We have measured the equivalent width of the Hα emission line for 11 006 galaxies brighter than Mb=−19 (ΩΛ= 0.7, Ωm= 0.3, H0= 70 km s−1 Mpc−1) at 0.05 < z < 0.1 in the 2dF Galaxy Redshift Survey (2dFGRS), in the fields of 17 known galaxy clusters. The limited redshift range ensures that our results are insensitive to aperture bias, and to residuals from night sky emission lines. We use these measurements to trace μ*, the star formation rate normalized to L*, as a function of distance from the cluster centre, and local projected galaxy density. We find that the distribution of μ* steadily skews toward larger values with increasing distance from the cluster centre, converging to the field distribution at distances greater than ∼3 times the virial radius. A correlation between star formation rate and local projected density is also found, which is independent of cluster velocity dispersion and disappears at projected densities below ∼1 galaxy Mpc−2 (brighter than Mb=−19). This characteristic scale corresponds approximately to the mean density at the cluster virial radius. The same correlation holds for galaxies more than two virial radii from the cluster centre. We conclude that environmental influences on galaxy properties are not restricted to cluster cores, but are effective in all groups where the density exceeds this critical value. The present‐day abundance of such systems, and the strong evolution of this abundance, makes it likely that hierarchical growth of structure plays a significant role in decreasing the global average star formation rate. Finally, the low star formation rates well beyond the virialized cluster rule out severe physical processes, such as ram pressure stripping of disc gas, as being completely responsible for the variations in galaxy properties with environment.

Several epidemiological studies have reported on the association between body mass index (BMI) and risk of esophageal cancer, but these were mostly in Western populations where many are overweight or obese. There is little direct evidence about the relationship in China where the mean BMI is relatively low and the disease rate is high. We examined the data from a populationbased prospective study of 220,000 Chinese men aged 40-79 without a previous history of cancer (mean BMI 21.7 kg/m 2 ), which included 1,082 esophageal cancer deaths during 10 years of follow-up. Adjusted hazard ratios for death from esophageal cancer by baseline BMI category were calculated using Cox proportional hazards models. Even among men with good self-assessed health and BMI 18.5 kg/m 2 , there was a strong inverse association between BMI and death from esophageal cancer, with each 5 kg/ m 2 higher BMI associated with 25% (95%CI: 11-36%) lower esophageal cancer mortality. This inverse association persisted when analysis was restricted to men who had never smoked or when the first 5 years of follow-up were excluded. The strength of the relationship was consistent with the pooled estimate for squamous cell carcinoma of the esophagus in a meta-analysis of prospective studies (31% lower relative risk per 5 kg/m 2 higher BMI; 95% CI: 25-37%), but contrasted with that for adenocarcinoma which showed a positive association with BMI. Together, these data provide reliable evidence that in many populations low BMI is associated with an increased risk of squamous cell carcinoma of the esophagus. ' 2007 Wiley-Liss, Inc.

