Employee Volunteering. Essence, Forms, Examples

Corporate volunteering is a social activity undertaken by employees with the support of their employer. Engaging in various charity actions is one of the most popular forms of implementing the principle of corporate social responsibility (CSR). In Poland, this institution has been known for a short time, but its importance and development are noticeable. The introduction of volunteering among employees takes various forms, depending on financial possibilities, commitment, free time and the needs of the beneficiaries. Volunteering also brings various benefits (both internal and external) as well as many difficulties and barriers that reduce the ability to engage in social projects.This article presents the essence of employee volunteering, as well as its typology, form and scale of dissemination in Poland. As a complement to the analysis, there are examples of completed corporate volunteering programs

Comparison of effects of anti-thrombin aptamers HD1 and HD22 on aggregation of human platelets, thrombin generation, fibrin formation, and thrombus formation under flow conditions

HD1 and HD22 are two of the most-studied aptamers binding to thrombin exosite I and exosite, respectively. To complete of their pharmacological profiles, the effects of HD1 and HD22 on thrombin-, ristocetin-, and collagen-induced human platelet aggregation, on thrombin generation and fibrin formation in human plasma, as well as on thrombus formation in human whole blood under flow conditions were assessed. The dissociation constants for HD1 and HD22 complexes with thrombin in simulated plasma ionic buffer were also evaluated. HD1 was more potent than HD22 in terms of inhibiting thrombin-induced platelet aggregation in platelet-rich plasma (PRP; 0.05-3 mu M) and in washed platelets (WPs; 0.005-3 mu M): approximately 8.31% (+/- 6.99% SD) and 89.53% (+/- 11.38% SD) for HD1 (0.5 mu M) and HD22 (0.5 mu M), respectively. Neither HD1 nor HD22 (3 mu M) did influence platelets aggregation induced by collagen. Both of them inhibited ristocetin-induced aggregation in PRP. Surprisingly, HD1 and HD22 aptamers (3 mu M) potentiated ristocetin-induced platelet aggregation in WP. HD1 reduced thrombin generation in a concentration-dependent manner [ETP at 3 mu M: 1677.53 +/- 55.77 (nM +/- min) vs. control 2271.71 +/- 423.66 (nM +/- min)], inhibited fibrin formation (lag time at 3 mu M: 33.70 min +/- 8.01 min vs. control 7.91 min +/- 0.91 min) and reduced thrombus formation under flow conditions [AUC(30) at 3 mu M: 758.30 +/- 344.23 (kPa +/- min) vs. control 1553.84 +/- 118.03 (kPa +/- min)]. HD22 (3 mu M) also delayed thrombin generation but increased the thrombin peak. HD22 (3 mu M) shortened the lag time of fibrin generation (5.40 min +/- 0.26 min vs. control 7.58 min +/- 1.14 min) but did not modify thrombus formation (3, 15 mu M). K-d values for the HD1 complex with thrombin was higher (257.8 +/- 15.0 nM) than the K-d for HD22 (97.6 +/- 2.2 nM). In conclusion, HD1 but not HD22 represents a potent anti-thrombotic agent, confirming the major role of exosite I in the action of thrombin. HD22 aptamer blocking exosite II displays weaker anti-platelet and anti-coagulant activity, with surprising activating effects on thrombin and fibrin generation most likely induced by HD22-induced allosteric changes in thrombin dynamic structure.</p

Comparison of Effects of Anti-thrombin Aptamers HD1 and HD22 on Aggregation of Human Platelets, Thrombin Generation, Fibrin Formation, and Thrombus Formation Under Flow Conditions

