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| 2. |
- Acosta, Stefan, et al.
(författare)
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Increasing incidence of ruptured abdominal aortic aneurysm : a population-based study
- 2006
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Ingår i: Journal of Vascular Surgery. - : Elsevier BV. - 0741-5214 .- 1097-6809. ; 44:2, s. 237-243
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Tidskriftsartikel (refereegranskat)abstract
- Objective: The aim of the present population-based study was to assess the trends of age- and gender-specific incidence of ruptured abdominal aortic aneurysm (rAAA). Methods. Patients with rAAA from the city of Malmo, Sweden, were studied between 2000 and 2004. An analysis of trends of incidence and mortality of rAAA in Malmo was possible because of a previous population-based study on patients with rAAA between 1971 and 1986 (autopsy rate 85% compared with 25% for the time period 2000 to 2004). The in-hospital registry of Malmo University Hospital and the databases at the Department of Pathology, Malmo, and the Institution of Forensic Medicine, Lund, identified patients with rAAA, and the in-hospital registry identified all elective repairs for AAA. Results. Compared with the time period 1971 to 1986, the overall incidence of rAAA significantly increased from 5.6 (95 % confidence interval [CI], 4.9 to 6.3) to 10.6 (95% CI, 8.9 to 12.4) per 100,000 person-years (standardized mortality ratio, 1.6; 95% CI, 1.0 to 2.1). In men aged 60 to 69 and 70 to 79 years, the incidence increased significantly from 16 (95% CI, 11 to 21) and 56 (95% Cl, 43 to 69) to 46 (95% Cl, 28 to 63) and 117 (95% CI, 84 to 149) per 100,000 person-years, respectively, whereas no increase in the age-specific incidence in women could be demonstrated. The overall incidence of elective repair of AAA increased significantly from 3.4 (95% CI, 2.8 to 4.0) to 7.0 (95% CI, 5.6 to 8.4) per 100,000 person-years and increased most significantly from 12 (95% CI, 3.4 to 32) to 68 (95% CI, 34 to 102) per 100,000 person-years in men aged 80 to 89 years and from 5.1 (95% CI, 2.4 to 9.3) to 28 (95% CI, 15 to 41) per 100,000 person-years in women aged 70 to 79 years. The elective-acute repair ratio in women increased from 2.4 to 5.6 and decreased in men from 2.1 to 1.0. Conclusions: Between 1971 to 1986 and 2000 to 2004, the incidence of rAAA increased significantly, despite a 100% increase in elective repairs and notwithstanding a potential for bias towards underestimation due to lower autopsy rates in recent years. The reason behind this increase is unclear, and further studies are needed to identify risk groups for direction of effective prevention and screening.
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| 4. |
- Alavian Ghavanini, Farzan, 1978, et al.
(författare)
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CMOS considerations in nanoelectromechanical carbon nanotube-based switches
- 2008
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Ingår i: Nanotechnology. - 1361-6528 .- 0957-4484.
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Tidskriftsartikel (refereegranskat)abstract
- In this paper, we focus on critical issues directly related to the viability of carbon nanotube-based nanoelectromechanical switches, to perform their intended functionality as logic and memory elements, through assessment of typical performance parameters with reference to complementary metal-oxide-semiconductor devices. A detailed analysis of performance metrics regarding threshold voltage control, static and dynamic power dissipation, speed, and integration density is presented. Apart from packaging and reliability issues, these switches seem to be competitive in low power, particularly low-standby power, logic and memory applications.
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| 5. |
- Amisten, Stefan, et al.
