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  1. Ali M, Wahab IBA, Huri HZ, Yusoff MS
    Syst Rev, 2024 Apr 02;13(1):99.
    PMID: 38566190 DOI: 10.1186/s13643-024-02478-4
    BACKGROUND: Personalised learning, an educational approach that tailors teaching and learning to individual needs and preferences, has gained attention in recent years, particularly in higher education. Advances in educational technology have facilitated the implementation of personalised learning in various contexts. Despite its potential benefits, the literature on personalised learning in health sciences higher education remains scattered and heterogeneous. This scoping review aims to identify and map the current literature on personalised learning in health sciences higher education and its definition, implementation strategies, benefits, and limitations.

    METHODS: A comprehensive search of electronic databases, PubMed, Scopus, Google Scholar, Educational Research Complete, and Journal Storage (JSTOR), will be conducted to identify relevant articles. The search will be limited to articles published in the English language between 2000 and 2023. The search strategy will be designed and adapted for each database using a combination of keywords and subject headings related to personalised learning and health sciences higher education. Eligibility criteria will be applied to screen and select articles. Data extraction and quality assessment will be performed, and thematic synthesis will be used to analyse the extracted data.

    DISCUSSION: The results of the scoping review will present a comprehensive and coherent overview of the literature on personalised learning in health sciences higher education. Key themes and topics related to personalised learning, its definitions, models, implementation strategies, benefits, and limitations, will be identified. The geographical and temporal distribution of research on personalised learning in health sciences higher education will also be described. This scoping review will provide a structured synthesis of the available evidence on personalised learning in health sciences higher education, highlighting potential gaps and areas for future research. The findings will contribute to ongoing scholarly and policy debates on personalised learning in higher education, informing the development of best practices, guidelines, and future research agendas.

  2. Bakar MH, Sarmidi MR, Kai CK, Huri HZ, Yaakob H
    Int J Mol Sci, 2014 Dec 02;15(12):22227-57.
    PMID: 25474091 DOI: 10.3390/ijms151222227
    A growing body of evidence suggests that activation of nuclear factor kappa B (NF-κB) signaling pathways is among the inflammatory mechanism involved in the development of insulin resistance and chronic low-grade inflammation in adipose tissues derived from obese animal and human subjects. Nevertheless, little is known about the roles of NF-κB pathways in regulating mitochondrial function of the adipose tissues. In the present study, we sought to investigate the direct effects of celastrol (potent NF-κB inhibitor) upon mitochondrial dysfunction-induced insulin resistance in 3T3-L1 adipocytes. Celastrol ameliorates mitochondrial dysfunction by altering mitochondrial fusion and fission in adipocytes. The levels of oxidative DNA damage, protein carbonylation and lipid peroxidation were down-regulated. Further, the morphology and quantification of intracellular lipid droplets revealed the decrease of intracellular lipid accumulation with reduced lipolysis. Moreover, massive production of the pro-inflammatory mediators tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were markedly depleted. Insulin-stimulated glucose uptake activity was restored with the enhancement of insulin signaling pathways. This study signified that the treatments modulated towards knockdown of NF-κB transcription factor may counteract these metabolic insults exacerbated in our model of synergy between mitochondrial dysfunction and inflammation. These results demonstrate for the first time that NF-κB inhibition modulates mitochondrial dysfunction induced insulin resistance in 3T3-L1 adipocytes.
  3. Huri HZ, Makmor-Bakry M, Hashim R, Mustafa N, Wan Ngah WZ
    Int J Clin Pharm, 2012 Dec;34(6):863-70.
    PMID: 22869200 DOI: 10.1007/s11096-012-9682-7
    BACKGROUND: Patients with type 2 diabetes mellitus (T2DM) are frequently admitted to the hospital with severe or acute hyperglycaemia secondary to an acute illness or disease. Uncontrolled glycaemia is a significant problem during severe or acute hyperglycaemia.

