Indicators of stress hematopoiesis in the blood predict COVID-19 progression in patients over 65 years old.

Objectives: Advanced age is a well-established risk factor for severe coronavirus disease 2019 (COVID-19). Exacerbated inflammation affects multiple organs, among which hematopoiesis responds by increased output of various cells. We aimed to determine the association between COVID-19 progression and large immature cell (LIC) counts, changes in erythrocyte and platelet distribution widths (RDW, PDW) with reference to patients' age.

The Multi-Faceted Nature of Renalase for Mitochondrial Dysfunction Improvement in Cardiac Disease.

The cellular mechanisms and signaling network that guide the cardiac disease pathophysiology are inextricably intertwined, which explains the current scarcity of effective therapy and to date remains the greatest challenge in state-of-the-art cardiovascular medicine. Accordingly, a novel concept has emerged in which cardiomyocytes are the centerpiece of therapeutic targeting, with dysregulated mitochondria as a critical point of intervention. Mitochondrial dysfunction pluralism seeks a multi-faceted molecule, such as renalase, to simultaneously combat the pathophysiologic heterogeneity of mitochondria-induced cardiomyocyte injury.

Renalase Challenges the Oxidative Stress and Fibroproliferative Response in COVID-19.

The hallmark of the coronavirus disease 2019 (COVID-19) pathophysiology was reported to be an inappropriate and uncontrolled immune response, evidenced by activated macrophages, and a robust surge of proinflammatory cytokines, followed by the release of reactive oxygen species, that synergistically result in acute respiratory distress syndrome, fibroproliferative lung response, and possibly even death. For these reasons, all identified risk factors and pathophysiological processes of COVID-19, which are feasible for the prevention and treatment, should be addressed in a timely manner. Accordingly, the evolving anti-inflammatory and antifibrotic therapy for severe COVID-19 and hindering post-COVID-19 fibrosis development should be comprehensively investigated.

The Scientific Rationale for the Introduction of Renalase in the Concept of Cardiac Fibrosis.

Cardiac fibrosis represents a redundant accumulation of extracellular matrix proteins, resulting from a cascade of pathophysiological events involved in an ineffective healing response, that eventually leads to heart failure. The pathophysiology of cardiac fibrosis involves various cellular effectors (neutrophils, macrophages, cardiomyocytes, fibroblasts), up-regulation of profibrotic mediators (cytokines, chemokines, and growth factors), and processes where epithelial and endothelial cells undergo mesenchymal transition. Activated fibroblasts and myofibroblasts are the central cellular effectors in cardiac fibrosis, serving as the main source of matrix proteins.

The Discriminatory Ability of Renalase and Biomarkers of Cardiac Remodeling for the Prediction of Ischemia in Chronic Heart Failure Patients With the Regard to the Ejection Fraction.

Renalase has been implicated in chronic heart failure (CHF); however, nothing is known about renalase discriminatory ability and prognostic evaluation. The aims of the study were to assess whether plasma renalase may be validated as a predictor of ischemia in CHF patients stratified to the left ventricular ejection fraction (LVEF) and to determine its discriminatory ability coupled with biomarkers representing a range of heart failure (HF) pathophysiology: brain natriuretic peptide (BNP), soluble suppressor of tumorigenicity (sST2), galectin-3, growth differentiation factor 15 (GDF-15), syndecan-1, and cystatin C. A total of 77 CHF patients were stratified according to the LVEF and were subjected to exercise stress testing.

Interaction of thrombophilic SNPs in patients with unexplained infertility-multifactor dimensionality reduction (MDR) model analysis.

Purpose: Our aim was to evaluate the frequency and SNP-SNP interactions between factor V Leiden (FVL) G1691A, prothrombin G20210A mutation, and C677T MTHFR and PAI-1 4G/5G gene polymorphisms in female IVF patients with unexplained infertility (UI) by using a multifactor dimensionality reduction (MDR) model analysis.

Methods: A total of 225 subjects were enrolled in the study. There were 105 females in UI group and 120 healthy controls.

Short-term dexamethasone plus acetylsalicylic acid treatment during in vitro fertilization procedure.

