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P. However (p + however)
Selected AbstractsImpact of Dredging on Phosphorus Transport in Agricultural Drainage Ditches of the Atlantic Coastal Plain,JOURNAL OF THE AMERICAN WATER RESOURCES ASSOCIATION, Issue 6 2008Francirose Shigaki Abstract:, Drainage ditches can be a key conduit of phosphorus (P) between agricultural soils of the Atlantic Coastal Plain and local surface waters, including the Chesapeake Bay. This study sought to quantify the effect of a common ditch management practice, sediment dredging, on fate of P in drainage ditches. Sediments from two drainage ditches that had been monitored for seven years and had similar characteristics (flow, P loadings, sediment properties) were sampled (0-5 cm) after one of the ditches had been dredged, which removed fine textured sediments (clay = 41%) with high organic matter content (85 g/kg) and exposed coarse textured sediments (clay = 15%) with low organic matter content (2.2 g/kg). Sediments were subjected to a three-phase experiment (equilibrium, uptake, and release) in recirculating 10-m-long, 0.2-m-wide, and 5-cm-deep flumes to evaluate their role as sources and sinks of P. Under conditions of low initial P concentrations in flume water, sediments from the dredged ditch released 13 times less P to the water than did sediments from the ditch that had not been dredged, equivalent to 24 mg dissolved P. However, the sediments from the dredged ditch removed 19% less P (76 mg) from the flume water when it was spiked with dissolved P to approximate long-term runoff concentrations. Irradiation of sediments to destroy microorganisms revealed that biological processes accounted for up to 30% of P uptake in the coarse textured sediments of the dredged ditch and 18% in the fine textured sediments of the undredged ditch. Results indicate that dredging of coastal plain drainage ditches can potentially impact the P buffering capacity of ditches draining agricultural soils with a high potential for P runoff. [source] Phosphorus and the regulation of nodulation in the actinorhizal symbiosis between Discaria trinervis (Rhamnaceae) and Frankia BCU110501NEW PHYTOLOGIST, Issue 1 2002Claudio Valverde Summary ,,After nitrogen (N), phosphorus (P) is the nutrient that most limits plant productivity. The role of P on growth and root nodulation was studied in the actinorhizal symbiosis between Discaria trinervis and Frankia, an intercellular infected N2,fixing association. ,,Growth, nodulation and nutrient content (N and P) were analysed in symbiotic plants receiving different supplies of P in nutrient solutions. The relative requirement of P for nodulation was analysed in P-deficient plants. ,,Nodule initiation was less impaired than general plant growth by low P. However, low P impaired nodule growth to a greater extent than plant growth. The proportion of nodule biomass, although not the number of nodules per plant, was stimulated by P supply. Autoregulation of nodulation was not affected by P. Use of N was limited by availability of P. Reserves of P in seeds were enough for the seedling to establish nodules. However nodule (and plant) growth was limited in the absence of exogenous P. ,,It is possible that P interacts with the feedback control of nodule growth that is associated with the plant demand for N. Leaf N : P ratio is negatively correlated with the proportion of nodule tissue. [source] Neurokinin-1 receptor desensitization to consecutive microdialysis infusions of substance P in human skinTHE JOURNAL OF PHYSIOLOGY, Issue 3 2005Brett J. Wong The neuropeptide substance P is known to be localized in nerve terminals in human skin and substance P-induced vasodilatation is believed to be partially dependent on nitric oxide (NO) and H1 histamine receptor activation. Unlike other neuropeptides investigated in human skin, substance P-induced vasodilatation has been shown to decline during continuous infusion, possibly suggestive of an internalization of neurokinin-1 (NK1) receptors, which are highly specific to substance P. However, questions remain regarding these mechanisms in human skin. Fifteen subjects participated in this series of studies designed to investigate the effect of consecutive infusions and possible mechanisms of substance P-induced vasodilatation in human skin. Two concentrations of substance P (10 ,m and 20 ,m) were tested via intradermal microdialysis in two groups of subjects. Site 1 served as a control and received substance P only. Site 2 received substance P combined with 10 mm l -NAME to inhibit NO synthase. Site 3 received substance P combined with 500 ,m pyrilamine, an H1 receptor antagonist. Site 4 received substance P combined with 10 mm l -NAME plus 500 ,m pyrilamine. Red blood cell (RBC) flux was measured via laser-Doppler