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Long-billed Curlew (Numenius americanus) typically nests in open grass habitat, such as native grassland, hayfields, or cow pasture. In May 2019, we discovered a Long-billed Curlew nest in the dense roadside shrub stubble near Prince George, British Columbia. The shrub stubble substrate for this nest appeared to be taller and denser than adjacent hayfields, which reduced the visibility of the nest site. The eggs in this nest were the first to hatch of the 11 curlew nests we monitored in the area.

Waterbirds are often used as indicators of ecosystem function across broad spatial and temporal scales. Resolving which species are declining and the ecological characteristics they have in common can offer insights into ecosystem changes and their underlying mechanisms. Using 20 years of citizen science data collected by the British Columbia Coastal Waterbird Survey, we examine species-specific trends in abundance of 50 species in the Salish Sea and 37 species along the outer Pacific Ocean coast that we considered to form the core wintering coastal bird community of British Columbia, Canada. Further, we explore whether ecological commonalities increase the likelihood of a species undergoing declines by testing the hypotheses that waterbird abundance trends are influenced by dietary specialization and migration distance to breeding grounds. Results suggest that most populations are stable (i.e., temporal trends are not significant) in both the Salish Sea (36 of 50 spp.) and Pacific coast (32 of 37 spp.) regions. Twelve species displayed significant decline trends in the Salish Sea, whereas two had significant increases. Along the Pacific coast, only three species displayed significant decline trends, and two significant increases. This result is corroborated by guild-specific trends indicating that waterbirds occupying the Salish Sea are faring significantly worse than those residing along the outer coastal regions, almost irrespective of dietary specialization or migration distance. Our results provide evidence that differential environmental pressures between the inner and outer coastal regions may be causing overall loss of wintering waterbirds within, or abundance shifts away from, the Salish Sea. Potential mechanisms responsible for these observed patterns are discussed, including environmental (e.g., climate) and human-induced (e.g., nutrient and chemical pollution) pressures. Collaborative, inter-disciplinary research priorities to help understand these mechanisms are suggested.

Many ecosystems have experienced anthropogenically induced changes in biodiversity, yet predicting these patterns has been difficult. Recently, individual behavioural and physiological measures have been proposed as more rapid links between environmental variation and fitness compared to demographics. Glucocorticoid hormones have received much attention given that they mediate energetic demands, metabolism, and foraging behaviour. However, it is currently unclear whether glucocorticoids can reliably predict environmental and fitness-related traits and whether they may be useful in specific groups of taxa. In particular, seabirds are a well-studied avian group often employed as biomonitoring tools for environmental change given their wide distribution and reliance on large oceanic patterns. Despite the increase in studies attempting to link variation in baseline corticosterone (the primary avian glucocorticoid) to variation in fitness-related traits in seabirds, there has been no comprehensive review of the relationship in this taxon. We present a phylogenetically controlled systematic review and meta-analysis of correlative and experimental studies examining baseline corticosterone as a predictor of fitness-related traits relevant to predicting seabird population health. Our results suggest that, while variation in baseline corticosterone may be a useful predictor of larger-scale environmental traits such as overall food availability and fitness-related traits such as reproductive success, this hormone may not be sensitive enough to detect variation in body condition, foraging effort, and breeding effort. Overall, our results support recent work suggesting that the use of baseline glucocorticoids as conservation biomarkers is complex and highly context dependent, and we suggest caution in their use and interpretation as simplified, direct biomarkers of fitness.

