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Träfflista för sökning "hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) hsv:(Cancer och onkologi) srt2:(2000-2004);srt2:(2004)"

Sökning: hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) hsv:(Cancer och onkologi) > (2000-2004) > (2004)

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31.
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32.
  • Rösch, Frank, et al. (författare)
  • Radiolanthanides in nuclear medicine.
  • 2004
  • Ingår i: Metal ions in biological systems. - 0161-5149. ; 42, s. 77-108
  • Forskningsöversikt (refereegranskat)
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33.
  • Tornblom, M, et al. (författare)
  • Lead time associated with screening for prostate cancer
  • 2004
  • Ingår i: International Journal of Cancer. - John Wiley and Sons Inc.. - 0020-7136. ; 108:1, s. 122-129
  • Tidskriftsartikel (refereegranskat)abstract
    • Screening serum levels of prostate-specific antigen (PSA) is now a major strategy for early detection of prostate cancer (PC). Quantification of the lead time thus obtained is important both for understanding the development of PC and for evaluating the advantages and disadvantages of widespread screening. In our study, 1,233 randomly selected men living in Stockholm in 1988 were invited to participate in an early detection (ED) program, in which suspicious findings provided by digital rectal examination (DRE), transrectal ultrasonography (TRUS) and/or a PSA value greater than or equal to10.0 ng/mL were followed up by biopsy. The cumulative incidence (Kaplan-Meier) of PC in the 946 participants (ED) during 12 years of follow-up was compared to that of an age-matched, randomly selected reference population (RP) of 657 men for whom PSA values (from frozen serum samples) could also be obtained. The PC incidence in men in the RP with PSA values >3.0 ng/mL reached the corresponding level for the ED group after 10.6 years (the "catch-up" point). After 12 years of follow-up, the estimated median lead time for men with PSA values in this interval was 4.5 years in the ED population, compared to 7.8 years in the RP. With 20 years of follow-up, the estimated median lead time of the RP was enhanced to 10.7 years. The lead time in connection with PC was influenced by the initial PSA level (although with large variations), length of follow-up and sensitivity of the ED procedure employed. The ED program described here was not associated with major overdetection.
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34.
  • Ahlberg, Karin, 1965-, et al. (författare)
  • Fatigue, psychological distress, coping and quality of life in patients with uterine cancer.
  • 2004
  • Ingår i: Journal of advanced nursing. - 0309-2402. ; 45:2, s. 205-13
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Cancer-related fatigue (CRF) is a subjectively experienced symptom that is multidimensional and multifactorial. Patients with cancer have identified fatigue as one of the major troubling symptoms and the primary cause of distress in their lives. AIMS: The major aim of the study was to examine how patients diagnosed with uterine cancer describe their experience of fatigue, psychological distress, coping resources and quality of life. A secondary aim was to describe the relationship between selected variables. METHOD: A descriptive and correlational design was used and the study was conducted at a university hospital in Sweden. The study population consisted of women, diagnosed with uterine cancer, who where scheduled to receive curative external radiation therapy. Sixty women participated in the study and data were collected through self-report instruments. Demographic and clinical data were extracted from patient records. The data were collected during year 2000-2002. The Conceptual Model of Symptom Management was used as a framework to guide the study. FINDINGS: Patients experienced a low grade of fatigue and psychological distress, but their functional status and global quality of life was high. Significant correlations were found between general fatigue and anxiety and also between general fatigue and depression. There was a significant negative correlation between general fatigue and coping resources. Depression explained 44% of the variance in general fatigue. CONCLUSIONS: The findings provide knowledge about predictors of CRF in women with uterine cancer, and can serve as a basis for future longitudinal studies in which different prophylactic strategies against therapy-related fatigue are prospectively studied.
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35.
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36.
  • Alonso, A, et al. (författare)
  • VHY, a novel myristoylated testis-restricted dual specificity protein phosphatase related to VHX
  • 2004
  • Ingår i: Journal of Biological Chemistry. - ASBMB. - 1083-351X. ; 279:31, s. 32586-32591
  • Tidskriftsartikel (refereegranskat)abstract
    • The human DUSP15 gene encodes an uncharacterized 235-amino acid member of the subfamily of small dual specificity protein phosphatases related to the Vaccinia virus VH1 phosphatase. Similar to VHR-related MKPX (VHX) (DUSP22), the predicted protein has an N-terminal myristoylation recognition sequence, and we show here that both are indeed modified by the attachment of a myristate to Gly-2. In recognition of this relatedness to VHX, we refer to the DUSP15-encoded protein as VH1-related member Y (VHY). We report that VHY is expressed at high levels in the testis and barely detectable levels in the brain, spinal cord, and thyroid. A VHY-specific antiserum detected a protein with an apparent molecular mass of 26 kDa, and histochemical analysis showed that VHY was readily detectable in pachytene spermatocytes (midstage of meiotic division I) and round spermatids and weakly in Leydig cells ( somatic cells outside of the seminiferous tubules). When expressed in 293T or NIH-3T3 cells, VHY was concentrated at the plasma membrane with some staining of vesicular structures in the Golgi region. Mutation of the myristoylation site Gly-2 abrogated membrane location. Finally, we demonstrate that VHY is an active phosphatase in vitro. We conclude that VHY is a new member of a subgroup of myristoylated VH1-like small dual specificity phosphatases.
