21 results on '"Rosengren L"'
Search Results
2. Glial fibrillary acidic protein: a potential biomarker for progression in multiple sclerosis
- Author
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Axelsson, M., Malmeström, C., Nilsson, S., Haghighi, S., Rosengren, L., and Lycke, J.
- Published
- 2011
- Full Text
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3. Serum levels of S100B, S100A1B and S100BB are all related to outcome after severe traumatic brain injury
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Nylén, K., Öst, M., Csajbok, L. Z., Nilsson, I., Hall, C., Blennow, K., Nellgård, B., and Rosengren, L.
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- 2008
- Full Text
- View/download PDF
4. Increased cerebrospinal fluid levels of glial fibrillary acidic protein (GFAp) in Lyme neuroborreliosis
- Author
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Dotevall, L., Hagberg, L., and Rosengren, L. E.
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- 1996
- Full Text
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5. Chlorpromazine treatment of blood-brain barrier dysfunction a quantitative and fluorescence microscopical study on small cerebral stab wounds in the rat
- Author
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Rosengren, L. E. and Persson, L. I.
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- 1979
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6. The influence of early protein-calorie malnutrition and postnatal rehabilitation on levels of a brain-specific protein (S 100) in discrete rat brain areas
- Author
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Wroński, A., Haglid, K. G., Rosengren, L., Rönnbäck, L., and Sourander, P.
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- 1982
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7. Exposure of the cat brain surface to neurosurgical irrigation fluids, hydrogen peroxide and air. Quantitative assay of blood-brain barrier dysfunction
- Author
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Vällfors, B., Rosengren, L. E., and Persson, L. I.
- Published
- 1982
- Full Text
- View/download PDF
8. Decreased morphine intake by opiate addicted rats administered zimelidine, a 5-HT uptake inhibitor
- Author
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Rönnbäck, L., Zeuchner, J., Rosengren, L., Wronski, A., and Ögren, S. O.
- Published
- 1983
- Full Text
- View/download PDF
9. Effects of trichloroethylene inhalation on proteins of the gerbil brain
- Author
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Haglid, K. G., Kjellstrand, P., Rosengren, L., Wroński, A., and Briving, C.
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- 1980
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10. Fettbestimmung
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Gottlieb-Röse, Eichloff, Grimmer, Röhrig, van Lennep, D. P. Ross, Ruys, J. D., Bremer, W., Greifenhagen, W., Huyge, C., Bonnema, A. A., König, C. J., Moog, W. C., Orla-Jensen, van Haarst, J., Siegfeld, M., Richter, O., Droop Ross, H., Gerber, Wendler, Sichler, A., Golding, J., Hesse, Kundrat, Fr., Rosam, A., Bloor, W. R., Lellan, B. G., Harding, E. P., Parkin, G., Porcher, Ch., Utt, A. A. A., Halverson, J. O., Redmond, N. G., Klein, Janoss, Lichtenberg, H. F., Rosengren, L. Fr., Weibull, Mats, Rusche, Lindet, L., Boes, J., and Weyland, H.
- Published
- 1919
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11. Zur Untersuchung und Beurteilung der Milch Konservierung der für die Analyse bestimmten Milchproben
- Author
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Rocques, X., Hinard, G., Corlay, Denigès, G., Tillmans, J., Splittgerber, A., Riffart, H., Dubosq, Kooper, W. D., Sirot, M., Joret, G., Heckmann, E., Jordis, E., Winter, J., Parmentier, E., Winter, J., Pritzker, J., Stoecklin, Fischer, Ph., Henderson, J. B., Meston, L. A., Pliester, A. C., Monier-Williams, G. W., Mollenhauer, Emil, Binaghi, R., Flohil, J. Th., Jackson, L. C., McNab, L., Rothera, A. C., Ackermann, E., Mai, Rothenfusser, Wiegner, Georg, Bull, Sleeter, Lührig, H., Kressner, L., Gerb, W., Lieber, G. D., Pfyl, B., Turnau, R., Kreidl, A., Lenk, E., Sobbe, O. v., Eichloff, Grimmer, Adorjan, J., van Lennep, D. P. Ross, Ruys, J. D., Brewer, W., Greifenhagen, W., Huyge, C., Bonnema, A. A., König, C. J., Moog, W. C., Orla-Jensen, van Haarst, J., Siegfeld, M., Richter, O., Droop, H., Richmond, Gerber, Wendler, Sichler, A., Golding, J., Hesse, Kundrat, Fr., Rosam, A., Bloor, W. R., McLellan, B. G., Harding, E. P., Parkin, G., Porcher, Ch., Utt, C. A. A., Halvesonm, J. O., Redmond, G., Klein, Janoss, Hesse, Lichtenberg, H. F., Rosengren, L. Fr., Rusche, Lindet, L., Hesse, Boes, J., and Weyland, H.
