Collective Bargaining Attitudes of Registered Nurses in the United States and Canada: A Wisconsin-Ontario Comparison

Bien que la condition des infirmières autorisées du Canada et des États-Unis se ressemble sous plusieurs aspects, elle diffère énormément quant au taux de syndicalisation. Soixante-quinze pour cent des infirmières autorisées du Canada sont syndiquées comparativement à moins de quinze pour cent aux États-Unis. L'explication la plus plausible d'une différence aussi marquée dans le pourcentage de syndicalisation d'un pays à l'autre provient de disparités législatives. Jusqu'à 1974, les infirmières américaines (et les autres employés des hôpitaux d'ailleurs) étaient exclues des dispositions duNational Labor Relations Act. Au contraire, les infirmières canadiennes n'étaient pas soumises à de pareilles restrictions, car on leur avait accordé depuis longtemps déjà les mêmes droits que la majorité des salariés du secteur privé de se former en syndicats, d'être accréditées et de négocier des conventions collectives de travail.Dans cette étude, les auteurs se demandent s'il n'est pas possible que, outre les motifs d'ordre juridique, le taux plus bas de syndicalisation des infirmières des États-Unis ne soit pas aussi attribuable au fait que les infirmières américaines perçoivent la négociation collective comme un mécanisme moins avantageux pour faire valoir leurs besoins que ne l'estiment les infirmières canadiennes.Pour jeter un peu de lumière sur cette question, on a comparé les comportements d'un échantillon d'infirmières de l'État du Wisconsin et de l'Ontario (tableau no 1). Strictement parlant, les infirmières interrogées ne constituaient pas un échantillon représentatif de l'ensemble des infirmières canadiennes et américaines. Toutefois, les types de syndicalisme chez les infirmières et les conditions de l'exercice de la profession dans les deux régions ressemblaient à ce qui existait ailleurs dans les deux pays. On a estimé, cependant, que dans la mesure où le faible taux de syndicalisation des infirmières américaines était relié à des attitudes défavorables à la négociation collective, on aurait pu s'attendre qu'il en ressortirait que les infirmières du Wisconsin étaient beaucoup moins sympathiques au syndicalisme que leurs collègues de l'Ontario.Les données furent recueillies au moyen d'un questionnaire en dix points présenté sous la forme d'affirmations relatives au syndicalisme et à la négociation collective. Les réponses à ces dix affirmations furent mesurées à l'aide d'une échelle en cinq points (très favorable, favorable, indifférent, en désaccord et totalement en désaccord). L'analyse des réponses (tableau no 2) a montré que le seul aspect de la négociation collective où les infirmières du Wisconsin avaient une attitude plus négative que celles de l'Ontario avait trait à la coopération possible avec les employés non-professionnels. Sur tous les autres points, les perceptions des deux groupes étaient semblables où les infirmières du Wisconsin se montraient plus favorables.Ces résultats tendent à nier dans une certaine mesure le postulat selon lequel les attitudes des infirmières aux États-Unis constituent un obstacle majeur à la syndicalisation. Ces constatations confirment plutôt la thèse traditionnelle voulant que la différence de climat politique dans les deux pays ait été la cause principale pour laquelle les infirmières américaines tardent davantage à recourir à la négociation collective.This paper compares the attitudes to collective bargaining of a sample of Ontario and Wisconsin registered nurses. Contrary to expectations (in view of the general low rate of American nursing unionism), the Wisconsin nurses who where surveyed viewed collective bargaining at least as favourably as their Ontario counterparts

Comparative study of platelet indices in cirrhosis, cirrhosis with sepsis and normal population

Background: Platelet indices are the first hematologic indices to be affected in cirrhosis. Cirrhosis patients are particularly susceptible to bacterial infections. The incidence of sepsis in cirrhosis is estimated to be at least 30-50% of hospital admissions. Sepsis also causes alterations in platelet indices. We studied and compared the platelet indices namely platelet count, mean platelet volume (MPV), platelet distribution width (PDW) and platecrit in cirrhosis, cirrhosis with sepsis and normal control population.Methods: This observational study included forty cirrhosis, forty three cirrhosis with sepsis and sixty one controls. Platelet indices were reviewed and compared between the groups and correlation of platelet indices with CTP score, MELD, platelet count and spleen size was also evaluated.Results: Platelet indices were significantly altered in cirrhosis compared to normal population. MPV and PDW were significantly higher in cirrhosis compared to control population. Platelet count and platecrit were significantly lower in cirrhosis compared to control population. CTP score and MELD showed significant positive correlation with MPV and platelet count showed significant negative correlation with PD. Sepsis in cirrhosis was associated with significant decrease in platelet count and platecrit but caused significant increase in PDW compared to cirrhosis without sepsis. Cirrhosis with sepsis group had four patients with variceal bleeding with significantly higher mean PDW(19%) and significantly lower mean platecrit (0.04) compared to nonbleeding group (p value <0.05).Conclusions: Platelet indices are useful parameters in cirrhosis. Other than platelet count, PDW and platecrit are useful indices to be monitored in cirrhosis with sepsis

