bluuebunny/crossref_metadata_2025_split huggingface dataset:
First Report of Kidney Bean Little Leaf Disease Associated with 16SrII Group Phytoplasma in China
Authors: Dong J. H. , Zhang L. , McBeath J. H. , Zhang Z. K. 
Published: December 2009

Kidney bean (Phaseolus vulgaris) is an important cash crop in China. It is widely grown in the Yunnan Province in the southwest region. In November of 2008, a new disease was observed on kidney bean plants grown in Yuanmou County. Affected plants displayed symptoms that included numerous twisted lateral shoots with abundant, tiny trifoliate leaves that were approximately one-tenth the size of healthy leaves. Some affected leaves, which were slightly distorted and oblong to oval, were evident on diseased plants and appeared pale green. On plants with little leaf symptoms, flowers were poorly formed, withered or aborted, and no pods were present. Surveys conducted in areas affected by disease revealed the presence of the disease in approximately 10% of the plants. DNA was extracted from 0.1 g of petioles and midveins harvested from both diseased and symptomless plants with the Qiagen DNeasy Plant Mini Kit (Qiagen, Hilden, Germany). Plants were evaluated for phytoplasma infection by a nested PCR assay with phytoplasma specific ribosomal operon primer pair P1/Tint followed by R16F2/R16R2 (2,3). An rDNA product of approximately 1,250 bp was amplified from seven of seven diseased plants, whereas no products were amplified from symptomless plants or a negative control devoid of DNA. Digests of nested PCR products (approximately 200 ng) with endonucleases AluI, ScaI, or EcoRI revealed no differences in restriction fragment length polymorphism (RFLP) among diseased plants. The amplicon was cloned and sequenced (GenBank Accession No. GQ336993). Comparison of in silico RFLP profiles with published profiles showed that kidney bean little leaf phytoplasma is a member of peanut witches' broom group 16SrII. Blast analysis of the kidney bean little leaf phytoplasma 16S rDNA sequence revealed that this strain is most similar (99.0%) to Syringa oblata yellows phytoplasma (Accession No. FJ263629) and to other phytoplasmas classified as group 16SrII members. Previously, phytoplasmas identified as 16SrII strains have been reported as probable cause of cactus witches' broom (1) and crotalaria witches' broom (4) in China. To our knowledge, this is the first report of a 16SrII phytoplasma infecting the kidney bean in China. References: (1) H. Cai et al. Plant Pathol. 51:394, 2002. (2) I.-M Lee et al. Phytopathology 83:834, 1993. (3) C. D. Smart et al. Appl. Environ. Microbiol. 62:2988, 1996 (4) Z. H. Wang et al. Plant Pathol. 57:364, 2008.
First Report of Blight of Common Bean Caused by Phytophthora capsici in Connecticut
Authors: LaMondia J. A. , Li D. W. , Vossbrinck C. R. 
Published: December 2009