HD1 and HD22 are two of the most-studied aptamers binding to thrombin exosite I and exosite, respectively. To complete of their pharmacological profiles, the effects of HD1 and HD22 on thrombin-, ristocetin-, and collagen-induced human platelet aggregation, on thrombin generation and fibrin formation in human plasma, as well as on thrombus formation in human whole blood under flow conditions were assessed. The dissociation constants for HD1 and HD22 complexes with thrombin in simulated plasma ionic buffer were also evaluated. HD1 was more potent than HD22 in terms of inhibiting thrombin-induced platelet aggregation in platelet-rich plasma (PRP; 0.05–3 μM) and in washed platelets (WPs; 0.005–3 μM): approximately 8.31% (±6.99% SD) and 89.53% (±11.38% SD) for HD1 (0.5 μM) and HD22 (0.5 μM), respectively. Neither HD1 nor HD22 (3 μM) did influence platelets aggregation induced by collagen. Both of them inhibited ristocetin-induced aggregation in PRP. Surprisingly, HD1 and HD22 aptamers (3 μM) potentiated ristocetin-induced platelet aggregation in WP. HD1 reduced thrombin generation in a concentration-dependent manner [ETP at 3 μM: 1677.53 ± 55.77 (nM⋅min) vs. control 2271.71 ± 423.66 (nM⋅min)], inhibited fibrin formation (lag time at 3 μM: 33.70 min ± 8.01 min vs. control 7.91 min ± 0.91 min) and reduced thrombus formation under flow conditions [AUC30 at 3 μM: 758.30 ± 344.23 (kPa⋅min) vs. control 1553.84 ± 118.03 (kPa⋅min)]. HD22 (3 μM) also delayed thrombin generation but increased the thrombin peak. HD22 (3 μM) shortened the lag time of fibrin generation (5.40 min ± 0.26 min vs. control 7.58 min ± 1.14 min) but did not modify thrombus formation (3, 15 μM). Kd values for the HD1 complex with thrombin was higher (257.8 ± 15.0 nM) than the Kd for HD22 (97.6 ± 2.2 nM). In conclusion, HD1 but not HD22 represents a potent anti-thrombotic agent, confirming the major role of exosite I in the action of thrombin. HD22 aptamer blocking exosite II displays weaker anti-platelet and anti-coagulant activity, with surprising activating effects on thrombin and fibrin generation most likely induced by HD22-induced allosteric changes in thrombin dynamic structure

phi YeO3-12 phage tail fiber Gp17 as a promising high specific tool for recognition of Yersinia enterocolitica pathogenic serotype O : 3

Yersiniosis is an infectious zoonotic disease caused by two enteropathogenic species of Gram-negative genus Yersinia: Yersinia enterocolitica and Yersinia pseudotuberculosis. Pigs and other wild and domestic animals are reservoirs for these bacteria. Infection is usually spread to humans by ingestion of contaminated food. Yersiniosis is considered a rare disease, but recent studies indicate that it is overlooked in the diagnostic process therefore the infections with this bacterium are not often identified. Reliable diagnosis of Yersiniosis by culturing is difficult due to the slow growth of the bacteria easily overgrown by other more rapidly growing microbes unless selec-tive growth media is used. Phage adhesins recognizing bacteria in a specific manner can be an excellent diagnostic tool, es-pecially in the diagnosis of pathogens difficult for culturing. In this study, it was shown that Gp17, the tail fiber protein (TFP) of phage phi YeO3-12, specifically recognizes only the pathogenic Yersinia enterocolitica serotype O:3 (YeO:3) bacteria. The ELISA test used in this work confirmed the specific interaction of this protein with YeO:3 and demonstrated a promising tool for developing the pathogen recognition method based on phage adhesins.Peer reviewe

Temporal relationship between systemic endothelial dysfunction and alterations in erythrocyte function in a murine model of chronic heart failure

