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Sökning: WFRF:(Järemo Petter)

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1.
  • Järemo, Petter, et al. (författare)
  • A significant relationship between Chlamydia pneumoniae seroreactivity and the severity of coronary atherosclerosis
  • Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
    • Background. Clinical evidence supporting a causal role of Chlamydia pneumoniae in the process of atherosclerosis is limited. It is also uncertain if the organism participates in the inflammatory response in stable angina pectoris. The current study investigates C. pneumoniae IgG and markers reflecting the inflammatory response in stable angina pectoris. The data were subsequently compared with the extent of coronary atherosclerosis.Setting. Department of Cardiology, Linköping University Hospital, Linköping, Sweden.Experimental protocol. We investigated 92 patients with stable angina pectoris subject to coronary angiography to assess chest pain Before angiography C. pneumoniae IgG, neutrophil count and plasma levels of myeloperoxidase and interleukin 6 were analysed. The number of major coronary arteries (1-3) having at least one diameter narrowing(=> 50%) stenosis was determined. The patients were divided into two equal sized groups according to C. pneumoniae IgG levels.Results. Subjects with higher antibody concentrations had a more severe disease. The number of diseased arteries was 2.1±0.8(SD) and 1.4±0.6(SD) for the two groups, respectively. The difference proved to he highly significant (p<0.0001). The groups did not differ with respect to inflammatory parameters.Conclusion. This study with 92 consented individuals with stable angina pectoris suggests a causative relationship between C. pneumoniae IgG seroreactivity and the degree of coronary atherosclerosis. It does not, however, prove causality. Thus, it is likely that C. pneumoniae participates in the progression of atherosclerosis.
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2.
  • Järemo, Petter, et al. (författare)
  • Alzheimer's disease and granulocyte density diversity
  • 2013
  • Ingår i: European Journal of Clinical Investigation. - : John Wiley & Sons. - 0014-2972 .- 1365-2362. ; 43:6, s. 545-548
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND:The current study investigates circulating eosinophils and neutrophils in Alzheimer's (AD) type dementia with respect to density (kg/L). The existence of β-amyloid plaques in the brain is a feature of AD. Sporadic scientific reports indicate that the disease affects circulating neutrophils. In contrast, numerous publications investigate inflammatory reactions in AD brains. Locally, the plaques evoke a substantial inflammatory response involving activated microglia and astrocytes.METHODS:Subjects with probable AD (n = 39) were included and compared with elderly individuals (n = 22) lacking apparent memory problems. We sampled 10 mL venous blood in citrate. Granulocytes were separated according to density in linear Percoll™ gradients. Subsequently, the gradients were divided into density subfractions (n = 16). In every fraction, determination of eosinophil and neutrophil counts was carried out.RESULTS:AD sufferers displayed less granulocytes in fractions nos. 13-15 containing light cells. For these fractions, the P-values proved to be (P < 0·001; not significant; P = 0·03) and (P = 0·01; P = 0·01; not significant), for eosinophils and neutrophils, respectively.CONCLUSIONS:The present work describes that less circulating light granulocytes are a feature of AD demented individuals. It is to hypothesize that it is a sign of impaired granulocyte turnover and cell damage. It is concluded that AD affects inflammatory cells in the periphery and that the behaviour of granulocytes in dementia is worthwhile further studies.
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  • Järemo, Petter (författare)
  • Computerised method for recording platelet density distribution
  • 1995
  • Ingår i: European Journal of Haematology. - : Wiley. - 0902-4441 .- 1600-0609. ; 54:5, s. 304-309
  • Tidskriftsartikel (refereegranskat)abstract
    • In the present study a computerized apparatus was employed for scanning light transmission variations along test tubes containing density-separated platelets. The device consists of a stepping motor, a stationary halogen lamp and a photopotentiometer connected to a personal computer. Anticoagulated whole blood was layered on a preformed continuous Percoll gradient having a density span from 1090 kg/l (bottom) to 1040 kg/l (top). After centrifugation at 3400g for 1.5 hours, high-density cells (i.e. erythrocytes) pass through to the bottom of the test tube and the lighter platelets remain in the gradient. The test tube is moved by the computer between the halogen lamp and the photopotentiometer. Transmission variations along the gradient were recorded and registered in the computer. Density markers beads were used as an internal standard and platelet peak density was determined. After perforating the test tube the gradient was divided into 45 aliquots. In all fractions determination of platelet counts and mean platelet volume was carried out. In addition, in the aliquots having a platelet count > 20 × 1012/l the ratio β-thromboglobulin per platelet was also determined. The platelet distribution in the gradient was illustrated graphically. A good agreement was found when comparing platelet distributions in the gradients and light transmission variations along the test tubes.
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7.
