| 1. |
|
|
| 2. |
- Falkenström, Erica, 1966-, et al.
(författare)
-
På spaning efter etik : Etisk kompetens och ansvarstagande för ledning och styrning av hälso- och sjukvården
- 2018
-
Bok (övrigt vetenskapligt/konstnärligt)abstract
- Kraven på vårdens professioner och chefer är höga. De förväntas ge en god och säker vård på lika villkor till hela befolkningen, administrera, prioritera och arbeta kostnadseffektivt. Men hälso- och sjukvården fungerar inte som den ska. Arbetsmiljön är osund, sjuksköterskor lämnar yrket, vården är ojämlik och svårt sjuka patienter får vänta i långa köer. Detta gör att människors liv, hälsa och värdighet står på spel.På spaning efter etik uppmärksammar tre nyckelgrupper av aktörer som genom sina beslut har ett stort inflytande över vårdens villkor: politiker, opolitiska chefstjänstemän och vårdgivarnas högsta chefer i landstingets ledningsorganisation. Hur ser de på sitt etiska ansvar för hälso- och sjukvården? Vilka etiska bedömningar och konsekvensanalyser gör de? Och vilken etisk kompetens fordras för att de ska kunna ta ett etiskt ansvar för vårdens villkor genom ledning, styrning och organisation på den regionala nivån – och därmed för att samhällsmedborgarna ska kunna känna tillit till att vården fungerar som den ska?Boken är ett resultat av ett tvärvetenskapligt empirisk forskningsprojekt, finansierat av AFA Försäkring, som har bedrivits på Stockholms centrum för forskning om offentlig sektor, Score.
|
|
| 3. |
- Olsson, Ulf
(författare)
-
OM FRISKVÅRDSPEDAGOGIK I ARBETSLIVET. : EN O/RÄTTVIS BETRAKTELSE.
- 1993
-
Licentiatavhandling (övrigt vetenskapligt/konstnärligt)abstract
- I fokus för detta arbete står friskvård inom arbetslivet som pedagogisk praktik med hälsoprofilsbedömning, en metod för undersökning och påverkan av människors hälsostatus och hälsovanor, som konkret exempel. En bakgrund till detta är framväxten av insatser för folkhälsa och den ökade betoning av friskvård inom arbetslivet som skett inom såväl privat som offentlig sektor. Friskvård handlar om människors levnadsvanor när det gäller kost, motion, stress, alkohol, tobak m.m.Hälsoprofilsbedömning och friskvårdspedagogik inom arbetslivet ses här ur två olika perspektiv. Ur det ena perspektivet behandlas verksamheten på dess egna villkor - som en metod att inom ramen för arbetslivet få till stånd ner hälsosamma livsstilar genom kontrakt mellan självständiga parter. Det andra perspektivet kan ses som kritiskt granskande. Här ifrågasätts premissema för hälsoprofilsbedömningen utifrån begrepp som makt och disciplinering. En inspirationskälla har därvid bland annat Michel Foucaults arbeten varit. Som empiriskt material för analysen används två avhandlingar som presenterar hälsoprofilbedömningen som metod.Ur dessa båda perspektiv erhålles två olika betraktelser om hälsoprofilsbedömning och friskvårdspedagogik inom arbetslivet - en rättvis och en orättvis. På basis av en kritisk pragmatisk ansats diskuteras möjligheten till ett samtal baserad på relationen mellan de båda betrakelserna.
|
|
| 4. |
|
|
| 5. |
- Chiaka Akuwudike, Pamela, 1987-
(författare)
-
Cellular effects of ionizing radiation : Relevant for understanding cancer risk after medical and environmental radiation exposures
- 2023
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Radiation-induced cancers are stochastic and delayed effects of exposure to ionizing radiation. The dose-response relationship for radiation-induced cancers at both low dose/low dose rates and high doses (doses encountered during radiotherapy) remains unclear. Uncertainties observed in epidemiological studies at low doses and dose rates hamper cancer risk estimation at this dose level. Assessing dose-response relationships for radiotherapy-induced cancers is also complicated due to the inherent difficulty in assessing the doses absorbed by tissues at the site of tumours. In addition, the modulatory effect of chemotherapy on the incidence of radiotherapy-induced cancer risk has been debated. Although included as a modifying factor of the incidence of radiotherapy-induced cancers, results from epidemiological studies do not provide sufficient evidence to support this claim. This thesis summarizes studies conducted to improve the understanding of the association of cancer incidence and radiation dose at clinically relevant (high) doses, low doses and low dose rates, as well as the modulatory role of platinum-based chemotherapy on radiation-induced carcinogenesis. In Paper I, we investigated the competitive relationship between cell killing and the accumulation of DNA damage and genomic instability using two normal cell types (VH10 fibroblasts and AHH-1 lymphoblasts). Dose fractionation schemes were designed based on the cell growth characteristics of each cell type. Cells were irradiated at 0.25, 0.5, 1.0, or 2 Gy per fraction, representing the various dose levels within a radiation field, to simulate the heterogeneous dose distribution across normal tissue during radiotherapy. Following fractionated radiation exposure, the effects on cell growth, cell survival, radiosensitivity, and the accumulation of residual DNA damage and genomic instability were analyzed as a function of dose per fraction and the total absorbed dose. The accumulation of DNA damage and markers of genomic instability associated with DNA damage depended on cell type-specific factors.In Paper II, we investigated the modulatory effects of combining cisplatin and radiation on the accumulation of micronuclei (a biomarker of DNA damage and carcinogenesis) in peripheral blood lymphocytes of patients receiving treatment for gynaecological cancers. We also determined the modulatory effects of the combination of both agents on cell death and cell proliferation, by scoring the frequency of apoptotic and binucleated cells. We compared the frequency of these markers between