@article{4040, abstract = {A plane geometric graph C in ℝ2 conforms to another such graph G if each edge of G is the union of some edges of C. It is proved that, for every G with n vertices and m edges, there is a completion of a Delaunay triangulation of O(m2 n) points that conforms to G. The algorithm that constructs the points is also described.}, author = {Edelsbrunner, Herbert and Tan, Tiow}, issn = {0179-5376}, journal = {Discrete & Computational Geometry}, number = {1}, pages = {197 -- 213}, publisher = {Springer}, title = {{An upper bound for conforming Delaunay triangulations}}, doi = {10.1007/BF02573974}, volume = {10}, year = {1993}, } @article{4041, abstract = {The zone theorem for an arrangement of n hyperplanes in d-dimensional real space says that the total number of faces bounding the cells intersected by another hyperplane is O(n(d-1)). This result is the basis of a time-optimal incremental algorithm that constructs a hyperplane arrangement and has a host of other algorithmic and combinatorial applications. Unfortunately, the original proof of the zone theorem, for d greater-than-or-equal-to 3, turned out to contain a serious and irreparable error. This paper presents a new proof of the theorem. The proof is based on an inductive argument, which also applies in the case of pseudohyperplane arrangements. The fallacies of the old proof along with some ways of partially saving that approach are briefly discussed.}, author = {Edelsbrunner, Herbert and Seidel, Raimund and Sharir, Micha}, issn = {0097-5397}, journal = {SIAM Journal on Computing}, number = {2}, pages = {418 -- 429}, publisher = {SIAM}, title = {{On the zone theorem for hyperplane arrangements}}, doi = {10.1137/0222031}, volume = {22}, year = {1993}, } @article{4042, abstract = {It is shown that a triangulation of a set of n points in the plane that minimizes the maximum edge length can be computed in time 0(n2). The algorithm is reasonably easy to implement and is based on the theorem that there is a triangulation with minmax edge length that contains the relative neighborhood graph of the points as a subgraph. With minor modifications the algorithm works for arbitrary normed metrics.}, author = {Edelsbrunner, Herbert and Tan, Tiow}, issn = {0097-5397}, journal = {SIAM Journal on Computing}, number = {3}, pages = {527 -- 551}, publisher = {SIAM}, title = {{A quadratic time algorithm for the minmax length triangulation}}, doi = {10.1137/0222036 }, volume = {22}, year = {1993}, } @article{4044, abstract = {Edge insertion iteratively improves a triangulation of a finite point set in ℜ2 by adding a new edge, deleting old edges crossing the new edge, and retriangulating the polygonal regions on either side of the new edge. This paper presents an abstract view of the edge insertion paradigm, and then shows that it gives polynomial-time algorithms for several types of optimal triangulations, including minimizing the maximum slope of a piecewise-linear interpolating surface.}, author = {Bern, Marshall and Edelsbrunner, Herbert and Eppstein, David and Mitchell, Stephen and Tan, Tiow}, issn = {0179-5376}, journal = {Discrete & Computational Geometry}, number = {1}, pages = {47 -- 65}, publisher = {Springer}, title = {{Edge insertion for optimal triangulations}}, doi = {10.1007/BF02573962}, volume = {10}, year = {1993}, } @article{4045, abstract = {We apply Megiddo's parametric searching technique to several geometric optimization problems and derive significantly improved solutions for them. We obtain, for any fixed ε>0, an O(n1+ε) algorithm for computing the diameter of a point set in 3-space, an O(8/5+ε) algorithm for computing the width of such a set, and on O(n8/5+ε) algorithm for computing the closest pair in a set of n lines in space. All these algorithms are deterministic.}, author = {Chazelle, Bernard and Edelsbrunner, Herbert and Guibas, Leonidas and Sharir, Micha}, issn = {0179-5376}, journal = {Discrete & Computational Geometry}, number = {1}, pages = {183 -- 196}, publisher = {Springer}, title = {{Diameter, width, closest line pair, and parametric searching}}, doi = {10.1007/BF02573973}, volume = {10}, year = {1993}, } @article{4175, abstract = {We have studied the effects of different neurotrophins on the survival and proliferation of rat cerebellar granule cells in culture. These neurons express trkB and trkC, the putative neuronal receptors for brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) respectively. Binding studies using iodinated BDNF and NT-3 demonstrated that both BDNF and NT-3 