Phytophthora capsici Leonion was first identified on pepper (Capsicum annuum L.) and is widespread on solanaceous and cucurbitaceous crops. It was first documented on Phaseolus lunatus L. in Delaware in 2002 (1), followed by reports on snap beans (Phaseolus vulgaris L.) in Michigan in 2003 (2), and on Long Island, NY in 2008 ( http://vegetablemdonline.ppath.cornell.edu/ NewsArticles/Bean_phytoJune09.html ). In 2009, we observed snap and wax beans in commercial production with water-soaked lesions on foliage, stems, and pods. Twelve to sixteen hectares were affected in the flood plain of the Connecticut River in central Connecticut. Weather conditions had been warm and very wet. Lesions displayed white mycelia and sporangia. P. capsici was isolated from surface-sterilized tissue on potato dextrose agar (PDA) and malt extract agar. Hyphal tips were subcultured onto V8 media for further analysis. To confirm Koch's postulates, two isolates were tested for pathogenicity against bean (cv. Valentino) and pepper (cv. Cayenne) by placing colonized PDA plugs or PDA alone next to the crown or in stem branches. Symptoms similar to those observed in the field on bean and pepper developed on inoculated plants and the pathogen was reisolated. Controls did not develop disease. Sporangia of P. capsici growing on V8 medium were ellipsoid, ovoid, pyriform, but occasionally irregular, papillate, and 54.0 ± 5.7 × 31.1 ± 4.7 μm (n = 31) with a length/width (L/W) ratio of 1.8 ± 0.3. The papillae were 5.4 ± 0.9 μm (n = 31) and the pedicels were 24.5 ± 12.6 × 3.0 ± 1.0 μm. Sporangia collected from bean plants were smaller with longer pedicels; the sporangia were 44.9 ± 9.1 × 26.0 ± 2.8 μm with a L/W ratio of 1.7 ± 0.2; papillae were 4.6 ± 1.0 μm; and the pedicels were 49 ± 20.0 × 2.8 ± 0.9 μm (n = 20). To confirm the identity of our isolate genetically, DNA was extracted from one P. capsici isolate and the nuclear ribosomal internal transcribed spacer (ITS) region was amplified and sequenced (GenBank Accession No. GU011684). The ITS sequence was identical to sequences of P. capsisci in GenBank and confirmed our identification of this new isolate as P. capsici. To our knowledge, this is the first report of P. capsici infecting Phaseolus vulgaris in Connecticut and New England. References: (1) C. R. Davidson et al. Plant Dis. 85:886, 2002. (2) A. J. Gevens et al. Plant Dis. 92:201, 2008.
Biased usage of BV gene families of T‐cell receptors of WT1 (Wilms’ tumor gene)‐specific CD8+ T cells in patients with myeloid malignancies
Authors: Tanaka‐Harada Yukie , Kawakami Manabu , Oka Yoshihiro , Tsuboi Akihiro , Katagiri Takamasa , Olga Elisseeva , Nishida Sumiyuki , Shirakata Toshiaki , Hosen Naoki , Fujiki Fumihiro , Murao Ayako , Nakajima Hiroko , Oji Yusuke , Kanda Yoshinobu , Kawase Ichiro , Sugiyama Haruo 
Published: December 2009

(Cancer Sci 2010; 101: 594–600)WT1 (Wilms’ tumor gene 1) protein is a potent pan‐tumor‐associated antigen (TAA) and WT1‐specific cytotoxic T lymphocytes (WT1 tetramer+ CD8+ T cells) are spontaneously induced in patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS). We conducted a single‐cell level comparative analysis of T‐cell receptor β‐chain variable region (TCR‐BV) gene families of a total of 1242 spontaneously induced WT1 tetramer+ CD8+ T cells in HLA‐A*2402+ patients with AML or MDS and those in healthy donors (HDs). This is the first report of direct usage analysis of TCR‐BV gene families of individual TAA‐specific CD8+ T cells at single‐cell level. Usage analysis using single‐cell RT‐PCR of TCR‐BV gene families of individual FACS‐sorted WT1 tetramer+ CD8+ T cells showed for the first time (i) that BVs 5, 6, 20, and 27 were commonly biased in both HDs and patients; (ii) that BV4 was commonly biased in HDs and MDS patients; (iii) that BV19 was commonly biased in the patients; and (iv) that BVs 7 and 28, BVs 9 and 15, and BVs 12 and 29 were specifically biased in HDs, AML, and MDS patients, respectively. However, statistical analysis of similarity among HD, AML, and MDS of individual usage frequencies of 24 kinds of TCR‐BV gene families indicated that the usage frequencies of TCR‐BV gene families in AML and MDS patients reflect those in HDs. These findings represent a novel insight for a better understanding of WT1‐specific immune response.
Augmentation of 3‐methylcholanthrene‐induced bioactivation in the human hepatoma cell line HepG2 by the calcium channel blocker nicardipine
Authors: Hosaka Takuomi , Sekimoto Masashi , Nemoto Kiyomitsu , Degawa Masakuni 
Published: December 2009

