Climate change is intensifying occupational heat exposure, posing risks not only for heat-related illness but also for sleep, which is essential for recovery, safety, and productivity. Heat-exposed workers are highly vulnerable due to prolonged exposure, limited access to cooling, and poor housing. This systematic review aimed to synthesise global evidence on how occupational heat exposure affects sleep quality among workers across different occupations and settings. A systematic review was conducted following Synthesis without Meta-Analysis (SWiM) guidelines. PubMed, Scopus, and Google Scholar were searched (2000–2025) for studies involving adult workers (≥18 years) reporting both heat exposure and sleep outcomes. The review was registered with PROSPERO (ID: CRD420251125735). Of 7,108 records screened, 11 studies met the inclusion criteria. Studies spanned Asia, Australia, North America, and global cohorts. Heat exposure consistently impaired sleep quality and duration. Using Pittsburgh Sleep Quality Index, Actigraphy, and self-reports, common complaints included difficulty falling asleep (64%), restlessness (54%), non-restorative sleep (54%), night sweats (36%), and reduced total sleep time (45%). Night-time temperatures above 25°C and high workplace wet bulb globe temperature values were strongly linked with reduced sleep efficiency and delayed sleep onset. Vulnerable groups included shift workers, petrochemical and steel labourers, women, older adults, and low-income workers in urban heat islands and poorly ventilated housing. Occupational heat exposure disrupts sleep, compounding daytime strain and creating a dual burden for workers. Integrating sleep into heat stress management through cooling interventions, better housing, and revised work–rest schedules is critical for workers well-being in a warming climate.

Cardiovascular disease (CVD) related mortality and morbidity heavily strain society. The relationship between external risk factors and our genetics have not been well established.It is widely acknowledged that environmental influence and individual behaviours play a significant role in CVD vulnerability, leading to the development of polygenic risk scores (PRS). We employed the PRISMA search method to locate pertinent research and literature to extensively review artificial intelligence (AI)-based PRS models for CVD risk prediction.Furthermore, we analyzed and compared conventional vs. AI-based solutions for PRS. We summarized the recent advances in our understanding of the use of AI-based PRS for risk prediction of CVD. Our study proposes three hypotheses: i) Multiple genetic variations and risk factors can be incorporated into AI-based PRS to improve the accuracy of CVD risk predicting. ii) AI-based PRS for CVD circumvents the drawbacks of conventional PRS calculators by incorporating a larger variety of genetic and non-genetic components, allowing for more precise and individualised risk estimations. iii) Using AI approaches, it is possible to significantly reduce the dimensionality of huge genomic datasets, resulting in more accurate and effective disease risk prediction models. Our study highlighted that the AI-PRS model outperformed traditional PRS calculators in predicting CVD risk. Furthermore, using AI-based methods to calculate PRS may increase the precision of risk predictions for CVD and have significant ramifications for individualized prevention and treatment plans.

BACKGROUND: Tissue engineering centers on creating a niche similar to the natural one, with a purpose of developing an organ construct. A natural scaffold can replace none while creating a scaffold unique to each tissue in composition, architecture and cues that regulate the character of cells. METHODS: Whole pancreas from mouse was decellularized using detergent and enzymes, followed by recellularizing with MSC from human placenta. This construct was transplanted in streptozotocin induced diabetic mice. Histopathology of both decellularized and recellularized transplanted pancreas and qPCR analysis were performed to assess its recovery. RESULTS: Decellularization removes the cells leaving behind extracellular matrix rich natural scaffold. After reseeding with mesenchymal stem cells, these cells differentiate into pancreas specific cells. Upon transplantation in streptozotocin induced diabetic mice, this organ was capable of restoring its histomorphology and functioning. Restoration of endocrine (islets), the exocrine region (acinar) and vascular network was seen in transplanted pancreas. The process of functional recovery of endocrine system took about 20 days when the mice start showing blood glucose reduction, though none achieved gluconormalization. CONCLUSION Natural decellularized scaffolds of soft organs can be refunctionalized using recipient’s mesenchymal stem cells to restore structure and function; and counter immune problems arising during transplantation.

BACKGROUND: Tissue engineering centers on creating a niche similar to the natural one, with a purpose of developing an organ construct. A natural scaffold can replace none while creating a scaffold unique to each tissue in composition, architecture and cues that regulate the character of cells. METHODS: Whole pancreas from mouse was decellularized using detergent and enzymes, followed by recellularizing with MSC from human placenta. This construct was transplanted in streptozotocin induced diabetic mice. Histopathology of both decellularized and recellularized transplanted pancreas and qPCR analysis were performed to assess its recovery. RESULTS: Decellularization removes the cells leaving behind extracellular matrix rich natural scaffold. After reseeding with mesenchymal stem cells, these cells differentiate into pancreas specific cells. Upon transplantation in streptozotocin induced diabetic mice, this organ was capable of restoring its histomorphology and functioning. Restoration of endocrine (islets), the exocrine region (acinar) and vascular network was seen in transplanted pancreas. The process of functional recovery of endocrine system took about 20 days when the mice start showing blood glucose reduction, though none achieved gluconormalization. CONCLUSION Natural decellularized scaffolds of soft organs can be refunctionalized using recipient’s mesenchymal stem cells to restore structure and function; and counter immune problems arising during transplantation.