37.
  • Alvarado-Kristensson, Maria, et al. (författare)
  • p38-MAPK Signals Survival by Phosphorylation of Caspase-8 and Caspase-3 in Human Neutrophils.
  • 2004
  • Ingår i: Journal of Experimental Medicine. - Rockefeller University Press. - 1540-9538. ; 199:4, s. 449-458
  • Tidskriftsartikel (refereegranskat)abstract
    • Neutrophil apoptosis occurs both in the bloodstream and in the tissue and is considered essential for the resolution of an inflammatory process. Here, we show that p38–mitogen-activated protein kinase (MAPK) associates to caspase-8 and caspase-3 during neutrophil apoptosis and that p38-MAPK activity, previously shown to be a survival signal in these primary cells, correlates with the levels of caspase-8 and caspase-3 phosphorylation. In in vitro experiments, immunoprecipitated active p38-MAPK phosphorylated and inhibited the activity of the active p20 subunits of caspase-8 and caspase-3. Phosphopeptide mapping revealed that these phosphorylations occurred on serine-364 and serine-150, respectively. Introduction of mutated (S150A), but not wild-type, TAT-tagged caspase-3 into primary neutrophils made the Fas-induced apoptotic response insensitive to p38-MAPK inhibition. Consequently, p38-MAPK can directly phosphorylate and inhibit the activities of caspase-8 and caspase-3 and thereby hinder neutrophil apoptosis, and, in so doing, regulate the inflammatory response. This research was originally published in The Journal of Experimental Medicine.
38.
  • Alvarado-Kristensson, Maria (författare)
  • Regulation of neutrophil apoptosis
  • 2004
  • Doktorsavhandling (övrigt vetenskapligt)abstract
    • Popular Abstract in Swedish Humana neutrofiler är vita blodkroppar med den kortaste livslängden. Varje dag frisätts det miljoner neutrofiler från benmärgen till blodet. Från blodbanan är neutrofiler de första celler som anländer och samlas i en infekterad vävnad. Neutrofiler är mest kända för deras anti-mikrobiella funktion. Dessa celler är rustade med olika proteiner för att kunna hitta och döda mikroorganismer. Olyckligtvis, kan inte dessa “vapen” särskilja mellan värdvävnaderna och inkräktarna. Därför leder en förlängd neutrofilreaktion till oavbruten utsöndring av toxiska ämnen som förstör värdvävnader och orsakar organdysfunktion under sjukdomstillstånd som: glomerulonefrit, reumatoid arthrit, hjärtinfarkt, ateroskleros, astma, kronisk bronkit, emfysem och ARDS (akut respiratory distress syndrome). Rekryterade neutrofiler återvinns aldrig till blodet och elimineringen av dessa celler från infektionshärden kommer att avgöra hur snabbt en inflammation läker ut samt graden av vävnadsskada. I blodet och i vävnaderna elimineras neutrofiler antingen genom nekros eller spontan apoptos. I händelse av nekros kommer neutrofilernas innehåll att läcka ut till omgivningen, vilket kommer att ge upphov till än mer vävnadsskada och en förlängd inflammationsreaktion. Om apoptos initieras i cellerna kommer vissa karakteristiska förändringar på cellytan att ske så att omgivande celler kommer att ta upp de apoptotiska neutrofilerna. På så sätt hindras neutrofilernas farligt innehåll att komma i kontakt med omgivningen, samtidigt som cellerna elimineras. Detta kommer att bidra till att begränsa och avsluta inflammationsreaktionen. Valet mellan apoptos eller nekros regleras av lokala faktorer i inflammationshärden. Ett exempel på en sådan faktor är ett protein som heter Fas. Syftet med mina doktorandstudier har varit att studera vilka signalvägar som deltar i regleringen av såväl spontan- som Fas-receptor-potentierad apoptos i humana neutrofiler. I våra utförda studier konstaterar vi att såväl spontan- som Fas-receptor-potentierad apoptos av neutrofiler gynnas av en tillfällig deaktivering av proteinet p38 (p38 mitogen activated protein kinase), samt att proteinet Fas tillfälligt aktiverar ytterligare ett protein, PI3K (phosphatidyl inositol 3-kinase), vilket påskyndar apoptosen än mer i neutrofilerna. Vi har också visat att p38 motverkar Fas-receptor-potentierad aktivering av caspase 8 och caspase 3 (proteiner vilka verkställer apoptos) genom direkt fosforylering (biokemisk förändring som ändrar funktionen hos ett protein) av aminosyrorna serine-364 och serine-150, respektive. Vidare