@inbook{2494, abstract = {This chapter focuses on metabotropic glutamate receptors (mGluRs). These receptors are linked to several intracellular signal transduction mechanisms via G-protein and are implicated in diverse functions of the mammalian central nervous system (CNS). These functions include mediation of slow excitatory and inhibitory responses; regulation of calcium channels, potassium channels, and non-selective cation channels; inhibition and facilitation of transmitter release; induction of long-term potentiation and long-term depression; and regulation of neuronal development. Functional diversity of the metabotropic glutamate receptor is reflected in molecular diversity of receptor subtypes. The sites of action of mGluRs are widely found throughout different membrane compartments of neuronal and glial cells. The chapter reviews the differential subcellular localization of metabotropic glutamate receptors in relation to transmitter release sites. Patterns of subcellular localization of mGluRs are different among three subgroups: group I and III mGluRs are mainly localized to somatodendritic and axonal domains of neurons, respectively, while group II mGluRs are extensively localized to both domains as well as to glial cell processes.}, author = {Shigemoto, Ryuichi and Mizuno, Noboru}, booktitle = {Glutamate}, issn = {0924-8196}, pages = {63 -- 98}, publisher = {Elsevier}, title = {{Chapter III Metabotropic glutamate receptors - immunocytochemical and in situ hybridization analyses}}, doi = {10.1016/S0924-8196(00)80044-5}, volume = {18}, year = {2000}, } @article{2598, abstract = {There are many types of cerebellar ataxia, including ataxia due to congenital or metabolic disorders and a paraneoplastic form in patients with gynecologic cancer, breast cancer, lung cancer, or Hodgkin's disease.1 This paraneoplastic syndrome is the only type of cerebellar ataxia associated with autoantibodies against neuronal antigens. Often, the neuronal antigens are aberrantly expressed by the tumor cells.2-4 The antineuronal autoantibodies are believed to cause cerebellar ataxia, but this is unproved.5,6 In Hodgkin's disease, the lymphoma precedes the ataxia by months to years in 80 percent of patients, and ataxia often occurs during a prolonged complete remission.4 Among patients with this type of ataxia, 30 percent have anti–Purkinje-cell antibodies, some of which have the features of the neuronal antibody anti-Tr.4,7 We identified a new autoantibody in two patients with severe cerebellar ataxia that developed while they were in remission from Hodgkin's disease. The antibody reacts specifically with the metabotropic glutamate receptor mGluR1 in mouse brain. Metabotropic glutamate receptors belong to a large family of cell-surface receptors that transmit signals into the cell by coupling to guanine nucleotide-binding proteins (G proteins) in the cytoplasm. Purified IgG from the serum of both patients blocked the glutamate-stimulated formation of inositol phosphates in Chinese-hamster-ovary (CHO) cells that expressed mGluR1α, and the injection of IgG from serum or cerebrospinal fluid into the cerebellar subarachnoid space of mice caused severe, reversible ataxia. These results indicate that antineuronal autoantibodies can cause disease of the central nervous system by blocking neuronal receptors.}, author = {Sillevis Smitt, Peter and Kinoshita, Ayae and De Leeuw, Bertie and Moll, Wiebe and Coesmans, Michiel and Jaarsma, Dick and Henzen Logmans, Sonja and Vecht, Charles and De Zeeuw, Chris and Sekiyama, Naotaka and Nakanishi, Shigetada and Shigemoto, Ryuichi}, issn = {0028-4793}, journal = {New England Journal of Medicine}, number = {1}, pages = {21 -- 27}, publisher = {Massachussetts Medical Society}, title = {{Paraneoplastic cerebellar ataxia due to autoantibodies against a glutamate receptor}}, doi = {10.1056/NEJM200001063420104}, volume = {342}, year = {2000}, } @article{2599, abstract = {The synaptic relationship between substance P (SP) and its receptor, i.e., neurokinin-1 