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Maternal protein restriction is often associated with structural and functional sequelae in offspring, particularly affecting growth and renal-cardiovascular function. However, there is little understanding as to whether hypertension and kidney disease occur because of a primary nephron deficit or whether controlling postnatal growth can result in normal renal-cardiovascular phenotypes. To investigate this, female Sprague-Dawley rats were fed either a low-protein (LP, 8.4% protein) or normal-protein (NP, 19.4% protein) diet prior to mating and until offspring were weaned at postnatal day (PN) 21. Offspring were then fed a non ‘growth’ (4.6% fat) which ensured that catch-up growth did not occur. Offspring growth was determined by weight and dual energy X-ray absorptiometry. Nephron number was determined at PN21 using the disector-fractionator method. Kidney function was measured at PN180 and PN360 using clearance methods. Blood pressure was measured at PN360 using radio-telemetry. Body weight was similar at PN1, but by PN21 LP offspring were 39% smaller than controls (Pdiet < 0.001). This difference was due to proportional changes in lean muscle, fat, and bone content. LP offspring remained smaller than NP offspring until PN360. In LP offspring, nephron number was 26% less in males and 17% less in females, than NP controls (Pdiet < 0.0004). Kidney function was similar across dietary groups and sexes at PN180 and PN360. Blood pressure was similar in LP and NP offspring at PN360. These findings suggest that remaining on a slow growth trajectory after exposure to a suboptimal intrauterine environment does not lead to the development of kidney dysfunction and hypertension.
The rocky shores of the north-east Atlantic have been long studied. Our focus is from Gibraltar to Norway plus the Azores and Iceland. Phylogeographic processes shape biogeographic patterns of biodiversity. Long-term and broadscale studies have shown the responses of biota to past climate fluctuations and more recent anthropogenic climate change. Inter- and intra-specific species interactions along sharp local environmental gradients shape distributions and community structure and hence ecosystem functioning. Shifts in domination by fucoids in shelter to barnacles/mussels in exposure are mediated by grazing by patellid limpets. Further south fucoids become increasingly rare, with species disappearing or restricted to estuarine refuges, caused by greater desiccation and grazing pressure. Mesoscale processes influence bottom-up nutrient forcing and larval supply, hence affecting species abundance and distribution, and can be proximate factors setting range edges (e.g., the English Channel, the Iberian Peninsula). Impacts of invasive non-native species are reviewed. Knowledge gaps such as the work on rockpools and host–parasite dynamics are also outlined.
Stroke is one of the leading causes of death worldwide. Currently more than two thirds of the burden of stroke occurs in developing countries. Development of strategies for prevention and management of stroke in these countries requires data on incidence, risk factors and management practices that are relevant to the specific socioeconomic and cultural factors present in these populations. Yet currently available data come almost exclusively from developed countries. Herein, we aim to discuss some of the issues, impediments and opportunities faced by researchers undertaking population-based studies on the burden of stroke in developing countries. Important criteria to be addressed include the establishment of productive working relationships with both local collaborators and the community; the identification of an appropriate population group; and development of a working protocol which takes into account potential language barriers and the need for cultural sensitivity. When possible the protocol should include similar methods to studies conducted elsewhere so that comparisons can be made between regions. Furthermore, the results of such studies should be disseminated in an appropriate and timely manner to the local community and appropriate government and nongovernment organisations. This will enable the development and implementation of prevention and intervention programs to reduce the impact of stroke in these nations.
We investigated how sympathetic nerve activity and vasoactive hormones interact in controlling renal haemodynamics in pentobarbitone-anaesthetized rabbits. Renal blood flow was progressively reduced by electrical stimulation (0.5-3 Hz) of the renal nerves, during renal arterial infusion of saline, vasoconstrictors (angiotensin II and [Phe2,Ile3,Orn8]-vasopressin), or vasodilators (acetylcholine, adrenomedullin and the nitric oxide donor methylamine hexamethylene NONOate (MAHMA NONOate). A frequency-rich stimulus was also applied to test whether the vasoactive agents affect the dynamic control of renal blood flow by sympathetic nerve activity. The vasodilators tended to increase renal blood flow, but only the effect of MAHMA NONOate was statistically significant. [Phe2,Ile3,Orn8]-vasopressin reduced medullary perfusion (by 61 ± 12 %) but not renal blood flow or cortical perfusion. Angiotensin II reduced renal blood flow (33 ± 3 %) and cortical perfusion (14 ± 5 %) but not medullary perfusion. Steady-state responses of renal blood flow and cortical perfusion during renal nerve stimulation were attenuated during infusion of acetylcholine and [Phe2,Ile3,Orn8]-vasopressin, while angiotensin II attenuated responses of medullary perfusion, and MAHMA NONOate and adrenomedullin had no significant effects. The dynamic response to sympathetic nerve activity (renal blood flow responded as a low pass filter with a pure time delay of ~664 ms) was not altered by the vasoactive agents. We conclude that some vasoactive agents can modulate steady-state renal haemodynamic responses to sympathetic nerve activity in a regionally specific manner, independent of their effects on baseline renovascular tone. However, they have little impact on the dynamic response of renal blood flow to sympathetic nerve activity. Experimental Physiology (2003) 88.2, 229-241.
Excavations in 1972–75 on behalf of the Department of the Environment revealed an extensive Iron Age settlement and traces of widespread Roman agricultural and industrial activity at Wakerley, Northamptonshire (FIG. 2). The settlement was situated in Wakerley parish, immediately to the south of the road running between the villages of Wakerley and Harringworth and nine miles north-northeast of Corby (FIG. 3). It was sited on sloping ground, overlooking the valley of the River Welland, and some ½ mile from the river itself. From the site there are extensive views of the river valley to the north and west and of the hills and dales of Rutland that lie beyond. A deep natural gully occurs in the hillside, just to the west of the settlement and, as a result, the site is in an open position and fully exposed to the westerly winds. The settlement was located between the 250 and 300 ft. contours on a wide expanse of Lower Lincolnshire Limestone. Clays of the LowerEstuarine Series and outcrops of Northampton Sand and Ironstone occur on the lower slopes of the valley below the site and in the adjacent gully to the west. It is likely that a convenient supply of water would have been available in this gully in earlier periods, but this has been piped away in modern times.
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