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    <title>HeRA Institution: Hospitals</title>
    <link>http://hdl.handle.net/10143/11958</link>
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      <title>The Institution's search engine</title>
      <description>Search the Channel</description>
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      <link>http://hera.helsebiblioteket.no/hera/simple-search</link>
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    <item>
      <title>Experiences of existential problems and psychiatric nurses' ways of addressing them</title>
      <link>http://hdl.handle.net/10143/144129</link>
      <description>Title: Experiences of existential problems and psychiatric nurses' ways of addressing them&lt;br/&gt;&lt;br/&gt;Authors: Bjelland, Stine Dyste; Severinsson, Elisabeth&lt;br/&gt;&lt;br/&gt;Abstract: Research on patients’ experiences of existential problems in psychiatric care is scarce. The aim of this study was to create a synthesis of published research about how psychiatric nurses address patients’ existential problems. Fourteen papers met the criteria for this review. Four were empirical papers focusing on patients in psychiatric care, eight had a theoretical approach, while two were on the subject of psychiatric nursing care. The findings revealed that the patients’ existential problems were related to lack of self-confidence, self-reflection, social relationships and inability to make choices. In addition, they found it difficult to take an interest in other people and felt alienated from themselves and others. Self-reflection is important for strengthening the identity of patients suffering from existential problems. Psychiatric nurses can promote a stronger identity in their patients by raising questions with a focus on self-reflection, by being present, inviting the patients into a dialogue and using different theories and models to achieve mental health. In conclusion, psychiatric nursing needs to focus to a greater extent on existential problems in order to support patients to discuss and deal with such concerns.</description>
      <pubDate>Fri, 29 Oct 2010 22:58:59 GMT</pubDate>
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      <title>High mortality explained by mildly elevated blood pressure in Scandinavian adolescent conscripts: a plea for early drug treatment?</title>
      <link>http://hdl.handle.net/10143/143320</link>
      <description>Title: High mortality explained by mildly elevated blood pressure in Scandinavian adolescent conscripts: a plea for early drug treatment?&lt;br/&gt;&lt;br/&gt;Authors: Kjeldsen, Sverre E; Oparil, Suzanne; Narkiewicz, Krzysztof; Hedner, Thomas</description>
      <pubDate>Fri, 29 Jul 2011 22:58:59 GMT</pubDate>
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      <title>Surgical treatment of endometrial cancer and atypical hyperplasia: a trend shift from laparotomy to laparoscopy.</title>
      <link>http://hdl.handle.net/10143/143319</link>
      <description>Title: Surgical treatment of endometrial cancer and atypical hyperplasia: a trend shift from laparotomy to laparoscopy.&lt;br/&gt;&lt;br/&gt;Authors: Qvigstad, Erik; Lieng, Marit&lt;br/&gt;&lt;br/&gt;Abstract: Background. Laparoscopic hysterectomy has proved to be a safe alternative to open surgery in women with benign indications. Few studies compare laparotomy and laparoscopy in gynecologic oncology, and the objective of this study was to analyze the feasibility and development of laparoscopic surgery in endometrial cancer patients. Material and Methods. Records from all women having a hysterectomy due to premalignant or malignant endometrial changes during the years 2002-2009 were examined retrospectively. Results. A total of 521 hysterectomies were performed during the study period. Laparoscopy was performed in about 20% of the cases in the first two years, increasing to 83% in the last year of the period. Moreover, the laparoscopic technique was increasingly applied in older women, more obese women and in women with high-risk preoperative diagnosis, without increasing the complication rate. Conclusions. As for benign indications, laparoscopic hysterectomy in endometrial cancer patients should be preferred whenever possible.</description>
      <pubDate>Fri, 29 Oct 2010 22:58:59 GMT</pubDate>
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    <item>
      <title>Advanced Clinical Medicine Requires Advanced Clinical Ethics.</title>
      <link>http://hdl.handle.net/10143/143339</link>