- Published
- 1919
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12. Do patients with large vessel occlusion ischemic stroke harboring prestroke disability benefit from thrombectomy?
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Larsson A, Karlsson C, Rentzos A, Schumacher M, Abrahamson M, Allardt A, Brederlau A, Ceder E, Davidson M, Dunker D, Gunnarsson T, Holmegaard L, Jerndal M, Karlsson JE, Nordanstig A, Redfors P, Rosengren L, Tatlisumak T, and Jood K
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- Female, Humans, Retrospective Studies, Thrombectomy, Treatment Outcome, Brain Ischemia complications, Brain Ischemia surgery, Endovascular Procedures, Ischemic Stroke, Stroke complications, Stroke surgery
- Abstract
Objectives: Evidence of endovascular treatment (EVT) for acute large vessel occlusion (LVO) ischemic stroke in patients harboring substantial prestroke disability is lacking due to their exclusion from randomized trials. Here, we used routine care observational data to compare outcomes in patients with and without prestroke disability receiving EVT for LVO ischemic stroke., Methods: Consecutive patients undergoing EVT for acute LVO ischemic stroke at the Sahlgrenska University Hospital from January 1st, 2015 to March 31st, 2018 were registered in the Sahlgrenska Stroke Recanalization Registry. Pre- and poststroke functional levels were assessed by the modified Rankin Scale (mRS). Outcomes were recanalization rate (mTICI = 2b/3), symptomatic intracranial hemorrhage [sICH], complications during hospital stay, and return to prestroke functional level and mortality at 3 months., Results: Among 591 patients, 90 had prestroke disability (mRS ≥ 3). The latter group were older, more often female, had more comorbidities and higher NIHSS scores before intervention compared to patients without prestroke disability. Recanalization rates (80.0% vs 85.0%, p = 0.211), sICH (2.2% vs 6.3% p = 0.086) and the proportion of patients returning to prestroke functional level (22.7% vs 14.8% p = 0.062) did not significantly differ between those with and without prestroke disability. Patients with prestroke disability had higher complication rates during hospital stay (55.2% vs 40.1% p < 0.01) and mortality at 3 months (48.9% vs 24.3% p < 0.001)., Conclusion: One of five with prestroke disability treated with thrombectomy for a LVO ischemic stroke returned to their prestroke functional level. However, compared to patients without prestroke disability, mortality at 3 months was higher.
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- 2020
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13. Circulating neurofilament light in ischemic stroke: temporal profile and outcome prediction.