Solvatochromism, aggregation and photochemical properties of Fullerenes, C<SUB>60</SUB> and C<SUB>70</SUB>, in solution

Fullerenes, C60 and C70, display interesting physicochemical properties in solutions, especially due to their unique chemical structures and their good electron accepting abilities. Solubility of fullerenes in different organic solvents and their unusual solvatochromic behavior, the ability of the fullerenes to form aggregates in solutions, and their electron transfer and charge transfer interactions with variety of electron donors, are the subjects of extensive research activities for more than one decade. Many research groups including ours have contributed substantially in the understanding of the solvatochromism, aggregation behavior, and the photoinduced electron transfer and charge transfer chemistry of fullerenes, in condensed phase. Present article is aimed to summarize the important results reported on the above aspects of fullerenes, subsequent to the earlier report from our group. (D.K. Palit and J.P. Mittal, Full. Sci. &amp; Tech. 3, 1995, 643-659)

Angiopoietin-like protein 3, an emerging cardiometabolic therapy target with systemic and cell-autonomous functions

Angiopoietin like protein 3 (ANGPTL3) is best known for its function as an inhibitor of lipoprotein and endothelial lipases. Due to the capacity of genetic or pharmacologic ANGPTL3 suppression to markedly reduce circulating lipoproteins, and the documented cardioprotection upon such suppression, ANGPTL3 has become an emerging therapy target for which both antibody and antisense oligonucleotide (ASO) therapeutics are being clinically tested. While the antibody is relatively selective for circulating ANGPTL3, the ASO also depletes the intra-hepatocellular protein, and there is emerging evidence for cell-autonomous functions of ANGPTL3 in the liver. These include regulation of hepatocyte glucose and fatty acid uptake, insulin sensitivity, LDL/VLDL remnant uptake, VLDL assembly/secretion, polyunsaturated fatty acid (PUFA) and PUFA-derived lipid mediator content, and gene expression. In this review we elaborate on (i) why ANGPTL3 is considered one of the most promising new cardiometabolic therapy targets, and (ii) the present evidences for its intra-hepatocellular or cell-autonomous functions.Peer reviewe

Angiopoietin-like 8 (Angptl8) controls adipocyte lipolysis and phospholipid composition

Angiopoietin-like 8 (Angptl8) inhibits lipolysis in the circulation together with Angplt3 and controls post-prandial fat storage in white adipose tissue (WAT). It is strongly induced by insulin in vivo in WAT and in vitro in adipocytes. In this study we addressed the function of Angptl8 in adipocytes by its stable lentivirus-mediated knock-down in 3T3-L1 cells, followed by analyses of triglyceride (TG) storage, lipid droplet (LD) morphology, the cellular lipidome, lipolysis, and gene expression. Depletion of Angptl8 did not drastically affect the adipocyte differentiation of 3T3-L1 cells but resulted in a moderate (18-19%) reduction of stored TGs. The lipidome analysis revealed a reduction of alkyl-phosphatidylcholines (PCs) and phosphatidylethanolamine (PE) plasmalogens, as well as saturated PCs and PEs. Importantly, the Angptl8 depleted cells displayed enhanced lipolysis as measured by release of non-esterified fatty acids (NEFA5). Consistently, mRNAs encoding Angptl4 and Leptin, which facilitate lipolysis, as well as Cpt1a, Cpt1b, and Pgc-1 alpha involved in FA oxidation, were elevated. The Angptl8 mRNA itself was suppressed by pharmacologic treatments inducing lipolysis: stimulation with the beta-adrenergic agonist isoproterenol or with the adenylate cyclase activator forskolin. To conclude, knock-down of Angptl8 in adipocytes suggests that the protein acts to inhibit intracellular lipolysis, analogous to its activity in the circulation. Depletion of Angptl8 results in an altered cellular phospholipid composition. The findings identify Angptl8 as a central insulin-regulated controller of adipocyte lipid metabolism. (C) 2017 Elsevier B.V. All rights reserved.Peer reviewe

