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Biomedical subjects

R Kettunen

Publications and source records attributed to R Kettunen.

At least 19 recordsLinked to original sources

Evaluation of the current status of operating and closed landfills in Russia, Finland and Ireland with regard to water pollution and methane emission.

The annual production of municipal solid wastes (MSW) in Russia, Finland and Ireland in the late 1990s accounts for 37.5, 2.5 and 2.05 min. tonnes or 252, 488 and 566 kg per capita, respectively. 96.5, 64 and 91% of these wastes (for Russia, Finland and Ireland, correspondingly) are currently disposed of via landfilling. However, nowadays, MSW management in these countries is undergoing drastic changes (source separation, closure of old landfills, reduction of the number of landfills etc.) forced by recent legislation set by the European Union and Russian authorities. This paper evaluates the current status of MSW landfills, as well as information on current leachate and methane emissions in the three above mentioned countries. Landfill leachates are highly variable in each country and between different countries due to different rainfall and climatic conditions and also due to poor landfill top insulation/cover. Leachates in poorly structured landfills are very dilute, whereas leachates with total COD and nitrogen contents as high as 33,700 mg COD/l and 4,030 mg N/l, respectively, have been detected from state-of-the-art sites. Currently, on-site treatment of leachates exists at only a few landfills in Russia, Finland and Ireland but this situation will be considerably improved during the next years. The annual methane emissions from landfills are estimated as 500-900 and 77 ktonnes for Russia and Finland, respectively. Recent estimates from Ireland suggest an annual landfill methane emission of c. 2.1 Mt CO2 equivalent. Several systems of methane recovery have been developed in all three countries and these are currently in different stages of implementation.

Environmental Monitoring↗

Prediction of atrial fibrillation after coronary artery bypass grafting by measuring atrial peptide levels and preoperative atrial dimensions.

OBJECTIVE: We prospectively tested the hypothesis that atrial enlargement and increased level of atrial natriuretic peptide, N-terminal atrial natriuretic peptide and brain natriuretic peptide would predict atrial fibrillation after coronary artery bypass grafting. METHODS: Eighty-eight elective coronary artery bypass grafting patients had preoperative echocardiographic assessment. The level of atrial natriuretic peptide, N-terminal atrial natriuretic peptide and brain natriuretic peptide were measured preoperatively. Patients were ECG- monitored during the whole hospital stay. RESULTS: Thirty one (35.2%) patients had postoperative atrial fibrillation. In univariate analysis increased age (P=0.003), enlargement of left and right atria (P=0.002 and P=0.004, respectively) and increased level of preoperative atrial natriuretic peptide and N-terminal atrial natriuretic peptide (P=0.016 and P=0.03, respectively) were associated with postoperative atrial fibrillation. There was correlation between the age and level of N-terminal atrial natriuretic peptide (r=0.45 and P<0.001). In multivariate analysis only age and the left atrial enlargement were independent predictors of postoperative atrial fibrillation (P=0.02 and P=0.01). CONCLUSION: Left atrial enlargement was independent predictor for postoperative atrial fibrillation. However, atrial peptides were associated with age and did not independently predict postoperative atrial fibrillation. In addition, the wide variation of the peptide levels renders the implementation of this measure in clinical practice superfluous.

Age Factors↗

Adverse ocular effects of flecainide.

PURPOSE: To study if flecainide has ocular adverse effects. METHODS: Both eyes of 38 flecainide medicated patients were thoroughly examined including colour vision, contrast sensitivity and visual fields. RESULTS: 10.5% of the patients had blurred vision on lateral gaze lasting for a couple of seconds. Small corneal deposits were found in 14.5% of the patients. All visual function tests were normal. CONCLUSION: Flecainide seems to be a safe drug with minimal ocular adverse effects.

Adult↗

Cardiac adrenergic denervation in patients with non-Q-wave versus Q-wave myocardial infarction.

