Spatiotemporal trends of illegal activities from ranger-collected data in a Ugandan national park.

Within protected areas, biodiversity loss is often a consequence of illegal resource use. Understanding the patterns and extent of illegal activities is therefore essential for effective law enforcement and prevention of biodiversity declines. We used extensive data, commonly collected by ranger patrols in many protected areas, and Bayesian hierarchical models to identify drivers, trends, and distribution of multiple illegal activities within the Queen Elizabeth Conservation Area (QECA), Uganda. Encroachment (e.g., by pastoralists with cattle) and poaching of noncommercial animals (e.g., snaring bushmeat) were the most prevalent illegal activities within the QECA. Illegal activities occurred in different areas of the QECA. Poaching of noncommercial animals was most widely distributed within the national park. Overall, ecological covariates, although significant, were not useful predictors for occurrence of illegal activities. Instead, the location of illegal activities in previous years was more important. There were significant increases in encroachment and noncommercial plant harvesting (nontimber products) during the study period (1999-2012). We also found significant spatiotemporal variation in the occurrence of all activities. Our results show the need to explicitly model ranger patrol effort to reduce biases from existing uncorrected or capture per unit effort analyses. Prioritization of ranger patrol strategies is needed to target illegal activities; these strategies are determined by protected area managers, and therefore changes at a site-level can be implemented quickly. These strategies should also be informed by the location of past occurrences of illegal activity: the most useful predictor of future events. However, because spatial and temporal changes in illegal activities occurred, regular patrols throughout the protected area, even in areas of low occurrence, are also required.

Does climate change explain the decline of a trans-Saharan Afro-Palaearctic migrant?

There is an urgent need to understand how climate change will impact on demographic parameters of vulnerable species. Migrants are regarded as particularly vulnerable to climate change; phenological mismatch has resulted in the local decline of one passerine, whilst variations in the survival of others have been related to African weather conditions. However, there have been few demographic studies on trans-Saharan non-passerine migrants, despite these showing stronger declines across Europe than passerines. We therefore analyse the effects of climate on the survival and productivity of common sandpipers Actitis hypoleucos, a declining non-passerine long-distant migrant using 28 years' data from the Peak District, England. Adult survival rates were significantly negatively correlated with winter North Atlantic Oscillation (NAO), being lower when winters were warm and wet in western Europe and cool and dry in northwest Africa. Annual variation in the productivity of the population was positively correlated with June temperature, but not with an index of phenological mismatch. The 59% population decline appears largely to have been driven by reductions in adult survival, with local productivity poorly correlated with subsequent population change, suggesting a low degree of natal philopatry. Winter NAO was not significantly correlated with adult survival rates in a second, Scottish Borders population, studied for 12 years. Variation in climatic conditions alone does not therefore appear to be responsible for common sandpiper declines. Unlike some passerine migrants, there was no evidence for climate-driven reductions in productivity, although the apparent importance of immigration in determining local recruitment complicates the assessment of productivity effects. We suggest that further studies to diagnose common sandpiper declines should focus on changes in the condition of migratory stop-over or wintering locations. Where possible, these analyses should be repeated for other declining migrants.

The menopause and the cardiovascular system.

Combining the wealth of epidemiological, metabolic and recent mechanistic data, it would appear biologically plausible that HRT, either oestrogen alone or in combination with progestogen, is cardioprotective. Further research is required, as information is lacking on cardiovascular effects of HRT instigated at an older age. There is a need to identify cardiovascular benefit, indirect and/or direct, of combined oestrogen/progestogen therapy using randomized trials. The various progestogen types and doses also need to be investigated. Studies are also required to investigate the effect of HRT use in higher risk patients with established CVD. There is scant information on the effect of HRT on blood pressure of patients with hypertension. Cardiovascular risk factor profiles and incidence surveys need to be conducted in developing countries to characterize their female population and to identify the prevalence of CVD; this needs to be undertaken before widespread recommendations on CVD prevention and the role of HRT can be made. If HRT is to be used effectively in the future treatment of heart disease in women these questions need to be addressed. At present HRT is indicated for the relief of menopausal symptoms and the prevention of osteoporosis. In women without these indications, ORT may be recommended in those who have had a premature menopause, and possibly in those who have established CHD or who are at high risk of developing CHD. It is too early to suggest a blanket recommendation for the use of HRT in the treatment of the symptoms of women with established CVD, but HRT after the menopause may at least be safely used in the secondary prevention of CHD.

Oestrogen as a calcium channel blocker.

This paper reviews the evidence for calcium-antagonist properties of oestrogen which may offer long-term protective effects on the cardiovascular system in postmenopausal women. Oestrogen has already been shown to have a beneficial effect on cholesterol metabolism and deposition, thereby inhibiting the formation of atherosclerotic plaque and coronary atheroma. Calcium antagonism, resulting in both acute and chronic modulation of coronary and peripheral vasomotion, is another mechanism by which oestrogens may provide cardiovascular benefits to women, including those with existing cardiovascular disease.

Cardioprotective effects of ovarian hormones.

