bluuebunny/crossref_metadata_2025_split huggingface dataset:
Correlation of basic fibroblast growth factor expression with the invasion and the prognosis of oral squamous cell carcinoma
Authors: Hase Takashi , Kawashiri Shuichi , Tanaka Akira , Nozaki Shinichi , Noguchi Natsuyo , Kato Koroku , Nakaya Hiromitsu , Nakagawa Kiyomasa 
Published: February 2006

Background:  The aim of this study was to evaluate the relationship between the expression of basic fibroblast growth factor (bFGF) and fibroblast growth factor receptor‐1 (FGFR‐1) in cancer cells and fibroblasts at the invasive front of oral squamous cell carcinoma (OSCC), and the pathologic and clinical characteristics.Methods:  Sections of 61 biopsy specimens of primary OSCC were immunostained to assess the expression of bFGF and FGFR‐1 in cancer cells and fibroblasts at the invasive front.Results:  The bFGF and FGFR‐1 expressions in the cancer cells were evident in all specimens, whilst, in fibroblasts, they were detected in 41 (67%) of 61 specimens. These expressions in the fibroblasts occurred notably more often in high‐invasive OSCC specimens than low‐invasive OSCC specimens. The prevalence of bFGF and FGFR‐1 expressions in cases with lymph node metastasis was significantly higher (P < 0.05) than in cases without metastasis. Moreover, these expressions were well correlated with patient prognosis.Conclusion:  This study concludes that bFGF and FGFR‐1 expressions in fibroblasts at the invasive front are linked to the mode of invasion and the prognosis in OSCC.
Analysis of apoptosis‐associated genes and pathways in oral cancer cells
Authors: Gibson Sandra , Shillitoe Edward J. 
Published: February 2006

Background:  Cancer cells can resist apoptosis that is induced by stimuli such as detachment or differentiation, but may be more susceptible to apoptosis when exposed to chemotherapeutic drugs. The pattern of gene expression that produces this phenotype is unknown.Methods:  We compared gene expression patterns of normal human epidermal keratinocytes (NHEK cells) and the oral cancer cell line Tu183 when the cells were exposed to different apoptosis‐inducing stimuli.Results:  Pathway analysis revealed that the phenotype difference could be best explained by the simultaneous existence of both proapoptosis and antiapoptosis signals in the cancer cells. Microarray analysis, supported by immunoblotting, showed that one gene that was likely to be involved in the proapoptosis signal was TNFRSF5, which encodes the receptor CD40. When Tu183 cells were exposed to the CD40 ligand they showed apoptosis, while NHEK cells did not.Conclusions:  The effects of different apoptotic stimuli on normal cells and oral cancer cells can be explained by expression of proapoptosis genes, including the gene that encodes CD40.
Experience of Urgent Reconstruction of Electrical Injuries
Authors: ZHU ZHI‐XIANG , XU XIAO‐GUANG , ZHANG YUE‐AN , CHEN LI‐YING , LIU TIAN‐YI , LI WEI‐PING 
Published: February 2006

ABSTRACT: Although there have been great advances in the treatment of electrical injuries in the last 20 years, the extremity loss ratio in electrical injuries remains at an unacceptably high level. The primary reason for this is the progressive tissue necrosis and enlargement of the necrosis in the wound. The goal in this study is to examine possible ways to break the necrotic malignancy circle and save the form and function of damaged extremities. As a result of systematic experimental and clinical research, a comprehensive urgent reconstruction alternative for electrical injuries has been proposed. The alternative includes the following principles: debriding the wound as early as possible after injury; preserving as much as possible the vital tissue structures, such as nerve, vessels, joints, tendons, and bone, even when they have undergone devitalization or local necrosis; transplanting these vital tissues during the first surgery if the functional reconstruction requires; nourishing the wound bed by covering with tissue flaps that have rich blood supply; improving flap survival by continuous irrigations with a compound medicine beneath the flaps for a 24‐ to 72‐hour period after surgery; providing general treatment with vasoactive agents and antibiotics.This paper summarizes our experience of using this method in the treatment of 105 electrical injury patients (a total of 309 wounds) in the time period from 1 January 1986 to 31 December 1996. Satisfying results were obtained, with the extremity loss ratio decreasing to 7% as compared to 41.5% during the 10 years preceding 1984 at the same hospital. Thus, the urgent comprehensive reconstruction alternative presented here is an effective and workable method to manage electrical injuries.
Factors in Xenograft Rejection
Authors: ROBSON SIMON C. , AM ESCH JAN SCHULTE , BACH FRITZ H. 
Published: February 2006

