68 research outputs found

    Developing an eMental health monitoring module for older mourners using fuzzy cognitive maps

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    Objective: Effective internet interventions often combine online self-help with regular professional guidance. In the absence of regularly scheduled contact with a professional, the internet intervention should refer users to professional human care if their condition deteriorates. The current article presents a monitoring module to recommend proactively seeking offline support in an eMental health service to aid older mourners. Method: The module consists of two components: a user profile that collects relevant information about the user from the application, enabling the second component, a fuzzy cognitive map (FCM) decision-making algorithm that detects risk situations and to recommend the user to seek offline support, whenever advisable. In this article, we show how we configured the FCM with the help of eight clinical psychologists and we investigate the utility of the resulting decision tool using four fictitious scenarios. Results: The current FCM algorithm succeeds in detecting unambiguous risk situations, as well as unambiguously safe situations, but it has more difficulty classifying borderline cases correctly. Based on recommendations from the participants and an analysis of the algorithm's erroneous classifications, we propose how the current FCM algorithm can be further improved. Conclusion: The configuration of FCMs does not necessarily demand large amounts of privacy-sensitive data and their decisions are scrutable. Thus, they hold great potential for automatic decision-making algorithms in mental eHealth. Nevertheless, we conclude that there is a need for clear guidelines and best practices for developing FCMs, specifically for eMental health.</p

    a case study

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    This paper is based on an explorative case study of all.department e-mails that were sent on the Intranet of a Danish university department. Following a social constructionist approach, our analysis assumes that language use shapes relations, identities, and representations. We thus investigate which social relations are expressed and constructed in the e-mail discourse and how the organizational world of the department is represented in the all.department e-mails. Our analyses of the e-mails show that the managerial voices are dominant as well as the perception of e-mail communication as a tool of information transmission. However, a few e-mails sent by employees without specific organizational functions differ significantly from the "managerial" mails. In these mails employee voices articulate a latent and unfulfilled need for a community and a forum for dialogue. The usage of the all.department e-mail communication is also related to the ongoing change of managing university departments in Denmark

    Effects of the TLR2 Agonists MALP-2 and Pam3Cys in Isolated Mouse Lungs

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    Background: Gram-positive and Gram-negative bacteria are main causes of pneumonia or acute lung injury. They are recognized by the innate immune system via toll-like receptor-2 (TLR2) or TLR4, respectively. Among all organs, the lungs have the highest expression of TLR2 receptors, but little is known about the pulmonary consequences of their activation. Here we studied the effects of the TLR2/6 agonist MALP-2, the TLR2/1 agonist Pam 3Cys and the TLR4 agonist lipopolysaccharide (LPS) on pro-inflammatory responses in isolated lungs. Methodology/Principal Findings: Isolated perfused mouse lungs were perfused for 60 min or 180 min with MALP-2 (25 ng/ mL), Pam3Cys (160 ng/mL) or LPS (1 mg/mL). We studied mediator release by enzyme linked immunosorbent assay (ELISA), the activation of mitogen activated protein kinase (MAPK) and AKT/protein kinase B by immunoblotting, and gene induction by quantitative polymerase chain reaction. All agonists activated the MAPK ERK1/2 and p38, but neither JNK or AKT kinase. The TLR ligands upregulated the inflammation related genes Tnf, Il1b, Il6, Il10, Il12, Ifng, Cxcl2 (MIP-2a) and Ptgs2. MALP-2 was more potent than Pam 3Cys in inducing Slpi, Cxcl10 (IP10) and Parg. Remarkable was the strong induction of Tnc by MALP2, which was not seen with Pam 3Cys or LPS. The growth factor related genes Areg and Hbegf were not affected. In addition, all three TLR agonists stimulated the release of IL-6, TNF, CXCL2 and CXCL10 protein from the lungs

    Prognostic model to predict postoperative acute kidney injury in patients undergoing major gastrointestinal surgery based on a national prospective observational cohort study.