(författare)
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Gene expression profiling for the identification of G-protein coupled receptors in human platelets
- 2008
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Ingår i: Thrombosis Research. - : Elsevier BV. - 1879-2472 .- 0049-3848. ; 122:1, s. 47-57
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Tidskriftsartikel (refereegranskat)abstract
- INTRODUCTION AND MATERIALS AND METHODS: G-protein coupled receptors (GPCRs) play an important role in platelet aggregation. To identify new platelet GPCRs, a platelet gene expression profile was generated and validated using quantitative real-time PCR. RESULTS: In total, mRNA of 28 GPCR genes was detected in human platelets. The 12 most abundant platelet GPCR transcripts were: thrombin receptor PAR1 (1865+/-178%), ADP receptor P2Y(12) (459+/-88%), succinate receptor 1 (257+/-48%), ADP receptor P2Y(1) (100%), orphan P2RY(10) (68.2+/-3.3%), lysophosphatidic acid receptors GPR23 (48.2+/-11%) and GPR92 (26.1+/-3.3%), adrenergic receptor alpha(2A) (18.4+/-4.4%), orphan EBI2 (6.31+/-0.42), adenosine receptors A(2A) (2.94+/-0.24%) and A(2B) (2.88+/-0.16%) and lysophosphatidic acid receptor LPA(1) (2.59+/-0.39%) (% relative to the chosen calibrator P2Y(1)). A surprising G-protein coupled receptor redundancy was found: two ADP receptors (P2Y(1) and P2Y(12)), three adenosine receptors (A(2A), A(2B), and A(1)), four lysophosphatidic acid receptors (LPA(1), LPA(3), GPR23 and GPR92), two l-glutamate receptors (mGlu(3) and mGlu(4)) and two serotonin receptors (5-HT(1F) and 5-HT(4)). The adenosine receptor A(2B) gene expression was validated with protein expression and functional studies. Western blot confirmed A(2B) receptor protein expression and platelet flow cytometry demonstrated inhibition of the effect of NECA by the adenosine A(2B)-antagonist MRS1754. CONCLUSIONS: We have detected several GPCRs not previously known to be expressed in platelets, including a functional adenosine A(2B) receptor. The findings could improve our understanding of platelet aggregation and provide new targets for drug development.
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| 6. |
- Arvidsson, Susann, 1965-, et al.
(författare)
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Upplevelse av hälsobefrämjande egenvård vid reumatisk sjukdom
- 2009
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Konferensbidrag (refereegranskat)abstract
- BakgrundPersoner med reumatiska sjukdomar skattar sitt hälsostatus lågt. Hälsostatus och tron på den egna förmågan att kunna påverka hälsan påverkar i sin tur valet av egenvårdsbeteenden. Egenvårdsbeteenden är vanliga och kan förhindra försämrad hälsa och förlust av värdefull fysisk och psykisk aktivitet. Kunskaperna är små om hur personer med reumatiska sjukdomar upplever att utföra egenvård. Syftet är därmed att beskriva hur personer med reumatiska sjukdomar erfar att utföra egenvård för att nå hälsa.MetodStudien har en kvalitativ design med en fenomenlogisk ansats och en livsvärldsteoretisk grund. Data har samlats in genom ostrukturerade och öppna intervjuer med 12 personer med olika diagnostiserade reumatiska sjukdomar.ResultatPersoner med reumatiska sjukdomar upplever att egenvård är ett sätt att leva och att det innebär att ständigt vara redo för att förstå och reagera på signaler från den levda kroppen. Egenvård upplevs som en inre dialog inom den levda kroppen, men också en yttre dialog med närmiljön. Egenvård beskrivs också som en maktkamp där personen strävar efter och tvingar sig att kämpa mot sjukdomen och dess konkreta konsekvenser. Egenvården kräver också att val görs. Avgörande för valet är att personen har tillit till sig själv och tror på sin egen förmåga att välja hälsobefrämjande egenvård. Personer med reumatiska sjukdomar prioriterar egenvård som upplevs som positiv och/eller ger en belöning till den levda kroppen.SammanfattningPersoner med reumatiska sjukdomar upplever egenvård som ett sätt att leva och det innebär att vara i beredskap för att förstå och reagera på signaler som den levda kroppen sänder ut. Egenvård kräver dialog, maktkamp och val. Denna kunskap bidrar till en mer fullständig förståelse av faktorer som från ett patientperspektiv är viktiga för hälsan vid kronisk reumatisk sjukdom.
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| 7. |
- Asplund Persson, Anna, 1966-, et al.