    OBJECTIVE: This study sought to identify demographic, clinical, and genetic factors that may contribute to increased insulin resistance or worsening of glycaemic control in patients with T2DM.

    SETTING: This prospective cohort study included 156 patients with T2DM and severe or acute hyperglycaemia who were treated with insulin at any medical ward of the National University of Malaysia Medical Centre.

    METHOD: Insulin resistance was determined using the homeostatic model assessment-insulin resistance index. Glycaemic control during the episode of hyperglycaemia was assessed as the degree to which the patient achieved the target glucose levels. The polymerase chain reaction-restriction fragment length polymorphism method was used to identify polymorphisms in insulin receptor substrate (IRS) genes.

    MAIN OUTCOME MEASURE: Identification of possible predictors (demographic, clinical, or genetic) for insulin resistance and glycaemic control during severe/acute hyperglycaemia.

    RESULTS: A polymorphism in IRS1, r.2963 G>A (p.Gly972Arg), was a significant predictor of both insulin resistance [odds ratios (OR) 4.48; 95 % confidence interval (CI) 1.2-16.7; P = 0.03) and worsening of glycaemic control (OR 6.04; 95 % CI 0.6-64.6; P = 0.02). The use of loop diuretics (P < 0.05) and antibiotics (P < 0.05) may indirectly predict worsening of insulin resistance or glycaemic control in patients with severe/acute hyperglycaemia.

    CONCLUSION: Clinical and genetic factors contribute to worsening of insulin resistance and glycaemic control during severe/acute hyperglycaemia in patients with T2DM. Early identification of factors that may influence insulin resistance and glycaemic control may help to achieve optimal glycaemic control during severe/acute hyperglycaemia.

  4. Jamaluddin JL, Huri HZ, Vethakkan SR
    Pharmacogenomics, 2016 06;17(8):867-81.
    PMID: 27249660 DOI: 10.2217/pgs-2016-0010
    AIM: To determine the clinical and genetic predictors of the dipeptidyl peptidase-4 (DPP-4) inhibitor treatment response in Type 2 diabetes mellitus (T2DM) patients.

    PATIENTS & METHODS: DPP4, WFS1 and KCNJ11 gene polymorphisms were genotyped in a cohort study of 662 T2DM patients treated with DPP-4 inhibitors sitagliptin, vildagliptin or linagliptin. Genotyping was performed by Applied Biosystems TaqMan SNP genotyping assay.

    RESULTS: Patients with triglyceride levels less than 1.7 mmol/l (odds ratio [OR]: 2.2.; 95% CI: 1.031-4.723), diastolic blood pressure (DBP) less than 90 mmHg (OR: 1.7; 95% CI: 1.009-2.892) and KCNJ11 rs2285676 (genotype CC) (OR: 2.0; 95% CI: 1.025-3.767) were more likely to response to DPP-4 inhibitor treatment compared with other patients, as measured by HbA1c levels.

    CONCLUSION: Triglycerides, DBP and KCNJ11 rs2285676 are predictors of the DPP-4 inhibitor treatment response in T2DM patients.

  5. Degaga A, Sirgu S, Huri HZ, Sim MS, Kebede T, Tegene B, et al.
    Diabetes Metab Syndr Obes, 2023;16:2523-2535.
    PMID: 37641646 DOI: 10.2147/DMSO.S426632
    OBJECTIVE: This study aimed to evaluate whether the M420del variants of SLC22A1 (rs72552763) is associated with metformin treatment response in Ethiopian patients with type 2 diabetes mellitus (T2DM).

