Khairul Bariah Ahmad Amin Noordin

Clinical reasoning and diagnostic competencies are widely recognized as essential components in dental and medical education yet remain difficult to achieve effective outcomes. Case-Based Learning (CBL) has been adopted as a structured pedagogical approach to address several challenges in engaging students in real clinical scenarios. In recent years, Artificial Intelligence (AI)-assisted tools, particularly those designed for clinical case development and information curation, have been introduced to support CBL without displacing traditional instructional methods. This narrative review synthesizes current literature to examine the role of AI-assisted approaches in enhancing undergraduates' learning experiences, in terms of engagement, motivation, knowledge integration, and improvement of diagnostic reasoning within CBL frameworks. The present review further highlights the practical consideration for dental and medical educators, and curriculum designers to focus on the integration of AI-assisted tools as a means of strengthening clinical education practices while maintaining educational integrity and learner-centered outcomes in higher education.

This review provides an overview of the integrin signaling pathways and their roles in mesenchymal stem cell differentiation into adipocytes, chondrocytes, and osteoblasts. In these three differentiated cells, the cell extracellular matrix plays an important role in regulating the integrin signaling pathway, as the presence of growth factors and other molecules in the extracellular matrix will affect the cell differentiation. The focus of this review is to elucidate the role of the integrin signaling pathway in adipogenesis, chondrogenesis, and osteogenesis, highlighting its diverse contributions to tissue homeostasis and repair. By synthesizing current knowledge, this paper aims to inspire further research into the therapeutic potential of targeting integrin pathways in stem cell-based tissue engineering.

Dental pulp stem cells (DPSCs) are widely available sources of stem cells that have been extensively studied for its capacity to differentiate into osteoblasts and endothelial cells and to support bone repair and regeneration. Collagen type 1 (Col-1) is a well-known extracellular matrix component, which plays a vital role in regulating the signaling pathway for osteoinduction of bone progenitor cells. However, the exact mechanism of Col-1 activation during stem cell osteogenesis remains unclear. Objectives This study aims to identify the key signalling pathway and proteins interaction associated with Col-1-induced osteogenesis of DPSCs. Methodology The localization of OCN protein was assessed by immunocytochemistry analysis, followed by Western blot analysis on OCN, AKT, p- AKT, Smad2/3, p-Smad2/3, ERK1/2, and p-ERK1/2 pathways. Protein profiling was performed using gel-free digestion and LC-MS/MS, followed by protein-protein interaction analysis using STRING online tools to assist in determination of link between various pathways. Results The data indicated that the PI3K/AKT pathway is the key signaling pathway involved in Col-1-induced DPSC, showing a significant impact and potential crosstalk with TGF-b/Smad and MAPK/ERK mainly via focal adhesion protein complexes. Conclusion The evidence suggests that PI3K/AKT signaling pathway is more dominant than the TGF-β/Smad and MAPK/ERK pathways, acting via stimulation of the focal adhesion protein complex. Together, these findings may provide deeper insight into cellular biology of differentiated cells for potential manipulation in bone tissue repair and regeneration.

Longevity has been associated with morbidity and an increase in age-related illnesses, linked to tissue degeneration and gradual loss of biological functions. Bone is an important organ that gradually degenerates with increasing lifespan. The remodeling phase plays a huge role in maintaining the ability of bone to regenerate and maintain its stability and function throughout life. Hence, bone health represents one of the major challenges to elderly citizens due to the increase of injury associated with bone degeneration, such as fragility and risks of fractures. In the virtue of improving the regenerative function of bone tissues, a specialized field of bone tissue engineering (BTE) has been introduced to improve the current strategies in treating bone degenerative disorders. Most of the research performed in BTE focuses on the optimization of key components to generate new bone formation, including the scaffold. A scaffold plays a significant role in establishing the structural form that interconnects major elements of the tissue engineering triad. To date, many types of biomaterials have been explored in BTE, ranging from natural and synthetic materials to nanocomposites. However, ideal scaffolds that display excellent biocompatibility and mechanical properties, approved for clinical practices are yet available. This paper aims to describe the up-to-date advancements in scaffold for new bone generation, highlighting the essential elements and strategies in selecting suitable biomaterials for bone repair.

Steadily rising population ageing is a global demographic trend due to the advancement of new treatments and technologies in the medical field. This trend also indicates an increasing prevalence of age-associated diseases, such as loss of muscle mass (sarcopenia), which tends to afflict the older population. The deterioration in muscle function can cause severe disability and seriously affects a patient’s quality of life. Currently, there is no treatment to prevent and reverse age-related skeletal muscle ageing frailty. Existing interventions mainly slow down and control the signs and symptoms. Mesenchymal stem cell-derived extracellular vesicle (MSC-EV) therapy is a promising approach to attenuate age-related skeletal muscle ageing frailty. However, more studies, especially large-scale randomised clinical trials need to be done in order to determine the adequacy of MSC-EV therapy in treating age-related skeletal muscle ageing frailty. This review compiles the present knowledge of the causes and changes regarding skeletal muscle ageing frailty and the potential of MSC-EV transplantation as a regenerative therapy for age-related skeletal muscle ageing frailty and its clinical trials.