ABSTRACT: Important mechanisms underlying immediate xenograft loss by hyperacute rejection (HAR), in the pig‐to‐primate combination, have been recently delineated. There are now several proposed therapies that deal with the problem of complement activation and xenoreactive natural antibody (XNA) binding to the vasculature that have been shown to prevent HAR. However, vascularized xenografts are still lost, typically within days, by delayed xenograft rejection (DXR), alternatively known as acute vascular rejection (AVR). This process is characterized by endothelial cell (EC) perturbation, localization of XNA within the graft vasculature, host NK cell and monocyte activation with platelet sequestration and vascular thrombosis. Alternative immunosuppressive strategies, additive anti‐complement therapies with the control of any resulting EC activation processes and induction of protective responses have been proposed to ameliorate this pathological process.In addition, several potentially important molecular incompatibilities between activated human coagulation factors and the natural anticoagulants expressed on porcine EC have been noted. Such incompatibilities may be analogous to cross‐species alterations in the function of complement regulatory proteins important in HAR. Disordered thromboregulation is potentially relevant to the progression of inflammatory events in DXR and the disseminated intravascular coagulation seen in primate recipients of porcine renal xenografts. We have recently demonstrated the inability of porcine tissue factor pathway inhibitor (TFPI) to adequately neutralize human factor Xa (FXa), the aberrant activation of both human prothrombin and FXa by porcine EC and the failure of the porcine natural anticoagulant, thrombomodulin to bind human thrombin and hence activate human protein C. The enhanced potential of porcine von Willebrand factor to associate with human platelet GPIb has been demonstrated to be dependent upon the isolated A1 domain of von Willebrand factor. In addition, the loss of TFPI and vascular ATPDase/CD39 activity following EC activation responses would potentiate any procoagulant changes within the xenograft. These developments could exacerbate vascular damage from whatever cause and enhance the activation of platelets and coagulation pathways within xenografts resulting in graft infarction and loss.Analysis of these and the other putative factors underlying DXR should lead to the development and testing of genetic approaches that, in conjunction with selected pharmacological means, may further prolong xenograft survival to a clinically relevant extent.
Bioreactors for Hybrid Liver Support: Historical Aspects and Novel Designs
Authors: BUSSE BENEDIKT , GERLACH JÖRG C. 
Published: February 2006

ABSTRACT: A novel bioreactor construction has been designed for the utilization of hepatocytes and sinusoidal endothelial cells. The reactor is based on capillaries for hepatocyte aggregate immobilization. Three separate capillary membrane systems, each permitting a different function are woven in order to create a three dimensional network. Cells are perfused via independent capillary membrane compartments. Decentralized oxygen supply and carbon dioxide removal with low gradients are possible. The use of identical parallel units to supply hepatocytes facilitates scale up. In vitro studies demonstrate long‐term external metabolic function in primary isolated hepatocytes within bioreactors. These systems are capable of supporting essential liver functions. Animal experiments have verified the possibility of scaling‐up the bioreactors for clinical treatment. However, since there is no reliable animal model for investigation of the treatment of acute liver failure, the promising results obtained from these studies have limited relevance. The small number of clinical studies performed so far is not sufficient to reach conclusions about improvements in the therapy of acute liver failure. Although important progress has been made in the development of these systems, various hepatocyte culture models and bioreactor constructions are being discussed in the literature, which indicates competition in this field of medical research.An overview, which emphasizes the development of hepatocyte culture models for bioreactors, subsequent In vitro studies, animal studies, and clinical application, is also provided.
Human Nerve Pathology Caused by Different Mutational Mechanisms of the PMP22 Gene
Authors: GABREËLS‐FESTEN ANNEKE , VAN DE WETERING RUDI 
Published: February 2006

