Integration of micro-gravity and geodetic data to constrain shallow system mass changes at Krafla Volcano, N Iceland

New and previously published micro-gravity data are combined with InSAR data, precise levelling and GPS measurements to produce a model for the processes operating at Krafla volcano, 20 years after its most recent eruption. The data have been divided into two periods: from 1990 to 1995 and from 1996 to 2003 and show that the rate of deflation at Krafla is decaying exponentially. The net micro-gravity change at the centre of the caldera is shown, using the measured Free Air Gradient, to be -85 μGal for the first and -100 μGal for the second period. After consideration of the effects of water extraction by the geothermal power station within the caldera, the net gravity decreases are -73 ± 17 μGal for the first and -65 ± 17 μGal for the second period. These decreases are interpreted in terms of magma drainage. Following a Mogi point source model we calculate the mass decrease to be ~2 x 1010 kg/yr reflecting a drainage rate of ~0.23 m3/s, similar to the ~0.13 m3/s drainage rate previously found at Askja volcano, N-Iceland. Based on the evidence for deeper magma reservoirs and the similarity between the two volcanic systems, we suggest a pressure-link between Askja and Krafla at deeper levels (at the lower crust or the crust-mantle boundary). After the Krafla fires, co-rifting pressure decrease of a deep source at Krafla stimulated the subsequent inflow of magma, eventually affecting conditions along the plate boundary in N-Iceland, as far away as Askja. We anticipate that the pressure of the deeper reservoir at Krafla will reach a critical value and eventually magma will rise from there to the shallow magma chamber, possibly initiating a new rifting episode. We have demonstrated that by examining micro-gravity and geodetic data, our knowledge of active volcanic systems can be significantly improved

Systematic review with meta-analysis of the epidemiological evidence relating smoking to COPD, chronic bronchitis and emphysema

<p>Abstract</p> <p>Background</p> <p>Smoking is a known cause of the outcomes COPD, chronic bronchitis (CB) and emphysema, but no previous systematic review exists. We summarize evidence for various smoking indices.</p> <p>Methods</p> <p>Based on MEDLINE searches and other sources we obtained papers published to 2006 describing epidemiological studies relating incidence or prevalence of these outcomes to smoking. Studies in children or adolescents, or in populations at high respiratory disease risk or with co-existing diseases were excluded. Study-specific data were extracted on design, exposures and outcomes considered, and confounder adjustment. For each outcome RRs/ORs and 95% CIs were extracted for ever, current and ex smoking and various dose response indices, and meta-analyses and meta-regressions conducted to determine how relationships were modified by various study and RR characteristics.</p> <p>Results</p> <p>Of 218 studies identified, 133 provide data for COPD, 101 for CB and 28 for emphysema. RR estimates are markedly heterogeneous. Based on random-effects meta-analyses of most-adjusted RR/ORs, estimates are elevated for ever smoking (COPD 2.89, CI 2.63-3.17, n = 129 RRs; CB 2.69, 2.50-2.90, n = 114; emphysema 4.51, 3.38-6.02, n = 28), current smoking (COPD 3.51, 3.08-3.99; CB 3.41, 3.13-3.72; emphysema 4.87, 2.83-8.41) and ex smoking (COPD 2.35, 2.11-2.63; CB 1.63, 1.50-1.78; emphysema 3.52, 2.51-4.94). For COPD, RRs are higher for males, for studies conducted in North America, for cigarette smoking rather than any product smoking, and where the unexposed base is never smoking any product, and are markedly lower when asthma is included in the COPD definition. Variations by sex, continent, smoking product and unexposed group are in the same direction for CB, but less clearly demonstrated. For all outcomes RRs are higher when based on mortality, and for COPD are markedly lower when based on lung function. For all outcomes, risk increases with amount smoked and pack-years. Limited data show risk decreases with increasing starting age for COPD and CB and with increasing quitting duration for COPD. No clear relationship is seen with duration of smoking.</p> <p>Conclusions</p> <p>The results confirm and quantify the causal relationships with smoking.</p

The Role of Gut Dysfunction and Nutritional Factors in Liver Cirrhosis

Malnutrition is a common finding in patients with liver cirrhosis. Malnutrition has been shown to be associated with increased morbidity and mortality. Its pathogenesis remains unclear but both poor dietary intake and increased energy expenditure have been reported. Spontaneous bacterial peritonitis is an important clinical problem in cirrhotics. It may occur as a consequence of repeated access of bacteria from the intestinal lumen (translocation) to the mesenteric lymph nodes. One of the mechanisms proposed to explain bacterial translocation in cirrhosis includes increased intestinal permeability. The aims of the present study were to evaluate GI symptoms in cirrhotic patients and their possible relation to nutritional status, to assess whether gastric sensorimotor dysfunction or metabolic disturbances are associated with reduced food intake, and to investigate the role of ascites in intestinal permeability in patients with liver cirrhosis. Gastrointestinal symptoms and health-related quality of life (HRQOL) were assessed with the aid of two questionnaires. Gastric sensorimotor function was measured by means of an electronic barostat. Food intake, as assessed with a food diary, was related to fasting and postprandial glucose, insulin, leptin, and ghrelin concentrations. Intestinal permeability was evaluated by a 51Cr-EDTA permeability test. Cirrhotics were found to have increased severity of GI symptoms compared with reference values from the general population. A relationship between GI symptoms and compromised HRQOL as well as weight loss was observed. Proximal stomach relaxation to a meal was increased in patients with liver cirrhosis as compared with healthy controls but the relation between gastric accommodation and energy intake was found to be disturbed in these patients. Gastric sensitivity to distension was shown to be related to GI symptom severity and to liver cirrhosis severity scores. Patients with liver cirrhosis exhibited higher postprandial insulin and glucose concentrations compared to controls. Cirrhotics had higher fasting leptin that fell significantly postmeal and they showed an attenuated increase of ghrelin before the next expected meal. Altered glucose and hormonal levels in patients with cirrhosis were associated with poor food intake. Only a few patients with cirrhosis had increased intestinal permeability, as assessed by a 51Cr-EDTA test, which was not influenced to a major extent by ascites. Conclusions: In patients with liver cirrhosis GI symptom severity is high and it is associated with impaired HRQOL and weight loss. Gastric accommodation is not involved in the poor food intake observed in cirrhotics and gastric sensitivity seems to be a relevant factor for GI symptom generation in these patients. Altered postprandial glucose, leptin, and ghrelin levels are correlated to reduced energy intake in this patient group. Increased intestinal permeability is probably of limited importance in the pathophysiology of bacterial infections in patients with liver cirrhosis and ascites