Environmental drivers of increased ecosystem respiration in a warming tundra.

Arctic and alpine tundra ecosystems are large reservoirs of organic carbon1,2. Climate warming may stimulate ecosystem respiration and release carbon into the atmosphere3,4. The magnitude and persistency of this stimulation and the environmental mechanisms that drive its variation remain uncertain5-7. This hampers the accuracy of global land carbon-climate feedback projections7,8. Here we synthesize 136 datasets from 56 open-top chamber in situ warming experiments located at 28 arctic and alpine tundra sites which have been running for less than 1 year up to 25 years. We show that a mean rise of 1.4 °C [confidence interval (CI) 0.9-2.0 °C] in air and 0.4 °C [CI 0.2-0.7 °C] in soil temperature results in an increase in growing season ecosystem respiration by 30% [CI 22-38%] (n = 136). Our findings indicate that the stimulation of ecosystem respiration was due to increases in both plant-related and microbial respiration (n = 9) and continued for at least 25 years (n = 136). The magnitude of the warming effects on respiration was driven by variation in warming-induced changes in local soil conditions, that is, changes in total nitrogen concentration and pH and by context-dependent spatial variation in these conditions, in particular total nitrogen concentration and the carbon:nitrogen ratio. Tundra sites with stronger nitrogen limitations and sites in which warming had stimulated plant and microbial nutrient turnover seemed particularly sensitive in their respiration response to warming. The results highlight the importance of local soil conditions and warming-induced changes therein for future climatic impacts on respiration.

Suicide methods in Europe: a gender-specific analysis of countries participating in the "European Alliance Against Depression".

OBJECTIVE: To identify the most frequent gender-specific suicide methods in Europe. DESIGN: Proportions of seven predominant suicide methods utilised in 16 countries participating in the European Alliance Against Depression (EAAD) were reported in total and cross-nationally. Relative risk (RR) relating to suicide methods and gender was calculated. To group countries by pattern of suicide methods, hierarchical clustering was applied. SETTING AND PARTICIPANTS: Data on suicide methods for 119,122 male and 41,338 female cases in 2000-4/5 from 16 EAAD countries, covering 52% of European population were obtained. RESULTS: Hanging was the most prevalent suicide method among both males (54.3%) and females (35.6%). For males, hanging was followed by firearms (9.7%) and poisoning by drugs (8.6%); for females, by poisoning by drugs (24.7%) and jumping from a high place (14.5%). Only in Switzerland did hanging rank as second for males after firearms. Hanging ranked first among females in eight countries, poisoning by drugs in five and jumping from a high place in three. In all countries, males had a higher risk than females of using firearms and hanging and a lower risk of poisoning by drugs, drowning and jumping. Grouping showed that countries might be divided into five main groups among males; for females, grouping did not yield clear results. CONCLUSIONS: Research on suicide methods could lead to the development of gender-specific intervention strategies. Nevertheless, other approaches, such as better identification and treatment of mental disorders and the improvement of toxicological aid should be put in place.

Cationic ester-containing gemini surfactants: chemical hydrolysis and biodegradation.

Two cationic gemini surfactants having ester bonds between the hydrophobic tail and the cationic moiety have been synthesized. The ester bonds were either with the ester carbonyl group away from the positive charge (esterquat type arrangement) or facing the positive charge (betaine ester type arrangement). The chemical hydrolysis of the surfactants was investigated and compared with the hydrolysis of the corresponding monomeric surfactants. The betaine ester type of surfactants was found to hydrolyze much faster than the esterquat surfactants. It was also seen that above the critical micelle concentration the gemini surfactants were much more susceptible to alkaline hydrolysis than the corresponding monomeric surfactants. The biodegradation of the geminis and the monomeric surfactants were also studied. It was found that whereas the monomeric surfactants were rapidly degraded, the two gemini surfactants were more resistant to biodegradation and could not be classified as readily biodegradable. The 60% biodegradation was reached after 35-40 days. Thus, there was no correlation between rate of chemical hydrolysis and rate of biodegradation.