    PATIENTS AND METHODS: A prospective observational cohort study was conducted on 86 patients with T2DM who had been receiving metformin monotherapy for <1 year. Patients showing ≥0.5% reduction in HbA1c levels from baseline within 3 months and remained low for at least another 3 months were defined as responders while those patients with <0.5% reduction in HbA1c levels and/or those whom started a new class of glucose-lowering drug(s) because of unsatisfactory reduction were defined as non-responders. In addition, good glycemic control was observed when HbA1c ≤7.0%, and the above values were regarded as poor. Genotyping of rs72552763 SNP was performed using TaqMan® Drug Metabolism Enzyme Genotyping Assay and its association with metformin response and glycemic control were assessed by measuring the change in HbA1c and fasting blood glucose levels using Chi-square, logistic regression and Mann-Whitney U-test. Statistical significance was set at p <0.05.

    RESULTS: The minor allele frequency of the rs72552763 SNP of SLC22A1 was 9.3%. Metformin response was significantly higher in deletion_GAT (del_G) genotypes as compared to the wild-type GAT_GAT (G_G) genotypes. Furthermore, a significantly lower median treatment HbA1 level was found in del_G genotypes as compared to G_G genotypes. However, the association of rs72552763 with metformin response was not replicated at the allele level. In contrast, the minor del_allele was significantly associated with good glycemic control compared to the G_allele, though not replicated at del_G genotypes level.

    CONCLUSION: This study demonstrated that metformin response was significantly higher in study participants with a heterozygous carrier of M420del variants of SLC22A1 as compared to the wild-type G_G genotypes after 3 months of treatment.

  6. Zaini S, Guan NC, Sulaiman AH, Zainal NZ, Huri HZ, Shamsudin SH
    Curr Drug Targets, 2018;19(12):1431-1455.
    PMID: 29484993 DOI: 10.2174/1389450119666180226125026
    Cancer patients are commonly associated with various physical and psychological symptoms. In palliative setting, the aims are to relieve those symptoms, improve quality of life, and increase medication adherence among cancer patients. Antidepressants are generally accepted for the treatment of depression among patients with or without cancer. Some other potential benefits of the antidepressants have been reported in cancer patients.

    OBJECTIVE: This study aims to review the use of antidepressants for physical and psychological symptoms in cancer patients.

    RESULTS: Our findings showed the mixed result of positive and negative findings in various symptoms associated with cancer patients. These studies are categorised according to the hierarchy of evidence from high to low level, namely randomised controlled trials, cohort studies, case-control studies, case series, case reports, as well as other type of publications. The majority of antidepressants used in cancer patients seem to be beneficial for the treatment of depression, anxiety, hot flashes and other symptoms such as sexual dysfunction, fatigue, nicotine dependence, vasomotor symptoms, executive functions, sleep problems, pruritus, as well as for hypochondriasis. While fluoxetine was found to be associated with the reduction of antiemetic property in ondansetron, mirtazapine was identified to be a good alternative in treating nausea and cachexia among cancer patients.

    CONCLUSION: More research studies with adequate statistical power are warranted to validate the use of antidepressants among cancer patients in treating these physical and psychological symptoms.

  7. Elnaem MH, Mohamed MHN, Huri HZ, Shah ASM
    Ther Clin Risk Manag, 2019;15:137-145.
    PMID: 30705590 DOI: 10.2147/TCRM.S182716
    Background: Cardiovascular diseases (CVDs) are the main complication leading to morbidity and mortality among patients with type 2 diabetes mellitus (T2DM). There is a large amount of evidence to support the use of lipid-lowering therapy (LLT) for the prevention of CVD. This study aimed to assess the effectiveness and prescription quality of LLT among T2DM patients and to identify its associated factors.

    Methods: A multicenter cross-sectional study included 816 T2DM patients from four different primary care centers in Pahang, Malaysia. We involved LLT-eligible T2DM patients as per the national clinical practice guidelines (CPG). The assessment of therapy effectiveness focused on the attainment of target lipid measures stated in the CPG. Evaluation of the prescription quality was classified into appropriate, potentially inappropriate, and inappropriate, based on the compliance with guidelines and existence of potential safety concerns. Binomial logistic regression was employed to identify the predictors of LLT effectiveness and prescription quality.

