| 1. |
- Warkentin, Siegbert, et al.
(författare)
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rCBF pathology in Alzheimer's disease is associated with slow processing speed
- 2008
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Ingår i: Neuropsychologia. - : Elsevier BV. - 1873-3514 .- 0028-3932. ; 46:5, s. 1193-1200
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Tidskriftsartikel (refereegranskat)abstract
- Decreased information processing speed (mental slowing) is a known sequelae of many brain disorders, and can be assessed by continuous naming tasks. Functional imaging studies have shown that pause and articulation times in continuous speech are normally associated with different brain regions, but knowledge about such association in dementia is lacking. We therefore tested the hypothesis that perfusion deficits in Alzheimer's disease (AD) are not only associated with slower processing, but also with these speech measures. Using regional cerebral blood flow (rCBF) measurements during the performance of a continuous colour and form-naming task, we found that naming speed was substantially slower in AD patients than in controls. This slower naming was exclusively determined by an increase in mean pause time, and only to a limited extent by articulation time. The increased pause time was uniquely associated with temporo-parietal rCBF reductions of the patients, while articulation was not. By contrast, the rCBF of healthy elderly control subjects was consistently accompanied by substantially shorter articulation and pause times, although the naming measures were not statistically associated with rCBF. These findings suggest that pause time (in contrast to articulation time) may serve as a sensitive measure in the assessment of information processing speed deficits in dementia, by virtue of its close association with brain pathology. (C) 2007 Elsevier Ltd. All rights reserved.
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| 2. |
- Möller, Karin, 1962, et al.
(författare)
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Avanta versus Swanson silicone implants in the MCP joint--a prospective, randomized comparison of 30 patients followed for 2 years
- 2005
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Ingår i: J Hand Surg [Br]. - : SAGE Publications. - 0266-7681. ; 30:1, s. 8-13
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Tidskriftsartikel (refereegranskat)abstract
- The results of Swanson and Avanta metacarpophalangeal joint arthroplasties in rheumatoid patients were compared in a prospective, randomized study of 30 patients (120 implants). At 2-year follow-up, grip strength was measured, hand function was assessed with the Sollerman test and the subjective outcome was determined with visual analogue scores. With both implants ulnar deviation and flexion deformities decreased, and there was no difference between the groups. The increase in range of motion was 7 degrees greater with Avanta implants than with Swanson implants. Grip strength and hand function were unaltered but the visual analogue scales showed decreased pain levels and subjective improvements in hand function, grip strength and cosmesis. Twenty-four of 30 patients were satisfied. Fracture of the silicone spacer occurred with 12 Avanta (20%) and eight Swanson implants (13%), with a higher fracture frequency in men.
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| 3. |
- Aldonyte, Ruta, et al.
(författare)
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Concentration-dependent effects of native and polymerised alpha 1-antitrypsin on primary human monocytes, in vitro
- 2004
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Ingår i: BMC Cell Biology. - : Springer Science and Business Media LLC. - 1471-2121. ; 5
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Tidskriftsartikel (refereegranskat)abstract
- Background: alpha1-antitrypsin (AAT) is one of the major serine proteinase inhibitors controlling proteinases in many biological pathways. There is increasing evidence that AAT is able to exert other than antiproteolytic effects. To further examine this question we compared how various doses of the native (inhibitory) and the polymerised (non- inhibitory) molecular form of AAT affect pro-inflammatory responses in human monocytes, in vitro. Human monocytes isolated from different donors were exposed to the native or polymerised form of AAT at concentrations of 0.01, 0.02, 0.05, 0.1, 0.5 and 1 mg/ml for 18 h, and analysed to determine the release of cytokines and to detect the activity of NF-kappaB. Results: We found that native and polymerised AAT at lower concentrations, such as 0.1 mg/ml, enhance expression of TNFalpha (10.9- and 4.8-fold, p < 0.001), IL-6 (22.8- and 23.4-fold, p < 0.001), IL-8 (2.4- and 5.5-fold, p < 0.001) and MCP-1 (8.3- and 7.7-fold, p < 0.001), respectively, compared to buffer exposed cells or cells treated with higher doses of AAT ( 0.5 and 1 mg/ml). In parallel to increased cytokine levels, low concentrations of either conformation of AAT (0.02-0.1 mg/ml) induced NF-kappaB p50 activation, while 1 mg/ml of either conformation of AAT suppressed the activity of NF-kappaB, compared to controls. Conclusions: The observations reported here provide further support for a central role of AAT in inflammation, both as a regulator of proteinase activity, and as a signalling molecule for the expression of pro-inflammatory molecules. This latter role is dependent on the concentration of AAT, rather than on its proteinase inhibitory activity.
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| 4. |
- Subramaniyam, Devipriya, et al.