The GALNT3 gene encodes GalNAc-T3, which prevents degradation of the phosphaturic hormone, fibroblast growth factor 23 (FGF23). Biallelic mutations in either GALNT3 or FGF23 result in hyperphosphatemic familial tumoral calcinosis or its variant, hyperostosis-hyperphosphatemia syndrome. Tumoral calcinosis is characterized by the presence of ectopic calcifications around major joints, whereas hyperostosis-hyperphosphatemia syndrome is characterized by recurrent long bone lesions with hyperostosis. Here we investigated four patients with hyperphosphatemia and clinical manifestations including tumoral calcinosis and/or hyperostosis-hyperphosphatemia syndrome to determine underlying genetic cause and delineate phenotypic heterogeneity of these disorders. Mutational analysis of FGF23 and GALNT3 in these patients revealed novel homozygous mutations in GALNT3. Although the presence of massive calcifications, cortical hyperostosis, or dental anomalies was not shared by all patients, all had persistent hyperphosphatemia. Three of the patients also had inappropriately normal 1,25-dihyroxyvitamin D [1,25(OH)(2)D] and confirmed low circulating intact FGF23 concentrations. The four novel GALNT3 mutations invariably resulted in hyperphosphatemia as a result of low intact FGF23, but other clinical manifestations were variable. Therefore, tumoral calcinosis and hyperostosis-hyperphosphatemia syndrome represent a continuous spectrum of the same disease caused by increased phosphate levels, rather than two distinct disorders.

Field studies involving the effects of growing sweet corn (Zea mays var. Jubilee sweet corn and var. Jubilee super-sweet corn) as a green manure for 2 or 3 seasons demonstrated both suppression of verticillium wilt by 60–70% (Verticillium dahliae Kleb.) and increased potato yields. Although these treatments showed no direct effect on V. dahliae soil populations, the colonization of V. dahliae on potato feeder-roots and in potato tissue of stem apices were reduced. Feeder-root colonization by V. dahliae was positively correlated with verticillium wilt incidence (P ≤ 0.05 to P ≤ 0.01) and negatively correlated with yield (P ≤ 0.05). Corn green manures additionally increased populations of several soilborne fungi which included Ulocladium, and Fusarium equiseti. Specific nutritional and microbial effects were secondary to the effects of cropping practices. When compared with the fallow treatments for 1994, 1995, and 1997, the percentage yield increases for 1994 were: +34% for total yield, +57% for U.S. #1’s, and +127% for tubers >280 g; for 1995 (a year of reduced degree-days and decreased verticillium incidence): +14% for total yields, +15% for U.S. #1 yields, and +21% for tubers >280 g; for 1997: +24% for yield totals, +74% for U.S. #1’s and +179% for tubers >280 g. For establishing these yield benefits, stalks with and without ears of corn were used as green manures. Corn varieties differed for effectiveness as a green manure, which could be accounted for by differences of biomass. When compared with the super-sweet corn, the sweet corn produced an increase (>2-fold) of biomass with less than half of the resulting wilt incidence. When potato was grown consecutively for 2 years, the benefits from green manures became mostly eliminated. However, following 2 consecutive years of potato, a single green manure of sweet corn was sufficient to return the potato crop to the original benefits of verticillium suppression and increased yields. This occurred even though soilborne V. dahliae inoculum levels had increased by >4-fold from 45 to 182 cfu g−1 of soil. Results of this study demonstrate the importance of green manures and soil-ecology to the management of the Russet Burbank potato.

Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is a rare metabolic disorder, characterized by hypophosphatemia and rickets/osteomalacia with increased serum 1,25-dihydroxyvitamin D [1,25-(OH)(2)D] resulting in hypercalciuria.Our objective was to determine whether mutations in the SLC34A3 gene, which encodes sodium-phosphate cotransporter type IIc, are responsible for the occurrence of HHRH.Mutation analysis of exons and adjacent introns in the SLC34A3 gene was conducted at an academic research laboratory and medical center.Members of two unrelated families with HHRH participated in the study.Two affected siblings in one family were homozygous for a 101-bp deletion in intron 9. Haplotype analysis of the SLC34A3 locus in the family showed that the two deletions are on different haplotypes. An unrelated individual with HHRH was a compound heterozygote for an 85-bp deletion in intron 10 and a G-to-A substitution at the last nucleotide in exon 7. The intron 9 deletion (and likely the other two mutations) identified in this study causes aberrant RNA splicing. Sequence analysis of the deleted regions revealed the presence of direct repeats of homologous sequences.HHRH is caused by biallelic mutations in the SLC34A3 gene. Haplotype analysis suggests that the two intron 9 deletions arose independently. The identification of three independent deletions in introns 9 and 10 suggests that the SLC34A3 gene may be susceptible to unequal crossing over because of sequence misalignment during meiosis.