    Results: The overall percentage of T2DM patients receiving statin therapy was 87.6% (715/816). Statin therapy was appropriately prescribed in 71.5% of the cases. About 17.5% of the LLT prescriptions have at least one significant drug interaction with co-prescribed medications. The achievement of the primary target of low-density lipoprotein cholesterol (LDL-C) levels was observed in only 37% of T2DM patients. The LLT indication and appropriateness of prescription were significantly associated with the attainment of LDL-C treatment goals. Primary prevention, Malay race, and hypertension were identified as predictors for appropriate prescribing of LLT among T2DM subjects.

    Conclusion: There is a need to enhance the quality of LLT prescribing in the primary care setting to cover all eligible high-risk patients and ensure patient safety. Strategies to improve the achievement of LDL-C goals among patients with T2DM, such as investigating the potential role of the combination therapy and high-intensity statin therapy, are required.
  8. Yugavathy N, Huri HZ, Kun LS, Bin Abdul Gafor AH, Geot WM, Bavanandan S, et al.
    Biomark Med, 2020 08;14(12):1099-1108.
    PMID: 32969247 DOI: 10.2217/bmm-2020-0205
    Aim: To determine the clinical and genetic markers associated with erythropoietin deficiency anemia in predialysis individuals. Materials & methods: Patients were categorized into cases and control group. Demographic characteristics and clinical parameters were obtained from medical record review and serum EPO and ferritin were obtained with ELISA. HIF-1α (rs2057482), IL-1β (rs1143627) and EPO (rs1617640) gene polymorphism were genotyped. Results: Female gender, glomerular filtration rate, treatment with hematinics, anticoagulant and diuretic were strong predictors of EPO-deficient anemia in predialysis chronic kidney disease patients. Genetic polymorphism in the HIF-1α recessive model was associated with non-EPO-deficiency, followed by EPO recessive allele associated with low-serum erythropoietin and IL-1β recessive model with low hemoglobin level. Conclusion: EPO-deficiency anemia can be diagnosed more conveniently in the presence of biomarkers.
  9. Ahmed RH, Huri HZ, Muniandy S, Al-Hamodi Z, Al-Absi B, Alsalahi A, et al.
    Clin Biochem, 2017 Sep;50(13-14):746-749.
    PMID: 28288852 DOI: 10.1016/j.clinbiochem.2017.03.008
    OBJECTIVES: Soluble DPP4 (sDPP4) is a novel adipokine that degrades glucagon-like peptide (GLP-1). We evaluated the fasting serum levels of active GLP-1 and sDPP4 in obese, overweight and normal weight subjects to assess the association between sDPP4 levels, active GLP-1 levels and insulin resistance in obese subjects.

    METHODS: The study involved 235 Malaysian subjects who were randomly selected (66 normal weight subjects, 97 overweight, 59 obese subjects, and 13 subjects who were underweight). Serum sDPP4 and active GLP-1 levels were examined by enzyme-linked immunosorbent assay (ELISA). Also, body mass index kg/m(2) (BMI), lipid profiles, insulin and glucose levels were evaluated. Insulin resistance (IR) was estimated via the homeostasis model assessment for insulin resistance (HOMA-IR).

    RESULTS: Serum sDPP4 levels were significantly higher in obese subjects compared to normal weight subjects (p=0.034), whereas serum levels of active GLP-1 were lower (p=0.021). In obese subjects, sDPP4 levels correlated negatively with active GLP-1 levels (r(2)=-0.326, p=0.015). Furthermore, linear regression showed that sDPP4 levels were positively associated with insulin resistance (B=82.28, p=0.023) in obese subjects.

    CONCLUSION: Elevated serum sDPP4 levels and reduced GLP-1 levels were observed in obese subjects. In addition, sDPP4 levels correlated negatively with active GLP-1 levels but was positively associated with insulin resistance. This finding provides evidence that sDPP4 and GLP-1 may play an important role in the pathogenesis of obesity, suggesting that sDPP4 may be valuable as an early marker for the augmented risk of obesity and insulin resistance.

