The pharmaceutical industry is the key player in the healthcare sector but faces significant challenges in terms of sustainability. As the industry evolves with Industry 4.0, integrating green chemistry principles and sustainable practices is imperative. This review explores the intersection of advanced digital technologies and sustainable production, focusing on cleaner manufacturing, green raw materials, and eco-friendly packaging. The adoption of Industry 4.0 technologies such as artificial intelligence, Internet of Things (IoT), and blockchain enhances transparency, efficiency, and environmental impact tracking throughout the pharmaceutical supply chain. Green chemistry approaches, including the use of renewable feedstocks, atom economy, and safer solvents, are discussed as key strategies to minimize the environmental footprint of pharmaceutical production. Additionally, the implementation of green raw materials and innovative packaging solutions is highlighted as a means to reduce waste and promote circular economy practices. This review also addresses the environmental fate and toxicity of pharmaceuticals, emphasizing the need for responsible disposal and waste management. The findings suggest that a comprehensive, technology-driven approach is essential for advancing sustainability in the pharmaceutical industry, ensuring that it can meet both current and future environmental and health challenges.

Food colors derived from natural sources are in high demand currently due to the industries and health-conscious consumers. Cyanobacteria are well-suited for the development of effective natural colorants; however, they are often neglected due to low yields and limited genetic tools. Phycoerythrin (PE) is an essential colorant that has a wide range of industrial applications, including food, cosmetics, agriculture, horticulture, and human health. Despite the high demand for PE, it is difficult to achieve higher levels of production, extraction efficiency, and stability under normal conditions. However, if low-cost cyanobacterial platforms are used, it is expected that the use of PE will increase in the near future. This review addresses the most recent studies on potential new PE producers, as well as their distinctive structure and properties that are responsible for novel biological activities. Additionally, newly discovered nutritional and process parameters for improving PE production in raceway ponds and photobioreactors are highlighted. The improvement of previously developed processes for extracting and purifying PE from cyanobacterial biomass is also thoroughly explained. Additionally, the recently reported biotechnological applications of cyanobacterial PE are discussed. Furthermore, a critical analysis is also given of the market and difficulties involved in developing a system for producing PE using cyanobacteria.

Tumor microenvironment (TME) plays a particularly important role in the pathogenesis and drug resistance of lung cancer. This article provides a framework that allows us to view lung cancer through the lens of cancer stem cells (CSCs) and angiogenesis, with the aim of enhancing both clinical and laboratory insights. It critically examines the bidirectional interactions between CSCs and other components of the TME, highlighting their combined contributions to tumor aggressiveness and angiogenic processes. We discuss the mechanisms by which CSCs influence angiogenesis, including the release of growth factors and cytokines, while also emphasizing how angiogenic factors, in turn, modulate CSC behavior and help maintain a microenvironment that supports tumor growth. Potential biomarkers and therapeutic targets- such as CD133, ALDH1, and VEGF-are explored as valuable not only for disease management but also for the development of targeted therapies for lung cancer. This article ultimately provides a foundation for researchers to further investigate these interconnected processes and for clinicians to consider therapeutic strategies when managing patients with lung cancer. Given the multifaceted nature of lung cancer biology and the numerous molecules involved, we advocate for a panel-centered approach in both research and clinical management, while underscoring the importance of carefully considering toxicity risks and variability in molecular expression.

The SARS-CoV-2 pandemic has highlighted the need for society, as a whole, to be prepared against potential pandemics caused by a variety of different viral families of concern. Here, we describe a roadmap towards the identification and validation of conserved T cell epitope regions from Viral Families of Pandemic Potential (VFPP). For each viral family, we select a prototype virus, the sequence of which could be utilized in epitope identification screens. Examples of viral families considered and their respective prototypes (species/ subspecies) are Coronaviridae (Severe Acute Respiratory Syndrome-related Coronavirus/ SARS-CoV-2), Flaviviridae (Dengue virus/DENV2), Togaviridae (Chikungunya virus/ CHIKV), Paramyixoviridae (Morbillivirus/measles), Arenaviridae (Mammarenavirus/ Lassa), and Picornaviridae (Enterovirus C/poliovirus). The peptide sequences encoded in each prototype virus are then analyzed to determine their conservation across different viral taxonomic groups and viral variants derived from each of the VFPP. We outline available methodologies for epitope discovery based on panels of overlapping peptides and bioinformatics- based predictions of HLA-peptide binding, along with high-throughput in vitro assays, with emphasis on addressing coverage of the general worldwide population. Validation can be achieved by a variety of methodologies, including determining HLA restriction and recognition in samples from volunteers convalescent from previous infections or immunized with approved or experimental vaccines, and immunophenotyping of responding T cells. The capacity of these regions to induce crossreactive T cell responses can be tested experimentally with homologous peptides derived from the various viral species of interest. Importantly, they could be considered as a component of pan-viral family vaccines. Conversely, immunogenic regions that are highly specific to a given virus could be of interest for diagnostic applications.