Familial tumoral calcinosis is characterized by ectopic calcifications and hyperphosphatemia. The disease is caused by inactivating mutations in fibroblast growth factor 23 (FGF23), Klotho (KL), and uridine diphosphate-N-acetyl-α-D-galactosamine:polypeptide N-acetylgalactosaminyltransferase 3 (GALNT3). In vitro studies indicate that GALNT3 O-glycosylates a phosphaturic hormone, FGF23, and prevents its proteolytic processing, thereby allowing secretion of intact FGF23. In this study we generated mice lacking the Galnt3 gene, which developed hyperphosphatemia without apparent calcifications. In response to hyperphosphatemia, Galnt3-deficient mice had markedly increased Fgf23 expression in bone. However, compared with wild-type and heterozygous littermates, homozygous mice had only about half of circulating intact Fgf23 levels and higher levels of C-terminal Fgf23 fragments in bone. Galnt3-deficient mice also exhibited an inappropriately normal 1,25-dihydroxyvitamin D level and decreased alkaline phosphatase activity. Furthermore, renal expression of sodium-phosphate cotransporters and Kl were elevated in Galnt3-deficient mice. Interestingly, there were sex-specific phenotypes; only Galnt3-deficient males showed growth retardation, infertility, and significantly increased bone mineral density. In summary, ablation of Galnt3 impaired secretion of intact Fgf23, leading to decreased circulating Fgf23 and hyperphosphatemia, despite increased Fgf23 expression. Our findings indicate that Galnt3-deficient mice have a biochemical phenotype of tumoral calcinosis and provide in vivo evidence that Galnt3 plays an essential role in proper secretion of Fgf23 in mice.

X-linked hypophosphatemic rickets (XLH) is a dominantly inherited disorder characterized by renal phosphate wasting, aberrant vitamin D metabolism, and abnormal bone mineralization. XLH is caused by inactivating mutations in PHEX (phosphate-regulating gene with homologies to endopeptidases on the X chromosome). In this study, we sequenced the PHEX gene in subjects from 26 kindreds who were clinically diagnosed with XLH. Sequencing revealed 18 different mutations, of which thirteen have not been reported previously. In addition to deletions, splice site mutations, and missense and nonsense mutations, a rare point mutation in the 3'-untranslated region (3'-UTR) was identified as a novel cause of XLH. In summary, we identified a wide spectrum of mutations in the PHEX gene. Our data, in accord with those of others, indicate that there is no single predominant PHEX mutation responsible for XLH.

Familial tumoral calcinosis is characterized by ectopic calcifications and hyperphosphatemia due to inactivating mutations in FGF23 or UDP-N-acetyl-alpha-D-galactosamine:polypeptide N-acetylgalactosaminyltransferase 3 (GALNT3). Herein we report a homozygous missense mutation (H193R) in the KLOTHO (KL) gene of a 13-year-old girl who presented with severe tumoral calcinosis with dural and carotid artery calcifications. This patient exhibited defects in mineral ion homeostasis with marked hyperphosphatemia and hypercalcemia as well as elevated serum levels of parathyroid hormone and FGF23. Mapping of H193R mutation onto the crystal structure of myrosinase, a plant homolog of KL, revealed that this histidine residue was at the base of the deep catalytic cleft and mutation of this histidine to arginine should destabilize the putative glycosidase domain (KL1) of KL, thereby attenuating production of membrane-bound and secreted KL. Indeed, compared with wild-type KL, expression and secretion of H193R KL were markedly reduced in vitro, resulting in diminished ability of FGF23 to signal via its cognate FGF receptors. Taken together, our findings provide what we believe to be the first evidence that loss-of-function mutations in human KL impair FGF23 bioactivity, underscoring the essential role of KL in FGF23-mediated phosphate and vitamin D homeostasis in humans.

