[1] Hydrographs from shallow wells in vegetated riparian zones frequently display a distinctive pattern of diurnal water table fluctuations produced by variations in plant water use. A multisite investigation assessed the major controls on these fluctuations and the ecohydrologic insights that can be gleaned from them. Spatial and temporal variations in the amplitude of the fluctuations are primarily a function of variations in (1) the meteorological drivers of plant water use, (2) vegetation density, type, and vitality, and (3) the specific yield of sediments in the vicinity of the water table. Past hydrologic conditions experienced by the riparian zone vegetation, either in previous years or earlier within the same growing season, are also an important control. Diurnal water table fluctuations can be considered a diagnostic indicator of groundwater consumption by phreatophytes at most sites, so the information embedded within these fluctuations should be more widely exploited in ecohydrologic studies.
Studies involving pharmacologic or molecular biologic manipulation of Group VIA phospholipase A 2 (iPLA 2 ) activity in pancreatic islets and insulinoma cells suggest that iPLA 2  participates in insulin secretion. It has also been suggested that iPLA 2  is a housekeeping enzyme that regulates cell 2-lysophosphatidylcholine (LPC) levels and arachidonate incorporation into phosphatidylcholine (PC). We have generated iPLA 2 -null mice by homologous recombination and have reported that they exhibit reduced male fertility and defective motility of spermatozoa. Here we report that pancreatic islets from iPLA 2 -null mice have impaired insulin secretory responses to D-glucose and forskolin. Electrospray ionization mass spectrometric analyses indicate that the abundance of arachidonate-containing PC species of islets, brain, and other tissues from iPLA 2 -null mice is virtually identical to that of wild-type mice, and no iPLA 2  mRNA was observed in any tissue from iPLA 2 -null mice at any age. Despite the insulin secretory abnormalities of isolated islets, fasting and fed blood glucose concentrations of iPLA 2 -null and wild-type mice are essentially identical under normal circumstances, but iPLA 2 -null mice develop more severe hyperglycemia than wild-type mice after administration of multiple low doses of the -cell toxin streptozotocin, suggesting an impaired islet secretory reserve. A high fat diet also induces more severe glucose intolerance in iPLA 2 -null mice than in wild-type mice, but PLA 2 -null mice have greater responsiveness to exogenous insulin than do wild-type mice fed a high fat diet. These and previous findings thus indicate that iPLA 2 -null mice exhibit phenotypic abnormalities in pancreatic islets in addition to testes and macrophages.
. Glucose homeostasis, insulin secretion, and islet phospholipids in mice that overexpress iPLA2 in pancreatic -cells and in iPLA2-null mice. Am J Physiol Endocrinol Metab 294: E217-E229, 2008. First published September 27, 2007 doi:10.1152/ajpendo.00474.2007.-Studies with genetically modified insulinoma cells suggest that group VIA phospholipase A2 (iPLA2) participates in amplifying glucose-induced insulin secretion. INS-1 insulinoma cells that overexpress iPLA 2, for example, exhibit amplified insulin-secretory responses to glucose and cAMPelevating agents. To determine whether similar effects occur in whole animals, we prepared transgenic (TG) mice in which the rat insulin 1 promoter (RIP) drives iPLA 2 overexpression, and two characterized TG mouse lines exhibit similar phenotypes. Their pancreatic islet iPLA2 expression is increased severalfold, as reflected by quantitative PCR of iPLA 2 mRNA, immunoblotting of iPLA2 protein, and iPLA2 enzymatic activity. Immunofluorescence microscopic studies of pancreatic sections confirm iPLA2 overexpression in RIPiPLA 2-TG islet -cells without obviously perturbed islet morphology. Male RIP-iPLA 2-TG mice exhibit lower blood glucose and higher plasma insulin concentrations than wild-type (WT) mice when fasting and develop lower blood glucose levels in glucose tolerance tests, but WT and TG blood glucose levels do not differ in insulin tolerance tests. Islets from male RIP-iPLA 2-TG mice exhibit greater amplification of glucose-induced insulin secretion by a cAMP-elevating agent than WT islets. In contrast, islets from male iPLA 2-null mice exhibit blunted insulin secretion, and those mice have impaired glucose tolerance. Arachidonate incorporation into and the phospholipid composition of RIP-iPLA2-TG islets are normal, but they exhibit reduced Kv2.1 delayed rectifier current and prolonged glucose-induced action potentials and elevations of cytosolic Ca 2ϩ concentration that suggest a molecular mechanism for the physiological role of iPLA2 to amplify insulin secretion. transgenic mice; glucose tolerance; insulin tolerance GLUCOSE HOMEOSTASIS REQUIRES that pancreatic -cells secrete insulin when blood glucose concentrations exceed 5 mM. Autoimmune -cell destruction causes type 1 diabetes mellitus, and in type 2 diabetes mellitus, there is 50% loss of -cell mass and impaired insulin secretion and action (12,15). Intensive insulin therapy reduces diabetic complications but increases risks of hypoglycemia (16), and -cell replacement might someday be a superior therapy (59,62).Understanding control of -cell growth, death, and secretion might permit iterative introduction of genes into -cell lines or precursors to optimize secretion, proliferation, and resistance to injury (24,69). Combined with empirical selection and encapsulation, such -cell engineering might someday provide a renewable source of -cells for replacement therapy (44,45). Developing such potential future therapies requires increased understanding of the genes and gene products that gov...
