bluuebunny/crossref_metadata_2025_split huggingface dataset:
Use of Paraffin-Embedded Tissue for Identification of
Saccharomyces cerevisiae
in a Baker's Lung Nodule by Fungal PCR and Nucleotide Sequencing
Authors: Ren Ping , Sridhar Sundara , Chaturvedi Vishnu 
Published: June 2004

ABSTRACT

A 40-year-old healthy male employed in a bakery presented with a single lung nodule and underwent investigations to rule out pulmonary carcinoma. Biopsy was positive for yeast cells, which did not match common fungal pathogens. PCR assay of paraffin-embedded tissue and nucleotide sequencing with ribosomal
ITS1
-
ITS2
universal primers revealed the presence of
Saccharomyces cerevisiae
.
A Case of Epstein-Barr Virus (EBV)-Associated Thymic Carcinoid and Investigation of Existence of EBV-Infected Cells in Thymus and Thymic Tumors
Authors: Takeuchi Hiroaki , Fujita Hiroshi , Iwasaki Fumio , Takeuchi Takako , Imadome Ken-Ichi , Okumiya Toshika , Matsui Tomohiro , Takahashi Mutsuo 
Published: June 2004

ABSTRACT
We describe the first case of Epstein-Barr virus (EBV)-associated thymic carcinoid tumor found by in situ hybridization (ISH) on paraffin-embedded sections. ISH revealed that both tumor cells and infiltrated lymphocytes were EBV positive, while a few EBV-infected lymphocytes were detected in 2 of 11 thymuses and 1 of 11 thymomas.
First Case Report of Catheter-Related Bacteremia Due to “
Mycobacterium lacticola
”
Authors: Kiska Deanna L. , Turenne Christine Y. , Dubansky A. Stephen , Domachowske Joseph. B. 
Published: June 2004

ABSTRACT

This is the first report of infection caused by “
Mycobacterium lacticola
,” a rapidly growing, scotochromogenic mycobacterium that was isolated from the blood of an immunosuppressed child. The organism was identified by sequence analysis of >1,400 bp of the 16S rRNA gene. The clinical relevance of this isolate, coupled with its unique 16S rRNA gene sequence, should prompt further investigation to establish this organism as a valid mycobacterial species.
Hernia Repair Mesh-AssociatedMycobacterium goodiiInfection
Authors: Sohail Muhammad R. , Smilack Jerry D. 
Published: June 2004

ABSTRACTWe report on a patient with an abdominal wall abscess that developed after an inguinal hernia repair that utilized synthetic mesh.Mycobacterium goodii, a recently recognized, rapidly growing mycobacterium related toM. smegmatis, was isolated both from the abdominal wall aspirate and from surgically drained material. Infection resolved following thorough debridement, mesh removal, and prolonged antimicrobial therapy. This case report extends our understanding of the spectrum ofM. goodiiinfection.
Hepatitis B Surface Antigen Variant with Multiple Mutations in the
a
Determinant in an Agammaglobulinemic Patient
Authors: Alexopoulou Alexandra , Baltayiannis Gerasimos , Jammeh Saffie , Waters Jenny , Dourakis Spyros P. , Karayiannis Peter 
Published: June 2004

ABSTRACT

A patient with agammaglobulinemia developed acute hepatitis that progressed to chronic liver disease with high levels of hepatitis B virus (HBV) DNA in the absence of detectable HBsAg. Sequencing of the
a
determinant region of HBsAg revealed multiple amino acid substitutions that, unusually, also included a substitution at position 122 that defines subtype specificity. All of these mutations had a profound effect on the antigenicity of this region, which led to the complete failure of variant detection by commercially available routine diagnostic assays or laboratory-based monoclonal antibody assays.
Fatal Case of Toxic Shock-Like Syndrome Due to Group C Streptococcus Associated with Superantigen Exotoxin
Authors: Korman Tony M. , Boers Anthony , Gooding Travis M. , Curtis Nigel , Visvanathan Kumar 
Published: June 2004

