bluuebunny/crossref_metadata_2025_split huggingface dataset:
NOTES ON SEVERAL SPECIES OF APHIDS COLLECTED ON POPULUS ANGUSTIFOLIA IN IDAHO
Authors: Miller Forrest W. 
Published: January 2010

Aphis populifoliae Fitch, Rept. Reg. N. Y. St. Cab. Nat. Hist., p. 66; 1851.Color:—Head and thorax reddish-brown, abdomen light green with light shadings, powdery on intersegmental lines. Legs, antennae and cornicles yellow to light brown.Structural details:—Hairs numerous and erect with lengths from .69mm. to .79 on antenna, approximately the same length on vertex. Secondary sensoria from 16-19 in number on III on alatae and arranged in an irregular row, absent in apterae.
ADDITIONAL NOTES ON TROPAEA LUNA (LEPID)
Authors: Wickwire Harriet A. , Calale Adele 
Published: January 2010

Robert E. Birdsong published some notes on Tropaca luna in the November 1932 issue of this magazine, which were of especial interest to us as we have been working along the same lines.In addition to the variations in ova-coloration which were mentioned the article, we have obtained ova which ranged in color from sky-blue to apple-green. In one of the few cases in which we obtained pure white ova, they turned green after a few days and never hatched. We have not noticed black micropyles.
CD72 Negatively Regulates KIT-Mediated Responses in Human Mast Cells
Authors: Kataoka Tatsuki R. , Kumanogoh Atsushi , Bandara Geethani , Metcalfe Dean D. , Gilfillan Alasdair M. 
Published: January 2010

Abstract
KIT activation, through binding of its ligand, stem cell factor, is crucial for normal mast cell growth, differentiation, and survival. Furthermore, KIT may also contribute to mast cell homing and cytokine generation. Activating mutations in KIT lead to the dysregulated mast cell growth associated with the myeloproliferative disorder, mastocytosis. We investigated the potential of downregulating such responses through mast cell inhibitory receptor activation. In this study, we report that the B cell-associated ITIM-containing inhibitory receptor, CD72, is expressed in human mast cells. Ligation of CD72 with the agonistic Ab, BU40, or with recombinant human CD100 (rCD100), its natural ligand, induced the phosphorylation of CD72 with a resulting increase in its association with the tyrosine phosphatase SH2 domain-containing phosphatase-1. This, in turn, resulted in an inhibition of KIT-induced phosphorylation of Src family kinases and extracellular-regulated kinases (ERK1/2). As a consequence of these effects, KIT-mediated mast cell proliferation, chemotaxis, and chemokine production were significantly reduced by BU40 and rCD100. Furthermore, BU40 and rCD100 also downregulated the growth of the HMC1.2 human mast cell line. Thus, targeting CD72 may provide a novel approach to the suppression of mast cell disease such as mastocytosis.
Absence of SHIP-1 Results in Constitutive Phosphorylation of Tank-Binding Kinase 1 and Enhanced TLR3-Dependent IFN-β Production
Authors: Gabhann Joan Ní , Higgs Rowan , Brennan Kiva , Thomas Warren , Damen Jacqueline E. , Ben Larbi Nadia , Krystal Gerald , Jefferies Caroline A. 
Published: January 2010

