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Perceived parenting style of fathers and adolescents' locus of control in a collectivist culture of Malaysia: the moderating role of fathers' education

Keshavarz S, Baharudin R, Mounts NS

J Genet Psychol, 2013 May-Jun;174(3):253-70.
PMID: 23991523

The authors investigated the moderating role of father's education on the associations between perceived paternal parenting styles and locus of control among 382 Malaysian adolescents with an average age of 14.27. Data were collected by means of adolescents' self-report using standardized instruments (i.e., parental authority questionnaire and Nowicki-Strickland Internal-External Control Scale for Children). Results revealed that there were significant negative relationships between fathers' authoritative parenting style (r = -.243, p < .001) and authoritarian parenting style (r = -.130, p < .01) with adolescents' internal locus of control. Furthermore, the findings indicated that father's high level of education moderated the relationship between perceived paternal authoritarian parenting and locus of control (b = -0.147, p < .001). The findings underscore the need to include the role of parents' education when assessing the links between parenting styles and adolescents' locus of control.
Effectiveness of health education module on work safety culture in improving knowledge, attitudes and practices: a cluster randomized controlled trial among public sector administrative workers in Nigeria

Odu JO, Hamedon TR, Mahmud A, Baharudin R

Med J Malaysia, 2023 May;78(3):308-317.
PMID: 37271840

INTRODUCTION: Studies have shown that a workplace safety culture (WSC) is lacking among the general workforce in Nigeria. Poor WSC can adversely impact workers' health and high remedial costs for employers. To improve WSC, workers need to improve related knowledge, attitude, and practices (KAP) towards WSC through effective health interventional programs at the workplace. The main objective of this study is to develop, implement and evaluate the effectiveness of the Work Safety Culture Health Education Module (WSCHEM). The specific goals are to improve KAP related to office ergonomics towards WSC among public sector administrative workers in Abeokuta, Nigeria MATERIALS AND METHODS: The study was a two-armed, singleblinded cluster randomised controlled trial (CRCT) involving 247 public sector administrative workers from clusters of 20 ministries in Abeokuta, Southwestern Nigeria. The intervention group was given WSCHEM, whereas the waitlist group received a seminar on team building and leadership skills and received the WSCHEM after the intervention program ended. The evaluation was done three times using the first formal validated, self-administered Work Safety Culture Questionnaire (WSCQ) among the administrative workers: first at baseline, second at 1 month, and third at 3 months post-intervention.
RESULT: The results showed no statistically significant differences between groups regarding the respondents' characteristics (socio-demographic and occupational/officerelated ergonomic factors) and the outcome variables KAP towards WSC at baseline. For practices towards WSC, both intervention (β 6.8, 95%CI 4.85, 8.72) and time (β 6.2, 95%CI 4.49, 7.94) significantly improved the respondents' practices towards WSC in the per-protocol analysis. In the secondary outcomes, both knowledge of WSC, intervention (β 3.5, 95%CI 2.8, 4.2) and time (β 3.4, 95%CI 2.7, 5.9); and attitudes towards WSC, intervention (β1.7, 95%CI 1.25, 2.23) and time (β 2.3, 95%CI 1.92, 2.76) significantly improved the respondents' level of knowledge and attitudes respectively towards WSC.
CONCLUSION: The intervention, WSCHEM, was effective in improving the administrative workers' KAP towards WSC, as demonstrated by the significance between and within-group differences.
Fulltext Epigenetics of SFRP1: The Dual Roles in Human Cancers

Baharudin R, Tieng FYF, Lee LH, Ab Mutalib NS

Cancers (Basel), 2020 Feb 14;12(2).
PMID: 32074995 DOI: 10.3390/cancers12020445

Secreted frizzled-related protein 1 (SFRP1) is a gene that belongs to the secreted glycoprotein SFRP family. SFRP1 has been classified as a tumor suppressor gene due to the loss of expression in various human cancers, which is mainly attributed by epigenetic inactivation via DNA methylation or transcriptional silencing by microRNAs. Epigenetic silencing of SFRP1 may cause dysregulation of cell proliferation, migration, and invasion, which lead to cancer cells formation, disease progression, poor prognosis, and treatment resistance. Hence, restoration of SFRP1 expression via demethylating drugs or over-expression experiments opens the possibility for new cancer therapy approach. While the role of SFRP1 as a tumor suppressor gene is well-established, some studies also reported the possible oncogenic properties of SFRP1 in cancers. In this review, we discussed in great detail the dual roles of SFRP1 in cancers-as tumor suppressor and tumor promoter. The epigenetic regulation of SFRP1 expression will also be underscored with additional emphasis on the potentials of SFRP1 in modulating responses toward chemotherapeutic and epigenetic-modifying drugs, which may encourage the development of novel drugs for cancer treatment. We also present findings from clinical trials and patents involving SFRP1 to illustrate its clinical utility, extensiveness of each research area, and progression toward commercialization. Lastly, this review provides directions for future research to advance SFRP1 as a promising cancer biomarker.
Fulltext Identification of Predictive DNA Methylation Biomarkers for Chemotherapy Response in Colorectal Cancer

Baharudin R, Ab Mutalib NS, Othman SN, Sagap I, Rose IM, Mohd Mokhtar N, et al.

