Universities and colleges play a pivotal role in the pursuit of a future that is sustainable through their pedagogical efforts and the execution of state-of-the-art research endeavors aimed at mitigating the effects of climate change. Higher Education Institutions (HEIs) serve as crucial catalysts in advancing sustainable development. HEIs are increasingly embracing precise measures to reduce their carbon footprint (CF) while also educating students on global sustainability. These nano-methods provide a quantitative framework for assessing a campus's sustainability efforts in line with Green Campus (GC) initiatives to lower carbon emissions align with GC goals. This study employs K-means clustering to analyze the integration of green and low-carbon principles in higher education political and ideological studies. Its goal is to identify patterns, assess teaching effectiveness, and improve sustainability education, aligning with Green Campus initiatives to enhance institutional contributions to sustainable growth through informed pedagogical strategies. Input data includes curriculum content, teaching methods, student engagement, and institutional goals related to sustainability. Seeking to improve sustainability education align with Green Campus initiatives, higher education can strategically enhance their contributions to long-term sustainability and growth through effective pedagogical approaches. Cluster 3 has the lowest WCSS value of 1200, indicating tighter cohesion and less variability within this cluster compared to Cluster 1 (1500) and Cluster 2 (1800). Cluster 3 stands out with the highest silhouette score of 0.7, suggesting well-defined and distinct clusters, while Cluster 2 has the lowest score of 0.4, indicating some overlap or ambiguity in data points. Cluster 1 has the lowest Davies-Bouldin Index of 0.4, implying better separation between clusters compared to Cluster 2 (0.6) and Cluster 3 (0.5). Cluster 3 is well-defined and cohesive, showing strong integration of green practices. Cluster 1 displays good separation and cohesion, while Cluster 2 requires refinement due to potential overlap in sustainability integration.

The mathematical modeling and analysis of within-host or between-host coronavirus disease 2019 (COVID-19) dynamics are considered robust tools to support scientific research. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of COVID-19. This paper proposes and investigates a within-host COVID-19 dynamics model with latent infection, the logistic growth of healthy epithelial cells and the humoral (antibody) immune response. Time delays can affect the dynamics of SARS-CoV-2 infection predicted by mathematical models. Therefore, we incorporate four time delays into the model: (i) delay in the formation of latent infected epithelial cells, (ii) delay in the formation of active infected epithelial cells, (iii) delay in the activation of latent infected epithelial cells, and (iv) maturation delay of new SARS-CoV-2 particles. We establish that the model’s solutions are non-negative and ultimately bounded. This confirms that the concentrations of the virus and cells should not become negative or unbounded. We deduce that the model has three steady states and their existence and stability are perfectly determined by two threshold parameters. We use Lyapunov functionals to confirm the global stability of the model’s steady states. The analytical results are enhanced by numerical simulations. The effect of time delays on the SARS-CoV-2 dynamics is investigated. We observe that increasing time delay values can have the same impact as drug therapies in suppressing viral progression. This offers some insight useful to develop a new class of treatment that causes an increase in the delay periods and then may control SARS-CoV-2 replication.

Coronavirus disease 2019 (COVID-19) is a new viral disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Malaria is a parasitic disease caused by Plasmodium parasites. In this paper, we explore a within-host model of SARS-CoV-2/malaria coinfection. This model consists of seven ordinary differential equations that study the interactions between uninfected red blood cells, infected red blood cells, free merozoites, uninfected epithelial cells, infected epithelial cells, free SARS-CoV-2 particles, and antibodies. We show that the model has bounded and nonnegative solutions. We compute all steady state points and derive their existence conditions. We use appropriate Lyapunov functions to confirm the global stability of all steady states. We enhance the reliability of the theoretical results by performing numerical simulations. The steady states reflect the monoinfection and coinfection with malaria and SARS-CoV-2. The shared immune response reduces the concentrations of malaria merozoites and SARS-CoV-2 particles in coinfected patients. This response reduces the severity of SARS-CoV-2 infection in this group of patients.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a new virus which infects the respiratory system and causes the coronavirus disease 2019 (COVID-19). The coinfection between malaria and COVID-19 has been registered in many countries. This has risen an urgent need to understand the dynamics of coinfection. In this paper, we construct a reaction–diffusion in-host malaria/COVID-19 model. The model includes seven-dimensional partial differential equations that explore the interactions between seven compartments, healthy red blood cells (RBCs), infected RBCs, free merozoites, healthy epithelial cells (ECs), infected ECs, free SARS-CoV-2 particles, and antibodies. The biological validation of the model is confirmed by establishing the nonnegativity and boundedness of the model’s solutions. All equilibrium points with the corresponding existence conditions are calculated. The global stability of all equilibria is proved by picking up appropriate Lyapunov functionals. Numerical simulations are used to enhance and visualize the theoretical results. We found that the equilibrium points show the different cases when malaria and SARS-CoV-2 infections occur as mono-infection or coinfection. The shared antibody immune response decreases the concentrations of SARS-CoV-2 and malaria merozoites. This can have an important role in reducing the severity of SARS-CoV-2 if the immune response works effectively.

The coronavirus disease 2019 (COVID-19) is a respiratory disease that appeared in 2019 caused by a virus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is still spreading and causing deaths around the world. There is a real concern of SARS-CoV-2 coinfection with other infectious diseases. Tuberculosis (TB) is a bacterial disease caused by Mycobacterium tuberculosis (Mtb). SARS-CoV-2 coinfection with TB has been recorded in many countries. It has been suggested that the coinfection is associated with severe disease and death. Mathematical modeling is an effective tool that can help understand the dynamics of coinfection between new diseases and well-known diseases. In this paper, we develop an in-host TB and SARS-CoV-2 coinfection model with cytotoxic T lymphocytes (CTLs). The model investigates the interactions between healthy epithelial cells (ECs), latent Mtb-infected ECs, active Mtb-infected ECs, SARS-CoV-2-infected ECs, free Mtb, free SARS-CoV-2, and CTLs. The model’s solutions are proved to be nonnegative and bounded. All equilibria with their existence conditions are calculated. Proper Lyapunov functions are selected to examine the global stability of equilibria. Numerical simulations are implemented to verify the theoretical results. It is found that the model has six equilibrium points. These points reflect two states: the mono-infection state where SARS-CoV-2 or TB occurs as a single infection, and the coinfection state where the two infections occur simultaneously. The parameters that control the movement between these states should be tested in order to develop better treatments for TB and COVID-19 coinfected patients. Lymphopenia increases the concentration of SARS-CoV-2 particles and thus can worsen the health status of the coinfected patient.