bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reproducibility of facial soft tissue landmarks on 3D laser‐scanned facial images
Authors: Toma AM , Zhurov A , Playle R , Ong E , Richmond S 
Published: January 2009

Structured AbstractAuthors –  Toma AM, Zhurov A, Playle R, Ong E, Richmond SBackground –  The three‐dimensional (3D) measuring technology is useful to inspect facial shape in three planes of space (X, Y, and Z). Recent work has been directed to analyse craniofacial morphology using facial soft tissue landmarks to identify facial differences among population. The reproducibility of facial landmarks is almost necessary to ensure accurate 3D facial measurements.Objective –  The aim of this study is to assess the reproducibility of facial soft tissue landmarks using laser‐scan 3D imaging technology.Subjects and Methods –  Facial landmarks were assessed for 30 15½‐year‐old British‐Caucasian children (15 males and 15 females). The sample was recruited from the Avon Longitudinal Study of Parents and Children (ALSPAC). The 3D facial images were acquired for each subject using two high‐resolution Konica/Minolta laser scanners. Twenty‐one facial landmarks (63 X, Y, and Z coordinates) were identified and recorded on each 3D facial image by two examiners. The reproducibility of landmarks identification at 2‐week interval was assessed for one of the examiners (intra‐examiner). In addition, the reproducibility of landmarks was assessed between the two examiners (inter‐examiner). Using Bland‐Altman plots, both intra‐ and inter‐examiner assessments had evaluated landmarks reproducibility in three dimensions for the sample divided by gender. The reproducibility of the 3D‐coordinates for each landmark was considered under three categories (< 0.5 mm, < 1 mm, and >1 mm) for both intra‐ and inter‐examiner reproducibility assessments.Results –  The distribution of coordinates at the three levels of reproducibility show the following percentages: intra‐examiner: < 0.5 mm (38%), < 1 mm (51%), >1 mm (11%); inter‐examiner: < 0.5 mm (35%), < 1 mm (48%), >1 mm (17%). Generally, 10 landmarks were reproducible to less than 1 mm for both intra‐ and inter‐examiner reproducibility assessments. The Labiale Superius was the most reproducible and Palebrale Superius was the least reproducible landmark. Some landmarks showed greater reliability in certain planes of space; the Glabella was more reliable in the Z than the Y axis. Gender differences were found; Subnasale was more reproducible in the Y‐axis in males compared with females.Conclusions –  The reproducibility of facial landmarks should be considered in the three planes of space. The majority of X‐Y‐Z coordinates taken to the 21 facial landmarks were reproducible to < 1 mm which is clinically acceptable. The accuracy of landmarks identification ranged from 0.39 to 1.49 mm. The reliability in identification depends on the clarity and definition of each landmark as well as gender characteristics. The different landmarks reproducibility should be considered when evaluating changes related to growth and healthcare interventions.
Intolerance reactions to knee arthroplasty in patients with nickel/cobalt allergy and disappearance of symptoms after revision surgery with titanium‐based endoprostheses
Authors: Dietrich Karin‐Almut , Mazoochian Farhad , Summer Burkhard , Reinert Mark , Ruzicka Thomas , Thomas Peter 
Published: January 2009

SummaryIntolerance reactions to metal implants may present as dermatitis, impaired wound healing, effusions, pain or loosening. The clinical relevance of metal allergy in the differential diagnosis is often unclear and patients may even tolerate implants containing metals to which they are allergic. We present four patients with knee arthroplasty in whom after exclusion of infection or mechanical causes, a nickel/cobalt allergy led to replacement surgery with titanium‐based prostheses. The subsequent alleviation of symptoms underlined the relevance and usefulness of allergological diagnostics in selected cases of complicated arthroplasty.
High prevalence of cardio‐metabolic risk factors among adolescents with intellectual disability
Authors: Wallén Eva Flygare , Müllersdorf Maria , Christensson Kyllike , Malm Gunilla , Ekblom Örjan , Marcus Claude 
Published: January 2009