receptor (NK1R), was examined in the striatum of the rat by confocal laser-scanning microscopy and electron microscopy. For confocal laser-scanning microscopy, triple-immunofluorescence histochemistry was performed to label NK1R, SP, and vesicular acetylcholine transporter (a specific marker for cholinergic neurons). In electron microscopic double- immunolabeling study, immunoreactivity for NK1R was detected with the silver- intensified gold method, while immunoreactivity for SP was detected with peroxidase immunohistochemistry. Simultaneous immunolabeling of NK1R and SP revealed significant mismatch at the synaptic level: although some SP- immunopositive axon terminals were in synaptic contact with NK1R- immunopositive sites of plasma membrane, NK1R-immunoreactivity was observed at both synaptic and non-synaptic sites of plasma membrane. Thus, SP released from the sites remote from NK1Rs might diffuse in the extracellular fluid to act, as a paracrine neurotransmitter, on NK1Rs distant from its releasing site. SP neurotransmission in the striatum might occur not only synaptically but also extrasynaptically. The SP-NK1R system might constitute an association system within the striatum.}, author = {Li, Jin and Wang, Dan and Kaneko, Takeshi and Shigemoto, Ryuichi and Nomura, Sakashi and Mizuno, Noboru}, issn = {0021-9967}, journal = {Journal of Comparative Neurology}, number = {2}, pages = {156 -- 163}, publisher = {Wiley-Blackwell}, title = {{Relationship between neurokinin-1 receptor and substance P in the striatum: Light and electron microscopic immunohistochemical study in the rat}}, doi = {10.1002/(SICI)1096-9861(20000306)418:2<156::AID-CNE3>3.0.CO;2-Z}, volume = {418}, year = {2000}, } @article{2600, abstract = {The synaptic relationship between substance P (SP) and its receptor, i.e. neurokinin-1 receptor (NK1R), was examined in the superficial laminae of the caudal subnucleus of the spinal trigeminal nucleus (medullary dorsal horn; MDH) of the rat. For confocal laser-scanning microscopy, double-immunofluorescence histochemistry for NK1 and SP was performed. In electron microscopic double-immunolabeling study, immunoreactivity for NK1R was detected with the silver-intensified gold method, while immunoreactivity for SP was detected with peroxidase immunohistochemistry. SP-immunoreactive axon terminals were observed to be in synaptic (mostly asymmetric) contact with NK1R-immunoreactive neuronal profiles in lamina I and lamina IIo. Although some SP-immunoreactive axon terminals were in synaptic contact with NK1R-immunoreactive sites of plasma membranes, NK1R-immunoreactivity was observed at both synaptic and non-synaptic sites of plasma membrane. Thus, SP released from axon terminals might not only act on NK1Rs facing the SP-containing axon terminals, but also diffuse in the extracellular fluid for distances larger than the synaptic cleft to act on NK1Rs at some distances from the synaptic sites. }, author = {Li, Jin and Wang, Dan and Kaneko, Takeshi and Shigemoto, Ryuichi and Nomura, Sakashi and Mizuno, Noboru}, issn = {0168-0102}, journal = {Neuroscience Research}, number = {4}, pages = {327 -- 334}, publisher = {Elsevier}, title = {{The relationship between neurokinin-1 receptor and substance P in the medullary dorsal horn: A light and electron microscopic immunohistochemical study in the rat}}, doi = {10.1016/S0168-0102(00)00095-X}, volume = {36}, year = {2000}, } @article{2601, abstract = {Targeted deletion of metabotropic glutamate receptor-subtype 1 (mGluR1) gene can cause defects in development and function in the cerebellum. We introduced the mGluR1α transgene into mGluR1-null mutant [mGluR1 (-/-)] mice with a Purkinje cell (PC)-specific promoter. mGluR1-rescue mice showed normal cerebellar long-term depression and regression of multiple climbing fiber innervation, events significantly impaired in mGluR1 (-/-) mice. The impaired motor coordination was rescued by this transgene, in a dose-dependent manner. We propose that mGluR1 in PCs is a key molecule for normal synapse formation, synaptic plasticity, and motor control in the cerebellum.