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This article presents key concepts for collaboration, participation and co-production in practice research, based on a cross-analysis of three research cases. The article aims to explore questions such as: 1) Who should be involved? 2) What preconditions are necessary from all participants? 3) What nuances arise in the process of becoming a partner? The article investigates how partnerships, participation and knowledge production can be performed in social work practice research, and highlights that any collaborative process is complex, and the questions may thus be intertwined. Such processes require researchers to be aware of the communicative, power-relational, dialogical and democratic processes involved. One of the key takeaways from the cross-analysis is that successful collaboration demands conscious attention and effort towards effective communication, power-sharing and democratic processes. [ABSTRACT FROM AUTHOR]

Inflammasomes are crucial gatekeepers of the immune response, but their maladaptive activation associates with inflammatory pathologies. Besides canonical activation, monocytes can trigger non-transcriptional or rapid inflammasome activation that has not been well defined in the context of acute myocardial infarction (AMI). Rapid transcription-independent inflammasome activation induced by simultaneous TLR priming and triggering stimulus was measured by caspase-1 (CASP1) activity and interleukin release. Both classical and intermediate monocytes from healthy donors exhibited robust CASP1 activation, but only classical monocytes produced high mature interleukin-18 (IL18) release. We also recruited a limited number of coronary artery disease (CAD, n=31) and AMI (n=29) patients to evaluate their inflammasome function and expression profiles. Surprisingly, monocyte subpopulations isolated from blood collected during percutaneous coronary intervention (PCI) from AMI patients presented diminished CASP1 activity and abrogated IL18 release despite increased NLRP3 gene expression. This unexpected attenuated rapid inflammasome activation was accompanied by a significant increase of TNFAIP3 and IRAKM expression. Moreover, TNFAIP3 protein levels of circulating monocytes showed positive correlation with high sensitive troponin T (hsTnT), implying an association between TNFAIP3 upregulation and the severity of tissue injury. We suggest this monocyte attenuation to be a protective phenotype aftermath following a very early inflammatory wave in the ischemic area. Damage-associated molecular patterns (DAMPs) or other signals trigger a transitory negative feedback loop within newly recruited circulating monocytes as a mechanism to reduce post-injury tissue damage. [ABSTRACT FROM AUTHOR]

Summary: This article focuses on user involvement in social work innovations in the public sector and provides an overview of how public innovation via user involvement in social work has been studied to date. Through analyses based on a systematic review combined with a narrative review of the identified literature, we offer a typology of social work innovations. The article concludes by discussing possibilities and barriers inherent in user involvement in social work and suggesting topics for future research. Findings: Through a systematic review we identify the relevant literature describing different kinds of user involvement in social work innovation. In the narrative review, we analyze the literature and identify three types of innovation: user-centered innovation, co-produced innovation, and citizen-driven innovation. With empirical examples we illustrate the different types of innovation and the citizen's role in the different innovation processes. Application: The typology provides an analytic tool to differentiate types of innovation and user involvement, but it may also function as inspiration to practitioners to reflect more about the roles of users and frontline workers and to be more aware of existing barriers when designing new social initiatives in the public sector. [ABSTRACT FROM AUTHOR]

We analyze coping strategies emerging as responses to relative poverty in families with children who receive the lowest benefits in Denmark. We use complementary theoretical perspectives, including Bourdieu's theory of practice, Archer's perspective on reflectivity as inner conversations, and Lazarus' psychological views on coping. We focus on two very different families coping with poverty and show how the parents' dispositions, the structured situations in which they act, the individuals' unique characteristics, and their choices shape their coping strategies. This paper offers social workers a theoretical framework to familiarize themselves with both the living conditions and the strategies of poor parents. [ABSTRACT FROM AUTHOR]

Copyright of Dansk Sociologi is the property of Djøf Forlag and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Aggravated endothelial injury and impaired endothelial repair capacity contribute to the high cardiovascular risk in patients with type 2 diabetes (T2D), but the underlying mechanisms are still incompletely understood. Here we describe the functional role of a mature form of miRNA (miR) 483-3p, which limits endothelial repair capacity in patients with T2D. Expression of human (hsa)-miR-483-3p was higher in endothelial-supportive M2-type macrophages (M2MΦs) and in the aortic wall of patients with T2D than in control subjects without diabetes. Likewise, the murine (mmu)-miR-483* was higher in T2D than in nondiabetic murine carotid samples. Overexpression of miR-483-3p increased endothelial and macrophage apoptosis and impaired reendothelialization in vitro. The inhibition of hsa-miR-483-3p in human T2D M2MΦs transplanted to athymic nude mice (NMRI-Foxn1ν/Foxn1ν ) or systemic inhibition of mmu-miR-483* in B6.BKS(D)-Leprdb /J diabetic mice rescued diabetes-associated impairment of reendothelialization in the murine carotid-injury model. We identified the endothelial transcription factor vascular endothelial zinc finger 1 (VEZF1) as a direct target of miR-483-3p. VEZF1 expression was reduced in aortae of diabetic mice and upregulated in diabetic murine aortae upon systemic inhibition of mmu-483*. The miRNA miR-483-3p is a critical regulator of endothelial integrity in patients with T2D and may represent a therapeutic target to rescue endothelial regeneration after injury in patients with T2D. [ABSTRACT FROM AUTHOR]

Copyright of Dansk Sociologi is the property of Djøf Forlag and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Abstract: Background: Flow-mediated dilation (FMD) of human conduit arteries is, in part, related to shear stress-induced release of endothelium-derived nitric oxide (NO). However, NO synthase inhibitors do not completely abolish this FMD-response. Recently, a cytochrome P450 (CYP) epoxygenase of the 2C family was linked to NO- and prostacyclin-independent relaxation of conduit arteries. We therefore evaluated the contribution of CYP 2C9 to FMD in humans. Methods and results: FMD of the radial artery was determined in 12 healthy volunteers by high-resolution ultrasound and analyzed before and after intra-arterial infusion of sulfaphenazole, a specific CYP 2C9 inhibitor, l-NMMA (NO synthase inhibitor) and co-infusion of both. Endothelium-independent vasodilation was characterized after intra-arterial infusion of SNP. FMD was reduced after sulfaphenazole (11.5±0.87% vs. 7.4±0.95%, p <0.01), after l-NMMA (6.0±0.71%; p <0.01), and after co-infusion 3.9±0.73% (p <0.05 vs. l-NMMA; p <0.01 vs. sulfaphenazole). Sulfaphenazole had no effect on endothelium-independent vasodilation. In patients with chronic heart failure, the portion of FMD blocked by sulfaphenazole was not affected. CYP 2C was detected by immunohistochemistry in radial artery samples obtained from patients undergoing coronary bypass surgery. Conclusions: FMD in human conductance arteries is reduced after inhibition of CYP 2C9, supporting the concept that CYP 2C metabolites contribute to endothelium-mediated vasodilation of peripheral conduit arteries in vivo. In patients with heart failure, the CYP-dependent FMD appears to be preserved. [Copyright &y& Elsevier]