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Biomedical subjects

M Mänttäri

Publications and source records attributed to M Mänttäri.

At least 19 recordsLinked to original sources

Water circuit closure with membrane technology in the pulp and paper industry.

In this study, membrane filtration as an internal purification method, "the kidney", in the pulp and paper industry is discussed. Membrane filtration is economically competitive and a very versatile process. It can be used to remove the enriched organic and/or inorganic loads either partially or totally from, for example, the mechanical pulping and paper making water circuits and it can be applied to various points within the process. With the so-called shear enhanced membrane modules very high fluxes, in ultrafiltration about 400 L/(m2h) and in nanofiltration fluxes almost 200 L/(m2h), have been obtained. Depending on the membrane, suspended solids (microfiltration), polysaccharides, extractives and high molar mass lignous substances (ultrafiltration) and multivalent salts (nanofiltration) can be removed. Ultrafiltration permeate can well be used in paper machine showers to replace fresh water. The quality of the nanofiltration permeate is significantly higher than that of ultrafiltration. The membrane processes can be enhanced by various pre-treatment techniques to produce higher permeate fluxes and to eliminate membrane fouling. Such pre-treatment methods are, e.g., chemical treatment, ozonation and biological treatment. The most cost-effective processes were chemical flocculation, pH adjustment and thermophilic aerobic biological treatment.

Filtration↗

Ultrafiltration and nanofiltration in the pulp and paper industry using cross-rotational (CR) filters.

Ultra- and nanofiltration with high shear CR-filters have been utilized for cleaning of clear filtrates and effluents from the pulp and paper industry. The aim was to find out how different nanofiltration membranes operate at high shear conditions. The filtration efficiency of the membranes was evaluated by measuring flux, retention and fouling at various recovery and pH conditions. High fluxes (approximately 100 L/(m2h)) for nanofiltration membranes were measured when circulation waters from the paper machine were filtered at neutral conditions. In the filtration of discharge of external activated sludge treatment plants we measured fluxes around 150 L/(m2h) even at a concentration factor of 12. The best NF membranes removed over 80% of the organic carbon and of the conductivity and almost completely eliminated the color. With acidic waters fluxes and retentions were significantly lower. The NF270 membrane from Dow and the Desal-5 membranes from Osmonics had the highest flux and retention properties. However, the Desal-5 membrane lost its retention properties slowly, which restricts its use in the high shear CR-filter. CR-nanofiltration can be used in the pulp and paper industry without feed pre-treatment by ultrafiltration. This increases the attractiveness of high shear CR-nanofiltration.

Carbon↗

Thrombolytic treatment of acute myocardial infarction after out-of-hospital cardiac arrest.

OBJECTIVE: To investigate the safety and efficacy of thrombolytic treatment for an acute myocardial infarction (AMI) immediately after resuscitation in the out-of-hospital setting. DESIGN: Retrospective. SETTING: A middle-sized urban city (population 540000) served by a single emergency medical system using a tiered response with physicians in field. PATIENTS AND METHODS: Sixty-eight patients with an initial diagnosis of AMI who received thrombolytic treatment in an out-of-hospital setting after cardiac arrest and cardiopulmonary resuscitation (CPR) between January 1st 1994 and December 31st 1998. An ECG and the myocardial enzymes (CK, CK-MB, Troponin-T) were used to diagnose AMI. Myocardial reperfusion was assessed by resolution of the ST-segment elevation. Side effects and complications were studied. The quality of secondary survival was evaluated. The Utstein style was used for a uniform style of reporting the cardiac arrest data. RESULTS: The accuracy of prehospital diagnosis was found to be excellent. Retrospective analysis revealed that thrombolytic therapy had been appropriately administered in 64 (94%) of the 68 patients actually treated. Reperfusion was achieved in 71% of the patients. Haemorrhagic complications were few, and included intracranial haemorrhage (one patient), gastrointestinal bleeding (two patients), bleeding from the puncture site (one patient) and epistaxis (one patient). The incidence of hypotension during streptokinase infusion was 22%. Sixty-three (93%) of the patients were admitted alive to the hospital, with 36 subsequently surviving to discharge. CONCLUSIONS: Thrombolytic treatment is a safe and effective treatment in AMI even after out-of-hospital cardiopulmonary resuscitation.