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    Background: Acute illness, existing co-morbidities and surgical stress response can all contribute to postoperative acute kidney injury (AKI) in patients undergoing major gastrointestinal surgery. The aim of this study was prospectively to develop a pragmatic prognostic model to stratify patients according to risk of developing AKI after major gastrointestinal surgery. Methods: This prospective multicentre cohort study included consecutive adults undergoing elective or emergency gastrointestinal resection, liver resection or stoma reversal in 2-week blocks over a continuous 3-month period. The primary outcome was the rate of AKI within 7 days of surgery. Bootstrap stability was used to select clinically plausible risk factors into the model. Internal model validation was carried out by bootstrap validation. Results: A total of 4544 patients were included across 173 centres in the UK and Ireland. The overall rate of AKI was 14·2 per cent (646 of 4544) and the 30-day mortality rate was 1·8 per cent (84 of 4544). Stage 1 AKI was significantly associated with 30-day mortality (unadjusted odds ratio 7·61, 95 per cent c.i. 4·49 to 12·90; P < 0·001), with increasing odds of death with each AKI stage. Six variables were selected for inclusion in the prognostic model: age, sex, ASA grade, preoperative estimated glomerular filtration rate, planned open surgery and preoperative use of either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker. Internal validation demonstrated good model discrimination (c-statistic 0·65). Discussion: Following major gastrointestinal surgery, AKI occurred in one in seven patients. This preoperative prognostic model identified patients at high risk of postoperative AKI. Validation in an independent data set is required to ensure generalizability

    Regulation of acute lung injury by the sympathetic nervous system and neuropeptide Y

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    The acute respiratory distress syndrome (ARDS) is a life-threatening medical condition caused by insults to the lung. Since ventilation strategies are critical for the outcome of ARDS patients, experimental models of ventilator-induced lung injury (VILI) are frequently used. Unfortunately, many models of VILI are poorly defined. There is a strong need for models, which focus on oxygenation, the most important clinical aspect of ARDS and also provide substantial information about relevant physiological parameters. Consequently, one aim was to develop an experimental VILI model that is characterised by ARDS-like hypoxemia and controlled by inflammation. This study shows that lung failure occurs rapidly once peak airway pressure exceeds 24 cmH2O and leads to diminished pulmonary compliance, hypoxemia and edema formation. Alongside several inflammatory mediators, neuropeptide Y (NPY) expression was strongly increased. Anti-inflammatory treatment with steroids attenuated inflammation, but did not prevent lung injury, strongly indicating a mechanical failure of the lung. Moreover, the present study demonstrates that maximising the duration of experimental ventilation protocols is crucial.The sympathetic nervous system (SNS) acts via the neurotransmitters norepinephrine, adenosine triphosphate and NPY, which are co-released. The SNS innervates the lung and is involved in different inflammatory processes. Most immune-modulatory effects of NPY are mediated by the Y1 receptor. One goal of the present study was to address the role of NPY and its receptor in ARDS. This thesis reports that ventilation together with a second insult (acid inspiration) is leading to a mild lung injury with increased levels of NPY. Administration of an Y1 receptor agonist is leading to increased pro-inflammatory mediators and deteriorated lung functions. Similar effects were obtained with an Y1 receptor antagonist. This could be due to increased signalling via the Y2/Y5 receptors and needs further research.A further common cause of ARDS is pneumonia induced by influenza virus infection. Therefore, the present study aimed to investigate the participation of NPY in the pathogenesis of ARDS caused by influenza virus. In summary, it was shown that besides well-known pro-inflammatory mediators pulmonary NPY levels were increased as well. Knockout of NPY significantly improved survival of mice infected with influenza viruses. Virus replication decreased while anti-viral and anti-inflammatory genes showed increased expression.Overall, this study demonstrates that NPY is activated in inflammatory processes in the lung and holds a crucial role in regulating respiratory infections
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