bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evolution of development in the sea star genus Patiriella: clade‐specific alterations in cleavage
Authors: Cerra Anna , Byrne Maria 
Published: February 2004

SummaryExamination of early development in five species of the Patiriella sea star species complex indicates that the ancestral‐type radial holoblastic cleavage (Type I) is characteristic of P. regularis and P. exigua, whereas cleavage in species from the calcar clade followed multiple alternatives (Types II–IV) from holoblastic to meroblastic. Considering that invariant radial cleavage is thought to play a role in embryonic axis formation in echinoderms, we documented the details of blastomere formation in Patiriella sp. and followed development of the embryos. In Type II cleavage, the first and second cleavage planes appeared simultaneously at one pole of the embryo, dividing it directly into four equally sized blastomeres. In Type III cleavage, the first and second cleavage planes appeared simultaneously, followed promptly by the third cleavage plane, dividing the embryo directly into eight equally sized blastomeres. In Type IV cleavage, numerous furrows appeared simultaneously at one end of the embryo, dividing it into 32–40 equally sized blastomeres. Confocal sections revealed that embryos with cleavage Types II–IV were initially syncytial. The timing of karyokinesis in embryos with Types II and III cleavage was similar to that seen in clutch mates with Type I cleavage. Karyokinesis in embryos with Type IV cleavage, however, differed in timing compared with Type I clutch mates. Alteration in cleavage was not associated with polarized distribution of maternally provided nutrients. For each cleavage type, development was normal to the competent larval stage. Although variable blastomere configuration in the calcar clade may be linked to possession of a lecithotrophic development, other Patiriella species with this mode of development have typical cleavage. The presence of variable cleavage in all calcar clade species indicates that phylogenetic history has played a role in the distribution of this embryonic trait in Patiriella. The plasticity in early cleavage in these sea stars indicates that this aspect of early development is not constrained against change and that there are many ways to achieve multicellularity.
Transcatheter Coil Closure of Pulmonary Arteriovenous Malformations in Children
Authors: ABUSHABAN LULU , UTHAMAN BABU , ENDRYS JERRY 
Published: February 2004

Pulmonary arteriovenous fistula (PAVF) is a rare vascular malformation of the lung that may lead to cyanosis, epistaxis, hemoptysis, and neurological deficits or cerebral abscess. The purpose of this study is to assess the effectiveness of percutaneous transcatheter embolization of PAVF in pediatric patients. Transcatheter embolization of PAVF using spring coils was performed in three patients (two males and one female) who presented between 1989 and 1999. The age at presentation ranged from 8 months to 3 years (mean 19.6 months). All patients had cyanosis and clubbing. Neurological, dermatological, or other cardiac manifestations were absent. The arterial oxygen saturations at presentation ranged from 60 to 72% (mean 64%). During eight procedures, multiple coils (total of 41 coils, average 14 coils per patient) were delivered to occlude the fistulas successfully. There was complete occlusion of the fistulas in all patients after the multiple interventions. The aortic saturations increased from a mean of 66% to a mean of 95%. Chest radiographs demonstrated dramatic regression of the pulmonary shadows in all three patients. There were no complications encountered during the procedures or during follow‐up. Transcatheter coil embolization of PAVF is a safe and effective method of treatment in the pediatric age group. Patients may require multiple procedures to completely occlude the fistulas. Long‐term follow‐up is essential to ensure absence of recurrence due to recanalization. (J Interven Cardiol 2004;17:23–26)
Matrix Metalloproteinases in Patients with Myocardial Infarction and Percutaneous Revascularization
Authors: ECKART ROBERT E. , UYEHARA CATHERINE F.T. , SHRY ERIC A. , FURGERSON JAMES L. , KRASUSKI RICHARD A. 
Published: February 2004