- Author
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Pedersen A, Stanne TM, Nilsson S, Klasson S, Rosengren L, Holmegaard L, Jood K, Blennow K, Zetterberg H, and Jern C
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- Adult, Aged, Brain Ischemia blood, Female, Humans, Male, Middle Aged, Recovery of Function, Biomarkers blood, Neurofilament Proteins blood, Stroke blood
- Abstract
Background and Purpose: Neurofilament light chain (NfL) is a marker of neuroaxonal damage. We aimed to study associations between serum NfL (sNfL) concentrations at different time points after ischemic stroke and outcomes., Methods: We prospectively included ischemic stroke cases (n = 595, mean age 59 years, 64% males) and assessed outcomes by both the modified Rankin Scale (mRS) and the NIH stroke scale (NIHSS) at 3 months and by mRS at 2 years. In a subsample, long-term (7-year) outcomes were also assessed by both mRS and NIHSS. We used the ultrasensitive single-molecule array assay to measure sNfL in the acute phase (range 1-14, median 4 days), after 3 months and 7 years in cases and once in controls (n = 595)., Results: Acute-phase sNfL increased by the time to blood-draw and highest concentrations were observed at 3 months post-stroke. High sNfL associated to stroke severity and poor outcomes, and both associations were strongest for 3-month sNfL. After adjusting for age, previous stroke, stroke severity, and day of blood draw, 3-month sNfL was significantly associated to both outcomes at all time points (p < 0.01 throughout). For all main etiological subtypes, both acute phase and 3-month sNfL were significantly higher than in controls, but the dynamics of sNfL differed by stroke subtype., Conclusions: The results from this study inform on sNfL in ischemic stroke and subtypes over time, and show that sNfL predicts short- and long-term neurological and functional outcomes. Our findings suggest a potential utility of sNfL in ischemic stroke outcome prediction.
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- 2019
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14. Serum S-100B protein levels in patients with herpes simplex encephalitis and tick-borne encephalitis--a marker of CNS damage during the initial stage of disease.
- Author
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Studahl M, Günther G, and Rosengren L
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- Adult, Aged, Aged, 80 and over, Disease Progression, Encephalitis, Herpes Simplex cerebrospinal fluid, Encephalitis, Tick-Borne cerebrospinal fluid, Female, Follow-Up Studies, Humans, Male, Middle Aged, Nerve Growth Factors cerebrospinal fluid, S100 Calcium Binding Protein beta Subunit, S100 Proteins cerebrospinal fluid, Time Factors, Encephalitis, Herpes Simplex blood, Encephalitis, Tick-Borne blood, Nerve Growth Factors blood, S100 Proteins blood
- Abstract
Background and Purpose: This study was mainly aimed at the comparative analysis of serum S-100B protein in patients with herpes simplex encephalitis (HSE) and tick-borne encephalitis (TBE). S-100B protein is an established biochemical marker of astroglial damage in central nervous system (CNS) injury., Methods: Serum levels of S-100B were measured using a commercial immunolumino-metric assay (LIA)., Results: Patients with HSE (n = 17) had significantly higher levels of S-100B with median 0.351 microg/l (range 0.017-0.636) compared to patients with TBE (n = 15), who had 0.04 microg/l (range 0.001-0.542) (p < 0.001), as well as controls (n = 17) 0.054 (range 0.004-0.214) (p < 0.001). 11/17 patients with HSE had serum S-100B levels above 0.2 microg/l, in contrast to 1/15 patients with TBE and 1/17 of the control patients. The patients with HSE with serum levels below 0.2 microg/l had a mean 3.2 days disease duration, while patients with levels above 0.2 microg/l had 6 days disease duration., Conclusions: The serum levels of S-100B in the acute stage of disease were significantly higher in patients with HSE than in patients with TBE or controls. A role for the use of serum S-100B in monitoring CNS damage during initial stage of disease in HSE is suggested.
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- 2009
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15. Explorative investigation of biomarkers of brain damage and coagulation system activation in clinical stroke differentiation.