patients receiving treatment with radiotherapy alone and a combination of cisplatin and radiotherapy. There was a decline in the frequency of micronuclei in patients receiving a combination of cisplatin and radiotherapy.We conducted in vitro experiments in Paper III using AHH-1 and VH10 cells. We investigated the effects of the concurrent combination of cisplatin treatment and multifractionated radiation exposure at 1 Gy per fraction on cell growth, cell survival, cell death, changes in radiosensitivity, accumulation of DNA damage, and other markers of genomic instability as well as the expression of cancer stem cell markers. We also investigated the interaction between cisplatin and radiation exposure in our schedule. The concurrent combination of cisplatin and radiation did not increase the accumulation of markers of genomic instability.In Paper IV, we investigated the short and long-term effects of radiation exposure at low doses and low dose rates on global gene expression, cell growth and cell survival of VH10 fibroblasts to identify unique dose rate signatures that could be useful biomarkers in determining if the application of DDREF is accurate. Except for the differential expression of DMXL2, the long-term effects of LDLDR exposure on global gene expression, cell growth and cell survival of VH10 fibroblasts were negligible. These results suggest that the accumulation of DNA damage and other markers of genomic instability is regulated by cell type-specific factors at these dose levels.
|
|
| 6. |
- López Riego, Milagrosa, 1992-
(författare)
-
Biomarkers of ionising radiation relevant to carcinogenesis : Dose, dose rate and LET dependency of the responses
- 2023
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- A better understanding of the relationship between ionising radiation (IR) dose, dose rate and radiation quality, and the risk of stochastic effects would improve risk extrapolation from atomic bomb survivors’ data. Owing to insufficient statistical power of epidemiological studies to detect excess incidence of cancer following low doses of IR delivered at low dose rates (LDLDR), as typically encountered in most common human exposure scenarios, radiobiological experiments are fundamental to describe the biological effectiveness of LDLDR and to define the underlying molecular mechanisms. DNA damage and downstream effects are major contributors to radiation carcinogenesis, and as such, these processes have been investigated in the context of plausible mechanisms of radiation-induced health effects in the studies compiled in this thesis, using different cell models and appropriate radiation sources. In Paper I, we characterized the energy, activity and dose rate of new low activity gamma and alpha sources of IR, expected to promote small-scale radiation protection research, and used to demonstrate that LDLDR led to an increased micronucleus frequency, a marker of DNA damage, in human osteosarcoma cells as compared to control cells. In Paper II, we used blood from patients undergoing radiological imaging procedures, i.e. PET-CT and scintigraphy, to investigate whether candidate IR biomarkers, i.e. ROS, γH2AX, and expression of a panel of radiation-responsive genes, are altered following in vivo low dose exposure as compared to control samples obtained before the diagnostic procedure. We showed that radiological imaging generally induced weak γH2AX, ROS, and gene expression fold changes at the selected timepoints, although few donors presented stronger responses. The observed mild increase in DNA damage was, nevertheless, coherent with a subsequent DNA damage response. This study also indicated that owing to the heterogeneity of the response across individuals, the discrimination of exposed samples might be complicated in the absence of a control for low dose exposures. The current risk assessment approach for mixed beam exposures, as encountered in space and other exposure scenarios, assumes additivity of effects of each radiation quality component, but some reports, which show synergistic effects instead, are in conflict with this assumption and indicate a potential underestimation of the corresponding cancer risk. In Paper III, we investigated the consistency of the interaction between low and high LET IR in two healthy donors who presented the largest inter- and intra-donor variability following mixed beam exposure in a previous study. Based on nine biological replicates, this study confirmed that combined alpha particles and photon radiation led to a higher cytogenetic damage and gene expression responses than those expected based on simple additivity of effects, but that the interaction was prone to seasonal intra-donor and inter-donor variation for both endpoints. This study additionally showed that IR exposure modified alternative transcription of FDXR and MDM2 in a radiation quality-dependent manner, albeit alternative transcription did not coincide with the mode of interaction between the different radiation qualities. In light of these results, we suggest that the possible interaction between low and high LET IR should be considered in calculating uncertainty of risk for mixed exposures. In Paper IV, we investigated the early- and long-term biological effects of LDLDR gamma radiation as compared to the same doses delivered acutely in human AHH-1 lymphoblasts, using relevant endpoints related to carcinogenesis, i.e. cell viability, clonogenic survival, chromosomal aberrations, cell growth and global gene expression. The results presented in this study are coherent with a potential detrimental effect of 100 mGy, delivered either chronically or acutely, with a clear dose rate effect for chromosomal aberrations and gene expression, which may modulate cancer risk by dose rate-dependent mechanisms.
|
|
| 7. |
|
|
| 8. |
|
|
| 9. |
|
|
| 10. |
|
|
