bluuebunny/crossref_metadata_2025_split huggingface dataset:
A robust identification and detection assay to discriminate the cucumber pathogens Fusarium oxysporum f. sp. cucumerinum and f. sp. radicis‐cucumerinum
Authors: Lievens Bart , Claes Loes , Vakalounakis Demetrios J. , Vanachter Alfons C. R. C. , Thomma Bart P. H. J. 
Published: May 2007

SummaryThe fungal species Fusarium oxysporum is a ubiquitous inhabitant of soils worldwide that includes pathogenic as well as non‐pathogenic or even beneficial strains. Pathogenic strains are characterized by a high degree of host specificity and strains that infect the same host range are organized in so‐called formae speciales. Strains for which no host plant has been identified are believed to be non‐pathogenic strains. Therefore, identification below the species level is highly desired. However, the genetic basis of host specificity and virulence in F. oxysporum is so far unknown. In this study, a robust random‐amplified polymorphic DNA (RAPD) marker‐based assay was developed to specifically detect and identify the economically important cucumber pathogens F. oxysporum f. sp. cucumerinum and F. oxysporum f. sp. radicis‐cucumerinum. While the F. oxysporum radicis‐cucumerinum strains were found to cluster in a separate clade based on elongation factor‐1α phylogeny, strains belonging to F. oxysporum f. sp. cucumerinum were found to be genetically more diverse. This is reflected in the observation that specificity testing of the identified markers using a broad collection of F. oxysporum strains with all known vegetative compatibility groups of the target formae speciales, as well as representative strains belonging to other formae speciales, resulted in two cross‐reactions for the F. oxysporum f. sp. cucumerimum marker. However, no cross‐reactions were observed for the F. oxysporum f. sp. radicis‐cucumerimum marker. This F. oxysporum f. sp. radicis‐cucumerimum marker shows homology to Folyt1, a transposable element identified in the tomato pathogen F. oxysporum f. sp. lycopersici and may possibly play a role in host‐range specificity in the target forma specialis. The markers were implemented in a DNA array that enabled parallel and sensitive detection and identification of the pathogens in complex samples from diverse origins.
Migration Rates and Genetic Structure of two Hungarian Ethnic Groups in Transylvania, Romania
Authors: Brandstätter A. , Egyed B. , Zimmermann B. , Duftner N. , Padar Z. , Parson W. 
Published: May 2007

SummaryTransylvania's ethnic mosaic is composed of Romanians, German Saxons and Hungarians. The ethnic groups of the Hungarian minority that settled in Romania show differences in dialects, customs and religious affiliations. In this study entire mtDNA control region sequences from 360 individuals of Hungarian ethnicity from two populations (the Csángó and the Székely), settled in the historical region of Transylvania in Romania, were generated and analyzed following high quality sequencing standards. Phylogenetic analyses were used for haplogroup determination, quasi‐median network analyses were applied for the visualization of character conflicts, and median joining reconstructions were used for depicting haplotype structures. Affiliation of haplotypes to major west Eurasian haplogroups was confirmed using coding region SNPs. Gene flow between the two populations was low and biased towards a higher migration rate from the Csángó to the Székely than vice versa. Phylogeographic analyses revealed effects of genetic isolation within the Csángó population, which is, in its genetic structure, clearly different from the Székely population. The pronounced genetic divergence between the two populations is in sharp contrast to the expectation of high genetic similarity due to the close geographic proximity of their native homelands. The population data will be incorporated in the EMPOP database (http://www.empop.org).
An immunohistochemical study of the triangular fibrocartilage complex of the wrist: regional variations in cartilage phenotype
Authors: Milz S. , Sicking B. , Sprecher C. M. , Putz R. , Benjamin M. 
Published: May 2007

