Professional identity of future financiers as the basis of professional culture

Розкрито суть професійної ідентичності як складного, багатофункціонального явища, яке тісно пов’язано з професійним самовизначенням і формується в процесі професійної підготовки майбутніх фінансистів. З'ясовано, що за своєю суттю професійна ідентичність має тісний взаємозв’язок із загальною культурою, системою цінностей, професіоналізмом і компетентностями фахівця, пов’язана зі змінами в структурі особистості. Автор вважає, що цілком ймовірно розглядати її як основу формування професійної культури майбутніх молодших фахівців з фінансів і кредиту.The essence of professional identity as a complex, multifunctional phenomenon, which is closely connected with professional self-determination and is formed in the process of professional training of future financiers, is disclosed. It has been found out that, in essence, professional identity has a close relationship with the general culture, system of values, professionalism and competence of a specialist associated with changes in the structure of the individual. The author believes that it is quite possible to consider it as the basis for the formation of a professional culture of future junior specialists in finance and credit

Different pharmacological responses of atrium and ventricle: Studies with human cardiac tissue

It has been recently reported that 5-hydroxytryptamine (5-HT) increases force of contraction in atrial tissue but not in ventricular tissue. In the present study with trabeculae obtained from non-diseased human hearts, we investigated whether this difference in the contractile response is specific for 5-HT or is also observed for other substances: calcitonin gene-related peptide (CGRP), angiotensin II, adenosine, somatostatin and acetyllcholine. CGRP (10−9 to 10−7 M) and angiotensin II (10−9 to 10−5 M) caused concentration-dependent increases in force of contraction in atrial trabeculae (up to36 ± 8%and42 ± 8% of the response to 10−5 M noradrenaline, respectively). Similar to 5-HT, no effects were observed with CGRP and angiotensin II in ventricular trabeculae. Adenosine (10−8 to 10−5 M) and somatostatin (10−8 to 10−6 M) caused concentration-dependent negative inotropic effects on baseline atrial contractility (−54 ± 17%and−51 ± 25%, respectively, but no response was found on baseline ventricular contractility. Adenosine, but not somatostatin, reduced force of contraction after pre-stimulation with 10−5 M noradrenaline in atrial tissue and, to a lesser extent, in ventricular tissue. Acethlcholine exhibited a biphasic concentration-response curve in the atrial tissue, consisting of an initial negative inotropic response (10−9 to 10−7 M, from 120 ± 41mg at baseline to48 ± 16mg at 10 −7 M, fol lowed by a positive inotropic response (10−6 to 10−3 M, from 48 ± 16 mg at 10−7 M to77 ± 55mg). On the baseline ventricular for foce of contraction, acetylcholine (10−9 to 10−4 M) induced only a positive inotropic effect, starting at 10−9 M (from 252 ± 65mg at baseline to353 ± 71mg at 10−4M). After pre-stimulation with 10−5 M noradrenaline, acethylcholine reduced force of contraction in both tissue at 10−3 M(atrium: −14 ± 4%,ventricle: −61 ± 5%). The data indicate that, in atrial tissue, force of contraction can be affected by either postive or negative inotropic agents. However, in ventricular tissue only positive inotropic effects could be detected. Since atrial and ventricular tissues display different responses to the above biogenic substances, a different mechnism of regulation of contractility seems feasible

Characterization of the positive and negative inotropic effects of acetylcholine in the human myocardium

In the human isolated myocardium, acetylcholine (10−9 to 10−3 M) elicited a biphasic inotropic effect (a decrease in the lower and an increase in the higher concentration range) in atrial and a positive inotropic effect in ventricular trabeculae. However, under conditions of raised contractility achieved by exposure to noradrenaline (10−5 M), only negative inotropic effects were observed in both atria and ventricles. Atropine (10−6 M), but not propranolol (10−6 M), antagonized both positive and negative inotropic effects of acetylcholine, thus showing that the responses were mediated by muscarinic acetylcholine receptors. The use of subtype selective muscarinic receptor antagonists (10−7 to 10−5 M), pirenzepine (M1 > M3 > M2), AF-DX 116 (11-({2-[(diethylamino)-methyl]-1-piperidyl}acetyl)-5,11-dihydro-6H-pyridol[2,3-b][1,4]benzodiazepine-6-one base; M2 > M1 > M and HHSiD (p-fluorohexahydro-siladifenidol hydrochloride; M3 ≥ M1 ⪢ M2) revealed that the negative inotropic effect of acetylcholine in atrial as well as the positive inotropic effect in ventricular trabeculae were best antagonized by AF-DX 116 and not by pirenzepine, suggesting the involvement of the muscarinic M2 receptor subtype, possibly linked to different second messenger systems. On the other hand, the positive inotropic effect of acetylcholine (10−6 to 10−3 M) in the atrial tissue, observed only in preparation with depressed contractility, was not effectively antagonized by either AF-DX 116 or HHSiD, but was significantly reduced by pirenzepine. Furthermore, the selective muscarinic M1 receptor agonist McN-A-343 (4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethyl ammonium chloride; 10−9 to 10−3 M), which failed to significantly change the baseline contractility in either atrial or ventricular trabeculae, produced a positive inotropic effect in atrial preparations when contractility had been depressed by prior treatment with acetylcholine (10−9 to 10−7 M). This effect of McN-A-343 was effectively antagonized by pirenzepine (10−5 M). These data show that, besides the muscarinic M2 receptor mediating both negative (atria) and positive (ventricle) inotropic effects, muscarinic M1 receptors, capable of reversing depressed atrial contractility, are present in the human heart

The efficacy of anti-inflammatory medication in postoperative cognitive decline: A meta-analysis

Objective: Post-operative cognitive decline is a surgical complication involving chronic impairments in different cognitive domains. Although the exact mechanisms behind postoperative cognitive decline are still unknown, there is increasing evidence for a key role of neuroinflammation. This meta-analysis aims to investigate the efficacy of anti-inflammatory treatment on postoperative cognitive decline. Participants and Methods: An electronic search was performed using PubMed, Psychinfo, EmBase, Cochrane Database of Systematic Reviews and clinicaltrial.gov (until November 2019). No year or language restrictions were applied. Only randomized, double-blind, placebocontrolled studies that investigated clinical outcome in adult patients who underwent surgery under general anaesthesia (except brain surgery) were included. The search yielded 574 papers, of which nineteen fulfilled the inclusion criteria. Results: The current meta-analysis found a significant effect of different anti-inflammatory agents on the incidence of POCD (OR=0.67, p=0.010). Administration of COX-2 inhibitors (OR=0.31, p<0.0001), ketamine (OR=0.44, p=0.38) and lidocaine (OR=0.79, p=0.33) showed better results than placebo in a meta-analysis of at least two studies. Erythromycin (OR=0.14, p=0.006), erythropoietin (OR=0.15, p=0.07) and dexmedetomidine (OR=0.58, p=0.03) were significant in single studies. No beneficial effects on cognition were found for magnesium, 17βestradiol, dexamethasone and melatonin. Conclusion: The results of this meta-analysis provide evidence for a potential efficacy of anti-inflammatory agents on POCD, but further research is necessary to determine which agents are most appropriate for clinical application