(författare)
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TNF-alpha-induced self expression in human lung endothelial cells is inhibited by native and oxidized alpha 1-antitrypsin
- 2008
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Ingår i: International Journal of Biochemistry & Cell Biology. - : Elsevier BV. - 1878-5875 .- 1357-2725. ; 40:2, s. 258-271
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Tidskriftsartikel (refereegranskat)abstract
- Endothelial cells are among the main physiological targets of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha). In endothelial cells TNF-alpha elicits a broad spectrum of biological effects including differentiation, proliferation and apoptosis. alpha 1-antitrypsin (AAT), an endogenous inhibitor of serine proteases plays a vital role in protecting host tissue from proteolytic injury at sites of inflammation. Recently, it has been shown that AAT can be internalized by pulmonary endothelial cells, raising speculation that it may modulate endothelial cell function in addition to suppressing protease activity. Using Affymetrix microarray technology, real time PCR and ELISA methods we have investigated the effects of AAT on un-stimulated and TNF-alpha stimulated human primary lung microvascular endothelial cell gene expression and protein secretion. We find that AAT and TNF-alpha generally induced expression of distinct gene families with AAT exhibiting little activity in terms of inflammatory gene expression. Approximately 25% of genes up regulated by TNF-alpha were inhibited by co-administration of AAT including TNF-alpha-induced self expression. Surprisingly, the effects of AAT on TNF-alpha-induced self expression was inhibited equally well by oxidized AAT, a modified form of AAT, which lacks serine protease inhibitor activity. Overall, the pattern of gene expression regulated by native and oxidized AAT was similar with neither inducing pro-inflammatory gene expression. These findings suggest that inhibitory effects of native and oxidized forms of AAT on TNF-alpha stimulated gene expression may play an important role in limiting the uncontrolled endothelial cell activation and vascular injury in inflammatory disease.
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| 5. |
- Hadimeri, Henrik, et al.
(författare)
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Dimensions of Arteriovenous Fistulas in Patients with Autosomal Dominant Polycystic Kidney Disease
- 2000
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Ingår i: Nephron. Clinical practice. - Basel : S. Karger. - 1660-8151 .- 2235-3186. ; 85:1, s. 50-53
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Tidskriftsartikel (refereegranskat)abstract
- Background/Aim: Aneurysms are known manifestations of autosomal dominant polycystic kidney disease (ADPKD). We investigated whether the dimensions of arteriovenous fistulas created for performance of haemodialysis were affected by the original disease.Methods: The lumen diameter of the fistula was studied by ultrasound in 19 patients with ADPKD and in 19 control patients. The patients’ sex, age, the duration of their fistulas, haemoglobin values and blood pressure levels were similar in both groups. The monitoring was performed along the forearm part of the vein, and the maximal diameter was measured. The diameters at the two needle insertion sites were also measured.Results: The ADPKD patients had a significantly higher fistula diameter than the control patients: 12 (range 8–19) mm versus 8 (range 6–24) mm at the widest level (p = 0.003). There were no significant differences in the diameters at the needle insertion sites.Conclusion: The receiving veins of arteriovenous fistulas in patients with ADPKD have an abnormality that causes a greater than normal dilatation in response to the arterialization. We postulate that this phenomenon is linked with the increased prevalence of aneurysms in ADPKD.
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| 6. |
- Heyde, Christoph-E, et al.
(författare)
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Pitfalls and complications in the treatment of cervical spine fractures in patients with ankylosing spondylitis.
- 2008
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Ingår i: Patient safety in surgery. - : Springer Science and Business Media LLC. - 1754-9493. ; 2
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Forskningsöversikt (refereegranskat)abstract
- Patients with ankylosing spondylitis are at significant risk for sustaining cervical spine injuries following trauma predisposed by kyphosis, stiffness and osteoporotic bone quality of the spine. The risk of sustaining neurological deficits in this patient population is higher than average. The present review article provides an outline on the specific injury patterns in the cervical spine, diagnostic algorithms and specific treatment modalities dictated by the underlying disease in patients with ankylosing spondylitis. An emphasis is placed on the risks and complication patterns in the treatment of these rare, but challenging injuries.
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| 7. |
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| 8. |
- Askling, Johan, et al.
(författare)
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Cancer risk in patients with rheumatoid arthritis treated with anti-tumor necrosis factor alpha therapies : does the risk change with the time since start of treatment?