AbstractThe triangular fibrocartilage complex (TFCC) transmits load from the wrist to the ulna and stabilizes the distal radioulnar joint. Damage to it is a major cause of wrist pain. Although its basic structure is well established, little is known of its molecular composition. We have analysed the immunohistochemical labelling pattern of the extracellular matrix of the articular disc and the meniscal homologue of the TFCC in nine elderly individuals (age range 69–96 years), using a panel of monoclonal antibodies directed against collagens, glycosaminoglycans, proteoglycans and cartilage oligomeric matrix protein (COMP). Although many of the molecules (types I, III and VI collagen, chondroitin 4 sulphate, dermatan sulphate and keratan sulphate, the oversulphated epitope of chondroitin 6 sulphate, versican and COMP) were found in all parts of the TFCC, aggrecan, link protein and type II collagen were restricted to the articular disc and to entheses. They were thus not a feature of the meniscal homologue. The shift in tissue phenotype within the TFCC, from a fibrocartilaginous articular disc to a more fibrous meniscal homologue, correlates with biomechanical data suggesting that the radial region is stiff and subject to considerable stress concentration. The presence of aggrecan, link protein and type II collagen in the articular disc could explain why the TFCC is destroyed in rheumatoid arthritis, given that it has been suggested that autoimmunity to these antigens results in the destruction of articular cartilage. The differential distribution of aggrecan within the TFCC is likely to be reflected by regional differences in water content and mobility on the radial and ulnar side. This needs to be taken into account in the design of improved MRI protocols for visualizing this ulnocarpal complex of the wrist.
Comparative anatomy of the foramen ovale in the hearts of cetaceans
Authors: Macdonald Alastair A. , Carr Peter A. , Currie Richard J. W. 
Published: May 2007

AbstractThe structure of the cardiac foramen ovale from 17 species representing six cetacean families, the Monodontidae, Phocoenidae, Delphinidae, Ziphiidae, Balaenidae and the Balaenopteridae, was studied using the scanning electron microscope. Eight white whale fetuses (Delphinapterus leucas) and a narwhal fetus (Monodon monoceros) represented the Monodontidae; one fetal and nine neonatal harbour porpoises (Phocoena phocoena) and a finless porpoise fetus (Neophocoena phocoenoides) represented the Phocoenidae; two white‐beaked dolphin fetuses (Lagenorhynchus albirostris), four fetal and one neonatal Atlantic white‐sided dolphins (Lagenorhynchus acutus), a Risso's dolphin fetus (Grampus griseus), two common bottle‐nosed dolphin neonates (Tursiops truncatus), a female short‐beaked common dolphin fetus (Delphinus delphis), four killer whale fetuses (Orcinus orca) and two long‐finned pilot whale fetuses (Globicephala melas) represented the Delphinidae; two northern bottlenose whale fetuses (Hyperoodon ampullatus) represented the Ziphiidae; one bowhead whale fetus (Balaena mysticetus) represented the Balaenidae and five Common minke whale fetuses (Balaenoptera acutorostrata), one blue whale fetus (Balaenoptera musculus), nine fin whale fetuses (Balaenoptera physalus) and four humpback whale fetuses (Megaptera novaeangliae) represented the Balaenopteridae. The hearts of an additional two incompletely identified toothed and four baleen whale fetuses were also studied. In each species the fold of tissue derived from the cardiac septum primum and subtended by the foramen ovale had the appearance of a short tunnel or sleeve which was fenestrated at its distal end. In the toothed whales the tissue fold was tunnel‐shaped with the interatrial septum as the floor whereas in baleen whales it was more sleeve‐like. In toothed whales thin threads extended from the fold to insert into the interatrial septum whereas a network of threads covered the distal end of the sleeve in the baleen whales. Similar structures were present in the corresponding cardiac tissues of neonatal Hippopotamidae.
Epidermal differentiation in embryos of the tuatara Sphenodon punctatus (Reptilia, Sphenodontidae) in comparison with the epidermis of other reptiles
Authors: Alibardi L. , Gill B. J. 
Published: May 2007