Background: Extracellular matrix remodeling is a component of coronary artery disease (CAD). Matrix metalloproteinases (MMPs) are enzymes involved in extracellular matrix degradation. The extrapolation of the role MMPs play in the clinical setting of acute coronary syndromes has not yet been defined. Methods: Samples from 100 subjects undergoing cardiac catheterization were analyzed for serum levels of MMP‐1, MMP‐2, and MMP‐9. These markers were assessed before, immediately after, and 24 hours after cardiac catheterization. Relationships among MMP levels, baseline characteristics, angiography findings and clinical course were assessed. Results: Comparing subjects with myocardial infarction versus those without, baseline MMP‐1 levels were not different at baseline but increased during the hospital stay, MMP‐2 levels were higher at baseline and throughout the monitoring period and MMP‐9 levels lower and decreased over time. MMP‐1 was higher 24 hours after catheterization in subjects undergoing revascularization. Subjects undergoing percutaneous revascularization had higher MMP‐9 levels following revascularization than those subjects undergoing angiography without angioplasty. Conclusions: Serial monitoring of MMPs indicates a differential subtype response to myocardial infarction and percutaneous revascularization. Results of this study indicate that MMP subtypes may play differing roles in the manifestation of acute coronary syndromes and response to revascularization. (J Interven Cardiol 2004;17:27–31)
Applications of Magnetic Resonance Imaging for Cardiac Stem Cell Therapy
Authors: RICKERS CARSTEN , GALLEGOS ROBERT , SEETHAMRAJU RAVI TEJA , WANG XIAOEN , SWINGEN CORY , JAYASWAL AVINASH , RAHRMANN ERIC P. , KASTENBERG ZACHARY J. , CLARKSON CHRISTINA E. , BIANCO RICHARD , O'BRIAN TIM , VERFAILLIE CATHERINE , BOLMAN R. MORTON , WILKE NORBERT , JEROSCH‐HEROLD MICHAEL 
Published: February 2004

Background: The latest generation of interactive cardiac magnetic resonance (MR) scanners has made cardiac interventions with real‐time MRI possible. To date, cardiac MRI has been mostly applied to measure myocardial perfusion, viability, and regional function, but now the application of cardiac MRI can be extended to cardiovascular interventions. The purpose of this article is to illustrate the potential of MRI in stem cell therapy for cardiac restoration.
Methods: We have applied MRI to (1) interactively target myocardial injections with a novel stem cell delivery catheter, and to compare gadolinium/blue dye injections to pathology; (2) assess myocardial perfusion with MR first pass imaging in an infarct model treated with stem cell therapy versus control animals; (3) measure regional functional changes using myocardial tissue tagging in the same animals.
Results: We were able to demonstrate the feasibility and safety of myocardial injections under MR fluoroscopy. The intramyocardial distribution of the blue dye at necropsy correlated well with the extent of gadolinium, as detected with a three‐dimensional inversion recovery MR pulse sequence for late enhancement immediately after contrast injection. Preliminary results show that myocardial perfusion reserve and regional wall motion improved in the stem‐cell‐treated group, compared to a control group.
Conclusions: These preliminary results suggest that (1) injections into the LV myocardium can be performed under real‐time MRI guidance using a directed catheter approach, and (2) regional myocardial perfusion and function, measured with MRI, both improve after stem cell therapy. This ongoing study demonstrates the potential of MRI for image‐guided interventions, combined with detailed evaluation of anatomy, function, perfusion, and viability. (J Interven Cardiol 2004;17:37–46)
Does Significance Matter?
Authors: Reese R. Allan 
Published: February 2004

AbstractThe name of this magazine was the subject of fierce debate. Although “significance” is a word often associated with statistics, it is very often misapplied or misunderstood. Its technical implications differ from the everyday use of the word and competing schools of thought within statistics have varying views on the correct usage. As the magazine is launched, R. Allan Reese examines some of these ideas from the viewpoint of a pragmatic data ­analyst.
Interferon-Dependent Immunity Is Essential for Resistance to Primary Dengue Virus Infection in Mice, Whereas T- and B-Cell-Dependent Immunity Are Less Critical
Authors: Shresta Sujan , Kyle Jennifer L. , Snider Heidi M. , Basavapatna Manasa , Beatty P. Robert , Harris Eva 
Published: February 2004

ABSTRACT

Dengue virus (DEN) causes dengue fever and dengue hemorrhagic fever/dengue shock syndrome, which are major public health problems worldwide. The immune factors that control DEN infection or contribute to severe disease are neither well understood nor easy to examine in humans. In this study, we used wild-type and congenic mice lacking various components of the immune system to study the immune mechanisms in the response to DEN infection. Our results demonstrate that alpha/beta interferon (IFN-α/β) and IFN-γ receptors have critical, nonoverlapping functions in resolving primary DEN infection. Furthermore, we show that IFN-α/β receptor-mediated action limits initial DEN replication in extraneural sites and controls subsequent viral spread into the central nervous system (CNS). In contrast, IFN-γ receptor-mediated responses seem to act at later stages of DEN disease by restricting viral replication in the periphery and eliminating virus from the CNS. Mice deficient in B, CD4
+
T, or CD8
+
T cells had no increased susceptibility to DEN; however, RAG mice (deficient in both B and T cells) were partially susceptible to DEN infection. In summary, (i) IFN-α/β is critical for early immune responses to DEN infection, (ii) IFN-γ-mediated immune responses are crucial for both early and late clearance of DEN infection in mice, and (iii) the IFN system plays a more important role than T- and B-cell-dependent immunity in resistance to primary DEN infection in mice.
Human Rhinovirus Type 2-Antibody Complexes Enter and Infect Cells via Fc-γ Receptor IIB1
Authors: Baravalle Günther , Brabec Marianne , Snyers Luc , Blaas Dieter , Fuchs Renate 
Published: February 2004