ABSTRACT: The study of the morphological phenotypes in patients with different mutations of the PMP22 gene gives additional insights into the role of the protein in myelin function. The pathology in young patients is in some aspects different from the pathology in older patients, providing essential and additional information about the early disease processes in humans induced by different PMP22 mutational mechanisms.Duplication of chromosome 17p11.2, causing an overexpression of the PMP22 gene, results in early hypermyelination. This suggests that PMP22 has a function in establishing the proper myelin thickness, probably in response to an axonal signal. Demyelination and remyelination with gradual formation of onion bulbs occur apparently as secondary processes, but these processes subside at the end of the first decade. PMP22 missense mutations usually result in a more severe phenotype showing an early hypomyelination and onion bulb formation, likely disturbing normal myelin formation and maintenance. The morphological differences with duplication cases underline the essential difference in pathogenesis between duplication and missense mutations despite the large overlap in clinical and electrophysiological phenotypes. The reciprocal deletion of chromosome 17p11.2, resulting in an underexpression of the PMP22 gene, is responsible for the clinical phenotype of HNPP. As the nerve abnormalities in HNPP show a marked resemblance to the changes in experimental and genuine human entrapment neuropathies, it is postulated that PMP22 has a function in adhesion of myelin lamellae, preventing mutual longitudinal sliding. Deletion of one PMP22 copy results in increased susceptibility for mechanical forces through which already minor nerve injuries might induce a longitudinal displacement of myelin lamellae. The frame shift mutation Gly94(insG) combines a loss of function like in the common deletion HNPP with a mild CMT1 phenotype, likely inducing a (mild) toxic gain of function by disturbing myelin formation and maintenance, comparable to the effect in missense mutations.
Some Design Concepts for Electrical Impedance Measurement
Authors: GOOVAERTS H. G. , FAES TH. J. C. , RAAIJMAKERS E. , HEETHAAR R. M. 
Published: February 2006

Abstract: Design concepts for the implementation of two basic functions for measurement of electrical impedance are presented: current injection and voltage measurement. At relatively high frequencies, the application of an alternating current through the body or a body segment results in electromagnetic stray fields that reduce the amount of current actually injected into the tissue under study. It is shown that electrical isolation and small dimensions of the isolated section are indispensable in order to substantially reduce these stray currents. The paper describes a new wideband current source configuration driven by direct digital sine wave synthesis (DDS) presenting very low stray currents due to a symmetrical layout. Two implementations of the actual current source circuit are presented: (1) a voltage‐controlled system and (2) a current conveyor‐based circuit.A wideband input amplifier with transformer coupling is described. The current source, amplifier, and (in case of tomography) multiplexer are also situated on an electrically isolated front end. The presented concepts are applied in a new electrical impedance tomograph (EIT) presently under construction in our department.
Purified Excreted-Secreted Antigens from
Trypanosoma cruzi
Trypomastigotes as Tools for Diagnosis of Chagas' Disease
Authors: Berrizbeitia Mariolga , Ndao Momar , Bubis José , Gottschalk Marcelo , Aché Alberto , Lacouture Sonia , Medina Mehudy , Ward Brian J. 
Published: February 2006

ABSTRACT

There is currently no “gold standard” test for the diagnosis of late-stage Chagas' disease. As a result, protection of the blood supply in areas where Chagas' disease is endemic remains problematic. A panel of 709 serum samples from subjects with confirmed Chagas' disease (
n
= 195), healthy controls (
n
= 400), and patients with other parasitic diseases (
n
= 114) was used to assess enzyme-linked immunosorbent assays (ELISAs) based on a concentrated extract of excretory-secretory antigens from either Brazil or Tulahuen strain
Trypanosoma cruzi
trypomastigotes (total trypomastigote excretory-secretory antigens [TESAs]). The total TESA-based assays had excellent overall sensitivity (100%) and specificity (>94%), except for cross-reactivity with
Leishmania
-infected sera. In an attempt to increase the specificity of the assay, immunoaffinity chromatography was used to purify the TESA proteins (TESA
IA
proteins). By Western blotting, a series of polypeptide bands with molecular masses ranging from 60 to 220 kDa were recognized by pooled sera positive for Chagas' disease. An ELISA based on TESA
IA
proteins had a slightly lower sensitivity (98.6%) but an improved specificity (100%) compared to the sensitivity and specificity of the total TESA protein-based ELISAs. A 60-kDa polypeptide was identified as a major contributor to the cross-reactivity with
Leishmania
. These data suggest the need for field validation studies of TESA- and TESA
IA
-based assays in regions where Chagas' disease is endemic.
Restricted Infectivity of a Human-Lineage H3N2 Influenza A Virus in Pigs Is Hemagglutinin and Neuraminidase Gene Dependent
Authors: Landolt Gabriele A. , Karasin Alexander I. , Schutten Melissa M. , Olsen Christopher W. 
Published: February 2006

