113 resultados para Coral mortality


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Background: Trends in cardiovascular risk factors among UK adults present a complex picture. Ominous increases in obesity and diabetes among young adults raise concerns about subsequent coronary heart disease (CHD) mortality rates in this group.

Objective: To examine recent trends in age-specific mortality rates from CHD, particularly those among younger adults.

Methods and results: Mortality data from 1984 to 2004 were used to calculate age-specific mortality rates for British adults aged 35+ years, and joinpoint regression was used to assess changes in trends. Overall, the age-adjusted mortality rate decreased by 54.7% in men and by 48.3% in women. However, among men aged 35–44 years, CHD mortality rates in 2002 increased for the first time in over two decades. Furthermore, the recent declines in CHD mortality rates seem to be slowing in both men and women aged 45–54. Among older adults, however, mortality rates continued to decrease steadily throughout the period.

Conclusions: The flattening mortality rates for CHD among younger adults may represent a sentinel event. Deteriorations in medical management of CHD appear implausible. Thus, unfavourable trends in risk factors for CHD, specifically obesity and diabetes, provide the most likely explanation for the observed trends.

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Background--Diabetes mellitus increases the risk of cardiovascular disease (CVD) and all-cause mortality. The relationship between milder elevations of blood glucose and mortality is less clear. This study investigated whether impaired fasting glucose and impaired glucose tolerance, as well as diabetes mellitus, increase the risk of all-cause and CVD mortality.

Methods and Results
--In 1999 to 2000, glucose tolerance status was determined in 10 428 participants of the Australian Diabetes, Obesity, and Lifestyle Study (AusDiab). After a median follow-up of 5.2 years, 298 deaths occurred (88 CVD deaths). Compared with those with normal glucose tolerance, the adjusted all-cause mortality hazard ratios (HRs) and 95% confidence intervals (CIs) for known diabetes mellitus and newly diagnosed diabetes mellitus were 2.3 (1.6 to 3.2) and 1.3 (0.9 to 2.0), respectively. The risk of death was also increased in those with impaired fasting glucose (HR 1.6, 95% CI 1.0 to 2.4) and impaired glucose tolerance (HR 1.5, 95% CI 1.1 to 2.0). Sixty-five percent of all those who died of CVD had known diabetes mellitus, newly diagnosed diabetes mellitus, impaired fasting glucose, or impaired glucose tolerance at baseline. Known diabetes mellitus (HR 2.6, 95% CI 1.4 to 4.7) and impaired fasting glucose (HR 2.5, 95% CI 1.2 to 5.1) were independent predictors for CVD mortality after adjustment for age, sex, and other traditional CVD risk factors, but impaired glucose tolerance was not (HR 1.2, 95% CI 0.7 to 2.2).

Conclusions--This study emphasizes the strong association between abnormal glucose metabolism and mortality, and it suggests that this condition contributes to a large number of CVD deaths in the general population. CVD prevention may be warranted in people with all categories of abnormal glucose metabolism.

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Aims/hypothesis We assessed whether the relationships between insulin sensitivity and all-cause mortality as well as fatal or non-fatal cardiovascular disease (CVD) events are independent of elevated blood glucose, high blood pressure, dyslipidaemia and body composition in individuals without diagnosed diabetes.
Methods
Between 1999 and 2000, baseline fasting insulin, glucose and lipids, 2 h plasma glucose, HbA1c, anthropometrics, blood pressure, medication use, smoking and history of CVD were collected from 8,533 adults aged >35 years from the population-based Australian Diabetes, Obesity and Lifestyle study. Insulin sensitivity was estimated by HOMA of insulin sensitivity (HOMA-%S). Deaths and fatal or non-fatal CVD events were ascertained through linkage to the National Death Index and medical records adjudication.
Results
After a median of 5.0 years there were 277 deaths and 225 CVD events. HOMA-%S was not associated with all-cause mortality. Compared with the most insulin-sensitive quintile, the combined fatal or non-fatal CVD HR (95% CI) for quintiles of decreasing HOMA-%S were 1.1 (0.6–1.9), 1.4 (0.9–2.3), 1.6 (1.0–2.5) and 2.0 (1.3–3.1), adjusting for age and sex. Smoking, CVD history, hypertension, lipid-lowering medication, total cholesterol and waist-to-hip ratio moderately attenuated this relationship. However, the association was rendered non-significant by adding HDL. Fasting plasma glucose, but not HOMA-%S significantly improved the prediction of CVD, beyond that seen with other risk factors.
Conclusions/interpretation In this cohort, HOMA-%S showed no association with all-cause mortality and only a modest association with CVD events, largely explained by its association with HDL. Fasting plasma glucose was a better predictor of CVD than HOMA-%S.