ABSTRACT

Group C streptococci have been reported to cause invasive disease similar to that classically associated with group A streptococcus (GAS). We describe a fatal case of toxic shock-like syndrome due to
Streptococcus equi
subsp.
zooepidemicus
. The causative organism did not possess any known GAS superantigen exotoxin genes but did show evidence of superantigen production.
Bacteremia Caused by
Gordonia bronchialis
in a Patient with Sequestrated Lung
Authors: Sng Li-Hwei , Koh T. H. , Toney S. R. , Floyd M. , Butler W. R. , Tan B. H. 
Published: June 2004

ABSTRACT

Gordonia
species have been recognized as pathogens in immunocompromised and immunocompetent patients. We report the first case of bacteremia due to
Gordonia bronchialis
in a diabetic patient with a sequestrated lung. Species identification was confirmed with mycolic acid analysis by high-performance liquid chromatography and sequencing of the 16S rRNA gene.
Prosthetic Joint Infection Due to “
Helcococcus pyogenica
”
Authors: Panackal Anil A. , Houze Yolanda B. , Prentice Jennifer , Leopold Seth S. , Cookson Brad T. , Liles W. Conrad , Limaye Ajit P. 
Published: June 2004

ABSTRACT

Helcococci have previously been associated with the colonization of ulcers and infections of the skin and soft tissues. We describe a case of prosthetic joint infection due to a previously undescribed organism that is genetically most closely related to
Helcococcus
.
INNOVATION AND ORGANISATIONAL SIZE IN IRISH SMES: AN EMPIRICAL STUDY
Authors: MCADAM RODNEY , REID RENEE S. , GIBSON DAVID A. 
Published: June 2004

The aim of this paper is to conduct an empirical study to explore the influence of size category on innovation incorporation in Irish SMEs. Changes in markets and in large organisation strategies have resulted in the need for SMEs to re-examine and modify their competitive strategies to increase innovation. Although there is some literature on innovation incorporation in SMEs, there is a lack of direct studies on this issue, with a reliance on related but indirect studies such as Reengineering and New product development in SMEs. Furthermore, there is a paucity of studies and data on the innovation incorporation in different organisational size categories within SMEs.This study uses a grounded SME innovation model developed from earlier studies as the basis of a questionnaire survey of 2086 SMEs in Northern Ireland. The results indicate that SME organisational size categories has a significant effect on innovation incorporation in relation to leadership, people and culture, TQM/CI, product and process and Knowledge and information management.
Tissue factor messenger RNA levels in leukocytes compared with tissue factor antigens in plasma from patients in hypercoagulable state caused by various diseases
Authors: Sase Tomohiro , Kamikura Yuko , Kaneko Toshihiro , Abe Yasunori , Nishioka Junji , Nobori Tsutomu , Shiku Hiroshi , Wada Hideo 
Published: June 2004

SummaryWe compared the levels of tissue factor (TF) mRNA in leukocytes with plasma TF antigens of patients in hypercoagulable state caused by various diseases. Flow cytometric analysis showed absence of TF antigen expression on neutrophils and monocytes in healthy subjects but strong expression in both cell types of patients with infections. TF mRNA levels in leukocytes were low in healthy subjects but they were significantly elevated in patients with underlying diseases of disseminated intravascular coagulation (DIC), especially in acute myeloid leukaemia (AML) and infections. TF mRNA levels in leukocytes were significantly high in patients with all diseases except those with thrombosis, and plasma TF antigen levels were significantly high in all diseases. TF mRNA in leukocytes and plasma TF antigen levels were significantly high in patients with overt-DIC, and TF mRNA/antigen ratio was significantly high in patients with overt-DIC. In patients with solid cancers, TF mRNA and TF mRNA/antigen ratio were significantly higher in patients with metastases than those without. TF mRNA levels in leukocytes and plasma levels of TF antigen did not correlate in normal subjects and all patients, but they tended to be correlated in patients with AML, infections or overt-DIC. Our analysis suggests that TF expression in leukocytes plays an important role in various diseases but the expression level does not always correlate with plasma levels of TF antigen.
Platelet activation, coagulation and angiogenesis in breast and prostate carcinoma
Authors: Caine Graham , Lip Gregory , Stonelake Paul , Ryan Peter , Blann Andrew 
Published: June 2004

