International Journal of Preventive Medicine (Int J Prev Med)2008-78021592024112029332933School of Population Health, Faculty of Health Sciences, Curtin University, Perth, Western AustraliaSydney School of Public Health, Faculty of Health Sciences, University of Sydney, Sydney, New South WalesCentre for Work Health and Safety, Sydney, New South WalesSchool of Population Health, Faculty of Health Sciences, Curtin University, Perth, Western Australia20241120Background: Artificial ultraviolet radiation (UVR) is produced during welding and can cause damage to both the eyes (ocular) and the skin (dermal). We aimed to investigate the protection used by welders to reduce their exposure to ocular and dermal UVR. Methods: We conducted a cross‑sectional online survey in Australia that asked welders about their welding tasks and the control measures they used to protect against UVR exposure. Results: There were 634 respondents, of whom 411 undertook welding themselves, 36 supervised other welders, and 130 both supervised and welded. Dermal UVR exposure occurred in 7.8% of welders and 14.4% of supervisors, whereas ocular UVR exposure occurred in 16.8% of welders and 33.1% of supervisors. The use of personal control measures was much lower among supervisors than welders; however, the presence of warning signs or barriers was reported more often by supervisors. Conclusions: Despite the well‑known acute and chronic effects of exposure to UVR from welding, there are still many welders and supervisors who do not use adequate protection.http://ijpm.mui.ac.ir/index.php/ijpm/article/view/2933http://ijpm.mui.ac.ir/index.php/ijpm/article/download/2933/717718774

International Journal of Preventive Medicine (Int J Prev Med)2008-78021592024112029362936College of Medicine, Shahid Beheshti University of Medical Sciences, Tehran1Life Sciences Institute, University of Michigan, Ann Arbor, MI2Chronic Respiratory Disease Research Center (CRDRC), National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran20241120Background: Nicotine is a behavioral stimulant that in high doses, through the neuro‑inflammatory and oxidative stress pathway, can induce apoptosis and autophagy leading to cell death. Previous data indicate that crocin has neuroprotective properties. The aim of the current study is to investigate crocin’s neuroprotective effects against nicotine‑triggered neuro‑inflammation, apoptosis, and autophagy in rat hippocampus. Methods: Seventy adult male Wistar rats were divided into the following seven groups: Group one received normal saline (0.2 ml/rat), group two was treated with nicotine 10 mg/kg intraperitoneally, groups 3 to 6 were treated simultaneously with nicotine and crocin (10, 20, 40, and 80 mg/kg, intraperitoneally), group 7 was treated with crocin‑alone (80 mg/kg, intraperitoneally). The period of the mentioned agent administration was 21 days. On the 22nd day, an open field test (OFT) was used for evaluation of anxiety and motor activity changes. Inflammatory and oxidative stress factors and also apoptosis and autophagy biomarkers were evaluated. Results: All mentioned doses of crocin could decrease the nicotine‑induced OFT behavioral changes. Crocin also could decrease levels of hippocampal TNF/TNF‑α (tumor necrosis factor), IL1B/IL‑1β (interleukin 1 beta), oxidized glutathione (GSSG), unphosphorylated and phosphorylated forms of JNK, BECN1 (beclin 1), BAX (BCL2 associated X, apoptosis regulator), and phosphorylated/inactive forms of BCL2 (BCL2 apoptosis regulator) in nicotine‑dependent rats. Crocin treatments also caused increases in the reduced form of glutathione (GSH) content and activity of CAT (catalase) and mitochondrial complex enzymes in nicotine‑addicted subjects. Conclusions: Crocin can modulate JNK‑BCL2‑BECN1 or JNK‑BCL2‑BAX signaling pathways and reduce neuronal oxidative stress, neuro‑inflammation, and mitochondrial respiratory chain enzymes and exert neuroprotective effects against nicotine‑induced neurodegeneration.http://ijpm.mui.ac.ir/index.php/ijpm/article/view/2936http://ijpm.mui.ac.ir/index.php/ijpm/article/download/2936/717718777