  10. Huri HZ, Ling CF, Razack AH
    Ther Clin Risk Manag, 2017;13:407-419.
    PMID: 28408836 DOI: 10.2147/TCRM.S118010
    This study was conducted in a tertiary medical center in Kuala Lumpur, Malaysia. A total of 200 erectile dysfunction (ED) patients with 499 cases who had received pharmacological treatments for their ED participated in this study. Types, causes and factors associated with drug-related problems (DRPs) in ED patients with multiple comorbidities were assessed. A total of 244 DRPs with an average of 1.2±2.1 DRPs per patient were identified. Drug interaction contributed the most to DRPs occurrence. There was a significant higher risk of DRPs in patients with benign prostatic hyperplasia, lower urinary tract infection and elderly and end-stage renal disease. Early identification of types of DRPs and factors associated may enhance their prevention and management.
  11. Jamaluddin JL, Huri HZ, Vethakkan SR, Mustafa N
    Pharmacogenomics, 2014 Feb;15(2):235-49.
    PMID: 24444412 DOI: 10.2217/pgs.13.234
    In the adult pancreas, the expression of the genes PAX4, KCNQ1, TCF7L2, KCNJ11, ABCC8, MTNR1B and WFS1 are mainly restricted to β cells to maintain glucose homeostasis. We have identified these genes as the main regulators of incretin-mediated actions, and therefore they may potentially influence the response of DPP-4 inhibitors. This review represents the first detailed exploration of pancreatic β-cell genes and their variant mechanisms, which could potentially affect the response of DPP-4 inhibitors in Type 2 diabetes. We have focused on the signaling pathways of these genes to understand their roles in gastrointestinal incretin-mediated effects; and finally, we sought to associate gene mechanisms with their Type 2 diabetes risk variants to predict the responses of DPP-4 inhibitors for this disease.
  12. Ahmed RH, Huri HZ, Al-Hamodi Z, Salem SD, Muniandy S
    PLoS One, 2015;10(10):e0140618.
    PMID: 26474470 DOI: 10.1371/journal.pone.0140618
    BACKGROUND: A soluble form of CD26/dipeptidyl peptidase-IV (sCD26/DPP-IV) induces DPP-IV enzymatic activity that degrades incretin. We investigated fasting serum levels of sCD26/DPP-IV and active glucagon-like peptide-1 (GLP-1) in Malaysian patients with type 2 diabetes mellitus (T2DM) with and without metabolic syndrome (MetS), as well as the associations between sCD26/DPP-IV levels, MetS, and antidiabetic therapy.

    METHODS: We assessed sCD26/DPP-IV levels, active GLP-1 levels, body mass index (BMI), glucose, insulin, A1c, glucose homeostasis indices, and lipid profiles in 549 Malaysian subjects (including 257 T2DM patients with MetS, 57 T2DM patients without MetS, 71 non-diabetics with MetS, and 164 control subjects without diabetes or metabolic syndrome).

    RESULTS: Fasting serum levels of sCD26/DPP-IV were significantly higher in T2DM patients with and without MetS than in normal subjects. Likewise, sCD26/DPP-IV levels were significantly higher in patients with T2DM and MetS than in non-diabetic patients with MetS. However, active GLP-1 levels were significantly lower in T2DM patients both with and without MetS than in normal subjects. In T2DM subjects, sCD26/DPP-IV levels were associated with significantly higher A1c levels, but were significantly lower in patients using monotherapy with metformin. In addition, no significant differences in sCD26/DPP-IV levels were found between diabetic subjects with and without MetS. Furthermore, sCD26/DPP-IV levels were negatively correlated with active GLP-1 levels in T2DM patients both with and without MetS. In normal subjects, sCD26/DPP-IV levels were associated with increased BMI, cholesterol, and LDL-cholesterol (LDL-c) levels.