ABSTRACT

HeLa cells were stably transfected with a cDNA clone encoding the B1 isoform of the mouse FcγRII receptor (hereafter referred to as HeLa-FcRII cells). The receptor was expressed at high level at the plasma membrane in about 90% of the cells. These cells bound and internalized mouse monoclonal virus-neutralizing antibodies 8F5 and 3B10 of the subtype immunoglobulin G2a (IgG2a) and IgG1, respectively. Binding of the minor-group human rhinovirus type 2 (HRV2) to its natural receptors, members of the low-density lipoprotein receptor family, is dependent on the presence of Ca
2+
ions. Thus, chelating Ca
2+
ions with EDTA prevented HRV2 binding, entry, and infection. However, upon complex formation of
35
S-labeled HRV2 with 8F5 or 3B10, virus was bound, internalized, and degraded in HeLa-FcRII cells. Furthermore, challenge of these cells with HRV2-8F5 or HRV2-3B10 complexes resulted in de novo synthesis of viral proteins, as shown by indirect immunofluorescence microscopy. These data demonstrate that minor-group receptors can be replaced by surrogate receptors to mediate HRV2 cell entry, delivery into endosomal compartments, and productive uncoating. Consequently, the conformational change and uncoating of HRV2 appears to be solely triggered by the low-pH (pH ≤ 5.6) environment in these compartments.
Interactions Required for Binding of Simian Virus 40 T Antigen to the Viral Origin and Molecular Modeling of Initial Assembly Events
Authors: Reese Danielle K. , Sreekumar Kodangattil R. , Bullock Peter A. 
Published: February 2004

ABSTRACT
The purified T-antigen origin binding domain binds site specifically to site II, the central region of the simian virus 40 core origin. However, in the context of full-length T antigen, the origin binding domain interacts poorly with DNA molecules containing just site II. Here we investigate the contributions of additional core origin regions, termed the flanking sequences, to origin recognition and the assembly of T-antigen hexamers and double hexamers. Results from these studies indicate that in addition to site-specific binding of the T-antigen origin binding domain to site II, T-antigen assembly requires non-sequence-specific interactions between a basic finger in the helicase domain and particular flanking sequences. Related studies demonstrate that the assembly of individual hexamers is coupled to the distortions in the proximal flanking sequence. In addition, the point in the double-hexamer assembly process that is regulated by phosphorylation of threonine 124, the sole posttranslational modification required for initiation of DNA replication, was further analyzed. Finally, T-antigen structural information is used to model various stages of T-antigen assembly on the core origin and the regulation of this process.
RNA Recombination Plays a Major Role in Genomic Change during Circulation of Coxsackie B Viruses
Authors: Oberste M. Steven , Peñaranda Silvia , Pallansch Mark A. 
Published: February 2004

ABSTRACT
RNA recombination has been shown to occur during circulation of enteroviruses, but most studies have focused on poliovirus. To examine the role of recombination in the evolution of the coxsackie B viruses (CVB), we determined the partial sequences of four genomic intervals for multiple clinical isolates of each of the six CVB serotypes isolated from 1970 to 1996. The regions sequenced were the 5′-nontranslated region (5′-NTR) (350 nucleotides [nt]), capsid (VP4-VP2, 416 nt, and VP1, ∼320 nt), and polymerase (3D, 491 nt). Phylogenetic trees were constructed for each genome region, using the clinical isolate sequences and those of the prototype strains of all 65 enterovirus serotypes. The partial VP1 sequences of each CVB serotype were monophyletic with respect to serotype, as were the VP4-VP2 sequences, in agreement with previously published studies. In some cases, however, incongruent tree topologies suggested that intraserotypic recombination had occurred between the sequenced portions of VP2 and VP1. Outside the capsid region, however, isolates of the same serotype were not monophyletic, indicating that recombination had occurred between the 5′-NTR and capsid, the capsid and 3D, or both. Almost all clinical isolates were recombinant relative to the prototype strain of the same serotype. All of the recombination partners appear to be members of human enterovirus species B. These results suggest that recombination is a frequent event during enterovirus evolution but that there are genetic restrictions that may influence recombinational compatibility.
The Truncated Form of Glycoprotein gp2 of Equine Herpesvirus 1 (EHV-1) Vaccine Strain KyA Is Not Functionally Equivalent to Full-Length gp2 Encoded by EHV-1 Wild-Type Strain RacL11
Authors: von Einem Jens , Wellington Janet , Whalley J. Millar , Osterrieder Kerstin , O'Callaghan Dennis J. , Osterrieder Nikolaus 
Published: February 2004