AbstractStudying the epidermis in primitive reptiles can provide clues regarding evolution of the epidermis during land adaptation in vertebrates. With this aim, the development of the skin of the relatively primitive reptile Sphenodon punctatus in representative embryonic stages was studied by light and electron microscopy and compared with that of other reptiles previously studied. The dermis organizes into a superficial and deep portion when the epidermis starts to form the first layers. At embryonic stages comparable with those of lizards, only one layer of the inner periderm is formed beneath the outer periderm. This also occurs in lizards and snakes so far studied. The outer and inner periderm form the embryonic epidermis and accumulate thick, coarse filaments (25–30 nm thick) and sparse alpha‐keratin filaments as in other reptiles. Beneath the embryonic epidermis an oberhautchen and beta‐cells form small horny tips that represent overlapping borders along the margin of beta‐cells that overlap other beta‐cells (in a tile‐like arrangement). The tips resemble those of agamine lizards but at a small scale, forming a lamellate‐spinulated pattern as previously described in adult epidermis. The embryonic epidermis matures by the dispersion of coarse filaments among keratin at the end of embryonic development and is shed around hatching. The presence of these matrix organelles in the embryonic epidermis of this primitive reptile further indicates that amniote epidermis acquired interkeratin matrix proteins early for land adaptation. Unlike the condition in lizards and snakes, a shedding complex is not formed in the epidermis of embryonic S. punctatus that is like that of the adult. Therefore, as in chelonians and crocodilians, the epidermis of S. punctatus also represents an initial stage that preceded the evolution of the shedding complex for moulting.
µMRI–HREM pipeline for high‐throughput, high‐resolution phenotyping of murine embryos
Authors: Pieles Guido , Geyer Stefan H. , Szumska Dorota , Schneider Jürgen , Neubauer Stefan , Clarke Kieran , Dorfmeister Karl , Franklyn Angela , Brown Steve D. , Bhattacharya Shoumo , Weninger Wolfgang J. 
Published: May 2007

AbstractRapid and precise phenotyping analysis of large numbers of wild‐type and mutant mouse embryos is essential for characterizing the genetic and epigenetic factors regulating embryogenesis. We present a novel methodology that permits precise high‐throughput screening of the phenotype of embryos with both targeted and randomly generated mutations. To demonstrate the potential of this methodology we show embryo phenotyping results produced in a large‐scale ENU‐mutagenesis study. In essence this represents an analysis pipeline, which starts with simultaneous micro‐magentic resonance imaging (µMRI) screening (voxel size: 25.4 × 25.4 × 24.4 µm) of 32 embryos in one run. Embryos with an indistinct phenotype are then cut into parts and suspect organs and structures are analysed with HREM (high‐resolution episcopic microscopy). HREM is an imaging technique that employs ‘positive’ eosin staining and episcopic imaging for generating three‐dimensional (3D) high‐resolution (voxel size: 1.07 × 1.07 × 2 µm) digital data of near histological contrast and quality. The results show that our method guarantees the rapid availability of comprehensive phenotype information for high numbers of embryos in, if necessary, histological quality and detail. The combination of high‐throughput µMRI with HREM provides an alternative screening pipeline with advantages over existing 3D phenotype screening methods as well as traditional histology. Thus, the µMRI‐HREM phenotype analysis pipeline recommends itself as a routine tool for analysing the phenotype of transgenic and mutant embryos.
Rituximab for warm‐type idiopathic autoimmune hemolytic anemia: a retrospective study of 11 adult patients
Authors: D’Arena Giovanni , Califano Catello , Annunziata Mario , Tartarone Alfredo , Capalbo Silvana , Villani Oreste , Amendola Giovanni , Pietrantuono Giuseppe , Ferrara Felicetto , Pinto Antonio , Musto Pellegrino , D’Arco Alfonso Maria , Cascavilla Nicola 
Published: May 2007

