bluuebunny/crossref_metadata_2025_split huggingface dataset:
Haptoglobin from psoriatic patients exhibits decreased activity in binding haemoglobin and inhibiting lecithin‐cholesterol acyltransferase activity
Authors: Cigliano L , Maresca B , Salvatore A , Nino M , Monfrecola G , Ayala F , Carlucci A , Pugliese RC , Pedone C , Abrescia P 
Published: September 2007

AbstractObjective  The aim of this work was to assess whether psoriasis is associated with phenotype prevalence and altered activity of haptoglobin (Hpt).Background  Hpt is a plasma acute‐phase glycoprotein, displaying in humans three phenotypes. Phenotype prevalence or structure modification of Hpt was associated with several diseases. The Hpt main function is to bind and carry to the liver free haemoglobin for degradation and iron recycling. Hpt was recently found able to bind the apolipoprotein A‐I (ApoA‐I), thus impairing its stimulation on the activity of the enzyme lecithin‐cholesterol acyl‐transferase (LCAT).Study design  Hpt was isolated from patients with psoriasis vulgaris, and its activity in haemoglobin or ApoA‐I binding and LCAT inhibition was compared with that of normal protein.Methods  Two affinity chromatography steps, the first using resin‐coupled haemoglobin and the second anti‐Hpt antibodies, were used to purify Hpt. The protein phenotype was assessed by electrophoresis. Binding experiments were performed by Enzyme‐linked immunosorbent assay with stationary haemoglobin or ApoA‐I, Hpt in solution and anti‐Hpt antibodies for detection of bound Hpt. Standard LCAT assays were carried out in the presence of Hpt purified from patients or healthy subjects.Results  Phenotype prevalence of Hpt in psoriasis was not found. After affinity chromatography by haemoglobin, albumin and ApoA‐I were routinely found heavily contaminating only Hpt from normal subjects. Isolated Hpt from patients had lower activity than normal protein in both haemoglobin binding and LCAT inhibition.Conclusions  In psoriasis, Hpt displays some structure modification(s), which might be associated with the protein function in the disease.
Elastosis Perforans Serpiginosa
Authors: Suneja Tina , Zelonis Beth , Hurley M. Yadira , Youker Summer R. 
Published: September 2007

A 41‐year‐old white man with Down syndrome presented with a slightly pruritic, papular eruption on bilateral forearms of several years' duration. Physical examination revealed multiple 2‐ to 3‐mm keratotic, umbilicated pink papules in an annular configuration distributed symmetrically on the flexural surfaces of the forearms (Figure 1). The skin surrounding these papules was noted to be hyperpigmented and somewhat atrophic. The remainder of his skin examination was unremarkable. A shave biopsy of 1 papule was performed and stained with hematoxylin‐eosin. Hematoxylin‐eosin‐stained sections showed clumps of bright red fibers being extruded through an acanthotic epidermis with a central invagination (Figure 2). Verhoeff‐van Gieson stain confirmed these fibers to be elastin (Figure 3). Elastosis perforans serpiginosa was diagnosed. The clinical image of elastosis perforans serpiginosa is shown here. image A shave biopsy yielded this histologic section of elastosis perforans serpiginosa (hematoxylin‐eosin stain, original magnification ×10). image In this case of elastosis perforans serpiginosa, the fibers were confirmed to be elastin (elastic fibers are black) (Verhoeff‐van Gieson stain, original magnification ×20). image
Atopic Dermatitis and Vα24+ Natural Killer T Cells
Authors: Ilhan Fulya , Kandi Basak , Akbulut Handan , Turgut Dilara , Cicek Demet 
Published: September 2007

Objective.

Atopic dermatitis is a chronic inflammatory skin disease associated with cutaneous hyperreactivity to environmental triggers and is often the first step in the atopic march that results in asthma and allergic rhinitis. Helper T cells and their cytokines, in addition to IgE and eosinophils, play a major role in the pathogenesis of atopic dermatitis. Natural killer T (NKT) cells may play a role in atopic dermatitis status.
Methods.