AbstractAdults with intellectual disabilities (IDs) have poor lifestyle‐related health compared with the general population. Our aim was to study whether such differences are present already in adolescents.Aim: To compare the prevalence and severity of cardio‐metabolic risk factors and cardio‐vascular fitness in adolescents with and without IDs.Methods: Intellectual disability (ID) students (n = 66) and non‐intellectual disability (non‐ID) students from practical (non‐ID‐p) (n = 34) and theoretical (non‐ID‐t) (n = 56) programmes were recruited from three upper secondary schools. Anthropometric data, blood pressure, body composition, fasting‐insulin, fasting‐glucose, fasting‐lipids and cardio‐vascular fitness were measured.Results: Participants with and without ID differed significantly in the prevalence of cardio‐metabolic risk factors with participants with ID having a higher percentage of total fat mass, wider waist circumferences (WCs), lower levels of fat‐free mass (FFM), lower bone mineral density (BMD) and higher insulin and homeostasis model assessment of insulin resistance (HOMA) levels and poorer cardio‐vascular fitness. The healthiest levels were found in the non‐ID‐t group compared to the group with ID and the group with non‐ID‐p in between.Conclusion: The prevalence of cardio‐metabolic risk factors and poor cardio‐vascular fitness was found to be high in this young population with intellectual disabilities. Measures should be taken to improve the health messages directed towards children and adolescents with intellectual disabilities.
Immunolocalization of Fascin, an Actin‐Bundling Protein and Glial Fibrillary Acidic Protein in Human Astrocytoma Cells
Authors: Mondal Soma , Dirks Peter , Rutka James T. 
Published: January 2009

AbstractFascin is a 55‐kDa globular protein that functions to organize filamentous‐actin into parallel bundles. A role for fascin in cell migration has led to its study in many tumor types. In this report, we investigate fascin in astrocytomas. We show that fascin is expressed in astrocytes and in a panel of human astrocytoma cell lines. Immunofluorescence analysis demonstrates that fascin and the intermediate filament protein, glial fibrillary acidic protein (GFAP), are both expressed in the perinuclear region and within cytoplasmic processes of astrocytes and astrocytoma cells. Amino acid residues within the NH2 terminus of GFAP can undergo phosphorylation; these modifications regulate intermediate filament disassembly and occur during cytokinesis. We show that fascin and specific phosphorylated species of GFAP colocalize within dividing cells. Finally, we demonstrate that fascin co‐immunoprecipitates with GFAP and that immunocomplex formation is preferential for GFAP phosphorylated at serine residues 8 and 13. These data show that fascin and GFAP are immunolocalized regionally within cells and tumors of astrocytic origin and suggest that their binding may occur during dynamic reorganization of intermediate filaments.
Genomic Comparison of PE and PPE Genes in theMycobacterium aviumComplex
Authors: Mackenzie Nick , Alexander David C. , Turenne Christine Y. , Behr Marcel A. , De Buck Jeroen M. 
Published: January 2009

ABSTRACTTheMycobacterium aviumcomplex (MAC) comprises genomically similar but phenotypically divergent bacteria that inhabit diverse environments and that cause disease in different hosts. In this study, a whole-genome approach was used to examine the polymorphic PE (Pro-Glu) and PPE (Pro-Pro-Glu) gene families, implicated in immunostimulation and virulence. The four major groups of MAC organisms were examined, including the newly sequenced type strains ofM. intracellulareandM. aviumsubsp.avium, plusM. aviumsubsp.paratuberculosisandM. aviumsubsp.hominissuis, for the purpose of finding genetic differences that could be exploited to design diagnostic tests specific to these groups and that could help explain their divergence in pathogenesis and host specificity. Unique and missing PPE genes were found in all MAC members exceptM. aviumsubsp.avium. OnlyM. intracellularehad a unique PE gene. Apart from this, most PE and PPE sequences were conserved, with average nucleotide sequence identities of 99.1 and 98.1%, respectively, among theM. aviumsubspecies, but only 82.9 and 79.7% identities with the PE and PPE sequences ofM. intracellulare, respectively. A detailed analysis of the amino acid sequences was performed betweenM. aviumsubsp.paratuberculosisandM. aviumsubsp.hominissuis. Most differences were detected in the PPE proteins, with amino acid substitutions and frame shifts leading to unique amino acid sequences. In conclusion, several unique PPE proteins were identified in MAC organisms next to numerous polymorphisms in both the PE and PPE gene families. These substantial differences could help explain the divergence in phenotypes within the MAC and could lead to diagnostic tests with better discriminatory abilities.
Biofilm Formation by
Staphylococcus haemolyticus
Authors: Fredheim Elizabeth Gladys Aarag , Klingenberg Claus , Rohde Holger , Frankenberger Stephanie , Gaustad Peter , Flægstad Trond , Sollid Johanna Ericson 
Published: January 2009