Neurodegenerative diseases are a group of life-threatening conditions characterized by gradual and severe neuronal degeneration, posing a significant global health challenge. Many neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease, share identical and recognizable etiologies, such as neuronal degeneration, apoptosis, oxidative stress, lipid peroxidation, Ca2+ overload, neuroinflammation, protein aggregation, endoplasmic reticulum stress, and mitochondrial dysfunction. Among these etiologies, oxidative stress and mitochondrial dysfunction are the primary contributing factors, involving several enzymes and signaling molecules in the underlying mechanism of disease progression. Globally available treatments provide only temporary symptomatic relief with side effects, and yet there is no medication to eradicate the disease-related cause. Extensive research has explored novel herbal medications offered as neuroprotective against these debilitating conditions, aiming to reverse or halt the disease progression with minimal adverse effects. Pinostrobin is a major bioactive flavonoid primarily isolated from Boesenbergia rotunda (Fingerroot). Established research has reported that pinostrobin exhibits a wide array of pharmacological activities, including anti-inflammatory, antileukemia, antioxidant, antimicrobial properties, as well as protective effects against mitochondrial dysfunction and neurodegeneration. Based on preclinical studies, we have summarised the current knowledge of pinostrobin's neuroprotective actions, highlighting its effectiveness in mitigating neuronal damage, preserving synaptic function, reducing oxidative stress, neuroinflammation, protein aggregation, mitochondrial apoptosis, and calcium overload. These mechanisms collectively support its therapeutic potential in modulating the molecular pathways underlying Alzheimer's and Parkinson's disease. This review offers a comprehensive analysis of pinostrobin and its molecular pathways in combating neurodegenerative diseases, highlighting its promising effectiveness as a natural neuroprotective agent in Alzheimer's and Parkinson's disease by modulating mitochondrial and oxidative stress-mediated pathways.

Non-small cell lung cancer (NSCLC) is among the most aggressive malignancies threatening human health. Histone deacetylase inhibitors (HDACi) have been shown to suppress epidermal growth factor receptor (EGFR) signaling, making them promising candidates for NSCLC therapy. This study aimed to evaluate the effects of Entinostat on NSCLC. The anti-proliferative effect of Entinostat was assessed using MTT assays, with four other HDAC inhibitors (the pan-HDAC inhibitor SAHA and selective HDAC inhibitors BRD73954, BG45, and NKL22) as controls. EGFR expression and phosphorylation of STAT3, AKT, and p38 were measured in vitro and in vivo via Western blot. Apoptosis was analyzed by flow cytometry, and expression of apoptosis regulators p53 and p21 was assessed by Western blot. The in vivo anti-tumor activity of Entinostat was evaluated using NSCLC xenograft models. Entinostat exhibited more potent anti-NSCLC activity than the other HDAC inhibitors in H460 and H1975 cell lines, with IC50 values of 0.69±0.03 μM and 0.20±0.01 μM, respectively. Western blot analysis demonstrated that Entinostat reduced EGFR expression and decreased phosphorylation of STAT3, AKT, and p38, indicating suppression of EGFR signaling both in vitro and in vivo. In xenograft models, treatment with 40 mg/kg Entinostat significantly inhibited tumor growth, though it also affected mouse body weight. Entinostat demonstrates strong anti-NSCLC activity by suppressing EGFR expression and downstream signaling, highlighting its potential as a therapeutic agent.

