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ABSTRACTRemote sensing has long been used to study wildlife; however, manual methods of detecting wildlife in aerial imagery are often time-consuming and prone to human error, and newer computer vision techniques have not yet been extensively applied to wildlife surveys. We used the object-based image analysis (OBIA) software eCognition to detect laughing gull (Leucophaeus atricilla) nests in Jamaica Bay as part of an ongoing monitoring effort at the John F. Kennedy International Airport. Our technique uses a combination of high resolution 4-band aerial imagery captured via manned aircraft with a multispectral UltraCam Falcon M2 camera, LiDAR point cloud data, and land cover data derived from a bathymetric LiDAR point cloud to classify and extract laughing gull nests. Our ruleset uses the site (topographic position of nest objects), tone (spectral characteristic of nest objects), shape, size, and association (nearby objects commonly found with the objects of interest that help identify them) elements of image interpretation, as well as NDVI and a sublevel object examination to classify and extract nests. The ruleset achieves a producer’s accuracy of 98% as well as a user’s accuracy of 65% and a kappa of 0.696, indicating that it extracts a majority of the nests in the imagery while reducing errors of commission to only 35% of the final results. The remaining errors of commission are difficult for the software to differentiate without also impacting the number of nests successfully extracted and are best addressed by a manual verification of output results as part of a semi-automated workflow in which the OBIA is used to complete the initial search of the imagery and the results are then systematically verified by the user to remove errors. This eliminates the need to manually search entire sets of imagery for nests, resulting in a much more efficient and less error prone methodology than previous unassisted image interpretation techniques. Because of the extensibility of OBIA software and the increasing availability of imagery due to small unmanned aircraft systems (sUAS), our methodology and its benefits have great potential for adaptation to other species surveyed using aerial imagery to enhance wildlife population monitoring.

[3,4-Difluoro-2-(2-fluoro-4-iodo-phenylamino)-phenyl]-((S)-3-hydroxy-3-piperidin-2-yl-azetidin-1-yl)-methanone (GDC-0973) is a potent and highly selective inhibitor of mitogen-activated protein kinase(MAPK)/extracellular signal-regulated kinase (ERK) 1/2 (MEK1/2), a MAPK kinase that activates ERK1/2. The objectives of these studies were to characterize the disposition of GDC-0973 in preclinical species and to determine the relationship of GDC-0973 plasma concentrations to efficacy in Colo205 mouse xenograft models. The clearance (CL) of GDC-0973 was moderate in mouse (33.5 ml · min–1· kg–1), rat (37.9 ± 7.2 ml · min–1· kg–1), and monkey (29.6 ± 8.5 ml · min–1· kg–1). CL in dog was low (5.5 ± 0.3 ml · min–1· kg–1). The volume of distribution across species was large, 6-fold to 15-fold body water; half-lives ranged from 4 to 13 h. Protein binding in mouse, rat, dog, monkey, and human was high, with percentage unbound, 1 to 6%. GDC-0973-related radioactivity was rapidly and extensively distributed to tissues; however, low concentrations were observed in the brain. In rats and dogs, [14C]GDC-0973 was well absorbed (fraction absorbed, 70–80%). The majority of [14C]GDC-0973-related radioactivity was recovered in the bile of rat (74–81%) and dog (65%). The CL and volume of distribution of GDC-0973 in human, predicted by allometry, was 2.9 ml · min–1· kg–1and 9.9 l/kg, respectively. The predicted half-life was 39 h. To characterize the relationship between plasma concentration of GDC-0973 and tumor growth inhibition, pharmacokinetic-pharmacodynamic modeling was applied using an indirect response model. The KC50value for tumor growth inhibition in Colo205 xenografts was estimated to be 0.389 μM, and the predicted clinical efficacious dose was ∼10 mg. Taken together, these data are useful in assessing the disposition of GDC-0973, and where available, comparisons with human data were made.