    CONCLUSION: Serum sCD26/DPP-IV levels increased in T2DM subjects with and without MetS. Active GLP-1 levels decreased in T2DM patients both with and without MetS. In addition, sCD26/DPP-IV levels were associated with Alc levels and negatively correlated with active GLP-1 levels. Moreover, metformin monotherapy was associated with reduced sCD26/DPP-IV levels. In normal subjects, sCD26/DPP-IV levels were associated with increased BMI, cholesterol, and LDL-c.

  13. Ahmed RH, Huri HZ, Al-Hamodi Z, Salem SD, Al-Absi B, Muniandy S
    PLoS One, 2016;11(4):e0154369.
    PMID: 27111895 DOI: 10.1371/journal.pone.0154369
    BACKGROUND: Genetic polymorphisms of the Dipeptidyl Peptidase 4 (DPP4) gene may play a role in the etiology of type 2 diabetes mellitus (T2DM). This study aimed to investigate the possible association of single nucleotide polymorphisms (SNPs) of the DPP4 gene in Malaysian subjects with T2DM and evaluated whether they had an effect on the serum levels of soluble dipeptidyl peptidase 4 (sDPP-IV).

    METHOD: Ten DPP4 SNPs were genotyped by TaqMan genotyping assays in 314 subjects with T2DM and 235 controls. Of these, 71 metabolic syndrome (MetS) subjects were excluded from subsequent analysis. The odds ratios (ORs) and their 95% confidence interval (CIs) were calculated using multiple logistic regression for the association between the SNPs of DPP4 and T2DM. In addition, the serum levels of sDPP-IV were investigated to evaluate the association of the SNPs of DPP4 with the sDPP-IV levels.

    RESULTS: Dominant, recessive, and additive genetic models were employed to test the association of DPP4 polymorphisms with T2DM, after adjusting for age, race, gender and BMI. The rs12617656 was associated with T2DM in Malaysian subjects in the recessive genetic model (OR = 1.98, p = 0.006), dominant model (OR = 1.95, p = 0.008), and additive model (OR = 1.63, p = 0.001). This association was more pronounced among Malaysian Indians, recessive (OR = 3.21, p = 0.019), dominant OR = 3.72, p = 0.003) and additive model (OR = 2.29, p = 0.0009). The additive genetic model showed that DPP4 rs4664443 and rs7633162 polymorphisms were associated with T2DM (OR = 1.53, p = 0.039), and (OR = 1.42, p = 0.020), respectively. In addition, the rs4664443 G>A polymorphism was associated with increased sDPP-IV levels (p = 0.042) in T2DM subjects.

    CONCLUSIONS: DPP4 polymorphisms were associated with T2DM in Malaysian subjects, and linked to variations in sDPP-IV levels. In addition, these associations were more pronounced among Malaysian Indian subjects.

  14. Huri HZ, Mat Sanusi ND, Razack AH, Mark R
    Patient Prefer Adherence, 2016;10:807-23.
    PMID: 27257374 DOI: 10.2147/PPA.S99544
    BACKGROUND: Erectile dysfunction (ED) is one of the most common health problems in men. ED can significantly affect a man's psychological well-being and overall health.

    PURPOSE: To investigate the association of psychological factors, patients' knowledge, and management among ED patients.

    PATIENTS AND METHODS: A total of 93 patients with an age range from 31 to 81 years who have undergone treatment for ED were included in this study.

    RESULTS: It was found that the feeling of blame (P=0.001), guilt (P=0.001), anger or bitterness (P=0.001), depression (P=0.001), feeling like a failure (P=0.001), and the feeling of letting down a partner during intercourse (P=0.001) were significantly associated with ED. Age was also found to be significantly associated with patients' psychological scale (P=0.004). In addition, the majority of patients in this study practice the right method of administration of ED therapy. However, no significant correlation was found between patients' knowledge of ED therapy and demographic characteristics.

