Time lower bounds for nonadaptive turnstile streaming algorithms

We say a turnstile streaming algorithm is "non-adaptive" if, during updates, the memory cells written and read depend only on the index being updated and random coins tossed at the beginning of the stream (and not on the memory contents of the algorithm). Memory cells read during queries may be decided upon adaptively. All known turnstile streaming algorithms in the literature are non-adaptive. We prove the first non-trivial update time lower bounds for both randomized and deterministic turnstile streaming algorithms, which hold when the algorithms are non-adaptive. While there has been abundant success in proving space lower bounds, there have been no non-trivial update time lower bounds in the turnstile model. Our lower bounds hold against classically studied problems such as heavy hitters, point query, entropy estimation, and moment estimation. In some cases of deterministic algorithms, our lower bounds nearly match known upper bounds

Overview of the PALM model system 6.0

In this paper, we describe the PALM model system 6.0. PALM (formerly an abbreviation for Parallelized Largeeddy Simulation Model and now an independent name) is a Fortran-based code and has been applied for studying a variety of atmospheric and oceanic boundary layers for about 20 years. The model is optimized for use on massively parallel computer architectures. This is a follow-up paper to the PALM 4.0 model description in Maronga et al. (2015). During the last years, PALM has been significantly improved and now offers a variety of new components. In particular, much effort was made to enhance the model with components needed for applications in urban environments, like fully interactive land surface and radiation schemes, chemistry, and an indoor model. This paper serves as an overview paper of the PALM 6.0 model system and we describe its current model core. The individual components for urban applications, case studies, validation runs, and issues with suitable input data are presented and discussed in a series of companion papers in this special issue

Developing a research strategy to better understand, observe, and simulate urban atmospheric processes at kilometer to subkilometer scales

A Met Office/Natural Environment Research Council Joint Weather and Climate Research Programme workshop brought together 50 key international scientists from the UK and international community to formulate the key requirements for an Urban Meteorological Research strategy. The workshop was jointly organised by University of Reading and the Met Office

EXPLORING THE MAMMALIAN NEUROMUSCULAR SYSTEM BY ANALYSIS OF MUTATIONS - SPINAL MUSCULAR-ATROPHY AND MYOTONIA

Jockusch H, KAUPMANN K, GRONEMEIER M, SCHLEEF M, KLOCKE R. EXPLORING THE MAMMALIAN NEUROMUSCULAR SYSTEM BY ANALYSIS OF MUTATIONS - SPINAL MUSCULAR-ATROPHY AND MYOTONIA. PROGRESS IN NEUROBIOLOGY. 1994;42(2):313-317.Any biological structure can be studied using mutations that interfere either with its emergence or its function. We investigate spontaneous and induced mutations in the mouse that affect neuromuscular development and function. The wobbler mouse (phenotype WR, genotype wr/wr) suffers from muscular atrophy because of the degeneration of 20-40% of the motoneurones; it is also unable to produce functional spermatozoa. As a step towards positional cloning of the wr gene, we have mapped the locus to proximal chromosome 11, thus excluding CNTF and its receptor as candidates, and suggesting the closely-linked Rab I gene encoding a GTP-binding protein as a possibility. In the case of the adr (arrested development of righting response) mouse, which shows hyperexcitability of mature muscle fibres due to a reduction of the 'dampening' function of chloride conductance at resting potential, we have shown that the defect is in the chloride channel gene adr/Clc-1 on chromosome 6. This allowed us to predict via synteny the chromosomal location of human Thomsen's and Becker's myotonias as close to the TCRB gene on human chromosome 7q. The combination of these approaches with gene-targeting approaches will allow genetic analysis of the establishment and structure of the neuromuscular system

Zero-Information Protocols and Unambiguity in Arthur-Merlin Communication

We study whether information complexity can be used to attack the long-standing open problem of proving lower bounds against Arthur–Merlin (AM) communication protocols. Our starting point is to show that—in contrast to plain randomized communication complexity— every boolean function admits an AM communication protocol where on each yes-input, the distribution of Merlin’s proof leaks no information about the input and moreover, this proof is unique for each outcome of Arthur’s randomness. We posit that these two properties of zero information leakage and unambiguity on yes-inputs are interesting in their own right and worthy of investigation as new avenues toward AM. • Zero-information protocols (ZAM). Our basic ZAM protocol uses exponential com-munication for some functions, and this raises the question of whether more efficient protocols exist. We prove that all functions in the classical space-bounded complexity classes NL and ⊕L have polynomial-communication ZAM protocols. We also prove that ZAM complexity is lower bounded by conondeterministic communication complexity. • Unambiguous protocols (UAM). Our most technically substantial result is a Ω(n) lower bound on the UAM complexity of the NP-complete set-intersection function; the proof uses information complexity arguments in a new, indirect way and overcomes the “zero-information barrier” described above. We also prove that in general, UAM complexity is lower bounded by the classic discrepancy bound, and we give evidence that it is not generally lower bounded by the classic corruption bound

CHLORIDE CHANNEL-2 GENE (CLC2) MAPS TO CHROMOSOME-16 OF THE MOUSE, EXTENDING A REGION OF CONSERVED SYNTENY WITH HUMAN-CHROMOSOME-3Q