Blood Circulation↗

Joint effects of C-reactive protein and other risk factors on acute coronary events.

BACKGROUND: Elevated serum C-reactive protein (CRP) is a predictor of coronary heart disease in population samples. We studied the contribution of the simultaneous presence (joint effects) of elevated CRP and the classic as well as some new risk factors on acute coronary events. METHODS: With a nested case-control design and logistic regression analyses, we measured baseline and pre-event CRP levels in patients who had myocardial infarction or coronary death (cases) during an 8.5-year follow-up in the Helsinki Heart Study, a coronary primary prevention trial in dyslipidemic middle-aged men. The control patients were participants remaining free of coronary events. RESULTS: Baseline and pre-event CRP levels were higher in cases than in control patients (4.4 vs 2.0 mg/L, P <.001 and 6.0 vs 3.6 mg/L, P <.001). The relative risk attributed to elevated CRP was 40% higher with chronic elevation (odds ratio [OR], 3.34) compared with high baseline (OR, 2.24) or pre-event (OR, 2.26) level only. Hypertension, low high-density lipoprotein cholesterol, and high leukocyte count increased the risk only marginally without simultaneous occurrence of high CRP, whereas the joint effects of CRP and these classic risk factors suggested additive effects on coronary risk. In contrast, high levels of immunoglobulin G-class antibodies to oxidized low-density lipoprotein and antiprothrombin antibodies as well as high total immunoglobulin G level increased the risk irrespective of CRP. CONCLUSIONS: Elevated CRP enhances the risks attributed to classic coronary risk factors.

Adult↗

Infections, inflammation, and the risk of coronary heart disease.

BACKGROUND: The role of infections and inflammation in the pathophysiology of coronary heart disease is emerging. We studied the independent and joint effects of these 2 components on coronary risk. METHODS AND RESULTS: We measured baseline levels of C-reactive protein (CRP) and antibodies to adenovirus, enterovirus, cytomegalovirus, and herpes simplex virus as well as to Chlamydia pneumoniae (Cpn) and Helicobacter pylori in 241 subjects who suffered either myocardial infarction or coronary death during the 8.5-year trial in the Helsinki Heart Study, a coronary primary prevention trial. The 241 controls in this nested case-control study were subjects who completed the study without coronary events. Antibody levels to herpes simplex type I (HSV-1) and to Cpn were higher in cases than in controls, whereas the distributions of antibodies to other infectious agents were similar. Mean CRP was higher in cases (4.4 versus 2.0 mg/L; P<0.001), and high CRP increased the risks associated with smoking and with high antimicrobial antibody levels. The odds ratios in subjects with high antibody and high CRP levels were 25.4 (95% CI 2.9-220.3) for HSV-1 and 5.4 (95% CI 2.4-12.4) for Cpn compared with subjects with low antibody levels and low CRP. High antibody levels to either HSV-1 or to Cpn increased the risk independently of the other, and their joint effect was close to additive. CONCLUSIONS: Two chronic infections, HSV-1 and Cpn, increase the risk of coronary heart disease. The effect is emphasized in subjects with ongoing inflammation, denoted by increased CRP levels.

Adult↗

Left ventricular calcification following resuscitation.

In this paper we report a case of 34-year-old man with a severe septic shock. Because of profound hypotension he was given massive amounts of catecholamines for 10 days. After a short recovery the function of his heart started to deteriorate again and clear calcification around the left ventricle was disclosed by computer tomography. Catecholamines are known to induce myocardial injury resulting in a special form of cardiomyopathy with eventual calcification, but there are no previous reports of myocardial calcification to this extent.