      <description>Title: Advanced Clinical Medicine Requires Advanced Clinical Ethics.&lt;br/&gt;&lt;br/&gt;Authors: Hansen, Thor Willy Ruud&lt;br/&gt;&lt;br/&gt;Abstract: Many advances have occurred in clinical medicine in the last decades. Solid organ transplants, corrective surgery for congenital malformations, improved cytostatic regimes for children with cancer, and respiratory care for premature infants are but a few examples of the changing face of medical practice. Such changes have added years to life. But along the way many patients have paid a price, both in terms of loss of life and of added suffering. Even today, some survivors are faced with a life of impairment and suffering. Follow-up studies of extremely low-birth-weight infants show that the smallest infants have a high rate of severe sequelae. Some argue that such suffering should be sufficient reason to make us desist from further attempts to advance the frontiers of therapy. This paper seeks to reflect on the character of advanced medicine and on how we relate to patients and their kin in our quest for further improvements in therapy. The price for continued advances will inevitably be paid by some patients who will not profit from them. Therefore, patients who are asked to participate in such a quest must receive honest and transparent information, including a discussion about where and how they would draw the limits. Clinical competency is a core concept in advanced medicine, but a caring comportment also demands that our relationship to the patient be characterized by honesty, integrity, and decency. In dialogue with parents, finding the right balance between parental exercise of autonomy and safe-guarding the best interest of the child remains a challenge.</description>
      <pubDate>Mon, 25 Jul 2011 22:58:59 GMT</pubDate>
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      <title>Resuscitation of newborn piglets. short-term influence of FiO2 on matrix metalloproteinases, caspase-3 and BDNF.</title>
      <link>http://hdl.handle.net/10143/142909</link>
      <description>Title: Resuscitation of newborn piglets. short-term influence of FiO2 on matrix metalloproteinases, caspase-3 and BDNF.&lt;br/&gt;&lt;br/&gt;Authors: Solberg, Rønnaug; Løberg, Else Marit; Andresen, Jannicke H; Wright, Marianne S; Charrat, Eliane; Khrestchatisky, Michel; Rivera, Santiago; Saugstad, Ola Didrik&lt;br/&gt;&lt;br/&gt;Abstract: Perinatal hypoxia-ischemia is a major cause of mortality and cerebral morbidity, and using oxygen during newborn resuscitation may further harm the brain. The aim was to examine how supplementary oxygen used for newborn resuscitation would influence early brain tissue injury, cell death and repair processes and the regulation of genes related to apoptosis, neurodegeneration and neuroprotection.; Anesthetized newborn piglets were subjected to global hypoxia and then randomly assigned to resuscitation with 21%, 40% or 100% O(2) for 30 min and followed for 9 h. An additional group received 100% O(2) for 30 min without preceding hypoxia. The left hemisphere was used for histopathology and immunohistochemistry and the right hemisphere was used for in situ zymography in the corpus striatum; gene expression and the activity of various relevant biofactors were measured in the frontal cortex. There was an increase in the net matrix metalloproteinase gelatinolytic activity in the corpus striatum from piglets resuscitated with 100% oxygen vs. 21%. Hematoxylin-eosin (HE) staining revealed no significant changes. Nine hours after oxygen-assisted resuscitation, caspase-3 expression and activity was increased by 30-40% in the 100% O(2) group (n = 9/10) vs. the 21% O(2) group (n = 10; p&lt;0.04), whereas brain-derived neurotrophic factor (BDNF) activity was decreased by 65% p&lt;0.03.; The use of 100% oxygen for resuscitation resulted in increased potentially harmful proteolytic activities and attenuated BDNF activity when compared with 21%. Although there were no significant changes in short term cell loss, hyperoxia seems to cause an early imbalance between neuroprotective and neurotoxic mechanisms that might compromise the final pathological outcome.</description>
      <pubDate>Thu, 29 Oct 2009 22:58:59 GMT</pubDate>
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      <title>Listeria monocytogenes infection affects a subset of Ly49-expressing NK cells in the rat.</title>
      <link>http://hdl.handle.net/10143/142889</link>