Abstract
Autoimmune diseases, such as systemic lupus erythematosus and rheumatoid arthritis, result from a loss of tolerance to self-antigens and immune-mediated injury precipitated by the overproduction of type I IFN and inflammatory cytokines. We have identified the inositol 5′ phosphatase SHIP-1 as a negative regulator of TLR3-induced type I IFN production. SHIP-1–deficient macrophages display enhanced TLR-induced IFN-β production, and overexpression of SHIP-1 negatively regulates the ability of TLR3 and its adaptor, Toll/IL-1 receptor domain-containing adaptor-inducing IFN-β, to induce IFN-β promoter activity, indicating that SHIP-1 negatively regulates TLR-induced IFN-β production. Further dissection of the IFN-β pathway implicates TANK-binding kinase 1 (TBK1) as the target for SHIP-1. Critically, in the absence of SHIP-1, TBK1 appears to be hyperphosphorylated both in unstimulated cells and following TLR3 stimulation. In addition, TBK1 appears to be constitutively associated with Toll/IL-1 receptor domain-containing adaptor-inducing IFN-β and TNFR-associated factor 3 in SHIP-1 deficient cells, whereas in wild-type cells this association is inducible following TLR3 stimulation. In support of a role for SHIP-1 in regulating complex formation, confocal microscopy demonstrates that TBK1 distribution in the cell is significantly altered in SHIP-1–deficient cells, with more prominent endosomal staining observed, compared with wild-type controls. Taken together, our results point to SHIP-1 as a critical negative regulator of IFN-β production downstream of TLR3 through the regulation of TBK1 localization and activity.
The CCL3/Macrophage Inflammatory Protein-1α–Binding Protein Evasin-1 Protects from Graft-versus-Host Disease but Does Not Modify Graft-versus-Leukemia in Mice
Authors: Castor Marina G. M. , Rezende Bárbara , Resende Carolina B. , Alessandri Ana L. , Fagundes Caio T. , Sousa Lirlândia P. , Arantes Rosa M. E. , Souza Danielle G. , Silva Tarcília A. , Proudfoot Amanda E. I. , Teixeira Mauro M. , Pinho Vanessa 
Published: January 2010

Abstract
CCL3 is a protein of the CC chemokine family known to be important for T cell recruitment in inflammatory diseases. The aim of the current study was to evaluate the effects and putative mechanism of action of evasin-1, a novel CCL3-binding protein, in the pathogenesis of acute graft-versus-host disease (GVHD). GVHD was induced by the transplantation of splenocytes from C57BL/6J to B6D2F1 mice. Treatment of recipient mice with evasin-1 prevented mortality associated with GVHD. This was correlated with reduced weight loss and clinical disease severity. Analysis of the small intestine showed that evasin-1 treatment reduced the histopathological score and decreased levels of IFN-γ and CCL5. Mechanistically, evasin-1 treatment reduced the number of CD4+ and CD8+ T cells infiltrating the small intestine, as assessed by immunohistochemistry, and the adhesion of leukocytes to intestinal venules of recipient mice, as assessed by intravital microscopy. Evasin-1 was also able to decrease liver damage, as seen by reduction of inflammatory infiltrate and IFN-γ levels. Treatment with evasin-1 did not interfere with graft-versus-leukemia. Altogether, our studies demonstrate that CCL3 plays a major role in mediating GVHD, but not graft-versus-leukemia in mice and suggest that blockade of CCL3 with evasin-1 has potential therapeutic application in patients undergoing bone marrow transplantation.
Structural Basis for Lipid-Antigen Recognition in Avian Immunity
Authors: Dvir Hay , Wang Jing , Ly Nary , Dascher Christopher C. , Zajonc Dirk M. 
Published: January 2010

Abstract
CD1 proteins present self- and foreign lipid Ags to activate specific T cells in the mammalian immune system. These T cells play an important role in controlling autoimmune diseases, suppression of tumor growth, and host defense against invading pathogens. Humans use five CD1 isoforms, whereas only two exist in birds. Unlike mammals’ CD1, the structure of chicken CD1-2 showed a primitive lipid-binding groove, suggesting that chicken may only recognize single-chain lipids. In contrast, the crystal structure of the second chicken CD1 isoform, chCD1-1, reported in this study at 2.2 Å resolution, reveals an elaborated binding groove with a dual-pocket, dual-cleft architecture. The A’ and F’ deep pockets are separated from each other, but each is connected to a hydrophobic surface cleft, which may participate in lipid binding. The long endogenous ligand found inside the binding groove of chCD1-1, together with binding data on various glycolipids and mycolic acid, strongly suggest that the unique avian CD1 family could bind long dual- and possibly triacyl-chain lipids.
Preparation of 4‐Spirocyclohexyloxazolidinone by
C
‐
H
Bond Nitrene Insertion
Authors: Huard Kim , Lebel Hélène 
Published: January 2010