  • Järemo, Petter, et al. (författare)
  • Elevated inflammatory parameters are associated with lower platelet density in acute myocardial infarctions with ST-elevation
  • 2000
  • Ingår i: Thrombosis Research. - 0049-3848 .- 1879-2472. ; 100:6, s. 471-478
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Platelets and granulocytes play important roles in coronary disorders. We therefore, investigated platelet and granulocyte alterations in myocardial infarctions (MIs).Patients and study design: A total of 36 individuals having MI with raised ST-segments who were receiving thrombolytic therapy were studied. Sampling was carried out after thrombolysis within 24 h after hospital admission. After 3 to 6 months of recovery, 25 patients were reinvestigated. At the infarction, peak platelet density was determined using a special designed computerised apparatus. In addition, we did counts on platelets, neutrophils and monocytes. Moreover, plasma levels of soluble P-selectin, myeloperoxidase and interleukin 6 were determined to estimate the degree of platelet, neutrophil and monocyte activation, respectively. Peak platelet density was analysed at the MI. All other parameters were determined at the acute event and at recovery.Results: At the MI, compared to the recovery, platelet counts were lower (P<.001). In addition, increased neutrophil counts (P<.001), elevated monocyte counts (P<.001), enhanced myeloperoxidase (P<.001) and interleukin 6 (P<.001) levels were demonstrated. We failed to show elevated soluble P-selectin. Compared to individuals with ST-segment elevations and low platelet density (≤1.058 kg/l), patients having peak platelet densities >1.058 kg/l displayed lower neutrophil counts (P<.01) and decreased interleukin 6 levels (P<.01). Furthermore, we demonstrate that individuals with higher inflammatory response at the MI had higher neutrophil (r=.6; P<.01) and higher monocyte counts (r=.6; P<.001) at recovery.Conclusion: We conclude that MI is associated with an inflammatory response. However, a subgroup of patients having MI with ST-elevations and low peak platelet density was identified. Compared to subjects with higher platelet density, they had more severe inflammatory characteristics. The differences persisted during recovery.
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8.
  • Järemo, Petter, et al. (författare)
  • Elevated platelet reactivity in stable angina pectoris without significant coronary flow obstruction
  • 2008
  • Ingår i: Journal of Cardiovascular Medicine. - : Lippincott Williams & Wilkins. - 1558-2027. ; 9:2, s. 129-130
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND:There are many different causes of angina pectoris without significant coronary flow obstruction in major coronary arteries. Examples include Prinzmetal angina and small vessel atherosclerotic disease.METHODS:We investigated individuals with stable angina pectoris subject to elective coronary angiography. To keep the study group as homogeneous as possible, patients with diabetes mellitus were excluded. Subjects with normal coronary angiograms (n = 13) or insignificant (< 50%) coronary flow obstruction(s) (n = 4) were grouped together. The remaining cohort (n = 96) with at least one significant (> or = 50%) flow obstruction in at least one major coronary artery served as controls.RESULTS:Before angiography, platelet activity in vitro on stimulation with a thrombin-receptor activating peptide (TRAP-6) (57 micromol/l and 74 micromol/l) and ADP (1.7 micromol/l and 8.5 micromol/l) was determined. Angina pectoris individuals without significant flow obstruction in major coronary arteries had enhanced platelet reactivity both when stimulated with TRAP-6 and ADP (P < 0.01 for both TRAP-6 concentrations and P < 0.05 for both ADP concentrations, respectively.CONCLUSIONS:It is concluded that angina pectoris without significant flow impediment in major epicardial arteries is associated with augmented platelet reactivity.
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  • Järemo, Petter (författare)
  • Evidence that Chlamydia pneumoniae affects platelet activity in patients with acute myocardial infarction and ST-segment elevations
  • 2001
  • Ingår i: Scandinavian Journal of Infectious Diseases. - : Informa UK Limited. - 0036-5548 .- 1651-1980. ; 33:10, s. 747-748
  • Tidskriftsartikel (refereegranskat)abstract
    • This study concerns platelet activity at myocardial infarctions and possible relationships with Chlamydia pneumoniae seroreactivity. Fourteen patients with acute myocardial infarction and ST-segment elevations were enrolled. They all received thrombolytic therapy. The subjects were examined within 24 h after hospital admission (Day 1) and after 6 months of recovery. On Day 1, C. pneumoniae IgM antibody titres were analysed and on Day 1 and during recovery C. pneumoniae IgG and soluble P-selectin were determined. P-selectin was used to estimate platelet activation. C. pneumoniae IgM titres at the infarction were closely related to both Day 1 IgG titres (r = 0.6; p < 0.05) and to IgG levels after 6 months (r = 0.8; p < 0.01). These results indicate a possible reactivation of a chronic infection. C. pneumoniae IgM was related to platelet activation. The correlation coefficient was r = 0.7 (p < 0.01) when comparing IgM titres with Day 1 plasma P-selectin. A similar relationship was found when comparing IgM and recovery P-selectin (r = 0.8; p < 0.01). The pathogen appears to contribute to platelet responses occurring during myocardial infarctions with ST-segment elevations. It is concluded that an ongoing reactivation of a chronic infection is related to increased platelet activity.
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