Elevated atmospheric humidity shapes the carbon cycle of a silver birch forest ecosystem: A FAHM study.

Processes determining the carbon (C) balance of a forest ecosystem are influenced by a number of climatic and environmental factors. In Northern Europe, a rise in atmospheric humidity and precipitation is predicted. The study aims to ascertain the effect of elevated atmospheric humidity on the components of the C budget and on the C-sequestration capacity of a young birch forest. Biomass production, soil respiration, and other C fluxes were measured in young silver birch (Betula pendula Roth) stands growing on the Free Air Humidity Manipulation (FAHM) experimental site, located in South-East Estonia. The C input fluxes: C sequestration in trees and understory, litter input into soil, and methane oxidation, as well as C output fluxes: soil heterotrophic respiration and C leaching were estimated. Humidified birch stands stored C from the atmosphere, but control stands can be considered as C neutral. Two years of elevated air humidity increased C sequestration in the understory but decreased it in trees. Humidification treatment increased remarkably the C input to the soil. The main reason for such an increase was the higher root litter input into the soil, brought about by the more than two-fold increase of belowground biomass production of the understory in the humidification treatment. Elevated atmospheric humidity increased C sequestration in young silver birch stands, mitigating increasing CO2 concentration in the atmosphere. However, the effect of elevated atmospheric humidity is expected to decrease over time, as plants and soil organisms acclimate, and new communities emerge.

A comparative perspective on longevity: the effect of body size dominates over ecology in moths.

Both physiologically and ecologically based explanations have been proposed to account for among-species differences in lifespan, but they remain poorly tested. Phylogenetically explicit comparative analyses are still scarce and those that exist are biased towards homoeothermic vertebrates. Insect studies can significantly contribute as lifespan can feasibly be measured in a high number of species, and the selective forces that have shaped it may differ largely between species and from those acting on larger animals. We recorded adult lifespan in 98 species of geometrid moths. Phylogenetic comparative analyses were applied to study variation in species-specific values of lifespan and to reveal its ecological and life-history correlates. Among-species and between-gender differences in lifespan were found to be notably limited; there was also no evidence of phylogenetic signal in this trait. Larger moth species were found to live longer, with this result supporting a physiological rather than ecological explanation of this relationship. Species-specific lifespan values could not be explained by traits such as reproductive season and larval diet breadth, strengthening the evidence for the dominance of physiological determinants of longevity over ecological ones.

Clinical and laboratory-reconfirmed myasthenia gravis: a population-based study.

The aim of this study was to compare the clinically based prevalence of myasthenia gravis (MG) with the prevalence of laboratory-confirmed cases. All patients with a diagnosis of MG living in Estonia as on 1 January 1997 were asked to participate in re-examination. The criteria for laboratory-supported MG were weakness and rapid fatigue and a positive outcome of at least one of three laboratory tests: (i) blinded acetylcholinesterase inhibitor test; (ii) determination of antibodies to acetylcholine receptor and (iii) neurophysiological examination using repetitive nerve stimulation and single-fibre EMG. Eighty-nine patients were re-examined and 70 patients (79%) fulfilled the criteria of laboratory-supported MG. The corrected prevalence ratio was 78 per million. In the non-confirmed MG group, there was more women (92%) than men (43%) whose diagnosis was established within 1 year from onset of symptoms (P = 0.016). In all women with non-confirmed MG the diagnosis was established within 1 year from referral to the physician, whereas 68% of women with confirmed MG was diagnosed within 1 year (P < 0.0001). Thus, we conclude that, in Estonia the prevalence of MG based on medical records seems overestimated by 21% and women are at higher risk of obtaining an uncertain diagnosis of MG.

Structural and functional adaptations of striated muscles to CK deficiency.