In spite of smaller infarct size and better preserved left ventricular function the long-term prognosis after a non-Q-wave infarction is not better than after a Q-wave infarction. In fact, the risk of sudden cardiac death is higher in patients with a non-Q-wave infarction than in patients with a Q-wave infarction. One possible reason for postinfarction arrhythmias is cardiac adrenergic denervation resulting from myocardial infarction. In this study we compared cardiac adrenergic innervation after non-Q-wave and Q-wave infarctions. Single-photon emission tomography using iodine-123 metaiodobentzylguanidine (MIBG) and technetium-99m sestamibi (MIBI) tracers were conducted in order to compare cardiac adrenergic denervation and myocardial perfusion in 12 patients with a non-Q-wave infarction and 15 patients with a Q-wave infarction. MIBG and MIBI defects were determined as regional uptake < or = 30% of maximal myocardial activity. The size of MIBI defects calculated as a percentage of left ventricular mass was significantly smaller in patients with a non-Q-wave infarction than in patients with a Q-wave infarction (4%+/-3% vs 9%+/-7%, P<0.05, respectively). According to the maximal serum creatine kinase activity, less myocardium was damaged in patients with a non-Q-wave infarction than in patients with a Q-wave infarction (502+/-436 IU/l vs 1878+/-1265 IU/l, P<0.001). In spite of this, the extent of MIBG defects was similar in patients with a non-Q-wave and patients with a Q-wave infarction (21%+/-18% vs 23%+/-12%, respectively). In addition, the size of MIBG defect correlated with the infarct size (maximal creatine kinase activity) (r=0.52, P<0.05) after a Q-wave infarction but not after a non-Q-wave infarction. In conclusion, despite a smaller infarct size in non-Q-wave infarct patients, the extent of cardiac adrenergic denervation was similar in patients with a non-Q-wave and patients with a Q-wave infarction. In addition, the extent of cardiac adrenergic denervation was related to the infarct size in patients with a Q-wave infarction but not in patients with a non-Q-wave infarction.

3-Iodobenzylguanidine↗

Cardiac adrenergic innervation within the first 3 months after acute myocardial infarction.

It is widely accepted that myocardial infarction results in adrenergic denervation of the infarcted and peri-infarcted myocardium. On the contrary, the concept of re-innervation of adrenergic nerve fibres is less well established. Although there is evidence of partial re-innervation occuring several months after myocardial infarction, the extent and time scale of re-innervation are only poorly known. In this study we investigated changes in cardiac adrenergic innervation and myocardial perfusion during the early convalescence period (the first 3 months) after an acute myocardial infarction. Single-photon emission computed tomographic imaging was conducted in 15 men 1 week and 3 months after an acute myocardial infarction with I123-metaiodobentzylguanidine (MIBG) and Tc99m-sestamibi (MIBI) to determine the extent of adrenergic denervation and impaired perfusion, respectively. A MIBG and MIBI defect was determined as regional uptake </=30% of maximal myocardial activity. The size of the MIBG defect calculated as a percentage of left ventricular mass remained unchanged between 1 week and 3 months after myocardial infarction (31.1 +/- 17.3% vs. 30. 5 +/- 16.8%, respectively). Accordingly, MIBG activity of the infarct and peri-infarct zones (expressed as a percentage of MIBG activity of the myocardium with normal perfusion) showed no significant change (23.7 +/- 10.0% vs. 25.3 +/- 11.0% and 39.0 +/- 11.3% vs. 40.8 +/- 12.8%, respectively) during the follow-up. On the other hand, the size of MIBI defect decreased significantly during the follow-up (14.2 +/- 11.5% vs. 11.4 +/- 9.7%, P<0.05, respectively) indicating improved myocardial perfusion. The results demonstrate that cardiac adrenergic re-innervation is a slow process; despite a significant increase in myocardial perfusion we found no evidence of adrenergic re-innervation during the first 3 months after acute myocardial infarction.

3-Iodobenzylguanidine↗

Ozone-sensitive arabidopsis rcd1 mutant reveals opposite roles for ethylene and jasmonate signaling pathways in regulating superoxide-dependent cell death.