Context: Hyperostosis-hyperphosphatemia syndrome (HHS) is a rare metabolic disorder characterized by hyperphosphatemia and localized hyperostosis. HHS is caused by mutations in GALNT3, which encodes UDP-N-acetyl-α-d-galactosamine:polypeptide N- acetylgalactosaminyltransferase 3. Familial tumoral calcinosis (TC), characterized by ectopic calcifications and hyperphosphatemia, is caused by mutations in the GALNT3 or fibroblast growth factor 23 (FGF23) genes. Objective: Our objective was to identify mutations in FGF23 or GALNT3 and determine serum FGF23 levels in an HHS patient. Design: Mutation detection in FGF23 and GALNT3 was performed by DNA sequencing, and serum FGF23 concentrations were measured by ELISA. Patients or Other Participants: A 5-year-old French boy with HHS and his family members participated. Results: The patient presented with painful cortical lesions in his leg. Radiographs of the affected bone showed diaphyseal hyperostosis. The lesional tissue comprised trabeculae of immature, woven bone surrounded by fibrous tissue. Biochemistry revealed elevated phosphate, tubular maximum rate for phosphate reabsorption per deciliter of glomerular filtrate, and 1,25-dihydroxyvitamin D levels. The patient was a compound heterozygote for two novel GALNT3 mutations. His parents and brother were heterozygous for one of the mutations and had no biochemical abnormalities. Intact FGF23 level in the patient was low normal, whereas C-terminal FGF23 was elevated, a pattern similar to TC. Conclusion: The presence of GALNT3 mutations and elevated C-terminal, but low intact serum FGF23, levels in HHS resemble those seen in TC, suggesting that HHS and TC are different manifestations of the same disorder. The absence of biochemical abnormalities in the heterozygous individuals suggests that one normal allele is sufficient for secretion of intact FGF23.

Familial tumoral calcinosis (TC) is a rare autosomal recessive disorder characterized by metastatic calcifications, often periarticular. Biochemical findings include hyperphosphatemia, high 1,25-dihydroxyvitamin D levels, and elevated tubular maximum for phosphate reabsorption per deciliter of glomerular filtrate (TmP/GFR). TC is caused by biallelic mutations of the genes encoding either fibroblast growth factor 23 (FGF23) or uridine diphosphate-N-acetyl-alpha-D-galactosamine:polypeptide N-acetylgalactosaminyltransferase 3 (GalNAc transferase 3 or GALNT3).The objective was to identify mutations in FGF23 or GALNT3 responsible for a mild TC phenotype by DNA sequencing and to determine serum FGF23 levels by ELISA.The subject was a 25-yr-old Caucasian woman with eyelid calcifications and biochemical features of TC.Eyelid biopsy revealed superficial dermis calcifications. There was no history of metastatic calcifications, mineral homeostasis abnormalities, or renal dysfunction. Biochemistry revealed normal levels of calcium, creatinine, PTH, and 25-hydroxyvitamin D, with elevated phosphorous, TmP/GFR, and high normal 1,25-dihydroxyvitamin D levels. Intact FGF23 was undetectable (3 pg/ml), whereas C-terminal FGF23 was elevated (698.2 RU/ml). Mutation detection revealed compound heterozygosity for two novel mutations in the glycosyl transferase domain of the GALNT3 gene.Previously reported GALNT3 mutations in TC have been null mutations. This study shows that missense mutations affecting the glycosyl transferase domain of GalNAc transferase 3 also cause TC. Elevated C-terminal FGF23 fragments with undetectable intact FGF23 suggest that the mutant enzyme lacks the ability to glycosylate FGF23 and that glycosylation by GalNAc transferase 3 is necessary for secretion of functional full-length FGF23.