bind to the cerebellar granule neurons with a similar affinity of approximately 2 x 10(-9) M. The number of receptors per granule cell was surprisingly high, approximately 30 x 10(-4) and 2 x 10(5) for BDNF and NT-3, respectively. Both NT-3 and BDNF elevated c-fos mRNA in the granule neurons, but only BDNF up-regulated the mRNA encoding the low-affinity neurotrophin receptor (p75). In contrast to NT-3, BDNF acted as a survival factor for the granule neurons. BDNF also induced sprouting of the granule neurons and significantly protected them against neurotoxicity induced by high (1 mM) glutamate concentrations. Cultured granule neurons also expressed low levels of BDNF mRNA which were increased by kainic acid, a glutamate receptor agonist. Thus, BDNF, but not NT-3, is a survival factor for cultured cerebellar granule neurons and activation of glutamate receptor(s) up-regulates BDNF expression in these cells.}, author = {Lindholm, Dan and Dechant, Georg and Heisenberg, Carl-Philipp J and Thoenen, Hans}, issn = {0953-816X}, journal = {European Journal of Neuroscience}, number = {11}, pages = {1455 -- 1464}, publisher = {Wiley-Blackwell}, title = {{Brain-derived neurotrophic factor is a survival factor for cultured rat cerebellar granule neurons and protects them against glutamate-induced neurotoxicity}}, doi = {10.1111/j.1460-9568.1993.tb00213.x}, volume = {5}, year = {1993}, } @article{4177, abstract = {Thyroid hormones play an important role in brain development, but the mechanism(s) by which triiodothyronine (T3) mediates neuronal differentiation is poorly understood. Here we demonstrate that T3 regulates the neurotrophic factor, neurotrophin-3 (NT-3), in developing rat cerebellar granule cells both in cell culture and in vivo. In situ hybridization experiments showed that developing Purkinje cells do not express NT-3 mRNA but do express trkC, the putative neuronal receptor for NT-3. Addition of recombinant NT-3 to cerebellar cultures from embryonic rat brain induces hypertrophy and neurite sprouting of Purkinje cells, and upregulates the mRNA encoding the calcium-binding protein, calbindin-28 kD. The present study demonstrates a novel interaction between cerebellar granule neurons and developing Purkinje cells in which NT-3 induced by T3 in the granule cells promotes Purkinje cell differentiation.}, author = {Lindholm, Dan and Castrén, Eero and Tsoulfas, Pantelis and Kolbeck, Roland and Berzaghi, Maria and Leingärtner, Axel and Heisenberg, Carl-Philipp J and Tesarollo, Lino and Parada, Luis and Thoenen, Hans}, issn = {0021-9525}, journal = {Journal of Cell Biology}, number = {2}, pages = {443 -- 450}, publisher = {Rockefeller University Press}, title = {{Neurotrophin-3 induced by tri-iodothyronine in cerebellar granule cells promotes Purkinje cell differentiation}}, doi = {10.1083/jcb.122.2.443}, volume = {122}, year = {1993}, } @article{4299, abstract = {Evolutionary explanations of aging (or senescence) fall into two classes. First, organisms might have evolved the optimal life history, in which survival and fertility late in life are sacrificed for the sake of early reproduction or high pre-adult survival. Second, the life history might be depressed below this optimal compromise by the influx of deleterious mutations; since selection against late-acting mutations is weaker, deleterious mutations will impose a greater load on late life. We discuss ways in which these theories might be investigated and distinguished, with reference to experimental work withDrosophila. While genetic correlations between life history traits determine the immediate response to selection, they are hard to measure, and may not reflect the fundamental constraints on life history. Long term selection experiments are more likely to be informative. The third approach of using experimental manipulations suffers from some of the same problems as measures of genetic correlations; however, these two approaches may be fruitful when used together. The experimental results so far suggest that aging inDrosophila has evolved in part as a consequence of selection for an optimal life history, and in part as a result of accumulation of predominantly late-acting deleterious mutations. Quantification of these effects presents a major challenge for the future.