Adsorption of ethoxylated cationic surfactants on self-assembled monolayers of alkanethiols on gold using surface plasmon resonance detection.

Adsorption of a series of ethoxylated cationic surfactants at model surfaces of alkanethiol self-assembled monolayers was studied by the surface plasmon resonance technique. Model surfaces were tailor-made by choosing alkanethiols or mixtures of alkanethiols with methyl, hydroxyl, carboxyl, and trimethylammonium groups in terminal position. The ethoxylated and quaternized cationic surfactants having from 2 to 18 oxyethylene units, showed a decrease in adsorbed amount with increasing oxyethylene chain length for both hydrophobic and hydrophilic surfaces. On a negatively charged surface, containing carboxylate groups, the surfactant with only two oxyethylene groups adsorbed strongly due to electrostatic attraction and the adsorption increased with increasing amount of surface carboxylate groups. This work shows the usefulness of self-assembled alkanethiols on gold as a tool for performing surfactant adsorption studies on surfaces with variable hydrophobicity and charge.

Self-assembled Gemini surfactant film-mediated dispersion stability.

The force-distance curves of 12-2-12 and 12-4-12 Gemini quaternary ammonium bromide surfactants on mica and silica surfaces obtained by atomic force microscopy (AFM) were correlated with the structure of the adsorption layer. The critical micelle concentration was measured in the presence or absence of electrolyte. The electrolyte effect (the decrease of CMC) is significantly more pronounced for Gemini than for single-chain surfactants. The maximum compressive force, F(max), of the adsorbed surfactant aggregates was determined. On the mica surface in the presence of 0.1 M NaCl, the Gemini micelles and strong repulsive barrier appear at surfactant concentrations 0.02-0.05 mM, which is significantly lower than that for the single C(12)TAB (5-10 mM). This difference between single and Gemini surfactants can be explained by a stronger adsorption energy of Gemini surfactants. The low concentration of Gemini at which this surfactant forms the strong micellar layer on the solid/solution interface proves that Gemini aggregates (micelles) potentially act as dispersing agent in processes such as chemical mechanical polishing or collector in flotation. The AFM force-distance results obtained for the Gemini surfactants were used along with turbidity measurements to determine how adsorption of Gemini surfactants affects dispersion stability. It has been shown that Gemini (or two-chain) surfactants are more effective dispersing agents, and that in the presence of electrolyte, the silica dispersion stability at pH 4.0 can also be achieved at very low surfactant concentrations ( approximately 0.02 mM).

Antioxidant therapy attenuates JNK activation and apoptosis in the remote noninfarcted myocardium after large myocardial infarction.

We hypothesized that the concomitant occurrence of increased oxidative stress, JNK activation, and myocyte apoptosis in the remote myocardium (RM) following a large myocardial infarction (MI) are causally related. Three days following coronary ligation, rats were randomized to treatment with probucol and PDTC (MI-T) or vehicle (MI). Control rats (C) underwent sham operation. At 7 weeks, TBARS assay showed increased level of lipid-peroxidation within the RM in the MI group vs C, which was completely inhibited in the MI-T group. Similarly, Western blot analysis showed a twofold increase in p-JNK in the MI group, vs C, which was attenuated in MI-T, a result confirmed by a JNK-kinase activity. Furthermore, apoptosis was increased within the RM in MI vs C, while this was inhibited in MI-T. We conclude that long-term antioxidant therapy with probucol and PDTC attenuates oxidative stress, JNK activation, and myocyte apoptosis within the RM after large MI.

Antioxidants attenuate myocyte apoptosis in the remote non-infarcted myocardium following large myocardial infarction.

