Background Diabetes mellitus (DM) affects hundreds of millions of people worldwide. Genetic research plays a cru-cial role in managing diabetes by providing valuable insights into genetic predispositions, facilitating early diagno-sis, and enabling personalized treatment strategies. Identification of important genetic markers has paved the way for the creation of targeted therapies, enhancing treatment outcomes and promoting preventive care for both type 1 diabetes mellitus ( T1DM) and type 2 diabetes mellitus ( T2DM). The aim of this study is to explore the role of different genes in the development of DM and its related complications. Methodology A comprehensive literature search was conducted from October 27 to November 14, 2024, to enlist articles related to genes involved in development of DM and its complications in search engines including PubMed, Medline, Google Scholar, and Scopus. We included original articles, case–control studies, cohort studies, review arti-cles, systematic review, and meta-analysis published between January 1, 2014, and November 14, 2024 in our study. Results In T1DM; research has historically concentrated on the role of HLA class II genes. However, recent studies have brought attention to the role of HLA class I genes in the disease’s development, suggesting a broader role of genetics than previously understood. CTLA4, IL2RA, and PTPN22, genes were also significantly linked to T1DM. In T2DM; TCF7L2 was found to be the most potent gene for its development among others genes such as LCAT, APOE, FTO. For gesta-tional diabetes mellitus (GDM), MTNR1B, CDKAL1, and IRS1 genes played an important role. Conclusion Genetics played an important role in the understanding of DM. Researchers have identified new genetic loci that can serve as diagnostic markers for DM and its associated compilations such as diabetic kidney disease (DKD), diabetic neuropathy (DN), diabetic retinopathy (DR) and cardiovascular diseases (CVDs). TCF7L2 and HLA class II are the strongest risk factors for T2DM and T1DM, respectively. Understanding the genetics of DM and its complications is essential for improving early detection, enhancing treatment outcomes, and developing targeted therapies for DM patients.

This study is motivated by the need to understand complex thermal and hydrodynamic behaviors of couple stress fluids, which commonly occur in lubrication systems, microfluidic devices, and polymeric material processing. Its significance lies in modeling non-isothermal couple stress fluid flow through an inclined Poiseuille channel bounded by two heated parallel plates, a configuration relevant to advanced heat and mass transfer applications. The aim is to determine the velocity profile, temperature distribution, volumetric flow rate, average velocity, and shear stress for the incompressible fluid. To achieve this, the highly nonlinear coupled ordinary differential equations governing the system are solved using the Optimal Homotopy Asymptotic Method and the Homotopy Perturbation Method, which provide accurate approximate solutions without linearization. The major findings show excellent agreement between the two approaches, confirming their validity, while parametric studies reveal how physical factors such as couple stress effects, plate inclination, and thermal gradients influence the flow. The specific applications of this work include lubrication processes, thermal energy devices, and fluid transport systems requiring precise control of flow and heat transfer.

This paper develops and analyzes a fractional-order predator–prey model with Holling type III functional response, incorporating the transmission of a contagious disease between both populations. We first establish the existence, uniqueness, non-negativity, and boundedness of solutions for the fractional-order system. The local stability of the model’s equilibrium points is examined, and the global stability is rigorously proved using a suitable Lyapunov function. We also investigate the effects of disease transmission on the predator–prey dynamics by identifying multiple equilibria, threshold parameters, and stability conditions. In particular, we analyze the existence of Hopf bifurcation at the endemic equilibrium point through bifurcation analysis, revealing the possible emergence of periodic oscillations. Analytical results are complemented by numerical simulations, highlighting the importance of incorporating both Holling type III predation and disease transmission when assessing prey–predator coexistence.