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Self-compatible, hermaphroditic marine invertebrates have the potential to self-fertilize in the absence of mates or under sperm-limited conditions, and outcross when sperm is available from a variety of males. Hence, many hermaphroditic marine invertebrates may have evolved mixed-mating systems that involve facultative self-fertilization. Such mixed-mating strategies are well documented for plants but have rarely been investigated in animals. Here, I use allozyme markers to make estimates of selfing from population surveys of reef slope and reef flat sites, and contrast this with direct estimates of selfing from progeny-array analysis, for the brooding coral Seriatopora hystrix. Consistent heterozygote deficits previously reported for S. hystrix suggests that inbreeding (including the extreme of selfing) may be common in this species. I detected significant levels of inbreeding within populations (FIS=0.48) and small but significant differentiation among all sites (FST=0.04). I detected no significant differentiation among habitats (FHT=0.009) though among site differentiation did occur within the reef slope habitat (FSH=0.06), but not within the reef flat habitat (FSH=0.015). My direct estimates of outcrossing for six colonies and their progeny from a single reef flat site revealed an intermediate value (tm (±s.d.)=0.53±0.20). Inbreeding coefficients calculated from progeny arrays (Fe=0.31) were similar to indirect estimates based on adult genotype frequencies for that site (FIS=0.38). This study confirms that the mating system of this brooding coral is potentially variable, with both outcrossing and selfing.

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We have investigated the relationship between genotypic diversity, the mode of production of brooded larvae and disturbance in a range of reef habitats, in order to resolve the disparity between the reproductive mode and population structure reported for the brooding coral Pocillopora damicornis. Within 14 sites across six habitats, the ratio of the observed (G o) to the expected (G e) genotypic diversity ranged from 69 to 100% of that expected for random mating. At three other sites in two habitats the G o /G e ranged from 35 to 53%. Two of these sites were recently bleached, suggesting that asexual recruitment may be favoured after disturbance. Nevertheless, our data suggest that brooded larvae, from each of five habitats surveyed, were asexually produced. While clonal recruitment may be important in disturbed habitats, the lack of clonality detected, both in this and earlier surveys of 40 other sites, implies that a disturbance is normally insufficient to explain this species’ continued investment in clonal reproduction.

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Body condition scoring is widely used for sheep and cattle but the practice is included in only one Code of Practice for the welfare of goats in Australia. There is no published scientific evidence to support or defend its use in the assessment of welfare risks to farmed goats.

PROCEDURE: The significance of stocking rate, grazing system, body condition score (CS) and live weight were investigated in explaining the risk of mortality of individual and flocks of grazing Angora goats from hypothermia following a severe weather event in April. This event occurred 5 weeks after shearing the goats. Angora goats and Saxon Merino sheep were grazed alone, or mixed together in equal numbers at each of three stocking rates.

RESULTS: There was no mortality amongst Angora goats provided they grazed at the lowest stocking rate even when their CS was < or = 2.0. Mortality in flocks of Angora goats was most related to the CS reached during the preceding 2 months. For flocks of Angora goats there was no mortality at CS > or = 2.5 and mortality increased sharply at mean CS < 2.0. For individual Angora goats, mortality increased as CS declined and stocking rate and grazing combinations were additive in effect on mortality. Grazing with sheep increased mortality of Angora goats at higher stocking rates. The individual goat mortality rate was not dependent on individual plot effects suggesting that these results are applicable widely. Live weight loss was not related to mortality rates of goats once CS had been accounted for.
CONCLUSION: It was concluded that CS and stocking rate were highly significant determinants of welfare risk in Angora goats.

