E-procurement in Public Organization

Tampereen kaupungin kokonaishankinnoista vain kaksi prosenttia tehtiin toiminnanohjausjärjestelmällä vuonna 2013. Järjestelmän matalasta käyttöasteesta johtuen hankintatiedot puuttuvat järjestelmästä, mikä hankaloittaa hankintojen strategista johtamista. Työn taustalla on tarve tehostaa toimintoja ja saada aikaan kustannussäästöjä sekä saada hankinnoista enemmän tietoa niiden tehokkaammaksi johtamiseksi. Tutkimuksen tarkoituksena oli tunnistaa keinoja, joiden avulla Tampereen kaupungin ostamista voidaan kehittää sähköisellä ostojärjestelmällä. Päätavoitteena oli kaupungin ostamisen nykytilan selvittäminen ja siihen soveltuvan sähköisen ratkaisun vaatimusten määrittely. Tässä työssä keskityttiin työn toimeksiantajan Tampereen Logistiikan valitsemien Tampereen kaupungin yksiköiden Infran, Kotihoidon ja Tilakeskuksen ostamisen kehittämiseen. Tutkimus toteutettiin laadullisena monimenetelmäisenä tapaustutkimuksena. Aineistona käytettiin kirjallisuutta, vanhoja Tampereen kaupungin selvityksiä sekä kohdeyksiköiden ja muiden kaupunkien hankinnoista vastaavien henkilöiden haastatteluja. Aikaisempi kirjallisuus on käsitellyt ostamisen suhdetta hankintoihin ja toimitusketjuun sekä tarkastellut sähköistä ostamista keinona tehostaa hankintoja. Tutkimuksen empiriaosuus esittelee ensin havaintoja aikaisemmista tutkimuksista sekä muiden kaupunkien benchmark-analyysistä. Toisessa osassa käsitellään ostotoimintaa ja sen kehitysmahdollisuuksia kohdeorganisaation valikoiduissa yksiköissä. Aineistoanalyysin tuloksena tunnistettiin ostamisen ongelmaksi kirjavat ostoprosessit sekä niistä aiheutuvat prosessikustannukset. Tuloksina saatiin ostamisen asettamia vaatimuksia ostojärjestelmälle, joita ovat noutojen kirjaus ja mobiilikäyttömahdollisuus. Ratkaisuehdotuksena annettiin malli uudesta prosessista, johon sitoutuu vähemmän työaikaa aikaisempaan verrattuna sekä ehdotettiin katalogien käyttöönottamista kaupungin omassa järjestelmässä

Analysis of the potential of cancer cell lines to release tissue factor-containing microvesicles: correlation with tissue factor and PAR2 expression

BackgroundDespite the association of cancer-derived circulating tissue factor (TF)-containing microvesicles and hypercoagulable state, correlations with the incidence of thrombosis remain unclear.MethodsIn this study the upregulation of TF release upon activation of various cancer cell lines, and the correlation with TF and PAR2 expression and/or activity was examined. Microvesicle release was induced by PAR2 activation in seventeen cell lines and released microvesicle density, microvesicle-associated TF activity, and phoshpatidylserine-mediated activity were measured. The time-course for TF release was monitored over 90 min in each cell line. In addition, TF mRNA expression, cellular TF protein and cell-surface TF activities were quantified. Moreover, the relative expression of PAR2 mRNA and cellular protein were analysed. Any correlations between the above parameters were examined by determining the Pearson’s correlation coefficients.ResultsTF release as microvesicles peaked between 30–60 min post-activation in the majority of cell lines tested. The magnitude of the maximal TF release positively correlated with TF mRNA (c = 0.717; p

Discovery of Molecular DNA Methylation-Based Biomarkers through Genome-Wide Analysis of Response Patterns to BCG for Bladder Cancer

Background: Bacillus Calmette-Guérin (BCG) immunotherapy, the standard adjuvant intravesical therapy for some intermediate and most high-risk non-muscle invasive bladder cancers (NMIBCs), suffers from a heterogenous response rate. Molecular markers to help guide responses are scarce and currently not used in the clinical setting. Methods: To identify novel biomarkers and pathways involved in response to BCG immunotherapy, we performed a genome-wide DNA methylation analysis of NMIBCs before BCG therapy. Genome-wide DNA methylation profiles of DNA isolated from tumors of 26 BCG responders and 27 failures were obtained using the Infinium MethylationEPIC BeadChip. Results: Distinct DNA methylation patterns were found by genome-wide analysis in the two groups. Differentially methylated CpG sites were predominantly located in gene promoters and gene bodies associated with bacterial invasion of epithelial cells, chemokine signaling, endocytosis, and focal adhesion. In total, 40 genomic regions with a significant difference in methylation between responders and failures were detected. The differential methylation state of six of these regions, localized in the promoters of the genes GPR158, KLF8, C12orf42, WDR44, FLT1, and CHST11, were internally validated by bisulfite-sequencing. GPR158 promoter hypermethylation was the best predictor of BCG failure with an AUC of 0.809 (p-value < 0.001). Conclusions: Tumors from BCG responders and BCG failures harbor distinct DNA methylation profiles. Differentially methylated DNA regions were detected in genes related to pathways involved in bacterial invasion of cells or focal adhesion. We identified candidate DNA methylation biomarkers that may help to predict patient prognosis after external validation in larger, well-designed cohorts

Hereditary thrombophilia and fetal loss: a prospective follow-up study

Background: As the placental vessels are dependent on the normal balance of procoagulant and anticoagulant mechanisms, inherited thrombophilia may be associated with fetal loss. Objectives: We performed a prospective study to investigate the relation between inherited thrombophilia and fetal loss, and the influence of thromboprophylaxis on pregnancy outcome. Patients and methods: Women were enrolled in the European Prospective Cohort on Thrombophilia (EPCOT). These included women with factor (F)V Leiden or a deficiency of antithrombin, protein C or protein S. Controls were partners or acquaintances of thrombophilic individuals. A total of 191 women (131 with thrombophilia, 60 controls) had a pregnancy outcome during prospective follow-up. Risk of fetal loss and effect of thromboprophylaxis were estimated by frequency calculation and Cox regression modelling. Results: The risk of fetal loss appeared slightly increased in women with thrombophilia without a previous history of fetal loss who did not use any anticoagulants during pregnancy (7/39 vs. 7/51; relative risk 1.4; 95% confidence interval 0.4, 4.7). Per type of defect the relative risk varied only minimally from 1.4 for FV Leiden to 1.6 for antithrombin deficiency compared with control women. Prophylactic anticoagulant treatment during pregnancy in 83 women with thrombophilia differed greatly in type, dose and duration, precluding solid conclusions on the effect of thromboprophylaxis on fetal loss. No clear benefit of anticoagulant prophylaxis was apparent. Conclusions: Women with thrombophilia appear to have an increased risk of fetal loss, although the likelihood of a positive outcome is high in both women with thrombophilia and in controls