1,403 research outputs found

    Spatial Patterns in the Distribution of Tropical Tree Species

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    Inflight and ground-based simulation of handling qualities of very large airplanes in landing approach

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    Inflight and ground based simulation of Boeing 367-80 variable stability aircraft handling qualities during landing approac

    Simulation of three supersonic transport configurations with the Boeing 367-80 in-flight dynamic simulation airplane

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    In-flight dynamic simulator used to evaluate problems of low-speed approach and landing of supersonic transpor

    The Vaccinia Virus Bifunctional Gene J3 (Nucleoside-2′-O-)-methyltransferase and Poly(A) Polymerase Stimulatory Factor Is Implicated as a Positive Transcription Elongation Factor by Two Genetic Approaches

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    AbstractVaccinia virus genes A18 and G2 affect the elongation and termination of postreplicative viral gene transcription in opposite ways. Viruses with mutations in gene A18 produce abnormally long transcripts, indicating that A18 is a negative transcription elongation factor. Viruses containing mutations in gene G2 produce transcripts that are abnormally short, truncated specifically from their 3′ ends, indicating that G2 is a positive transcription elongation factor. Despite the fact that both A18 and G2 are essential genes, A18-G2 double-mutant viruses are viable, presumably because the effects of the mutations are mutually compensatory. In addition, the anti-poxviral drug isatin-β-thiosemicarbazone (IBT) seems to enhance elongation during a vaccinia infection: IBT treatment of a wildtype vaccinia infection induces a phenotype identical to an A18 mutant infection, and G2 mutant viruses are dependent on IBT for growth, presumably because IBT restores the G2 mutant truncated transcripts to a normal length. These observations inspire two independent genetic selections that have now been used to identify an additional vaccinia gene, J3, that regulates postreplicative transcription elongation. In the first selection, a single virus that contains an extragenic suppressor of the A18 temperature-sensitive mutant, Cts23, was isolated. In the second selection, several spontaneous IBT-dependent (IBTd) mutant viruses were isolated and characterized genetically. Marker rescue mapping and DNA sequence analysis show that the extragenic suppressor of Cts23 contains a point mutation in the J3 gene, while each of seven new IBTd mutants contains null mutations in the J3 gene. The J3 protein has previously been identified as a (nucleoside-2′-O-)-methyltransferase and as a processivity subunit for the heterodimeric viral poly(A) polymerase. The nature of the two independent selections used to isolate the J3 mutants strongly suggests that the J3 protein serves as a positive postreplicative transcription elongation factor during a normal virus infection

    Chronic Pancreatitis Progressing to Duodenal Obstruction in the Absence of Classic Symptoms

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    We report the case of a 34-year-old alcoholic who was initially seen in March 1985 because of acute pancreatitis. A mass was demonstrated in the head of the pancreas. Serial sonogram and computed tomography scans over 4 1/2 years revealed progressive encroachment of the duodenum without symptoms attributable to obstruction. In 1989, three separate endoscopies with multiple biopsies showed chronic inflammation and strictures. Hypotonic duodenography confirmed stricture and obstructed duodenum. Surgical intervention is being considered. Duodenal obstruction secondary to chronic pancreatitis is rare. It may proceed subclinically for several years independent of continued alcohol use. Only when obstruction became severe in our patient did the classic symptoms of postprandial nausea, emesis, and weight loss become manifest. Obstructive jaundice from chronic pancreatitis due to stricture in the pancreatic portion of the common bile duct is uncommon

    Characterizing extinction debt following habitat fragmentation using neutral theory

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    Habitat loss leads to species extinctions, both immediately and over the long-term as “extinction debt” is repaid. The same quantity of habitat can be lost in different spatial patterns with varying habitat fragmentation. How this translates to species loss remains an open problem requiring an understanding of the interplay between community dynamics and habitat structure across temporal and spatial scales. Here we develop formulas that characterize extinction debt in a spatial neutral model after habitat loss and fragmentation. Central to our formulas are two new metrics, which depend on properties of the taxa and landscape: “effective area”, measuring the remaining number of individuals; and “effective connectivity”, measuring individuals’ ability to disperse through fragmented habitat. This formalizes the conventional wisdom that habitat area and habitat connectivity are the two critical requirements for long term preservation of biodiversity. Our approach suggests that mechanistic fragmentation metrics help resolve debates about fragmentation and species loss

    Interaction between the J3R Subunit of Vaccinia Virus Poly(A) Polymerase and the H4L Subunit of the Viral RNA Polymerase

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    AbstractJ3R, the 39-kDa subunit of vaccinia virus poly(A) polymerase, is a multifunctional protein that catalyzes (nucleoside-2′-O-)-methyltransferase activity, serves as a poly(A) polymerase stimulatory factor, and acts as a postreplicative positive transcription elongation factor. Prior results support an association between poly(A) polymerase and the virion RNA polymerase. A possible direct interaction between J3R and H4L subunit of virion RNA polymerase was evaluated. J3R was shown to specifically bind to H4L amino acids 235–256, C terminal to NPH I binding site on H4L. H4L binds to the C-terminal region of J3R between amino acids 169 and 333. The presence of a J3R binding site near to the NPH I binding region on H4L led us to evaluate a physical interaction between NPH I and J3R. The NPH I binding site was located on J3R between amino acids 169 and 249, and J3R was shown to bind to NPH I between amino acids 457 and 524. To evaluate a role for J3R in early gene mRNA synthesis, transcription termination, and/or release, a transcription-competent extract prepared from cells infected with mutant virus lacking J3R, J3-7. Analysis of transcription activity demonstrated that J3R is not required for early mRNA synthesis and is not an essential factor in early gene transcription termination or transcript release in vitro. J3R interaction with NPH I and H4L may serve as a docking site for J3R on the virion RNA polymerase, linking transcription to mRNA cap formation and poly(A) addition
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