Occupational health and psychological wellbeing in first line nurses during health crisis periods: reliability study of the SOIC tool.

Background: In 2020, the emergence of the new Coronavirus has put health professionals under enormous pressure, as they had to work in difficult and often disadvantaged situations. Prevention of symptoms such as stress, anxiety and burnout therefore become important health management goals. Aim: The aim of this pilot cross-sectional study was to assess the reliability and feasibility of a tool on Occupational Health Nurses after a Pandemic Period such as the COVID-19 pandemic (Salute Oc-cupazionale negli Infermieri in Periodo Pandemico Covid19 - SOIC) that aims to assess the occupational health and psychological wellbeing of nurses during periods of health crisis. Methods: This study was conducted from September to November 2022. The SOIC tool is composed by two preliminary sections and a third part including five validated questionnaires (measuring burnout, work engagement, psychological symptoms, resilience, and mindful awareness). An opportunistic sample of 202 nurses working in a Teaching Hospital of Rome and members of NurSind union were invited to participate: of these, 24 nurses completed the SOIC in two subsequent occasions (T1 and T2). Results: The test-retest assessment showed no differences between the two waves (T1 and T2) in terms of median scores for all questionnaires included in the SOIC tool. The Cronbach alphas, considering all items of each questionnaire included in the SOIC tool, showed good or excellent internal consistencies. Conclusion: The test-retest assessments and the reliability analyses encouraged the usability of the SOIC tool. Furthermore, consistent associations between the five questionnaires were obtained.

Primary Aldosteronism and Drug Resistant Hypertension: A "Chicken-Egg" Story.

Drug-resistant arterial hypertension (RH) is a major risk factor for cardiovascular disease, often due to overlooked underlying causes. Identification of such causes poses significant clinical challenges. In this setting, primary aldosteronism (PA) is a frequent cause of RH and its prevalence in RH patients is likely higher than 20%.The pathophysiological link between PA and the development and maintenance of RH involves target organ damage and the cellular and extracellular effects of aldosterone excess that promote pro-inflammatory and pro-fibrotic changes in the kidney and vasculature.The feasibility of adrenal vein sampling in PA patients with RH, and the clinical benefit achieved by adrenalectomy, further emphasize the need to implement systematic screening for this common form of secondary hypertension in the management of a high-risk population as RH patients.: We herein review the current knowledge of the factors that contribute to the RH phenotype with a focus on PA and discuss the issues regarding the screening for PA in this setting and the therapeutic approaches (surgical and medical) aimed at resolving RH caused by PA.

Impact of nursing students on the quality of care perceived by patients: a systematic review of the literature.

OBJECTIVE: The quality assessment process, based on customer satisfaction, is fundamental in the delivery of the best care services. This is most evident in care settings where trainee students are allowed to assist the patients. The purpose of this review is to clarify whether nursing students have an impact on patients' assessment of the quality of their nursing care. MATERIALS AND METHODS: A systematic literature search was carried out using the PRISMA (Preferred Reporting Items for Systematic reviews and Meta-Analyses) guidelines in six databases: PubMed, CINAHL, Cochrane, Web of Science, Scopus, and PsycInfo. Two co-authors independently screened titles, abstracts, and full-text articles, following explicit exclusion and inclusion criteria. Analyses included non-randomized and non-homogeneous samples, involving both selected patients and methods for assessing their satisfaction. RESULTS: After full-text screening, 30 articles were identified, but only 11 were considered pertinent to the topic of the review. The trainee-patient relationship is based on mutual help and can improve the patient experience and trainee learning. The instruments used to measure perceived quality were found to be valid and reliable. CONCLUSIONS: The studies under review show high levels of satisfaction among patients when nursing care is delivered through training, particularly when the patients who agree to be treated by nursing trainees have previous experience of hospitalization and relationships with trainees. Educational background and the empathy and communication skills of both professional nurses and trainees influence patients' perception of the quality of care and their satisfaction with it.

NAMI-A inhibits the PMA-induced ODC gene expression in ECV304 cells: involvement of PKC/Raf/Mek/ERK signalling pathway.

Imidazolium trans-imidazole dimethyl sulfoxide tetrachlororuthenate (NAMI-A) is a new compound active against lung metastasis of solid metastasizing tumours. While its in vivo effect has been studied, the molecular insights that underlie its action are largely unknown. Among the possible pathways responsible for malignant transformation, PKC arose as one of the most promising targets for new antineoplastic drugs. We demonstrated the capability of NAMI-A of inhibiting PMA induced-PKC activity in ECV304 in a dose-dependent fashion. Furthermore, NAMI-A through modulation of PKC activity has been proved capable of reducing the phorbol ester induced expression of ornithine decarboxilase (ODC) gene and to abrogate the activation of the Raf/MEK/ERK pathway. Taken together these results suggest that many of the in vivo outcomes of NAMI-A treatment may be the result of a direct action on PKC.