Mechanotransduction is the process by which physical force is converted into a biochemical signal that is used in development and physiology; meanwhile, it is intended for the ability of cells to sense and respond to mechanical forces by activating intracellular signals transduction pathways and the relative phenotypic adaptation. It encompasses the role of mechanical stimuli for developmental, morphological characteristics, and biological processes in different organs; the response of cells to mechanically induced force is now also emerging as a major determinant of disease. Due to fluid shear stress caused by blood flowing tangentially across the lumen surface, cells of the cardiovascular system are typically exposed to a variety of mechanotransduction. In the body, tissues are continuously exposed to physical forces ranging from compression to strain, which is caused by fluid pressure and compressive forces. Only lately, though, has the importance of how forces shape stem cell differentiation into lineage-committed cells and how mechanical forces can cause or exacerbate disease besides organizing cells into tissues been acknowledged. Mesenchymal stem cells (MSCs) are potent mediators of cardiac repair which can secret a large array of soluble factors that have been shown to play a huge role in tissue repair. Differentiation of MSCs is required to regulate mechanical factors such as fluid shear stress, mechanical strain, and the rigidity of the extracellular matrix through various signaling pathways for their use in regenerative medicine. In the present review, we highlighted mechanical influences on the differentiation of MSCs and the general factors involved in MSCs differentiation. The purpose of this study is to demonstrate the progress that has been achieved in understanding how MSCs perceive and react to their mechanical environment, as well as to highlight areas where more research has been performed in previous studies to fill in the gaps.

Background: This study aimed to identify new genes associated with CRC in patients with normal mismatch repair (MMR) protein expression. Method: Whole-genome sequencing (WGS) was performed in seven early-age-onset Malay CRC patients. Potential germline genetic variants, including single-nucleotide variations and insertions and deletions (indels), were prioritized using functional and predictive algorithms. Results: An average of 3.2 million single-nucleotide variations (SNVs) and over 800 indels were identified. Three potential candidate variants in three genes—IFNE, PTCH2 and SEMA3D—which were predicted to affect protein function, were identified in three Malay CRC patients. In addition, 19 candidate genes—ANKDD1B, CENPM, CLDN5, MAGEB16, MAP3K14, MOB3C, MS4A12, MUC19, OR2L8, OR51Q1, OR51AR1, PDE4DIP, PKD1L3, PRIM2, PRM3, SEC22B, TPTE, USP29 and ZNF117—harbouring nonsense variants were prioritised. These genes are suggested to play a role in cancer predisposition and to be associated with cancer risk. Pathway enrichment analysis indicated significant enrichment in the olfactory signalling pathway. Conclusion: This study provides a new spectrum of insights into the potential genes, variants and pathways associated with CRC in Malay patients.

Purpose: Small interfering RNA (siRNA) has the potential as a therapeutic approach against selective pathways in colorectal cancer. EPCAM, a transmembrane glycoprotein mediating cell adhesion, was known to be involved in suppressing Wnt/β-catenin pathway, an important pathway for tumour progression in colon cancer cells. EPCAM deletions caused a transcriptional read-through that may silence its neighbouring gene, MSH2. This study aimed to investigate the effect of co-siRNA targeted genes, MSH2 and EPCAM, in colon cancer cell line, HCT116, and their effect in regulating the Wnt/β-catenin pathway. Methods: Pre-designed siRNA of MSH2 and EPCAM were transfected into HCT116 cells. The cells were divided into six group of treatments: untreated cell group, cells treated with negative control siRNA, MSH2-siRNA treated cells, EPCAM-siRNA treated cells, cells treated with both EPCAM and MSH2-siRNA, and cells treated with transfection reagent (mock control). The mRNA and protein expression following the individual and combined siRNA treatments were assessed by quantitative polymerase chain reaction and Western blot. Results: The mRNA and protein expression levels of MSH2, EPCAM and β-catenin were reduced in the individual MSH2 and EPCAM-siRNA treated samples as compared to the untreated sample. Further reduction of mRNA and protein expressions for MSH2, EPCAM and β-catenin were identified in combined siRNA treatments. Conclusion: Reduction of β-catenin expression by simultaneous silencing of MSH2 and EPCAM suggested that these genes may play a role in supressing the Wnt/β-catenin pathway in cancer cells.