Abstract

Rhodium(II) acetate

Triphenylacetic acid

Rhodium (II) tetrakis(triphenylacetate)

Cyclohexylmethyl
N‐
hydrocarbamate

1,1‐Carbonyldiimadole

Cyclohexanemethanol

Hydroxylamine hydrochloride

Imidazole

p‐
Toluenesulfonyl chloride

Triethylamine

Cyclohexylmethyl
N'‐
tosylcarbamate

4‐Spirocyclohexyloxazolidinone

Potassium carbonate
Synthesis of Polyynes by In Situ Desilylative Bromination and Palladium‐Catalyzed Coupling: (7‐(Benzyloxy)Hepta‐1,3,5‐Triynyl)Triisopropylsilane
Authors: Hwang Soonho , Ryong Kang Hee , Kim Sanghee 
Published: January 2010

Abstract

Benzyl propargyl ether

N‐
Bromosuccinimide

Silver nitrate

(Trispropylsilyl)acetylene

Dichlorbis(triphenylphosphine)palladium(II)

Copper(I) iodide

Diisopropylamine

Silver(I) fluoride
Robust adaptive output‐feedback control for a class of nonlinear systems with time‐varying actuator faults
Authors: Zhang Zhengqiang , Xu Shengyuan , Guo Yu , Chu Yuming 
Published: January 2010

AbstractA robust adaptive output‐feedback control scheme is proposed for a class of nonlinear systems with unknown time‐varying actuator faults. Additional unmodelled terms in the actuator fault model are considered. A new linearly parameterized model is proposed. The boundedness of all the closed‐loop signals is established. The desired control performance of the closed‐loop system is guaranteed by appropriately choosing the design parameters. The properties of the proposed control algorithm are demonstrated by two simulation examples. Copyright © 2010 John Wiley & Sons, Ltd.
Stretchable, Curvilinear Electronics Based on Inorganic Materials
Authors: Kim Dae‐Hyeong , Xiao Jianliang , Song Jizhou , Huang Yonggang , Rogers John A. 
Published: January 2010

AbstractAll commercial forms of electronic/optoelectronic technologies use planar, rigid substrates. Device possibilities that exploit bio‐inspired designs or require intimate integration with the human body demand curvilinear shapes and/or elastic responses to large strain deformations. This article reviews progress in research designed to accomplish these outcomes with established, high‐performance inorganic electronic materials and modest modifications to conventional, planar processing techniques. We outline the most well developed strategies and illustrate their use in demonstrator devices that exploit unique combinations of shape, mechanical properties and electronic performance. We conclude with an outlook on the challenges and opportunities for this emerging area of materials science and engineering.
Heat transfer during microwave combination heating: Computational modeling and MRI experiments
Authors: Rakesh Vineet , Seo Youngseob , Datta Ashim K. , McCarthy Kathryn L. , McCarthy Michael J. 
Published: January 2010