(Cancer Sci2010; 101: 652–657)The abilities of the dihydropyridine calcium channel blocker nicardipine (Nic) to induce cytochrome P450 1 family enzymes (CYP1s) and to enhance the 3‐methylcholanthrene (MC)‐mediated induction of CYP1s and formation of MC‐DNA adduct were examined in the human hepatoma cell line HepG2. The results from real time RT‐PCR analysis demonstrated that Nic could induce CYP1 mRNAs and enhance the MC‐mediated induction of the CYP1 mRNAs. The luciferase‐reporter gene assay using the HepG2‐A10 cell line, which has been previously established for the screening of aryl hydrocarbon receptor (AhR) activators, also indicated the augmentation of MC‐mediated activation of AhR (induction of luciferase) by Nic, although Nic showed limited capacity for the activation of AhR. Furthermore, the results from the Western blot analysis of CYP1s, the enzyme activity assay, and the assay for MC‐DNA adduct formation indicated that Nic could enhance the MC‐mediated induction of CYP1s, especially CYP1A1. Furthermore, the intracellular accumulation level of [3H]MC after treatment of HepG2 cells with [3H]MC significantly increased in the presence of Nic. The present findings demonstrate that Nic can enhance the MC‐mediated induction of CYP1s, especially CYP1A1, and the formation of MC‐DNA adduct in HepG2 cells. Furthermore, the augmentation of the MC‐mediated bioactivation by Nic is demonstrated to occur mainly through an increase in intracellular accumulation of MC.
Altered expression of glycan genes in cancers induced by epigenetic silencing and tumor hypoxia: Clues in the ongoing search for new tumor markers
Authors: Kannagi Reiji , Sakuma Keiichiro , Miyazaki Keiko , Lim Khe‐Ti , Yusa Akiko , Yin Jun , Izawa Mineko 
Published: December 2009

(Cancer Sci 2010; 101: 586–593)The glycan molecules that preferentially appear in cancers are clinically utilized as serum tumor markers. The exact reason, however, why glycans are useful as tumor markers remain elusive. Here, we will summarize lessons learned from well‐established cancer‐associated glycans, and propose strategies to develop new cancer markers. Our recent results on cancer‐associated glycans, sialyl Lewis A and sialyl Lewis X, indicated that the repressed transcription of some glycan genes by epigenetic silencing during early carcinogenesis, and the transcriptional induction of some other glycan genes by tumor hypoxia accompanying cancer progression at locally advanced stages, are two major factors determining cancer‐associated glycan expression. Multiple genes are involved in glycan synthesis, and epigenetic silencing of a part of such genes leads to accumulation of glycans having truncated incomplete structures, which are readily detected by specific antibodies. Glycans are very unique and advantageous as marker molecules because they are capable of reflecting epigenetic silencing in their structures. Transcriptional induction of some glycan genes by tumor hypoxia at the later stages produces further glycan modifications, such as an unusual increase of the N‐glycolyl sialic acid residues in the glycan molecules. The entire process of malignant transformation thus creates abnormal glycans, whose structures reveal the effects of both epigenetic silencing and tumor hypoxia. The second advantage of a glycan marker over a proteinous marker is that they can reflect the plurality of genetic anomalies in a singular molecule, as it is synthesized by the cooperative action of multiple genes. Glycans are sometimes covalently bound to well‐known cancer‐associated proteins, such as CD44v, and this eventually contributes to a high cancer specificity and functional relevancy in cancer progression.
Age dependence of radiation‐induced renal cell carcinomas in an Eker rat model
Authors: Kokubo Toshiaki , Kakinuma Shizuko , Kobayashi Toshiyuki , Watanabe Fumiko , Iritani Riichirou , Tateno Kaori , Nishimura Mayumi , Nishikawa Tetsu , Hino Okio , Shimada Yoshiya 
Published: December 2009

