Tietosuoja-asetuksen vaatimusten täyttyminen Turun yliopiston henkilörekistereissä

Tämän tutkielman tarkoitus on tutkia Turun yliopiston valmiutta vastata Euroopan parlamentin ja neuvoston asetuksen (EU) 2016/679 eli yleisemmin Tietosuoja-asetuksen asettamiin haasteisiin henkilötietojen käsittelystä organisaation henkilörekistereissä. Tutkielmassa käydään läpi myös yleisemmin suuren organisaation haasteita suoriutua henkilötietojen käsittelystä asetuksen vaatimalla tavalla. Tutkielmassa keskitytään ensin käsittelemään yliopistoa organisaationa sekä sen luonnetta julkisena organisaationa sekä sen keskeisimpiä henkilörekistereitä. Näiden henkilörekisterien henkilötiedon käsittelyn analysoinnin kautta tutkielma pyrkii muodostamaan kuvan yliopistosta henkilötietojen käsittelijänä yleisemmin ilman, että läpikäynti ulotettaisiin jokaiseen organisaation henkilörekisteriin. Tutkielmassa käydään läpi Tietosuoja-asetuksen sisältö niiltä osin kuin sen katsotaan koskettavan tutkielmassa käsiteltäviä henkilörekistereitä. Lisäksi tutkielma keskittyy myös vertaamaan Tietosuoja-asetuksen sisältöä sen edeltäjään, vuonna 1995 julkaistuun Euroopan parlamentin ja neuvoston direktiiviin 95/46/EY. Lopuksi jokainen tutkielmaan valittu henkilörekisteri peilataan Tietosuoja-asetuksen vaatimuksiin ja analysoidaan niiden kyvykkyys vastata henkilötiedon käsittelylle asetettuihin vaatimuksiin laeissa ja asetuksissa. Osana analyysiä käydään läpi myös tutkimuksen aikana henkilötietojen käsittelyyn tehdyt kehitystoimet. Tutkimuksen teoreettinen osuus pohjautuu kokonaisuudessaan Tietosuoja-asetukseen ja sen pohjalta tehtyihin tietosuojaan liittyviin linjauksiin sekä tietosuojalakiin. Tutkielman tuloksena todetaan Turun yliopiston kyenneen vastaamaan Tietosuoja-asetuksen vaatimuksiin kaikkiaan hyvin, mutta tutkielman tuloksena syntyy myös lista henkilörekisterien puutteista ja kehitysehdotuksista kutakin henkilörekisteriä kohden

Pathogenesis of Age-Related Osteoporosis: Impaired Mechano-Responsiveness of Bone Is Not the Culprit

BACKGROUND: According to prevailing understanding, skeletal mechano-responsiveness declines with age and this apparent failure of the mechano-sensory feedback system has been attributed to the gradual bone loss with aging (age-related osteoporosis). The objective of this study was to evaluate whether the capacity of senescent skeleton to respond to increased loading is indeed reduced as compared to young mature skeleton. METHODS AND FINDINGS: 108 male and 101 female rats were randomly assigned into Exercise and Control groups. Exercise groups were subjected to treadmill training either at peak bone mass between 47-61 weeks of age (Mature) or at senescence between 75-102 weeks of age (Senescent). After the training intervention, femoral necks and diaphysis were evaluated with peripheral quantitative computed tomography (pQCT) and mechanical testing; the proximal tibia was assessed with microcomputed tomography (microCT). The microCT analysis revealed that the senescent bone tissue was structurally deteriorated compared to the mature bone tissue, confirming the existence of age-related osteoporosis. As regards the mechano-responsiveness, the used loading resulted in only marginal increases in the bones of the mature animals, while significant exercise-induced increases were observed virtually in all bone traits among the senescent rats. CONCLUSION: The bones of senescent rats displayed a clear ability to respond to an exercise regimen that failed to initiate an adaptive response in mature animals. Thus, our observations suggest that the pathogenesis of age-related osteoporosis is not attributable to impaired mechano-responsiveness of aging skeleton. It also seems that strengthening of even senescent bones is possible--naturally provided that safe and efficient training methods can be developed for the oldest old

