The hallmark of multiple myeloma is myeloma related bone disease. Interactions between myeloma plasma cells (MPCs), stromal cells, and the bone marrow (BM) microenvironment play a critical role in the pathogenesis of MBD. Bone remodeling is severely dysregulated with the prevalence of osteoclast activity. We aimed to assess circulating levels of sRANKL, periostin, and osteopontin as osteoclast activators in NDMM patients at diagnosis and in the course of treatment, correlations with clinical and laboratory data, and to evaluate their potential as additional biomarkers for the assessment of MBD. The current study involved 74 subjects (41 NDMM patients, 33 controls). MBD was assessed by whole-body low-dose computed tomography. sRANKL, periostin, and osteopontin were assayed by commercial ELISA kits. At diagnosis, all tested parameters were significantly higher in NDMM patients compared to the controls (p < 0.0001), correlating with disease stage, MBD grade, and BM infiltration by MPCs. During therapy, the serum levels of all tested proteins decrease, most prominently after autologous stem cell transplantation (p < 0.0001). A significant reduction was established in patients achieving complete and very-good partial response compared to all others (p < 0.05). In conclusion, sRANKL, periostin, and osteopontin reflect MBD severity and could be promising markers for MBD monitoring and the effect of myeloma treatment.

Cyanoprokaryotes are distributed worldwide and they produce various bioactive compounds, including cyanotoxins. The major route of human exposure to cyanotoxins is the oral intake by using contaminated drinking water, by incidental intake of contaminated water during recreational and professional activities, and by consuming contaminated food or dietary supplements prepared from cyanobacteria. The prolonged chronic exposure to low concentrations of cyanotoxins provokes cell damage and may increase the risk for cancer development. Due to the variety of cyanotoxin chemical structures, different mechanisms of their toxic effects are known. At the same time, some of the natural compounds produced by cyanoprokaryotes have anticancer potential and are promising sources for the development of novel drugs. This chapter is dedicated to the target mechanisms behind the effects of the widely distributed cyanotoxins with an impact on human health, microcystins, nodularins, and cylindrospermopsin.

Eutrophication of water bodies and the bloom of toxin-producing cyanoprokaryotes raise health concerns. Various cyanoprokaryotes species, including Microcystis, Raphidiopsis, Nodularia, and Chrysosporum, release toxins into the aquatic environment, which can reach concentrations toxic to humans and animals. Rising temperatures and human activities are primary drivers behind the increasing frequency of toxic cyanobacterial blooms. The Word Health Organization (WHO) has established provisional guideline values for cyanotoxins in drinking water and water used for other purposes in daily human activities, and has published guidance for identifying hazards and managing risks posed by cyanobacteria and their toxins. There are currently no acceptable limit values for cyanotoxins. To address monitoring needs, contemporary strategies now incorporate molecular genetics, immunoassays, biochemical profiling, and emerging machine-learning frameworks. This paper reviews current early detection methods for harmful cyanobacterial blooms, highlighting their practical advantages and drawbacks.

Objectives: Matrix Gla protein (MGP) is a calcification inhibitor that plays a role in preventing soft tissue calcification and local mineralization of the vascular wall. The present study aimed to assess the expression of MGP in Peripheral Blood Mononuclear Cells (PBMC) in adult patients with CVD pathologies and its association with the presence and severity of coronary artery calcium score (CACS) and conventional CVD risk factors. Methods: MGP expression was measured in 87 individuals using real time qPCR. Subgrouping was performed according etiologic and metabolic CVD risk factors. Results: A clear trend for a decreased MGP expression was observed in all subgroups with high CVD risk. This decrease was significant in abdominally obese hypertensive individuals and in those with dyslipidemia. MGP expression was significantly lower in patients representing high Total cholesterol and LDL cholesterol levels. A positive correlation between MGP expression and smoking status in patients with coronary calcium and in the CVD group was established. Atrial hypertension duration correlated negatively with MGP expression in the group without coronary calcium deposits. Conclusions: The current study supports the hypothesis that MGP expression in PBMC probably reflects CVD pathology and is related to lipid metabolism dysregulation.

Background: Cardiovascular diseases (CVDs) are the major cause of death globally. Among them, heart failure (HF) and atrial fibrillation (AF) result in poor prognosis and quality of life. Standard methods for assessing AF and HF, through history and physical examination, have limited sensitivity and specificity, which lead to delayed diagnosis and high risk of mortality. The identification of biomarkers able to detect the early stages of disease and/or their progression is of great importance for improving the clinical outcome. As AF and HF often coexist, it would be of great importance to find a biomarker with diagnostic utility in predicting HF in AF patients. Soluble suppression of tumorigenesis-2 (sST2) is a part of the cardioprotective IL-33/ST2 signaling pathway and may serve as a candidate biomarker for HF and AF. We aimed to evaluate sST2 serum levels in patients with AF and HF with preserved ejection fraction (HFpEF) and to explore potential relationships with traditional CVD risk factors and with novel biomarkers for vascular calcification such as undercarboxylated matrix Gla-protein (ucMGP). Materials and Methods: This study included 99 patients stratified into three groups: HFpEF (n=19), paroxysmal or persistent AF in sinus rhythm (n=33), and control group without CVD but at moderate-to-high CVD risk (n=47). Hemodynamic and anthropometric measures, coronary artery calcification (CAC), routine laboratory parameters, circulating ucMGP, and sST2 were measured. Results: sST2 levels were highly elevated in HFpEF patients. Significant positive correlation was found between sST2 and CAC-score (r=0.237, p=0.039), negative relations with serum lipids in AF patients, and positive association with serum C-reactive protein (r=0.609, p=0.018) in HFpEF patients. Soluble ST2 positively correlates with ucMGP in the entire studied population (r=0.252, p=0.006) and in the combined CVD group (AF+HFpEF) (r=0.254, p=0.036). Conclusions: sST2 levels emerge as a novel biomarker in CVD and may have prognostic importance for HF prediction in AF patients.