AbstractWarm‐type idiopathic autoimmune hemolytic anemia (AIHA) is a relatively common hematologic disorder resulting from autoantibody production against red blood cells. Steroids represent the first‐line therapeutic option, and immunosuppressive agents as well as splenectomy are used for refractory cases. Recently, the anti‐CD20 monoclonal antibody rituximab has been shown to control autoimmune hemolysis in patients with refractory chronic disease. We report results from a retrospective analysis of 11 adult patients receiving rituximab for steroid‐refractory AIHA of the warm type at a mean age of 55 yr (range 23–81 yr). All patients were given methyl‐prednisolone as first‐line treatment and some of them also received azathioprine and intravenous high‐dose immunoglobulins. One patient underwent splenectomy. All patients were considered refractory to steroids and/or immunosuppressive drugs and all were then given weekly rituximab (375 mg/m2) for four consecutive weeks. An increase in hemoglobin (Hgb) levels in response to rituximab, with a mean increment of 3.3 g/dL (95% CI 2.1–4.4), was observed in all cases. Four patients required packed red cell transfusions before starting rituximab and all became transfusion‐free. At a mean follow‐up of 604 d (range 30–2884 d) since the treatment of AIHA with rituximab, all patients are alive, eight (73%) of them in complete remission (CR) and three (27%) in partial remission (PR). A moderate hemolysis still persisted in six (54%) patients. In conclusion, our experience clearly demonstrates that anti‐CD20 monoclonal antibody rituximab is an effective and safe alternative treatment option for idiopathic AIHA, in particular, for steroid‐refractory disease.
The effect of ranitidine on antibody responses to polysaccharide vaccines in patients with B‐cell chronic lymphocytic leukaemia
Authors: Van der Velden Ankie M. T. , Van Velzen‐Blad Heleen , Claessen Anke M. E. , Van der Griend René , Oltmans Ruud , Rijkers Ger T. , Biesma Douwe H. 
Published: May 2007

Abstract Objectives: To analyse the effects of ranitidine treatment on vaccination induced antibody responses in patients with chronic lymphocytic leukaemia (CLL).Methods: Fifty CLL patients were vaccinated with tetanus conjugated Hib vaccine and a 23‐valent pneumococcal polysaccharide vaccine with (n = 25) or without (n = 25) ranitidine treatment in a matched case‐‐control setting. Anti tetanus toxoid (TT), anti‐Hib and anti‐pneumococcal antibody levels were determined before and after vaccination. Additionally, cytokine levels were assessed in patients treated with ranitidine.Results: Vaccination‐induced increases in anti‐Hib and anti‐TT antibody levels were higher in the ranitidine group compared with the control group. Anti‐pneumococcal antibody responses were not improved by administration of ranitidine. Higher levels of IL‐18 were found in patients treated with ranitidine compared with healthy controls. Levels of IL‐6, IL‐8, IL‐18, RANTES, IP‐10, sVCAM‐1 and sICAM‐1 were within normal ranges and did not change during ranitidine treatment.Conclusion: Ranitidine treatment improves vaccination‐induced T‐cell dependent antibody responses in patients with CLL but has no beneficial effect on the response to vaccination with unconjugated polysaccharide antigens.
Immunophenotypic analysis of Epstein–Barr virus (EBV)‐infected CD8+ T cells in a patient with EBV‐associated hemophagocytic lymphohistiocytosis
Authors: Wada Taizo , Kurokawa Toshiro , Toma Tomoko , Shibata Fumie , Tone Yumi , Hashida Yoko , Kaya Hiroyasu , Yoshida Takashi , Yachie Akihiro 
Published: May 2007

