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  • 1.
    Blom, Hans
    et al.
    KTH, School of Engineering Sciences (SCI), Applied Physics, Cell Physics. KTH, Centres, Science for Life Laboratory, SciLifeLab.
    Brismar, Hjalmar
    KTH, School of Engineering Sciences (SCI), Applied Physics, Cell Physics. KTH, Centres, Science for Life Laboratory, SciLifeLab.
    STED microscopy: increased resolution for medical research?2014In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 276, no 6, p. 560-578Article, review/survey (Refereed)
    Abstract [en]

    Optical imaging is crucial for addressing fundamental problems in all areas of life science. With the use of confocal and two-photon fluorescence microscopy, complex dynamic structures and functions in a plethora of tissue and cell types have been visualized. However, the resolution of classical' optical imaging methods is poor due to the diffraction limit and does not allow resolution of the cellular microcosmos. On the other hand, the novel stimulated emission depletion (STED) microscopy technique, because of its targeted on/off-switching of fluorescence, is not hampered by a diffraction-limited resolution barrier. STED microscopy can therefore provide much sharper images, permitting nanoscale visualization by sequential imaging of individual-labelled biomolecules, which should allow previous findings to be reinvestigated and provide novel information. The aim of this review is to highlight promising developments in and applications of STED microscopy and their impact on unresolved issues in biomedical science.

  • 2.
    Grankvist, R.
    et al.
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neuroradiol, S-17176 Stockholm, Sweden..
    Jensen-Urstad, M.
    Karolinska Inst, Karolinska Univ Hosp, Dept Cardiol, Stockholm, Sweden..
    Clarke, J.
    Karolinska Inst, Dept Cell & Mol Biol & Med, Stockholm, Sweden..
    Lehtinen, M.
    Karolinska Inst, Dept Cell & Mol Biol & Med, Stockholm, Sweden..
    Little, P.
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neuroradiol, S-17176 Stockholm, Sweden..
    Lundberg, J.
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neuroradiol, S-17176 Stockholm, Sweden..
    Arnberg, F.
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neuroradiol, S-17176 Stockholm, Sweden..
    Jonsson, Stefan
    KTH, School of Industrial Engineering and Management (ITM), Materials Science and Engineering. Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neuroradiol, S-17176 Stockholm, Sweden.
    Chien, K. R.
    Karolinska Inst, Dept Cell & Mol Biol & Med, Stockholm, Sweden..
    Holmin, S.
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neuroradiol, S-17176 Stockholm, Sweden..
    Superselective endovascular tissue access using trans-vessel wall technique: feasibility study for treatment applications in heart, pancreas and kidney in swine2019In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 285, no 4, p. 398-406Article in journal (Refereed)
    Abstract [en]

    Objectives. With the emergence of targeted cell transplantation and gene therapy, there is a need for minimally invasive tissue access to facilitate delivery of therapeutic substrate. The objective of this study was to demonstrate the suitability of an endovascular device which is able to directly access tissue and deliver therapeutic agent to the heart, kidney and pancreas without need to seal the penetration site. Methods. In vivo experiments were performed in 30 swine, including subgroups with follow-up to evaluate complications. The previously described trans-vessel wall (VW) device was modified to be sharper and not require tip detachment to seal the VW. Injections into targets in the heart (n = 13, 24-h follow-up n = 5, 72-h follow-up n = 3), kidney (n = 8, 14-day follow-up n = 3) and pancreas (n = 5) were performed. Some animals were used for multiple organ injections. Follow-up consisted of clinical monitoring, angiography and necropsy. Transvenous (in heart) and transarterial approaches (in heart, kidney and pancreas) were used. Injections were targeted towards the subepicardium, endomyocardium, pancreas head and tail, and kidney subcapsular space and cortex. Results. Injections were successful in target organs, visualized by intraparenchymal contrast on fluoroscopy and by necropsy. No serious complications (defined as heart failure or persistent arrhythmia, haemorrhage requiring treatment or acute kidney injury) were encountered over a total of 157 injections. Conclusions. The trans-VW device can achieve superselective injections to the heart, pancreas and kidney for delivery of therapeutic substances without tip detachment. All parts of these organs including the subepicardium, pancreas tail and renal subcapsular space can be efficiently reached.