OBJECTIVE: Increased oxidative stress and myocyte apoptosis co-exist in the remote non-infarcted myocardium (RM) following a large myocardial infarction. We proposed that these phenomena are causally related. METHODS AND RESULTS: On day 3 after induction of myocardial infarction, Sprague-Dawley rats were randomized to receive probucol and pyrrolidine dithiocarbamate (MI-T), or vehicle only (MI) for 7 weeks. Control rats (C) received vehicle. At 7 weeks, lipidperoxidation within the RM was assessed by measuring thiobarbituric acid reactive substances, which were significantly increased in MI vs. C, while MI-T was not different from C. There was a significant increase in cardiac myocytes positive for in situ TdT-UTP nick-end labeling within the RM in MI vs. C, which was inhibited in MI-T. Furthermore, internucleosomal DNA fragmentation was clearly demonstrated on agarose gels from RM in the MI group, while it was much less apparent on gels from RM in the C and MI-T groups. Western blot analysis showed a significant increase in p53, Bax and caspase-3 protein expression within the RM of MI vs. C, all of which were inhibited in the MI-T group. Furthermore, there was evidence for an increase in caspase-3 activity within the RM from MI vs. C, which was normalized in the MI-T group. CONCLUSIONS: Long-term treatment with the antioxidants probucol and pyrrolidine dithiocarbamate attenuates oxidative stress, myocyte apoptosis, caspase-3 like activity and the expression of p53, bax and caspase-3 within RM in rats after a large myocardial infarction.

Lack of seasonal mood change in the Icelandic population: results of a cross-sectional study.

OBJECTIVE: The prevalence of seasonal affective disorder-as measured by the Seasonal Pattern Assessment Questionnaire-has been found to be unexpectedly low among Icelanders. The aim of this cross-sectional study was to measure seasonal variations in the prevalence of anxiety and depression among Icelanders assessed with the Hospital Anxiety and Depression Questionnaire. METHOD: Four 1, 000-person cohorts, age 20-70 years, selected at random from the Icelandic National Register, were sent the Hospital Anxiety and Depression Scale by mail in either January, April, July, or October. Only responses from the 4-week period after each mailing were considered in the subsequent analysis. RESULTS: The mean anxiety and depression scores in winter were not higher than those in summer for either sex. There was no significant difference between winter and summer in rates of actual or borderline cases of anxiety or depression or for the two categories combined. CONCLUSIONS: This lack of seasonality in anxiety and depression is in sharp contrast to findings from similar cross-sectional studies and may reflect the low propensity for seasonal affective disorder that has been described in the Icelandic population.

Effect of protein kinase C and phospholipase A2 inhibitors on the impaired ability of human diabetic platelets to cause vasodilation.

1. The aim of this study was to examine the mechanism of impaired platelet-mediated endothelium-dependent vasodilation in diabetes. Exposure of human platelets to high glucose in vivo or in vitro impairs their ability to cause endothelium-dependent vasodilation. While previous data suggest that the mechanism for this involves increased activity of the cyclo-oxygenase pathway, the signal transduction pathway mediating this effect is unknown. 2. Platelets from diabetic patients as well as normal platelets and normal platelets exposed to high glucose concentrations were used to determine the role of the polyol pathway, diacylglycerol (DAG) production, protein kinase C (PKC) activity and phospholipase A2 (PLA2) activity on vasodilation in rabbit carotid arteries. 3. We found that two aldose-reductase inhibitors, tolrestat and sorbinil, caused only a modest improvement in the impairment of vasodilation by glucose exposed platelets. However, sorbitol and fructose could not be detected in the platelets, at either normal or hyperglycaemic conditions. We found that incubation in 17 mM glucose caused a significant increase in DAG levels in platelets. Furthermore, the DAG analog 1-oleoyl-2-acetyl-sn-glycerol (OAG) caused significant impairment of platelet-mediated vasodilation. The PKC inhibitors calphostin C and H7 as well as inhibitors of PLA2 activity normalized the ability of platelets from diabetic patients to cause vasodilation and prevented glucose-induced impairment of platelet-mediated vasodilation in vitro. 4. These results suggest that the impairment of platelet-mediated vasodilation caused by high glucose concentrations is mediated by increased DAG levels and stimulation of PKC and PLA2 activity.

Activation of JNK in the remote myocardium after large myocardial infarction in rats.