Endothelial dysfunction (ED) and red blood cell distribution width (RDW) are both prognostic factors in heart failure (HF), but the relationship between them is not clear. In this study, we used a unique mouse model of chronic HF driven by cardiomyocyte-specific overexpression of activated Gαq protein (Tgαq*44 mice) to characterise the relationship between the development of peripheral ED and the occurrence of structural nanomechanical and biochemical changes in red blood cells (RBCs).Systemic ED was detected in vivo in 8-month-old Tgαq*44 mice, as evidenced by impaired acetylcholine-induced vasodilation in the aorta and increased endothelial permeability in the brachiocephalic artery. ED in the aorta was associated with impaired nitric oxide (NO) production in the aorta and diminished systemic NO bioavailability. ED in the aorta was also characterised by increased superoxide and eicosanoid production. In 4- to 6-month-old Tgαq*44 mice, RBC size and membrane composition displayed alterations that did not result in significant changes in their nanomechanical and functional properties. However, 8-month-old Tgαq*44 mice presented greatly accentuated structural and size changes and increased RBC stiffness. In 12-month-old Tgαq*44 mice, the erythropathy was featured by severely altered RBC shape and elasticity, increased RDW, impaired RBC deformability, and increased oxidative stress (GSH/GSSH ratio). Moreover, RBCs taken from 12-month-old Tgαq*44 mice, but not from 12-month-old FVB mice, co-incubated with aortic rings from FVB mice, induced impaired endothelium-dependent vasodilation and this effect was partially reversed by an arginase inhibitor (ABH, 2(S)-amino-6-boronohexanoic acid).In the Tgαq*44 murine model of HF, systemic endothelial dysfunction accelerates erythropathy and, conversely, erythropathy may contribute to endothelial dysfunction. These results suggest that erythropathy may be regarded as a marker and a mediator of systemic endothelial dysfunction in HF. In particular, targeting RBC arginase may represent a novel treatment strategy for systemic endothelial dysfunction in HF. RBC arginase and possibly other RBC-mediated mechanisms may represent novel therapeutic targets for systemic endothelial dysfunction in HF.Endothelial dysfunction (ED) and red blood cell distribution width (RDW) both have prognostic value for heart failure (HF), but it is not known whether these pathologies are related. We comprehensively characterized endothelial and RBC functional status in a unique murine model of chronic heart failure with a prolonged time course of HF progression. Our results suggest that ED accelerates erythropathy and, conversely, erythropathy may contribute to ED. Accordingly, erythropathy in HF reflects ED and involves various changes (in functional, structural, nanomechanical, and biochemical levels) that could have diagnostic and therapeutic significance for HF

Determination of physicochemical properties of anthracycline antibiotics using a potentiometric titration method and capillary electrophoresis

Doksorubicyna (DOX) i daunorubicyna (DAU) należą do grupy antybiotyków antarcyklinowych, leków o właściwościach cytostatycznych, które są szeroko stosowane w terapii przeciwnowotworowej. Ich aktywność biologiczna, wychwyt przez komórki nowotworowe, transport w organizmie i selektywność w stosunku do komórek nowotworowych są zależne od właściwości fizykochemicznych, w tym także od wykładnika stałej dysocjacji (pKa). Istnieje szereg metod stosowanych do wyznaczania pKa, między innymi metoda potencjometryczna, konduktometryczna lub spektrofotometryczna. Niestety większość z tych metod ma poważne ograniczenia, które powodują, że nie zawsze są one odpowiednie do wyznaczania pKa. Za pomocą elektoforezy kapilarnej możemy badać związki w zanieczyszczonej matrycy, słabo rozpuszczalne w wodzie oraz próbki o nieznanym stężeniu substancji czynnej. W takich wypadkach metody potencjometryczne nie mają zastosowania.Przeprowadzone badania polegały na doświadczalnym wyznaczeniu wartości pKa dla 10 antybiotyków antracyklinowych: DOX, DAU i ich enencjomerów EDOX i EDAU oraz pochodnych z dołączonym pierścieniem piperydynowym (FPIP) i morfolinowym (FMOR) za pomocą elektroforezy kapilarnej (CE) oraz metodą miareczkowania potencjometrycznego. Stosując CE dla każdego związku wyznaczono dwie wartości pKa, zgodnie z przyjętym założeniem o dwóch stanach jonizacji związku. Związki amfoteryczne w niższym pH są naładowane dodatnio i migrują szybciej niż markery obojętne, w pH=pI związek wykazuje charakter obojętny, natomiast w wysokim pH cząsteczki będą naładowane ujemnie i w związku z tym będą przemieszczały się wolniej niż marker obojętny. Stosując metodę potencjometryczną otrzymano tylko jedną wartość pKa, będącą w przybliżeniu średnią z wartości uzyskanych za pomocą CE. Wykładniki stałych dysocjacji badanych pochodnych różniły się od wykładników stałych dysocjacji leków modelowych. Otrzymane wyniki badań będą pomocne w lepszym zrozumieniu procesu dystrybucji antybiotyków antarcyklinowych do komórek nowotworowych oraz znalezieniu zależności między wartościami pKa tych leków oraz ich selektywnością w stosunku do komórek nowotworowych.Doxoribicin (DOX) and daunorubicin (DAU) belong to anthracyclines – a group of antitumor antibiotics, which are widely used in cancer therapy. Biological activity of these drugs, uptake by tumor tissue, transport rate and cancer cell selectivity are determined also by the physicochemical properties including pKa. There are some methods to determine pKa values, for example potentiometry, conductometry or spectrophotometry. However, sometimes they cannot be applied for pKa determination because they may be not enough accurate. Dissociation constants of DOX, DAU and number of their derivatives, such as enantiomers: EDOX and EDAU, and derivatives with piperidine (FPIP) or morpholine (FMOR) ring are determined using capillary zone electrophoresis (CZE) and potentiometric titrations. The advantages of CZE can be utilized in those fields where potentiometry has limitations (sample quantity, solubility, purity).In this study we experimentally determined pKa values of 10 anthracycline antibiotics. Using CZE two pKa values for each compounds were determined, according to the assumption of two ionization states of samples. Ampholytes can have a positive charge in low pH values and migrate quicker than a neutral marker, at pH=pI drug can be neutral, and negatively charged in high pH values, migrating slower than the neutral marker. The results of potentiometric measurments gave only one value of pKa, being approximately average of the two values determined using CZE. The pKa values of parent drugs differ from chose of their derivatives. The results of the present study may help to better understand intracellular distribution of anthracyclines within cancer cells and to find a relationship between drugs pKa values and their selectivity to cancer cells