The authors examined the percentage of Vα24+CD161+ NKT cells and CD3+CD16+ CD56+ NKT cells in peripheral blood from 23 patients with atopic dermatitis aged 8 to 35 years (mean, 21.77±2.88 years) and 30 healthy controls aged 18 to 32 years (mean, 24.32±2.44 years) by using flow cytometric analysis. The mean percentages of Vα24+CD161+ NKT cell subtypes in the atopic dermatitis group and the healthy group were 0.29%±0.02% and 0.42%±0.05%, respectively (P<.001).
Results.

Percentages of Vα24+CD161+ NKT cell subtypes are significantly lower in patients with atopic dermatitis than healthy individuals. On the other hand, the CD3+CD16+CD56+ NKT cell subtype does not differ between the groups.
Conclusions.

The reduction of Vα24+CD161+ NKT cells subtypes may be involved in the immunopathogenesis of atopic dermatitis.
Epitope Specificities of the Group Y and W-135 Polysaccharides ofNeisseria meningitidis
Authors: Moore Samuel L. , Uitz Catherine , Ling Chang-Chun , Bundle David R. , Fusco Peter C. , Michon Francis 
Published: September 2007

ABSTRACTPrevious studies have identified the length dependency of several polysaccharide (PS) protective epitopes. We have investigated whether meningococcal polysaccharides Y and W-135 possess such epitopes. Oligosaccharides (OSs) consisting of one or more disaccharide repeating units (RU) were derived from the capsular PSs of group Y and W-135 meningococci (GYMP and GWMP, respectively) by mild acid hydrolysis. The relative affinities of anticapsular antibodies binding to derivative OSs of different chain lengths were measured in inhibition enzyme-linked immunosorbent assays. As OS size increased from two to three RU, there was a notable increase in binding inhibition of rabbit anti-group Y antiserum. This pattern of antibody binding inhibition was also observed for rabbit antiserum to group W-135, though the inhibition increase was much more pronounced. In the cases of both OS species, the concentration of inhibiting antigen required to achieve 50% inhibition of rabbit immunoglobulin binding increased progressively as the inhibiting disaccharide chain length increased from 1 RU through greater than 50 RU. These data suggest that antibodies directed against both of these meningococcal PSs recognize conformational epitopes only fully expressed in higher-molecular-weight forms of these antigens.
Comparative Evaluation of the Automated Roche TaqMan Real-Time Quantitative Human Immunodeficiency Virus Type 1 RNA PCR Assay and the Roche AMPLICOR Version 1.5 Conventional PCR Assay
Authors: Oliver Anthony R. , Pereira Spyridon F. , Clark Duncan A. 
Published: September 2007

ABSTRACT

The need to evaluate antiviral treatment response and the emergence of resistance have made the human immunodeficiency virus (HIV) viral load assay a major feature of the diagnostic monitoring of HIV-infected individuals. The objective of this study was to evaluate the utility of the recently In Vitro Diagnostic Medical Devices Directive-approved Roche COBAS AmpliPrep/TaqMan96 real-time PCR assay by comparison with the existing Roche COBAS AmpliPrep/AMPLICOR MONITOR conventional PCR assay. EDTA-treated plasma samples from 191 HIV-1-infected individuals were tested for HIV-1 RNA by the AMPLICOR assay and the TaqMan assay. This was a prospective study using 191 pairs of samples from the same bleed per patient. The correlation coefficient of the assays was 98.08%. The mean difference between the assays was 0.05 log
10
copy/ml plasma, with a standard deviation (SD) of 0.27 log
10
copy/ml plasma. Thirteen samples gave results with variances greater than 0.5 log
10
copy/ml plasma, which is our clinical cutoff. Two samples were more than 3 SD different (0.81 log
10
copy/ml plasma). The TaqMan assay appeared to be slightly more sensitive at the lower end of the dynamic range. The assays correlated significantly (
P
> 0.95) with each other, and the regression analysis was also highly significant (
R
2
> 0.95).
Rapid Multiplex Nested PCR for Detection of Respiratory Viruses
Authors: Lam W. Y. , Yeung Apple C. M. , Tang Julian W. , Ip Margaret , Chan Edward W. C. , Hui Mamie , Chan Paul K. S. 
Published: September 2007