Adult↗

Joint effects of an aldosterone synthase (CYP11B2) gene polymorphism and classic risk factors on risk of myocardial infarction.

BACKGROUND: The -344C allele of a 2-allele (C or T) polymorphism in the promoter of the gene encoding aldosterone synthase (CYP11B2) is associated with increased left ventricular size and mass and with decreased baroreflex sensitivity, known risk factors for morbidity and mortality associated with myocardial infarction (MI). We hypothesized that this polymorphism was a risk factor for MI. METHODS AND RESULTS: We used a nested case-control design to investigate the relationships between this polymorphism and the risk of nonfatal MI in 141 cases and 270 matched controls from the Helsinki Heart Study, a coronary primary prevention trial in dyslipidemic, middle-aged men. There was a nonsignificant trend of increasing risk of MI with number of copies of the -344C allele. However, this allele was associated in a gene dosage-dependent manner with markedly increased MI risk conferred by classic risk factors. Whereas smoking conferred a relative risk of MI of 2.50 (P=0.0001) compared with nonsmokers in the entire study population, the relative risk increased to 4.67 in -344CC homozygous smokers (relative to nonsmokers with the same genotype, P=0.003) and decreased to 1.09 in -344TT homozygotes relative to nonsmokers with this genotype. Similar joint effects were noted with genotype and decreased HDL cholesterol level as combined risk factors. CONCLUSIONS: Smoking and dyslipidemia are more potent risk factors for nonfatal MI in males who have the -344C allele of CYP11B2.

Adult↗

Prediction of myocardial infarction in dyslipidemic men by elevated levels of immunoglobulin classes A, E, and G, but not M.

BACKGROUND: Immune mechanisms have been suggested to play an important role in the development of coronary atherosclerosis and its thrombotic complications. We evaluated the predictive value of the levels of various serum immunoglobulin classes in middle-aged men at increased risk of myocardial infarction. METHODS: Using nested case-control design and logistic regression analysis, we estimated the association between serum immunoglobulins and the risk of coronary end points (nonfatal or fatal myocardial infarction or sudden cardiac death) in dyslipidemic men (levels of non-high-density lipoprotein cholesterol >5.2 mmol/L [>201 mg/dL]) participating in the Helsinki Heart Study. The cases consisted of 135 subjects in whom a coronary end point occurred during the 5-year observation period of the study, and the controls were 135 subjects who did not suffer coronary end points during this period. Levels of IgA, IgE, IgG, and IgM were determined in serum samples collected at study entry. RESULTS: Levels of IgA, IgE, and IgG, but not IgM, were significantly higher in cases than in controls. After adjustment for other risk factors, such as age, smoking, and blood pressure, the risk of coronary disease showed a significant relation to the levels of IgA, IgE, and IgG. The risk in the highest quartile of each distribution as compared with the lowest quartile was 2.2-fold for IgA (95% confidence interval, 1.0-4.5), 2.8-fold for IgE (1.3-5.9), and 2.8-fold for IgG (1.3-5.9). Hypertriglyceridemia and a low level of high-density lipoprotein cholesterol were associated with increased risk of a coronary end point only if the levels of IgA, IgE, or IgG were also elevated. CONCLUSION: Elevated levels of IgA, IgE, and IgG are associated with myocardial infarction and cardiac death in men with dyslipidemia. The present data suggest that, for dyslipidemia to cause coronary atherothrombosis, an immune response reflected by elevated levels of these immunoglobulin classes is an important determinant.

Adult↗

Antibodies to prothrombin crossreact with plasminogen in patients developing myocardial infarction.