A large myocardial infarction (MI) causes a chronic hemodynamic load on the uninjured remote myocardium (RM). This may lead to oxidative stress, activation of stress-induced cell signaling and increase in myocyte apoptosis. MI was produced in 6 rats (INF) while 4 rats underwent sham operation (CON). At four weeks, there was 128% increase in right ventricular hypertrophy in the hearts from INF vs. CON. Western blot analysis showed 3.8 fold increase in JNK phosphorylation within the RM from INF vs. CON, confirmed by a 4.2 fold increase in JNK kinase activity. There was a 52% increase in TBARS within the RM from INF vs. CON, suggesting increased lipid peroxidation. Furthermore, there was a twofold increase in myocyte apoptosis within the RM in INF vs. CON. We conclude that the RM from INF is associated with activation of JNK, increased oxidative stress and enhanced myocyte apoptosis.

Diabetic human platelets release a substance that inhibits platelet-mediated vasodilation.

This study was performed to investigate the mechanism for impaired vasodilation in response to activated diabetic human platelets. As observed previously, diabetic platelets failed to cause vasorelaxation, whereas normal platelets produced normal vasodilation. However, when activated and perfused through quiescent, NG-nitro-L-arginine-pretreated arteries, diabetic and normal platelets caused similar degrees of vasoconstriction. Inhibition of serotonergic and thromboxane A2 receptors in preconstricted normal arteries also failed to improve vasodilatory responses to diabetic platelets. The amount of ADP released into the supernatant from activated diabetic and normal platelets was similar. Concomitant perfusion of activated diabetic platelets impaired vasodilation produced by abluminally applied acetylcholine but perfusion of normal platelets did not. Whereas activated diabetic platelets failed to produce vasodilation, supernatant from the same platelets caused normal vasorelaxation. Dimethylthiourea and Tiron, intracellular free radical scavengers, normalized the vasodilatory response to diabetic platelets, whereas superoxide dismutase, catalase, and mannitol did not. We conclude that the impaired vasorelaxation in response to activated diabetic platelets is caused by an unidentified, short-acting, platelet-derived substance(s) that interferes with the normal dilatory response.

Cyclosporine impairs the ability of human platelets to mediate vasodilation.

Cyclosporine causes various platelet abnormalities. Whether it affects the ability of platelets to mediate vasodilation is unknown. Platelets were isolated from healthy volunteers and 13 heart transplant patients on cyclosporine. When perfused through preconstricted normal rabbit carotid arteries, activated platelets from transplant patients failed to cause vasorelaxation, whereas normal platelets produced significant vasodilation (-4.0 +/- 1.9% versus 30 +/- 3% [P < .0001] change in vessel diameter, respectively). When normal platelets were exposed to cyclosporine in vitro, they lost their ability to cause vasodilation in a dose- and time-dependent fashion. However, when activated and perfused through quiescent, N omega-nitro-L-arginine-pretreated arteries, platelets from transplant patients and normal platelets caused similar degrees of vasoconstriction. The amount of adenosine triphosphate in the supernatant from activated cyclosporine-exposed and control platelets was similar (1.7 +/- 0.4 versus 1.5 +/- 0.3 mumol/L [P = NS], respectively). However, concomitant perfusion of activated platelets from transplant patients impaired acetylcholine-mediated, endothelium-dependent vasodilation but perfusion of normal platelets did not. Although cyclosporine-exposed platelets showed an impaired ability to produce vasorelaxation, supernatant from the same platelets caused near normal vasodilation. Human platelets exposed to cyclosporine have an impaired ability to mediated vasodilation. This is not due to increased platelet-mediated vasoconstriction or a decrease in the release of platelet-derived nucleotides but rather to a short-acting compound released by cyclosporine-exposed platelets that interferes with endothelium-dependent vasodilation.

The effect of aminophylline on pharmacological stress with intravenous adenosine.