ABSTRACT

Infections due to coagulase-negative staphylococci (CoNS) most frequently occur after the implantation of medical devices and are attributed to the biofilm-forming potential of CoNS.
Staphylococcus haemolyticus
is the second most frequently isolated CoNS from patients with hospital-acquired infections. There is only limited knowledge of the nature of
S. haemolyticus
biofilms. The aim of this study was to characterize
S. haemolyticus
biofilm formation. We analyzed the biofilm-forming capacities of 72 clinical
S. haemolyticus
isolates. A detachment assay with NaIO
4
, proteinase K, or DNase was used to determine the main biofilm components. Biofilm-associated genes, including the
ica
operon, were analyzed by PCR, and the gene products were sequenced. Confocal laser scanning microscopy (CLSM) was used to elucidate the biofilm structure. Fifty-three isolates (74%) produced biofilms after growth in Trypticase soy broth (TSB) with glucose, but only 22 (31%) produced biofilms after growth in TSB with NaCl. It was necessary to dissolve the biofilm in ethanol-acetone to measure the optical density of the full biofilm mass. DNase, proteinase K, and NaIO
4
caused biofilm detachment for 100%, 98%, and 38% of the isolates, respectively.
icaRADBC
and polysaccharide intercellular adhesin (PIA) production were found in only two isolates. CLSM indicated that the biofilm structure of
S. haemolyticus
clearly differs from that of
S. epidermidis
. We conclude that biofilm formation is a common phenotype in clinical
S. haemolyticus
isolates. In contrast to
S. epidermidis
, proteins and extracellular DNA are of functional relevance for biofilm accumulation, whereas PIA plays only a minor role. The induction of biofilm formation and determination of the biofilm mass also needed to be optimized for
S. haemolyticus
.
MDM2-Dependent Inhibition of p53 Is Required for Epstein-Barr Virus B-Cell Growth Transformation and Infected-Cell Survival
Authors: Forte Eleonora , Luftig Micah A. 
Published: January 2009

ABSTRACT
Epstein-Barr virus (EBV) growth transformation of primary B lymphocytes into indefinitely proliferating lymphoblastoid cell lines (LCLs) depends on the concerted activities of a subset of viral proteins expressed during latency. EBV drives quiescent B cells into S phase, and consequently, a host response is activated that includes expression of p53 and its target genes. Since LCLs retain wild-type p53, it was of interest to determine what contribution the p53 pathway may have in controlling established LCL growth and EBV-mediated transformation of primary B cells. We found that liberation of p53 through chemical antagonism of one of its major ubiquitin ligases, MDM2, using the small-molecule Nutlin-3 led to apoptosis of established LCLs and suppressed EBV-mediated transformation of primary B cells. The activation of latent p53 induced target genes associated with apoptosis. Furthermore, MDM2 antagonism synergized with NF-κB inhibition in killing LCLs. NF-κB was important to increase steady-state MDM2 protein levels rather than in affecting p53-dependent transcription, suggesting a unique mechanism by which LCLs survive in the presence of a primed p53 pathway. Nutlin sensitivity of EBV-infected cells provides a novel system for studying the pathways that dictate LCL survival and regulate EBV transformation. Finally, MDM2 antagonists may be considered for therapeutic intervention in EBV-associated malignancies expressing wild-type p53.
Identification of Novel Epstein-Barr Virus MicroRNA Genes from Nasopharyngeal Carcinomas
Authors: Zhu Jia Yun , Pfuhl Thorsten , Motsch Natalie , Barth Stephanie , Nicholls John , Grässer Friedrich , Meister Gunter 
Published: January 2009