      <description>Title: Listeria monocytogenes infection affects a subset of Ly49-expressing NK cells in the rat.&lt;br/&gt;&lt;br/&gt;Authors: Shegarfi, Hamid; Naper, Christian; Rolstad, Bent; Inngjerdingen, Marit&lt;br/&gt;&lt;br/&gt;Abstract: NK cells are protective against certain bacterial and viral infections, and their production of IFN-γ is important for the early innate immune defence against L. monocytogenes. We have previously shown that depletion of NK cells in rats leads to increased bacterial burden upon L. monocytogenes infection, and that a subset of NK cells encompassing the majority of Ly49 receptors (Ly49s3+ NK cells) contributed to this effect. In this study, we have further investigated how the Ly49s3+ NK cell subset is affected by L. monocytogenes infection. We observed an increased percentage of Ly49s3+ NK cells in the spleen and a reduction in the bone marrow within the first 48 hrs of L. monocytogenes infection. Concomitantly, we observed increased expression levels of the inflammatory chemokine receptors CCR5 and CXCR3 by Ly49s3+ bone marrow NK cells, as compared to Ly49s3- NK cells, suggesting involvement of Ly49s3+ NK cells in the early phase of infection. However, NK cell production of IFN-γ was independent of Ly49 receptor expression. Furthermore, we observed increased expression levels of MHC class I molecules on both macrophages and NK cells during the first 48 hrs of infection, paralleled by a reduction in the surface expression of Ly49s3 on NK cells. In conclusion, L. monocytogenes infection modulates the tissue distribution of Ly49s3+ NK cells, and induces increased MHC class I expression and hence reduced surface expression of Ly49 receptors on NK cells. These changes indicate that L. monocytogenes infection may have multiple effects on NK cells in vivo, and suggests the involvement of Ly49-expressing NK cells in the immune responses towards L. monocytogenes.</description>
      <pubDate>Thu, 29 Oct 2009 22:58:59 GMT</pubDate>
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      <title>Tiling array analysis of UV treated Escherichia coli predicts novel differentially expressed small peptides.</title>
      <link>http://hdl.handle.net/10143/142390</link>
      <description>Title: Tiling array analysis of UV treated Escherichia coli predicts novel differentially expressed small peptides.&lt;br/&gt;&lt;br/&gt;Authors: Thomassen, Gard O S; Weel-Sneve, Ragnhild; Rowe, Alexander D; Booth, James A; Lindvall, Jessica M; Lagesen, Karin; Kristiansen, Knut I; Bjørås, Magnar; Rognes, Torbjørn&lt;br/&gt;&lt;br/&gt;Abstract: Despite comprehensive investigation, the Escherichia coli SOS response system is not yet fully understood. We have applied custom designed whole genome tiling arrays to measure UV invoked transcriptional changes in E. coli. This study provides a more complete insight into the transcriptome and the UV irradiation response of this microorganism.; We detected a number of novel differentially expressed transcripts in addition to the expected SOS response genes (such as sulA, recN, uvrA, lexA, umuC and umuD) in the UV treated cells. Several of the differentially expressed transcripts might play important roles in regulation of the cellular response to UV damage. We have predicted 23 novel small peptides from our set of detected non-gene transcripts. Further, three of the predicted peptides were cloned into protein expression vectors to test the biological activity. All three constructs expressed the predicted peptides, in which two of them were highly toxic to the cell. Additionally, a remarkably high overlap with previously in-silico predicted non-coding RNAs (ncRNAs) was detected. Generally we detected a far higher transcriptional activity than the annotation suggests, and these findings correspond with previous transcription mappings from E. coli and other organisms.; Here we demonstrate that the E. coli transcriptome consists of far more transcripts than the present annotation suggests, of which many transcripts seem important to the bacterial stress response. Sequence alignment of promoter regions suggest novel regulatory consensus sequences for some of the upregulated genes. Finally, several of the novel transcripts identified in this study encode putative small peptides, which are biologically active.</description>
      <pubDate>Thu, 29 Oct 2009 22:58:59 GMT</pubDate>
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      <title>A novel method for the efficient and selective identification of 5-hydroxymethylcytosine in genomic DNA.</title>
      <link>http://hdl.handle.net/10143/142370</link>