}, author = {Partridge, Linda and Barton, Nicholas H}, issn = {0016-6707}, journal = {Genetica}, number = {1-3}, pages = {89 -- 98}, publisher = {Springer}, title = {{Evolution of aging: Testing the theory using Drosophila}}, doi = {10.1007/BF01435990}, volume = {91}, year = {1993}, } @article{4300, abstract = {Evolutionary explanations of ageing fall into two classes. Organisms might have evolved the optimal life history, in which survival and fertility late in life are sacrificed for the sake of early reproduction and survival. Alternatively, the life history might be depressed below this optimal compromise by deleterious mutations: because selection against late-acting mutations is weaker, these will impose a greater load on late life. Evidence for the importance of both is emerging, and unravelling their relative importance presents experimentalists with a major challenge.}, author = {Partridge, Linda and Barton, Nicholas H}, issn = {0028-0836}, journal = {Nature}, pages = {305 -- 311}, publisher = {Nature Publishing Group}, title = {{Optimality, mutation and the evolution of ageing}}, doi = {10.1038/362305a0}, volume = {362}, year = {1993}, } @inbook{4301, author = {Barton, Nicholas H and Gale, Katherine}, booktitle = {Hybrid zones and the evolutionary process}, editor = {Harrison, Richard}, isbn = { 0-19-506917-X}, pages = {13 -- 45}, publisher = {Oxford University Press}, title = {{Genetic analysis of hybrid zones}}, doi = {10.1046/j.1420-9101.1994.7050631.x}, year = {1993}, } @misc{4302, author = {Barton, Nicholas H}, booktitle = {Genetical Research}, issn = {0016-6723}, number = {1}, pages = {77 -- 85}, publisher = {Cambridge University Press}, title = {{Review of "The causes of molecular evolution" by J.H. Gillespie}}, doi = {10.1017/S001667230003158X }, volume = {62}, year = {1993}, } @article{4303, abstract = {In a stably subdivided population with symmetric migration, the chance that a favoured allele will be fixed is independent of population structure. However, random extinction introduces an extra component of sampling drift, and reduces the probability of fixation. In this paper, the fixation probability is calculated using the diffusion approximation; comparison with exact solution of the discrete model shows this to be accurate. The key parameters are the rates of selection, migration and extinction, scaled relative to population size (S = 4Ns, M = 4Nm, Λ = 4Nλ); results apply to a haploid model, or to diploids with additive selection. If new colonies derive from many demes, the fixation probability cannot be reduced by more than half. However, if colonies are initially homogeneous, fixation probability can be much reduced. In the limit of low migration and extinction rates (M, Λ 1), it is 2s/{1 + (Λ/MS)(1 −exp(−S))}, whilst in the opposite limit (S 1), it is 4sM/{Λ(Λ + M)}. In the limit of weak selection (M, Λ 1), it is 4sM/{Λ(Λ + M)}. These factors are not the same as the reduction in effective population size (Ne/N), showing that the effects of population structure on selected alleles cannot be understood from the behaviour of neutral markers.}, author = {Barton, Nicholas H}, issn = {0016-6723}, journal = {Genetics Research}, number = {2}, pages = {149 -- 158}, publisher = {Cambridge University Press}, title = {{The probability of fixation of a favoured allele in a subdivided population}}, doi = {10.1017/S0016672300031748}, volume = {62}, year = {1993}, } @article{4304, author = {Barton, Nicholas H}, issn = {0960-9822}, journal = {Current Biology}, number = {11}, pages = {797 -- 799}, publisher = {Cell Press}, title = {{Why species and subspecies?}}, doi = {10.1016/0960-9822(93)90036-N}, volume = {3}, year = {1993}, } @inproceedings{4506, abstract = {We propose a formal framework for designing hybrid systems by stepwise refinement. Starting with a specification in hybrid temporal logic, we make successively more transitions explicit until we obtain an executable system.}, author = {Henzinger, Thomas A and Manna, Zohar and Pnueli, Amir}, booktitle = {International Hybrid Systems Workshop}, editor = {Grossman, Robert and Nerode, Anil and Ravn, Anders and Rischel, Hans}, isbn = {978-3-540-57318-0}, pages = {60 -- 76}, publisher = {Springer}, title = {{Towards refining temporal specifications into hybrid systems}}, doi = {10.1007/3-540-57318-6_24}, volume = {736}, year = {1993}, } @article{2484, abstract = {Three cDNA clones, mGluR2, mGluR3, and mGluR4, were isolated from a rat brain cDNA library by cross-hybridization with the cDNA for a metabotropic glutamate receptor (mGluR1). The cloned receptors show considerable sequence similarity with mGluR1 and possess a large extracellular domain preceding the seven putative membrane-spanning segments. mGluR2 is expressed in some particular neuronal cells different from those expressing mGluR1 and mediates an efficient inhibition of forskolin-stimulated cAMP formation in cDNA- transfected cells. The mGluRs thus form a novel family of G protein-coupled receptors that differ in their signal transduction and expression patterns.