ABSTRACT
Most equine herpesvirus 1 (EHV-1) strains, including the naturally occurring virulent RacL11 isolate, encode a large glycoprotein, gp2 (250 kDa), which is expressed from gene 71. Besides other alterations in the viral genome, the avirulent strain KyA harbors an in-frame deletion of 1,242 nucleotides in gene 71. To examine the contributions of gp2 variation to virus growth and virulence, mutant RacL11 and KyA viruses expressing full-length or truncated gp2 were generated. Western blot analyses demonstrated expression of a 250-kDa gp2 in cells infected with RacL11 virus or a mutant KyA virus harboring full-length gene 71, whereas a 75- to 80-kDa gp2 was detected in cells infected with KyA or mutant RacL11 virus expressing KyA gp2. The RacL11 gp2 precursor of 250 kDa in size and its truncated KyA counterpart of 80 kDa, as well as the 42-kDa carboxy-terminal gp2 subunit, were incorporated into virus particles. Absence of gp2 in RacL11 resulted in a 6-fold reduction of extracellular virus titers and a 13% reduction of plaque diameters, whereas gp2-negative KyA exhibited a 55% reduction in plaque diameter and a 51-fold decrease in extracellular virus titers. The massive growth defects of gp2-negative KyA could be restored by reinsertion of the truncated but not the full-length gp2 gene. The virulence of the generated gp2 mutant viruses was compared to the virulence of KyA and RacL11 in a murine infection model. RacL11 lacking gp2 was apathogenic for BALB/c mice, and insertion of the truncated KyA gp2 gene into RacL11 was unable to restore virulence. Similarly, replacement in the KyA genome of the truncated with the full-length RacL11 gene 71 did not result in the generation of virulent virus. From the results we conclude that full-length and truncated EHV-1 gp2 are not functionally equivalent and cannot compensate for the action of their homologues in allogeneic virus backgrounds.
Norovirus Capture with Histo-Blood Group Antigens Reveals Novel Virus-Ligand Interactions
Authors: Harrington Patrick R. , Vinjé Jan , Moe Christine L. , Baric Ralph S. 
Published: February 2004

ABSTRACT

Noroviruses are genetically diverse, uncultivable, positive-sense RNA viruses and are the most common cause of epidemic acute gastroenteritis in humans in the United States. Recent studies of norovirus attachment in vitro by using recombinant virus-like particles (VLPs) suggest that various norovirus strains exhibit different patterns of attachment to ABH histo-blood group antigens, which are carbohydrate epitopes present in high concentrations on mucosal cell surfaces of the gut. However, attachment of live norovirus strains to histo-blood group antigens has not been investigated to date. Utilizing a newly designed magnetic bead-virus capture method, we characterized histo-blood group antigen attachment properties of various norovirus strains obtained from clinical stool specimens to compare the attachment properties of wild-type virus and VLPs and to further map norovirus attachment. Consistent with previous reports using VLPs, various strains of noroviruses exhibited different patterns of attachment to histo- blood group antigens. Norwalk virus bound specifically to H type 1, H type 3, and Le
b
. Two genogroup II noroviruses, one representing the Toronto genotype and the other from a novel genotype, bound specifically to Le
b
. A Desert Shield-like strain did not attach to H types 1, 2, or 3, H type 1 and 3 precursors, Le
a
, or Le
b
. Surprisingly, wild-type Snow Mountain virus (SMV) attached specifically to H type 3, which contradicted previous findings with SMV VLPs. On further investigation, we found that stool components promote this attachment, providing the first known observation that one or more components of human feces could promote and enhance norovirus attachment to histo-blood group antigens.
Infectious Salmon Anemia Virus Specifically Binds to and Hydrolyzes 4-O-Acetylated Sialic Acids
Authors: Hellebø Audny , Vilas Ulrike , Falk Knut , Vlasak Reinhard 
Published: February 2004