AbstractHemophagocytic lymphohistiocytosis (HLH) is a severe and often fatal condition characterized by uncontrolled activation of T cells and macrophages. In Epstein–Barr virus (EBV)‐associated HLH (EBV‐HLH), the pathogenic roles of ectopic EBV infection in the T‐cell population and of clonal proliferation of EBV‐infected T cells has been described. However, the immunophenotype of EBV‐infected T cells has not been fully characterized. Here we describe a case of EBV‐HLH presenting with a massive clonal proliferation of CD8+ T cells with TCR VB14. Analysis of in situ hybridization for EBV‐encoded small RNA1 showed that only CD8+ T cells harbored EBV in this patient. The EBV‐infected TCR VB14+ CD8+ T cells exhibited unique immunophenotypic features including lacked CD5 expression and a markedly bright expression of HLA‐DR. After initiation of treatment with prednisolone, etoposide, and cyclosporin A, the percentage of infected cells declined progressively in parallel with other serum markers such as ferritin. These findings suggest that lacking expression of CD5 on CD8+ T cells with specific TCR VB may serve as a useful marker of dysregulated T‐cell activation and proliferation in EBV‐HLH.
Effects of estradiol and 4-hydroxytamoxifen on the conformation, thermal stability, and DNA recognition of estrogen receptor β
Authors: Vijayanathan Veena , Greenfield Norma J. , Thomas T. J. , Ivanova Margarita M. , Tyulmenkov Valentyn V. , Klinge Carolyn M. , Gallo Michael A. , Thomas Thresia 
Published: May 2007

Estrogen receptors (ERα and ERβ) are ligand-activated transcription factors. We examined the effects of estradiol (E2), 4-hydroxytamoxifen (HT), and the estrogen response element (ERE) on the helical content and thermal unfolding of ERβ. A circular dichroism (CD) spectrum of ERβ showed changes at 210 and 222 nm that were due to the presence of E2, which is indicative of partial unfolding. In contrast, HT did not alter the CD spectrum of ERβ. The addition of E2 + ERE caused an increase in the α-helical content and an increase in the temperature midpoint of folding transition (TM) from 39 ± 0.7 °C to 57.2 ± 1 °C. The addition of E2 + mutant ERE, or E2 + control oligonucleotide, increased the TMof ERβ to 45 ± 2 °C only. In the presence of HT, ERβ yielded similar TMvalues (55–58 °C) with ERE, mutant ERE, or control oligodeoxynucleotide. The binding affinity of ERβ for ERE increased 125.7-fold as a result of the presence of E2, but only 4-fold as a result of HT. These results demonstrate coupled effects of E2and ERE on ERβ stability and binding affinity. The increased thermal stability of HT–ERβ–ERE was associated with reduced specificity of ERβ–ERE recognition, illustrating profound differences in conformational states of ERβ induced by E2and HT.
The inhibitory effect of simvastatin on the ADMA-induced inflammatory reaction is mediated by MAPK pathways in endothelial cells
Authors: Jiang Jun-Lin , Wang Shan , Li Nian-Sheng , Zhang Xiao-Hong , Deng Han-Wu , Li Yuan-Jian 
Published: May 2007

Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, is emerging as a key contributor for endothelial dysfunction associated with inflammation. Statins can inhibit vascular inflammatory reaction and improve endothelial function. The aim of this study was to investigate in human endothelial cells the signaling pathways of ADMA-induced inflammatory reaction and potential inhibitory effects of simvastatin. Endothelial cells were cultured and used for all of the studies. Tumor necrosis factor-α (TNF-α) and soluble intercellular adhesion molecule-1 (sICAM-1) were determined by enzyme-linked immunosorbent assay. Nuclear factor-κB (NF-κB) was assayed by electrophoretic mobility shift assay. The activation of mitogen-activated protein kinases (MAPKs), including p38 MAPK and extracellular signal-related kinase (ERK1/2), were characterized by Western blot analysis. Treatment with ADMA (3–30 µmol/L) increased the concentration of sICAM-1 in a dose-dependent manner. ADMA (30 µmol/L) significantly enhanced the concentrations of TNF-α and sICAM-1, the activity of NF-κB and the phosphorylation of p38 MAPK and ERK1/2. The increased secretion of TNF-α and sICAM-1 and the increased activity of NF-κB by ADMA were altered by SB203580 (5 µmol/L) or PD98059 (20 µmol/L), but not by LY294002 (20 µmol/L). Simvastatin (0.1, 0.5, or 2.5 µmol/L) markedly inhibited the elevated concentrations of TNF-α and sICAM-1, the activity of NF-κB, and the phosphorylation of p38 MAPK and ERK1/2 induced by ADMA. Simvastatin inhibited ADMA-induced inflammatory reaction by p38 MAPK and ERK1/2 pathways in cultured endothelial cells.
Mitochondria-independent morphological and biochemical apoptotic alterations promoted by the anti-tumor agent bleomycin inSaccharomyces cerevisiae
Authors: Aouida Mustapha , Mekid Halima , Belhadj Omrane , Mir Lluis M. , Tounekti Omar 
Published: May 2007

Bleomycin is a highly potent cytotoxic and genotoxic agent used in the chemotherapy of various types of tumors. It is a radiomimetic anticancer drug that produces single- and double-stranded DNA breaks in a catalytic way. Using Saccharomyces cerevisiae as a model system, we show that when a high amount of bleomycin molecules is internalized (100 µmol/L), morphological changes identical to those usually associated with apoptosis, i.e., a sub-G1region peak, chromatin condensation, and very rapid DNA fragmentation into oligonucleosomal-sized fragments, are observed. The known bleomycin inhibitors cobalt and EDTA were able to prevent bleomycin nucleasic activity and thus apoptotic cell death. However, both oligomycin, a potent inhibitor of the mitochondial F0F1-ATPase, and antimycin, a drug affecting mitochondria respiration, were unable to prevent the bleomycin-induced apoptotic-like cell death. These results suggest that high bleomycin concentrations induce an apoptosis-like mitochondria-independent cell death in yeast.
A 27.368 kDa retinal reductase in New Zealand white rabbit liver cytosol encoded by the peroxisomal retinol dehydrogenase–reductase cDNA: purification and characterization of the enzymeThis paper is one of a selection of papers in this Special Issue, entitled International Symposium on Recent Advances in Molecular, Clinical, and Social Medicine, and has undergone the Journal's usual peer-review process.
Authors: Du Kun , Liu Ge-Fei , Xie Jian-Ping , Song Xu-Hong , Li Rui , Liang Bin , Huang Dong-Yang 
Published: May 2007

We obtained a full-length cDNA based on a sequence deposited in GenBank (accession No. AB045133), annotated as rabbit peroxisomal NADP(H)-dependent retinol dehydrogenase–reductase (NDRD). The rabbit NDRD gene, like its mouse and human homologs, harbors 2 initiation sites, one of which theoretically encodes a 29.6 kDa protein with 279 amino acids, and the other encodes a 27.4 kDa protein with 260 amino acids. The purification of a rabbit cytosolic retinol oxidoreductase with a subunit molecular mass of 34 kDa and an N terminus that is not completely identical to that of NDRD, has been reported. An enzyme responsible for the all-trans retinal reductase activity in the liver cytosol of New Zealand white rabbit was purified to homogeneity using differential centrifugation and successive chromatographic analyses. The subunit molecular mass of the purified enzyme, revealed by SDS–PAGE, was approximately 27 kDa. The intact molecular mass, measured by MALDI–TOF mass spectrometry, was 27.368 kDa. The 60 kDa relative mobility observed in size-exclusion chromatography indicates that the native protein probably exists as a dimer. The purified enzyme was positively confirmed to be the product of NDRD by peptide mass fingerprinting, tandem mass spectrometry, and N-terminal sequencing. Taken together, the results suggested that the native protein is truncated at the N terminus.