ABSTRACT

Respiratory tract infections can be caused by a heterogeneous group of viruses and bacteria that produce similar clinical presentations. Specific diagnosis therefore relies on laboratory investigation. This study developed and evaluated five groups of multiplex nested PCR assays that could simultaneously detect 21 different respiratory pathogens: influenza A virus (H1N1, H3N2, and H5N1); influenza B virus; parainfluenza virus types 1, 2, 3, 4a, and 4b; respiratory syncytial virus A and B; human rhinoviruses; human enteroviruses; human coronaviruses OC43 and 229E; severe acute respiratory syndrome coronavirus; human metapneumoviruses;
Mycoplasma pneumoniae
;
Chlamydophila pneumoniae
;
Legionella pneumophila
; and adenoviruses (A to F). These multiplex nested PCRs adopted fast PCR technology. The high speed of fast PCR (within 35 min) greatly improved the efficiency of these assays. The results show that these multiplex nested PCR assays are specific and more sensitive (100- to 1,000-fold) than conventional methods. Among the 303 clinical specimens tested, the multiplex nested PCR achieved an overall positive rate of 48.5% (95% confidence interval [CI], 42.9 to 54.1%), which was significantly higher than that of virus isolation (20.1% [95% CI, 15.6 to 24.6%]) and that of direct detection by immunofluorescence assay (13.5% [95% CI, 9.7 to 17.4%]). The improved sensitivity was partly due to the higher sensitivity of multiplex nested PCR than that of conventional methods in detecting cultivatable viruses. Moreover, the ability of the multiplex nested PCR to detect noncultivatable viruses, particularly rhinoviruses, coronavirus OC43, and metapneumoviruses, contributed a major gain (15.6%) in the overall positive rate. In conclusion, rapid multiplex nested PCR assays can improve the diagnostic yield for respiratory infections to allow prompt interventive actions to be taken.
Highly Sensitive and Broadly Reactive Quantitative Reverse Transcription-PCR Assay for High-Throughput Detection of Rift Valley Fever Virus
Authors: Bird Brian H. , Bawiec Darcy A. , Ksiazek Thomas G. , Shoemaker Trevor R. , Nichol Stuart T. 
Published: September 2007

ABSTRACT
Rift Valley fever (RVF) virus is a mosquito-borne virus associated with large-scale epizootics/epidemics throughout Africa and the Arabian peninsula. Virus infection can result in economically disastrous “abortion storms” and high newborn mortality in livestock. Human infections result in a flu-like illness, with 1 to 2% of patients developing severe complications, including encephalitis or hemorrhagic fever with high fatality rates. There is a critical need for a highly sensitive and specific molecular diagnostic assay capable of detecting the natural genetic spectrum of RVF viruses. We report here the establishment of a pan-RVF virus quantitative real-time reverse transcription-PCR assay with high analytical sensitivity (∼5 RNA copies of in vitro-transcribed RNA/reaction or ∼0.1 PFU of infectious virus/reaction) and efficiency (standard curve slope = −3.66). Based on the alignments of the complete genome sequences of 40 ecologically and biologically diverse virus isolates collected over 56 years (1944 to 2000), the primer and probe annealing sites targeted in this assay are known to be located in highly conserved genomic regions. The performance of this assay relative to serologic assays is illustrated by testing of known RVF case materials obtained during the Saudi Arabia outbreak in 2000. Furthermore, analysis of acute-phase blood samples collected from human patients (25 nonfatal, 8 fatal) during that outbreak revealed that patient viremia at time of presentation at hospital may be a useful prognostic tool in determining patient outcome.
Mycobacterium alsiense, a Novel, Slowly Growing Species Isolated from Two Patients with Pulmonary Disease
Authors: Richter Elvira , Tortoli Enrico , Fischer Arno , Hendricks Oliver , Engel Regina , Hillemann Doris , Schubert Sabine , Kristiansen Jette E. 
Published: September 2007