(författare)
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Cross-talk between adenosine and the oxatriazole derivative GEA 3175 in platelets
- 2005
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Ingår i: European Journal of Pharmacology. - : Elsevier BV. - 0014-2999 .- 1879-0712. ; 517:3, s. 149-157
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Tidskriftsartikel (refereegranskat)abstract
- We examined the interplay between adenosine and the nitric oxide (NO)-containing oxatriazole derivative GEA 3175 in human platelets. The importance of cyclic guanosine 3′5′-monophosphate (cGMP)-inhibited phosphodiesterases (PDEs) was elucidated by treating the platelets with adenosine combined with either GEA 3175 or the PDE3-inhibitor milrinone. The drug combinations provoked similar cyclic adenosine 3′5′-monophosphate (cAMP) responses. On the contrary, cGMP levels were increased only in GEA 3175-treated platelets. Both drug combinations reduced P-selectin exposure, platelet adhesion and fibrinogen-binding. However, adenosine together with GEA 3175 was more effective in inhibiting platelet aggregation and ATP release. Thrombin-induced rises in cytosolic Ca2+ were suppressed by the two drug combinations. Adenosine administered with GEA 3175 was, however, more effective in reducing Ca2+ influx.In conclusion, the interaction between adenosine and GEA 3175 involves cGMP-mediated inhibition of PDE3. The results also imply that inhibition of Ca2+ influx represent another cGMP-specific mechanism that enhances the effect of adenosine.
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| 8. |
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| 9. |
- Bengtsson, Eva, et al.
(författare)
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Cystatin C and cathepsins in cardiovascular disease.
- 2008
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Ingår i: Frontiers in Bioscience. - 1093-9946. ; 13:1, s. 5780-5786
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Tidskriftsartikel (refereegranskat)abstract
- Cystatin C and cathepsins could play a role in almost all processes involved in atherosclerotic lesion formation by their degradation of extracellular matrix proteins and apolipoprotein B100, the protein moiety of LDL. Several cysteine cathepsins are upregulated in human lesions accompanied by a decrease in cystatin C, the major inhibitor of cysteine cathepsins. Recent research show that atherosclerotic mice deficient in cystatin C display increased elastic lamina degradation as well as larger plaque formation. Cathepsin S- and K-deficient atherosclerotic mice, on the other hand, both have less atherosclerosis, where cathepsin S-/- mice exhibited fewer plaque ruptures and cathepsin K-/- larger foam cells than control mice. This article reviews possible roles of cystatin C and cathepsins in different processes and stages of the atherosclerotic disease.
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| 10. |
- Bengtsson, Eva, et al.
(författare)
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Lack of the Cysteine-Protease Inhibitor Cystatin C Promotes Atherosclerosis in Apolipoprotein E-Deficient Mice.
- 2005
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Ingår i: Arteriosclerosis, Thrombosis and Vascular Biology. - 1524-4636. ; 25:10, s. 2151-2156
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Tidskriftsartikel (refereegranskat)abstract
- Objective - Degradation of extracellular matrix plays an important role in growth and destabilization of atherosclerotic plaques. Cystatin C, inhibitor of the collagen- and elastin-degrading cysteine proteases of the cathepsin family, is produced by virtually all cell types. It is present in the normal artery wall but severely reduced in human atherosclerotic lesions. Methods and Results - To determine the functional role of cystatin C in atherosclerosis, we crossed cystatin C - deficient ( cysC(-/-)) mice with apolipoprotein E - deficient ( apoE(-/-)) mice. After 25 weeks of atherogenic diet, mice lacking apoE and cystatin C (cysC(-/-) apoE(-/-)) had larger subvalvular plaques compared with cysC(+/+) apoE(-/-) mice (766 000 +/- 20 000 mu m(2) per section versus 662 000 +/- 19 000 mu m(2) per section; P = 0.001), suggesting an atheroprotective role of cystatin C. The plaques from cysC(-/-) apoE(-/-) mice were characterized by increased total macrophage content. To determine which cellular source is important for the antiatherosclerotic effect of cystatin C, we performed bone marrow transplantations. ApoE(-/-) mice were transplanted with either cysC(-/-) apoE(+/+) or cysC(+/+) apoE(-/-) bone marrow. No significant differences in plaque area, macrophage, collagen, or lipid content of subvalvular lesions between the 2 groups were detected. Conclusions - The result suggests that the protective role of cystatin C in atherosclerosis is dependent primarily on its expression in nonhematopoietic cell types.
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