Community resilience and cultural sustainability in two Finnish urban neighbourhoods

This study explores how urban cultural environments, and particularly their cultural provision and forms of participation, can foster cultural sustainability in urban communities, namely neighbourhoods. Conceptually, the article situates cultural sustainability within the concept of community resilience to facilitate an understanding of the everyday lives of residents and concerns residents' expectations of the cultural environment and opportunities for cultural participation in two case neighbourhoods in Jyväskylä Finland. Drawing on the mixed-methods approach of the study our findings show that different cultural activities and communities can be central to promoting sustainable urban development. Community resilience as a sense of belonging like neighbourhood-related identity and also as a sense of ownership of place seems strong in various ways, and relation to the cultural participation can be identified. However, from urban cultural policy perspective, the low-threshold participation and opportunities for grassroots cultural activity seem an underexploited resource in the cities, especially when the concept of sustainability is under consideration. Moreover, the negotiation and communication between community actors and public officials deserves a lot of attention while the implementation of urban cultural policy is on focus. From urban cultural policy perspective, it is important to find new ways to measure the direct and indirect impacts of policies. According to findings of the study holistic analysis of residents, actors and institutions viewpoints helps us to understand the practises and processes related to community resilience. All this deserves multidisciplinary research and joint reflection. This approach assists to make sense of how urban cultural policy and cultural participation can support community resilience at community level

Injury incidence and prevalence in Finnish top-level football - one-season prospective cohort study

Ojective: To investigate the injury characteristics in Finnish male football players. Design: One-season prospective epidemiological study. Data were collected via injury reports from the medical staff and directly from the players using the Olso Sports Trauma Research Center Health Questionnaire. Participants: The first team squads of Finnish football league (n = 12 teams, 236 players). Main outcome measurement: Injury incidence. Results: A total of 541 injuries occurred during the exposure of 62 878 hours. Injury incidence per 1000 exposure hours was 8.6 (30.6 in matches and 3.4 in training). A player sustained on average 2.3 (median 2, range 0-13) injuries during the study. Thigh and ankle were the most commonly injured body parts for acute injuries and hip/groin were the most commonly injured body part for overuse injuries. The median absence time for all injuries was 12 (range 0-107) days, 12 (range 0-107) for acute, and 8 (range 0-61) for overuse injuries. Thigh injuries caused the greatest consequences in terms of absence from full participation (median 5 days, range 0-88). Conclusion: Lower limb muscle injuries were the most prevalent injuries in the study. Collecting data directly from the players enabled to report more injuries compared to what was reported only by the medical staff.Peer reviewe

Tenascin-C and fibronectin in normal esophageal mucosa, Barrett's esophagus, dysplasia and adenocarcinoma.

