Archives and libraries of the people, by the people, for the people : how to open collections by crowdsourcing at the special library

Archives and libraries have been a storage for the centuries. In the 20th century they were seen as memory organizations, where memories were stored, but also new ones were created. The next step for the librarians and archivists was to be active to collect many kinds of materials about the surrounding society, paying attention to minorities as well. The last step has been to open organizations to co-operate with the clients. Internet has given new kind of possibilities for the participation in the libraries, like crowdsourcing. In this representation I will talk about co-operation and participation and the roles which the librarian can have in co-operation. There can be many kind of motivations for the library and for the clients to cooperate. As a case study I will introduce a collection of rare maps which were donated to the Lapland Department at Rovaniemi City Library. The staff wanted that the maps will be findable, available and usable, so the library co-operated with donator and his fellow experts to make a traditional exhibition and also a webexhibition.publishedVersio

HIF-mediated metabolic switching in bladder outlet obstruction mitigates the relaxing effect of mitochondrial inhibition.

Prior work demonstrated increased levels of hypoxia-inducible factor-1α (HIF-1α) in the bladder following outlet obstruction, associated with bladder growth and fibrosis. Here we hypothesized that HIF induction in outlet obstruction also switches energetic support of contraction from mitochondrial respiration to glycolysis. To address this hypothesis, we created infravesical outlet obstruction in female Sprague-Dawley rats and examined HIF induction and transcriptional activation. HIF-1α increased after 6 weeks of outlet obstruction as assessed by western blotting and yet transcription factor-binding site analysis indicated HIF activation already at 10 days of obstruction. Accumulation HIF-2α and of Arnt2 proteins were found at 10 days, providing an explanation for the lack of correlation between HIF-1α protein and transcriptional activation. HIF signature targets, including Slc2a1, Tpi1, Eno1 and Ldha increased in obstructed compared with sham-operated bladders. The autophagy markers Bnip3 and LC3B-II were also increased at 6 week of obstruction, but electron microscopy did not support mitophagy. Mitochondria were, however, remodeled with increased expression of Cox4 compared with other markers. In keeping with a switch toward glycolytic support of contraction, we found that relaxation by the mitochondrial inhibitor cyanide was reduced in obstructed bladders. This was mimicked by organ culture with the HIF-inducer dimethyloxalylglycine, which also upregulated expression of Ldha. On the basis of these findings, we conclude that HIF activation in outlet obstruction involves mechanisms beyond the accumulation of HIF-1α protein and that it results in a switch of the energetic support of contraction to anaerobic glycolysis. This metabolic adaptation encompasses increased expression of glucose transporters and glycolytic enzymes combined with mitochondrial remodeling. Together, these changes uphold contractility when mitochondrial respiration is limited.Laboratory Investigation advance online publication, 3 March 2014; doi:10.1038/labinvest.2014.48

Non-uniform changes in membrane receptors in the rat urinary bladder following outlet obstruction.

The aim of the present study was to investigate the expression and distribution of membrane receptors after bladder outlet obstruction (BOO). Partial bladder outlet obstruction (BOO) was induced in female rats and bladders were harvested after either 10 days or 6 weeks of BOO. The expression of different receptors was surveyed by microarrays and corroborated by immunohistochemistry and western blotting. A microarray experiment identified 10 membrane receptors that were differentially expressed compared to sham-operated rats including both upregulated and downregulated receptors. Four of these were selected for functional experiments on the basis of magnitude of change and relevance to bladder physiology. At 6 weeks of BOO, maximal contraction was reduced for neuromedin B and vasopressin (AVP), consistent with reductions of receptor mRNA levels. Glycine receptor-induced contraction on the other hand was increased and receptor mRNA expression was accordingly upregulated. Maximal relaxation by the β3-adrenergic receptor agonist CL316243 was reduced as was the receptor mRNA level. Immunohistochemistry supported reduced expression of neuromedin B receptors, V1a receptors and β3-adrenergic receptors, but glycine receptor expression appeared unchanged. Western blotting confirmed repression of V1a receptors and induction of glycine receptors in BOO. mRNA for vasopressin was detectable in the bladder, suggesting local AVP production. We conclude that changes in receptor expression following bladder outlet obstruction are non-uniform. Some receptors are upregulated, conferring increased responsiveness to agonist, whereas others are downregulated, leading to decreased agonist-induced responses. This study might help to select pharmacological agents that are effective in modulating lower urinary tract symptoms in BOO