Myocardial perfusion imaging with adenosine pharmacological stress may be useful in patients with obstructive lung disease who are unable to exercise. However, these patients are often treated with medications containing theophylline, which is an adenosine antagonist. This study assessed the effect of aminophylline on coronary vasodilation produced by intravenous adenosine as commonly used during cardiac imaging. Changes in coronary flow velocity (measured by intracoronary Doppler catheter) heart rate, arterial pressure and changes in coronary resistance were measured during intravenous infusion of adenosine at 140 micrograms/kg/min before and after aminophylline, 6 mg/kg intravenously in 12 patients. After aminophylline infusion, the theophylline level averaged 14 +/- 1 microgram/mL. The coronary hemodynamic effects of adenosine were markedly attenuated by aminophylline. Adenosine increased coronary blood flow velocity by 192 +/- 39% at control and 78 +/- 16% after aminophylline (P < .05 v control). Adenosine produced a 63 +/- 5% decrease in coronary vascular resistance at control and 40 +/- 6% (P < .05) after aminophylline. The utility of myocardial imaging techniques using coronary vasodilation with intravenous adenosine may be reduced in patients treated with theophylline-containing preparations.

Does pharmacologic coronary flow reserve reflect vasodilator responsiveness to increased myocardial demand in humans?

OBJECTIVE: To assess the relationship between maximal pharmacologic coronary flow reserve and metabolic coronary vasodilation in nonstenotic coronary arteries. BACKGROUND: Evaluation of the coronary microcirculation in humans during cardiac catheterization is commonly performed by assessment of coronary hemodynamics during administration of potent coronary vasodilators. However, the relationship between maximal pharmacologic vasodilation and flow increases occurring in response to increased myocardial demand has not been evaluated. METHODS: The coronary blood flow responses to a maximally dilating dose of intracoronary adenosine or papaverine and to a standardized atrial pacing stress were assessed in 49 patients using intracoronary Doppler velocimetry. The blood flow responses to a maximally dilating dose of intracoronary adenosine and to intravenous infusion of dobutamine were determined in 13 patients. RESULTS: The maximal pharmacologic coronary flow reserve averaged 3.2 +/- 0.1 (mean +/- SEM). The coronary blood flow velocity increased by 32 +/- 3% during atrial pacing, and the change in coronary flow velocity was correlated with the change in the mean arterial pressure x heart rate product during pacing. Regression analysis revealed no relationship between the pharmacologic coronary flow reserve and the change in coronary flow velocity during atrial pacing or the response of the flow to pacing normalized with respect to the magnitude of stress reflected by the change in rate x pressure product. The coronary blood flow velocity increased by 135 +/- 16% during dobutamine infusion. Regression analysis revealed no relationship between the pharmacologic coronary flow reserve and the change in coronary flow velocity during dobutamine infusion. CONCLUSIONS: Knowledge of the maximal pharmacologic coronary flow reserve is an inadequate surrogate for assessment of coronary vasodilation in response to increases in myocardial metabolic demand in nonstenotic arteries.

Platelets from patients with diabetes mellitus have impaired ability to mediate vasodilation.

OBJECTIVES: The purpose of this study was to examine vasomotor responses mediated by platelets from patients with diabetes mellitus. BACKGROUND: Diabetes mellitus is associated with increased cardiovascular morbidity and mortality, which in part may be due to a variety of abnormalities reported in diabetic platelets. However, the effects of diabetic platelets on vasomotor tone have not been characterized. METHODS: We compared platelet-mediated vasodilation elicited by platelets isolated from 30 healthy volunteers and 29 patients with diabetes mellitus as they were perfused through a preconstricted normal rabbit carotid artery. RESULTS: Platelets from the diabetic patients mediated an impaired dilatory response in comparison with normal platelets: 2.7 +/- 2% versus 15.8 +/- 3.4% (p < 0.001) and 4.1 +/- 2.7% versus 32.7 +/- 3.3% (p < 0.001) (mean +/- SEM) increase in vessel diameter, for 5 X 10(7) and 1 X 10(8) platelets per milliliter perfused, respectively. The degree of impairment was similar for type I (insulin-dependent) and type II (non-insulin-dependent) diabetes mellitus. Normal platelets incubated in high D-glucose concentrations lost their ability to mediate dilation in a concentration-dependent and time-dependent manner. This was not true for incubation of normal platelets in high concentrations of L-glucose or insulin. However, there was not a significant correlation between glucose control in the diabetic patients and the ability of their platelets to mediate vasodilation. CONCLUSIONS: Platelets from patients with diabetes mellitus have an impaired ability to mediate vasodilation. This impairment appears to be mediated by high glucose concentration. Further work is needed to elucidate the mechanisms for this abnormality in diabetic platelets.