    CONCLUSION: This study concluded that ED does affect psychological well-being of people. In addition, patient's knowledge about ED and its management is also crucial in ensuring that the patient achieves optimal therapeutic outcomes from ED therapy.

  15. Huri HZ, Lim LP, Lim SK
    Drug Des Devel Ther, 2015;9:4355-71.
    PMID: 26300627 DOI: 10.2147/DDDT.S85676
    BACKGROUND: Good glycemic control can delay the progression of kidney diseases in type 2 diabetes mellitus (T2DM) patients with renal complications. To date, the association between antidiabetic agents and glycemic control in this specific patient population is not well established.

    PURPOSE: This study aimed to identify antidiabetic regimens as well as other factors that associated with glycemic control in T2DM patients with different stages of chronic kidney disease (CKD).

    PATIENTS AND METHODS: This retrospective, cross-sectional study involved 242 T2DM inpatients and outpatients with renal complications from January 2009 to March 2014 and was conducted in a tertiary teaching hospital in Malaysia. Glycated hemoglobin (A1C) was used as main parameter to assess patients' glycemic status. Patients were classified to have good (A1C <7%) or poor glycemic control (A1C ≥7%) based on the recommendations of the American Diabetes Association.

    RESULTS: Majority of the patients presented with CKD stage 4 (43.4%). Approximately 55.4% of patients were categorized to have poor glycemic control. Insulin (57.9%) was the most commonly prescribed antidiabetic medication, followed by sulfonylureas (43%). Of all antidiabetic regimens, sulfonylureas monotherapy (P<0.001), insulin therapy (P=0.005), and combination of biguanides with insulin (P=0.038) were found to be significantly associated with glycemic control. Other factors including duration of T2DM (P=0.004), comorbidities such as anemia (P=0.024) and retinopathy (P=0.033), concurrent medications such as erythropoietin therapy (P=0.047), α-blockers (P=0.033), and antigouts (P=0.003) were also correlated with A1C.

    CONCLUSION: Identification of factors that are associated with glycemic control is important to help in optimization of glucose control in T2DM patients with renal complication.

