In search of dermatophytes – frequency and etiology of fungal infections in patients with and without diabetes mellitus

Introduction: Onychomycosis is a frequent nail disorder, accounting for up to 50% of all nail problems. Treatment of onychomycosis is expensive and requires a long time of antifungal medications. Consequently, a proper and faster diagnosis is necessary. Especially for those patients with diabetes mellitus, where onychomycosis is among the most significant predictors of foot ulcer and possible severe complications.Aim: To compare the sensitivity, specificity, and turnaround time between direct microscopy, culture, histology, and real-time PCR. In addition, to compare the frequency and etiology of onychomycosis in patients with and without DM.Materials and methods: This study included 102 patients, divided into two groups. One group consisted of patients with diabetes mellitus and the other – without diabetes. Nail samples were collected and examined by direct KOH microscopic examination, culture, histology, and real-time PCR.Results: From the 102 patients with clinical onychomycosis, positive KOH was found in 38 (37.3%). Culture – 82 out of 102 samples (80.4%) were positive for dermatophytes, yeasts, and/or NDM. Positive histology samples were 32 (41.6%). The PCR was positive in 57 (55.9%) out of the 102. We discovered that there is no significant statistical difference in the etiology of the fungal infections between the two groups.Conclusions: All mycological investigations have their place in the diagnosis of onychomycosis. Direct microscopy, culture, and histology are useful methods for clinicians to diagnose and follow up the post-treatment period. The advantages of RT-PCR include obtaining results faster and accurately identifying fungi, thus becoming more valued in the diagnosis of OM

YKL-40 and neuron-specific enolase in neurodegeneration and neuroinflammation

Abstract Neurodegenerative diseases comprise a large number of disorders with high impact on human health. Neurodegenerative processes are caused by various etiological factors and differ in their clinical presentation. Neuroinflammation is widely discussed as both a cause and a consequence in the manifestation of these disorders. The interplay between the two entities is considered as a major contributor to the ongoing disease progression. An attentive search and implementation of new and reliable markers specific for the processes of inflammation and degeneration is still needed. YKL-40 is a secreted glycoprotein produced by activated glial cells during neuroinflammation. Neuron-specific enolase (NSE), expressed mainly by neuronal cells, is a long-standing marker for neuronal damage. The aim of this review is to summarize, clarify, and evaluate the potential significance and relationship between YKL-40 and NSE as biomarkers in the monitoring and prognosis of a set of neurological diseases, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and multiple sclerosis. YKL-40 appears to be a more reliable biomarker in neurological diseases than NSE. The more prominent expression pattern of YKL-40 could be explained with the more obvious involvement of glial cells in pathological processes accompanying each neurodegenerative disease, whereas reduced NSE levels are likely related to low metabolic activity and increased death of neurons.</jats:p

The lncRNAs/miR-30e/CHI3L1 Axis Is Dysregulated in Systemic Sclerosis

Systemic sclerosis (SSc) is an autoimmune disease with completely undefined etiology and treatment difficulties. The expression of both protein coding and non-coding RNAs is dysregulated during disease development. We aimed to examine a possible regulatory axis implemented in the control of chitinase-3 like protein 1 (CHI3L1) or YKL-40, an inflammation-associated glycoprotein, shown to be elevated in SSc. A panel of seven miRNAs and three lncRNAs potentially involved in the control of CHI3L1 were selected on the basis of in silico analysis. TagMan assay was used to evaluate the expression levels of miRNAs and RT-qPCR for lncRNAs in white blood cells (WBCs) and plasma from SSc patients and healthy controls. Among the eight screened miRNAs, miR-30e-5p (p = 0.04) and miR-30a-5p (p = 0.01) were significantly downregulated in WBCs and plasma of SSc patients, respectively. On the contrary, the expression of the metastasis associated lung adenocarcinoma transcript 1 (MALAT1) (p = 0.044) and the Nuclear enriched abundant transcript 1 (NEAT1) (p = 0.008) in WBCs was upregulated compared to the controls. Increased levels of MALAT1 and NEAT1 could be associated with the downregulation of miR-30e-5p and miR-30a-5p expression in WBCs and plasma. We present novel data on the involvement of a possible regulatory axis lncRNAs/miR-30e/CHI3L1 in SSc and hypothesize that MALAT1 and NEAT1 could act as miR-30e-5p and miR-30a-5p decoys. This may be a reason for the increased serum levels of CHI3L1 in SSc patients.</jats:p