ABSTRACT
Influenza A viruses cause pandemics at sporadic intervals. Pandemic viruses can potentially be introduced into the human population through in toto transfer of an avian influenza virus or through reassortment between avian and human strains. Pigs are believed to play a central role in the creation of pandemic viruses through reassortment because of their susceptibility to infection with both avian and human influenza viruses. However, we recently found that a human-lineage H3N2 influenza virus was highly restricted in its ability to infect pigs after intranasal inoculation. We hypothesized that this restricted infectivity phenotype was controlled by the hemagglutinin (HA) and neuraminidase (NA). To test this, we infected pigs with reverse genetics-created HA plus NA reassortant viruses. Specifically, introduction of the HA and NA genes of a contemporary H3N2 swine virus into the genetic background of the wholly human virus resulted in a significant increase in virus shedding and pathogenicity. These data indicate that the HA/NA can play important roles in controlling human influenza virus infectivity in pigs. The results further support the premise that a barrier exists to human influenza virus infection in pigs, which may limit the role of pigs in pandemic virus creation through reassortment of human and avian influenza viruses.
Rapid Detection of
Mycobacterium tuberculosis
Beijing Genotype Strains by Real-Time PCR
Authors: Hillemann Doris , Warren Rob , Kubica Tanja , Rüsch-Gerdes Sabine , Niemann Stefan 
Published: February 2006

ABSTRACT

Mycobacterium tuberculosis
strains of the Beijing genotype were first identified in China and neighboring countries and have attracted special attention due to their global emergence and association with drug resistance. To further analyze the spread and special characteristics of Beijing genotype strains, accurate, rapid and sensitive methods that overcome the drawbacks of the classical methods such as IS
6110
DNA fingerprinting or spoligotyping for the identification of strains of this genotype are needed. Based on the nucleotide sequences of
M. tuberculosis
SAWC0780 and H37Rv, primers and fluorogenic 5′ nuclease (TaqMan) probes for real-time PCR assays specific for Beijing and non-Beijing strains, respectively, were designed. The detection limits for the real-time PCR assays were about 5 and 10 copies of chromosomal DNA, respectively. In mixtures of Beijing and non-Beijing DNA, a multiplex assay was able to detect (i) one copy of Beijing DNA in approximately 1,000 copies of non-Beijing DNA and (ii) one copy of non-Beijing DNA in approximately 2,000 copies of Beijing DNA. In a blinded analysis of a collection of 103 multidrug-resistant strains isolated in Germany in 2001, all 62 Beijing and all 41 non-Beijing strains were correctly identified. In conclusion, the real-time assay allows for the rapid and specific detection of Beijing and non-Beijing strains. The major advantages of this test in comparison to other methods used for the identification of Beijing strains are its simplicity and sensitivity and the fact that amplification and detection occur within one reaction tube.
Isolation ofCorynebacterium tuscaniaesp. nov. from Blood Cultures of a Patient with Endocarditis
Authors: Riegel Philippe , Creti Roberta , Mattei Romano , Nieri Alfredo , von Hunolstein Christina 
Published: February 2006

ABSTRACTA strain of an unknown coryneform bacterium was repeatedly isolated in pure culture from the blood of a patient affected by endocarditis. Comparative 16S rRNA gene sequence analysis revealed that this isolate represented a new subline within the genusCorynebacterium. This new taxon can be identified by the presence of corynomycolic acids and its enzymatic activities and fermentation of sugars. Acid production from glucose and maltose, pyrazinamidase and alkaline phoshatase activities, and hippurate hydrolysis were the most characteristic phenotypic features of the bacterium. On the basis of both phenotypic and phylogenetic evidence, it is proposed that this isolate be classified as a novel species,Corynebacterium tuscaniaesp. nov. The type strain, ISS-5309, has been deposited in the American Type Culture Collection (ATCC BAA-1141) and in the Culture Collection of the University of Göteborg (CCUG 51321).
Shiga Toxins Present in the Gut and in the Polymorphonuclear Leukocytes Circulating in the Blood of Children with Hemolytic-Uremic Syndrome
Authors: Brigotti Maurizio , Caprioli Alfredo , Tozzi Alberto E. , Tazzari Pier Luigi , Ricci Francesca , Conte Roberto , Carnicelli Domenica , Procaccino Maria Antonietta , Minelli Fabio , Ferretti Alfonso V. S. , Paglialonga Fabio , Edefonti Alberto , Rizzoni Gianfranco 
Published: February 2006