Accuracy achievable in estimation of an unknown parameter \theta is considered when the intensity function of an observed Poisson process is given as \alpha + \beta f(t - \theta) , where \alpha and \beta are known positive constants and f is a step function or a rectangular pulse.

The plasma kinetics of timolol administered orally and intravenously to 5 male subjects were examined. Bioavailability was reduced by 25% when the drug was taken orally. Mean plasma half-life after oral dosing was 4.86 h, and after intravenous administration it was 4.56 h; the difference was not significant. The volume of distribution was 3.5 1/k. It is suggested that timolol is little affected by the 'first pass effect', even though there is marked interindividual variation in availability and peak plasma level.

Paternalism in the medical care of children is appropriate and ethically justifiable. However, dilemmatic disagreement by paternalistic agents as to which clinical choice is in the child's best interest may occur because of the underlying conflict between two rival standards for the moral value of life: longevity versus quality. Neither standard is unreasonable. Either could be the basis for choice of medical care by the parents or by the pediatrician. Having the child choose between options disputed by his parents and the pediatrician is unlikely to resolve their conflict. Exercise of informed consent by the adolescent requires agreement by his parents to relinquish their paternalistic veto. The probable best-interest choice by the child when he has matured could be reasonably made from either standard. Therefore, the longevity/quality of life question ought not ordinarily to be foreclosed by paternalistic authority which opts for one standard to the exclusion of the other. Medical interventions, paternalistically determined, are justified in the face of deteriorating quality, but only as long as the interventions themselves do not cause deterioration. Application of this limitation of paternalism to the zone of agreement between the rival life standards is made to clinical case examples. Multiple extrinsic criteria may measure the quality of life. Three quality factors, sensation of pain, capacity to communicate and physical functioning are considered. The extent of the zone of agreement between the two life standards varies because quality of life is a relative good, contingent both upon which extrinsic criteria are selected to assess it and upon the priorities which are set among these criteria.

This is the first of a two-part series based on a roundtable discussion held at the 21st IEEE Conference on Decision and Control and organized by the Control Systems Society Professional Activities Committee. Part I is based on prepared statements by the first five roundtable participants, while Part II is based on Leo Fanning's review of the activities of the IEEE Washington Office in the areas of technology policy.

Knowledge of the probability density function of the state conditioned on all available measurement data provides the most complete possible description of the state, and from this density any of the common types of estimates (e.g., minimum variance or maximum a posteriori) can be determined. Except in the linear Gaussian case, it is extremely difficult to determine this density function. In this paper an approximation that permits the explicit calculation of the a posteriori density from the Bayesian recursion relations is discussed and applied to the solution of the nonlinear filtering problem. In particular, it is noted that a weighted sum of Gaussian probability density functions can be used to approximate arbitrarily closely another density function. This representation provides the basis for procedure that is developed and discussed.

For linear systems the error covariance matrix for the unbiased, minimum variance estimate of the state does not depend upon any specific realization of the measurement sequence. Thus it can be examined to determine the expected behavior of the error in the estimate before actually using the filter in practice. In this paper, the general linear system that contains both plant and measurement noise is shown to exhibit a decomposition property that permits the derivation of upper and lower bounds upon the error covariance matrix. This decomposition allows systems containing either plant or measurement noise, but not both, to be considered separately. Some general characteristics of these simpler systems are discussed and conditions for the positive definiteness and vanishing of the error covariance matrix are established. It is seen that the presence of plant noise, in general, prevents the error from vanishing. Alternatively, the condition of q -stage observability is seen to be sufficient to insure that the error covariance matrix asymptotically approaches the zero matrix for systems with noise-free plants. These results are used to establish very specific lower bounds. Through the application of the duality principle, they can be applied directly to the analysis of the linear regulator problem.

The efficacy of Geoffrion's taxonomy of large-scale mathematical programming is being investigated in the context of state-constrained optimal control problems. One algorithm which can be synthesized from this taxonomy is called Generalized Benders Decomposition. In this paper, we first consider its direct application to optimal control. Numerical experience indicates the best performance is achieved when the dynamics are non-linear in the control and relatively few state-constraints are violated during the iteration process. To combat this latter difficulty, the algorithm is combined with parametric penalty methods. Some guidelines are provided on how to achieve improved numerical performance using this combined approach.