BACKGROUND: Tenascin-C and fibronectin are adhesive glycoproteins modulating the structure of the extracellular matrix and cellular functions. Their expression and function in esophageal adenocarcinoma is poorly known. The aim of this study was to evaluate the expression of tenascin-C and fibronectin in esophageal adenocarcinoma and its precursor stages. RESULTS: Stromal tenascin-C and fibronectin expression were found in all evaluated lesion types. Expression of both molecules increased from gastric metaplasia towards adenocarcinoma (p<0.05). In carcinomas, tenascin-C expression in the bulk was associated with T-stage (p=0.006), presence of lymph node (p=0.004) and distant organ metastases (p=0.007). Abundant tenascin-C expression associated with poor survival (p=0.034) in univariate analysis. Fibronectin expression associated to T-stage (p=0.030). Expression of tenascin-C or fibronectin in the tumor invasive front was not associated to clinicopathological variables or survival. No significant correlation with tumor/stroma percentage, cancer-associated fibroblasts or mean vascular density was observed with either tenascin-C or fibronectin. METHODS: Tenascin-C and fibronectin were stained immunohistochemically and assessed in esophageal specimens from patients with esophageal adenocarcinoma (n=90) or dysplasia (n=30). Structures and lesion were evaluated including normal esophagus (n=77), gastric (n=61) or intestinal (n=51) metaplasia without dysplasia, and low-grade (n=42) or high-grade (n=34) dysplasia, and esophageal adenocarcinoma (n=90). In carcinomas, both bulk and invasive front were separately evaluated. In addition, tumor/stroma percentage, cancer-associated fibroblasts and mean vascular density were evaluated. CONCLUSIONS: Tenascin-C and fibronectin are upregulated in esophageal adenocarcinoma when compared to Barrett's esophagus and dysplasia. Increased tenascin-C expression is associated with metastasis and poor prognosis in esophageal adenocarcinoma.Orion Research FoundationThelma Mäkikyrö FoundationPäivikki and Sakari Sohlberg FoundationGeorg C. and Mary Ehrnroot FoundationSigrid Juselius FoundationThe Finnish Medical FoundationEmil Aaltonen FoundationPublishe

Expression of R-Spondin 1 in Apc(Min/+) Mice Suppresses Growth of Intestinal Adenomas by Altering Wnt and Transforming Growth Factor Beta Signaling

BACKGROUND & AIMS: Mutations in the APC gene and other genes in the Wnt signaling pathway contribute to development of colorectal carcinomas. R-spondins (RSPOs) are secreted proteins that amplify Wnt signaling in intestinal stem cells. Alterations in RSPO genes have been identified in human colorectal tumors. We studied the effects of RSPO1 overexpression in ApcMin/thorn mutant mice. METHODS: An adeno associated viral vector encoding RSPO1-Fc fusion protein, or control vector, was injected into ApcMin/thornmice. Their intestinal crypts were isolated and cultured as organoids. which were incubated with or without RSPO1-Fc and an inhibitor of transforming growth factor beta receptor (TGFBR). Livers were collected from mice and analyzed by immunohistochemistry. Organoids and adenomas were analyzed by quantitative reverse-transcription PCR, single cell RNA sequencing, and immunohistochemistry. RESULTS: Intestines from Apcthorn/thorn mice injected with the vector encoding RSPO1-Fc had significantly deeper crypts, longer villi, with increased EdU labeling, indicating increased proliferation of epithelial cells, in comparison to mice given control vector. AAV-RSPO1-Fctransduced ApcMin/thorn mice also developed fewer and smaller intestinal tumors and had significantly longer survival times. Adenomas of ApcMin/thorn mice injected with the RSPO1-Fc vector showed a rapid increase in apoptosis and in the expression of Wnt target genes, followed by reduced expression of messenger RNAs and proteins regulated by the Wnt pathway, reduced cell proliferation, and less crypt branching than adenomas of mice given the control vector. Addition of RSPO1 reduced the number of adenoma organoids derived from ApcMin/thorn mice and suppressed expression of Wnt target genes but increased phosphorylation of SMAD2 and transcription of genes regulated by SMAD. Inhibition of TGFBR signaling in organoids stimulated with RSPO1-Fc restored organoid formation and expression of genes regulated by Wnt. The TGFBR inhibitor restored apoptosis in adenomas from ApcMin/thorn mice expressing RSPO1Fc back to the same level as in the adenomas from mice given the control vector. CONCLUSIONS: Expression of RSPO1 in ApcMin/thorn mice increases apoptosis and reduces proliferation and Wnt signaling in adenoma cells, resulting in development of fewer and smaller intestinal tumors and longer mouse survival. Addition of RSPO1 to organoids derived from adenomas inhibits their growth and promotes proliferation of intestinal stem cells that retain the APC protein; these effects are reversed by TGFB inhibitor. Strategies to increase the expression of RSPO1 might be developed for the treatment of intestinal adenomas.Peer reviewe