ABSTRACT

Hemolytic-uremic syndrome, the main cause of acute renal failure in early childhood, is caused primarily by intestinal infections from some
Escherichia coli
strains that produce Shiga toxins. The toxins released in the gut are targeted to renal endothelium after binding to polymorphonuclear leukocytes. The presence of Shiga toxins in the feces and the circulating neutrophils of 20 children with hemolytic uremic syndrome was evaluated by the Vero cell cytotoxicity assay and flow cytometric analysis, respectively. The latter showed the presence of Shiga toxins on the polymorphonuclear leukocytes of 13 patients, 5 of whom had no other microbiologic or serologic evidence of infection by Shiga toxin-producing
Escherichia coli
. A positive relationship was observed between the amounts of Shiga toxins released in the intestinal lumen and those released in the bloodstream. The toxins were detectable on the neutrophils for a median period of 5 days after they were no longer detectable in stools. This investigation confirms that the immunodetection of Shiga toxins on neutrophils is a valuable tool for laboratory diagnosis of Shiga toxin-producing
Escherichia coli
infection in hemolytic-uremic syndrome and provides clues for further studies on the role of neutrophils in the pathogenesis of this syndrome.
Evaluation of the Invader Assay for Genotyping Hepatitis C Virus
Authors: Germer Jeffrey J. , Majewski David W. , Yung Billy , Mitchell P. Shawn , Yao Joseph D. C. 
Published: February 2006

ABSTRACT

The Invader 1.0 assay (Invader HCV Genotyping Assay, version 1.0; Third Wave Technologies, Inc., Madison, WI) has been developed for the rapid differentiation of hepatitis C virus (HCV) genotypes 1 to 6 based on sequence variation within the HCV 5′ noncoding (NC) region. In the present study, we evaluated the compatibility of Invader 1.0 with the COBAS MONITOR (COBAS AMPLICOR HCV MONITOR Test, version 2.0; Roche Molecular Systems, Inc., Branchburg, NJ), COBAS AMPLICOR (COBAS AMPLICOR Hepatitis C Virus Test, version 2.0; Roche Molecular Systems, Inc.), and COBAS TaqMan (COBAS TaqMan HCV Test; Roche Molecular Systems, Inc.) assays. The minimum HCV RNA titers required for successful HCV genotyping (≥90% success rate) were 1,000 IU/ml for COBAS MONITOR, 100 IU/ml for COBAS AMPLICOR, and 10 IU/ml for COBAS TaqMan. Invader 1.0 results obtained from unpurified COBAS TaqMan amplification products of 111 retrospectively selected clinical serum specimens (genotypes 1 to 6, with virus titers ranging from 15.1 to 2.1 × 10
7
IU/ml) showed 98% concordance with results obtained from the TRUGENE
HCV 5
′
NC
Genotyping Kit (Bayer HealthCare LLC, Tarrytown, NY), used in conjunction with COBAS AMPLICOR. Although the assay is sensitive, accurate, and easy to perform, additional optimization of the Invader 1.0 interpretive software (Invader Data Analysis Worksheet) may be necessary to reduce potential misidentification of HCV genotypes in low-titer specimens. In summary, Invader 1.0 is compatible with a variety of commercially available PCR-based HCV 5′ NC region amplification assays and is suitable for routine HCV genotyping in clinical laboratories.
Emergence of a New Norovirus Genotype II.4 Variant Associated with Global Outbreaks of Gastroenteritis
Authors: Bull Rowena A. , Tu Elise T. V. , McIver Christopher J. , Rawlinson William D. , White Peter A. 
Published: February 2006

ABSTRACT
Norovirus (NoV) is highly infectious and is the major cause of outbreak gastroenteritis in adults, with pandemic spread of the virus being reported in 1995 and 2002. The NoV genome is genetically diverse, which has hampered development of sensitive molecular biology-based methods. In this study we report on a nested reverse transcriptase PCR (nRT-PCR) that was designed to amplify the highly conserved 3′ end of the polymerase region and the 5′ end of the capsid gene of NoV genogroup II (GII). The nRT-PCR was validated with strains isolated from sporadic and outbreak cases between 1997 and 2004 in New South Wales, Australia. Phylogenetic analysis identified six genotypes circulating in New South Wales, GII.1, GII.3, GII.4, GII.6, GII.7, and GII.10, with GII.4 being the predominant genotype. In 2004, there was a marked increase in NoV GII activity in Australia, with a novel GII.4 variant being identified as the etiological agent in 18 outbreaks investigated. This novel GII.4 variant, termed Hunter virus, differed by more than 5% at the amino acid level across the capsid from any other NoV strain in the GenBank and EMBL databases. The Hunter virus was subsequently identified as the etiological agent in large epidemics of gastroenteritis in The Netherlands, Japan, and Taiwan in 2004 and 2005.