[Ni(R2pipdt)2](BF4)2 (R2pipdt = 1,4-disubstituted-piperazine-3,2-dithione) as useful precursors of mixed-ligand dithiolenes of interest for non-linear optics.

A simple method to obtain in high yields mixed-ligand nickel-dithiolene complexes, which show strong negative solvatochromism and negative first molecular hyperpolarizability, and the use of Raman spectroscopy to establish the extent of electronic delocalisation in these complexes, are reported.

Elf-pulsed magnetic fields modulate opioid peptide gene expression in myocardial cells.

OBJECTIVES: Magnetic fields have been shown to affect cell proliferation and growth factor expression in cultured cells. Although the activation of endorphin systems is a recurring motif among the biological events elicited by magnetic fields, compelling evidence indicating that magnetic fields may modulate opioid gene expression is still lacking. We therefore investigated whether extremely low frequency (ELF) pulsed magnetic fields (PMF) may affect opioid peptide gene expression and the signaling pathways controlling opioid peptide gene transcription in the adult ventricular myocyte, a cell type behaving both as a target and as a source for opioid peptides. METHODS: Prodynorphin gene expression was investigated in adult rat myocytes exposed to PMF by the aid of RNase protection and nuclear run-off transcription assays. In PMF-exposed nuclei, nuclear protein kinase C (PKC) activity was followed by measuring the phosphorylation rate of the acrylodan-labeled MARCKS peptide. The effect of PMF on the subcellular distribution of different PKC isozymes was assessed by immunoblotting. A radioimmunoassay procedure coupled to reversed-phase high performance liquid chromatography was used to monitor the expression of dynorphin B. RESULTS: Here, we show that PMF enhanced myocardial opioid gene expression and that a direct exposure of isolated myocyte nuclei to PMF markedly enhanced prodynorphin gene transcription, as in the intact cell. The PMF action was mediated by nuclear PKC activation but occurred independently from changes in PKC isozyme expression and enzyme translocation. PMF also led to a marked increase in the synthesis and secretion of dynorphin B. CONCLUSIONS: The present findings demonstrate that an opioid gene is activated by myocyte exposure to PMF and that the cell nucleus and nuclear embedded PKC are a crucial target for the PMF action. Due to the wide ranging importance of opioid peptides in myocardial cell homeostasis, the current data may suggest consideration for potential biological effects of PMF in the cardiovascular system.

Heparin down-regulates the phorbol ester-induced protein kinase C gene expression in human endothelial cells: enzyme-mediated autoregulation of protein kinase C-alpha and -delta genes.

Overexpression of protein kinase C-alpha and protein kinase C-delta has been shown to modulate a number of biological effects, including the cell growth and differentiation. We hypothesized that heparin, a potent antimitogenic drug, could affect the cell proliferation by inhibiting the expression of specific protein kinase C genes. Heparin, markedly but not completely, inhibited the serum-stimulated protein kinase C-alpha and -delta mRNA expression. Protein kinase C inhibition or down-regulation significantly decreased the serum-induced protein kinase C isoenzyme gene expression. Heparin failed to inhibit the residual effect of serum that was resistant to the above-mentioned treatments. Phorbol 12-myristate 13-acetate elicited an increase of protein kinase C isoenzyme gene expression that was completely prevented by protein kinase C inhibition or down-regulation. Heparin dose-dependently counteracted and ultimately abolished the increase in the protein kinase C isoenzyme gene expression elicited by phorbol 12-myristate 13-acetate. These results suggest that the inhibition of an autoregulatory role wielded by protein kinase C on the protein kinase C-alpha and -delta gene expression might represent a possible mechanism by which glycosaminoglycans modulate the cell growth.

Nuclear opioid receptors activate opioid peptide gene transcription in isolated myocardial nuclei.

Opioid-binding sites were identified in highly purified nuclei isolated from hamster ventricular myocardial cells. A significant increase in the maximal binding capacity for a kappa opioid receptor ligand was observed in myocardial nuclei from BIO 14.6 cardiomyopathic hamsters, as compared with nuclei obtained from normal myocytes of the F1B strain. The exposure of isolated nuclei to dynorphin B, a natural agonist of kappa opioid receptors, markedly increased opioid peptide gene transcription. The transcriptional effect was mediated by nuclear protein kinase C activation and occurred at a higher rate in nuclei from cardiomyopathic myocytes than in nuclei isolated from normal cells. Thus, a nuclear endorphinergic system may play an intracrine role in the regulation of gene transcription under both normal and pathological conditions.