A comparison of the filter structures resulting from the consideration of different systems, both nonlinear models and linear models with correlated noise sequences, show an interesting similarity. Compared with the Kalman filter, these filter structures cause an apparent change in the linear system matrices, the noise covariance matrices, and in the form of the one-stage prediction. These modifications have interesting implications relative to adaptive filtering methods and system identification techniques.

In this paper a computational method to obtain the solution to an unconstrained stochastic optimization problem is presented. A conjugate gradient scheme is applied to generate a sequence of random variables approximating the optimum solution to the problem. Under certain conditions, this, sequence converges to the optimum solution in the mean-square sense. Since a random variable is completely defined by its probability distribution the stochastic optimization problem is treated as a problem of obtaining the probability distribution for the optimum solution. This can be achieved by generating probability distributions for the convergent sequence of random variables obtained in the conjugate gradient scheme. A computational scheme to obtain the probability-density function for the limiting random variable is derived by using finite sums of Gaussian density to approximate the probability densities for the convergent sequence of random variables.

A class of Newton-like methods is introduced which is feasible for large scale minimization problems. The methods are essentially an imbedding of Gauss-Newton or Newton-type nonlinear algorithms into any of several well known linear iterative methods. The resulting composite algorithms are simple to implement, converge quickly, and require only reasonable amounts of computer storage. Numerical comparisons indicate that for optimal control problems such an approach can be superior to the conjugate direction methods in Rn.

A sum of weighted gaussian probability density functions can be used to approximate another density function. This representation provides the basis for a procedure for computing the conditional density p(xk|zk) of the state xk of a nonlinear dynamical system given all available measurement data zk. As is well-known, estimates of the state xk for any performance criterion can be determined in a relatively straight forward manner if one has p(xk|zk). Consequently, knowledge of this density function essentiaUy constitutes a solution of the general nonlinear filtering problem.

The equations for a recursive extended Kalman filter with exponential age-weighting of data and dynamics are derived. A similar result is given for a second-order filter. It is seen that the filter equations are essentially of the same form as their unfaded counterparts. This technique offers promise in controlling the divergence problem that recursive filtering often encounters.

A forty-year-old man who had been stabbed in the chest was brought to the emergency room of a metropolitan hospital by the police. He was bleeding and his blood pressure was low. A physician applied manual pressure to the wound and administered fluid intravenously to restore blood volume. When the pressure was released to allow a surgeon to inspect the wound, bleeding immediately resumed, and pressure was reapplied. The patient was told that an artery had been cut and that he needed an immediate, potentially life-saving operation to tie the bleeding vessel and to determine whether there was a more serious, underlying injury. To everyone's surprise, the patient would not consent to the operation. Holding up his left hand to show three flexed and immobile fingers, he said that ten years earlier he had agreed, against his better judgment, to an operation on his hand. Now the hand was useless. He did not be

Both 9-anthrylacetaldehyde and phenylacetaldehyde undergo stereoselective self-condensation in the presence of base to give (E)- 2,4-di(9-anthryl)but-2-enal (2a), and (E)-2,4-diphenylbut-2-enal (2b) respectively, as established by single-crystal X-ray structure determination. Crystals of (2a) are monoclinic, P21/n, Z 8, a 10.638(9), b 20.68(1), c 20.41(2)Ǻ, β 92.36(5)°; R was 0.061 for No 3476 'observed' reflections. Crystals of (2b) are monoclinic, P21/c, Z 4, a 5.781(2), b 23.163(8), c 9.297(5)Ǻ, β 91.54(4)°; R 0.037 for No 1174. In both compounds, the enal moiety assumes a virtually planar s-trans conformation, with the angles between the planes of the olefinic double bond and the adjacent aromatic π-system around 70°.