- Author
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Undén J, Strandberg K, Malm J, Campbell E, Rosengren L, Stenflo J, Norrving B, Romner B, Lindgren A, and Andsberg G
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- Aged, Biomarkers blood, Brain, Brain Injuries blood, Brain Injuries metabolism, Brain Ischemia blood, Brain Ischemia diagnosis, Brain Ischemia metabolism, Cerebral Hemorrhage blood, Cerebral Hemorrhage diagnosis, Cerebral Hemorrhage metabolism, Diagnosis, Differential, Enzyme-Linked Immunosorbent Assay, Female, Humans, Male, Middle Aged, Prospective Studies, S100 Calcium Binding Protein beta Subunit, Stroke blood, Stroke metabolism, Brain Injuries diagnosis, Glial Fibrillary Acidic Protein blood, Nerve Growth Factors blood, Phosphopyruvate Hydratase blood, Protein C Inhibitor blood, S100 Proteins blood, Stroke diagnosis
- Abstract
Introduction: A simple and accurate method of differentiating ischemic stroke and intracerebral hemorrhage (ICH) is potentially useful to facilitate acute therapeutic management. Blood measurements of biomarkers of brain damage and activation of the coagulation system may potentially serve as novel diagnostic tools for stroke subtypes., Methods: Ninety-seven stroke patients were prospectively investigated in a multicenter design with blood levels of brain biomarkers S100B, neuron specific enolase (NSE), glial fibrillary acidic protein (GFAP) as well as a coagulation biomarker, activated protein C-protein C inhibitor complex (APC-PCI), within 24 hours of symptom onset., Results: Eighty-three patients (86%) had ischemic stroke and fourteen patients (14%) had ICH. There were no differences in S100B (p=0.13) and NSE (p=0.67) levels between patients with ischemic stroke or ICH. However, GFAP levels were significantly higher in ICH patients (p=0.0057). APC-PCI levels were higher in larger ischemic strokes (p=0.020). The combination of GFAP and APC-PCI levels, in patients with NIHSS score more than 3, had a sensitivity and negative predictive value of 100% for ICH in our material (p=0.0052)., Conclusion: This exploratory study indicated that blood levels of biomarkers GFAP and APC-PCI, prior to neuroimaging, may rule out ICH in a mixed stroke population.
- Published
- 2009
- Full Text
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16. CSF neurofilament protein (NFL) -- a marker of active HIV-related neurodegeneration.
- Author
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Abdulle S, Mellgren A, Brew BJ, Cinque P, Hagberg L, Price RW, Rosengren L, and Gisslén M
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- AIDS Dementia Complex cerebrospinal fluid, AIDS Dementia Complex complications, AIDS Dementia Complex therapy, AIDS-Related Opportunistic Infections cerebrospinal fluid, AIDS-Related Opportunistic Infections complications, AIDS-Related Opportunistic Infections therapy, Antiretroviral Therapy, Highly Active methods, CD4-Positive T-Lymphocytes pathology, Cell Count methods, Enzyme-Linked Immunosorbent Assay methods, HIV Infections therapy, Humans, Neurodegenerative Diseases therapy, Statistics, Nonparametric, HIV Infections cerebrospinal fluid, HIV Infections complications, Neurodegenerative Diseases cerebrospinal fluid, Neurodegenerative Diseases etiology, Neurofilament Proteins cerebrospinal fluid
- Abstract
Background and Methods: The light subunit of the neurofilament protein (NFL), a major structural component of myelinated axons, is a sensitive indicator of axonal injury in the central nervous system (CNS) in a variety of neurodegenerative disorders. Cerebrospinal fluid (CSF) NFL concentrations were measured by ELISA (normal < 250 ng/l) in archived samples from 210 HIV-infected patients not taking antiretroviral treatment: 55 with AIDS dementia complex (ADC), 44 with various CNS opportunistic infections/tumours (CNS OIs), 95 without neurological symptoms or signs, and 16 with primary HIV infection (PHI). The effect of highly active antiretroviral treatment (HAART) was studied by repeated CSF sampling in four of the ADC patients initiating treatment., Results: CSF NFL concentrations were significantly higher in patients with ADC (median 2590 ng/l, IQR 780-7360) and CNS OIs (2315 ng/l, 985-7390 ng/l) than in neuroasymptomatic patients (<250 ng/l, <250-300) or PHI (<250 ng/l, <250-280), p < 0.001. Among patients with ADC, those with more severe disease (stage 2-4) had higher levels than those with milder disease (stage 0.5-1), p < 0.01. CSF NFL declined during HAART to the limit of detection in parallel with virological response and neurological improvement in ADC.CSF NFL concentrations were higher in neuroasymptomatic patients with lower CD4-cell strata than higher, p < 0.001. This increase was less marked than in the ADC patients and noted in 26/58 neuroasymptomatic patients with CD4 counts <200/microl compared to 1/37 with CD4-cells > or =200/microl., Conclusions: The findings of this study support the value of CSF NFL as a useful marker of ongoing CNS damage in HIV infection. Markedly elevated CSF NFL concentrations in patients without CNS OIs are associated with ADC, follow the grade of severity, and decrease after initiation of effective antiretroviral treatment. Nearly all previously suggested CSF markers of ADC relate to immune activation or HIV viral load that do not directly indicate brain injury. By contrast NFL is a sensitive marker of such injury, and should prove useful in evaluating the presence and activity of ongoing CNS injury in HIV infection.