      <description>Title: A novel method for the efficient and selective identification of 5-hydroxymethylcytosine in genomic DNA.&lt;br/&gt;&lt;br/&gt;Authors: Robertson, Adam B; Dahl, John A; Vågbø, Cathrine B; Tripathi, Pankaj; Krokan, Hans E; Klungland, Arne&lt;br/&gt;&lt;br/&gt;Abstract: Recently, 5-hydroxymethylcytosine (5hmC) was identified in mammalian genomic DNA. The biological role of this modification remains unclear; however, identifying the genomic location of this modified base will assist in elucidating its function. We describe a method for the rapid and inexpensive identification of genomic regions containing 5hmC. This method involves the selective glucosylation of 5hmC residues by the β-glucosyltransferase from T4 bacteriophage creating β-glucosyl-5-hydroxymethylcytosine (β-glu-5hmC). The β-glu-5hmC modification provides a target that can be efficiently and selectively pulled down by J-binding protein 1 coupled to magnetic beads. DNA that is precipitated is suitable for analysis by quantitative PCR, microarray or sequencing. Furthermore, we demonstrate that the J-binding protein 1 pull down assay identifies 5hmC at the promoters of developmentally regulated genes in human embryonic stem cells. The method described here will allow for a greater understanding of the temporal and spatial effects that 5hmC may have on epigenetic regulation at the single gene level.</description>
      <pubDate>Tue, 29 Mar 2011 22:58:59 GMT</pubDate>
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      <title>Role of the C-terminal domain of PCSK9 in degradation of the LDL receptors.</title>
      <link>http://hdl.handle.net/10143/142389</link>
      <description>Title: Role of the C-terminal domain of PCSK9 in degradation of the LDL receptors.&lt;br/&gt;&lt;br/&gt;Authors: Holla, Oystein L; Cameron, Jamie; Tveten, Kristian; Strøm, Thea Bismo; Berge, Knut Erik; Laerdahl, Jon K; Leren, Trond P&lt;br/&gt;&lt;br/&gt;Abstract: Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to the low density lipoprotein receptor (LDLR) at the cell surface and disrupts the normal recycling of the LDLR. In this study, we investigated the role of the C-terminal domain for the activity of PCSK9. Experiments in which conserved residues and histidines on the surface of the C-terminal domain were mutated indicated that no specific residues of the C-terminal domain, apart from those responsible for maintaining the overall structure, are required for the activity of PCSK9. Rather, the net charge of the C-terminal domain is important. The more positively charged the C-terminal domain, the higher the activity toward the LDLR. Moreover, replacement of the C-terminal domain with an unrelated protein of comparable size led to significant activity of the chimeric protein.We conclude that the role of the evolutionary, poorly conserved C-terminal domain for the activity of PCSK9 reflects its overall positive charge and size and not the presence of specific residues involved in protein-protein interactions.</description>
      <pubDate>Wed, 28 Sep 2011 22:58:59 GMT</pubDate>
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      <title>Mycoplasma contamination revisited: mesenchymal stromal cells harboring Mycoplasma hyorhinis potently inhibit lymphocyte proliferation in vitro.</title>
      <link>http://hdl.handle.net/10143/142369</link>
      <description>Title: Mycoplasma contamination revisited: mesenchymal stromal cells harboring Mycoplasma hyorhinis potently inhibit lymphocyte proliferation in vitro.&lt;br/&gt;&lt;br/&gt;Authors: Zinöcker, Severin; Wang, Meng-Yu; Gaustad, Peter; Kvalheim, Gunnar; Rolstad, Bent; Vaage, John T&lt;br/&gt;&lt;br/&gt;Abstract: Mesenchymal stromal cells (MSC) have important immunomodulatory effects that can be exploited in the clinical setting, e.g. in patients suffering from graft-versus-host disease after allogeneic stem cell transplantation. In an experimental animal model, cultures of rat T lymphocytes were stimulated in vitro either with the mitogen Concanavalin A or with irradiated allogeneic cells in mixed lymphocyte reactions, the latter to simulate allo-immunogenic activation of transplanted T cells in vivo. This study investigated the inhibitory effects of rat bone marrow-derived MSC subsequently found to be infected with a common mycoplasma species (Mycoplasma hyorhinis) on T cell activation in vitro and experimental graft-versus-host disease in vivo.; We found that M. hyorhinis infection increased the anti-proliferative effect of MSC dramatically, as measured by both radiometric and fluorimetric methods. Inhibition could not be explained solely by the well-known ability of mycoplasmas to degrade tritiated thymidine, but likely was the result of rapid dissemination of M. hyorhinis in the lymphocyte culture.; This study demonstrates the potent inhibitory effect exerted by M. hyorhinis in standard lymphocyte proliferation assays in vitro. MSC are efficient vectors of mycoplasma infection, emphasizing the importance of monitoring cell cultures for contamination.</description>
      <pubDate>Fri, 29 Oct 2010 22:58:59 GMT</pubDate>
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