MiR-107 inhibits CDK6 expression, differentiation, and lipid storage in human adipocytes

MicroRNA-107 (miR-107) plays a regulatory role in obesity and insulin resistance, but the mechanisms of its function in adipocytes have not been elucidated in detail. Here we show that overexpression of miR-107 in pre- and mature human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes attenuates differentiation and lipid accumulation. Our results suggest that miR-107 controls adipocyte differentiation via CDK6 and Notch signaling. CDK6 is a validated target of miR-107 and was downregulated upon miR-107 overexpression. Notch3, a signaling receptor involved in adipocyte differentiation, has been shown to decrease upon CDK6 depletion; Here Notch3 and its target Hes1 were downregulated by miR-107 overexpression. In mature adipocytes, miR-107 induces a triglyceride storage defect by impairing glucose uptake and triglyceride synthesis. To conclude, our data suggests that miR-107 has distinct functional roles in preadipocytes and mature adipocytes; Its elevated expression at these different stages of adipocytes may on one hand dampen adipogenesis, and on the other, promote ectopic fatty acid accumulation and reduced glucose tolerance.Peer reviewe

Targeting EGF-receptor(s) - STAT1 axis attenuates tumor growth and metastasis through downregulation of MUC4 mucin in human pancreatic cancer.

Transmembrane proteins MUC4, EGFR and HER2 are shown to be critical in invasion and metastasis of pancreatic cancer. Besides, we and others have demonstrated de novo expression of MUC4 in ~70-90% of pancreatic cancer patients and its stabilizing effects on HER2 downstream signaling in pancreatic cancer. Here, we found that use of canertinib or afatinib resulted in reduction of MUC4 and abrogation of in vitro and in vivo oncogenic functions of MUC4 in pancreatic cancer cells. Notably, silencing of EGFR family member in pancreatic cancer cells decreased MUC4 expression through reduced phospho-STAT1. Furthermore, canertinib and afatinib treatment also inhibited proliferation, migration and survival of pancreatic cancer cells by attenuation of signaling events including pERK1/2 (T202/Y204), cyclin D1, cyclin A, pFAK (Y925) and pAKT (Ser473). Using in vivo bioluminescent imaging, we demonstrated that canertinib treatment significantly reduced tumor burden (P=0.0164) and metastasis to various organs. Further, reduced expression of MUC4 and EGFR family members were confirmed in xenografts. Our results for the first time demonstrated the targeting of EGFR family members along with MUC4 by using pan-EGFR inhibitors. In conclusion, our studies will enhance the translational acquaintance of pan-EGFR inhibitors for combinational therapies to combat against lethal pancreatic cancer

Avicin D, a Plant Triterpenoid, Induces Cell Apoptosis by Recruitment of Fas and Downstream Signaling Molecules into Lipid Rafts

Avicins, a family of triterpene electrophiles originally identified as potent inhibitors of tumor cell growth, have been shown to be pleiotropic compounds that also possess antioxidant, anti-mutagenic, and anti-inflammatory activities. We previously showed that Jurkat cells, which express a high level of Fas, are very sensitive to treatment with avicins. Thus, we hypothesized that avicins may induce cell apoptosis by activation of the Fas pathway. By using a series of cell lines deficient in cell death receptors, we demonstrated that upon avicin D treatment, Fas translocates to the cholesterol- and sphingolipid-enriched membrane microdomains known as lipid rafts. In the lipid rafts, Fas interacts with Fas-associated death domain (FADD) and Caspase-8 to form death-inducing signaling complex (DISC) and thus mediates cell apoptosis. Interfering with lipid raft organization by using a cholesterol-depleting compound, methyl-β-cyclodextrin, not only prevents the clustering of Fas and its DISC complex but also reduces the sensitivity of the cells to avicin D. Avicin D activates Fas pathways independent of the association between extracellular Fas ligands and Fas receptors. A deficiency in Fas and its downstream signaling molecules leads to the resistance of the cells to avicin D treatment. Taken together, our results demonstrate that avicin D triggers the redistribution of Fas in the membrane lipid rafts, where Fas activates receptor-mediated cell death