  • 3. Grans, H.
    et al.
    Nilsson, Peter
    KTH, School of Biotechnology (BIO), Proteomics.
    Evengard, B.
    Gene expression profiling in the chronic fatigue syndrome2005In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 258, no 4, p. 388-390Article in journal (Refereed)
  • 4.
    Hansson, Sven Ove
    KTH, School of Architecture and the Built Environment (ABE), Philosophy and History of Technology, Philosophy.
    Homoeopathy and consumers' right to know2013In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 274, no 5, p. 493-493Article in journal (Refereed)
  • 5.
    Hansson, Sven Ove
    KTH, School of Architecture and the Built Environment (ABE), Philosophy and History of Technology, Philosophy.
    Reply to the comment from C Fiori and D Martinez on my article 'Homoeopathy and consumers' right to know'2013In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 274, no 5, p. 495-495Article in journal (Refereed)
  • 6. Janszky, I
    et al.
    Ericson, Mats
    KTH, School of Technology and Health (STH), Ergonomics (Closed 20130701).
    Lekander, M
    Blom, M
    Buhlin, K
    Georgiades, A
    Ahnve, S
    Inflammatory markers and heart rate variability in women with coronary heart disease2004In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 256, no 5, p. 421-428Article in journal (Refereed)
    Abstract [en]

    Purpose. Both heart rate variability (HRV) and inflammatory markers are carrying prognostic information in coronary heart disease (CHD), however, we know of no studies examining their relation in CHD. The aim of this study, therefore, was,to assess the association between HRV and inflammatory activity, as reflected by the levels of interleukin-6 (IL-6), IL-1 receptor antagonist (IL-1ra) and C-reactive protein (CRP). Subjects and methods. Consecutive women patients who survived hospitalization for acute myocardial infarction, and/or underwent a percutaneous transluminal coronary angioplasty or a coronary artery bypass grafting were included and evaluated in a stable condition 1 year after the index events. An ambulatory 24-h ECG was recorded during normal activities. SDNN index (mean of the standard deviations of all normal to normal intervals for all 5-min segments of the entire recording) and the following frequency domain parameters were assessed: total power, high frequency (HF) power, low frequency (LF) power and very low frequency (VLF) power. Levels of high-sensitivity CRP were measured by nephelometry, IL-6 and IL-1ra concentrations were determined by enzyme immunoassay. Results. Levels of IL-6 showed an inverse relation with HRV measures even after controlling for potential confounding factors. The P-values were 0.02, 0.04, 0.01, 0.03, 0.18 for the multivariate association with SDDN index, total power, VLF power, LF power and HF power respectively. In contrast, the inverse relationship between HRV measures and CRP or IL-1ra levels were weak and nonsignificant. Correlation coefficients for the relationship between IL-6 and HRV measures were both uni- and multivariately higher than for the relationship between HRV measures and any other factors evaluated in this study. Conclusion. Concentration of IL-6 showed a negative, independent association with HRV in women with CHD. Thus, increased inflammatory activity, as reflected by IL-6 levels, may represent a new auxiliary mechanism linking decreased HRV to poor prognosis in CHD.

  • 7. Janszky, I.
    et al.
    Ericson, Mats
    KTH, School of Technology and Health (STH), Ergonomics (Closed 20130701).
    Mittleman, M. A.
    Wamala, S.
    Al-Khalili, F.
    Schenck-Gustafsson, K.
    Orth-Gomer, K.
    Heart rate variability in long-term risk assessment in middle-aged women with coronary heart disease: The Stockholm Female Coronary Risk Study2004In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 255, no 1, p. 13-21Article in journal (Refereed)
    Abstract [en]