Non-equilibrium capillary electrophoresis of equilibrium mixtures (NECEEM) method in quantitative characterization of aptamer-target integra

Aptamers are artificial nucleic acid (single-stranded DNA or RNA) ligands that bind to certain targets with high specificity. They have numerous advantages, including satisfactory stability, ease of chemical modification, and the ability to be synthetically created. Further, their low immunogenicity means they are often a more promising choice than antibodies. Quantification of new aptamer-target interactions is crucial for selection of appropriate sequences and further research. Capillary electrophoresis (CE) may be a suitable technique for determining the basic parameters of such biomolecular interactions. Today, several methods for studying binding parameters using the CE technique exist. In the case of aptamers, the NECEEM (non-equilibrium capillary electrophoresis of equilibrium mixtures) method is widely used. Based on fundamental parameters, such as peak area and migration time, obtained from a single electropherogram, the degree and strength of binding can be evaluated. Undoubtedly, further research into aptamers must be pursued to extend the frontiers of their bioapplications. Thus, the presented technique provides a highly efficient and versatile platform for the development and assessment of new ligands. © 2018 Nova Science Publishers, Inc

Simultaneous quantification of selected glycosaminoglycans by butanolysis-based derivatization and LC-SRM/MS analysis for assessing glycocalyx disruption in vitro and in vivo

Glycosaminoglycans (GAGs) constitute the main building blocks of the endothelial glycocalyx (GLX), and disruption of GLX initiates and promotes endothelial dysfunction. Here, we aimed to develop a novel, specific and accurate LC-SRM/MS-based method for glycosaminoglycans (GAGs) profiling. The method involved butanolysis derivatization to facilitate GAG-specific disaccharide generation and its subsequent retention in LC–reversed-phase mode followed by mass spectrometric detection performed in positive ion-selected reaction monitoring (SRM) mode. GAG contents were measured in media of endothelial cells (EA.hy926) subjected to various GAG-degrading enzymes, as well as in murine plasma and urine in apolipoprotein E/low‐density lipoprotein receptor‐deficient (ApoE/LDLR −/−) mice and age-matched wild-type C57BL/6 mice. Alternatively, GLX disruption was verified by atomic force microscopy (AFM)-based analysis of GLX thickness. The proposed assay to quantify GAG-specific disaccharides presented high sensitivity for each of the analytes (LLOQ: 0.05–0.1 μg/mL) as well as accuracy and precision (86.8–114.9% and 2.0–14.3%, respectively). In medium of EA.hy926 cells subjected to GAG-degrading enzymes various GAG-specific disaccharides indicating the degradation of keratan sulphate (KS), heparan sulphate (HS), chondroitin sulphate (CHS) or hyaluronan (HA) were detected as predicted based on the characteristics of individual enzyme activity. In turn, AFM-based assessment of GLX thickness was reduced to a similar extent by all single enzyme treatments, whereas the most prominent reduction of GLX thickness was detected following the enzyme mixture. Plasma measurements of GAGs revealed age- and hypercholesterolemia-dependent decrease in GAGs concentration. In summary, a novel LC-SRM/MS-based method for GAG profiling was proposed that may inform on GLX status in cell culture for both in vitro and in vivo conditions