(Cancer Sci 2010; 101: 616–623)Exposure to carcinogens early in life may contribute to cancer development later in life. The amount of radiation exposure children experience during medical procedures has been increasing, so it is important to evaluate the radiation risk of cancer in developing organs. Toward this goal, we assessed the risk of developing renal cell carcinoma using Eker rats as a kidney tumor model. F1 hybrids of male Eker (Tsc2 mutant) and female F344 rats were irradiated with 0.5 or 2 Gy gamma radiation on gestation days 15 and 19, and on postnatal days 5, 20, and 49. At 27 weeks of age, kidneys were examined for proliferative lesions. Preneoplastic lesions such as phenotypically altered tubules increased after postnatal irradiation as a function of age‐at‐irradiation, and hyperplasia were greatly increased after perinatal and postnatal irradiation. In contrast, development of adenoma and adenocarcinoma were evident in animals irradiated at perinatal ages, being maximal at gestational day 19. The frequency of LOH at the Tsc2 locus was unexpectedly low – 0% (0 of 4) for the unirradiated control, and 17% (6 of 35) for the irradiated group. Irrespective of LOH, the mTOR (mammalian target of rapamycin) pathway, which is negatively regulated by the Tsc1/2 complex, was activated in both benign and malignant lesions, as evidenced by phosphorylation of S6 ribosomal protein and 4E‐BP1. This suggests that the wild‐type Tsc2 allele may be functionally inactivated. In conclusion, actively growing kidneys in perinatal‐aged (F344 × Eker) F1 rats (Tsc2+/−) are at risk for radiation‐induced malignant transformation of the renal epithelium associated with mTOR activation.
High expression of BUBR1 is one of the factors for inducing DNA aneuploidy and progression in gastric cancer
Authors: Ando Koji , Kakeji Yosihiro , Kitao Hiroyuki , Iimori Makoto , Zhao Yan , Yoshida Rintaro , Oki Eiji , Yoshinaga Keiji , Matumoto Takuya , Morita Masaru , Sakaguchi Yoshihisa , Maehara Yoshihiko 
Published: December 2009

(Cancer Sci 2010; 101: 639–645)Gastric cancers show high frequency of DNA aneuploidy, a phenotype of chromosomal instability. It is suggested that the abnormal spindle assembly checkpoint is involved in DNA aneuploidy, but the underlying mechanism is still unclear. We studied the mechanism by assessing the expression of BUBR1 in gastric cancer. The DNA ploidy patterns of 116 gastric cancer samples obtained from the Department of Surgery and Science at Kyushu University Hospital were analyzed. Of those, DNA aneuploidy was seen in 70 (60.3%) cases of gastric cancer. The expression of BUBR1 was studied by immunohistochemistry in 181 gastric cancer samples and by real‐time RT‐PCR in several gastric cancer cell lines. Ninety‐one (50.3%) cases had high expression of BUBR1 and those cases correlated significantly with DNA aneuploidy (P < 0.05). Also high expression of BUBR1 cases had significant correlation with deep invasion, lymph node metastasis, liver metastasis, and poor prognosis. In gastric cancer cell lines, high expression of BUBR1 had a significant relationship with DNA aneuploidy (P < 0.05). Then, gastric cancer cell lines MKN‐28 and SNU‐1 were transfected with full‐length BUBR1 to observe the significance of the change in BUBR1 expression. Enforced expression of BUBR1 resulted in changes to the ploidy pattern and high Ki‐67 expression. Collectively, our clinical and in vitro data indicate that high expression of BUBR1 may be one of causative factors for the induction of DNA aneuploidy and progression of gastric cancer.
Advances in the understanding and management of angioimmunoblastic T‐cell lymphoma
Authors: De Leval Laurence , Gisselbrecht Christian , Gaulard Philippe 
Published: December 2009