    Objectives. Low heart rate variability (HRV) is associated with poor prognosis after acute coronary events in men. In women, the prognostic impact is not well documented. The objective of this study was to assess the long-term predictive power of HRV on mortality amongst middle-aged women with coronary heart disease (CHD). Design, Settings and Subjects. Consecutive women below 65 years hospitalized for an acute coronary syndrome during a 3-year period in Stockholm were examined for cardiovascular prognostic factors including HRV, and followed for a median of 9 years. An ambulatory 24-h electrocardiograph was recorded during normal activities, 3-6 months after hospitalization. SDNN index (mean of the standard deviations of all normal to normal intervals for all 5-min segments of the entire recording) and the following frequency domain parameters were assessed: total power, high-frequency (HF) power, low-frequency (LF) power, very-low frequency (VLF) power and LF/HF ratio. Using Cox proportional hazards regression, the hazard ratios (HR) for each 25% decrease of the HRV parameters were assessed. Results. After controlling for the independent, significant predictors of mortality amongst the clinical variables, the following HRV parameters were found to be significant predictors of all-cause mortality: SDNN index [HR 1.56, 95% confidence intervals (CI) 1.19-2.05], total power (HR 1.21, 95% CI 1.08-1.35), VLF power (HR 1.22, 95% CI 1.09-1.36), LF power (HR 1.18 95%, CI 1.07-1.30) and HF power (HR 1.18, 95% CI 1.05-1.33). The results were essentially the same when cardiovascular mortality was used as end-points. The HRV parameters were stronger predictors of mortality in the first 5 years following the index event. Conclusion. Low HRV is a predictor of long-term mortality amongst middle-aged women with CHD when measured 3-6 months after hospitalization for an acute coronary syndrome, even after controlling for established clinical prognostic markers.

  • 8. Jensen-Urstad, M
    et al.
    Jensen-Urstad, K
    Ericson, Mats
    KTH, School of Technology and Health (STH), Ergonomics.
    Johansson, J
    Heart rate variability is related to leucocyte count in men and to blood lipoproteins in women in a healthy population of 35-year-old subjects.1998In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 243, no 1, p. 33-40Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: To investigate if, in a healthy randomly-selected population of 35-year-old men and women, there already is a relation between decreased heart rate variability and conventional risk factors for cardiovascular disease.

    BACKGROUND: Analysis of heart rate variability (HRV) has been used for estimating tonic autonomic activity. HRV is reduced in patients with various cardiovascular diseases. If a decreased HRV is a late phenomenon in the progression of cardiovascular disease, or if it parallels or even precedes manifest disease is unknown.

    DESIGN: Spectral analysis of HRV was made from 24-hour ambulatory electrocardiograms in a randomised population of healthy 35-year-old men (n = 63) and women (n = 70). The different spectral indices of HRV were analysed against gender, leucocyte count (previously described as an independent risk factor for cardiovascular disease), blood lipoproteins, smoking, heredity, body mass index (BMI) and systolic blood pressure.

    SETTING: A research centre of general medicine and a university hospital.

    RESULTS: Mean heart rate was lower, total power (TP), very low frequency power (VLF) and low frequency power (LF) were higher in men than in women. In women TP, VLF and LF were negatively correlated to BMI, smoking, triglycerides and positively correlated to HDL cholesterol. TP and VLF were also negatively correlated to risk factor score. High frequency power (HF), a marker of parasympathetic activity, was positively related to HDL cholesterol. In men, at daytime, TP, VLF, LF and HF were negatively correlated to leucocyte count. TP, VLF and LF were also negatively correlated to triglycerides and VLF also to risk factor score.

    CONCLUSIONS: There are correlations between HRV and known risk factors for cardiovascular disease already in a healthy 35-year-old population. A novel observation is the relationship in men between leucocyte count and heart rate variability.