Contrast cine left ventriculography: comparison of two pigtail catheter shapes and analysis of factors determining the final quality.

Ventricular arrhythmias or inadequate opacification of the ventricular cavity during contrast-cine left ventriculography frequently interfere with evaluation of regional wall motion, ejection fraction or mitral regurgitation. In this prospective, randomized study traditional (straight) pigtail catheter was compared with a new, large loop pigtail catheter (both 6 French, large lumen) in terms of the quality of the cine left ventriculograms. Straight (Group I) and curved pigtail (Group II) groups were further subdivided randomly into a preset (13 cc per second for 3 seconds with a pressure rise time of 0.5 seconds) injection rate (Group IA, n = 46, and Group IIA, n = 48) or operator definded injection rate (Group IB, n = 49, and Group IIB, n = 45) subgroups. The ventricular tachycardia and couplets occurred at similar frequency among the groups. The curved pigtail subgroups showed significantly more frequent catheter induced mitral regurgitation. However, the opacification and overall quality of the left ventriculograms were distributed similarly between the groups. Because the catheter type and injection protocol did not affect the left ventriculogram quality in our study, variables determining opacification and overall quality rating are analyzed in the overall group of 190 patients. Left ventricular opacification was excellent in 72, acceptable in 108 and marginal in 10 patients. The patients with marginal opacification were significantly heavier (P = .004) with larger left ventricular enddiastolic volumes (P = .019), and smaller amount of contrast volume per enddiastolic volume (P = .005) and kilogram body weight (P = .003). The overall quality of left ventriculograms were excellent in 38, acceptable in 133, and marginal in 19 patients. The patients with excellent left ventriculograms were significantly younger (P = .019) and slightly less heavy (P = 0.09). Significantly more female patients were also in this group (P = .036). Ventricular tachycardia was the most common cause of unsatisfactory left ventriculograms. In the RAO view, deeper (more apical) placement of the catheter was associated with higher incidence of ventricular tachycardia (53%). The most "silent" area was the posterobasal area. In conclusion, the perfect left ventriculogram remains to be an elusive goal in routine clinical practice. When using 6F highflow pigtail catheters and nonionic contrast agents, more basal catheter position and higher contrast volume increase the quality of the left ventriculograms.

Hemodynamic changes pre- and post-pacing with complete heart block and aortic valve stenosis and regurgitation.

Conduction disturbances in the setting of calcific aortic valve disease have been well documented in the literature. In this report we describe a case of a patient who presented in complete heart block and dyspnea on exertion. Subsequent non-invasive and invasive studies revealed moderate aortic stenosis and regurgitation with preserved left ventricular function. Hemodynamically important physiological pressure waveform changes occurred before and after pacing the ventricles and are highlighted here.

[Quality management by physicians in Iceland.].

The Icelandic Medical Association appointed a committee in 1993 with the task of recommending how to introduce the concept of Total Quality Management into the Icelandic healthcare system. The first task was to conduct a mail survey of the current status of quality assurance. Heads of departments at the five major hospitals in Iceland were contacted as well as the chairmen of all the specialist societies. The response rate was only 37%, but compensated by two ameliorating facts; responses were obtained from most of the major departments, and there was a considerable overlap between hospital departments and specialty societies as well as between subspecialty societies. The results indicate that quality assurance is an ingrained part of Icelandic hospitals, mostly in the form of standards and retrospective audits, not prospective actions. Methods used are further detailed. Outside hospitals, the Icelandic Society of Family Physicians stands out amongst the specialty societies represented, by having organized and carried out several projects in quality assurance. It is recommended that more emphasis shall be put on prospective methods, the setting of practice guidelines, outcome studies and research in quality assurance. The lack of quality assurance in specialty practice outside hospitals needs to be addressed with vigour.