In a prospective study on healthy middle-aged men, high level of antibodies to prothrombin implied a risk of myocardial infarction. The possible mechanism(s) of these antibodies in coronary thrombosis are not known. Because prothrombin belongs to the kringle proteins and shares structural homology with a fibrinolytic kringle protein plasminogen, we studied whether antibodies to prothrombin crossreact with plasminogen. Sera from 17 healthy middle-aged men who later developed myocardial infarction were studied. Binding of antibodies to immobilized prothrombin (EIA) was inhibited by using soluble prothrombin, plasminogen and synthetic peptides of 20 amino acids from plasminogen kringle 5 (P304, P305) and from prothrombin kringle 2 (P302) as inhibitors. The peptides contained the conserved pentapeptide CRNPD of the kringle proteins. Soluble prothrombin inhibited up to 50% the binding of antibodies to immobilized prothrombin in all sera. Plasminogen inhibited binding in 9/17 (53%) sera (a decrease of at least 20%). P305 inhibited binding to prothrombin in 8/17 (47%), P304 in 4/17 (23%) and P302 in 6/17 (35%) sera. In structural analysis, presentation of the pentapeptide was conformationally different between the peptides. We conclude that crossreactive antibodies binding to prothrombin and plasminogen occur in sera of patients later developing myocardial infarction. The crossreactive epitope seems to be conformational and include the conserved pentapeptide of the kringle proteins. These antibodies may interfere with the fibrinolytic function of plasminogen and contribute to the development of myocardial infarction.

Antibodies↗

Alcohol and coronary heart disease: the roles of HDL-cholesterol and smoking.

OBJECTIVES: To study the role of HDL-cholesterol (HDLc) in the causal pathway mediating the effect of alcohol on coronary heart disease (CHD). DESIGN: Cox proportional hazard models were used to compare the relative CHD risks in various HDLc-smoking categories. SETTING: A prospective, multicentre, placebo-controlled, double-blind CHD primary prevention trial with gemfibrozil in primary (occupational) health care units, the Helsinki Heart Study. SUBJECTS: Dyslipidaemic middle-aged men with available alcohol consumption data (1924 of 2035) in the placebo arm of the 5-year study. MAIN OUTCOME MEASURES: Seventy-seven (of 84) cases of nonfatal myocardial infarction or cardiac death. RESULTS: A U-shaped association was detected between alcohol consumption and CHD. The protection was found both in subjects with low (mean 0.94 mmol L-1) and normal (mean 1.25 mmol L-1) HDLc with corresponding reductions of 23% and 36% in relative risks. In contrast to previous data, alcohol offered virtually no protection against CHD in non-smokers. In subjects consuming more than 800 g pure ethanol annually, the CHD incidence was 6/1000 in subjects with more than three weekly drinking occasions, compared to 11/1000 in 'weekend' drinkers. CONCLUSIONS: Our results confirm the protective effect of alcohol against CHD. However, in contrast to previous data the effect in our population is restricted to smokers and the role of HDLc in mediating the effect is less central than suggested previously.

Adult↗

QT dispersion as a risk factor for sudden cardiac death and fatal myocardial infarction in a coronary risk population.

OBJECTIVE: To test in a prospective study the hypothesis that increased QT dispersion in resting 12-lead ECG is a predictor of sudden cardiac death. DESIGN: A nested case-control study during a mean (SD) follow up time of 6.5 (2.8) years. SETTING: A prospective, placebo controlled, coronary prevention trial with gemfibrozil among dyslipidaemic middle aged men in primary (occupational) health care units: the Helsinki heart study. PATIENTS: 24 victims of fatal myocardial infarction, 48 victims of sudden cardiac death without acute myocardial infarction, and their matched controls. MAIN OUTCOME MEASURES: QT dispersion in baseline and pre-event electrocardiograms. RESULTS: At study baseline, QT dispersion was similar in all victims and controls. When estimated from the pre-event ECG on average 14 months before death, the risk of sudden cardiac death in the highest QTPEAK (up to the peak of the T wave) dispersion tertile (> or = 50 ms) was 6.2-fold (95% confidence interval 1.7 to 23.5) compared with the risk in the lowest tertile (< or = 30 ms), and 4.9-fold (1.2 to 19.5) after adjustment for the presence of left ventricular hypertrophy, while QTPEAK dispersion could not predict fatal myocardial infarction. QTEND dispersion (up to the end of the T wave) in pre-event ECGs could not discriminate victims of either sudden cardiac death or fatal myocardial infarction from their matched controls. CONCLUSIONS: In middle aged men with a normal conventional QT interval in 12-lead resting ECG, increased QTPEAK dispersion is an independent risk factor for sudden cardiac death, but not for fatal myocardial infarction.