International Journal of Preventive Medicine (Int J Prev Med)2008-78021592024112029372937Chronic Respiratory Disease Research Center (CRDRC), National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran1Faculty of Veterinary Medicine, Tehran University, Tehran2 Faculty of Veterinary Medicine, Semnan University, Semnan3Life Sciences Institute, University of Michigan, Ann Arbor, MIChronic Respiratory Disease Research Center (CRDRC), National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, TehranChronic Respiratory Disease Research Center (CRDRC), National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran4Department of Comparative Bioscience, Faculty of Veterinary Medicine, University of Tehran, Tehran5Division of Toxicology, Department of Comparative Bioscience, Faculty of Veterinary Medicine, University of Tehran, Tehran20241120Background: Previous evidence indicates that tramadol (TRA) can lead to neurodegenerative events and minocycline (MIN) has neuroprotective properties. Aim of the Study: The current research evaluated the neuroprotective effects of MIN for TRA‑promoted neurodegeneration. Methods: Sixty adult male rats were placed into the following groups: 1 (received 0.7 ml/rat of normal saline, IP), 2 (received 50 mg/kg of TRA, i.p.), 3, 4, 5 (administered TRA as 50 mg/kg simultaneously with MIN at 20, 40, and 60 mg/kg, IP, respectively), and 6 (received MIN alone as 60 mg/kg, IP). The treatment procedure was 21 days. An open field test (OFT) was used to measure motor activity and anxiety‑related behavior. Furthermore, oxidative stress; hippocampal inflammation; apoptotic parameters as well as activity of mitochondrial complexes I, II, III, and IV; ATP levels; and mitochondrial membrane potential (MMP) were evaluated. In addition, histomorphological alteration was assessed in two regions of the hippocampus: Cornu Ammonis (CA1) and dentate gyrus (DG). Results: MIN treatment could inhibit TRA‑induced anxiety and motor activity disturbances (P < 0.05). In addition, MIN could attenuate reactive oxygen species (ROS), H2 O2 , oxidized glutathione (GSSG), and malondialdehyde (MDA) level (P < 0.05), while there was increased reduced glutathione (GSH), total antioxidant capacity (TAC), ATP, MMP, and BCL2 levels (P < 0.05) and also elevation of SOD, GPX, GSR (P < 0.05), and mitochondrial complexes I, II, III, and IV activity (P < 0.05) in TRA‑treated rats. In consistence with these findings, MIN could reduce TNF/TNF‑α, IL1B/IL1‑β, BAX, and CASP3 levels (P < 0.05) in TRA‑treated rats. MIN also restored the quantitative (P < 0.05) and qualitative histomorphological sequels of TRA in both CA1 and DG areas of the hippocampus. Conclusions: MIN probably has repositioning capability for inhibition of TRA‑induced neurodegeneration via modulation of inflammation, oxidative stress, apoptosis, and mitochondrial disorders.http://ijpm.mui.ac.ir/index.php/ijpm/article/view/2937http://ijpm.mui.ac.ir/index.php/ijpm/article/download/2937/717718778

International Journal of Preventive Medicine (Int J Prev Med)2008-780215920241120293829381 Department of Community Medicine, JSS Medical College, JSS Academy of Higher Education and Research, Mysuru, Karnataka1 Department of Community Medicine, JSS Medical College, JSS Academy of Higher Education and Research, Mysuru, Karnataka2 Department of General Medicine, JSS Medical College, JSS Academy of Higher Education and Research, Mysuru, Karnataka1 Department of Community Medicine, JSS Medical College, JSS Academy of Higher Education and Research, Mysuru, Karnataka1 Department of Community Medicine, JSS Medical College, JSS Academy of Higher Education and Research, Mysuru, Karnataka1 Department of Community Medicine, JSS Medical College, JSS Academy of Higher Education and Research, Mysuru, Karnataka1 Department of Community Medicine, JSS Medical College, JSS Academy of Higher Education and Research, Mysuru, Karnataka20241120Background: Diabetes is a chronic medical condition with severe complications, mainly caused by unhealthy lifestyles in genetically susceptible individuals. There has been a growing interest in the role of mobile health technologies in achieving better self-efficacy in managing diabetes. This study attempts to assess the impact of a web-based model on improving the diabetes status among Type 2 diabetic patients attending a tertiary care hospital in southern India. Methods: A longitudinal study was conducted among patients with type 2 diabetes attending the outpatient department of a tertiary care hospital in Mysuru, southern India, for 6 months. Diabetes Care (https://www.diabetescare.co.in/), which is an online website that can be used as a risk prediction tool for uncontrolled diabetes and recommends lifestyle changes, was used by 456 diabetes patients for 6 months. We assessed the change in glycosylated haemoglobin levels at the beginning and after 6 months of using the software. Results: The mean HbA1c value at the start of the study was 8.039% ± 1.981. The HbA1c value assessed after 6 months post-intervention showed an improvement of 7.794% ± 1.853 with a mean difference of 0.245. A paired T-test showed a statistically significant association with a P value of 0.049. Conclusions: Evidence from this study suggests that intervention using a webbased model focusing on risk prediction and educational intervention showed an improvement in the diabetic status of the patients with T2DM.http://ijpm.mui.ac.ir/index.php/ijpm/article/view/2938http://ijpm.mui.ac.ir/index.php/ijpm/article/download/2938/717718779

International Journal of Preventive Medicine (Int J Prev Med)2008-78021592024112029342934Department of Nursing, School of Nursing, Larestan University of Medical Sciences, Laresta1Student Research Committee, Larestan University of Medical Sciences, Larestan20241120Dear Editor, Suicide is a set of actions to end life that a person consciously commits.[1] According to the studies of Yaghmour et al.,[2] suicide is the second leading cause of death in the USA. Also, the deaths of physician residents in Iran, which have occurred in recent years, have shocked both the public and the medical community.http://ijpm.mui.ac.ir/index.php/ijpm/article/view/2934http://ijpm.mui.ac.ir/index.php/ijpm/article/download/2934/717718775

International Journal of Preventive Medicine (Int J Prev Med)2008-780215920241120293529351 Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran, 2 Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan1 Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, IsfahanDepartment Neurology, University of Cincinnati, Cincinnati, OH1 Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran, 2 Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan20241120Dear Editor, Coronavirus disease 2019 (COVID‑19) is caused by the severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) infection. SARS‑CoV‑2 is a member of the RNA family called Coronaviridae, which has swept the world from December 2019 onward.[1] Due to the morbidity, mortality, no definite therapy, and multiple problems that the virus has caused worldwide, most countries have tried to make vaccines with various technologies and methods.[http://ijpm.mui.ac.ir/index.php/ijpm/article/view/2935http://ijpm.mui.ac.ir/index.php/ijpm/article/download/2935/717718776