Association of muscarinic M(3) receptors and Kir6.1 with caveolae in human detrusor muscle.

Caveolae are 50-100nm large membrane invaginations that play a role in cellular signaling. The aim of the present study was to assess whether muscarinic M(3) receptors and the K(ATP) channel subunit Kir6.1 are associated with human detrusor caveolae, and to pharmacologically assess the relevance of this organization for contractility. Detrusor strips were dissected and used in ultrastructural, biochemical and mechanical studies. Caveolae were manipulated by cholesterol desorption using mβcd (methyl-β-cyclodextrin). Mβcd disrupted caveolae and caused a cholesterol-dependent ~3-fold rightward shift of the concentration-response curve for the muscarinic receptor agonist carbachol. The effect of mβcd was inhibited by the K(ATP) blockers glibenclamide, repaglinide and PNU-37883, and it was mimicked by the K(ATP) activator levcromakalim. Immunoelectron microscopy showed muscarinic M(3) receptors and Kir6.1 to be enriched in caveolae. In conclusion, pharmacological K(ATP) channel inhibition antagonizes the effect of caveolae disruption on muscarinic contractility in the human detrusor, and the K(ATP) channel subunit Kir6.1 co-localizes with M(3) receptors in caveolae

Induction of angiotensin converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility.

MicroRNAs have emerged as regulators of smooth muscle cell phenotype with a role in smooth muscle-related disease. Studies have shown that miR-143 and miR-145 are the most highly expressed microRNAs in smooth muscle cells, controlling differentiation and function. The effect of miR-143/145 knockout has been established in the vasculature but not in smooth muscle from other organs. Using knockout mice we found that maximal contraction induced by either depolarization or phosphatase inhibition was reduced in vascular and airway smooth muscle but maintained in the urinary bladder. Furthermore, a reduction of media thickness and reduced expression of differentiation markers was seen in the aorta but not in the bladder. Supporting the view that phenotype switching depends on a tissue-specific target of miR-143/145, we found induction of angiotensin converting enzyme in the aorta but not in the bladder where angiotensin converting enzyme was expressed at a low level. Chronic treatment with angiotensin type-1 receptor antagonist restored contractility in miR-143/145-deficient aorta while leaving bladder contractility unaffected. This shows that tissue-specific targets are critical for the effects of miR-143/145 on smooth muscle differentiation and that angiotensin converting enzyme is one such target

Preoperative Posterior Tilt Increases the Risk of Later Conversion to Arthroplasty After Osteosynthesis for Femoral Neck Fracture

BackgroundFemoral neck fractures (FNFs) are one of the most common injuries in the elderly. Treatment is either internal fixation or primary arthroplasty. The main aim of this study is to assess the risk factors associated with fixation failure leading to further arthroplasty in FNFs treated with cannulated screws.MethodsData on internal fixations of FNFs performed at Turku University Hospital between January 1, 2012 and December 31, 2017 were collected retrospectively from the patient database. Radiographical measurements were performed for preoperative displacement and posterior tilt, postoperative displacement, reduction quality, and implant shaft angle.ResultsAltogether 301 cases were included in the study. The overall reoperation rate was 25% and conversion to arthroplasty was performed in 16% of cases. In the multiple variant analysis, adjusted for age and gender, nondisplaced fractures with a 0°-20° preoperative posterior tilt had a significantly lower risk of later conversion to arthroplasty than did nondisplaced fractures with a ≤0° or ≥20° posterior tilt (odds ratio [OR] 4.0, 95% confidence interval [Cl] 1.8-8.6, P = .0005) and displaced fractures (OR 7.2, 95% CI 3.0-17.4, P P = .2).ConclusionDisplaced fractures and fractures with a preoperative posterior tilt of 20° or Keywordsinternal fixationarthroplastyreoperationfixation failureposterior tiltfemoral neck fracture</div