  16. Baig S, Seevasant I, Mohamad J, Mukheem A, Huri HZ, Kamarul T
    Cell Death Dis, 2016;7:e2058.
    PMID: 26775709 DOI: 10.1038/cddis.2015.275
    Underneath the intricacy of every cancer lies mysterious events that impel the tumour cell and its posterity into abnormal growth and tissue invasion. Oncogenic mutations disturb the regulatory circuits responsible for the governance of versatile cellular functions, permitting tumour cells to endure deregulated proliferation, resist to proapoptotic insults, invade and erode normal tissues and above all escape apoptosis. This disruption of apoptosis has been highly implicated in various malignancies and has been exploited as an anticancer strategy. Owing to the fact that apoptosis causes minimal inflammation and damage to the tissue, apoptotic cell death-based therapy has been the centre of attraction for the development of anticancer drugs. Increased understanding of the molecular pathways underlying apoptosis has enabled scientists to establish unique approaches targeting apoptosis pathways in cancer therapeutics. In this review, we reconnoitre the two major pathways (intrinsic and extrinsic) targeted cancer therapeutics, steering toward chief modulators of these pathways, such as B-cell lymphoma 2 protein family members (pro- and antiapoptotic), inhibitor of apoptosis proteins, and the foremost thespian of extrinsic pathway regulator, tumour necrosis factor-related apoptosis-inducing agent. Together, we also will have a look from clinical perspective to address the agents (drugs) and therapeutic strategies adopted to target these specific proteins/pathways that have entered clinical trials.
  17. A Wahab I, Goh KW, Zainal ZA, Mohamed Yusof NS, Huri HZ, Jacob SA, et al.
    Int J Environ Res Public Health, 2022 Aug 05;19(15).
    PMID: 35954990 DOI: 10.3390/ijerph19159629
    The global depression burden has remained a challenge throughout the pre- and post-pandemic era. The pandemic effect has led to the spiraling of mental disorders among young people who will be the next generation of leaders. This study aims to identify university students’ sociodemographic, psychosocial and academic backgrounds and performance associated with depression symptoms for the development of primary and secondary preventive strategies for mental health. A cross-sectional study was conducted using an online questionnaire distributed to 19 institutions in Malaysia offering a Bachelor of Pharmacy degree program. The self-rated Depression Anxiety Stress Scale (DASS-42) was used to assess depression symptoms. Pearson’s chi-square test and Fisher’s exact test were used to assess the investigated variables with depression symptoms. Independent T-test and one-way ANOVA were used to compare means of depression score across variables. Binary logistic regression was employed to examine the relationship between the investigated variables and depression symptoms. A total of 610 pharmacy students participated, of which 47% (n = 289/610) were having depression symptoms. Students who smoke nicotine and those who have separated parents, family history of mental illness, and poor academic performance were associated with depression symptoms (p < 0.05). Differences in geographical areas, race and religion also showed significant associations with depression symptoms. Parental marital status, poor academic performance, history of mental illness and comorbidities were statistically predicting depression symptoms (p < 0.05). Primary preventive strategies allowing students to harness healthy coping skills for stress, nicotine-free campaigns and a holistic curriculum are warranted. Secondary measures on mindfulness and compassion skills activities to benefit students who experienced early life crises are highly recommended. Enforcing these targeted strategies in collaboration with health and social sectors should be the primary agenda of universities to ensure their uptake.
  18. Loganadan NK, Huri HZ, Vethakkan SR, Hussein Z
    Pharmacogenomics J, 2016 06;16(3):209-19.
    PMID: 26810132 DOI: 10.1038/tpj.2015.95
    The clinical response to sulphonylurea, an oral antidiabetic agent often used in combination with metformin to control blood glucose in type 2 diabetes (T2DM) patients, has been widely associated with a number of gene polymorphisms, particularly those involved in insulin release. We have reviewed the genetic markers of CYP2C9, ABCC8, KCNJ11, TCF7L2 (transcription factor 7-like 2), IRS-1 (insulin receptor substrate-1), CDKAL1, CDKN2A/2B, KCNQ1 and NOS1AP (nitric oxide synthase 1 adaptor protein) genes that predict treatment outcomes of sulphonylurea therapy. A convincing pattern for poor sulphonylurea response was observed in Caucasian T2DM patients with rs7903146 and rs1801278 polymorphisms of the TCF7L2 and IRS-1 genes, respectively. However, limitations in evaluating the available studies including dissimilarities in study design, definitions of clinical end points, sample sizes and types and doses of sulphonylureas used as well as ethnic variability make the clinical applications challenging. Future studies need to address these limitations to develop personalized sulphonylurea medicine for T2DM management.
  19. Loganadan NK, Huri HZ, Vethakkan SR, Hussein Z
    Pharmacogenomics, 2020 06;21(9):587-600.
    PMID: 32468916 DOI: 10.2217/pgs-2019-0171
    Background: Due to several limitations in the study designs of sulfonylurea pharmacogenomics studies, we investigated the clinical and genetic predictors of secondary sulfonylurea failure in Type 2 diabetes patients. Materials & methods: Patients receiving the maximum sulfonylurea and metformin doses for >1 year were enrolled. Secondary sulfonylurea failure was defined as HbA1c >7.0% (>53 mmol/mol) after a 12-month follow-up. Results: By multivariate analysis, increased insulin resistance (HOMA2-IR), baseline HbA1c >7.0%, residing in eastern Peninsular Malaysia, and the CC genotype of rs757110 ABCC8 gene polymorphism were independent predictors of secondary sulfonylurea failure (p 
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