The growth hormone receptor (GHR) cDNA was cloned from the liver of Rhesus macaque using polymerase chain reaction. As deduced from the nucleotide sequence, the mature GHR is a protein of 620 amino acids which presents 94.1% identity with the human receptor. The monkey GHR (mkGHR) expressed in 293 cells presented the expected specificity for a primate GHR and was able to transduce a transcriptional effect of GH. Human GH was able to activate tyrosine phosphorylation of both the tyrosine kinase JAK2 and the receptor in 293 cells co-transfected with mkGHR and JAK2 cDNAs. The GH binding protein (GHBP), the soluble short form of the GHR, was also present in monkey serum. Expression of the GHR cDNA in eucaryotic cells indicated that the GHBP can be produced by proteolytic cleavage of the membrane receptor. Northern blot analysis of GHR gene expression in different tissues allowed us to identify three different transcripts of 5.0 and 2.8 kilobase pairs and a smaller one of 1.7 kilobase pairs which could encode a GHBP. Rapid amplification of cDNA extremities (3'-RACE-polymerase chain reaction) was used to identify a cDNA encoding a protein in which the transmembrane and cytoplasmic domains of the receptor are substituted by a short sequence of 9 amino acids. This transcript was present in various tissues and could encode a GHBP as well, suggesting for the first time that two different mechanisms can coexist for the generation of the GHBP: proteolytic cleavage of the membrane receptor and a specific mRNA produced by alternative splicing.

Intracellular current-clamp recordings were performed using in vitro brainstem slice preparations to compare the actions of substance P, neurokinin B and their agonists on rat dorsal vagal nucleus neurons with or without antagonists of neurokinin 1 and 2 receptors. The agonists used were either [Sar9,Met(O2)11]substance P or septide for neurokinin 1 and [Nle10]neurokinin A(4–10) for neurokinin 2 receptors. The antagonists were spantide, SR 140333 or RP 67580 for neurokinin 1 receptors and SR 48968 for neurokinin 2 receptors. Identification of vagal neurons was achieved electrophysiologically by testing antidromic responses and confirmed morphologically by an intracellular injection of biocytin. Of the 70 neurons tested, substance P led to depolarization in 36, hyperpolarization in six and no effect in 28. Depolarization was concentration dependent and generally associated with an increase of the membrane input resistance. Addition of tetrodotoxin (1 μM) to the medium had no effect on depolarization. RP 67580 (1 μM) blocked depolarization, but spantide and SR 140333 (1 μM to 50 μM) did not. Hyperpolarization was never observed using agonists. Neurokinin A and neurokinin 2 agonist induced concentration-dependent depolarization associated with an increase in membrane input resistance in eight of 14 neurons and in four of nine neurons, respectively. Depolarization was only partially abolished by the neurokinin 2 antagonist SR 48968. Neurokinin B had no effect in any of the eight neurons tested.

The glomerular filtration rate (GFR) and maximum tubular reabsorption of glucose (TmG) were measured in 24 cases of diabetes mellitus. The patients, who were of different ages, varied with regard to the severity and duration of the disease and 11 patients showed clinical and functional evidence of vascular disease. The GFR and TmG were diminished in almost 50 per cent of cases, and the diminution of the two factors was closely correlated. The incidence of these renal functional changes was almost the same in the group of diabetics with vascular disease as in the group without complications. The GFR and TmG were not correlated with the age of the patients or with the severity of diabetes, though these factors were to some extent correlated with the duration of the disease. No relationship was observed between the incidence of impairment of the renal function and sex.The examinations carried out in this series of cases as well as in a number of normal subjects suggest various considerations with regard to the value of the various techniques which have been proposed for the measurement of the TmG.

A reduction in tubular phosphorus reabsorption caused by the effect of competition induced by the intravenous injection of a glucose load, may provide information on the state of phosphorus reabsorption before the introduction of the glucose.The authors use the term Cp1for the phosphorus clearance value in the basic condition and Cp2to indicate clearance modification brought about by glucose. The ratio Cp2/Cp1thus shows the increase over the basic clearance. For normal subjects (10 cases) the ratio varied between 1.7 and 3.7 (mean value 2.6); in simple renal calculus (10 cases), in osteoporosis (2 cases), in thyrotoxicosis (3 cases), and in prolonged heparin therapy (2 cases) the ratio was within the normal range; in acromegaly (4 cases) the values tended to be above normal. There was a characteristic increase in the value of the ratio only in the case of hypoparathyroidism (3 patients). The reduction in the ratio found in hyperparathyroidism (3 cases) cannot be considered as characteristic since a reduction was also observed on occasion in other diseases, namely Paget's disease (1 case out of 2) and osseous metastasis (2 cases out of 4).

The glomerular filtration rate and the maximum tubular reabsorption of phosphate were determined in 5 patients with acromegaly. In 4 cases these functions were increased proportionally. In the fifth case they were normal.The findings are discussed in relation to present knowledge of the nephrotropic action of growth hormone.

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