  • 9. Malarstig, A.
    et al.
    Silveira, A.
    Wagsater, D.
    Ohrvik, J.
    Backlund, A.
    Samnegård, Ann
    Khademi, M.
    Hellenius, M. -L
    Leander, K.
    Olsson, T.
    Uhlén, Mathias
    KTH, School of Biotechnology (BIO), Proteomics.
    de Faire, U.
    Eriksson, P.
    Hamsten, A.
    Plasma CD93 concentration is a potential novel biomarker for coronary artery disease2011In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 270, no 3, p. 229-236Article in journal (Refereed)
    Abstract [en]

    Objectives. A common nonsynonymous single nucleotide polymorphism (SNP) in the CD93 gene (rs3746731, Pro541Ser) has been associated with risk of coronary artery disease (CAD). CD93 is a transmembrane glycoprotein, which is detectable in soluble form in human plasma. We investigated whether the concentration of soluble CD93 in plasma is related to risk of myocardial infarction (MI) and CAD, using a case-control study of premature MI (n = 764) and a nested case-control analysis of a longitudinal cohort study of 60-year-old subjects (analysis comprising 844 of 4232 subjects enrolled at baseline). In addition, SNPs in the CD93 gene were studied in relation to plasma CD93 concentration and CD93 mRNA expression. Methods and Results. A sensitive and specific enzyme-linked immunosorbent assay was established for determination of the plasma CD93 concentration. Subjects were divided into three groups according to tertiles of the distribution of CD93 concentration. Lower odds ratios for risk of MI and incidence of CAD were observed in the middle CD93 tertile (142-173 mu g L(-1)): odds ratio (95% confidence interval), 0.69 (0.49-0.97) and 0.61 (0.40-0.94), respectively. These associations were independent of traditional CAD risk factors. The minor allele of a SNP in the 3' untranslated region of CD93(rs2749812) was associated with increased plasma CD93 concentrations (P = 0.03) and increased CD93 mRNA expression levels (P = 0.02). Conclusion. The results of the present study suggest that the concentration of soluble CD93 in plasma is a potential novel biomarker for CAD, including MI.

  • 10. Perisic, L.
    et al.
    Aldi, S.
    Sun, Y.
    Folkersen, L.
    Razuvaev, A.
    Roy, J.
    Lengquist, M.
    Akesson, S.
    Wheelock, C. E.
    Maegdefessel, L.
    Gabrielsen, A.
    Odeberg, Jacob
    KTH, School of Biotechnology (BIO), Proteomics and Nanobiotechnology. KTH, Centres, Science for Life Laboratory, SciLifeLab. Department of Medicine, Karolinska Institute, Stockholm, Sweden.
    Hansson, G. K.
    Paulsson-Berne, G.
    Hedin, U.
    Gene expression signatures, pathways and networks in carotid atherosclerosis2016In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 279, no 3, p. 293-308Article in journal (Refereed)
    Abstract [en]

    BackgroundEmbolism from unstable atheromas in the carotid bifurcation is a major cause of stroke. Here, we analysed gene expression in endarterectomies from patients with symptomatic (S) and asymptomatic (AS) carotid stenosis to identify pathways linked to plaque instability. MethodsMicroarrays were prepared from plaques (n = 127) and peripheral blood samples (n = 96) of S and AS patients. Gene set enrichment, pathway mapping and network analyses of differentially expressed genes were performed. ResultsThese studies revealed upregulation of haemoglobin metabolism (P = 2.20E-05) and bone resorption (P = 9.63E-04) in S patients. Analysis of subgroups of patients indicated enrichment of calcification and osteoblast differentiation in S patients on statins, as well as inflammation and apoptosis in plaques removed >1 month compared to <2 weeks after symptom. By prediction profiling, a panel of 30 genes, mostly transcription factors, discriminated between plaques from S versus AS patients with 78% accuracy. By meta-analysis, common gene networks associated with atherosclerosis mapped to hypoxia, chemokines, calcification, actin cytoskeleton and extracellular matrix. A set of dysregulated genes (LMOD1, SYNPO2, PLIN2 and PPBP) previously not described in atherosclerosis were identified from microarrays and validated by quantitative PCR and immunohistochemistry. ConclusionsOur findings confirmed a central role for inflammation and proteases in plaque instability, and highlighted haemoglobin metabolism and bone resorption as important pathways. Subgroup analysis suggested prolonged inflammation following the symptoms of plaque instability and calcification as a possible stabilizing mechanism by statins. In addition, transcriptional regulation may play an important role in the determination of plaque phenotype. The results from this study will serve as a basis for further exploration of molecular signatures in carotid atherosclerosis.