AbstractCombination of heating modes such as microwaves, convection, and radiant heating can be used to realistically achieve the quality and safety needed for cooking processes and, at the same time, make the processes faster. Physics‐based computational modeling used in conjunction with MRI experimentation can be used to obtain critical understanding of combination heating. The objectives were to: (1) formulate a fully coupled electromagnetics ‐ heat transfer model, (2) use magnetic resonance imaging (MRI) experiments to determine the 3D spatial and temporal variation of temperatures and validate the numerical model, (3) use the insight gained from the model and experiments to understand the combination heating process and to optimize it. The different factors that affect heating patterns during combination heating such as the type of heating modes used, placement of sample, and microwave cycling were considered. Objective functions were defined and minimized for design and optimization. The use of such techniques can lead to greater control and automation of combination heating process benefitting the food process and product developers immensely. © 2010 American Institute of Chemical Engineers AIChE J, 2010
Overlapping spectra of SMAD4 mutations in juvenile polyposis (JP) and JP–HHT syndrome
Authors: Gallione Carol , Aylsworth Arthur S. , Beis Jill , Berk Terri , Bernhardt Barbara , Clark Robin D. , Clericuzio Carol , Danesino Cesare , Drautz Joanne , Fahl Jeffrey , Fan Zheng , Faughnan Marie E. , Ganguly Arupa , Garvie John , Henderson Katharine , Kini Usha , Leedom Tracey , Ludman Mark , Lux Andreas , Maisenbacher Melissa , Mazzucco Sara , Olivieri Carla , Ploos van Amstel Johannes K. , Prigoda‐Lee Nadia , Pyeritz Reed E. , Reardon Willie , Vandezande Kirk , Waldman J. Deane , White Robert I. , Williams Charles A. , Marchuk Douglas A. 
Published: January 2010

AbstractJuvenile polyposis (JP) and hereditary hemorrhagic telangiectasia (HHT) are clinically distinct diseases caused by mutations in SMAD4 and BMPR1A (for JP) and endoglin and ALK1 (for HHT). Recently, a combined syndrome of JP–HHT was described that is also caused by mutations in SMAD4. Although both JP and JP–HHT are caused by SMAD4 mutations, a possible genotype:phenotype correlation was noted as all of the SMAD4 mutations in the JP–HHT patients were clustered in the COOH‐terminal MH2 domain of the protein. If valid, this correlation would provide a molecular explanation for the phenotypic differences, as well as a pre‐symptomatic diagnostic test to distinguish patients at risk for the overlapping but different clinical features of the disorders. In this study, we collected 19 new JP–HHT patients from which we identified 15 additional SMAD4 mutations. We also reviewed the literature for other reports of JP patients with HHT symptoms with confirmed SMAD4 mutations. Our combined results show that although the SMAD4 mutations in JP–HHT patients do show a tendency to cluster in the MH2 domain, mutations in other parts of the gene also cause the combined syndrome. Thus, any mutation in SMAD4 can cause JP–HHT. Any JP patient with a SMAD4 mutation is, therefore, at risk for the visceral manifestations of HHT and any HHT patient with SMAD4 mutation is at risk for early onset gastrointestinal cancer. In conclusion, a patient who tests positive for any SMAD4 mutation must be considered at risk for the combined syndrome of JP–HHT and monitored accordingly. © 2010 Wiley‐Liss, Inc.
Imperforate anus is a rare associated finding in blepharocheilodontic syndrome
Authors: Weaver K. Nicole , Rutledge Katherine D. , Grant John H. , Robin Nathaniel H. 
Published: January 2010

AbstractBlepharocheilodontic (BCD) syndrome is a rare autosomal‐dominant condition that is characterized by lower eyelid ectropion, upper eyelid distichiasis, euryblepharon, bilateral cleft lip and palate, and conical teeth. It exhibits considerable phenotypic variability among affected individuals. An additional rare associated manifestation is imperforate anus (IA), which has been reported in three cases [Guyuron et al. (1995); J Craniofac Surg 6:392–394; Gorlin et al. (1996); Am J Med Genet 65:109–112; da Silva Lopes et al. (2003); Am J Med Genet Part A 121A:266–270]. Here we report on a family with BCD that includes IA, confirming that anorectal anomalies are a part of BCD syndrome. © 2010 Wiley‐Liss, Inc.
Two siblings with alternate unbalanced recombinants derived from a large cryptic maternal pericentric inversion of chromosome 20
Authors: DeScipio Cheryl , Morrissette Jennifer D. , Conlin Laura K. , Clark Dinah , Kaur Maninder , Coplan James , Riethman Harold , Spinner Nancy B. , Krantz Ian D. 
Published: January 2010

