Patients with early diabetic heart disease demonstrate a normal myocardial response to dobutamine

OBJECTIVES We sought to use quantitative markers of the regional left ventricular (LV) response to stress to infer whether diabetic cardiomyopathy is associated with ischemia. BACKGROUND Diabetic cardiomyopathy has been identified in clinical and experimental studies, but its cause remains unclear. METHODS We studied 41 diabetic patients with normal resting LV function and a normal dobutamine echo and 41 control subjects with a low probability of coronary disease. Peak myocardial systolic velocity (Sm) and early diastolic velocity (Em) in each segment were averaged, and mean Sm and Em were compared between diabetic patients and controls and among different stages of dobutamine stress. RESULTS Both Sm and Em progressively increased from rest to peak dobutamine stress. In the diabetic group, Sm was significantly lower than in control subjects at baseline (4.2 +/- 0.9 cm/s vs. 4.7 +/- 0.9 cm/s, p = 0.012). However, Sin at a low dose (6.0 +/- 1.3), before peak (8.4 +/- 1.8), and at peak stress (8.9 +/- 1.8) in diabetic patients was not significantly different from that of controls (6.3 +/- 1.4, 8.9 +/- 1.6, and 9.6 +/- 2.1 cm/s, respectively). The Em (cm/s) in the diabetic group (rest: 4.2 +/- 1.2; low dose: 5.0 +/- 1.4; pre-peak: 5.3 +/- 1.1; peak: 5.9 +/- 1.5) was significantly lower than that of controls (rest: 5.8 +/- 1.5; low dose: 6.6 +/- 1.5; pre-peak: 6.9 +/- 1.3; peak: 7.3 +/- 1.7; all p < 0.001). However, the absolute and relative increases in Sm or Em from rest to peak stress were similar in diabetic and control groups. CONCLUSIONS Subtle LV dysfunction is present in diabetic patients without overt cardiac disease. The normal response to stress suggests that ischemia due to small-vessel disease may not be important in early diabetic heart muscle disease. (C) 2003 by the American College of Cardiology Foundation.

Plasma zinc and immune markers in runners in response to a moderate increase in training volume

Changes in plasma zinc concentration and markers of immune function were examined in a group of 10 male runners (n = 10) following a moderate increase in training over four weeks. Seven sedentary males acted as controls. Fasting blood samples were taken at rest, before (T0) and after T4) four weeks of increased (+ 16 %) training and after two weeks of reduced (- 31 %) training (W. Blood was analysed for plasma zinc concentration, differential leucocyte counts, lymphocyte subpopulations and lymphocyte proliferation using incorporation of H-3-thymidine. The runners increased their training volume by 16 % over the four weeks. When compared with the nonathletes, the runners had lower concentrations of plasma zinc (p = 0.012), CD3(+) (p = 0.042) and CD19(+) lymphocytes (p = 0.010) over the four weeks. Lymphocyte proliferation in response to Concanavalin A stimulation was greater in the runners (p = 0.0090). Plasma zinc concentration and immune markers remained constant during the study. Plasma zinc concentration correlated with total leucocyte counts in the athletes at T6 (r = -0.72, p < 0.05) and with Pokeweed mitogen stimulation in the nonathletes at T6 (r = -0.92, p < 0.05). Therefore, athletes are unlikely to benefit from zinc supplementation during periods of moderately increased training volume.

A global health problem caused by arsenic from natural sources

Arsenic is a carcinogen to both humans and animals. Arsenicals have been associated with cancers of the skin, lung, and bladder. Clinical manifestations of chronic arsenic poisoning include non-cancer end point of hyper- and hypo-pigmentation, keratosis, hypertension, cardiovascular diseases and diabetes. Epidemiological evidence indicates that arsenic concentration exceeding 50 mug l(-1) in the drinking water is not public health protective. The current WHO recommended guideline value for arsenic in drinking water is 10 mug l(-1), whereas many developing countries are still having a value of 50 mug 1(-1). It has been estimated that tens of millions of people are. at risk exposing to excessive levels of arsenic from both contaminated water and arsenic-bearing coal from natural sources. The global health implication and possible intervention strategies were also discussed in this review article. (C) 2003 Elsevier Ltd. All rights reserved.