visar våra studier att fosforylering av caspaserna påskyndar deras nedbrytning, vilket minskar deras aktivitet och därmed neutrofilernas apoptos. PP2A (Phospho-serine/-treonine Phosphatase, type 2A) är proteinet som tillfälligt deaktiverar p38 och på så sätt defosforyleras också caspaserna vilket leder till att apoptos påskyndas. Apoptotiska neutrofiler spelar en viktig roll för en snabb läkning av en inflammation. Vetskap om de molekulära mekanismerna som reglerar apotos i neutrofiler kommer att ge en bättre förståelse för ett inflammationsförlopp samt grundläggande kunskaper för utveckling av inflammationsreglerande läkemedel. Rubbningar i det apoptotiska programmet är kända för att vara involverade i många olika sjukdomsbilder. Minskad apoptos leder bl.a. till cancer och autoimmuna sjukdomar, medan en ökning av apoptos leder till neurodegenerativa sjukdomar och AIDS. Det är väldokumenterat att tillförsel av proteinet Fas är ett sätt att inducera apoptos under fysiologiska och patologiska tillstånd. Dysfunktion av Fas-pontentierad-apoptos har visat sig vara inblandad i bland annat carcinogenesis, cancercellers utvecklade resistens mot kemoterapeutiska läkemedel samt autoimmuna sjukdomar.
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39.
40.
  • Arbyn, M, et al. (författare)
  • Virologic versus cytologic triage of women with equivocal pap smears: A meta-analysis of the accuracy to detect high-grade intraepithelial neoplasia
  • 2004
  • Ingår i: Journal of the National Cancer Institute. - Oxford University Press. - 1460-2105. ; 96:4, s. 280-293
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The appropriate management of women with minor cytologic lesions in their cervix is unclear. We performed a meta-analysis to assess the accuracy of human papillomavirus (HPV) DNA testing as an alternative to repeat cytology in women who had equivocal results on a previous Pap smear. Methods: Data were extracted from articles published between 1992 and 2002 that contained results of virologic and cytologic testing followed by colposcopically directed biopsy in women with an index smear showing atypical cells of undetermined significance (ASCUS). Fifteen studies were identified in which HPV triage and the histologic outcome (presence or absence of a cervical intra-epithelial neoplasia of grade 11 or worse [CIN2+]) was documented. Nine, seven, and two studies also documented the accuracy of repeat cytology when the cutoff for abnormal cytology was set at a threshold of ASCUS or worse, low-grade squamous intraepithelial lesion (LSIL) or worse, or high-grade squamous intraepithelial lesion (HSIL) or worse, respectively. Random-effects models were used for pooling of accuracy parameters in case of interstudy heterogeneity. Differences in accuracy were assessed by pooling the ratio of the sensitivity (or specificity) of HPV testing to that of repeat cytology. Results: The sensitivity and specificity were 84.4% (95% confidence interval [CI] = 77.6% to 91.1%) and 72.9% (95% CI = 62.5% to 83.3%), respectively, for HPV testing overall and 94.8% (95% CI = 92.7% to 96.9%) and 67.3% (95% CI = 58.2% to 76.4%), respectively, for HPV testing in the eight studies that used the Hybrid Capture 11 assay. Sensitivity and specificity of repeat cytology at a threshold for abnormal cytology of ASCUS or worse was 81.8% (95% CI = 73.5% to 84.3%) and 57.6% (95% CI = 49.5% to 65.7%), respectively. Repeat cytology that used higher cytologic thresholds yielded substantially lower sensitivity but higher specificity than triage with the Hybrid Capture 11 assay. The ratio of the sensitivity of the Hybrid Capture 11 assay to that of repeat cytology at a threshold of ASCUS or worse pooled from the four studies that used both triage tests was 1.16 (95% CI = 1.04 to 1.29). The specificity ratio was not statistically different from unity. Conclusion: The published literature indicates that the Hybrid Capture 11 assay has improved accuracy (higher sensitivity, similar specificity) than the repeat Pap smear using the threshold of ASCUS for an outcome of CIN2+ among women with equivocal cytologic results. The sensitivity of triage at higher cytologic cutoffs is poor.
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