Adult↗

How to define coronary heart disease in register-based follow-up studies: experience from the Helsinki Heart Study.

Information on coronary heart disease (CHD) obtained from the Finnish Hospital Discharge and Cause-of-Death Registers was compared with that collected in the Helsinki Heart Study (HHS) during an 8.5-year follow-up. The purpose of the comparison was two-fold, firstly, to study the accuracy of registration of CHD and secondly, to find out what diagnostic codes to use for CHD in register-based follow-up studies. The HHS cases were used as the 'golden standard' and the CHD deaths and definite nonfatal acute myocardial infarctions (AMIs) (all diagnoses) were taken from the registers to establish the sensitivity of the Hospital Discharge and Cause-of-Death Registers combined. The sensitivity was 0.84 during the period 1980-86 and 0.87 during 1987-90, with the positive predictive values 0.94 and 0.92 respectively. The treatment effects seen in the HHS were compared with the effects that would have emerged, if register-based information only had been used with different definitions of CHD. Of the register-based calculations, the one with the definition 'all CHD deaths and hospitalizations with the ICD-8 code 410' came closest to the HHS result, with a 32% reduction (P=0.028 one-sided) of CHD incidence, while the original HHS result was a 34% reduction (P=0.008 one sided). However, when comparing Kaplan-Meier plots of cumulative hazards of CHD, the plot with a wider definition of CHD (ICD-8 and ICD-9 codes 410-414) came closest to the HHS experience, especially if revascularizations were included in the latter. Definite AMI as a single definition of CHD might thus not be sufficient when studying CHD risk, instead, at least two parallel definitions of CHD should be used.

Coronary Disease↗

Antibodies to prothrombin imply a risk of myocardial infarction in middle-aged men.

Antiphospholipid antibodies in patients with "antiphospholipid syndrome" may be directed at least in part against plasma phospholipid-binding proteins, such as beta 2-glycoprotein I or prothrombin, which are involved in the control of thrombosis and haemostasis. IgG-class antibodies against prothrombin and beta 2-glycoprotein I were measured by enzyme-linked immunoassay in initially healthy middle-aged dyslipidaemic men (non-high-density lipoprotein > 5.2 mml/l). Serum samples had been drawn at entry to a 5-year coronary primary-prevention trial with gemfibrozil from 106 subjects who experienced either a non-fatal myocardial infarction or cardiac death during the follow-up and from 106 subjects without coronary episodes, matched for treatment group (gemfibrozil/placebo) and geographical area. The antiprothrombin antibody level, as expressed in optical density units, was significantly higher in patients than in controls (0.26 +/- 0.17 versus 0.22 +/- 0.09; p < 0.02). A high level of antiprothrombin antibodies (highest tertile of distribution) predicted a 2.5-fold increase in the risk (95% confidence interval 1.2-5.3) of myocardial infarction or cardiac death. The distribution of IgG-class antibodies against beta 2-glycoprotein I did not differ significantly between cases and controls. The joint effect of antiprothrombin antibodies and other factors associated with hypercoagulative state: triglyceride level, lipoprotein(a) and smoking, was multiplicative for the risk. Antiprothrombin antibodies are a new immunological predictor of myocardial infarction and the effect of these antibodies may be mediated by hypercoagulative mechanisms.

Apolipoproteins↗