- 2009
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Ingår i: Arthritis and Rheumatism. - : Wiley. - 0004-3591 .- 1529-0131. ; 60:11, s. 3180-3189
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE:To determine the short-term and medium-term risks of cancer in patients receiving anti-tumor necrosis factor alpha (anti-TNFalpha) therapies that have proven effective in the treatment of chronic inflammatory conditions.METHODS:By linking together data from the Swedish Biologics Register, Swedish registers of RA, and the Swedish Cancer Register, we identified and analyzed for cancer occurrence a national cohort of 6,366 patients with RA who first started anti-TNF therapy between January 1999 and July 2006. As comparators, we used a national biologics-naive RA cohort (n = 61,160), a cohort of RA patients newly starting methotrexate (n = 5,989), a cohort of RA patients newly starting disease-modifying antirheumatic drug combination therapy (n = 1,838), and the general population of Sweden. Relative risks (RRs) were estimated using Cox regression analyses, examining overall RR as well as RR by time since the first start of anti-TNF therapy, by the duration of active anti-TNF therapy, and by the anti-TNF agent received.RESULTS:During 25,693 person-years of followup in 6,366 patients newly starting anti-TNF, 240 first cancers occurred, yielding an RR of 1.00 (95% confidence interval 0.86-1.15) versus the biologics-naive RA cohort, and similar RRs versus the other 2 RA comparators. RRs did not increase with increasing time since the start of anti-TNF therapy, nor with the cumulative duration of active anti-TNF therapy. During the first year following the first treatment start, but not thereafter, dissimilar cancer risks for adalimumab, etanercept, and infliximab were observed.CONCLUSION:During the first 6 years after the start of anti-TNF therapy in routine care, no overall elevation of cancer risk and no increase with followup time were observed.
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| 9. |
- Haglund, Marie, et al.
(författare)
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Kontrastnefropati efter datortomografi. Hydrering och anpassad kontrastmedelsdos ger bästa profylax
- 2005
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Ingår i: Läkartidningen. - 0023-7205. ; 102:40, s. 2864-2870
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Tidskriftsartikel (refereegranskat)abstract
- Nefrotoxicitet efter kontrastmedelstillförsel, räknat som en 25-procentig stegring av kreatinin i plasma, förekom hos 12 procent i en oselekterad grupp patienter som genomgått datortomografi. Generell arterioskleros kan läggas till övriga kända riskfaktorer för utveckling av kontrastmedelsnefrotoxicitet. Uppskattning av njurfunktion, t ex med hjälp av lämplig formel, bör göras före kontrastmedelstillförsel, särskilt hos patienter över 70 års ålder. För att minimera risken för njurpåverkan bör kontrastmedelsdosen uttryckt i gram jod understiga det numeriska värdet av den glomerulära filtrationshastigheten (GFR) uttryckt i ml/min.
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| 10. |
- Windahl, Sara H, 1971, et al.
(författare)
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Identification of Target Cells for the Genomic Effects of Estrogens in Bone
- 2007
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Ingår i: Endocrinology. - : The Endocrine Society. - 0013-7227 .- 1945-7170. ; 148:12, s. 5688-95
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Tidskriftsartikel (refereegranskat)abstract
- Estrogen has bone protective effects, but the exact mechanism behind these effects remains unclear. The aim of the present study was to identify the primary target cells in bone for the classical genomic effects of estrogens in vivo. For this purpose we have used reporter mice with a luciferase gene under the control of three estrogen-responsive elements (EREs), enabling detection of in vivo activation of gene transcription. Three-month-old ovariectomized mice were treated with a single dose (50microg/kg) 17beta-estradiol (E2). Luciferase activity was analysed in several tissues and in different bone marrow-derived lymphocyte enriched/depleted preparations using MacsMouse CD19 (for B lymphocytes) or CD90 (for T lymphocytes) MicroBeads. Histological characterization of cells with high luciferase content was performed using immunohistochemistry. Both cortical bone and bone marrow displayed a rapid (within 1h) and pronounced E2-induced increase in luciferase activity. The luciferase activity in total bone marrow and in bone marrow depleted of lymphocytes was increased 6-8 times more than in either B lymphocyte and T lymphocyte enriched cell fractions 4h after the E2-injection, demonstrating that mature lymphocytes are not major direct targets for the genomic effect of estrogens in bone. Immunohistochemistry identified clear luciferase staining in hypertrophic growth plate chondrocytes, megakaryocytes, osteoblasts and lining cells, while no staining was seen in proliferative chondrocyte. Although most of the osteocytes did not display any detectable luciferase staining, a subpopulation of osteocytes both in cortical and trabecular bone stained positive for luciferase. In conclusion, hypertrophic growth plate chondrocytes, megakaryocytes, osteoblasts, lining cells and a subpopulation of osteocytes were identified to respond to estrogen via the classical ERE-mediated genomic pathway in bone. Furthermore, our findings indicate that possible direct estrogenic effects on the majority of osteocytes, not staining positive for luciferase, on proliferative chondrocytes and on mature lymphocytes are mediated by non-ERE actions.
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