ABSTRACTA previously undescribed, slowly growingMycobacteriumspecies was isolated from pulmonary specimens of two patients, one from Denmark and one from Italy. The isolates showed unique 16S rRNA internal transcribed spacers andhsp65sequences: the 16S rRNA was most closely related toMycobacterium szulgaiandMycobacterium malmoense.
Clinical Features and Complete Genome Characterization of a Distinct Human Rhinovirus (HRV) Genetic Cluster, Probably Representing a Previously Undetected HRV Species, HRV-C, Associated with Acute Respiratory Illness in Children
Authors: Lau Susanna K. P. , Yip Cyril C. Y. , Tsoi Hoi-wah , Lee Rodney A. , So Lok-yee , Lau Yu-lung , Chan Kwok-hung , Woo Patrick C. Y. , Yuen Kwok-yung 
Published: September 2007

ABSTRACT
Although human rhinoviruses (HRVs) are common causes of respiratory illness, their molecular epidemiology has been poorly investigated. Despite the recent findings of new HRV genotypes, their clinical disease spectrum and phylogenetic positions were not fully understood. In this study, 203 prospectively collected nasopharyngeal aspirates (NPAs), negative for common respiratory viruses (83 were human bocavirus [HBoV] positive and 120 HBoV negative), from hospitalized children during a 1-year period were subjected to reverse transcription-PCR for HRV. HRV was detected in 14 NPAs positive and 12 NPAs negative for HBoV. Upon VP4 gene analysis, 5 of these 26 HRV strains were found to belong to HRV-A while 21 belonged to a genetic clade probably representing a previously undetected HRV species, HRV-C, that is phylogenetically distinct from the two known HRV species, HRV-A and HRV-B. The VP4 sequences of these HRV-C strains were closely related to the newly identified HRV strains from the United States and Australia. Febrile wheeze or asthma was the most common presentation (76%) of HRV-C infection, which peaked in fall and winter. Complete genome sequencing of three HRV-C strains revealed that HRV-C represents an additional HRV species, with features distinct from HRV-A and HRV-B. Analysis of VP1 of HRV-C revealed major deletions in regions important for neutralization in other HRVs, which may be signs of a distinct species, while within-clade amino acid variation in potentially antigenic regions may indicate the existence of different serotypes among HRV-C strains. A newly identified HRV species, HRV-C, is circulating worldwide and is an important cause of febrile wheeze and asthmatic exacerbations in children requiring hospitalization.
Simultaneous Infection with More than One Strain of
Burkholderia pseudomallei
Is Uncommon in Human Melioidosis
Authors: Limmathurotsakul Direk , Wuthiekanun Vanaporn , Chantratita Narisara , Wongsuvan Gumphol , Thanwisai Aunchalee , Biaklang Mayurachat , Tumapa Sarinna , Lee Sue , Day Nicholas P. J. , Peacock Sharon J. 
Published: September 2007

ABSTRACT

A prospective study was performed to determine the rate at which patients with melioidosis are infected with more than one strain of
Burkholderia pseudomallei
. Genotyping of 2,058 bacterial colonies isolated from 215 samples taken from 133 patients demonstrated that mixed infection is uncommon (2/133 cases [1.5%; 95% confidence interval, 0.2 to 5.3%]).
Interactions between Human Immunodeficiency Virus Type 1 and Vaccinia Virus in Human Lymphoid Tissue Ex Vivo
Authors: Vanpouille Christophe , Biancotto Angélique , Lisco Andrea , Brichacek Beda 
Published: September 2007