Heparin inhibits phorbol ester-induced ornithine decarboxylase gene expression in endothelial cells.

Glycosaminoglycans regulate angiogenesis by affecting the availability of different growth factors for the endothelial cell (EC). However, little is known about the molecular and functional consequences resulting from direct interaction of these polyelectrolytes with the EC. Here we show that heparin markedly inhibited serum-stimulated DNA synthesis and ornithine decarboxylase (ODC) mRNA expression in human endothelial cells (HEC). About 50% of the serum effect on DNA synthesis and ODC gene expression was prevented by the selective protein kinase C (PKC) inhibitor chelerythrine or by PKC down-regulation. Heparin was ineffective in counteracting that part of the effect of serum that was resistant to PKC inhibition or down-regulation. In serum-free cultured HEC, heparin completely abolished the increase in DNA synthesis and ODC mRNA expression elicited by a number of PKC activators. Cell exposure to difluoromethylornithine, an irreversible inhibitor of ODC enzyme, dramatically antagonised both serum- and phorbol 12-myristate 13-acetate (PMA)-stimulated DNA synthesis. These results suggest that inhibition of PKC-mediated ODC gene expression by glycosaminoglycans may represent an important mechanism in the regulation of HEC proliferation.

Opioid Peptide gene expression in the myocardial cell.

Both κ and δ opioid receptors have been identified in the myocardial cell. These receptors are coupled to phosphoinositide turnover and protein kinase C (PKC) activation, and their stimulation affects the cytosolic Ca(2+) and pH homeostasis as well as the contractility and the myofilament responsiveness to Ca(2+). Both the proenkephalin and the prodynorphin gene are expressed in cardiac myocytes. These cells are also able to synthetize and secrete dynorphin B, a biologically active end product of the prodynorphin gene binding selectively the κ opioid receptor. Prodynorphin mRNA and dynorphin B expression are markedly increased in ventricular myocytes isolated from Syrian cardiomyopathic hamsters (the hypertrophic BIO 14.6 strain), as compared with normal cells. Nuclear PKC activation and intracellular Ca(2+) overload have been shown to act as the two major signaling mechanisms involved in the increase in prodynorphin gene transcription observed in cardiomyopathic myocytes. In these cells, secreted dynorphin B activates κ opioid receptors at the cell surface and elicits an autocrine loop, leading to an increase in nuclear PKC activity and to a tonic feed-forward stimulation of prodynorphin gene transcription. The possibility that opioid genes may act in an autocrine fashion to affect myocardial Ca(2+) homeostasis, growth, and differentiation is also discussed.

Opioid peptide gene expression in the primary hereditary cardiomyopathy of the Syrian hamster. I. Regulation of prodynorphin gene expression by nuclear protein kinase C.

Prodynorphin gene expression was investigated in adult ventricular myocytes isolated from normal (F1B) or cardiomyopathic (BIO 14.6) hamsters. Prodynorphin mRNA levels were higher in cardiomyopathic than in control myocytes and were stimulated by treatment of control cells with the protein kinase C (PKC) activator 1, 2-dioctanoyl-sn-glycerol. Both chelerythrine and calphostin C, two PKC inhibitors, abolished the stimulatory effect of the diglyceride and significantly reduced prodynorphin gene expression in cardiomyopathic myocytes. Nuclear run-off experiments indicated that the prodynorphin gene was regulated at the transcriptional level and that treatment of nuclei isolated from control cells with 1, 2-dioctanoyl-sn-glycerol increased prodynorphin gene transcription, whereas chelerythrine or calphostin C abolished this transcriptional effect. Direct exposure of nuclei isolated from cardiomyopathic myocytes to these inhibitors markedly down-regulated the rate of gene transcription. The expression of PKC-alpha, -delta, and -epsilon, as well as PKC activity, were increased in nuclei of cardiomyopathic myocytes compared with nuclei from control cells. The levels of both intracellular and secreted dynorphin B, a biologically active product of the gene, were higher in cardiomyopathic than in control cells and were stimulated or inhibited by cell treatment with 1,2-dioctanoyl-sn-glycerol or PKC inhibitors, respectively.

Opioid peptide gene expression in the primary hereditary cardiomyopathy of the Syrian hamster. II. Role of intracellular calcium loading.