ABSTRACT
MicroRNAs (miRNAs) represent a conserved class of small noncoding RNAs that are found in all higher eukaryotes as well as some DNA viruses. miRNAs are 20 to 25 nucleotides in length and have important regulatory functions in biological processes such as embryonic development, cell differentiation, hormone secretion, and metabolism. Furthermore, miRNAs have been implicated in the pathology of various diseases, including cancer. miRNA expression profiles not only classify different types of cancer but also may even help to characterize distinct tumor stages, therefore constituting a valuable tool for prognosis. Here we report the miRNA profile of Epstein-Barr virus (EBV)-positive nasopharyngeal carcinoma (NPC) tissue samples characterized by cloning and sequencing. We found that all EBV miRNAs from the BART region are expressed in NPC tissues, whereas EBV miRNAs from the BHRF1 region are not found. Moreover, we identified two novel EBV miRNA genes originating from the BART region that have not been found in other tissues or cell lines before. We also identified three new human miRNAs which might be specific for nasopharyngeal tissues. We further show that a number of different cellular miRNAs, including miR-15a and miR-16, are up- or downregulated in NPC tissues compared to control tissues. We found that the tumor suppressor BRCA-1 is a target of miR-15a as well as miR-16, suggesting a miRNA role in NPC pathogenesis.
Vesicular Stomatitis Virus M Protein Mutant Stimulates Maturation of Toll-Like Receptor 7 (TLR7)-Positive Dendritic Cells through TLR-Dependent and -Independent Mechanisms
Authors: Ahmed Maryam , Mitchell Latoya M. , Puckett Shelby , Brzoza-Lewis Kristina L. , Lyles Douglas S. , Hiltbold Elizabeth M. 
Published: January 2009

ABSTRACT

Wild-type (wt) vesicular stomatitis virus (VSV) strains stimulate plasmacytoid dendritic cells (pDC) through Toll-like receptor 7 (TLR7) and its adaptor molecule, MyD88. Granulocyte-macrophage colony-stimulating factor-derived DC (G-DC), which do not express TLR7, are unresponsive to wt VSV due to inhibition of cellular gene expression by the matrix (M) protein. In contrast to its recombinant wt (rwt) counterpart, an M protein mutant of VSV, rM51R-M virus, stimulates maturation of G-DC independently of MyD88. These results suggest that, as in the case of G-DC, rM51R-M virus may stimulate pDC by mechanisms distinct from that by rwt virus. Studies presented here demonstrate that both rwt and rM51R-M viruses induced maturation of TLR7-positive DC derived by culture in the presence of Flt3L (F-DC), with the subsequent expression of type I interferon (IFN). F-DC are a mixture of myeloid (CD11b
+
) and plasmacytoid (B220
+
) DC, both of which respond to TLR7 ligands. Separated CD11b
+
and B220
+
F-DC responded to both rwt and rM51R-M viruses. Both viruses were also defective at inhibiting host gene expression in F-DC, including the expression of genes involved in the antiviral response. The data from F-DC generated from IFN receptor knockout mice demonstrated that the maturation of F-DC induced by rwt virus was dependent on the type I IFN response, while maturation induced by rM51R-M virus was partially dependent on this molecule. Therefore, activation of the type I IFN pathway appears to be important for not only inducing an antiviral response but also for stimulating maturation of F-DC upon virus infection. Importantly, F-DC from TLR7 and MyD88 knockout mice did not undergo maturation in response to rwt virus, while maturation induced by rM51R-M virus was largely independent of both molecules. These results indicate that although both viruses induce F-DC maturation, F-DC detect and respond to rM51R-M virus by means that are distinct from rwt virus. Specifically, this mutant virus appears capable of inducing DC maturation in a wide variety of DC subsets through TLR-dependent and independent mechanisms.
Determinants of the Establishment of Human Immunodeficiency Virus Type 1 Latency
Authors: Duverger Alexandra , Jones Jennifer , May Jori , Bibollet-Ruche Frederic , Wagner Frederic A. , Cron Randall Q. , Kutsch Olaf 
Published: January 2009

ABSTRACTRecent research has emphasized the notion that human immunodeficiency virus type 1 (HIV-1) latency is controlled by a restrictive histone code at, or DNA methylation of, the integrated viral promoter (long terminal repeat [LTR]). The present concept of HIV-1 latency has essentially been patterned from the principles of cellular gene regulation. Here we introduce an experimental system that allows for the qualitative and quantitative kinetic study of latency establishment and maintenance at the population level. In this system, we find no evidence that HIV-1 latency establishment is the consequence of downregulation of initial active infection followed by the establishment of a restrictive histone code at the viral LTR. Latent infection was established following integration of the virus in the absence of viral gene expression (silent integration) and was a function of the NF-κB activation level in the host cell at the time of infection. In the absence of a role for epigenetic regulation, we demonstrate that transcriptional interference, a mechanism that has recently been suggested to add to the stabilization of HIV-1 latency, is the primary mechanism to govern latency maintenance. These findings provide direct experimental evidence that the high number of viral integration events (>90%) found in actively expressed genes of CD4+memory T cells from highly active antiretroviral therapy-suppressed patients represent indeed latent infection events and that transcriptional interference may be the primary mechanism to control HIV-1 latency in vivo. HIV-1 latency may thus not be governed by the principles of cellular gene regulation, and therapeutic strategies to deplete the pool of latently HIV-1-infected cells should be reconsidered.
Translocation of Incoming Pseudorabies Virus Capsids to the Cell Nucleus Is Delayed in the Absence of Tegument Protein pUL37
Authors: Krautwald Mirjam , Fuchs Walter , Klupp Barbara G. , Mettenleiter Thomas C. 
Published: January 2009