SummaryIn health, haemostasis and angiogenesis are tightly regulated processes, but may become deregulated in cancer. Recent evidence suggests that platelet activation may link these processes as platelets can release angiogenic factors such as vascular endothelial growth factor (VEGF). Furthermore, inflammation has also been implicated in regulating both coagulation and angiogenesis, possibly by activating platelets directly and increasing, for example, plasma fibrinogen. We hypothesized relationships between plasma markers of the processes in two common forms of cancer. Plasma levels of VEGF (reflecting angiogenesis), soluble P-selectin, (marking platelet activation), tissue factor [TF], fibrinogen and fibrin D-dimer (coagulation markers), and serum levels of IL-6 (inflammation) were measured by ELISA in 30 patients with biopsy-proven breast cancer, 30 patients with biopsy-proven prostate cancer, and 30 ageand sex-matched controls for each group. Prostate specific antigen was also measured in the men. Release of VEGF from IL-6 stimulated platelets was assessed by ELISA. Plasma levels of IL-6 (P <0.02), VEGF, soluble P-selectin, fibrinogen, and fibrin D-dimer (all p <0.01) were significantly raised in breast cancer, whereas VEGF, soluble P-selectin, fibrin D-dimer (all p <0.01) and fibrinogen (p <0.05) were significantly raised in prostate cancer. Significant correlations were found between IL-6 and VEGF (p <0.01), and IL-6 and soluble P-selectin (p = 0.038) in breast cancer. Further experiments demonstrated an in vitro IL-6 induced dose-dependent release of VEGF from platelets. In conclusion, strong relationships between IL6 and VEGF, but not with coagulation or platelet markers, and release of VEGF from IL-6 stimulated platelets, suggest a role for inflammation and platelets in angiogenesis.
Manganese-induced integrin affinity maturation promotes recruitment of αVβ3 integrin to focal adhesions in endothelial cells: evidence for a role of phosphatidylinositol 3-kinase and Src
Authors: Dormond Olivier , Ponsonnet Lionel , Hasmim Meriem , Foletti Alessandro , Rüegg Curzio 
Published: June 2004

SummaryIntegrin activity is controlled by changes in affinity (i.e. ligand binding) and avidity (i.e. receptor clustering). Little is known, however, about the effect of affinity maturation on integrin avidity and on the associated signaling pathways. To study the effect of affinity maturation on integrin avidity, we stimulated human umbilical vein endothelial cells (HUVEC) with MnCl2 to increase integrin affinity and monitored clustering of β1 and β3 integrins. In unstimulated HUVEC, β1 integrins were present in fibrillar adhesions, while αVβ3 was detected in peripheral focal adhesions. Clustered β1 and β3 integrins expressed high affinity/ligand-induced binding site (LIBS) epitopes. MnCl2-stimulation promoted focal adhesion and actin stress fiber formation at the basal surface of the cells, and strongly enhanced mAb LM609 staining and expression of β3 high affinity/LIBS epitopes at focal adhesions. MnCl2-induced αVβ3 clustering was blocked by a soluble RGD peptide, by wortmannin and LY294002, two parmacological inhibitors of phosphatidylinositol 3-kinase (PI 3-K), and by over-expressing a dominant negative PI 3-K mutant protein. Conversely, over-expression of active PI 3-K and pharmacological inhibiton of Src with PP2 and CGP77675, enhanced basal and manganese-induced αVβ3 clustering. Transient increased phosphorylation of protein kinase B/Akt, a direct target of PI 3K, occurred upon manganese stimulation. MnCl2 did not alter β1 integrin distribution or β1 high-affinity/LIBS epitope expression. Based on these results, we conclude that MnCl2-induced αVβ3 integrin affinity maturation stimulates focal adhesion and actin stress fiber formation, and promotes recruitment of high affinity αVβ3 to focal adhesions. Affinity-modulated αVβ3 clustering requires PI3-K signaling and is negatively regulate by Src.
ADP secretion and subsequent P2Y12 receptor signalling play a crucial role in thrombin-induced ERK2 activation in human platelets
Authors: Fälker Knut , Lange Danica , Presek Peter 
Published: June 2004