In adult mammalian muscle cells, energy consuming processes are mainly localized to the sarcolemma, sarcoplasmic reticulum (SR) and myofibrillar compartments, while energy production occurs within mitochondria or glycolytic complexes. Due to the restricted diffusion of adenine nucleotides near the active sites of ATPases involved in contractile activity and calcium homeostasis, there are multiple local systems that can locally rephosphorylate ADP and provide ATP. The creatine kinase (CK) system, with specific isoenzymes localized within each compartment, efficiently controls local adenylate pools and links energy production and utilization. However, mice lacking one or both of the MM-CK and mi-CK isoforms (CK-/-) are viable and develop almost normal cardiac and skeletal muscle function under the conditions of moderate workload, suggesting adaptations or other mechanisms that may ensure efficient energy transfer. While fixed CK is essentially important, other systems could also be involved as well, such as bound glycolytic enzymes or adenylate kinase. We have shown that, additionally, a direct functional interplay exists between mitochondria and sarcoplasmic reticulum, or between mitochondria and myofilaments in muscle cells, that catalyzes direct energy and signal transfer between organelles. In cardiac cells of CK-/- mice, marked cytoarchitectural modifications were observed, and direct adenine nucleotide channeling between mitochondria and organelles was very effective to rescue SR and myofilament functions. In fast skeletal muscles, increased oxidative capacity also indicates compensatory mechanisms. In mutant mice, mitochondrial capacity increases and a direct energy channeling occurs between mitochondria on one hand and ATP consuming sites on the other. However, these systems appear to be insufficient to fully compensate for the lack of CK at high workload. It can be concluded that local rephosphorylation of ADP is a crucial regulatory point in highly differentiated and organized muscle cells to ensure contractile diversity and efficiency and that the CK system is important to control energy fluxes and energy homeostasis.

A population based epidemiological study on myasthenia gravis in Estonia.

OBJECTIVE: To describe the occurrence of myasthenia gravis in the Baltic area. METHODS: Data were obtained from hospital files recorded during the period 1942 to 1996 from neurologists and the patient organisation. Survival data were checked with the Estonian Citizenship and Migration Board. Prevalence was determined on 1 January 1997. A questionnaire on the course of myasthenia gravis was sent to all the prevalent patients. RESULTS: The size of the population surveyed was 1 462 130. The average annual incidence from 1970 to 1996 was 4.0 per million (women, 5.2; men, 2.6). The point prevalence was 99 per million (women, 133; men 59). The incidence in the younger age group (<50 years) was 3.4 per million (women, 4.8; men, 1.9) and in the older age group (>or=50 years), 5.5 (women, 5.9; men, 4.9). The prevalence ratio was twofold higher in the older age group (p<0.0001)-for men (p = 0.034) as well as for women (p<0.001). CONCLUSIONS: Prevalence and incidence values of myasthenia gravis from Estonia are similar to those reported in most studies from Europe and north America. However, there seems to be a higher frequency in the elderly (>or=50 years) in Estonia.

Decreased expression of phospholamban is not associated with lower beta-adrenergic activation in rat atria.

The aim of the study was to find out whether low phospholamban level in atria as compared with ventricles is associated with differences in sarcoplasmic reticular Ca2+-uptake and contractile performance. Relationship between phospholamban and beta-adrenergic stimulation in rat left atria and papillary muscles were examined by means of contractile measurements, sarcoplasmic reticular oxalate-supported Ca2+-uptake, and Western blotting of phosphorylated phospholamban. Phosphoprotein determination after beta-adrenergic stimulation demonstrated that the levels of Ser16 and Thr17 phosphorylated phospholamban in atria remained at about one-third of that in ventricles. However, comparison of sarcoplasmic reticular Ca2+-uptake in control and isoproterenol perfused preparations demonstrated that the effect of beta-adrenergic stimulation on sarcoplasmic reticular Ca2+-uptake was stronger in atrial preparations. Moreover, atria responded to isoproterenol with much larger increases in developed tension, contractility and relaxation rates than papillary muscles. Thus, despite lower level of phospholamban, the beta-adrenergic activation of sarcoplasmic reticular Ca2+-uptake and contractile indices are higher in atria.

Epilepsy in Estonia: a quality-of-life study.

PURPOSE: To study the impact of epilepsy and its treatment on people with epilepsy in Estonia and to analyze how it is affected by the characteristics of epilepsy. METHODS: Clinical and demographic data about patients were obtained from medical notes and mailed self-completed questionnaires (including the RAND 36-Items Health Survey 1.0 (RAND-36)). RESULTS: Information was collected from 203 patients aged 20-74 years, who all had active epilepsy. A third of the respondents had been seizure free during the last year. Eighty-four percent were receiving monotherapy. More than half of respondents felt stigmatized by epilepsy, 24.7% of them highly so. A third were working full-time, 31.9% were underemployed workers, and 11%, unemployed. Sixty-two percent of these same unemployed or underemployed workers considered their epilepsy to be a significant reason for this situation. Overall, 44% believed they had been treated unfairly at work or when trying to get a job. Study respondents scored lower in all domains on the RAND-36 than did persons from the control group. The biggest differences were found in five domains: Social functioning, Role limitations-physical, Role limitations-emotional, General health, and Vitality. CONCLUSIONS: The clinical characteristics of this study were similar to those of most other series of prevalence cases of epilepsy. The level of employment among persons with epilepsy was not lower than that in the general population. The percentage of stigmatization was high. There were significant differences in the way respondents scored on the stigma scale and on the RAND-36 domains when measuring their health status, depending above all on seizure frequency and type.