An experimental and numerical study on laminar flame characteristics of methane oxy-fuel mixtures highly diluted with CO 2 was conducted using a constant volume chamber and CHEMKIN package. The effects of high CO 2 dilution on combustion chemical reaction, flame instability, and flame radiation of CH 4 /CO 2 /O 2 mixtures were studied. The laminar burning velocities of CH 4 /CO 2 /O 2 mixtures decrease with the increase of the CO 2 fraction. CO 2 directly participates in the chemical reaction through the elementary reaction OH + CO = H + CO 2 and inhibits the combustion process by the competition of the H radical between the reverse reaction of OH + CO = H + CO 2 and the reaction H + O 2 = O + OH. This effect is more obvious for highly diluted CO 2 in the case of CH 4 /CO 2 /O 2 mixtures. CO 2 suppresses the flame instability by the combined effect of hydrodynamic and thermal-diffusive instabilities. The radiation of CH 4 oxy-fuel combustion is much stronger than that of CH 4 / air combustion mainly because of the existence of a large fraction of CO 2 in CH 4 /CO 2 /O 2 flames, which will influence the wall temperature and temperature distribution in the gas turbine combustor.
Studies involving pharmacologic inhibition or transient reduction of Group
Mouse macrophages undergo ER stress and apoptosis upon free cholesterol loading (FCL). We recently generated iPLA 2 -null mice, and here we demonstrate that iPLA 2 -null macrophages have reduced sensitivity to FCL-induced apoptosis, although they and wild-type (WT) cells exhibit similar increases in the transcriptional regulator CHOP. iPLA 2 -null macrophages are also less sensitive to apoptosis induced by the sarcoplasmic reticulum Ca 2؉ -ATPase inhibitor thapsigargin and the scavenger receptor A ligand fucoidan, and restoring iPLA 2 2  modulates mitochondrial cytochrome c release, and we find that thapsigargin and fucoidan induce mitochondrial phospholipid loss and cytochrome c release into WT macrophage cytosol and that these events are blunted in iPLA 2 -null cells. Immunoblotting studies indicate that iPLA 2  associates with mitochondria in macrophages subjected to ER stress. AA incorporation into glycerophosphocholine lipids is unimpaired in iPLA 2 -null macrophages upon electrospray ionization-tandem mass spectrometry analyses, and their complex lipid composition is similar to WT cells. These findings suggest that iPLA 2  participates in ER stress-induced macrophage apoptosis caused by FCL or thapsigargin but that deletion of iPLA 2  does not impair macrophage arachidonate incorporation or phospholipid composition.
Abstract. The flux along a horizontal well in uniform flow is examined using an analytic three-dimensional, steady model. Wells with uniform head and low pumping rates have gaining sections along which water enters the well and losing sections along which water exits. Such a well may provide a conduit for contaminated groundwater to be drawn into the well, conveyed a large distance, and injected into an uncontaminated region of an aquifer. Dimensionless ratios of the well's length L and radius R, aquifer thickness H, and uniform flow rate U are developed to quantify the minimum pumping rate Q min at which no losing section occurs. The ratio Qmin/(ULH) is presented as a nomograph using R/H and L/H for placement parallel to flow and is 6rrR/H for placement perpendicular to flow, and a parabolic relationship between these limiting cases is developed for placement oblique to flow. Capture zone geometry is quantified using Qmin/(ULH).
A newly identified genie male-sterile mutant in soybean [Glycine max (L.) Merr.] has high seed set under natural field conditions and is potentially useful in breeding programs. Meiosis is normal in the mutant line. Sterility in this mutant is caused by failure of cailose dissolution at the tetrad stage, which results in microspore abortion; however, little is known about the male-sterile gene at the molecular level. The objective of this study was to identify molecular markers linked with the male-sterile gene (ms) and to place the ms gene onto the soybean molecular genetic map. An F2 population of 107 individuals was constructed from a cross between the mutant msMOS (ms ms) and the cultivar Minsoy (Ms Ms). Two hundred seventy markers, including 219 RFLP and 51 SSRs, were evaluated. Of these, 102 RFLP probes and 31 SSR markers detected polymorphisms between the parents. The F2 population was screened for segregation of these polymorphic molecular markers. Analyses revealed that the male-sterile locus, designated 'ms', was located on linkage group D1b of the USDA/ISU soybean molecular genetic map. The availability of linked DNA markers will facilitate the genetic analysis of this male-sterility gene in relation to soybean breeding programs, and will be a starting point for the isolation of the ms gene by map-based cloning. Disciplines Agronomy and Crop Sciences | Botany | Plant Breeding and Genetics CommentsThis article is from Crop Science 38 (1998): 1681, doi: 10.2135/cropsci1998.0011183X003800060043x. RightsWorks produced by employees of the U.S. Government as part of their official duties are not copyrighted within the U.S. The content of this document is not copyrighted. (L.) Merr.] has high seed set under natural field conditions and is potentially useful in breeding programs. Meiosis is normal in the mutant line. Sterility in this mutant is caused by failure of cailose dissolution at the tetrad stage, which results in microspore abortion; however, little is known about the male-sterile gene at the molecular level. The objective of this study was to identify molecular markers linked with the male-sterile gene (ms) and to place the ms gene onto the soybean molecular genetic map. An F2 population of 107 individuals was constructed from a cross between the mutant msMOS (ms ms) and the cultivar Minsoy (Ms Ms). Two hundred seventy markers, including 219 RFLP and 51 SSRs, were evaluated. Of these, 102 RFLP probes and 31 SSR markers detected polymorphisms between the parents. The F2 population was screened for segregation of these polymorphic molecular markers. Analyses revealed that the male-sterile locus, designated 'ms', was located on linkage group Dlb of the USDA/ISU soybean molecular genetic map. The availability of linked DNA markers will facilitate the genetic analysis of this malesterility gene in relation to soybean breeding programs, and will be a starting point for the isolation of the ms gene by map-based cloning.
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