AbstractTwo brothers, with dissimilar clinical features, were each found to have different abnormalities of chromosome 20 by subtelomere fluorescence in situ hybridization (FISH). The proband had deletion of 20p subtelomere and duplication of 20q subtelomere, while his brother was found to have a duplication of 20p subtelomere and deletion of 20q subtelomere. Parental cytogenetic studies were initially thought to be normal, both by G‐banding and by subtelomere FISH analysis. Since chromosome 20 is a metacentric chromosome and an inversion was suspected, we used anchored FISH to assist in identifying a possible inversion. This approach employed concomitant hybridization of a FISH probe to the short (p) arm of chromosome 20 with the 20q subtelomere probe. We identified a cytogenetically non‐visible, mosaic pericentric inversion of one of the maternal chromosome 20 homologs, providing a mechanistic explanation for the chromosomal abnormalities present in these brothers. Array comparative genomic hybridization (CGH) with both a custom‐made BAC and cosmid‐based subtelomere specific array (TEL array) and a commercially available SNP‐based array confirmed and further characterized these rearrangements, identifying this as the largest pericentric inversion of chromosome 20 described to date. TEL array data indicate that the 20p breakpoint is defined by BAC RP11‐978M13, ∼900 kb from the pter; SNP array data reveal this breakpoint to occur within BAC RP11‐978M13. The 20q breakpoint is defined by BAC RP11‐93B14, ∼1.7 Mb from the qter, by TEL array; SNP array data refine this breakpoint to within a gap between BACs on the TEL array (i.e., between RP11‐93B14 and proximal BAC RP11‐765G16). © 2010 Wiley‐Liss, Inc.
Planar cell polarity pathway genes and risk for spina bifida
Authors: Wen Shu , Zhu Huiping , Lu Wei , Mitchell Laura E. , Shaw Gary M. , Lammer Edward J. , Finnell Richard H. 
Published: January 2010

AbstractSpina bifida, a neural tube closure defect (NTD) involving the posterior portion of what will ultimately give rise to the spinal cord, is one of the most common and serious birth defects. The etiology of spina bifida is thought to be multi‐factorial and involve multiple interacting genes and environmental factors. The causes of this congenital malformation remain largely unknown. However, several candidate genes for spina bifida have been identified in lower vertebrates, including the planar cell polarity (PCP) genes. We used data from a case–control study conducted in California to evaluate the association between variation within several key PCP genes and the risk of spina bifida. The PCP genes included in this study were the human homologs of the Xenopus genes Flamingo, Strabismus, Prickle, Dishevelled, and Scrib, two of the homologs of Xenopus Wnt genes, WNT5A and WNT11, and two of the homologs of Xenopus Frizzled, FZD3 and FZD6. None of the 172 SNPs that were evaluated were significantly associated with spina bifida in any racial/ethnic group after correction for multiple testing. However, several SNPs in the PRICKLE2 gene had unadjusted P‐value <0.01. In conclusion, our results, though largely negative, suggest that the PRICKLE2 gene may potentially modify the risk of spina bifida and deserves further investigation. © 2010 Wiley‐Liss, Inc.
Chromosomal breakpoints characterization of two supernumerary ring chromosomes 20
Authors: Guediche N. , Brisset S. , Benichou J.‐J. , Guérin N. , Mabboux P. , Maurin M.‐L. , Bas C. , Laroudie M. , Picone O. , Goldszmidt D. , Prévot S. , Labrune P. , Tachdjian G. 
Published: January 2010