}, author = {Tanabe, Yasuto and Masu, Masayuki and Ishii, Takahiro and Shigemoto, Ryuichi and Nakanishi, Shigetada}, issn = {0896-6273}, journal = {Neuron}, number = {1}, pages = {169 -- 179}, publisher = {Elsevier}, title = {{A family of metabotropic glutamate receptors}}, doi = {10.1016/0896-6273(92)90118-W}, volume = {8}, year = {1992}, } @article{2485, abstract = {Endothelins (ETs) are very potent vasoconstrictive peptides and have diverse functions in both vascular and nonvascular tissues. This investigation concerns the tissue distribution and cellular localization of rat mRNAs encoding two different subtypes of ET receptors (ET(A) and ET(B)). We isolated 46 cDNA clones from a rat lung cDNA library by hybridization with the bovine ET(A) cDNA. The characterization of these cDNA clones indicated that they represent either the ET(A) or ET(B) cDNA. In situ and blot hybridization analyses revealed that the rat ET(A) mRNA is predominantly expressed in vascular smooth muscle cells of a variety of tissues, bronchial smooth muscle cells, myocardium, and the pituitary gland. There is no significant expression of ET(B) mRNA in vascular smooth muscle cells, and ET(A), thus, plays a primary role in ET-induced vascular contraction. ET(B) mRNA is more widely distributed in various cell types of many tissues. Its prominent expression is seen in glial cells throughout the brain regions, epithelial cells of the choroid plexus, ependymal cells lining the ventricle, myocardium, endothelial cells of glomeruli, and epithelial cells of the thin segments of Henle's loops. Our investigation demonstrates that the mRNAs for the two subtypes of rat ET receptors show specialized expression patterns of cell types in both brain and peripheral tissues.}, author = {Hori, Seiji and Komatsu, Yasato and Shigemoto, Ryuichi and Mizuno, Noboru and Nakanishi, Shigetada}, issn = {0013-7227}, journal = {Endocrinology}, number = {4}, pages = {1885 -- 1895}, publisher = {The Endocrine Society}, title = {{Distinct tissue distribution and cellular localization of two messenger ribonucleic acids encoding different subtypes of rat endothelin receptors}}, doi = {10.1210/endo.130.4.1312429}, volume = {130}, year = {1992}, } @article{2486, abstract = {Distribution of the mRNA for a metabotropic glutamate receptor (mGluR1), which is linked to phosphoinositide (PI) hydrolysis, was investigated in adult and developing rat central nervous system (CNS) by in situ hybridization. Transcripts of mGluR1 were specifically localized to neurons and widely distributed throughout the adult rat brain. Most intensely labeled neurons were Purkinje cells of the cerebellum, mitral and tufted cells of the olfactory bulb, and neurons in the hippocampus, lateral septum, thalamus, globus pallidus, entopeduncular nucleus, ventral pallidum, magnocellular preoptic nucleus, substantia nigra, and dorsal cochlear nucleus. Moderately labeled neurons were seen in high density in the dentate gyrus, striatum, islands of Calleja, superficial layers of the retrosplenial, cingulate and entorhinal cortices, mammillary nuclei, red nucleus, and superior colliculus. In the developing rat brain, the level of mGluR1 expression gradually increased during early postnatal days in accordance with the maturation of neuronal elements. These results show prominent expression of mGluR1 in the major targets of putative glutamatergic pathways and unique distribution pattern of mGluR1 distinct from those reported for ionotropic subtypes of glutamate receptors, suggesting specific roles of mGluR1 in the glutamatergic system.}, author = {Shigemoto, Ryuichi and Nakanishi, Shigetada and Mizuno, Noboru}, issn = {0021-9967}, journal = {Journal of Comparative Neurology}, number = {1}, pages = {121 -- 135}, publisher = {Wiley-Blackwell}, title = {{Distribution of the mRNA for a metabotropic glutamate receptor (mGluR1) in the central nervous system: An in situ hybridization study in adult and developing rat}}, doi = {10.1002/cne.903220110}, volume = {322}, year = {1992}, } @article{2531, abstract = {The distribution of NMDA receptor (NMDAR1) on neurons in the peripheral ganglia was examined in the adult rat by in situ hybridization. NMDAR1 mRNA was expressed in all neurons in the sensory and autonomic ganglia examined; in the dorsal root, trigeminal, nodose, superior cervical, and sphenopalatine ganglia. Possible roles of the NMDA receptor on the sensory and autonomic ganglion neurons are discussed.