SummaryStimulating human platelets with thrombin induces the activation of the extra cellular signal-regulated kinase 2 (ERK2). We demonstrate that this effect is highly dependent on ADP secretion and P2Y12 receptor signalling. AR-C69931MX (10 µM), a specific antagonist of the Gi-coupled P2Y12 ADP receptor, inhibits ERK2 activation induced by thrombin. Antagonists of the Gq-coupled P2Y1 ADP receptor, A3P5P (500 µM) and MRS2179 (100 µM), have no effect. ADP and its more potent analogue 2-methylthio-ADP alone (both up to 100 µM) do not induce ERK2 activation. Furthermore, we show that the inhibitory effect of AR-C69931MX on ERK2 activation induced by 0.1 U/ml thrombin as well as on platelet aggregation can be bypassed by epinephrine (1 and 10 µM), whereas epinephrine alone has no effect. Epinephrine acts on platelets mainly via α2A-adrenergic receptors, which, like P2Y12 receptors, couple to inhibitory G proteins. In addition, 2-methylthioADP as well as epinephrine provoke ERK2 activation at a thrombin concentration that alone has no detectable effect (0.05 U/ml). Thromboxane A2 (TXA2), which, like ADP, is released by activated platelets, acts as a positive feedback mediator. Stimulating the Gq-coupled TXA2-receptor with U46619 (10 µM), which leads to ADP secretion and P2Y12 receptor dependent platelet aggregation, also induces P2Y12-related ERK2 activation. The inhibition of U46619-induced ERK2 activation and platelet aggregation by AR-C69931MX are also rescued by epinephrine. Pretreatment with aspirin inhibits ERK2 activation induced by 0.1 U/ml thrombin, but has no effect at high concentrations of thrombin. The combination of U46619 and thrombin, at concentrations which alone have no effect, provokes ERK2 activation, suggesting that thrombin and released TXA2 act synergistically. Our data indicate that both primary signalling through Gq, which evokes ADP secretion, as well as subsequent coupling via Gi by the P2Y12 receptor are required for ERK2 activation.
High factor VIII (FVIII) levels in venous thromboembolism: role of unbound FVIII
Authors: Grossmann Ralf , Zonnur Sarah , Berger Mario , Teuchert Kathleen , Spahn Alois , Walter Ulrich , Schambeck Christian 
Published: June 2004

SummaryTheoretically, von Willebrand factor (VWF) should be capable of binding all factor VIII (FVIII), but an unbound FVIII (uFVIII) plasma fraction remains. In patients’ status post deep-vein thrombosis (DVT), an altered uFVIII fraction and high FVIII levels might be indicative of dysfunctional FVIII regulation. Out of 928 consecutive DVT patients, 321 were found to have high FVIII levels. After excluding 183 patients with known causes for high FVIII levels, plasma samples with unexplainably high FVIII levels were available from 84 patients. To capture the FVIIIVWF-complex, superparamagnetic polystyrene beads with covalently attached streptavidin were coated with biotinylated anti-rabbit Ig and incubated with rabbit anti-human VWF-Ig. Slowly thawed plasma samples were added to cooled beads, which were then separated by a magnetic particle concentrator. The uFVIII fraction was calculated by dividing the FVIII activity in the supernatant of the FVIII-VWF-complex-free sample by the FVIII activity in the supernatant of the control sample. Additionally, the VWF residuum in the supernatant was determined. Compared to age- and sex-matched blood donors, thrombosis patients showed a significantly higher plasma FVIII/VWF ratio (median: 1.3 vs. 1.0, p<0.001). uFVIII fraction data were adjusted for VWF residuum. After forward stepwise logistic regression, uFVIII had an odds ratio of 0.48 (95% CI 0.34 – 0.65), i. e. the uFVIII fraction was reduced in thrombosis patients. Analysis of covariance confirmed these results: In thrombosis patients, the estimated mean of the uFVIII fraction was significantly lower (6.34% vs. 7.58%, p<0.001). In conclusion, thrombosis patients with high FVIII levels showed a higher FVIII/VWF ratio, similar to mice with defective FVIII clearance.The clearly reduced uFVIII fraction lends further support to the hypothesis of a modified FVIII clearance.
Mutation in the leucine-rich repeat C-flanking region of platelet glycoprotein Ibβ impairs assembly of von Willebrand factor receptor
Authors: Tang Jingrong , Stern-Nezer Sara , Liu Po-Ching , Matyakhina Ludmila , Riordan Michael , Luban Naomi , Steinbach Peter , Kaler Stephen 
Published: June 2004