AbstractThe occurrence of an additional ring chromosome 20 is a rare chromosome abnormality, and no common phenotype has been yet described. We report on two new patients presenting with a supernumerary ring chromosome 20 both prenatally diagnosed. The first presented with intrauterine growth retardation and some craniofacial dysmorphism, and the second case had a normal phenotype except for obesity. Conventional cytogenetic studies showed for each patient a small supernumerary marker chromosome (SMC). Using fluorescence in situ hybridization, these SMCs corresponded to ring chromosomes 20 including a part of short and long arms of chromosome 20. Detailed molecular cytogenetic characterization showed different breakpoints (20p11.23 and 20q11.23 for Patient 1 and 20p11.21 and 20q11.21 for Patient 2) and sizes of the two ring chromosomes 20 (13.6 Mb for case 1 and 4.8 Mb for case 2). Review of the 13 case reports of an extra r(20) ascertained postnatally (8 cases) and prenatally (5 cases) showed varying degrees of phenotypic abnormalities. We document a detailed molecular cytogenetic chromosomal breakpoints characterization of two cases of supernumerary ring chromosomes 20. These results emphasize the need to characterize precisely chromosomal breakpoints of supernumerary ring chromosomes 20 in order to establish genotype–phenotype correlation. This report may be helpful for prediction of natural history and outcome, particularly in prenatal diagnosis. © 2010 Wiley‐Liss, Inc.
The Roberts syndrome/SC phocomelia spectrum—A case report of an adult with review of the literature
Authors: Goh Elaine Suk‐Ying , Li Chumei , Horsburgh Sheri , Kasai Yumi , Kolomietz Elena , Morel Chantal France 
Published: January 2010

AbstractRoberts syndrome (RBS) (OMIM #268300) is a rare autosomal recessive disorder characterized by tetraphocomelia (symmetrical limb reduction), craniofacial anomalies, growth retardation, mental retardation, cardiac and renal abnormalities. The syndrome is caused by mutations in the ESCO2 (establishment of cohesion 1 homolog 2) (Entrez 609353) gene, which is located at 8p21.1, and encodes a protein essential in establishing sister chromatid cohesion during S phase. SC phocomelia (SC) (OMIM #269000), has less severe symmetric limb reduction, flexion contractures of various joints, minor facial anomalies, growth retardation and occasionally, mental retardation. These two syndromes can be considered part of a spectrum, with RBS at the most severe range in which severely affected infants may be stillborn or die in the post‐natal period, while individuals with SC phocomelia represent the milder end of the spectrum and typically survive to adulthood. In both presentations, karyotype investigations characteristically reveal premature centromere separation (PCS), otherwise known as heterochromatin repulsion or puffing. There is little literature about the follow‐up of adults with the spectrum of RBS/SC phocomelia or their recommended management. We report on an adult presentation of RBS/SC phocomelia spectrum disorder with a history of major cardiac malformation in childhood, normal limbs on physical examination, mild facial anomalies, mild learning difficulties, and PCS. Molecular studies of ESCO2 have confirmed the diagnosis. A literature review, focussing on adult manifestations of this condition and a discussion of follow‐up guidelines are presented. © 2010 Wiley‐Liss, Inc.
Analysis of genotype–phenotype correlations in human holoprosencephaly
Authors: Solomon Benjamin D. , Mercier Sandra , Vélez Jorge I. , Pineda‐Alvarez Daniel E. , Wyllie Adrian , Zhou Nan , Dubourg Christèle , David Veronique , Odent Sylvie , Roessler Erich , Muenke Maximilian 
Published: January 2010

AbstractSince the discovery of the first gene causing holoprosencephaly (HPE), over 500 patients with mutations in genes associated with non‐chromosomal, non‐syndromic HPE have been described, with detailed descriptions available in over 300. Comprehensive clinical analysis of these individuals allows examination for the presence of genotype–phenotype correlations. These correlations allow a degree of differentiation between patients with mutations in different HPE‐associated genes and for the application of functional studies to determine intragenic correlations. These early correlations are an important advance in the understanding of the clinical aspects of this disease, and in general argue for continued analysis of the genetic and clinical findings of large cohorts of patients with rare diseases in order to better inform both basic biological insight and care and counseling for affected patients and families. Published 2010 Wiley‐Liss, Inc.