}, author = {Ichise, Taeko and Kano, Masanobu and Hashimoto, Kouichi and Yanagihara, Dai and Nakao, Kazuki and Shigemoto, Ryuichi and Katsuki, Motoya and Aiba, Atsu}, issn = {0036-8075}, journal = {Science}, number = {5472}, pages = {1832 -- 1835}, publisher = {American Association for the Advancement of Science}, title = {{mGluR1 in cerebellar Purkinje cells essential for long-term depression, synapse elimination, and motor coordination}}, doi = {10.1126/science.288.5472.1832}, volume = {288}, year = {2000}, } @article{2602, abstract = {Although presynaptic localization of mGluR7 is well established, the mechanism by which the receptor may control Ca2+ channels in neurons is still unknown. We show here that cultured cerebellar granule cells express native metabotropic glutamate receptor type 7 (mGluR7) in neuritic processes, whereas transfected mGluR7 was also expressed in cell bodies. This allowed us to study the effect of the transfected receptor on somatic Ca2+ channels. In transfected neurons, mGuR7 selectively inhibited P/Q-type Ca2+ channels. The effect was mimicked by GTPγS and blocked by pertussis toxin (PTX) or a selective antibody raised against the G-protein αo subunit, indicating the involvement of a G(o)-like protein. The mGuR7 effect did not display the characteristics of a direct interaction between G-protein βγ subunits and the α1A Ca2+ channel subunit, but was abolished by quenching βγ subunits with specific intracellular peptides. Intracellular dialysis of G-protein βγ subunits did not mimic the action of mGluR7, suggesting that both G-protein βγ and αo subunits were required to mediate the effect. Inhibition of phospholipase C (PLC) blocked the inhibitory action of mGluR7, suggesting that a coincident activation of PLC by the G-protein βγ with αo subunits was required. The Ca2+ chelator BAPTA, as well as inhibition of either the inositol trisphosphate (IP3) receptor or protein kinase C (PKC) abolished the mGluR7 effect. Moreover, activation of native mGluR7 induced a PTX-dependent IP3 formation. These results indicated that IP3-mediated intracellular Ca2+ release was required for PKC-dependent inhibition of the Ca2+ channels. Possible control of synaptic transmission by the present mechanisms is discussed.}, author = {Perroy, Julie and Prezèau, Laurent and De Waard, Michel and Shigemoto, Ryuichi and Bockaërt, Joël and Fagni, Laurent}, issn = {0270-6474}, journal = {Journal of Neuroscience}, number = {21}, pages = {7896 -- 7904}, publisher = {Society for Neuroscience}, title = {{Selective blockade of P/Q-type calcium channels by the metabotropic glutamate receptor type 7 involves a phospholipase C pathway in neurons}}, doi = {10.1523/JNEUROSCI.20-21-07896.2000}, volume = {20}, year = {2000}, } @article{2603, abstract = {Aggregation of neurotransmitter receptors at pre- and postsynaptic structures is crucial for efficient neuronal communication. In contrast to the wealth of information about postsynaptic specializations, little is known about the molecular organization of presynaptic membrane proteins. We show here that the metabotropic glutamate receptor mGluR7a, which localizes specifically to presynaptic active zones, interacts in vitro and in vivo with PICK1. Coexpression in heterologous systems induces coclustering dependent upon the extreme C terminus of mGluR7a and the PDZ domain of PICK1. mGluR7a and PICK1 localize to excitatory synapses in hippocampal neurons. Furthermore, whereas transfected mGluR7a clusters at presynaptic sites, mGluR7aΔ3 lacking the PICK1 binding site targets to axons but does not cluster. These results suggest that PICK1 is a component of the presynaptic machinery involved in mGlUR7a aggregation and in modulation of glutamate neurotransmission.