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- 2007
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17. Incidence and pathogenesis of clinical relapse after herpes simplex encephalitis in adults.
- Author
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Sköldenberg B, Aurelius E, Hjalmarsson A, Sabri F, Forsgren M, Andersson B, Linde A, Strannegård O, Studahl M, Hagberg L, and Rosengren L
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- Adolescent, Adult, Aged, Aged, 80 and over, Case-Control Studies, Cytokines cerebrospinal fluid, Encephalitis, Herpes Simplex epidemiology, Encephalitis, Herpes Simplex physiopathology, Enzyme-Linked Immunosorbent Assay methods, Female, Follow-Up Studies, Glial Fibrillary Acidic Protein cerebrospinal fluid, Herpes Simplex genetics, Humans, Incidence, Male, Middle Aged, Phosphopyruvate Hydratase cerebrospinal fluid, Prospective Studies, RNA, Messenger biosynthesis, Recurrence, Retrospective Studies, Reverse Transcriptase Polymerase Chain Reaction methods, Time Factors, Encephalitis, Herpes Simplex cerebrospinal fluid, Encephalitis, Herpes Simplex pathology, Herpes Simplex cerebrospinal fluid
- Abstract
Objectives: To study the occurrence of relapse of herpes simplex encephalitis (HSE) and to find out whether soluble activity markers in cerebrospinal fluid (CSF) indicate direct viral or immune- mediated events., Methods: A consecutive series of 32 adult survivors of HSE were followed to determine the incidence of clinical relapse of HSE. Four patients had neurological deterioration interpreted as relapsing HSE. Four non-relapsing HSE cases were selected as matched controls. Fifty nine batched, paired CSF and serum samples from the eight HSE patients were analysed for soluble activity markers, predominantly cytokines and mediators (interferon-gamma, soluble CD8, tumour necrosis factor-alpha, and interleukin-10), amount of HSV-DNA and markers of glial and neuronal destruction (neurofilament protein, glial fibrillary acidic protein, S-100-beta, and neuron specific enolase)., Results: Relapse of HSE was diagnosed in 3 of 26 (12 %) acyclovir-treated patients (5 episodes during 6.1 years of followup) and in 1 of 6 vidarabine-recipients. All relapses occurred from 1 to 4 months after acute HSE, except for a second relapse after 3.3 years in one patient. Computer tomography at relapses revealed few abnormalities apart from those found during the primary disease. Intravenous acyclovir and corticosteroids were given for 7-21 days in all the relapse patients. All relapse patients seemed to recover to the pre-relapse condition. HSV-DNA was demonstrated in CSF in all patients during the acute stage but not in any of 13 CSF samples taken during relapse phases. The HSV viral load during the acute stage of HSE was not higher or of longer duration in the relapsing patients than in the non-relapsing HSE controls. The levels of sCD8 were increased in nearly all CSF samples tested with peaks of sCD8 at one month of acute HSE. In all episodes of relapse, sCD8 peaks were detected during the first week at high levels. CSF levels of neuron-specific enolase, S-100 and glial fibrillary acidic protein were markedly lower at relapse than at the acute stage of HSV-1 encephalitis., Conclusion: The lack of demonstrable HSV DNA in CSF, the lack of acute CSF signs and the lack of signs of neural and glia cells destruction indicate that a direct viral cytotoxicity is not the major pathogenic mechanism in relapse. Instead, the pronounced CSF proinflammatory immunological response and the relative lack of CSF anti-inflammatory cytokine IL-10 response suggest immunologically-mediated pathogenicity.
