Introduction: Due to the SARS-CoV-2 coronavirus pandemic, the wearing of masks has become a common phenomenon. Most of the undesirable effects of using a protective face covering are usually related to the prolonged time of its wearing, and the adverse consequences of face coverings should be considered two-fold. The aim of the study was to evaluate the rate of contamination of the three types of face coverings (surgical, N95, and FFP2 masks) with the microorganism—aerobic bacteria, yeasts, and molds—after the 3 h exposure time. The study aimed to investigate the effects of wearing FFP2 masks (KN95) on respiratory function and the acid–base balance of the human body. Results: The presence of S. aureus was confirmed in both nasal carriers and non-carriers which may demonstrate the cross-contamination and spread of this bacterium via hands. S. aureus was found on external and internal surfaces of face masks of each type, and therefore could also be transmitted via hands from external sources. The 3 h exposure time is not sufficient for Gram-negative rods and mold contamination. Moreover, there were no significant differences in most of the parameters studied between the first and second examinations, both in spirometry and capillary blood gas analysis (p > 0.05).
Multiple myeloma (MM) is a plasma cell malignancy with multifactorial etiology. One of the underlying mechanisms is immune system dysregulation. Immunotherapy is being widely introduced into various MM treatment protocols. Nevertheless, little is known about boosting the immune system with supportive treatment. Although classical actions of vitamin D (VD) are very well established, their non-classical actions related to the modulation of the immune system in MM are still a subject of ongoing research. In this literature review, we intend to summarize research conducted on VD and MM, both in vitro and in vivo, with particular emphasis on immune system modulation, the induction of the differentiation of malignant MM cells, synergic activity with anti-MM drugs, and MM-associated peripheral neuropathy.
The exact pathophysiology of severe COVID-19 is not entirely elucidated, but it has been established that hyperinflammatory responses and cytokine storms play important roles. The aim of this study was to examine CMV status, select chemokines, and complement components in COVID-19, and how concentrations of given molecules differ over time at both molecular and proteomic levels. A total of 210 COVID-19 patients (50 ICU and 160 non-ICU patients) and 80 healthy controls were enrolled in this study. Concentrations of select chemokines (CXCL8, CXCL10, CCL2, CCL3, CCR1) and complement factors (C2, C9, CFD, C4BPA, C5AR1, CR1) were examined at mRNA and protein levels with regard to a COVID-19 course (ICU vs. non-ICU group) and CMV status at different time intervals. We detected several significant differences in chemokines and complement profiles between ICU and non-ICU groups. Pro-inflammatory chemokines and the complement system appeared to greatly contribute to the pathogenesis and development of severe COVID-19. Higher concentrations of CXCL8 and CCL2 in the plasma, with reduced mRNA expression presumably through negative feedback mechanisms, as well as CMV-positive status, correlated with more severe courses of COVID-19. Therefore, CXCL8, CCL2, and CMV seropositivity should be considered as new prognostic factors for severe COVID-19 courses. However, more in-depth research is needed.
The launch of novel chemotherapeutic agents—in particular, proteasome inhibitors and immunomodulatory drugs—dramatically changed multiple myeloma (MM) therapy, improving the response rate and prolonging progression-free survival. However, none of the anti-MM drugs are deprived of side effects. Peripheral neuropathy (PN) seems to be one of the most pressing problems. Despite extensive research in this area, the pathogenesis of drug-induced peripheral neuropathy (DiPN) has not yet been fully elucidated. In the present study, we aimed to assess the potential relationship between proinflammatory factors and the development of PN in MM patients with particular emphasis on the application of VTD (bortezomib, thalidomide, dexamethasone) regimen. Our analysis identified increased concentrations of CCL2, IL-1β, and IFN-γ in plasma of MM patients during treatment, both with and without symptoms of PN, compared with untreated neuropathy-free MM patients. At the same time, the plasma concentration of IL-1β in patients with neuropathy was significantly increased compared with patients without PN before and during treatment. Moreover, the results were enhanced at the transcript level by performing global mRNA expression analysis using microarray technology. The most significant changes were observed in the expression of genes responsible for regulating immunological and apoptotic processes. An in-depth understanding of the mechanisms responsible for the development of DiPN might in the future reduce the incidence of PN and accelerate diagnosis, allowing the choice of neuropathy-free treatment strategies for MM.