}, author = {Boudin, Hélène and Doan, Andrew and Xia, Jun and Shigemoto, Ryuichi and Huganir, Richard and Worley, Paul and Craig, Ann}, issn = {0896-6273}, journal = {Neuron}, number = {2}, pages = {485 -- 497}, publisher = {Elsevier}, title = {{Presynaptic clustering of mGluR7a requires the PICK1 PDZ domain binding site}}, doi = {10.1016/S0896-6273(00)00127-6}, volume = {28}, year = {2000}, } @inbook{2710, abstract = {In this paper we describe an intrinsically geometric way of producing magnetic fields on §3 and $\R^3$ for which the corresponding Dirac operators have a non-trivial kernel. In many cases we are able to compute the dimension of the kernel. In particular we can give examples where the kernel has any given dimension. This generalizes the examples of Loss and Yau (Commun. Math. Phys. 104 (1986) 283-290).}, author = {Erdös, László}, booktitle = {Differential Equations and Mathematical Physics}, isbn = {9780821821572}, pages = {111 -- 119}, publisher = {American Mathematical Society}, title = {{The kernel of Dirac operators on S3 and R3}}, doi = {10.1090/amsip/016}, volume = {16}, year = {2000}, } @article{2731, abstract = {We study the time evolution of a quantum particle in a Gaussian random environment. We show that in the weak coupling limit the Wigner distribution of the wave function converges to a solution of a linear Boltzmann equation globally in time. The Boltzmann collision kernel is given by the Born approximation of the quantum differential scattering cross section.}, author = {Erdös, László and Yau, Horng}, issn = {0010-3640}, journal = {Communications on Pure and Applied Mathematics}, number = {6}, pages = {667 -- 735}, publisher = {Wiley-Blackwell}, title = {{Linear Boltzmann equation as the weak coupling limit of a random Schrödinger equation}}, doi = {10.1002/(SICI)1097-0312(200006)53:6<667::AID-CPA1>3.0.CO;2-5}, volume = {53}, year = {2000}, } @article{2732, abstract = {We consider a quantum particle moving in a harmonic exterior potential and linearly coupled to a heat bath of quantum oscillators. Caldeira and Leggett derived the Fokker Planck equation with friction for the Wigner distribution of the particle in the large-temperature limit: however, their (nonrigorous) derivation was not free of criticism, especially since the limiting equation is not of Lindblad form. In this paper we recover the correct form of their result in a rigorous way. We also point out that the source of the diffusion is physically restrictive under this scaling. We investigate the model at a fixed temperature and in the large-time limit, where the origin of the diffusion is a cumulative effect of many resonant collisions. We obtain a heat equation with a friction term for the radial process in phase space and we prove the Einstein relation in this case.}, author = {Castella, François and Erdös, László and Frommlet, Florian and Markowich, Peter}, issn = {0022-4715}, journal = {Journal of Statistical Physics}, number = {3-4}, pages = {543 -- 601}, publisher = {Springer}, title = {{Fokker-Planck equations as scaling limits of reversible quantum systems}}, doi = {10.1023/A:1018667323830}, volume = {100}, year = {2000}, } @article{2733, abstract = {The Li-Yau semiclassical lower bound for the sum of the first N eigenvalues of the Dirichlet–Laplacian is extended to Dirichlet–Laplacians with constant magnetic fields. Our method involves a new diamagnetic inequality for constant magnetic fields.}, author = {Erdös, László and Loss, Michael and Vougalter, Vitali}, issn = {0373-0956}, journal = {Annales de l'Institut Fourier}, number = {3}, pages = {891 -- 907}, publisher = {Association des Annales de l'Institut Fourier}, title = {{Diamagnetic behavior of sums Dirichlet eigenvalues}}, doi = {10.5802/aif.1777}, volume = {50}, year = {2000}, } @article{3149, abstract = {The prohormone convertases (PCs) are an evolutionarily ancient group of proteases required for the maturation of neuropeptide and peptide hormone precursors. In Drosophila melanogaster, the homolog of prohormone convertase 2, dPC2 (amontillado), is required for normal hatching behavior, and immunoblotting data indicate that flies express 80- and 75-kDa forms of this protein. Because