The lncRNAs/miR-30e/CHI3L1 Axis Is Dysregulated in Systemic Sclerosis

Systemic sclerosis (SSc) is an autoimmune disease with completely undefined etiology and treatment difficulties. The expression of both protein coding and non-coding RNAs is dysregulated during disease development. We aimed to examine a possible regulatory axis implemented in the control of chitinase-3 like protein 1 (CHI3L1) or YKL-40, an inflammation-associated glycoprotein, shown to be elevated in SSc. A panel of seven miRNAs and three lncRNAs potentially involved in the control of CHI3L1 were selected on the basis of in silico analysis. TagMan assay was used to evaluate the expression levels of miRNAs and RT-qPCR for lncRNAs in white blood cells (WBCs) and plasma from SSc patients and healthy controls. Among the eight screened miRNAs, miR-30e-5p (p = 0.04) and miR-30a-5p (p = 0.01) were significantly downregulated in WBCs and plasma of SSc patients, respectively. On the contrary, the expression of the metastasis associated lung adenocarcinoma transcript 1 (MALAT1) (p = 0.044) and the Nuclear enriched abundant transcript 1 (NEAT1) (p = 0.008) in WBCs was upregulated compared to the controls. Increased levels of MALAT1 and NEAT1 could be associated with the downregulation of miR-30e-5p and miR-30a-5p expression in WBCs and plasma. We present novel data on the involvement of a possible regulatory axis lncRNAs/miR-30e/CHI3L1 in SSc and hypothesize that MALAT1 and NEAT1 could act as miR-30e-5p and miR-30a-5p decoys. This may be a reason for the increased serum levels of CHI3L1 in SSc patients

YKL-40 and Lysosome-Associated Membrane Proteins as Potential Discriminative Biomarkers in Central Nervous System Infections

The aim of our study was to evaluate the discriminative value of gene and protein expression levels of the inflammatory marker (YKL-40) and lysosome-associated membrane protein 1 and 2 (LAMP-1 and LAMP-2) in patients with central nervous system (CNS) infections. Thirty hospitalized patients with CNS infections and undefined etiology, and 22 healthy subjects as a control group, were included in the study. Gene expression levels of YKL-40, LAMP-1 and LAMP-2 were determined by qPCR. Plasma and CSF concentrations of the tree proteins of interest were detected by ELISA. Our results showed that mRNA levels of YKL-40 were significantly downregulated in WBCs of patients compared to controls, while plasma YKL-40 concentrations were higher. LAMP-1 significantly increased in patients&rsquo; plasma and CSF was found. Patients were subdivided depending on the confirmed or presumed etiological agent into two subgroups groups&mdash;patients with bacterial or with viral neuroinfection. Differences between plasma levels of YKL-40 in the subgroups when matched with controls were detected. The concentrations of the glycoprotein were higher in patients with bacterial infections compared to those with the viral ones. We revealed that LAMP-1 plasma levels were also significantly increased in patients with viral infections in comparison to healthy individuals. We could speculate that YKL-40 plasma levels might serve as a fast discriminative tool to support the presence of viral or bacterial CNS infections

The Serum ACE2, CTSL, AngII, and TNF&alpha; Levels after COVID-19 and mRNA Vaccines: The Molecular Basis

Background: The SARS-CoV-2 virus as well as the COVID-19 mRNA vaccines cause an increased production of proinflammatory cytokines. Aim: We investigated the relationship between ACE2, CTSL, AngII, TNF&alpha; and the serum levels of IL-6, IL-10, IL-33, IL-28A, CD40L, total IgM, IgG, IgA and absolute count of T- and B-lymphocytes in COVID-19 patients, vaccinees and healthy individuals. Methods: We measured the serum levels ACE2, AngII, CTSL, TNF&alpha; and humoral biomarkers (CD40L, IL-28A, IL-10, IL-33) by the ELISA method. Immunophenotyping of lymphocyte subpopulations was performed by flow cytometry. Total serum immunoglobulins were analyzed by the turbidimetry method. Results: The results established an increase in the total serum levels for ACE2, CTSL, AngII and TNF&alpha; by severely ill patients and vaccinated persons. The correlation analysis described a positive relationship between ACE2 and proinflammatory cytokines IL-33 (r = 0.539) and CD40L (r = 0.520), a positive relationship between AngII and CD40L (r = 0.504), as well as between AngII and IL-33 (r = 0.416), and a positive relationship between CTSL, total IgA (r = 0.437) and IL-28A (r = 0.592). Correlation analysis confirmed only two of the positive relationships between TNF&alpha; and IL-28A (r = 0.491) and CD40L (r = 0.458). Conclusions: In summary, the findings presented in this study unveil a complex web of interactions within the immune system in response to SARS-CoV-2 infection and vaccination