Objectives: Embryo implantation represents the major limiting step during in vitro fertilization (IVF) procedure. Immu- nological and coagulation abnormalities were shown to have a substantial part in multifactorial etiology of IVF failure. We aimed to investigate the effect of short-term low-dose dexamethasone plus acetylsalicylic acid (ASA) treatment, starting at the time of embryo transfer, on the implantation and clinical pregnancy rates in general IVF population.

Mechanisms of plasminogen activator inhibitor 1 action in stromal remodeling and related diseases.

Plasminogen activator inhibitor type 1 (PAI-1) is the main physiologic inhibitor of fibrinolysis. However, it is also involved in many physiological processes such as extracellular matrix (ECM) proteolysis and remodeling, cell adhesion, motility, and apoptosis, angiogenesis, etc. The aim of the study was to summarize current knowledge and gain insights into the mechanisms of PAI-1 action in the processes of stromal remodeling and diseases with considerable matrix pathologies (atherosclerosis, tissue fibrosis, cancer metastasis, pregnancy related complications, etc).

Distribution of MEFV gene mutations and R202Q polymorphism in the Serbian population and their influence on oxidative stress and clinical manifestations of inflammation.

Background: The Mediterranean fever (MEFV) gene codes for protein pyrin, one of the regulators of inflammasome activity in innate immune cells. Mutations in this gene are considered the primary cause of Familial Mediterranean fever, but are also found in other monogenic and multifactorial autoinflammatory diseases. The aim of the study was to determine if healthy carriers of MEFV gene mutations and R202Q polymorphism have clinical manifestations of inflammation and impaired oxidative stress parameters.

CORRELATION OF C-REACTIVE PROTEIN AND COPD SEVERITY.

Chronic obstructive pulmonary disease (COPD) is a progressive pulmonary disease characterized by systemic inflammation. The aim of this study was to correlate the parameters of systemic inflammation, C-reactive protein (CPR) and total leukocyte count, with clinical indicators of the disease. Our study included 157 COPD patients, both outpatients and those hospitalized at the Knez Selo Department of Pulmonology of the Niš Clinical Centre during a six-month period, while in the phase of disease exacerbation.

Crosstalk of Various Biomarkers That Might Provide Prompt Identification of Acute or Chronic Cardiorenal Syndromes.

Introduction: Pathophysiological interaction between the heart and kidneys represents the basis for clinical entities called cardiorenal syndromes. The purpose of the study was to assess the relations between acute and chronic cardiorenal syndromes and biomarkers [advanced oxidation protein products, brain natriuretic peptide, malondialdehyde, xanthine oxidoreductase (XOD), xanthine oxidase, xanthine dehydrogenase, interleukin 8, cystatin C, plasminogen activator inhibitor-1, high-sensitive troponin T, C-reactive protein and glomerular filtration rate, measured by the Modification of Diet in Renal Disease (MDRD) formula], to hypothesize biomarkers that might provide a prompt identification of acute or chronic cardiorenal syndromes, and to distinguish acute versus chronic types of these syndromes.

Methods: A total of 114 participants were enrolled in this study, i.

Impact of Ki-67 and E-cadherin expression on lymphovascular invasion in upper urinary tract urothelial carcinoma.

Unlabelled: BACGROUND/AIM: Upper urinary tract urothelial carcinoma (UUT-UC) constitutes 5% of malignant neoplasms arising from transitional epithelium, but is more invasive than bladder cancer. Lzmphovascular invasion (LVI) is associated with biologically aggressive carcinoma and with occult metastases. The aim of this study was to investigate the correlation between LVI and immunohistochemical expression of two frequently routinely applied immunohistochemical biomarkers, Ki-67 and E-cadherin, in UUT-UC.

MDR1 gene polymorphisms and P-glycoprotein expression in respiratory diseases.

Background: P-glycoprotein (P-gp/MDR1), a member of the ATP-binding cassette (ABC) transporters super family, encoded by the ABCB1/MDR1 gene, is one of suggested respiratory tract protection components, found in various tissues with a barrier function, such as tracheobronchial epithelium and lung parenchyma. As an ATP-dependent pump, P-gp extrudes lipophilic particles out of cells and acts as a gatekeeper against numerous xenobiotics, with a protective role in mediating DNA damage, secretion of toxic compounds, apoptosis and the immune response. Therefore, a presence of MDR1 polymorphisms and altered P-gp expression may be important for pathogenesis of reduced lung inflammatory response on cigarette smoke exposure, as well as for the severity of chronic obstructive pulmonary disease and lung cancer pathogenesis and treatment efficacy.