on behalf of the Heart Protection Study Collaborative Group Background-Low-density lipoprotein (LDL) cholesterol and high-density lipoprotein (HDL) cholesterol are established risk factors for vascular disease, but lipoprotein particle concentrations may be stronger determinants of risk. Methods and Results-Associations between vascular events and baseline concentrations of cholesterol fractions, apolipoproteins B and A 1 , and lipoprotein particles assessed by nuclear magnetic resonance were considered in the Heart Protection Study randomized trial of simvastatin versus placebo (Ͼ5000 vascular events during 5.3 years of follow-up among 20 000 participants). Major occlusive coronary events were equally strongly associated with the cholesterol-and particle-based total LDL measures; adjusted hazard ratios per 1-SD-higher level were 1.25 (95% confidence interval [CI], 1.16 -1.34) for LDL cholesterol, 1.22 (95% CI, 1.14 -1.32) for non-HDL cholesterol, 1.23 (95% CI, 1.15-1.33) for apolipoprotein B, and 1.25 (95% CI, 1.16 -1.35) for LDL particle number. Given the total LDL particle number, the distribution between small and large particles did not add predictive value. Associations of these different LDL-related measures were similar with arterial revascularization procedures but much weaker or nonexistent with ischemic stroke and other cardiac events (mainly heart failure). After adjustment for LDL particle number, the hazard ratios for major occlusive coronary event per 1-SD-higher level were 0.91 (95% CI, 0.86 -0.96) for HDL cholesterol and 0.89 (95% CI, 0.85-0.93) for HDL particle number. Other cardiac events were inversely associated with total (hazard ratio, 0.84; 95% CI, 0.79 -0.90) and small (0.82; 95% CI, 0.76 -0.89) HDL particle number but only very weakly associated with HDL cholesterol (0.94; 95% CI, 0.88 -1.00). Conclusions-In a population at 2% average coronary event risk per year, cholesterol, apolipoprotein, and particle measures of LDL were strongly correlated and had similar predictive values for incident major occlusive vascular events. It is unclear whether the associations between HDL particle numbers and other cardiac events represent a causal or reverse-causal effect. Clinical Trial Registration-URL: http://www.isrctn.org/. Unique identifier: ISRCTN48489393. arge observational studies indicate strong positive associations between low-density lipoprotein (LDL) particles, which carry cholesterol, and the risk of coronary heart disease (CHD). 1,2 Randomized trials have demonstrated that lowering LDL cholesterol (LDL-C) with statins reduces the risk of CHD death, nonfatal myocardial infarction (MI), ischemic stroke, and the need for revascularization procedures, with less benefit apparent on deaths resulting from other cardiac disease (including sudden death, arrhythmia, and heart failure). [3][4][5] Observational studies, however, have typically reported weaker associations of LDL-C (or related measures) with ischemic stroke than with CHD, 1,2 which is discordant with the findings of randomized tri...

AimsPlasma levels of apolipoprotein B (apoB), the main surface protein on LDL particles, and LDL-C, the amount of cholesterol in those particles, are closely correlated and, considered separately, are positive risk factors. Plasma levels of apolipoprotein A1, the main surface protein on HDL particles, and HDL-C, the amount of cholesterol in those particles, are also closely correlated with each other and, considered separately, are negative risk factors. The interdependence of these four risk factors is unclear.Methods and resultsCase–control study among 3510 acute myocardial infarction patients (without prior vascular disease, diabetes, or statin use) in UK hospitals and 9805 controls. Relative risks (age, sex, smoking, and obesity-adjusted) were more strongly related to apoB than to LDL-C and, given apoB, more strongly negatively related to apoA1 than to HDL-C. The ratio apoB/apoA1 was uncorrelated with time since symptom onset in cases, was reproducible in samples collected a few years apart in controls (correlation 0.81), and encapsulated almost all the predictive power of these four measurements. Its effect was continuous, substantial throughout the UK normal range [relative risk, top vs. bottom decile of this ratio, 7.3 (95% CI 5.8–9.2)] and varied little with age. The ratio apoB/apoA1 was substantially more informative about risk (χ12 = 550) than were commonly used measures such as LDL-C/HDL-C, total/HDL cholesterol, non-HDL cholesterol, and total cholesterol (χ12 = 407, 334, 204, and 105, respectively). Given apoB and apoA1, the relationship with risk of LDL-C was reversed, and this reversal was strengthened by appropriate allowance for random measurement errors in two correlated variables. Given usual apoB, lower LDL-C (consistent with smaller LDL particles) was associated with higher risk (P < 0.0001). During the first 8 h after symptom onset HDL-C increased by about 10%, precluding reliable assessment of the joint relationship of apoA1 and pre-onset HDL-C with risk in such retrospective case–control studies.ConclusionApolipoprotein ratios are more informative about risk than lipid fractions are. This suggests that, among lipoprotein particles of a particular type (LDL or HDL), some smaller and larger subtypes differ in their effects on risk. Direct measurements of even more specific subtypes of lipoprotein particles may be even more informative about risk.

With the advent of very large redshift surveys of tens to hundreds of thousands of galaxies reliable techniques for automatically determining galaxy redshifts are becoming increasingly important. The most common technique currently in common use is the cross-correlation of a galactic spectrum with a set of templates. This series of papers presents a new method based on Principal Component Analysis. The method generalizes the cross-correlation approach by replacing the individual templates by a simultaneous linear combination of orthogonal templates. This effectively eliminates the mismatch between templates and data and provides for the possibility of better error estimates. In this paper, the first of a series, the basic mathematics are presented along with a simple demonstration of the application.