We have previously shown that prodynorphin gene expression was markedly increased in adult myocytes of BIO 14.6 cardiomyopathic hamsters and that nuclear protein kinase C (PKC) may be involved in the induction of this opioid gene. Here we report that the cytosolic Ca2+ concentration was significantly increased in resting and in KCl-depolarized cardiomyopathic myocytes compared with normal cells. In normal and in cardiomyopathic cells, KCl significantly increased prodynorphin mRNA levels and prodynorphin gene transcription. These effects were abolished by the Ca2+ channel blocker verapamil. In control myocytes, the KCl-induced increase in prodynorphin mRNA expression was in part attenuated by chelerythrine or calphostin C, two selective PKC inhibitors. In these cells, KCl induced the translocation of PKC-alpha into the nucleus, increasing nuclear PKC activity. In resting cardiomyopathic myocytes, the increase in prodynorphin mRNA levels and gene transcription were significantly attenuated by the intracellular Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetraacetoxy-methylester being completely abolished when the chelating agent was administered in the presence of PKC inhibitors. KCl and the PKC activator 1,2-dioctanoyl-sn-glycerol additively stimulated prodynorphin gene expression both in normal and in cardiomyopathic cells. Therefore, we conclude that PKC activation and intracellular Ca2+ overload may represent the two major signaling mechanisms involved in the induction of the prodynorphin gene in cardiomyopathic cells.

Opioid peptide gene expression in the primary hereditary cardiomyopathy of the Syrian hamster. III. Autocrine stimulation of prodynorphin gene expression by dynorphin B.

Prodynorphin mRNA and dynorphin B expression have been previously shown to be greatly increased in cardiac myocytes of BIO 14.6 cardiomyopathic hamsters. Here we report that exogenous dynorphin B induced a dose-dependent increase in prodynorphin mRNA levels and stimulated prodynorphin gene transcription in normal hamster myocytes. Similar responses were elicited by the synthetic selective kappa opioid receptor agonist U-50,488H. These effects were counteracted by the kappa opioid receptor antagonist Mr-1452 and were not observed in the presence of chelerythrine or calphostin C, two specific protein kinase C (PKC) inhibitors. Treatment of cardiomyopathic cells with Mr-1452 significantly decreased both prodynorphin mRNA levels and prodynorphin gene transcription. In control myocytes, dynorphin B induced the translocation of PKC-alpha to the nucleus and increased nuclear PKC activity without affecting the expression of PKC-delta, -epsilon, or -zeta. Acute release of either U-50,488H or dyn B over single normal or cardiomyopathic cells transiently increased the cytosolic Ca2+ concentration. A sustained treatment with each opioid agonist increased the cytosolic Ca2+ level for a more prolonged period in cardiomyopathic than in control myocytes and led to a depletion of Ca2+ from the sarcoplasmic reticulum in both groups of cells. The possibility that prodynorphin gene expression may affect the function of the cardiomyopathic cell through an autocrine mechanism is discussed.

Phorbol ester regulation of opioid peptide gene expression in myocardial cells. Role of nuclear protein kinase.

Opioid peptide gene expression was characterized in adult rat ventricular cardiac myocytes that had been cultured in the absence or the presence of phorbol 12-myristate 13-acetate. The phorbol ester induced a concentration- and time-dependent increase of prodynorphin mRNA, the maximal effect being reached after 4 h of treatment. The increase in mRNA expression was suppressed by incubation of cardiomyocytes with staurosporine, a putative protein kinase C inhibitor, and was not observed when the cells were cultured in the presence of the inactive phorbol ester 4 alpha-phorbol 12,13-didecanoate. Incubation of cardiac myocytes with phorbol 12-myristate 13-acetate also elicited a specific and staurosporine-sensitive increase in immunoreactive dynorphin B, a biologically active end product of the precursor, both in the myocardial cells and in the culture medium. In vitro run-off transcription assays indicated that transcription of the prodynorphin gene was increased both in nuclei isolated from phorbol ester-treated myocytes and in nuclei isolated from control cells and then exposed to phorbol 12-myristate 13-acetate. No transcriptional effect was observed when cardiac myocytes or isolated nuclei where exposed to 4 alpha-phorbol 12,13-didecanoate. The phorbol ester-induced increase in prodynorphin gene transcription was prevented by pretreatment of myocytes or isolated nuclei with staurosporine, suggesting that myocardial opioid gene expression may be regulated by nuclear protein kinase C. In this regard, cardiac myocytes expressed protein kinase C-alpha, -delta, -epsilon, and -zeta, as shown by immunoblotting. Only protein kinase C-delta and protein kinase C-epsilon were expressed in nuclei that have been isolated from control myocytes, suggesting that these two isotypes of the enzyme may be part of the signal transduction pathway involved in the effect elicited by the phorbol ester on opioid gene transcription in isolated nuclei. The incubation of myocardial nuclei isolated from control cells in the presence of a protein kinase C activator induced the phosphorylation of the myristoylated alanine-rich protein kinase C substrate peptide, a specific fluorescent substrate of the enzyme. The possibility that prodynorphin gene expression may control the heart function through autocrine or paracrine mechanisms is discussed.