SummaryWe describe a syndrome of thrombocytopenia, bleeding episodes, congenital heart disease and facial dysmorphism in a newborn infant, and trace the cause to mutations on chromosome 22 that involve the gene for platelet glycoprotein Ibβ (GPIbβ, Human Genome Organisation gene symbol GPIBB), a critical component of the von Willebrand factor (vWF) receptor. Fluorescence in situ hybridization in transformed lymphoblasts revealed hemizygous microdeletion of 22q11.2 containing the GP1BB locus. DNA sequencing revealed a C to T transition in the patient’s remaining GP1BB allele, predicting a novel proline to serine substitution (Pro96Ser) in the carboxyterminal flanking domain of a leucine-rich repeat. We characterized the mutant GP1BB allele by expression in a cell line (CHOαIX) that stably expresses two other components of the vWF receptor, GPIbα and GPIX. Flow cytometry and confocal imaging of transfected CHOαIX cells demonstrated that P96S GPIbβ abrogates surface assembly of the complex, consistent with platelet flow cytometry studies in the patient. Based on sequence homology to the known crystal structures of two other leucine-rich repeat proteins, the human Nogo receptor and GPIbα, we propose a new structural model of GPIbβ. The model refutes earlier assumptions about cysteine-cysteine interactions in the amino-terminal region of GPIbβ, and predicts a hydrophobic patch the burial of which may contribute to proper conformation of the fully assembled vWF receptor complex.
Periodontal disease, but not edentulism, is independently associated with increased plasma fibrinogen levels
Authors: Völzke Henry , Robinson Daniel , Luedemann Jan , Bernhardt Olaf , Gesch Dietmar , John Ulrich , Kocher Thomas , Schwahn Christian 
Published: June 2004

SummaryThe systemic response to periodontal disease was analyzed in the cross-sectional Study of Health in Pomerania (SHIP). The completed data of 2,738 subjects aged 20 to 59 years were used for logistic regression analysis with an increased plasma fibrinogen level (≥3.25 g/L according to Clauss) as the dependent variable. Participants were divided into four groups according to the number of periodontal pockets ≥ 4mm (0, 1-7, 8-14, ≥15 pocketing). An additional group comprised the 52 edentulous subjects. The adjusted odds ratio (OR) of ≥15 periodontal pockets for increased plasma fibrinogen levels was 1.88 (95% CI: 1.25-2.83). Edentulism per se was not associated with increased plasma fibrinogen levels but was contained in a two-way interaction with the number of cigarettes/day in current smokers (p = 0.031). For edentulous nonsmokers the adjusted OR was 1.10 (95% CI: 0.51-2.39). Furthermore, body mass index, the interaction between gender and body mass index, serum LDL cholesterol, medication, the interaction between LDL cholesterol and medication, aspirin, smoking, school education, chronic bronchitis, and the interaction between alcohol consumption and chronic gastritis were associated with plasma fibrinogen levels. Our results show that periodontal disease but not edentulism per se is associated with an increased plasma fibrinogen level.
CD14+CD16+ monocytes in coronary artery disease and their relationship to serum TNF-α levels
Authors: Blankenberg Stefan , Espinola-Klein Christine , Dopheide Joern , Bickel Christoph , Lackner Karl , Iz Mete , Meyer Juergen , Darius Harald , Rupprecht Hans , Schlitt Axel , Heine Gunnar 
Published: June 2004