Survival of patients with primary CNS tumours in Estonia.

We studied a population-based survey that included 1417 patients with a primary central nervous system (CNS) tumour diagnosed in Estonia between 1986 and 1996. Survival rates at 1 and 5 years and median survival by histology and patient's age at diagnosis were estimated. Median survival time for all tumours was 33.2 months and 1- and 5-year survival rates were 59.3 and 46.0%, respectively. In multivariate analysis, younger age, better clinical condition (i.e. a Karnofsky Performance Status (KPS) score of 60 and more) and tumour histology were all dependent prognostic factors for better survival. Risk of death was more than 8 times greater for glioblastoma (Risk Ratio (RR) 8.31) and approximately seven times greater for anaplastic astrocytoma (RR 7.22) and other gliomas (RR 5.74) compared with meningiomas. Comparing the first (1986-1989) and the third (1994-1996) time periods, statistically significant improvements in survival occurred for all tumours and astrocytomas. Declines in survival during the second period (1990-1993) were statistically significant for all the tumour groups, but the most striking decrease took place in patients with glioblastoma. Age-specific rates showed that the increase in survival was more evident for patients aged between 45 and 64 years.

Energetic crosstalk between organelles: architectural integration of energy production and utilization.

Cells with high and fluctuating energy demands such as cardiomyocytes need efficient systems to link energy production to energy utilization. This is achieved in part by compartmentalized energy transfer enzymes such as creatine kinase (CK). However, hearts from CK-deficient mice develop normal cardiac function under conditions of moderate workload. We have therefore investigated whether a direct functional interplay exists between mitochondria and sarcoplasmic reticulum or between mitochondria and myofilaments in cardiac cells that catalyzes direct energy and signal channeling between organelles. We used the selective permeabilization of sarcolemmal membranes with saponin to study the functional interactions between organelles within the cellular architecture. We measured contractile kinetics, oxygen consumption, and caffeine-induced tension transients. The results show that in hearts of normal mice, ATP produced by mitochondria (supplied with substrates, oxygen, and adenine nucleotides) was able to sustain calcium uptake and contractile speed. Moreover, direct mitochondrially supplied ATP was nearly as effective as CK-supplied ATP and much more effective than externally supplied ATP, suggesting that a direct ATP/ADP channeling exists between the sites of energy production (mitochondria) and energy utilization (sarcoplasmic reticulum and myofilaments). On the other hand, in cardiac cells of mice deficient in mitochondrial and cytosolic CK, marked cytoarchitectural modifications were observed, and direct adenine nucleotide channeling between mitochondria and organelles was still effective for sarcoplasmic reticulum and myofilaments. Such direct crosstalk between organelles may explain the preserved cardiac function of CK-deficient mice under moderate workloads.

Dehydroepiandrosterone sulphate prevents oxygen-glucose deprivation-induced injury in cerebellar granule cell culture.

Decreased levels of dehydroepiandrosterone sulphate have been hypothesized to contribute to increased vulnerability of the ageing or stressed human brain to ischemia. To help to address the question of whether of dehydroepiandrosterone sulphate has a possible neuroprotective effect against ischemic neuronal injury, we tested its effect on the neurodegeneration induced by oxygen-glucose deprivation in rat cultured cerebellar granule cells. Dehydroepiandrosterone sulphate added to the medium after injury demonstrated a neuroprotective effect with a median inhibitory concentration of 0.5 microM. At 10 microM concentration almost full neuroprotection was observed. Even more pronounced neuroprotective effect was found when dehydroepiandrosterone sulphate was added for 48h before injury. Furthermore, partial neuroprotection of dehydroepiandrosterone sulphate was also found against 1-methyl-4-phenylpyridinium, colchicine, glutamate and N-methyl-D-aspartate-induced toxicity. Further analysis demonstrated that dehydroepiandrosterone sulphate eliminated the apoptotic features of the oxygen-glucose deprivation-induced neuronal death: DNA fragmentation and nuclear condensation/fragmentation.Thus, our data suggest that dehydroepiandrosterone sulphate may have therapeutic potential in the prevention and treatment of ischemic/hypoxic neuronal damage. The neuroprotective action of dehydroepiandrosterone sulphate was inhibited by both a GABA(A) receptor-linked chloride channel agonist and an antagonist, pentobarbital and picrotoxin, respectively. It seems that GABA(A) receptor-mediated neuronal inhibition as well as neuronal excitation can reduce the neuroprotective action of dehydroepiandrosterone sulphate.