We have isolated a codominant Arabidopsis mutant, radical-induced cell death1 (rcd1), in which ozone (O(3)) and extracellular superoxide (O(2)(*)-), but not hydrogen peroxide, induce cellular O(2)(*)- accumulation and transient spreading lesions. The cellular O(2)(*)- accumulation is ethylene dependent, occurs ahead of the expanding lesions before visible symptoms appear, and is required for lesion propagation. Exogenous ethylene increased O(2)(*)--dependent cell death, whereas impairment of ethylene perception by norbornadiene in rcd1 or ethylene insensitivity in the ethylene-insensitive mutant ein2 and in the rcd1 ein2 double mutant blocked O(2)(*)- accumulation and lesion propagation. Exogenous methyl jasmonate inhibited propagation of cell death in rcd1. Accordingly, the O(3)-exposed jasmonate-insensitive mutant jar1 displayed spreading cell death and a prolonged O(2)(*)- accumulation pattern. These results suggest that ethylene acts as a promoting factor during the propagation phase of developing oxyradical-dependent lesions, whereas jasmonates have a role in lesion containment. Interaction and balance between these pathways may serve to fine-tune propagation and containment processes, resulting in alternate lesion size and formation kinetics.

Arabidopsis↗

Virus-specific capping of tobacco mosaic virus RNA: methylation of GTP prior to formation of covalent complex p126-m7GMP.

In capping cellular mRNAs, a covalent GMP-enzyme intermediate leads to formation of G(5')ppp(5')N at the 5' end of the RNA, which is modified by methylation catalyzed by guanine-7-methyltransferase. Here we show that isolated membranes from tobacco mosaic virus (TMV)-infected plant or insect cells expressing TMV replicase protein p126, synthesized m7GTP using S-adenosylmethionine (AdoMet) as the methyl donor, and catalyzed the formation of a covalent guanylate-p126 complex in the presence of AdoMet. The methyl group from AdoMet was incorporated into p126, suggesting that the complex consisted of m7GMP-p126. Thus, TMV and alphaviruses, despite their evolutionary distance, share the same virus-specific capping mechanism.

Amino Acid Sequence↗

Similar effect of revascularization on technetium-99m( )sestamibi and 15-(p-iodophenyl)pentadecanoic acid uptake in myocardial infarction patients.

To study its usefulness as a tracer for assessment of the perfusion and viability of myocardium, 15-(p-iodophenyl)pentadecanoic acid (IPPA) was compared with technetium-99m sestamibi (MIBI). Dual-tracer single-photon emission tomography rest imaging was performed no more than 2 months before and 3 months after coronary artery bypass grafting in 28 patients with previous anterior (n=13) or inferior (n=15) infarction. The size of MIBI and IPPA defects decreased from 14%+/-12% and 13%+/-9% to 10%+/-11% and 9%+/-7%, respectively (P<0.001 for both). The MIBI uptake increased in the infarct zones from 35%+/-11% to 43%+/-8% (P<0.001), and in the peri-infarct zones from 50%+/-11% to 55%+/-10% (P<0.05). The IPPA uptake increased in the infarct zones from 37%+/-11% to 44%+/-13% (P<0.001), and in the peri-infarct zones from 51%+/-11% to 57%+/-12% (P<0.05). In nine patients with improved regional echocardiographic wall motion score after bypass surgery, the pre-operative uptake values of both MIBI and IPPA in the infarct and peri-infarct zones were on average slightly but not significantly higher than in 19 patients with no observed improvement in regional wall motion score. In patients with improved regional wall motion, the MIBI scans and the IPPA scans showed (non-significant) decreases in defect size and increases in infarct and peri-infarct zone uptake after bypass surgery. Similar (in some cases significant) changes were observed in the patients without improvement in wall motion. Thus IPPA and MIBI provided similar information about perfusion and viability in pre- and postoperative evaluation of patients with clinically evident myocardial infarction and with normal global ejection fraction. Regardless of the tracer used, the resolution capability of the dual-tracer method with a rest imaging protocol was not sufficient to differentiate viable from non-viable infarction defects in unselected individual patients with a normal ejection fraction.

Coronary Artery Bypass↗

Transit time heterogeneity of bolus flow through the heart and lungs in patients with left-to-right intracardiac shunt.