  • 11. Pontén, F.
    et al.
    Schwenk, Jochen M.
    KTH, School of Biotechnology (BIO), Proteomics (closed 20130101). KTH, Centres, Science for Life Laboratory, SciLifeLab.
    Asplund, A.
    Edqvist, P. -HD.
    The Human Protein Atlas as a proteomic resource for biomarker discovery2011In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 270, no 5, p. 428-446Article, review/survey (Refereed)
    Abstract [en]

    The analysis of tissue-specific expression at both the gene and protein levels is vital for understanding human biology and disease. Antibody-based proteomics provides a strategy for the systematic generation of antibodies against all human proteins to combine with protein profiling in tissues and cells using tissue microarrays, immunohistochemistry and immunofluorescence. The Human Protein Atlas project was launched in 2003 with the aim of creating a map of protein expression patterns in normal cells, tissues and cancer. At present, 11 200 unique proteins corresponding to over 50% of all human protein encoding genes have been analysed. All protein expression data, including underlying high-resolution images, are published on the free and publically available Human Protein Atlas portal (http://www.proteinatlas.org). This database provides an important source of information for numerous biomedical research projects, including biomarker discovery efforts. Moreover, the global analysis of how our genome is expressed at the protein level has provided basic knowledge on the ubiquitous expression of a large proportion of our proteins and revealed the paucity of cell-andtissue-type-specific proteins.

  • 12. Sarkar, N.
    et al.
    Ruck, A.
    Kallner, G.
    Y-Hassan, S.
    Blomberg, P.
    Islam, K. B.
    Van Der Linden, J.
    Lindblom, D.
    Nygren, A. T.
    Lind, B.
    Brodin, Lars-Åke
    Drvota, V.
    Sylven, C.
    Effects of intramyocardial injection of phVEGF-A(165) as sole therapy in patients with refractory coronary artery disease - 12-month follow-up: Angiogenic gene therapy2001In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 250, no 5, p. 373-381Article in journal (Refereed)
    Abstract [en]

    Objective. To test the safety and bioactivity of phVEGF-A(165) after intramyocardial injection during 12-month follow-up. Design. Open-labelled study. Subjects. Inclusion criteria were angina pectoris, Canadian Cardiovascular Society (CCS) class III-IV, unamenable to further revascularization, ejection fraction (EF) >30%, perfusion defects extending over >10% of the anterolateral left ventricle wall detectable with adenosine single photon emission computerized tomography (SPECT) and at least one patent vessel visible by coronary angiography. Seven of 39 patients referred for gene therapy were included. Intervention. Via a mini-thoracotomy under general anaesthesia, phVEGF-A(165) was injected directly into the myocardium at four sites in the anterolateral region of the left ventricle. Results. Operative procedures were uneventful. Perioperative release of myocardial markers and electrocardiogram (ECG) changes were detected in two patients. There were no perioperative deaths but one patient died 7 months postoperatively because of myocardial infarction. Plasma vascular endothelial growth factor (VEGF)-A levels increased two to threefold peaking 6 days postoperatively (P<0.004) and returning to baseline by day 30. A significant reduction in angina pectoris was reported. The CCS class improved from 3.30.2 to 1.9 +/-0.3 (P<0.01) and nitroglycerine intake decreased from 3915 to 12 +/-5 tablets week(-1) (P<0.001) 2 months after gene transfer. Improvements remained after 12 months when nitroglycerine consumption approached zero. Improved myocardial function in the phVEGF-A(165) injection region was documented in all patients (P<0.016) by tissue velocity imaging (TVI). Reduced reversible ischaemia was detected by adenosine SPECT in four patients. Improved collateralization was detected in four patients with coronary angiography. Conclusion. Intramyocardial injection of phVEGF-A(165) is safe and may lead to improved myocardial perfusion and function with longstanding symptomatic relief in end-stage angina pectoris. Based on these results this therapeutic potential is being tested in a double-blind placebo controlled multicentre trial, EUROINJECT ONE.

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