SummaryMonocytes play a central role in the inflammatory disease atherosclerosis. CD14+CD16+ monocytes are considered proinflammatory monocytes, as they have an increased capacity to produce proinflammatory cytokines, such as TNF-α, and are elevated in various inflammatory diseases. We hypothesized that patients with coronary artery disease (CAD) have increased levels of CD14+CD16+ monocytes, and that CD14+CD16+ monocytes are associated with inflammation markers. We investigated CD14+CD16+ monocytes in 247 patients with CAD and 61 control subjects using flow cytometry. In addition serum concentrations of TNF-α, IL-6, and Hs-CRP were assessed. Patients with CAD had higher levels of CD14+CD16+ monocytes than controls (13.6% versus 11.4%; p<0.001). Logistic regression analysis including quartiles of CD14+CD16+ monocytes showed that CD14+CD16+ monocytes were associated with prevalence of CAD (OR 4.9, 95% CI 2.5–19.1, for subjects in the fourth quartile in comparison to subjects in the first quartile). The association between CD14+CD16+ monocytes and CAD remained independently significant after adjustment for most potential confounders (OR 5.0, 95% CI 1.2-20.0). Serum concentrations of TNF-α were elevated in subjects within the highest quartiles of CD14+CD16+ monocytes (p=0.018). Our study showed that increased numbers of CD14+CD16+ monocytes are associated with coronary atherosclerosis and TNF-α. In accordance, recent animal studies suggest a possibly important role of these monocytes in the development of atherosclerosis.
In vitro studies, pharmacokinetic studies and clinical use of a high purity double virus inactivated FVIII/VWF concentrate (Immunate) in the treatment of von Willebrand disease
Authors: Ver Elst Kristien , van Vliet Huub , Kappers-Klunne Mies , Leebeek Frank 
Published: June 2004

SummaryPatients with type 2 and 3 von Willebrand disease (VWD) are treated with factor VIII/VWF concentrate in case of bleeding or surgery. Immunate® (Baxter, Vienna, Austria) is a double virus inactivated FVIII/VWF concentrate and is registered in several countries for patients with VWD with reduced FVIII levels.We performed an in vitro, a pharmacokinetic and a clinical study to evaluate Immunate in VWD. In vitro studies showed a significant variation in VWF levels in 9 different batches. The median (range) values (in IU/mL) were 1.10 (0.98-1.30) for FVIII:C, 1.34 (0.95-1.61) for VWF:Ag, 0.60 (0.27-1.08) for VWF:CBA and 0.73 (0.59-0.94) for VWF:RCo. The relatively low VWF activity is mainly due to the lack of high molecular weight multimers (HMWM), as determined by electrophoresis. A pharmacokinetic study showed, based on a content of FVIII:C of 1 U/mL, in vivo recoveries (%) of 106 (56-150) (median and range) for FVIII:C, 105 (62-187) for VWF:Ag, 25 (7-41) for VWF:CBA and 43 (11-76) for VWF:RCo. Half-lives were 14.1 h (7.4-36.9) for FVIII:C, 10.8 h (7.7-26.2) for VWF:Ag, 15.3 h (7.8-44.6) for VWF:CBA and 16.4 h (4.2-26.5) for VWF:RCo. In a clinical study efficacy was determined after infusion given before surgery or dental extractions in ten patients. In two patients the hemostatic response was classified as inadequate. In conclusion, there is a wide variability in VWF concentration and activity in various batches of Immunate®. In the clinical study in which the dosage was based on FVIII:C contents of the concentrate, two out of ten patients had an insufficient haemostatic response. Therefore dosing of Immunate dosing should not be based on FVIII:C levels, but should be based on VWF activity of the individual batches. Future studies using a VWF activity-guided dosage regimen have to be performed to establish the efficacy of Immunate in the treatment of von Willebrand disease.