Seizure disorders in patients with brain tumors.

The aim of this study was to analyze the clinical data of patients with epileptic seizures and diagnosed brain tumors. Analysis included 711 patients with primary and secondary brain tumors. 165 (23%) patients had experienced at least one seizure before tumor diagnosis. The mean time from the first epileptic seizure to tumor diagnosis was 16 months. The patient's age, location and pathology of tumor were associated with occurrence of seizures. Seizures were more common in patients aged 30-50 years. Tumors involving the frontal, frontoparietal, temporal and frontotemporal lobes were associated with occurrence of seizures. According to the histological diagnosis, patients with mixed gliomas (62%), oligodendrogliomas (53%) and astrocytomas (42%) experienced seizures most frequently.

Epidemiology of primary central nervous system tumors in Estonia.

During the period from 1986 to 1996, 1,665 cases of primary central nervous system (CNS) tumors were identified in the resident population of Estonia. Histological verification was available in 81% of the cases. Gliomas were more common in men, while meningiomas and neurinomas were more common in women. No significant difference was observed between the sexes for all primary CNS tumors. The age-specific incidence increased from the age of 30, reached a maximum in the age range of 50-69 years and declined in the elderly which may reflect under-diagnosis. The age-adjusted incidence rate for CNS tumors was 8.5/100,000 population. A comparison of our results with those of a previous study carried out in Estonia revealed a significant histology-specific increase in incidence in all age groups.

Felt stigma and impact of epilepsy on employment status among Estonian people: exploratory study.

This article examines the impact of epilepsy and its treatment on employment status and the extent of stigma among patients with epilepsy. Clinical and demographic data concerning patients examined during a recent epidemiological survey were obtained from medical notes and postal self-completed questionnaires. Information was collected from 90 patients aged 16-70 years. A third of the respondents had been seizure-free during the last year. Thirty-nine percent were working full-time, 24% were working part-time and 11% were unemployed. Sixty-three percent from those working part-time or unemployed considered their epilepsy to be a significant reason for this. Overall, 55.4% believed they had been treated unfairly at work or when trying to get a job. Fifty-one percent of respondents felt stigmatized by epilepsy, 14% of them highly so. The level of employment among epileptic people was not lower than in the general population. The percentage of stigmatization in general and the percentage of the severely stigmatized was as high or even higher than in other studies. Occurrence of stigma and its severity depended first and foremost on the type of seizures. The frequency of seizures was not clearly related to this.

Neuroprotective action of group I metabotropic glutamate receptor agonists against oxygen-glucose deprivation-induced neuronal death.

The metabotropic glutamate receptor (mGluR) non-selective agonist (1S,3R)-1-aminocycloheptane-trans-1,3-dicarboxylic acid [(1S, 3R)ACPD] and group I selective receptor agonist 3, 5-dihydrophenylglycine (DHPG) effectively attenuated oxygen-glucose deprivation (OGD)-induced death of the cultured cerebellar granule cells. Furthermore, (1S,3R)ACPD (100 microM) reduced the number of apoptotic cells. Antiapoptotic action of (1S,3R)ACPD was prevented by the group I selective antagonist (RS)-1-aminoindan-1, 5-dicarboxylic acid (AIDA, 100 microM) and protein kinase C (PKC) inhibitor bisindolylmaleimide (BMI, 1 microM).

Do nuclear condensation or fragmentation and DNA fragmentation reflect the mode of neuronal death?

It is generally believed that nuclear condensation and fragmentation as well as DNA fragmentation reflect the events related to the neuronal apoptosis. Our report demonstrates that severe oxygen-glucose deprivation (OGD) induced condensation and fragmentation of nuclear chromatin of neurones in primary cultures of cerebellar granule cells without intemucleosomal DNA fragmentation. DNA fragmentation detected by TUNEL assay was seen only after mild OGD or after addition of colchicine but not after severe OGD. Thus, at least in primary cerebellar granule cell cultures, the chromatin condensation and fragmentation cannot be considered as a hallmark of apoptosis but rather reflect the neuronal death despite of its form.

Subcellular creatine kinase alterations. Implications in heart failure.