Knowledge of the contributions of transit time heterogeneity to the cardiopulmonary system is important for understanding cardiopulmonary function in patients with intracardiac shunt. We determined the heterogeneity of blood transit times occurring between the right atrium and the left ventricle. Eighty two patients with suspected left-to right shunt were investigated with first-pass 99mTc-labelled red blood cell radiocardiography at supine rest. Forty two of them had a pulmonary-to-systemic flow ratio (Qp:Qs) of less than 1.2 and they served as a control group. The remaining study subjects had a Qp:Qs ratio of 1.7 +/- 0.3 (mean +/- SD). The patients with shunt had significantly greater (p < 0.001) heterogeneity of transit times (49 +/- 9%) than in the controls (39 +/- 7%). Overall heterogeneity of cardiopulmonary transit times in patients with shunt showed a curvature relationship; the highest values were centred in patients with moderate to severe shunt (1.5 < Qp:Qs < 2.5). The results suggest that the increased heterogeneity of transit times mainly occurs within the pulmonary capillary bed in patients with intracardiac shunt. This is probably due to the recruitment of the open capillaries without vessel distension.

Adolescent↗

Cardiac sympathetic denervation in patients with coronary artery disease without previous myocardial infarction.

Myocardial infarction damages sympathetic nerve fibers coursing through the infarct zone. In this study we investigated whether coronary artery disease without myocardial infarction results in sympathetic denervation. We examined 12 patients without a history of previous myocardial infarction and 19 postinfarction patients. 1-123 metaiodobenzylguanidine (MIBG) and technetium-99m sestamibi (MIBI) single-photon emission tomography were conducted at rest to determine the extent of denervated myocardium and the extent of myocardium with reduced perfusion, respectively. In addition, myocardial perfusion during exercise was assessed with MIBI. A MIBG or MIBI defect was determined as being regional uptake of < or =30% of the maximal myocardial activity. All but 1 patient without previous infarction had MIBG defects. MIBG defects (10.3 +/- 8.5% of left ventricular mass) were significantly larger than MIBI defects at rest (2.4 +/- 3.2%, p <0.001) and during exercise (4.8 +/- 6.1%, p <0.05). In multiregression analysis, the size of an MIBG defect was associated with severity of coronary stenoses (> or =90% of lumen diameter; p <0.05), but not with age, number of significant stenoses (> or =50% of lumen diameter), left main disease, functional class, left ventricular ejection fraction, angina pectoris, maximal ST depression, or mean workload during exercise test. MIBG and MIBI defects were significantly larger in patients with severe coronary stenoses than in patients with moderate stenoses (50% to 89% of lumen diameter) (16.4 +/- 8.9% vs 6.0 +/- 5.2% [p <0.05] and 5.0 +/- 3.1% vs 0.6 +/- 1.3% [p <0.001], respectively). The size of MIBG (16.1 +/- 8.9%) and MIBI defects (7.3 +/- 6.5%) at rest in postinfarction patients did not differ from patients with severe stenoses. Our study demonstrates that cardiac adrenergic tissue is very sensitive to ischemia and that regional cardiac sympathetic denervation can occur in patients with stable coronary artery disease without previous myocardial infarction.

Adult↗

Transcriptional and translational adjustments of psbA gene expression in mature chloroplasts during photoinhibition and subsequent repair of photosystem II.