Front Pharmacol, 2017;8:47.
PMID: 28243201 DOI: 10.3389/fphar.2017.00047

Resistance to 5-Fluorouracil (5-FU) is a major obstacle to the successful treatment of colorectal cancer (CRC) and posed an increased risk of recurrence. DNA methylation has been suggested as one of the underlying mechanisms for recurrent disease and its contribution to the development of drug resistance remains to be clarified. This study aimed to determine the methylation phenotype in CRC for identification of predictive markers for chemotherapy response. We performed DNA methylation profiling on 43 non-recurrent and five recurrent CRC patients using the Illumina Infinium HumanMethylation450 Beadchip assay. In addition, CRC cells with different genetic backgrounds, response to 5-FU and global methylation levels (HT29 and SW48) were treated with 5-FU and DNA methylation inhibitor 5-aza-2'-deoxycytidine (5-azadC). The singular and combined effects of these two drug classes on cell viability and global methylation profiles were investigated. Our genome-wide methylation study on the clinical specimens showed that recurrent CRCs exhibited higher methylation levels compared to non-recurrent CRCs. We identified 4787 significantly differentially methylated genes (P < 0.05); 3112 genes were hyper- while 1675 genes were hypomethylated in the recurrent group compared to the non-recurrent. Fifty eight and 47 of the significantly hypermethylated and hypomethylated genes have an absolute recurrent/non-recurrent methylation difference of ≥20%. Most of the hypermethylated genes were involved in the MAPK signaling pathway which is a key regulator for apoptosis while the hypomethylated genes were involved in the PI3K-AKT signaling pathway and proliferation process. We also demonstrate that 5-azadC treatment enhanced response to 5-FU which resulted in significant growth inhibition compared to 5-FU alone in hypermethylated cell lines SW48. In conclusion, we found the evidence of five potentially biologically important genes in recurrent CRCs that could possibly serve as a new potential therapeutic targets for patients with chemoresistance. We postulate that aberrant methylation of CCNEI, CCNDBP1, PON3, DDX43, and CHL1 in CRC might be associated with the recurrence of CRC and 5-azadC-mediated restoration of 5-FU sensitivity is mediated at least in part by MAPK signaling pathway.
Fulltext Single Cell Transcriptome in Colorectal Cancer-Current Updates on Its Application in Metastasis, Chemoresistance and the Roles of Circulating Tumor Cells

Tieng FYF, Baharudin R, Abu N, Mohd Yunos RI, Lee LH, Ab Mutalib NS

Front Pharmacol, 2020;11:135.
PMID: 32174835 DOI: 10.3389/fphar.2020.00135

Colorectal cancer (CRC) is among the most common cancer worldwide, a challenge for research, and a model for studying the molecular mechanisms involved in its development. Previously, bulk transcriptomics analyses were utilized to classify CRC based on its distinct molecular and clinicopathological features for prognosis and diagnosis of patients. The introduction of single-cell transcriptomics completely turned the table by enabling the examination of the expression levels of individual cancer cell within a single tumor. In this review, we highlighted the importance of these single-cell transcriptomics analyses as well as suggesting circulating tumor cells (CTCs) as the main focus of single-cell RNA sequencing. Characterization of these cells might reveal the intratumoral heterogeneity present in CRC while providing critical insights into cancer metastasis. To summarize, we believed the analysis of gene expression patterns of CTC from CRC at single-cell resolution holds the potential to provide key information for identification of prognostic and diagnostic markers as well as the development of precise and personalized cancer treatment.
Fulltext Antimicrobial Susceptibility of Klebsiella pneumoniae and Escherichia coli with Extended-Spectrum β-lactamase associated Genes in Hospital Tengku Ampuan Afzan, Kuantan, Pahang

Mahdi Yahya Mohsen S, Hamzah HA, Muhammad Imad Al-Deen M, Baharudin R

Malays J Med Sci, 2016 Mar;23(2):14-20.
PMID: 27547110 MyJurnal

To assess antimicrobial susceptibility of extended-spectrum β-lactamase- (ESBL-) producing Klebsiella pneumoniae and Escherichia coli isolates from Hospital Tengku Ampuan Afzan (HTAA), as well as to identify ESBL genes.
Young adult survivors of childhood acute lymphoblastic leukemia show evidence of chronic inflammation and cellular aging

Ariffin H, Azanan MS, Abd Ghafar SS, Oh L, Lau KH, Thirunavakarasu T, et al.

Cancer, 2017 Nov 01;123(21):4207-4214.
PMID: 28654149 DOI: 10.1002/cncr.30857

BACKGROUND: Large epidemiologic studies have reported the premature onset of age-related conditions, such as ischemic heart disease and diabetes mellitus, in childhood cancer survivors, decades earlier than in their peers. The authors investigated whether young adult survivors of childhood acute lymphoblastic leukemia (ALL) have a biologic phenotype of cellular ageing and chronic inflammation.
METHODS: Plasma inflammatory cytokines were measured using a cytometric bead array in 87 asymptomatic young adult survivors of childhood ALL (median age, 25 years; age range, 18-35 years) who attended annual follow-up clinic and compared with healthy, age-matched and sex-matched controls. Leukocyte telomere length (LTL) was measured using Southern blot analysis.
RESULTS: Survivors had significant elevation of plasma interleukin-2 (IL-2), IL-10, IL-17a, and high-sensitivity C-reactive protein levels (all P 0.8 mg/dL) was related to increased odds of having metabolic syndrome (odds ratio, 7.256; 95% confidence interval, 1.501-35.074). Survivors also had significantly shorter LTL compared with controls (median, 9866 vs 10,392 base pairs; P = .021). Compared with published data, LTL in survivors was similar to that in healthy individuals aged 20 years older. Survivors who received cranial irradiation had shorter LTL compared with those who had not (P = .013).
CONCLUSIONS: Asymptomatic young adult survivors of childhood ALL demonstrate a biologic profile of chronic inflammation and telomere attrition, consistent with an early onset of cellular processes that drive accelerated aging. These processes may explain the premature development of age-related chronic conditions in childhood cancer survivors. Understanding their molecular basis may facilitate targeted interventions to disrupt the accelerated aging process and its long-term impact on overall health. Cancer 2017;123:4207-4214. © 2017 American Cancer Society.