- Published
- 2006
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18. Marked increase of beta-amyloid(1-42) and amyloid precursor protein in ventricular cerebrospinal fluid after severe traumatic brain injury.
- Author
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Olsson A, Csajbok L, Ost M, Höglund K, Nylén K, Rosengren L, Nellgård B, and Blennow K
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- Adult, Alzheimer Disease metabolism, Alzheimer Disease physiopathology, Amyloid beta-Peptides blood, Biomarkers blood, Biomarkers cerebrospinal fluid, Causality, Cerebral Ventricles metabolism, Diffuse Axonal Injury physiopathology, Disease Progression, Female, Humans, Male, Middle Aged, Peptide Fragments blood, Plaque, Amyloid metabolism, Up-Regulation physiology, Alzheimer Disease etiology, Amyloid beta-Peptides cerebrospinal fluid, Amyloid beta-Protein Precursor cerebrospinal fluid, Brain Injuries complications, Diffuse Axonal Injury cerebrospinal fluid, Diffuse Axonal Injury etiology, Peptide Fragments cerebrospinal fluid
- Abstract
Severe traumatic brain injury (TBI) may result in widespread damage to axons, termed diffuse axonal injury. Alzheimer's disease (AD) is characterised by synaptic and axonal degeneration together with senile plaques (SP). SP are mainly composed of aggregated beta-amyloid (Abeta), which are peptides derived from the amyloid precursor protein (APP). Apart from TBI in itself being considered a risk factor for AD, severe head injury seems to initiate a cascade of molecular events that are also associated with AD. We have therefore analysed the 42 amino acid forms of Abeta (Abeta1-42) and two soluble forms of APP (alpha-sAPP and ss-sAPP) in ventricular cerebrospinal fluid (VCSF) and Abeta(1-42) in plasma from 28 patients in a serial samples 0-11 days after TBI. The levels of alpha-sAPP, ss-sAPP and Abeta(1-42) were determined using ELISA assays. After TBI, there was a significant stepwise increase in VCSF-Abeta(1-42) up to 1173 % from day 0-1 to day 5-6 and in VCSF-beta-sAPP up to 2033 % increase from day 0-1 to day 7-11. There was also a slight but significant increase of VCSF-beta-sAPP from day 0-1 to day 5-6 and day 7-11. By contrast, the plasma- Abeta(1-42) level is unchanged after injury. The marked increase in VCSFAbeta(1-42) implies that increased Abeta expression may occur as a secondary phenomenon after TBI with axonal damage. The unchanged level of plasma-Abeta(1-42) in contrast to the marked increase in VCSF-Abeta(1-42) after severe TBI, supports the suggestion that plasma Abeta(1-42) does not reflect Abeta metabolism in the central nervous system (CNS).
- Published
- 2004
- Full Text
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19. Incidence of CSF abnormalities in siblings of multiple sclerosis patients and unrelated controls.
- Author
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Haghighi S, Andersen O, Rosengren L, Bergström T, Wahlström J, and Nilsson S
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- Adolescent, Adult, Aged, Antibody Formation, Autoimmune Diseases immunology, Case-Control Studies, Enzyme-Linked Immunosorbent Assay, Family Health, Female, Humans, Immunoglobulin G immunology, Male, Middle Aged, Multiple Sclerosis immunology, Phenotype, Immunoglobulin G cerebrospinal fluid, Measles immunology, Multiple Sclerosis genetics
- Abstract
We found that 19% (9/47) of healthy siblings of patients with clinically definite multiple sclerosis had an intrathecal immunological reaction with two or more 2 CSF-enriched oligoclonal bands (OCBs), in contrast to (4%) (2/50) unrelated healthy controls. Furthermore, in this group of nine healthy sibs the measles CSF IgG antibody titers were higher than that of the other sibs and that of controls. There were also differences in the serum titers for measles IgG antibody, which were higher in the group of all healthy sibs than in healthy volunteers, and (as with CSF titers) higher in the subgroup of healthy sibs with two or more 2 CSF-enriched OCBs than the other sibs. Thus a significant proportion of healthy siblings to MS patients have a partially hyperimmune condition similar to that occurring in MS, which in 19% manifested itself as an OCB reaction, in 9% as increased CSF measles IgG antibody titers, and in 21% as increased serum measles IgG antibody titers, these phenomena tending to occur in the same individuals. This condition is characterized by CSF-enriched OCBs with undefined specificity, although some increased antiviral reactivity is found both in the serum and CSF. While it needs further characterization, a genetic trait interacting with common infections is suggested. The recurrence risk of this condition is approximately five times higher than the 3-4% recurrence risk for manifest MS reported for sibs.