Bernstein fits implemented into R allow another route for Kruskal-Wallis power-study tool development. Monte-Carlo Kruskal-Wallis power studies were compared with measured power, a Monte-Carlo ANOVA equivalent and with an analytical method, with or without normalization, using four simulated runs, each with 60–100 populations (each population with N = 30,000 from a set of Pearson-type ranges): random selection gave 6300 samples analyzed for predictive power. Three medical-study datasets (Dialysis/systolic blood pressure; Diabetes/sleep-hours; Marital-status/high-density-lipoprotein cholesterol) were also analyzed. In three from four simulated runs (run_one, run_one_relaxed, and run_three) with Pearson types pooled, Monte-Carlo Kruskal-Wallis gave predicted sample sizes significantly slightly lower than measured but more accurate than with ANOVA methods; the latter gave high sample-size predictions. Populations (run_one_relaxed) with ANOVA assumptions invalid gave Kruskal-Wallis predictions similar to those measured. In two from three medical studies, Kruskal-Wallis predictions (Dialysis: similar predictions; Marital: higher than measured) were more accurate than ANOVA (both higher than measured) but in one (Diabetes) the reverse was found (Kruskal-Wallis: lower; Monte-Carlo ANOVA: similar to measured). These preliminary studies appear to show that Monte-Carlo Kruskal-Wallis power studies, based on Bernstein fits, might perform better than ANOVA equivalents in many settings (and provide reasonable results when ANOVA cannot be used); and both Monte-Carlo methods appeared to be considerably more accurate than the analytical version analyzed.
The management of patients undergoing stem cell transplantation requires a multipurpose central venous catheter (CVC) to facilitate drug administration, parenteral nutrition, transfusion of blood products, and collection of blood samples. Peripherally inserted central venous catheters (PICCs) appear to meet these requirements but are rarely used for stem cell infusion. We aimed to retrospectively assess the safety and feasibility of stem cell infusion through PICC and to evaluate its impact on transplantation kinetics. We retrospectively analyzed the outcomes of peripheral blood stem cell (PBSC) transplantation in patients receiving cryopreserved autologous or allogeneic PBSC by PICCs and compared the results with patients receiving transplants through a conventionally inserted central venous catheter (CICC). Despite statistically significant differences in CD34+ dose, infusion rate, and total length of administration, the clinical outcomes of transplantation, exemplified by platelet and neutrophil engraftment, along with the length of hospitalization, were not affected by the prolonged infusion time and lower infusion velocity in the PICC group. Our study showed that the clinical outcomes of PBSC transplantation did not differ between the PICC and CICC groups, suggesting that both types of catheters can be implemented in a PBSC transplantation setting.
Multiple myeloma (MM) remains an incurable hematological malignancy. Bortezomib (BTZ) is a proteasome inhibitor widely used in MM therapy whose potent activity is often hampered by the development of resistance. The immune system is vital in the pathophysiology of BTZ resistance. Vitamins D (VD) and K (VK) modulate the immune system; therefore, they are potentially beneficial in MM. The aim of the study was to evaluate the effect of BTZ therapy and VD and VK supplementation on the proliferation potential and gene expression profiles of MM cells in terms of the development of BTZ resistance. The U266 MM cell line was incubated three times with BTZ, VD and VK at different timepoints. Then, proliferation assays, RNA sequencing and bioinformatics analysis were performed. We showed BTZ resistance to be mediated by processes related to ATP metabolism and oxidative phosphorylation. The upregulation of genes from the SNORDs family suggests the involvement of epigenetic mechanisms. Supplementation with VD and VK reduced the proliferation of MM cells in both the non-BTZ-resistant and BTZ-resistant phenotypes. VD and VK, by restoring proper metabolism, may have overcome resistance to BTZ in vitro. This observation forms the basis for further clinical trials evaluating VD and VK as potential adjuvant therapies for MM patients.
Bortezomib-induced peripheral neuropathy (BiPN) occurs in approximately 40% of patients with multiple myeloma. The induction of severe neuropathy entails the dose reduction or complete elimination of bortezomib (BTZ). Interestingly, discontinuation of BTZ mostly results in a reduction or complete resolution of peripheral neuropathy (PN) symptoms. Therefore, it is likely that the BiPN mechanisms are based on temporary/reversible changes such as epigenetic alterations. In this study, we examined the effect of treating nerve cells, differentiated from the Lund human mesencephalic (dLUHMES) cell line, with several low-dose BTZ (0.15 nM) applications. We showed a significant decrease in global histone H3 acetylation as well as histone H3 lysine 9 acetylation. Moreover, analysis of the genetic microarray showed changes mainly in epigenetic processes related to chromatin rearrangement, chromatin silencing, and gene silencing. GSEA analysis revealed three interesting signaling pathways (SIRT1, B-WICH and, b-Catenin) that may play a pivotal role in PN development. We also performed an analysis of the miRNA microarray which showed the interactions of miR-6810-5p with the genes MSN, FOXM1, TSPAN9, and SLC1A5, which are directly involved in neuroprotective processes, neuronal differentiation, and signal transduction. The study confirmed the existence of BTZ-induced complex epigenetic alterations in nerve cells. However, further studies are necessary to assess the reversibility of epigenetic changes and their potential impact on the induction/resolution of PN.
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