Liselotte Schäfer Elinder

Prof. Liselotte Schäfer Elinder

orcid

Research Focus & Metrics

Academic Career Length

38Years (1989-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 November 1994 in The American Journal of Cardiology
Verified
Journal Article
Closed access
GWGöran Walldius
Göran Walldius
UEUno Erikson
Uno Erikson
AOAnders G. Olsson
Anders G. Olsson
LBLott Bergstrand
Lott Bergstrand
KHKarin Hådell
Karin Hådell
IHIngar Holme
Ingar Holme

1 May 1999 in Clinical and Experimental Immunology
Verified
Journal Article
Closed access
PDF file
YHY H Huang
Y H Huang
LELiselotte Schäfer Elinder
Liselotte Schäfer Elinder
RWR Wu
R Wu
HCHans-Erik Claesson
Hans-Erik Claesson
JFJohan Frostegard
Johan Frostegard

1 March 1997 in BMJ
Verified
Journal Article
Closed access
MKMargareta Kristenson
Margareta Kristenson
BZBo Ziedén
Bo Ziedén
ZKZita Kucinskienë
Zita Kucinskienë
AAAlgis Abaravicius
Algis Abaravicius
LRLaima Razinkovienë
Laima Razinkovienë
AOAnders G Olsson
Anders G Olsson
Objective: To investigate possible risk factors and mechanisms behind the four times higher and diverging mortality from coronary heart disease in Lithuanian compared with Swedish middle aged men. Design: Concomitant cross sectional comparison of randomly selected 50 year old men without serious acute or chronic disease. Methods and equipment were identical or highly standardised between the centres. Setting: LinkÖping (Sweden) and Vilnius (Lithuania). Subjects: 101 and 109 men aged 50 in LinkÖping and Vilnius respectively. Main outcome measures: Anthropometric data, blood pressure, smoking, plasma lipid and lipoprotein concentrations, susceptibility of low density lipoprotein to oxidation, and plasma concentrations of fat soluble antioxidant vitamins. Results: Systolic blood pressure was higher (141 v 133 mm Hg, P<0.01), smoking habits were similar, and plasma total cholesterol (5.10 v 5.49 mmol/l, P<0.01) and low density lipoprotein cholesterol (3.30 v 3.68 mmol/l, P<0.01) lower in men from Vilnius compared with those from LinkÖping. Triglyceride, high density lipoprotein cholesterol, and Lp(a) lipoprotein concentrations did not differ between the two groups. The resistance of low density lipoprotein to oxidation was lower in the men from Vilnius; lag phase was 67.6 v 79.5 minutes (P<0.001). Also lower in the men from Vilnius were mean plasma concentrations of lipid soluble antioxidant vitamins (ß carotene 377 v 510 nmol/l, P<0.01; lycopene 327 v 615 nmol/l, P<0.001; and lipid adjusted tocopherol 0.25 v 0.46 µmol/mmol, P<0.001. Tocopherol concentration did not differ). Regression analysis showed that the lag phase was still significantly shorter by 10 minutes in men from Vilnius when the influence of other known factors was taken into account. Conclusions: The high mortality from coronary heart disease in Lithuania is not caused by traditional risk factors alone. Mechanisms related to antioxidant state may be important. Key messages: Mortality from coronary heart disease in 50-54 year old men is four times higher in Lithuania than in Sweden Differences in traditional risk factors for coronary heart disease in 50 year old men in LinkÖping (Sweden) and Vilnius (Lithuania) were small–systolic blood pressure was higher in men from Vilnius, but total and low density lipoprotein cholesterol concentrations were lower and smoking habits similar The resistance of low density lipoprotein to oxidation was lower in men from Vilnius and remained after adjustment for antioxidant vitamin concentrations Plasma concentrations of the antioxidant vitamins, ß carotene, lycopene, and lipid adjusted tocopherol were lower in men from Vilnius; tocopherol did not differ Mechanisms related to antioxidant state may be important in explaining the much higher mortality from coronary heart disease in Lithuanian compared with Swedish middle aged men