Association of serum bilirubin and uric acid levels changes during neuroinflammation in patients with initial and relapsed demyelination attacks.

In order to examine the endogenous antioxidants values in the earliest phase of demyelination, we have determined bilirubin and uric acid (UA) serum values in the patients with clinically isolated syndrome (CIS) and relapsing remitting multiple sclerosis (RRMS), regarding their clinical disability, measured by Extended Disability Status Scale (EDSS), Magnetic Resonance Imaging (MRI), disease duration, gender and other parameters. The bilirubin and UA levels were lower in CIS and RRMS patients than in control group, whether male or female (p < 0.05).

Suppression of the lipid peroxidation process in the CNS reduces neurological expression of experimentally induced autoimmune encephalomyelitis.

Objective: Here we report the influence of malondialdehyde (MDA) as a measure of the lipid peroxidation process (LP), on multiple sclerosis (MS) pathogenesis and its neurological signs, during the treatment with aminoguanidine (AG) - a selective inducible nitric oxide synthase inhibitor and N-Acetyl cysteine (NAC) - an oxidative scavenger, in the experimental autoimmune encephalomyelitis (EAE), an animal model for studying MS.

Material And Methods: Encephalomyelitis induction by the subcutaneous injection of myelin basic protein of bovine type, dissolved in phosphate buffered saline (PBS) emulsified in equal volume of the complete Freund's adjuvant (CFA), was described in detail in our earlier published papers. Each of animals was randomly assigned to seven groups - control (PBS), EAE, CFA, EAE + AG, AG, EAE + NAC and NAC group.

Correlation of nitric oxide levels in the cerebellum and spinal cord of experimental autoimmune encephalomyelitis rats with clinical symptoms.

Experimental autoimmune encephalomyelitis (EAE) is a well-established cell-mediated autoimmune inflammatory disease of the CNS, which has been used as a model of the human demyelinating disease. EAE is characterized by infiltration of the CNS by lymphocytes and mononuclear cells, microglial and astrocytic hypertrophy, and demyelination which cumulatively contribute to clinical expression of the disease. EAE was induced in female Sprague-Dawley rats, 3 months old (300 g ± 20 g), by immunization with myelin basic protein (MBP) in combination with Complete Freund's adjuvant (CFA).

Frequency of the C1236T, G2677T/A and C3435T MDR1 gene polymorphisms in the Serbian population.

The multi-drug resistance 1 (MDR1) gene encodes for a P-glycoprotein (PGP), which acts as a gate-keeper against various kinds of xenobiotics. Several single nucleotide polymorphisms (SNPs) in the MDR1 gene that may influence PGP level and function have been identified. The aim of this study was to simultaneously analyze the three most important MDR1 SNPs, C3435T, G2677T/A and C1236T, in the Serbian population and to compare the results with those published for other ethnic groups.

PC-1 (ENPP1) K121Q polymorphism in overweight and obese type 2 diabetic coronary heart disease patients.

Aim: The aim of the present study was to investigate the prevalence of the PC-1 121Q allele and to test its association to cardiovascular risk factors in type 2 diabetes mellitus (DM) patients.

Methods: A total of 103 unrelated Caucasians from Serbia, including 71 DM patients without CHD (aged 59.4 +/- 8.

The association of PC-1 (ENPP1) K121Q polymorphism with metabolic syndrome in patients with coronary heart disease.

Background: Metabolic syndrome (MS) is a clinical feature, closely associated with insulin resistance, one of the prime underlying causes of overall cardiovascular morbidity, including coronary heart disease (CHD). Considering the association between PC-1 121Q genotype and insulin resistance phenotype, the aim of the present study was to investigate the contribution of PC-1 K121Q polymorphism to the development of MS and its concomitant disorders in CHD patients.

Methods: A total of 130 Caucasians from Serbia, including 80 CHD patients (aged 59.