The aim of this study was to develop a clinical application model for the rational use of caffeine. Caffeine is related to the incidence of neuro immune gastrointestinal diseases. Coffee consumption needs to be optimized in order to reduce the incidence rate. By using KEEG analysis to explore potential molecular signaling pathways involved in the progression of neurological immune gastrointestinal diseases, and analyzing the details of this signaling Pathway using molecular simulation results, which can support AI system for doctor. The research team designed a controlled experiment to analyze the differences in reward and reinforcement of Brain pleasure/addiction and dopamine related signaling pathways function between multiple groups of people with different coffee drinking habits and a blank control group. The study team used molecular dynamics methods to investigate the signaling route that links coffee with the binding of dopamine receptor D3.AI is used to predict the prevalence of gastric reflux disease. Human experiments have shown a correlation between caffeine intake and gastroesophageal reflux disease. AI algorithm results can provide clinical support, and molecular simulation results are consistent with human experimental results. Caffeine and DRD3 protein have a stable interaction system. The research team elucidated the intermolecular interaction between caffeine and DRD3, and AI algorithms can predict the likelihood of disease occurrence, providing a new strategy for clinical practice. This study has passed ethical approval at Chifeng Cancer Hospital, and the ethical documents for this study have been submitted to the World Health Organization for filing.

Nanoparticles used in enzyme immobilization offer a high surface area- to-volume ratio, high chemical and thermal stability, and resistance to microbial attack. The present investigation demonstrates the immobilization of Aspergillus oryzae β- galactosidase on silica nanoparticles via covalent binding. A greater yield of enzyme immobilization (89%) was attained on the developed nanobiocatalyst. It was observed that the immobilized and soluble enzymes had optimal pH and temperature values of 50°C and 4.5, respectively. It was monitored that at pH 4.0, soluble β- galactosidase (SβG) exhibited 59% activity. However, the immobilized enzyme showed 92% activity under identical conditions. Similarly, 41% enzyme activity was retained at 70 °C by the free enzyme. Conversely, immobilized β-galactosidase (IβG) retained 70% activity under similar experimental conditions. Additionally, it was observed that at 5% galactose concentration, IβG showed 55% activity under one hour of incubation. However, under comparable experimental conditions, SβG showed 24% activity. It was observed that the immobilized enzyme was reusable, maintaining 90% of its activity even after five uses. The soluble enzyme demonstrated 62% and 70% lactose hydrolysis under the same conditions after 8 hours, while IβG demonstrated 74% and 85% lactose hydrolysis at 40°C and 50°C, respectively, in a controlled batch reactor experiment that was run for 10 hours. Hence, owing to the greater reusability (90% after 5th repeated use) and excellent conversion of lactose at higher temperatures, the developed nanosupport may be used to produce lactose-free dairy products in continuous reactors on a large scale in biotechnology industries.

Diabetic Kidney Disease (DKD) is a major cause of End-Stage Renal Disease (ESRD) and lacks effective treatments. Tangmaikang Granules (TMK), a multi-herb traditional Chinese medicine formulation, have shown potential in managing DKD. However, the precise active components, molecular mechanisms, and therapeutic advantages of TMK remain unclear. This study tests the hypothesis that TMK granules exert protective effects on DKD by targeting multiple pathways involved in oxidative stress, inflammation, and apoptosis in podocytes through a multi-targeted approach. The aim was to identify TMK's bioactive components, evaluate its therapeutic potential, and uncover its molecular mechanisms in DKD. The bioactive constituents in TMK were determined through ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). Drug targets were identified using SwissTargetPrediction and SuperPred, whereas DKD-associated targets were obtained from the GeneCards, DisGeNET, OMIM, and TTD databases. A Protein-Protein Interaction (PPI) network was constructed, and key targets were identified via topological analysis. Molecular docking and dynamics simulations were performed to evaluate stable binding interactions. GO and KEGG pathway enrichment analyses were conducted to uncover relevant signaling pathways. TMK's effects on oxidative stress, inflammation, and apoptosis in podocytes were assessed using CCK-8, flow cytometry, RT-qPCR, ELISA, and Western blot assays. Thirty active compounds and 384 potential therapeutic targets were identified, with eight key targets. Pathway enrichment analysis revealed TMK's involvement in AGE-RAGE, EGFR, HIF-1, and apoptosis pathways, affecting inflammatory cytokine responses and oxidative stress. In vitro experiments demonstrated that TMK significantly reduced oxidative stress, inflammation, and apoptosis in podocytes by inhibiting the MAPK and NF-κB pathways. TMK granules target DKD through a multi-component, multi-target strategy, effectively mitigating oxidative stress and suppressing inflammatory and apoptotic pathways. This study integrates advanced computational and experimental methods, demonstrating TMK's unique therapeutic potential and providing a robust foundation for its clinical application in DKD management.