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The effects of animal species (AS; Angora goats, Merino sheep, mixed-grazed goats and sheep at the ratio of 1:1) and stocking rate (SR; 7.5, 10 and 12.5 animals/ha) on the liveweight, body condition score, carcass yield and mortality of goats and sheep were determined in a replicated experiment on improved annual temperate pastures in southern Australia from 1981 to 1984. The pattern of liveweight change was similar for both species with growth from pasture germination in autumn until maturation in late spring followed by weight loss. In winter, sheep grew faster than goats (65 versus 10 g/day, P < 0.05). In mixed-grazed treatments between November and December goats either grew when sheep were losing weight or goats lost less weight than sheep (P < 0.01). Both AS (P < 0.001) and SR (P < 0.001) affected liveweight of sheep and an AS SR interaction (P <  0.05) affected liveweight of goats. Mixed-grazed sheep were heavier than separately grazed sheep at all SR with a mean difference at 10 and 12.5/ha of 4.6 kg. Mixed-grazed goats at 10/ha were heavier than separately grazed goats from the end of the second year of the experiment, but at 12.5/ha, separately grazed goats maintained an advantage over mixed-grazed goats, with a 9.4-kg mean difference in December (P < 0.05). Body condition scores of goats and sheep declined with increasing SR; they were highest in late spring and were highly correlated with liveweight (r2 > 0.8). Both AS and SR affected (P < 0.001) carcass weight and GR tissue depth as a direct result of differences in liveweight. Adjusting for differences in carcass weight negated AS effects on GR tissue depth. The carcass weights of sheep and goats increased by similar amounts for each 1-kg increase in liveweight. Mortality of sheep (3.1% p.a.) was unaffected by AS or SR. An AS SR interaction indicated mortality of separately grazed goats at 12.5/ha and mixed-grazed goats at 10 and 12.5/ha were higher (P < 0.05) than all other goat (29 versus 9%) and sheep treatments, primarily because of increased susceptibility to cold stress. Disease prevalence differed between sheep and goats. Mixed grazing of Merino sheep and Angora goats produced complementary and competitive effects depending upon the SR. Goats used summer pasture better but winter pasture less well for liveweight gain than sheep. Angora goats should not be grazed alone or mixed grazed with sheep on annual temperate pastures at SR greater than that recommended for Merino sheep and the evidence indicates a lower SR will reduce risks associated with mortality.

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Indices of socio-economic deprivation are often used as a proxy for differences in the health behaviours of populations within small areas, but these indices are a measure of the economic environment rather than the health environment. Sets of synthetic estimates of the ward-level prevalence of low fruit and vegetable consumption, obesity, raised blood pressure, raised cholesterol and smoking were combined to develop an index of unhealthy lifestyle. Multi-level regression models showed that this index described about 50% of the large-scale geographic variation in CHD mortality rates in England, and substantially adds to the ability of an index of deprivation to explain geographic variations in CHD mortality rates.

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This study juxtaposed women's experiences of birth at home in rural Ethiopia where it is 'safe' with that in a modern health care setting where it is 'unsafe' because the distance from international maternal health policy to its implementation is vast and the 'pathway to maternal survival' can be circuitous.

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Background The aims of this study were to assess whether deprivation inequality at small area level in England is associated with coronary heart disease (CHD) mortality rates and to assess whether this provides evidence of an association between area-level and individual-level risk.

Methods Mortality rates for all wards in England were calculated using all CHD deaths between 2001 and 2006. Ward-level deprivation was measured using the Carstairs Index. Deprivation inequality within local authorities (LAs) was measured by the IQR of deprivation for wards within the LA. Relative deprivation for wards was measured as the modulus of the difference between deprivation for the ward and average deprivation for all neighbouring wards.

Results Deprivation inequality within LAs was positively associated with CHD mortality rates per 100 000 (eg, all men β; 95% CI=2.7; 1.1 to 4.3) after adjustment for absolute deprivation (p<0.001 for all models). Relative deprivation for wards was positively associated with CHD mortality rates per 100 000 (eg, all men 1.4; 0.7 to 2.1) after adjustment for absolute deprivation (p<0.001 for all models). Subgroup analyses showed that relative deprivation was independently associated with CHD mortality rates in both affluent and deprived wards.

Conclusions
Rich wards surrounded by poor areas have higher CHD mortality rates than rich wards surrounded by rich areas, and poor wards surrounded by rich areas have worse CHD mortality rates than poor wards surrounded by poor areas. Local deprivation inequality has a similar adverse impact on both rich and poor areas, supporting the hypothesis that income inequality of an area has an impact on individual-level health outcomes.