1 January 1991 in Journal of Investigative Dermatology
Verified
Journal Article
Closed access
LELiselotte Schäfer Elinder
Liselotte Schäfer Elinder
KKKnud Kragballe
Knud Kragballe

1 November 2013 in Research in Developmental Disabilities
Verified
Journal Article
Open access
HBHelena Bergström
Helena Bergström
MHMaria Hagstromer
Maria Hagstromer
JHJan Hagberg
Jan Hagberg
LELiselotte Schäfer Elinder
Liselotte Schäfer Elinder
People with ID have an increased risk for unhealthy diets, physical inactivity and weight disturbances. The aim of the current study was to investigate the effectiveness of a novel and complex intervention to improve diet and physical activity, targeting both caregivers and residents, in community residences for people with ID. A three component intervention based on Social Cognitive Theory was developed, including: (1) appointment of a health ambassador in each community residence attending network meetings, (2) a study circle for caregivers, and (3) a health course for the residents. The intervention lasted for 12-16 months and allowed for some local tailoring. A cluster randomised controlled trial, randomised at residence level, was conducted to evaluate the effects of the intervention. Thirty community residences for people with mild or moderate ID in Stockholm County, Sweden, were included. A total of 130 participants, 74 women and 56 men aged 20-66 years, entered, and 129 participants completed the study. The primary outcome was physical activity, measured by pedometry. Secondary outcomes were BMI, waist circumference, dietary quality measured by digital photography, satisfaction with life assessed with a scale, and work routines assessed with a questionnaire. Outcomes were related to intervention fidelity. A positive intervention effect was found on physical activity, with an average increase of 1608 steps/day among participants in the intervention group (P=0.045). The effect size was 0.29 (Cohen's d). The type of residence was found to be an effect moderator. A positive intervention effect was found as well on work routines, with an average increase of 7.1 percentage points on a self-assessment scale among residences in the intervention group (P=0.016). No significant effects were found on BMI, waist circumference, dietary quality, or satisfaction with life. In conclusion, this innovative intervention was effective in improving physical activity and work routines. It is likely that even greater effects could be achieved by improvements in implementation strategies, leading to higher fidelity.

1 May 1997 in Arteriosclerosis, Thrombosis, and Vascular Biology
Verified
Journal Article
Closed access
JFJohan Frostegard
Johan Frostegard
YHYi Hui Huang
Yi Hui Huang
JRJohan Rönnelid
Johan Rönnelid
LELiselotte Schäfer Elinder
Liselotte Schäfer Elinder
Platelet activating factor (PAF) is a phospholipid with proinflammatory and thrombogenic properties, which has been implicated in inflammatory disorders including vasculitis and asthma. PAF-like compounds are present in oxidized LDL (oxLDL), which has been detected in the atherosclerotic lesion, where it may activate monocytes, macrophages, and T cells. OxLDL may therefore both initiate and perpetuate inflammatory reactions in the artery wall. Herein we demonstrate that PAF has the capacity to induce enhanced interferon gamma (IFN-γ) secretion in peripheral blood mononuclear leukocytes (PBMCs), as does oxLDL. Both oxLDL- and PAF-induced IFN-γ secretions were inhibited by a specific PAF-receptor antagonist, WEB 2170. PAF-like lipids in oxLDL could thus be responsible for oxLDL-induced activation of immune-competent cells. The effects of PAF and oxLDL were inhibited by antibodies to major histocompatibility complex class II and thus depend on accessory cells like monocytes. Both PAF and oxLDL induced tumor necrosis factor-α (TNF-α) synthesis in peripheral blood. PAF-mediated TNF-α production was inhibited by WEB 2170, whereas oxLDL-induced TNF-α was only partially inhibited. These findings indicate that both PAF and oxLDL have the capacity to induce TNF-α, which may increase atherogenesis due to its pleiotropic proinflammatory effects. Our findings suggest that the PAF receptor plays an important role in the inflammatory component of atherosclerosis.