Regulation of smooth muscle dystrophin and synaptopodin 2 expression by actin polymerization and vascular injury

Producción CientíficaObjective: Actin dynamics in vascular smooth muscle is known to regulate contractile differentiation and may play a role in the pathogenesis of vascular disease. However, the list of genes regulated by actin polymerization in smooth muscle remains incomprehensive. Thus, the objective of this study was to identify actin-regulated genes in smooth muscle and to demonstrate the role of these genes in the regulation of vascular smooth muscle phenotype. Approach and Results: Mouse aortic smooth muscle cells were treated with an actin-stabilizing agent, jasplakinolide, and analyzed by microarrays. Several transcripts were upregulated including both known and previously unknown actin-regulated genes. Dystrophin and synaptopodin 2 were selected for further analysis in models of phenotypic modulation and vascular disease. These genes were highly expressed in differentiated versus synthetic smooth muscle and their expression was promoted by the transcription factors myocardin and myocardin-related transcription factor A. Furthermore, the expression of both synaptopodin 2 and dystrophin was significantly reduced in balloon-injured human arteries. Finally, using a dystrophin mutant mdx mouse and synaptopodin 2 knockdown, we demonstrate that these genes are involved in the regulation of smooth muscle differentiation and function. Conclusions: This study demonstrates novel genes that are promoted by actin polymerization, that regulate smooth muscle function, and that are deregulated in models of vascular disease. Thus, targeting actin polymerization or the genes controlled in this manner can lead to novel therapeutic options against vascular pathologies that involve phenotypic modulation of smooth muscle cells.Instituto de Salud Carlos III - Fondo Europeo de Desarrollo Regional (grant RD12/0042/0006)Ministerio de Economía, Industria y Competitividad (grants BFU2010-15898 and BFU2013-45867-R

Developmental regulation of smooth muscle contraction in the urinary bladder

Smooth muscle cells in the urinary bladder are involved in the control of urine filling and emptying. We have used mice to study the contractile regulation of urinary bladder smooth muscle during the fetal period. We found that nerve-induced contractions are mainly dependent on muscarinic receptor activation in the newborn whereas adult bladders are equally dependent on muscarinic and purinergic receptor activation. Muscarinic receptor-induced contractions are due to activation of the M3 subtype in both adults and newborns. Activator calcium is mainly recruited from the extracellular space via L-type calcium channels in both adult and newborn tissue. The contractile machinery of the newborn’s bladder tissue is more sensitive to calcium which enables contractions at lower intracellular and extracellular calcium concentrations. Non-muscle myosin is contributing to the force development in the newborn but is not the cause for the increased calcium sensitivity. The increased calcium sensitivity is due to a lower phosphatase activity and a lower expression of the myosin light chain phosphatase subunit MYPT1. The contractions induced by muscarinic receptor agonists are characterized by increased phasic activity in the newborn. This activity is not dependent on K+ channels, calcium release from the sarcoplasmic reticulum or gap junctional transmission. Muscarinic receptor stimulation activates T-type calcium channels in the newborn bladder but not in the adult. The main sensitizing pathways, involving protein kinase C (PKC) and Rho-kinase, are established in the newborn tissue. The effects of PKC activation on muscarinic receptor-induced responses differ in newborn and adult tissue. The muscarinic receptor-induced response of the newborn is abolished in the presence of high PKC activation (using PDBu) whereas the response is potentiated in the adult. The phasic component of the response in the newborn bladder is particularly inhibited due to activation of PKC