The D1 reaction centre protein of photosystem II (PSII), encoded by the plastid psbA gene, has the highest turnover rate of all thylakoid proteins, due to light-induced damage to D1. The expression of the psbA gene was studied in chloroplasts of fully developed pea (Pisum sativum L.) leaves during high-light photoinhibitory treatment and subsequent restoration of PSII function at low light. psbA transcript levels were determined and the translational activity was followed by in vivo pulse-labelling, by in vitro translations with intact chloroplasts, and by run-off translations on isolated thylakoid membranes. PSII photochemical efficiency was determined in vivo by monitoring the ratio of variable fluorescence to maximal fluorescence (F(V)/F(M)). Enhanced D1 synthesis in pea leaves, upon a shift first from darkness to growth light and subsequently to high light, was accompanied by a substantial increase in the total number of pshA transcripts and by the accumulation of psbA mRNA x initiation complexes on thylakoid membrane. This suggested that high-light illumination increased the transcriptional activity of the psbA gene in mature leaves, and that enhanced translational initiation of psbA mRNA was followed by docking of the initiation complexes to the thylakoid membrane. The high-light-induced increase in the number of thylakoid-associated psbA mRNA x initiation complexes, occurred in parallel with enhanced in vivo D1 synthesis. This, however, did not result in an enhanced accumulation of D1 translation products in in vitro run-off translations when pea leaves were shifted from growth light to high light. This may suggest that at high light only a portion of thylakoid-associated psbA mRNA can be under translational elongation at a given moment. When the leaves were shifted from high light to low light to allow repair of PSII, thylakoid-associated psbA mRNA was rapidly released from the membrane and the high-light-induced pool of psbA transcripts was degraded. The synthesis of the D1 protein decreased on the same time scale. However, the restoration of PSII photochemical function, measured as F(V)/F(M), took a substantially longer time. It is concluded that during changing light conditions, mature leaves are able to adjust psbA gene expression both at the transcriptional and at the translational level.

Chloroplasts↗

Synthesis and assembly of the D1 protein into photosystem II: processing of the C-terminus and identification of the initial assembly partners and complexes during photosystem II repair.

In previous studies [van Wijk, K. J., Bingsmark, S., Aro, E.-M., & Andersson, B. (1995) J. Biol. Chem. 270, 25685-25695; van Wijk, K. J., Andersson, B., & Aro, E.-M. (1996) J. Biol. Chem 271, 9627-9636], we have demonstrated that D1 protein synthesized in isolated chloroplasts and thylakoids is incorporated into the photosystem II (PSII) core complex. By pulse-chase experiments in these in vitro systems, followed by sucrose gradient fractionation of solubilized thylakoid membranes, it was shown that this assembly proceeded stepwise; first the D1 protein was incorporated to form a PSII reaction center complex (PSII rc), and through additional assembly steps the PSII core complex was formed. In this study, we have analyzed this assembly process in more detail, with special emphasis on the initial events, through further purification and analysis of the assembly intermediates by nondenaturing Deriphat-PAGE and by flatbed isoelectric focusing. The D2 protein was found to be the dominant PSII reaction center protein initially associating with the new D1 protein. This strongly suggests that the D2 protein is the primary "receptor" or stabilizing component during or directly after synthesis of the D1 protein. After formation of the D1-D2 heterodimer, cyt b559 became attached, whereas the psbI gene product was assembled as a subsequent step, thereby forming a PSII reaction center complex. Subsequent formation of the PSII core occurred by binding of CP47 and then CP43 to the PSII rc. The rapid radiolabeling of a minor population of a PSII core subcomplex without CP43 indicated that an association of newly synthesized D1 protein with a preexisting complex consisting of D2/cyt b55q/psbI gene product/CP47 was possibly occurring, in parallel to the predominant sequential assembly pathway. The kinetics of synthesis and processing of the precursor D1 protein were followed in isolated chloroplasts and were compared with its incorporation into PSII assembly intermediates. No precursor D1 protein was found in PSII core complexes, indicating either that incorporation into the PSII core complex facilitates the cleavage of the C-terminus or, more likely, that processing is more rapid than the assembly into the PSII core.

Centrifugation, Density Gradient↗

Differential D1 dephosphorylation in functional and photodamaged photosystem II centers. Dephosphorylation is a prerequisite for degradation of damaged D1.

