Introduction: Tobacco smoking causes various chronic diseases and adds costs to healthcare systems. The current smoking cessation interventions mostly target smokers who are ready to quit and are reactive in recruitment. Recently, mobile phones have become a new tool for promoting smoking cessation. The aim of this paper is to present a study protocol on a quasi-experimental study investigating the effects of a workplace mHealth intervention for smoking behaviour. Methods: A quasi-experimental study will be conducted among employees in an academic institution in Malaysia. The intervention group will receive a theory based WhaSTOP module via WhatsApp and will be compared with the control group (receive usual care). The primary outcomes are stage movement and the number of cigarettes per day. The secondary outcomes include knowledge of smoking, quit attempt, nicotine dependence, 7-day point prevalence of smoking abstinence, and the Transtheoretical Model constructs. A generalised estimating equation analysis will be performed to determine the effects of the intervention. Discussion: This protocol will provide a novel method to proactively approach smokers regardless of readiness to quit and to guide them through the stages of change so that they will be ready to take action to quit. This research will also provide insight into whether the intervention can be utilised as an additional tool for smokers at the workplace to quit smoking. Trial Registration: The trial was registered with the Iranian Registry of Clinical Trials (Registry Number IRCT20220415054539N1).

Introduction: Association studies between single nucleotide polymorphisms (SNPs) and type 2 diabetes mellitus (T2DM) have been abundant. However, there are limited reports on copy number variations (CNVs) of beta-defensins (DEFB) gene in relation to T2DM. In this study, DEFB copy numbers were quantified in T2DM with nephropathy, T2DM without nephropathy and non-diabetic control groups to investigate its influence in chronic inflammation in Malaysian individuals. Methods: DEFB copy number in Malaysian individuals were quantified by using paralogue ratio tests (PRT) which allow direct quantification of gene copy number by using PRT107A and HSPD21 PRT primers. The copy number generated was then validated from insertion/deletion ratio measurement 5DEL (rs5889219) and two microsatellite analyses (EPEV-1 and EPEV-3). Results: DEFB copy number was found extending from 2 to 8 copies in the non-diabetic group (n=146), while in T2DM group (n=392), copy numbers were more extensive, ranging between 1 and 12 copies; with 1, 10 and 12 copies detected in T2DM with nephropathy group (n=202). Statistically, there is no significant difference in DEFB copy number between T2DM and the non-diabetic group (p=0.209) as well as between diabetic nephropathy and without nephropathy of the T2DM group (p=0.522). However, significant white blood cell (WBC) count was found between T2DM groups with and without diabetic nephropathy (p=0.000). Conclusion: Extreme DEFB copy numbers in T2DM with nephropathy group suggest future studies with bigger sample size are necessary to elucidate the true impact of CNVs of DEFB gene in promoting early onset of nephropathy in T2DM.