flowmetry to provide an index of skin blood flow. Cutaneous vascular conductance was calculated as RBC flux/mean arterial pressure and was normalized to maximal vasodilatation via 28 mm sodium nitroprusside. Substance P was perfused through each microdialysis fibre at a rate of 4 ,l min,1 for 15 min. The subsequent increase in skin blood flow was allowed to return to baseline (,45,60 min) and a stable 5 min plateau was used as a new baseline (post-infusion baseline). A second dose of substance P was then delivered to the skin and skin blood flow was monitored for 45,60 min. Substance P produced a dose-dependent increase in skin blood flow with the concentrations of substance P tested, which was significantly attenuated in the presence of l -NAME and the combination of l -NAME plus pyrilamine. However, substance P-induced vasodilatation was unaffected in the presence of pyrilamine. There was no significant difference between the l -NAME-only sites and the l -NAME plus pyrilamine sites. Importantly, the second dose of substance P did not produce a significant increase in skin blood flow compared to the initial baseline or the post-infusion baseline. These data suggest substance P-induced vasodilatation delivered via microdialysis contains an NO component but does not contain an H1 receptor activation component at the doses tested. Additionally, these data provide evidence for NK1 receptor desensitization as there was no observable increase in skin blood flow following a second administration of substance P. This may provide a useful model for studying the role of substance P in the control of skin blood flow in humans. [source] Stoppage: An issue for segregation analysisGENETIC EPIDEMIOLOGY, Issue 3 2001S.L. Slager Abstract Segregation analysis assumes that the observed family-size distribution (FSD), i.e., distribution of number of offspring among nuclear families, is independent of the segregation ratio p. However, for certain serious diseases with early onset and diagnosis (e.g., autism), parents may change their original desired family size, based on having one or more affected children, thus violating that assumption. Here we investigate "stoppage," the situation in which such parents have fewer children than originally planned. Following Brookfield et al. [J Med Genet 25:181,185, 1988], we define a stoppage probability d that after the birth of an affected child, parents will stop having children and thus not reach their original desired family size. We first derive the full correct likelihood for a simple segregation analysis as a function of p, d, and the ascertainment probability ,. We show that p can be estimated from this likelihood if the FSD is known. Then, we show that under "random" ascertainment, the presence of stoppage does not bias estimates of p. However, for other ascertanment schemes, we show that is not the case. We use a simulation study to assess the magnitude of bias, and we demonstrate that ignoring the effect of stoppage can seroiusly bias the estimates of p when the FSD is ignored. In conclusion, stoppage, a realistic scenario for some complex diseases, can represent a serious and potentially intractable problem for segregation analysis. Genet. Epidemiol. 20:328,339, 2001. © 2001 Wiley-Liss, Inc. [source] SMR Analysis of Historical Follow-Up Studies with Missing Death CertificatesBIOMETRICS, Issue 4 2000Werner Rittgen Summary. The evaluation of epidemiological follow-up studies is frequently based on a comparison of the number O of deaths observed in the cohort from a specified cause with the expected number E calculated from person years in the cohort and mortality rates from a reference population. The ratio SMR = 100 ×O/E is called the standardized mortality ratio (SMR). While person years can easily be calculated from the cohort and reference rates are generally available from the national statistical offices or the World Health Organization (WHO), problems can arise with the accessibility of the causes of death of the deceased study participants. However, the information that a person has died may be available, e.g., from population registers. In this paper, a statistical model for this situation is developed to derive a maximum likelihood (ML) estimator for the true (but unknown) number O* of deaths from a specified cause, which uses the known number O of deaths from this cause and the proportion p of all known causes of death among all deceased participants. It is shown that the standardized mortality ratio SMR * based on this estimated number is just SMR *= SMR/p. Easily computable confidence limits can be obtained by dividing the usual confidence limits of the SMR by the opposite limit of the proportion p. However, the confidence level , has to be adjusted appropriately. [source] | ||||||||||