LENGELING A, GRONEMEIER M, RONSIEK M, THIEMANN A, JENTSCH TJ, Jockusch H. CHLORIDE CHANNEL-2 GENE (CLC2) MAPS TO CHROMOSOME-16 OF THE MOUSE, EXTENDING A REGION OF CONSERVED SYNTENY WITH HUMAN-CHROMOSOME-3Q. GENETICAL RESEARCH. 1995;66(02):175-178.The Clc2 gene of the mouse codes for the ubiquitously expressed chloride channel ClC-2, a member of a family of at least seven voltage gated chloride channels, some of which are implicated in hereditary diseases. Using a mouse interspecies back-cross panel, we have mapped Clc2 to Chr 16, proximal to the somatostatin gene Smst, extending a region of documented conserved synteny to human Chr 3q

NONSENSE AND MISSENSE MUTATIONS IN THE MUSCULAR CHLORIDE CHANNEL GENE CLC-1 OF MYOTONIC MICE

GRONEMEIER M, CONDIE A, PROSSER J, STEINMEYER K, JENTSCH TJ, Jockusch H. NONSENSE AND MISSENSE MUTATIONS IN THE MUSCULAR CHLORIDE CHANNEL GENE CLC-1 OF MYOTONIC MICE. JOURNAL OF BIOLOGICAL CHEMISTRY. 1994;269(8):5963-5967.In mature vertebrate muscle, the chloride channel Clc-1 is necessary for the stabilization of the resting potential. Its functional defect leads to the disease myotonia. The ADR mouse (phenotype ADR, genotype adr/adr) is an animal model for human myotonias. The adr gene is a member of a family of non-complementing recessive autosomal mutations (''alleles'' of adr) that cause myotonia in the mouse. The standard allele adr has arisen by the insertion of a retroposon into the chloride channel gene Clc-1 (Steinmeyer, K., Klocke, R., Ortland, C., Gronemeier, M., Jockusch, H., Grunder, S., and Jentsch, T. J. (1991) Nature 354, 304-308). In order to study the nature of two other alleles, adr(mto) and adr(K), we have analyzed overlapping Clc-1 cDNA amplification products by the hydroxylamine and osmium tetroxide modification technique and direct sequencing. A comparison between ADR*MTO and C57BL/6 wild type showed six base pair substitutions, one of which resulted in a stop codon in position 47, whereas the five others are either silent or lead to amino acid substitutions in non-conserved regions of the Clc-1 sequence and were already present in the wild type inbred SWR/J strain from which adr(mto) was derived. The detection of the stop codon in the adr(mto) allele is further indication of the identity of the Clc-1 chloride channel with the adr myotonia gene in the mouse, because a chain termination close to the N terminus would necessarily destroy gene function. For the ethylnitrosourea-induced mutation adr(K), an Ile --> Thr exchange in codon 553 was identified. As this affects a conserved residue within a highly conserved region of the Clc-1 gene, a functional significance of this residue is suggested

The mouse Clc1/myotonia gene: ETn insertion, a variable AATC repeat, and PCR diagnosis of alleles

Schnulle V, Antropova O, Gronemeier M, Wedemeyer N, Jockusch H, Bartsch JW. The mouse Clc1/myotonia gene: ETn insertion, a variable AATC repeat, and PCR diagnosis of alleles. Mammalian genome. 1997;8(10):718-725.Myotonias are muscle diseases in which the function of the muscular chloride channel ClC-1 is impaired. Null alleles of the corresponding Clc1 gene on mouse chromosome (Chr) 6 provide animal models for human myotonias. It was shown that the allele adr (Clc1(adr)) is due to an insertion of an ETn type transposon that is transcribed and leads to multiple splicing events; the allele mto (Clc1(adr-mto)) involves a stop codon near the N-terminus. We have determined the genomic organization of the mouse Clc1 gene and the sequence requirements for the transposon insertion in the Clc1(adr) allele. The mouse Clc1 gene is composed of 23 exons, ranging from 39 to 372 bp, and spans approximately 23 kb of genomic DNA. The exo/intron organization is highly homologous to that of the human CLCN1 gene; the homology of the coding sequence is 97% to rat and 89% to human. In the adr allele the ETn transposon is inserted into intron 12, the largest intron. Whereas the 5' and 3' LTR sequences of the ETn transposon are homologous to those reported for other insertional mutations of the mouse, no consensus motif for an insertion target site could be defined. On the basis of flanking sequences, we provide duplex PCR diagnoses for the adr, adr-mto, and wild-type alleles of Clc1. Close to the 3' end of intron 12, a tetranucleotide repeat (AATC)(n) was found that is polymorphic between mouse species Mus musculus, M. molossinus, M. castaneus, and M. spretus, and can thus be used for chromosomal mapping studies

CHROMOSOMAL MAPPING IN THE MOUSE OF 8 K+-CHANNEL GENES REPRESENTING THE 4 SHAKER-LIKE SUBFAMILIES SHAKER, SHAB, SHAW, AND SHAL

KLOCKE R, ROBERDS SL, TAMKUN MM, et al. CHROMOSOMAL MAPPING IN THE MOUSE OF 8 K+-CHANNEL GENES REPRESENTING THE 4 SHAKER-LIKE SUBFAMILIES SHAKER, SHAB, SHAW, AND SHAL. GENOMICS. 1993;18(3):568-574