- Published
- 2000
- Full Text
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20. Difference in pathogenesis between herpes simplex virus type 1 encephalitis and tick-borne encephalitis demonstrated by means of cerebrospinal fluid markers of glial and neuronal destruction.
- Author
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Studahl M, Rosengren L, Günther G, and Hagberg L
- Subjects
- Adult, Aged, Female, Humans, Male, Middle Aged, Neuroglia cytology, Neuroglia pathology, Neurons cytology, Neurons pathology, Biomarkers analysis, Encephalitis, Herpes Simplex physiopathology, Encephalitis, Tick-Borne physiopathology, Glial Fibrillary Acidic Protein cerebrospinal fluid, Herpesvirus 1, Human pathogenicity, Neurofilament Proteins cerebrospinal fluid, Phosphopyruvate Hydratase cerebrospinal fluid, S100 Proteins cerebrospinal fluid
- Abstract
We determined the extent of neuronal and glial cell destruction in 13 patients with herpes simplex type 1 (HSV-1) encephalitis, 15 patients with tick-borne encephalitis (TBE), and 20 noninfectious controls by analyzing the cerebrospinal fluid (CSF) concentrations of neurofilament protein (a marker of neurons, mainly axons), neuron-specific enolase (a marker of neurons, mainly somas), glial fibrillary acidic protein, and S-100 protein (markers of astrocytes). In addition, in patients with HSV-1 encephalitis CSF samples were collected serially before 7, 8-14, and 18-49 days and 3-10 months after the onset of neurological symptoms. In the acute stage of HSV-1 encephalitis we found markedly higher CSF levels of the cell damage markers than in patients with TBE. The concentration of cell damage markers in HSV-1 encephalitis decreased within 45 days after acute infection, except for neurofilament protein. The CSF concentrations of neurofilament protein increased during the second week, remained extremely high throughout the next month, and decrease thereafter. The changes in these markers of neuronal and glial destruction demonstrate the neuronal and astroglial cell damage during the first month after HSV-1 encephalitis. In contrast, most patients with TBE had signs only of slight astrogliosis, except for two patients with paresis.
- Published
- 2000
- Full Text
- View/download PDF
21. Decreased morphine intake by opiate addicted rats administered zimelidine, a 5-HT uptake inhibitor.
- Author
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Rönnbäck L, Zeuchner J, Rosengren L, Wronski A, and Ogren SO
- Subjects
- Animals, Dose-Response Relationship, Drug, Feeding Behavior drug effects, Female, Humans, Male, Morphine administration & dosage, Morphine Dependence etiology, Quinine administration & dosage, Rats, Rats, Inbred Strains, Receptors, Serotonin physiology, Morphine Dependence psychology, Zimeldine pharmacology
- Abstract
Zimelidine, a specific 5-HT uptake inhibitor, reduced peroral morphine consumption by morphine-addicted adult male and female Sprague-Dawley rats and old male rats in choice tests. The effect was dose dependent in male rats. Thus, the availability of central 5-HT appears to be important for the regulation of morphine preference in rat. The results are discussed in relation to recent literature where ethanol preference has been found to be attenuated by zimelidine. The results may provide insights into the complex cellular mechanisms underlying opiate addiction.
- Published
- 1984
- Full Text
- View/download PDF
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