mouse PC2 (mPC2) requires 7B2, a helper protein for productive maturation, we searched the fly data base for the 7B2 signature motif PPNPCP and identified an expressed sequence tag clone encoding the entire open reading frame for this protein. dPC2 and d7B2 cDNAs were subcloned into expression vectors for transfection into HEK-293 cells; mPC2 and rat 7B2 were used as controls. Although active mPC2 was detected in medium in the presence of either d7B2 or r7B2, dPC2 showed no proteolytic activity upon coexpression of either d7B2 or r7B2. Labeling experiments showed that dPC2 was synthesized but not secreted from HEK-293 cells. However, when dPC2 and either d7B2 or r7B2 were coexpressed in Drosophila S2 cells, abundant immunoreactive dPC2 was secreted into the medium, coincident with the appearance of PC2 activity. Expression and secretion of dPC2 enzyme activity thus appears to require insect cell-specific posttranslational processing events. The significant differences in the cell biology of the insect and mammalian enzymes, with 7B2 absolutely required for secretion of dPC2 and zymogen conversion occurring intracellularly in the case of dPC2 but not mPC2, support the idea that the Drosophila enzyme has specific requirements for maturation and secretion that can be met only in insect cells.}, author = {Hwang, Jae and Siekhaus, Daria E and Fuller, Robert and Taghert, Paul and Lindberg, Iris}, issn = {0021-9258}, journal = {Journal of Biological Chemistry}, number = {23}, pages = {17886 -- 17893}, publisher = {American Society for Biochemistry and Molecular Biology}, title = {{Interaction of Drosophila melanogaster prohormone convertase 2 and 7B2: Insect cell specific processing and secretion}}, doi = {10.1074/jbc.M000032200 }, volume = {275}, year = {2000}, } @article{11126, abstract = {Nuclear import of the two uracil-rich small nuclear ribonucleoprotein (U snRNP) components U1A and U2B′′ is mediated by unusually long and complex nuclear localization signals (NLSs). Here we investigate nuclear import of U1A and U2B′′ in vitro and demonstrate that it occurs by an active, saturable process. Several lines of evidence suggest that import of the two proteins occurs by an import mechanism different to those characterized previously. No cross competition is seen with a variety of previously studied NLSs. In contrast to import mediated by members of the importin-β family of nucleocytoplasmic transport receptors, U1A/U2B′′ import is not inhibited by either nonhydrolyzable guanosine triphosphate (GTP) analogues or by a mutant of the GTPase Ran that is incapable of GTP hydrolysis. Adenosine triphosphate is capable of supporting U1A and U2B′′ import, whereas neither nonhydrolyzable adenosine triphosphate analogues nor GTP can do so. U1A and U2B′′ import in vitro does not require the addition of soluble cytosolic proteins, but a factor or factors required for U1A and U2B′′ import remains tightly associated with the nuclear fraction of conventionally permeabilized cells. This activity can be solubilized in the presence of elevated MgCl2. These data suggest that U1A and U2B′′ import into the nucleus occurs by a hitherto uncharacterized mechanism.}, author = {HETZER, Martin W and Mattaj, Iain W.}, issn = {1540-8140}, journal = {Journal of Cell Biology}, keywords = {Cell Biology}, number = {2}, pages = {293--304}, publisher = {Rockefeller University Press}, title = {{An Atp-dependent, Ran-independent mechanism for nuclear import of the U1a and U2b′′ spliceosome proteins}}, doi = {10.1083/jcb.148.2.293}, volume = {148}, year = {2000}, } @article{11127, abstract = {Nuclear formation in Xenopus egg extracts requires cytosol and is inhibited by GTPγS, indicating a requirement for GTPase activity. Nuclear envelope (NE) vesicle fusion is extensively inhibited by GTPγS and two mutant forms of the Ran GTPase, Q69L and T24N. Depletion of either Ran or RCC1, the exchange factor for Ran, from the assembly reaction also inhibits this step of NE formation. Ran depletion can be complemented by the addition of Ran loaded with either GTP or GDP but not with GTPγS. RCC1 depletion is only complemented by RCC1 itself or by RanGTP. Thus, generation of RanGTP by RCC1 and GTP hydrolysis by Ran are both required for the extensive membrane fusion events that lead to NE formation.