ABSTRACT
After fusion of the envelope of herpesvirus particles with the host cell plasma membrane, incoming nucleocapsids are transported to nuclear pores. Inner tegument proteins pUL36, pUL37, and pUS3 remain attached to the nucleocapsid after entry and therefore might mediate interactions between the nucleocapsid and cellular microtubule-associated motor proteins during transport. To assay for the role of pUL37 in this process, we constructed a pUL37-deleted pseudorabies virus mutant, PrV-ΔUL37/UL35GFP, which expresses a fusion protein of green fluorescent protein (GFP) and the nonessential small capsid protein pUL35, resulting in the formation of fluorescently labeled capsids. Confocal laser-scanning microscopy of rabbit kidney cells infected with PrV-ΔUL37/UL35GFP revealed that, whereas penetration was not affected in the absence of pUL37, nuclear translocation of incoming particles was delayed by approximately 1 h compared to PrV-UL35GFP, but not abolished. In contrast, phenotypically complemented pUL37-containing virions of PrV-ΔUL37/UL35GFP exhibited wild type-like entry kinetics. Thus, the presence of pUL37 is required for rapid nuclear translocation of incoming nucleocapsids.
Age-Associated Aggravation of Clinical Disease after Primary Metapneumovirus Infection of BALB/c Mice
Authors: Darniot M. , Pitoiset C. , Petrella T. , Aho S. , Pothier P. , Manoha C. 
Published: January 2009

ABSTRACT

Human metapneumovirus (hMPV) is associated with respiratory tract infections among children and adults. Because hMPV induces significant morbidity and mortality in the elderly, a model of hMPV infection in aged BALB/c mice was established. Young (8 weeks old) and aged (18 months old) mice were intranasally inoculated with hMPV. The infected mice showed respiratory dysfunction, as measured by plethysmography, a marked loss in weight (up to 24%), and severe histopathological abnormalities including bronchiolitis obliterans organizing pneumonia. However, clinical severity was far higher in the aged mice, and none of the young infected mice died. Although virus replication in the lung was greater in the older mice, clearance of virus was not delayed compared to young mice. Production of virus-specific antibody as well as neutralizing antibody was lower. Gamma interferon and monocyte chemotactic protein-1 levels in bronchoalveolar lavage fluid were significantly lower in older mice, whereas interleukin-6 and interleukin-4 levels were significantly higher. We observed by flow cytometry a significant increase in the CD4
+
T lymphocytes (
P
< 0.05) of the aged mice and no difference in CD8
+
T-cell recruitment to the respiratory tract between the two groups. The present study investigated the effects of aging on the immunopathogenesis of hMPV infection and suggests that CD4
+
T lymphocytes, the cytokine response, or a defect in humoral response may be associated with the increased disease severity observed in the aged mice.
Interaction of Epstein-Barr Virus BZLF1 C-Terminal Tail Structure and Core Zipper Is Required for DNA Replication but Not for Promoter Transactivation
Authors: McDonald Carol M. , Petosa Carlo , Farrell Paul J. 
Published: January 2009

ABSTRACT

The Epstein-Barr virus (EBV) protein BZLF1 contains a bZIP DNA binding domain in which C-terminal tail residues fold back against a zipper region that forms a coiled coil and mediates dimerization. Point mutagenesis in the zipper region reveals the importance of individual residues within the
208
SSENDRLR
215
sequence that is conserved in C/EBP for transactivation and EBV DNA replication. The restoration of BZLF1 DNA replication activity by the complementation of two deleterious mutations (S208E and D236K) indicates that the interaction of the C-terminal tail and the core zipper is required for DNA replication, identifying a functional role for this structural feature unique to BZLF1.