SummaryAngioimmunoblastic T‐cell lymphoma (AITL) is a distinct peripheral T‐cell lymphoma (PTCL) entity with peculiar clinical and pathological features. The recent identification of follicular helper T (TFH) cell as the cell of origin of this neoplasm represents a major step in our understanding of the pathobiological characteristics of the disease and should, in the future, clarify the diagnostic criteria for AITL and help to delineate its spectrum, especially from PTCL, not otherwise specified (PTCL, NOS). Deciphering the pathogenesis of the disease is needed to identify targets for new therapies that are expected to improve the poor outcome of AITL patients, when treated with conventional chemotherapy regimens. In this respect, efforts will be needed to evaluate promising innovative therapies in prospective clinical trials.
Role of 5‐HT2A, 5‐HT4and 5‐HT7receptors in the antigen‐induced airway hyperresponsiveness in guinea‐pigs
Authors: Segura P. , Vargas M. H. , Córdoba‐Rodríguez G. , Chávez J. , Arreola J. L. , Campos‐Bedolla P. , Ruiz V. , García‐Hernández L. M. , Méndez C. , Montaño L. M. 
Published: December 2009

SummaryBackgroundA possible role of 5‐hydroxytryptamine (5‐HT) in the origin of antigen‐induced airway hyperresponsiveness (AI‐AHR) has been scarcely investigated.ObjectiveTo explore the participation of different 5‐HT receptors in the development of AI‐AHR in guinea‐pigs.MethodsLung resistance was measured in anaesthetized guinea‐pigs sensitized to ovalbumin (OVA). Dose–response curves to intravenous (i.v.) acetylcholine (ACh) were performed before and 1 h after antigenic challenge and expressed as the 200% provocative dose (PD200). Organ bath experiments, confocal microscopy and RT‐PCR were additionally used. The 5‐HT content in lung homogenates was measured by HPLC.ResultsAntigenic challenge significantly decreased PD200, indicating the development of AI‐AHR. This hyperresponsiveness was abolished by a combination of methiothepin (5‐HT1/5‐HT2/5‐HT5/5‐HT6/5‐HT7receptors antagonist) and tropisetron (5‐HT3/5‐HT4antagonist). Other 5‐HT receptor antagonists showed three different patterns of response. Firstly, WAY100135 (5‐HT1Aantagonist) and ondansetron (5‐HT3antagonist) did not modify the AI‐AHR. Secondly, SB269970 (5‐HT7antagonist), GR113808 (5‐HT4antagonist), tropisetron or methiothepin abolished the AI‐AHR. Thirdly, ketanserin (5‐HT2Aantagonist) produced airway hyporresponsiveness. Animals with bilateral vagotomy did not develop AI‐AHR. Experiments in tracheal rings showed that pre‐incubation with LP44 or cisapride (agonists of 5‐HT7and 5‐HT4receptors, respectively) induced a significant increase of the cholinergic contractile response to the electrical field stimulation. In sensitized lung parenchyma strips, ketanserin diminished the contractile responses to ACh. Sensitization was associated with a ninefold increase in the 5‐HT content of lung homogenates. Confocal microscopy showed that sensitization enhanced the immunolabelling and co‐localization of nicotinic receptor and 5‐HT in airway epithelium, probably located in pulmonary neuroendocrine cells (PNECs). RT‐PCR demonstrated that neither sensitization nor antigen challenge modified the 5‐HT2Areceptor mRNA levels.ConclusionsOur results suggested that 5‐HT was involved in the development of AI‐AHR to ACh in guinea‐pigs. Specifically, 5‐HT2A, 5‐HT4and 5‐HT7receptors seem to be particularly involved in this phenomenon. Participation of 5‐HT might probably be favoured by the enhancement of the PNECs 5‐HT content observed after sensitization.Cite this as: P. Segura, M. H. Vargas, G. Córdoba‐Rodríguez, J. Chávez, J. L. Arreola, P. Campos‐Bedolla, V. Ruiz, L. M. García‐Hernández, C. Méndez and L. M. Montaño,Clinical & Experimental Allergy, 2010 (40) 327– 338.
Systemic and local anti-C5 therapy reduces the disease severity in experimental autoimmune uveoretinitis
Authors: Copland D A , Hussain K , Baalasubramanian S , Hughes T R , Morgan B P , Xu H , Dick A D , Nicholson L B 
Published: December 2009