Neurodegenerative diseases (NDs) such as Alzheimer’s, Parkinson’s, Huntington’s disease, and amyotrophic lateral sclerosis are escalating worldwide, straining healthcare systems and leaving patients with therapies that are largely palliative. Emerging evidence positions diversified ultraviolet (UV) irradiation as a groundbreaking, non-invasive strategy to counter these disorders. Beyond its traditional use in sterilization, specific UV spectra, UV-B (280–320 nm), UV-C (200–280 nm), and far-UV (207–222 nm), are now recognized for modulating oxidative stress, restoring mitochondrial function, correcting apoptotic dysregulation, and enhancing DNA repair. Innovative approaches such as riboflavin-mediated phototherapy and photobiomodulation (PBM) show the capacity to disaggregate toxic protein aggregates like β-amyloid and α-synuclein, boost antioxidant defenses, stimulate neurotrophic factors, and quell neuroinflammation. Preclinical models and early clinical trials reveal preserved cognition, enhanced neurogenesis, and reduced disease biomarkers, suggesting real translational promise. From a public-health perspective, UV-based interventions offer a cost-effective, scalable option for aging populations and resource-limited settings, especially when integrated with community-level health technologies and remote delivery platforms. Continued investigation of optimal dosing, long-term safety, and mechanistic pathways will be pivotal to unlock the full therapeutic and population-wide impact of this novel modality.

The objective of this study is to analyze controllability results for time-varying linear and nonlinear fractional dynamical systems with multiple control delays within the framework of the Caputo fractional derivative. This paper focuses on examining control problems within a finite time interval, aiming to identify a control function that steers the system’s solution from a specified initial state to a targeted final state. For linear systems, the study establishes necessary and sufficient conditions for controllability by utilizing the Grammian matrix techniques. For nonlinear systems, the existence of a solution is ensured through an iterative technique, with completeness of the space guaranteed. With the help of this technique, we establish the sufficient conditions for the controllability of time-varying nonlinear fractional dynamical systems. The results show that the controllability of fractional dynamical systems can be effectively analyzed with the given framework, along with numerical simulations and graphical representations to clarify the theoretical findings.

Background: Current antivirals for orolabial Herpes simplex virus type 1 (HSV-1) often provide incomplete suppression and limited reactivation control, sustaining recurrent oral lesions and inflammation that compromise oral health. HSV-1 subverts host signaling networks to enhance its replication and trigger inflammation. Among these, the extracellular signal-regulated kinase 1/2 (ERK1/2) and phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathways are hijacked to facilitate viral gene expression and cell survival. Objectives: In this study, we employed U0126 [a mitogen-activated protein kinase 1/2 (MEK1/2) inhibitor] and LY294002 [a phosphatidylinositol 3-kinase (PI3K) inhibitor] as targeted pharmacological tools to intercept HSV-1’s exploitation of host keratinocyte signaling. Methods: Human HaCaT keratinocytes were infected with HSV-1 and treated with U0126 or LY294002. Western blotting was used to assess phosphorylation of ERK1/2 and activation of protein kinase B (AKT). MTT assays were performed to evaluate cell viability. Real-time PCR was utilized to quantify viral transcripts (ICP0, ICP4, gB, and gC) and inflammatory cytokines [interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α)]. Confocal microscopy was employed to visualize the intracellular distribution of phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2), phosphorylated activation of protein kinase B (p-AKT), and HSV-1 glycoprotein D (gD). Viral titers were determined using plaque assays. Results: The HSV-1 infection induced a time-dependent increase in phosphorylation of ERK1/2 and AKT, with p-ERK1/2 peaking at 12 h and p-AKT increasing 2.5-fold by 24 h. Cell viability declined from 100% at baseline to 45% at 24-hours post-infection (hpi). Treatment with U0126 and LY294002 reduced p-ERK1/2 and p-AKT levels to 25% and 30% of infected controls, respectively, restoring viability to 82 - 86%. Both inhibitors markedly suppressed viral gene expression (ICP0, ICP4, gB, gC down by 60 - 80%) and inflammatory cytokines (IL-6 and TNF-α reduced by > 50%). Plaque assays showed a strong decline in infectious titers — from 175 plaques per well in untreated infection to 60 and 45 plaques after U0126 and LY294002, respectively. Confocal imaging further revealed diminished nuclear accumulation of p-ERK1/2 and p-AKT, indicating disruption of post-entry signaling critical for viral replication. Conclusions: Targeting host signaling bottlenecks with U0126 and LY294002 offers a dual-pronged antiviral strategy against HSV-1 by dismantling the ERK/AKT axis critical for replication and inflammatory amplification. These findings position MEK1/2 and PI3K as promising therapeutic nodes for managing cutaneous HSV-1 infections. This host-directed dual-pathway inhibition may therefore help reduce recurrent orolabial HSV-1 lesions.