Effects of taurine and hypotaurine on lipid peroxidation.

It has been suggested that hypotaurine might inhibit lipid peroxidation in vivo by scavenging the initiator OH. The results presented demonstrate that hypotaurine affects other reactions relevant to the initiation, propagation and termination phases of lipid peroxidation. Hypotaurine a) decreases Fe2+ autoxidation, either spontaneous or catalyzed by Fe3+, that may generate perferryl iron; b) decreases Fe2+ oxidation, by cumene hydroperoxide, that forms the alkoxy radical; c) inhibits the lipid hydroperoxide dependent lipid peroxidation, favoring the onset of the termination phase. Hypotaurine does not affect the autoxidation of Fe2+ bound to phosphatidic acid containing liposomes. Taurine is ineffective in all the experimental systems tested.

Evaluation of opioid peptide gene expression by solution hybridization RNase protection.

The solution hybridization RNase protection assay may be considered a suitable method for both qualitative and quantitative analysis of mRNAs. In the present study we described an application of solution hybridization RNase protection assay to the quantitative analysis of prodynorphin mRNA, which encodes for the synthesis of prodynorphin, a common precursor for a number of opioid peptides. In the myocardial cell, stimulation of the K opioid is involved in the modulation of cytosolic calcium and pH homeostasis. In the present study, we found that prodynorphin mRNA, which encodes for the synthesis of a common precursor of opioid peptides interacting with K sites, is synthesized both in atrial and in ventricular tissue of the rat heart. In adult cultured rat ventricular cardiomyocytes, the level of prodynorphin mRNA did not differ from that detected in the original ventricular tissue. This finding indicates that the myocardial cell is an important source for prodynorphin gene expression and has the potential for an intrinsic synthesis of dynorphin-related peptides.

Dynorphin gene expression and release in the myocardial cell.

The expression of the prodynorphin gene was investigated in adult cultured rat ventricular cardiac myocytes by using a sensitive solution hybridization RNase protection assay for the quantitative analysis of prodynorphin mRNA. Myocyte culture in high KCl resulted, after 4 h, in a marked increase in cellular prodynorphin mRNA, while a KCl treatment for 6, 12, or 24 h progressively down-regulated the levels of prodynorphin mRNA below the control value. Immunoreactive dynorphin B, a biologically active end product of the precursor, was found to be present in the culture medium in significantly higher amounts than in the cardiac myocytes. The levels of this biologically active K opioid receptor agonist significantly increased after 4 h of KCl treatment and were markedly reduced following a 24-h exposure of the cardiac myocytes to KCl. These KCl-induced effects were all abolished by cell incubation in the presence of the calcium channel blocker verapamil. In single cardiac myocytes, acute stimulation of K opioid receptors with dynorphin B or with the selective agonist U-50,488H increased the level of cytosolic calcium. This effect was abolished by the specific K opioid receptor antagonist (Mr-1452) and was not affected by the removal of calcium from the bathing medium. These results suggest that an opioid gene may influence the myocardial function in an autocrine or paracrine fashion.

Polyamine levels during the onset of "CAM" inOpuntia F. indica (Miller).

Polyamines have been related to the "Crassulacean Acid Metabolism" (CAM) in higher plants. Such relationship was however observed in plants where CAM activity is inducible by external factors. Results presented here indicate that, inOpuntia F. indica, cladodes where onset of CAM is dependent on internal conditions, i.e. leaf age, the concentration of putrescine increases in parallel to the acidity of the cytoplasm. The parallel increase of putrescine concentration and acidity (malic acid concentration) can be best evaluated during the onset of CAM (young cladodes), while such correlation is not observed in mature cladodes where CAM is already in it's full function. Spermidine and spermine show no correlation with CAM activity neither during the onset of CAM nor during it's full function. However, spermidine levels correlate negatively to CAM activity when cladodes attain > 30 days of age. The results suggest that putrescine in free form could possibly counteract the increase of cellular acidity during onset of CAM inOpuntia F. indica; the possible roles of spermidine are discussed.