SummaryActivation of complement occurs during autoimmune retinal and intraocular inflammatory disease as well as neuroretinal degenerative disorders. The cleavage of C5 into fragments C5a and C5b is a critical event during the complement cascade. C5a is a potent proinflammatory anaphylatoxin capable of inducing cell migration, adhesion and cytokine release, while membrane attack complex C5b-9 causes cell lysis. Therapeutic approaches to prevent complement-induced inflammation include the use of blocking monoclonal antibodies (mAb) to prevent C5 cleavage. In these current experiments, the rat anti-mouse C5 mAb (BB5.1) was utilized to investigate the effects of inhibition of C5 cleavage on disease progression and severity in experimental autoimmune uveoretinitis (EAU), a model of organ-specific autoimmunity in the eye characterized by structural retinal damage mediated by infiltrating macrophages. Systemic treatment with BB5.1 results in significantly reduced disease scores compared with control groups, while local administration results in an earlier resolution of disease. In vitro, contemporaneous C5a and interferon-γ signalling enhanced nitric oxide production, accompanied by down-regulation of the inhibitory myeloid CD200 receptor, contributing to cell activation. These experiments demonstrate that C5 cleavage contributes to the full expression of EAU, and that selective C5 blockade via systemic and local routes of administration can suppress disease. This presents great therapeutic potential to protect against tissue damage during autoimmune responses in the retina or inflammation-induced degenerative disease.
Four integration patterns: a socio‐technical approach to integration in IS development projects
Authors: Bygstad Bendik , Nielsen Peter Axel , Munkvold Bjørn Erik 
Published: December 2009

AbstractThis paper aims to contribute to a theory of integration within the field of information systems (IS) project management. Integration is a key IS project management issue when new systems are developed and implemented into an increasingly integrated information infrastructure in corporate and governmental organizations. Expanding the perspective of traditional project management research, we draw extensively on central insights from IS research. Building on socio‐technical IS research and software engineering research, we suggest four generic patterns of integration: big bang, stakeholder integration, technical integration and socio‐technical integration. We analyse and describe the advantages and disadvantages of each pattern. The four patterns are ideal types. To explore the forces and challenges in these patterns, three longitudinal case studies were conducted. In particular we investigate the management challenges for each pattern. We find that the patterns are context‐sensitive and describe the different contexts where the patterns are applicable. For IS project management, the four integration patterns are a contribution to the management of integration risks – extending the vocabulary for assessing and mitigating these risks in IS development. For practitioners the four integration patterns represent an analytical framework to be used in planning modern IS development projects.
A comparative study of the spatial distribution of mast cells and microvessels in the foetal, adult human thymus and thymoma
Authors: Raica Marius , Cimpean Anca Maria , Nico Beatrice , Guidolin Diego , Ribatti Domenico 
Published: December 2009

SummaryMast cells (MCs) are widely distributed in human and animal tissues and have been shown to play an important role in angiogenesis in normal and pathological conditions. Few data are available about the relationship between MCs and blood vessels in the normal human thymus, and there are virtually no data about their distribution and significance in thymoma. The aim of this study was to analyse the spatial distribution of MCs and microvessels in the normal foetal and adult thymus and thymoma. Twenty biopsy specimens of human thymus, including foetal and adult normal thymus and thymoma were analysed. Double staining with CD34 and mast cell tryptase was used to count both mast cells and microvessels in the same fields. Computer‐assisted image analysis was performed to characterize the spatial distribution of MCs and blood vessels in selected specimens. Results demonstrated that MCs were localized exclusively to the medulla. Their number was significantly higher in thymoma specimens as compared with adult and foetal normal specimens respectively. In contrast the microvessel area was unchanged. The analysis of the spatial distribution and relationship between MCs and microvessels revealed that only in the thymoma specimens was there a significant spatial association between MCs and microvessels. Overall, these data suggest that MCs do not contribute significantly to the development of the vascular network in foetal and adult thymus, whereas in thymoma they show a close relationship to blood vessels. This could be an expression of their involvement not only in endothelial cells but also in tumour cell proliferation.