ABSTRACT

Vaccinia virus (VACV) has been attracting attention recently not only as a vector for various vaccines but also as an immunization tool against smallpox because of its potential use as a bioterrorism agent. It has become evident that in spite of a long history of studies of VACV, its tissue pathogenesis remains to be fully understood. Here, we investigated the pathogenesis of VACV and its interactions with human immunodeficiency virus type 1 (HIV-1) in the context of human lymphoid tissues. We found that ex vivo-cultured tonsillar tissue supports productive infection by the New York City Board of Health strain, the VACV strain of the Dryvax vaccine. VACV readily infected both T and non-T (B) lymphocytes and depleted cells of both of these subsets equally over a 12-day period postinfection. Among T lymphocytes, CD8
+
cells are preferentially depleted in accordance with their preferential infection: the probability that a CD8
+
T cell will be productively infected is almost six times higher than for a CD4
+
T cell. T cells expressing CCR5 and the activation markers CD25, CD38, and HLA-DR are other major targets for infection by VACV in lymphoid tissue. As a consequence, VACV predominantly inhibits the replication of the R5
SF162
phenotype of HIV-1 in coinfected tissues, as R5-tropic HIV-1 requires activated CCR5
+
CD4
+
cells for productive infection. Human lymphoid tissue infected ex vivo by VACV can be used to investigate interactions of VACV with other viruses, in particular HIV-1, and to evaluate various VACV vectors for the purpose of recombinant vaccine development.
Myc and Human Papillomavirus Type 16 E7 Genes Cooperate To Immortalize Human Keratinocytes
Authors: Liu Xuefeng , Disbrow Gary L. , Yuan Hang , Tomaić Vjekoslav , Schlegel Richard 
Published: September 2007

ABSTRACT
The E6 protein of the oncogenic human papillomaviruses (HPVs), in combination with the E7 protein, is essential for the efficient immortalization of human foreskin keratinocytes (HFKs). Since we recently demonstrated that E6 activates the human telomerase reverse transcriptase (hTERT) promoter via a Myc-dependent mechanism, we speculated that overexpressed Myc might be able to substitute for E6 in cell immortalization. Myc (similar to E6) was unable to immortalize HFKs when transduced alone, despite inducing high levels of telomerase activity. However, when transduced with E7, Myc immortalized HFKs following a brief but detectable crisis period. In contrast to E6 + E7-immortalized cells, the Myc + E7-immortalized cells expressed high levels of p53 protein as well as two p53-regulated proteins, p21 and hdm-2. The increase in p21 and hdm-2 proteins correlated directly with their mRNA levels, suggesting transcriptional activation of the respective genes by the overexpressed p53 protein. Interestingly, a significant proportion of the p53 protein in the Myc + E7-immortalized cells was localized to the cytoplasm, potentially due to interactions with the overexpressed hdm-2 protein. Regardless, cell immortalization by the Myc + E7 genes occurred independently of p53 degradation. Since we have already observed high-efficiency cell immortalization with the hTERT + E7 or E6 mutant (p53 degradation-defective) + E7 genes (i.e., no crisis period) that proceeds in the presence of high levels of p53, we hypothesize that the crisis period in the Myc + E7 cells is due not to the levels of the p53 protein but rather to unique properties of the Myc protein. The common factor in cell immortalization by the three gene sets (E6 + E7, Myc + E7, and hTERT + E7 genes) is the induction of telomerase activity.
Human Papillomavirus E6 Regulates the Cytoskeleton Dynamics of Keratinocytes through Targeted Degradation of p53
Authors: Cooper Brooke , Brimer Nicole , Vande Pol Scott B. 
Published: September 2007