}, author = {Shigemoto, Ryuichi and Ohishi, Hitoshi and Nakanishi, Shigetada and Mizuno, Noboru}, issn = {0304-3940}, journal = {Neuroscience Letters}, number = {1-2}, pages = {229 -- 232}, publisher = {Elsevier}, title = {{Expression of the mRNA for the rat NMDA receptor (NMDAR1) in the sensory and autonomic ganglion neurons}}, doi = {10.1016/0304-3940(92)90756-W}, volume = {144}, year = {1992}, } @article{2532, abstract = {In the present study, we have investigated the expression of both the erythrocyte-type (GLUT1) and the brain-type (GLUT3) glucose transporter isoforms in primary human brain tumors. In situ hybridization made it possible to localize and semiquantify both GLUT1 and GLUT3 mRNAs of individual cells in all 18 samples examined. More signals for GLUT3 mRNA than for GLUT1 mRNA were found over astrocytoma cells, while the reverse was the case in all 6 meningiomas. In astrocytomas, for both mRNAs, the density of silver grains over tumor cells was well correlated with the malignancy of the cells. This correlation was, as was also confirmed by Northern blot analysis, more marked with GLUT3 mRNA than with GLUT1 mRNA. In 2 of 5 anaplastic astrocytomas and in all 3 glioblastomas, numerous tumor cells with large amounts of both mRNAs tended to surround the perivascular regions. 'Tumor vessels' with endothelial proliferation, an almost pathognomonic feature of glioblastomas, expressed much GLUT3 mRNA but no significant GLUT1 mRNA, while a single- or a few-layered capillary endothelium expressed much GLUT1 mRNA. The distribution of both mRNAs was in good accordance with that of both proteins. Our results suggest that the expression of both glucose transporter isoforms may contribute to the maintenance of human brain tumors and that the expression of the GLUT3 isoform may be closely related to the malignant change of astrocytomas and particularly related to the aberrant neovascularization which accompanies glioblastomas.}, author = {Nishioka, Tatsuya and Oda, Yoshifumi and Seino, Yutaka and Yamamoto, Taizo and Inagaki, Nobuya and Yano, Hideki and Imura, Hiroo and Shigemoto, Ryuichi and Kikuchi, Haruhiko}, issn = {0008-5472}, journal = {Cancer Research}, number = {14}, pages = {3972 -- 3979}, publisher = {American Association for Cancer Research}, title = {{Distribution of the glucose transporters in human brain tumors}}, volume = {52}, year = {1992}, } @article{2533, abstract = {A cDNA clone for a new metabotropic glutamate receptor, mGluR5, was isolated through polymerase chain reaction-mediated DNA amplification by using primer sequences conserved among the metabotropic glutamate receptor (mGluR) family and by the subsequent screening of a rat brain cDNA library. The cloned receptor consists of 1171 amino acid residues and exhibits a structural architecture common to the mGluR family, possessing a large extracellular domain preceding the seven putative membrane-spanning segments. mGluR5 shows the highest sequence similarity to mGluR1 among the mGluR members and is coupled to the stimulation of phosphatidylinositol hydrolysis/ Ca2+ signal transduction in Chinese hamster ovary cells transfected with the cloned cDNA. This receptor also resembles mGluR1 in its agonist selectivity and antagonist responses; the potency rank order of agonists for mGluR5 was determined to be quisqualate > L-glutamate ≥ ibotenate > trans-1-aminocyclopentane-1,3-dicarboxylate. Blot and in situ hybridization analyses indicated that mGluR5 mRNA is widely distributed in neuronal cells of the central nervous system and is expressed differently from mGluR1 mRNA in many brain regions. This investigation thus demonstrates that there is an additional mGluR subtype which closely resembles mGluR1 in its signal transduction and pharmacological properties and is expressed in specialized neuronal cells in the central nervous system.}, author = {Abe, Takaaki and Sugihara, Hidemitsu and Nawa, Hiroyuki and Shigemoto, Ryuichi and Mizuno, Noboru and Nakanishi, Shigetada}, issn = {0021-9258}, journal = {Journal of Biological Chemistry}, number = {19}, pages = {13361 -- 13368}, publisher = {American Society for Biochemistry and Molecular Biology}, title = {{Molecular characterization of a novel metabotropic glutamate receptor mGluR5 coupled to inositol phosphate/Ca2+ signal transduction}}, doi = {10.1016/S0021-9258(18)42219-3}, volume = {267}, year = {1992}, }