In search of the ultimate ionosonde deduced equator

A further progress has been made in defining the ionosonde deduced equator (IDE) which characterises a latitudinal transition from the northern to southern hemisphere. It is now possible to define the global IDE location as the locus of the average position between geographic and geomagnetic equators. A more complete insight to the phenomenon of the third equator (i.e. after geographic and geomagnetic equators) was made possible due to availability of ionospheric height (h'F) data from three stations positioned close to the IDE in the American and the far-east sectors. The IDE ionospheric signature (or E-type signature), detected at these stations, consists of bi-annual h'F height increases. This signature however is not consistently observed during solar cycle and at times, particularly at sunspot minimum, a weak hemispheric signature is observed (i.e. the northern or southern hemisphere signature). In general, the height increase at the IDE are considerably smaller (by a factor of 4) than at other equatorial locations, indicating that the ionosphere at the IDE location becomes less disturbed. It is suggested that the equatorial longitudinal regions which can be associated with more consistent E-type signature are located in the central Pacific and at the east coast of America, close to the intersection points of the geographic and geomagnetic equators. (C) 2003 Elsevier Ltd. All rights reserved.

Measuring the accumulated hazards of smoking: global and regional estimates for 2000

Objective: Current prevalence of smoking, even where data are available, is a poor proxy for cumulative hazards of smoking, which depend on several factors including the age at which smoking began, duration of smoking, number of cigarettes smoked per day, degree of inhalation, and cigarette characteristics such as tar and nicotine content or filter type. Methods: We extended the Peto-Lopez smoking impact ratio method to estimate accumulated hazards of smoking for different regions of the world. Lung cancer mortality data were obtained from the Global Burden of Disease mortality database. The American Cancer Society Cancer Prevention Study, phase 11 (CPS-II) with follow up for the years 1982 to 1988 was the reference population. For the global application of the method, never-smoker lung cancer mortality rates were chosen based on the estimated use of coal for household energy in each region. Results: Men in industrialised countries of Europe, North America, and the Western Pacific had the largest accumulated hazards of smoking. Young and middle age males in many regions of the developing world also had large smoking risks. The accumulated hazards of smoking for women were highest in North America followed by Europe. Conclusions: In the absence of detailed data on smoking prevalence and history, lung cancer mortality provides a robust indicator of the accumulated hazards of smoking. These hazards in developing countries are currently more concentrated among young and middle aged males.

Estimates of global mortality attributable to smoking in 2000

Background Smoking is a risk factor for several diseases and has been increasing in many developing countries. Our aim was to estimate global and regional mortality in 2000 caused by smoking, including an analysis of uncertainty. Methods Following the methods of Peto and colleagues, we used lung-cancer mortality as an indirect marker for accumulated smoking risk. Never-smoker lung-cancer mortality was estimated based on the household use of coal with poor ventilation. Relative risks were taken from the American Cancer Society Cancer Prevention Study, phase II, and the retrospective proportional mortality analysis of Liu and colleagues in China. Relative risks were corrected for confounding and extrapolation to other regions. Results We estimated that in 2000, 4.83 (uncertainty range 3.94-5.93) million premature deaths in the world were attributable to smoking; 2.41 (1.80-3.15) million in developing countries and 2.43 (2.13-2.78) million in industrialised countries. 3.84 million of these deaths were in men. The leading causes of death from smoking were cardiovascular diseases (1.69 million deaths), chronic obstructive pulmonary disease (0.97 million deaths), and lung cancer (0.85 million deaths). Interpretation Smoking was an important cause of global mortality in 2000. In view of the expected demographic and epidemiological transitions and current smoking patterns in the developing world, the health loss due to smoking will grow even larger unless effective interventions and policies that reduce smoking among men and prevent increases among women in developing countries are implemented.