This paper reviews the evidence regarding the cardioprotective effects of oestrogen replacement therapy in postmenopausal women. Oestrogens have been shown to improve serum lipid profiles, carbohydrate metabolism, and insulin sensitivity; prevent the formation and development of atherosclerotic plaque; reduce blood pressure and plasma fibrinogen levels; and favourably affect overall cardiac function. Thus, oestrogen replacement therapy may prevent or inhibit the progression of existing coronary disease, and may also have a protective effect against acute cardiovascular and cerebrovascular ischaemic events.

Cyclical variation in paroxysmal supraventricular tachycardia in women.

BACKGROUND: Paroxysmal supraventricular tachycardia (SVT) in premenopausal women is often judged to be related to anxiety, and may be associated with the menstrual cycle. The aim of this study was to determine whether a cyclical variation of episodes of SVT exists and to correlate such variation with cyclical variation in plasma ovarian hormones. METHODS: 26 women (mean age 36 [SD 8] years; with paroxysmal SVT were screened; those with regular menses who experienced at least three episodes of paroxysmal SVT in two consecutive 48-hour ambulatory ECG recordings were included. 13 patients (aged 32 [6] years) met these criteria. Patients underwent 48-hour ambulatory ECG monitoring and determination of plasma concentrations of oestradiol-17 beta and progesterone on day 7, 14, 21, and 28 of their menstrual cycle. FINDINGS: An increase in the number and duration of episodes of paroxysmal SVT was observed on day 28 as compared to day 7 of the menstrual cycle. A significant positive correlation was found between plasma progesterone and number of episodes and duration of SVT (5.6 [2.2] ng/mL; r=0.83, p=0.0004; and r=0.82, p=0.0005), while a significant inverse correlation was found between plasma oestradiol-17 beta and number of episodes and duration of SVT (155 [22] pg/mL; r=0.89, p<0.0001; and r=0.81, p=0.0007). INTERPRETATION: Women with paroxysmal SVT and normal menses exhibit a cyclical variation in the occurrence of the arrhythmia with their menstrual cycle. There is a close correlation between the episodes of paroxysmal SVT and the plasma concentrations of ovarian hormones. These data suggest that changes in plasma levels of ovarian hormones (and their interaction) may be of importance in determining episodes of arrhythmia in such patients. The mechanisms of these effects are unknown.

17 beta-Estradiol attenuates acetylcholine-induced coronary arterial constriction in women but not men with coronary heart disease.

BACKGROUND: Women are protected from coronary artery disease until the menopause. Ovarian hormones are vasoactive substances that influence both hemodynamic parameters and atheroma formation. Intravenous ethinyl estradiol has been shown to reverse acetylcholine-induced vasoconstriction in cynomolgus monkeys and humans, and 17 beta-estradiol improves exercise-induced myocardial ischemia in female patients. We investigated the effect of the naturally occurring estrogen 17 beta-estradiol on the coronary circulation in postmenopausal women and men with coronary artery disease. METHODS AND RESULTS: We studied nine postmenopausal women 59 +/- 3 years old, mean +/- SEM, and seven men 52 +/- 4 years old with proven coronary artery disease. They underwent measurement of coronary artery diameter and coronary blood flow after intracoronary infusion of acetylcholine 1.6 and 16 micrograms/min before and 20 minutes after intracoronary administration of 2.5 micrograms of 17 beta-estradiol into atherosclerotic, nonstenotic coronary arteries. Changes in coronary artery diameter were measured by quantitative angiography, and changes in coronary blood flow were measured with an intracoronary Doppler catheter. In female patients, acetylcholine 1.6 and 16 micrograms/min caused constriction before the administration of 17 beta-estradiol (-6 +/- 2% and -8 +/- 5%, respectively, compared with baseline). This constrictor response was converted to dilatation after intracoronary administration of 17 beta-estradiol (+8 +/- 2% and +9 +/- 3%, respectively; P < .01 before versus after estrogen). Acetylcholine 1.6 and 16 micrograms/min increased coronary blood flow before and after the infusion of 17 beta-estradiol. However, the mean acetylcholine-induced increases in coronary flow were significantly greater (P < .009) after (126 +/- 37% and 248 +/- 89%, respectively) than before (94 +/- 31% and 143 +/- 49% mL/min, respectively) the administration of 17 beta-estradiol. 17 beta-Estradiol alone had no significant effect on coronary diameter or coronary blood flow (P > .05). Isosorbide dinitrate (1 mg) caused dilatation of the coronary arteries by 11 +/- 2% (P < .005). In men, acetylcholine 1.6 and 16 micrograms/min caused constriction both before and after the administration of 17 beta-estradiol and caused similar increases in coronary blood flow both before and after the intracoronary administration of 17 beta-estradiol. Infusion of intracoronary placebo in six female control patients 55 +/- 3 years old and six male control patients 56 +/- 3 years old did not change coronary diameter responses or coronary blood flow responses to acetylcholine. CONCLUSIONS: 17 beta-Estradiol modulates acetylcholine-induced coronary artery responses of female but not male atherosclerotic coronary arteries in vivo. These human data confirm reports from studies in cynomolgus monkeys that estrogen modulates the responses of atherosclerotic coronary arteries. An enhancement of endothelium-dependent relaxation by natural estrogen (as used in most hormone replacement therapy) may be important in postmenopausal women with established coronary heart disease and may contribute to the acute effect of 17 beta-estradiol on blood flow and its long-term protective effect on the development of coronary artery disease.