Wastewater monitoring provides essential information about water quality and the degree of contamination. Monitoring these waters helps identify and manage risks to public health, prevent the spread of disease, and protect the environment. Standardizing the appropriate and most accurate methods for the isolation and identification of viruses in wastewater is necessary. This review aims to present the major classes of viruses in wastewater, as well as the methods of concentration, isolation, and identification of viruses in wastewater to assess public health risks and implement corrective measures to prevent and control viral infections. Last but not least, we propose to evaluate the current strategies in wastewater treatment as well as new alternative methods of water disinfection.

Gastric cancer has remained in the top five cancers for over ten years, both in terms of incidence and mortality due to the shortage of biomarkers for disease follow-up and effective therapies. Aiming to fill this gap, we performed a bioinformatics assessment on our data and two additional GEO microarray profiles, followed by a deep analysis of the 40 differentially expressed genes identified. PPI network analysis and MCODE plug-in pointed out nine upregulated hub genes coding for proteins from the collagen family (COL12A1, COL5A2, and COL10A1) or involved in the assembly (BGN) or degradation of collagens (CTHRC1), and also associated with cell adhesion (THBS2 and SPP1) and extracellular matrix degradation (FAP, SULF1). Those genes were highly upregulated at the mRNA and protein level, the increase being correlated with pathological T stages. The high expression of BGN (p = 8 × 10⁻¹²), THBS2 (p = 1.2 × 10⁻⁶), CTHRC1 (p = 1.1 × 10⁻⁴), SULF1 (p = 3.8 × 10⁻⁴), COL5A1 (p = 1.3 × 10⁻⁴), COL10A1 (p = 5.7 × 10⁻⁴), COL12A1 (p = 2 × 10⁻³) correlated with poor overall survival and an immune infiltrate based especially on immunosuppressive M2 macrophages (p-value range 4.82 × 10⁻⁷–1.63 × 10⁻¹³). Our results emphasize that these genes could be candidate biomarkers for GC progression and prognosis and new therapeutic targets.

Immunotherapy has emerged as a promising approach to cancer treatment, but only a small percentage of cancer patients benefit from it. To enhance therapeutic outcomes, it is essential to understand factors influencing immune response and tumor progression. Soluble PD-L1 (sPD-L1) has been identified as an essential element in immune regulation, with potential implications in cancer biology and treatment. This manuscript explores the sources and mechanisms of sPD-L1 production, its role in immune evasion and tumor progression, and its clinical significance. Elevated sPD-L1 levels have been linked to disease severity, survival, and treatment response in various malignancies, and as a consequence, strategies for combinatorial targeting of sPD-L1 with other immunotherapies are considered. Further studies are needed to understand sPD-L1 dynamics and to clarify the mechanisms of sPD-L1-mediated immunosuppression and its therapeutic implications.

This manuscript assesses the critical role of exosomal PD-L1 (ExoPD-L1) in immune suppression, tumor progression, and resistance to therapy. ExoPD-L1 has been identified as a key mediator of tumor immune evasion, contributing to systemic immunosuppression beyond the tumor microenvironment (TME) due to its capacity to travel to distant anatomical sites. In this context, the review aims to elaborate on the mechanisms by which exosomal PD-L1 interacts with T cell receptors and modulates both the tumor microenvironment and immune responses, impacting patient outcomes. We further explore emerging therapeutic strategies that target ExoPD-L1 to enhance the effectiveness of immunotherapy. Blocking ExoPD-L1 offers a novel approach to counteracting immune escape in cancer. Promising strategies include inhibiting exosome biogenesis with GW4869 or Rab inhibitors, neutralizing ExoPD-L1 with targeted antibodies, and silencing PD-L1 expression through RNA interference (RNAi) or CRISPR-based methods. While each approach presents certain limitations, their integration into combination therapies holds significant potential to improve the efficacy of immune checkpoint inhibitors. Future research should focus on optimizing these strategies for clinical application, with particular attention to improving delivery specificity and minimizing off-target effects.

Experimental models of a clinical, pathophysiological context are used to understand molecular mechanisms and develop novel therapies. Previous studies revealed better outcomes for spinal cord injury chronic ethanol-consuming patients. This study evaluated cellular and molecular changes in a model mimicking spinal cord injury (hypoxic stress induced by treatment with deferoxamine or cobalt chloride) in chronic ethanol-consuming patients (ethanol-exposed neural cultures (SK-N-SH)) in order to explain the clinical paradigm of better outcomes for spinal cord injury chronic ethanol-consuming patients. The results show that long-term ethanol exposure has a cytotoxic effect, inducing apoptosis. At 24 h after the induction of hypoxic stress (by deferoxamine or cobalt chloride treatments), reduced ROS in long-term ethanol-exposed SK-N-SH cells was observed, which might be due to an adaptation to stressful conditions. In addition, the HIF-1α protein level was increased after hypoxic treatment of long-term ethanol-exposed cells, inducing fluctuations in its target metabolic enzymes proportionally with treatment intensity. The wound healing assay demonstrated that the cells recovered after stress conditions, showing that the ethanol-exposed cells that passed the acute step had the same proliferation profile as the cells unexposed to ethanol. Deferoxamine-treated cells displayed higher proliferative activity than the control cells in the proliferation–migration assay, emphasizing the neuroprotective effect. Cells have overcome the critical point of the alcohol-induced traumatic impact and adapted to ethanol (a chronic phenomenon), sustaining the regeneration process. However, further experiments are needed to ensure recovery efficiency is more effective in chronic ethanol exposure.

Despite being a “silent epidemic” disease, chronic kidney disease (CKD) is considered one of the major causes of mortality, together with its main complication, the cardiovascular disease, which contributes to the poor prognosis of these patients. Inflammation has been recognized as an essential part of CKD and is closely linked to cardiovascular complications. The identification of novel biomarkers using omics technologies is rapidly advancing and could improve the early detection in renal diseases. Omics approaches, including proteomics, could provide novel insights into disease mechanisms, identifying at the same time accurate inflammatory biomarker panels with an essential role in disease monitoring and follow-up. Recent advances highlight the gut microbiota as an important source of inflammation in kidney diseases. An increasing body of evidence reveals the cross talk between microbiota and host in CKD; in addition, gut dysbiosis may represent an underappreciated cause of inflammation and subsequently could lead to malnutrition, accelerated cardiovascular disease and CKD progression. This chapter discusses the relationship between inflammation and CKD and highlights the novel approaches regarding microbiota involvement in CKD pathology, as well as their potential to facilitate improving the quality of life.