ABSTRACT
The attachment and spreading of keratinocyte cells result from interactions between integrins and immobilized extracellular matrix molecules. Human papillomavirus type 16 (HPV-16) E6 augmented the kinetics of cell spreading, while E6 genes from HPV-11 or bovine papillomavirus type 1 did not. The ability of E6 to interact with the E6AP ubiquitin ligase and target p53 degradation was required to augment cell-spreading kinetics; dominant negative p53 alleles also enhanced the kinetics of cell spreading and the level of attachment of cells to hydrophobic surfaces. The targeted degradation of p53 by E6 may contribute to the invasive phenotype exhibited by cervical cells that contain high-risk HPV types.
Herpes Simplex Virus Remodels T-Cell Receptor Signaling, Resulting in p38-Dependent Selective Synthesis of Interleukin-10
Authors: Sloan Derek D. , Jerome Keith R. 
Published: September 2007

ABSTRACTHerpes simplex virus (HSV)-specific T cells are essential for viral clearance. However, T cells do not prevent HSV latent infection or reactivation, suggesting that HSV has the potential to modulate T-cell function. T-cell receptor (TCR) stimulation is a potent and specific means of activating T cells. To investigate how HSV affects T-cell function, we have analyzed how HSV affects TCR-stimulated intracellular signaling and cytokine synthesis in mock-infected and HSV-infected T cells. Mock-infected T cells stimulated through the TCR synthesized a broad range of cytokines that included the proinflammatory cytokines tumor necrosis factor alpha, gamma interferon, and interleukin-2. In contrast, HSV-infected T cells stimulated through the TCR selectively synthesized interleukin-10, a cytokine that suppresses cellular immunity and favors viral replication. To achieve selective interleukin-10 synthesis, HSV differentially affected TCR signaling pathways. HSV inhibited TCR-stimulated formation of the linker for activation of the T-cell signaling complex, and HSV inhibited TCR-stimulated NF-κB activation. At the same time, HSV activated the p38 and JNK mitogen-activated protein kinases as well as the downstream transcription factors ATF-2 and c-Jun. HSV did not inhibit TCR-stimulated activation of STAT3, a transcription factor involved in interleukin-10 synthesis. The activation of p38 was required for interleukin-10 synthesis in HSV-infected T cells. The ability of HSV to differentially target intracellular signaling pathways and transform an activating stimulus into an immunosuppressive response represents a novel strategy for pathogen-mediated immune modulation. Selective, TCR-stimulated interleukin-10 synthesis may play an important role in HSV pathogenesis.
Activation of the Beta Interferon Promoter by Unnatural Sendai Virus Infection Requires RIG-I and Is Inhibited by Viral C Proteins
Authors: Strähle Laura , Marq Jean-Baptiste , Brini Albert , Hausmann Stéphane , Kolakofsky Daniel , Garcin Dominique 
Published: September 2007

ABSTRACT

As infection with wild-type (wt) Sendai virus (SeV) normally activates beta interferon (IFN-β) very poorly, two unnatural SeV infections were used to study virus-induced IFN-β activation in mouse embryonic fibroblasts: (i) SeV-DI-H4, which is composed mostly of small, copyback defective interfering (DI) genomes and whose infection overproduces short 5′-triphosphorylated trailer RNAs (pppRNAs) and underproduces viral V and C proteins, and (ii) SeV-GFP(+/−), a coinfection that produces wt amounts of viral gene products but that also produces both green fluorescent protein (GFP) mRNA and its complement, which can form double-stranded RNA (dsRNA) with capped 5′ ends. We found that (i) virus-induced signaling to IFN-β depended predominantly on RIG-I (as opposed to mda-5) for both SeV infections, i.e., that RIG-I senses both pppRNAs and dsRNA without 5′-triphosphorylated ends, and (ii) it is the viral C protein (as opposed to V) that is primarily responsible for countering RIG-I-dependent signaling to IFN-β. Nondefective SeV that cannot specifically express C proteins not only cannot prevent the effects of transfected poly(I-C) or
ppp
RNAs on IFN-β activation but also synergistically enhances these effects. SeV-V
minus
infection, in contrast, behaves mostly like wt SeV and counteracts the effects of transfected poly(I-C) or
ppp
RNAs.