We have tested the hypothesis that decreased functioning of creatine kinase (CK) at sites of energy production and utilization may contribute to alterations in energy fluxes and calcium homeostasis in congestive heart failure (CHF). Heart failure was induced by aortic banding in 3-week-old rats. Myofilaments, sarcoplasmic reticulum (SR), mitochondrial functions, and CK compartmentation were studied in situ using selective membrane permeabilization of left ventricular fibers with detergents (saponin for mitochondria and SR and Triton X-100 for myofibrils). Seven months after surgery, animals were in CHF. A decrease in total CK activity could be accounted for by a 4-fold decrease in activity and content (Western blots) of mitochondrial CK and a 30% decrease in M isoform of CK (MM-CK) activity. In myofibrils, maximal force, crossbridge kinetics, and alpha-myosin heavy-chain expression decreased, whereas calcium sensitivity of tension development remained unaltered. Myofibrillar CK efficacy was unchanged. Calcium uptake capacities of SR were estimated from the surface of caffeine-induced tension transient (SCa) after loading with different substrates. In CHF, SCa decreased by 23%, and phosphocreatine was 2 times less efficient in enhancing calcium uptake. Oxidative capacities of the failing myocardium measured as oxygen consumption per gram of fiber dry weight decreased by 28%. Moreover, the control of respiration by creatine, ADP, and AMP was severely impaired. Our observations provide evidence that alterations in CK compartmentation may contribute to alterations of energy fluxes and calcium homeostasis in CHF.

Registry of first-ever stroke in Tartu, Estonia, 1991 through 1993: outcome of stroke.

OBJECTIVES: To provide information about the functional ability of the survivors of first-ever stroke in Estonia. PATIENTS AND METHODS: A population based epidemiological study 1991 through 1993 in Tartu. Herewith the data for 1991 and 1993 are presented. A total of 519 persons were registered; 82% of them were admitted (mean length 14 days), 66% were discharged home. RESULTS: During 6 months 41% of the patients died, the remaining 305 patients were interviewed about their living conditions, and functional ability using the Barthel ADL Index. Although 58% of patients responded to the questionnaire, no significant differences in several factors between the respondents and non-respondents were found. Thirty-eight percent of the patients were totally independent in ADL. CONCLUSION: The case-fatality rate at 6 months was high in Estonia and the proportion of totally independent patients 6 months after stroke is slightly lower compared to other studies. The short length of hospital treatment was possibly compensated by sufficient support by relatives after discharge.

The risk of motor neurone disease and multiple sclerosis is different in Estonians and Russians. Data from South Estonia.

Epidemiological studies were performed in South Estonia to establish the prevalence rate of multiple sclerosis (MS) and motor neurone disease (MND). The case finding method included information from the hospital records of the central hospital in the region-the University Hospital (for MS from 1942 to 1989), from all neurologists in the region, from the Estonian MS Society and Association of Muscular Disorders, and from nursing homes in the region. The prevalence day was 31 December 1989. MND incidence was established for the period of 1986-1995. The results demonstrated high prevalence rates of MS among native Estonians (55.3 per 100 000), somewhat lower prevalence among native-born representatives of other nationalities (43.6 per 100 000) and the lowest prevalence rate of MS among non-Estonian immigrants (26.6 per 100 000). The differences were not statistically significant. The results for MND demonstrated the opposite pattern. The mean annual incidence rate of MND for 10 years was statistically significantly higher among people of other nationalities (2.5 per 100 000) and Russians (2.6 per 100 000), and lower in native-born Estonians (1.1 per 100 000). No differences in health care or clinical picture were established. The reasons for the demonstrated differences in MND incidence remain unclear.

Nitric oxide inhibits cardiac energy production via inhibition of mitochondrial creatine kinase.

Nitric oxide biosynthesis in cardiac muscle leads to a decreased oxygen consumption and lower ATP synthesis. It is suggested that this effect of nitric oxide is mainly due to the inhibition of the mitochondrial respiratory chain enzyme, cytochrome c oxidase. However, this work demonstrates that nitric oxide is able to inhibit soluble mitochondrial creatine kinase (CK), mitochondrial CK bound in purified mitochondria, CK in situ in skinned fibres as well as the functional activity of mitochondrial CK in situ in skinned fibres. Since mitochondrial isoenzyme is functionally coupled to oxidative phosphorylation, its inhibition also leads to decreased sensitivity of mitochondrial respiration to ADP and thus decreases ATP synthesis and oxygen consumption under physiological ADP concentrations.