}, author = {HETZER, Martin W and Bilbao-Cortés, Daniel and Walther, Tobias C and Gruss, Oliver J and Mattaj, Iain W}, issn = {1097-2765}, journal = {Molecular Cell}, keywords = {Cell Biology, Molecular Biology}, number = {6}, pages = {1013--1024}, publisher = {Elsevier}, title = {{GTP hydrolysis by Ran is required for nuclear envelope assembly}}, doi = {10.1016/s1097-2765(00)80266-x}, volume = {5}, year = {2000}, } @article{11683, abstract = {The vertex connectivity κ of a graph is the smallest number of vertices whose deletion separates the graph or makes it trivial. We present the fastest known deterministic algorithm for finding the vertex connectivity and a corresponding separator. The time for a digraph having n vertices and m edges is O(min{κ3 + n, κn}m); for an undirected graph the term m can be replaced by κn. A randomized algorithm finds κ with error probability 1/2 in time O(nm). If the vertices have nonnegative weights the weighted vertex connectivity is found in time O(κ1nmlog(n2/m)) where κ1 ≤ m/n is the unweighted vertex connectivity or in expected time O(nmlog(n2/m)) with error probability 1/2. The main algorithm combines two previous vertex connectivity algorithms and a generalization of the preflow-push algorithm of Hao and Orlin (1994, J. Algorithms17, 424–446) that computes edge connectivity.}, author = {Henzinger, Monika H and Rao, Satish and Gabow, Harold N.}, issn = {0196-6774}, journal = {Journal of Algorithms}, keywords = {Computational Theory and Mathematics, Computational Mathematics, Control and Optimization}, number = {2}, pages = {222--250}, publisher = {Elsevier}, title = {{Computing vertex connectivity: New bounds from old techniques}}, doi = {10.1006/jagm.1999.1055}, volume = {34}, year = {2000}, } @article{11685, abstract = {We consider the problem of sampling URLs uniformly at random from the Web. A tool for sampling URLs uniformly can be used to estimate various properties of Web pages, such as the fraction of pages in various Internet domains or written in various languages. Moreover, uniform URL sampling can be used to determine the sizes of various search engines relative to the entire Web. In this paper, we consider sampling approaches based on random walks of the Web graph. In particular, we suggest ways of improving sampling based on random walks to make the samples closer to uniform. We suggest a natural test bed based on random graphs for testing the effectiveness of our procedures. We then use our sampling approach to estimate the distribution of pages over various Internet domains and to estimate the coverage of various search engine indexes.}, author = {Henzinger, Monika H and Heydon, Allan and Mitzenmacher, Michael and Najork, Marc}, issn = {1389-1286}, journal = {Computer Networks}, keywords = {URL sampling, Random walks, Internet domain distribution, Search engine size}, number = {1-6}, pages = {295--308}, publisher = {Elsevier}, title = {{On near-uniform URL sampling}}, doi = {10.1016/s1389-1286(00)00055-4}, volume = {33}, year = {2000}, } @article{11694, abstract = {We consider exploration problems where a robot has to construct a complete map of an unknown environment. We assume that the environment is modeled by a directed, strongly connected graph. The robot's task is to visit all nodes and edges of the graph using the minimum number R of edge traversals. Deng and Papadimitriou [Proceedings of the 31st Symposium on the Foundations of Computer Science, 1990, pp. 356-361] showed an upper bound for R ofd O(d)m and Koutsoupias (reported by Deng and Papadimitriou) gave a lower bound of Ω≠(d2m), where m is the number of edges in the graph and d is the minimum number of edges that have to be added to make the graph Eulerian. We give the 1rst subexponential algorithm for this exploration problem, which achieves an upper bound of dO(logd)m. We also show a matching lower bound of d≠(logd)m for our algorithm. Additionally, we give lower bounds of 2≠(d)m, respectively, d≠(logd)m for various other natural exploration algorithms.