 examined the dynamic properties of G6PD wild types and six G6PD variants from 23 different classes using molecular dynamic simulation (MDS). The wild-type and variant 24 G6PD structures unveil high fluctuations within the amino acid range of 274-515, the structural NADP+ binding site, pivotal for enzyme dimerization. Specifically, two variants, G6PDZacatecas (R257L) and G6PDDurham (K238R), demonstrate compromised structural stability at the dimer interface, attributable to the disruption of a salt bridge involving Glu 206 and Lys 407, along with the disturbance of hydrogen bonds formed by Asp 421 at the βN-βN sheets. Consequently, this impairment cascades to affect the binding affinity of crucial interactions, such as Lys 171-Glucose-6-Phosphate (G6P) and Lys 171-catalytic NADP+, leading to diminished enzyme activity. This study underscores the utility of computational in silico techniques in predicting the structural alterations and flexibility of G6PD variants. This insight holds promise for guiding future endeavors in drug development targeted at mitigating the impacts of G6PD deficiency.