Light dependence and kinetics of reversible phosphorylation of the D1 reaction center protein of Photosystem II was studied in pumpkin leaves. At growth light, maximal phosphorylation of D1 was observed after illumination of 1 h, with higher phosphorylation rates at stronger irradiances. 70-85% of D1 became phosphorylated, corresponding to the proportion of the protein in appressed thylakoid membranes. Comparison of the kinetics of D1 phosphorylation and photoinactivation of Photosystem II revealed that D1 phosphorylation became saturated before any significant photoinhibition of Photosystem II could be detected. Dephosphorylation of D1 in both dim light and darkness was determined in leaves preilluminated with high light for various periods. Similar rates of D1 dephosphorylation were observed after short preillumination conditions that induce no significant loss of functional Photosystem II centers. In contrast, photodamage to Photosystem II centers significantly decreased the dephosphorylation rate of D1 in darkness, and no dephosphorylation occurred in leaves containing mainly damaged Photosystem II centers. Darkness also blocked the degradation of damaged D1 after photoinhibitory preillumination. Degradation of damaged D1 could be prevented even in dim light by sodium fluoride, an inhibitor of protein phosphatases, indicating that dephosphorylation is a prerequisite for D1 proteolysis. We conclude that in higher plants (i) high light induced photodamage to Photosystem II occurs in the centers containing phosphorylated D1. (ii) Dephosphorylation of phosphorylated and photodamaged D1 is associated with the repair cycle of inactivated Photosystem II and is a light-dependent reaction in vivo. (iii) Dephosphorylation of D1 in functional Photosystem II centers, however, occurs rapidly and independent of light. We suggest that two reversible phosphorylation cycles with spatially segregated protein phosphatases are involved in dephosphorylation of functional and damaged phosphorylated D1, respectively.

Carbon Dioxide↗

Degradation pattern of photosystem II reaction center protein D1 in intact leaves. The major photoinhibition-induced cleavage site in D1 polypeptide is located amino terminally of the DE loop.

Photoinhibition-induced degradation of the D1 protein of the photosystem II reaction center was studied in intact pumpkin (Cucurbita pepo L.) leaves. Photoinhibition was observed to cause the cleavage of the D1 protein at two distinct sites. The main cleavage generated an 18-kD N-terminal and a 20-kD C-terminal degradation fragment of the D1 protein. this cleavage site was mapped to be located clearly N terminally of the DE loop. The other, less-frequent cleavage occurred at the DE loop and produced the well-documented 23-kD, N-terminal D1 degradation product. Furthermore, the 23-kD, N-terminal D1 fragment appears to be phosphorylated and can be detected only under severe photoinhibition in vivo. Comparison of the D1 degradation pattern after in vivo photoinhibition to that after in vitro acceptor-side and donor-side photoinhibition, performed with isolated photosystem II core particles, gives indirect evidence in support of donor-side photoinhibition in intact leaves.

Light↗

Methotrexate-linked ventricular arrhythmias.

A 36-year-old male, who 1 year previously had survived a large anterior myocardial infarction, followed by cardiac arrest, was treated a few months for psoriasis with oral methotrexate, at single weekly oral doses of up to 10 mg, when he had to be hospitalized due to anginal pain and palpitation. Repeated 24-hour electrocardiogram recordings revealed ventricular ectopy up to 580 premature beats per hour. The ventricular premature beats were almost completely abolished after a few days' discontinuation of methotrexate therapy but recurred a few hours after an attempt to restart it had been made. A coronary angiogram showed only minimal wall abnormalities. Electrophysiological testing and endomyocardial biopsy were normal.

Administration, Oral↗

Preoperative diagnosis of coronary artery disease in patients with valvular heart disease using technetium-99m isonitrile tomographic imaging together with high-dose dipyridamole and handgrip exercise.

Forty-seven consecutive patients (mean age 61 +/- 8 years) referred for cardiac catheterization due to moderate to severe aortic (n = 30) or mitral (n = 17) valvular heart disease were examined by technetium-99m isonitrile tomography together with a high-dose dipyridamole infusion (0.7 mg/kg) and handgrip stress. Tomography did not identify coronary artery disease (CAD) in 3 of the 21 patients with angiographically proven disease (sensitivity 86%) and suggested false positive results in 5 of the 26 without the disease (specificity 81% and negative predictive accuracy 88%). No patient without angina pectoris and with negative scintigraphy (n = 14) had angiographically significant (greater than or equal to 50% diameter stenosis) CAD. Overall vessel sensitivity was 63%, and specificity was 92%. The frequency of side effects during the dipyridamole-handgrip test was only 7%. No serious complications occurred during stress tests. Thus, technetium-99m isonitrile tomographic imaging, together with high-dose dipyridamole and handgrip exercise, is a useful noninvasive method in excluding significant CAD in patients with valvular heart disease.

Coronary Angiography↗