}, author = {Albers, Susanne and Henzinger, Monika H}, issn = {1095-7111}, journal = {SIAM Journal on Computing}, keywords = {directed graph, exploration algorithm}, location = {El Paso, TX, United States}, number = {4}, pages = {1164--1188}, publisher = {Society for Industrial and Applied Mathematics}, title = {{Exploring unknown environments}}, doi = {10.1137/s009753979732428x}, volume = {29}, year = {2000}, } @article{11770, abstract = {We compare several algorithms for identifying mirrored hosts on the World Wide Web. The algorithms operate on the basis of URL strings and linkage data: the type of information about Web pages easily available from Web proxies and crawlers. Identification of mirrored hosts can improve Web-based information retrieval in several ways: first, by identifying mirrored hosts, search engines can avoid storing and returning duplicate documents. Second, several new information retrieval techniques for the Web make inferences based on the explicit links among hypertext documents—mirroring perturbs their graph model and degrades performance. Third, mirroring information can be used to redirect users to alternate mirror sites to compensate for various failures, and can thus improve the performance of Web browsers and proxies. We evaluated four classes of “top-down” algorithms for detecting mirrored host pairs (that is, algorithms that are based on page attributes such as URL, IP address, and hyperlinks between pages, and not on the page content) on a collection of 140 million URLs (on 230,000 hosts) and their associated connectivity information. Our best approach is one which combines five algorithms and achieved a precision of 0.57 for a recall of 0.86 considering 100,000 ranked host pairs.}, author = {Bharat, Krishna and Broder, Andrei and Dean, Jeffrey and Henzinger, Monika H}, issn = {0002-8231}, journal = {Journal of the American Society for Information Science}, number = {12}, pages = {1114--1122}, publisher = {Wiley}, title = {{A comparison of techniques to find mirrored hosts on the WWW}}, doi = {10.1002/1097-4571(2000)9999:9999<::aid-asi1025>3.0.co;2-0}, volume = {51}, year = {2000}, } @article{842, author = {Wolf, Yuri and Kondrashov, Fyodor and Koonin, Eugene}, issn = {0168-9479}, journal = {Trends in Genetics}, number = {8}, pages = {333 -- 334}, publisher = {Elsevier}, title = {{No footprints of primordial introns in a eukaryotic genome}}, doi = {10.1016/S0168-9525(00)02059-X}, volume = {16}, year = {2000}, } @article{8525, abstract = {Let M be a smooth compact manifold of dimension at least 2 and Diffr(M) be the space of C r smooth diffeomorphisms of M. Associate to each diffeomorphism f;isin; Diffr(M) the sequence P n (f) of the number of isolated periodic points for f of period n. In this paper we exhibit an open set N in the space of diffeomorphisms Diffr(M) such for a Baire generic diffeomorphism f∈N the number of periodic points P n f grows with a period n faster than any following sequence of numbers {a n } n ∈ Z + along a subsequence, i.e. P n (f)>a ni for some n i →∞ with i→∞. In the cases of surface diffeomorphisms, i.e. dim M≡2, an open set N with a supergrowth of the number of periodic points is a Newhouse domain. A proof of the man result is based on the Gontchenko–Shilnikov–Turaev Theorem [GST]. A complete proof of that theorem is also presented.}, author = {Kaloshin, Vadim}, issn = {0010-3616}, journal = {Communications in Mathematical Physics}, keywords = {Mathematical Physics, Statistical and Nonlinear Physics}, pages = {253--271}, publisher = {Springer Nature}, title = {{Generic diffeomorphisms with superexponential growth of number of periodic orbits}}, doi = {10.1007/s002200050811}, volume = {211}, year = {2000}, }