ABSTRACT

Infectious salmon anemia virus (ISAV) is the causative agent of infections in farmed Atlantic salmon. ISAV presumably represents a new genus within the
Orthomyxoviridae
. ISAV has been shown earlier to exhibit a receptor-destroying activity, which was defined as an acetylesterase with unknown specificity. We have analyzed the substrate specificity of the ISAV esterase in detail. Purified ISAV hydrolyzed free 5-
N
-acetyl-4-
O
-acetyl neuraminic acid. In addition, the purified 9-O-acetylated sialic acid derivative was also hydrolyzed, but at lower rates. When we used a glycosidically bound substrate, ISAV was unable to hydrolyze 9-O-acetylated sialic acid, which represents the major substrate for the influenza C virus esterase. ISAV completely de-O-acetylated glycoprotein-bound 5-
N
-acetyl-4-
O
-acetyl neuraminic acid. Thus, the enzymatic activity of the hemagglutinin-esterase of ISAV is comparable to that of the sialate-4-O-esterases of murine coronaviruses and related group 2 coronaviruses. In addition, we found that ISAV specifically binds to glycoproteins containing 4-O-acetylated sialic acids. Both the ISAV esterase and recombinant rat coronavirus esterase specific for 4-O-acetylated sialic acids hydrolyzed ISAV receptors on horse and rabbit erythrocytes, indicating that this sialic acid represents a receptor determinant for ISAV.
Cholesterol Is Required for Endocytosis and Endosomal Escape of Adenovirus Type 2
Authors: Imelli Nicola , Meier Oliver , Boucke Karin , Hemmi Silvio , Greber Urs F. 
Published: February 2004

ABSTRACTThe species C adenovirus type 2 (Ad2) and Ad5 bind the coxsackievirus B Ad receptor and αv integrin coreceptors and enter epithelial cells by clathrin-mediated endocytosis. This pathway is rapid and efficient. It leads to cell activation and the cholesterol-dependent formation of macropinosomes. Macropinosomes are triggered to release their contents when incoming Ad2 escapes from endosomes. Here, we show that cholesterol extraction of epithelial cells by methyl-β-cyclodextrin (mβCD) treatment reduced Ad5-mediated luciferase expression ∼4-fold. The addition of cholesterol to normal cells increased gene expression in a dose-dependent manner up to threefold, but it did not restore gene expression in mβCD-treated cells. mβCD had no effect in the presence of excess cholesterol, indicating that the inhibition of gene expression was due specifically to cholesterol depletion. Cholesterol depletion inhibited rapid Ad2 endocytosis, endosomal escape, and nuclear targeting, consistent with the notion that clathrin-dependent endocytosis of Ad2 is cholesterol dependent. In cholesterol-reduced cells, Ad2 internalized at a low rate, suggestive of an alternative, clathrin-independent, low-capacity entry pathway. While exogenous cholesterol completely restored rapid Ad2 endocytosis, macropinocytosis, and macropinosome disruption, it did not, surprisingly, restore viral escape from endosomes. Our results indicate that macropinosome disruption and endosomal escape of Ad2 are independent events in cells depleted of and then refilled with cholesterol, suggesting that viral escape from endosomes requires lipid-controlled membrane homeostasis, trafficking, or signaling.
Rapid Uncoating of Vector Genomes Is the Key toEfficient Liver Transduction with Pseudotyped Adeno-Associated VirusVectors
Authors: Thomas Clare E. , Storm Theresa A. , Huang Zan , Kay Mark A. 
Published: February 2004

ABSTRACT
Transduction
of the liver with single-stranded adeno-associated virus
serotype 2 (AAV2) vectors is inefficient; less than 10% of
hepatocytes are permissive for stable transduction, and transgene
expression is characterized by a lag phase of up to 6 weeks. AAV2-based
vector genomes packaged inside AAV6 or AAV8 capsids can transduce the
liver with higher efficiency, but the molecular mechanisms underlying
this phenomenon have not been determined. We now show that the primary
barrier to transduction of the liver with vectors based on AAV2 capsids
is uncoating of vector genomes in the nucleus. The majority of AAV2
genomes persist as encapsidated single-stranded molecules within the
nucleus for as long as 6 weeks after vector administration.
Double-stranded vector genomes packaged inside AAV2 capsids are at
least 50-fold more active than single-stranded counterparts, but these
vectors also exhibit a lag phase before maximal gene expression. Vector
genomes packaged inside AAV6 or AAV8 capsids do not persist as
encapsidated molecules and are more biologically active than vector
genomes packaged inside AAV2 capsids. Our data suggest that the rate of
uncoating of vector genomes determines the ability of complementary
plus and minus single-stranded genomes to anneal together and convert
to stable, biologically active double-stranded molecular
forms.