bluuebunny/crossref_metadata_2025_split huggingface dataset:
First Report of Tomato chlorosis virus Infecting Tomato in Single and Mixed Infections with Tomato yellow leaf curl virus in Cuba
Authors: Martínez-Zubiaur Y. , Fiallo-Olivé E. , Carrillo-Tripp J. , Rivera-Bustamante R. 
Published: April 2008

Whitefly-transmitted viruses have caused severe losses in tomato crops (Solanum lycopersicum) in Cuba. In 2006 and 2007, tomato greenhouses across eastern Cuba exhibited high levels of Bemisia tabaci (B biotype) infestation. Some plants showed interveinal chlorosis and a severe yellow mosaic, combined with leaf brittleness. These symptoms were different from those induced by Tomato yellow leaf curl virus (TYLCV-IL(CU)). Only 12 of 31 symptomatic samples resulted in positive PCR assays with TYLCV-specific primers (CTGAATGTTTGGATGGAAATGTGC and GCTCGTAAGTTTCCTCAACGGAC). A reverse transcription (RT)-PCR analysis for Tomato chlorosis virus (ToCV) with generic (HS-11/HS-12) and specific primers (ToC-5/ToC-6) was also carried out (2). Sequence analysis of the cloned RT-PCR products (463 bp) confirmed the presence of ToCV in Cuba. The fragment had 97 to 98% identity with GenBank isolates from Spain (DQ136146), Florida (AY903448), and Reunion Island, France (AJ968396). Cloned TYLCV and ToCV amplicons were used as probes to reanalyze the selected 31 samples by a dot-blot hybridization assay in search of mixed infections (1). The assay showed 16 samples to be positive for ToCV, 4 for TYLCV, 8 for both, and 3 samples were negative. To our knowledge, this is the first report of ToCV and TYLCV/ToCV mixed infections in Cuba. References: (1) Y. Abou-Jawdha et al. Plant Dis. 90:378, 2006. (2) C. I. Dovas et al. Plant Dis. 86:1345, 2002.
Photodynamic therapy with recombinant adenovirus AdmIL‐12 enhances anti‐tumour therapy efficacy in human papillomavirus 16 (E6/E7) infected tumour model
Authors: Park Eun Kyung , Bae Su‐Mi , Kwak Sun‐Young , Lee Sung Jong , Kim Yong‐Wook , Han Chan‐Hee , Cho Hyun‐Jung , Kim Kyung Tae , Kim Young‐Jae , Kim Hyun‐Jung , Ahn Woong Shick 
Published: April 2008

SummaryImmunotherapy with photodynamic therapy (PDT) offers great promise as a new alternative for cancer treatment; however, its use remains experimental. Here we investigated the utility of adenoviral delivery of interleukin‐12 (AdmIL‐12) as an adjuvant for PDT in mouse tumour challenge model. PDT was performed by irradiating Radachlorin in C57BL/6 mice transplanted with TC‐1 cells. PDT plus AdmIL‐12 treatment for tumour suppression as well as specific immune responses were evaluated with the following tests: in vitro and in vivo tumour growth inhibition, interferon‐γ (IFN‐γ) and tumour necrosis factor‐α (TNF‐α) assay, and cytotoxic T lymphocyte (CTL) assay. Direct intratumoral injection of AdmIL‐12 resulted in a significant suppression of tumour growth compared to the control group. Treatment of PDT along with AdmIL‐12 further enhanced antitumour effects significantly higher than either AdmIL‐12 or PDT alone. This combined treatment resulted in complete regression of 9‐mm sized tumour in every animal. We also evaluated immune responses induced by these treatments. Combined treatment significantly increased the production level of IFN‐γ and TNF‐α compared with that by AdmIL‐12 or PDT alone. PDT plus AdmIL‐12 enhanced antitumour immunity through increased expansion of the CTL subset mediated by CD8+ T cells. Taken together, these results indicate that the high anti‐cancer activity of PDT with AdmIL‐12 is a powerful tool against cancer therapy and is a promising subject for further investigation.
Cachexia in the non‐obese diabetic mouse is associated with CD4+ T‐cell lymphopenia
Authors: Zhao Chunfang , Wang Zhuanzhi , Robertson Michael W. , Davies Joanna D. 
Published: April 2008

SummaryOne of the long‐term consequences of Type I diabetes is weight loss with muscle atrophy, the hallmark phenotype of cachexia. A number of disorders that result in cachexia are associated with immune deficiency. However, whether immune deficiency is a cause or an effect of cachexia is not known. This study examines the non‐obese diabetic mouse, the mouse model for spontaneous Type I diabetes, as a potential model to study lymphopenia in cachexia, and to determine whether lymphopenia plays a role in the development of cachexia. The muscle atrophy seen in patients with Type I diabetes involves active protein degradation by activation of the ubiquitin–proteasome pathway, indicating cachexia. Evidence of cachexia in the non‐obese diabetic mouse was determined by measuring skeletal muscle atrophy, activation of the ubiquitin–proteasome pathway, and apoptosis, a state also described in some models of cachexia. CD4+ T‐cell subset lymphopenia was measured in wasting and non‐wasting diabetic mice. Our data show that the mechanism of wasting in diabetic mice involves muscle atrophy, a significant increase in ubiquitin conjugation, and upregulation of the ubiquitin ligases, muscle RING finger 1 (MuRF1) and muscle atrophy F box/atrogin‐1 (MAFbx), indicating cachexia. Moreover, fragmentation of DNA isolated from atrophied muscle tissue indicates apoptosis. While CD4+ T‐cell lymphopenia is evident in all diabetic mice, CD4+ T cells that express a very low density of CD44 were significantly lost in wasting, but not non‐wasting, diabetic mice. These data suggest that CD4+ T‐cell subsets are not equally susceptible to cachexia‐associated lymphopenia in diabetic mice.
Differential regulation of SOCS‐1 signalling in B and T lymphocytes by hepatitis C virus core protein
Authors: Yao Zhi Qiang , Prayther Deborah , Trabue Christopher , Dong Zhi Ping , Moorman Jonathan 
Published: April 2008

SummaryHepatitis C virus (HCV) infection is characterized by a strong propensity toward chronicity, autoimmune phenomena and lymphomagenesis, supporting a role for lymphocyte dysregulation during persistent viral infection. We have shown that HCV core protein inhibits T‐cell functions through interaction with a complement receptor, gC1qR. Here, we further report that B cells also express gC1qR that can be bound by HCV core protein. Importantly, using flow cytometry, we demonstrated differential regulation of B and T lymphocytes by the HCV core–gC1qR interaction, with down‐regulation of CD69 activation in T cells but up‐regulation of CD69 activation and cell proliferation in B cells. HCV core treatment led to decreased interferon‐γ production in CD8+ T cells but to increased immunoglobulin M and immunoglobulin G production as well as cell surface expression of costimulatory and chemokine receptors, including CD86 (B7‐2), CD154 (CD40L) and CD195 (CCR5), in CD20+ B cells. Finally, we showed down‐regulation of suppressor of cytokine signalling‐1 (SOCS‐1) using real‐time reverse transcription–polymerase chain reaction, accompanied by up‐regulation of signal transducer and activator of transcription‐1 (STAT1) phosphorylation in B cells in response to HCV core protein, with the opposite pattern observed in HCV core‐treated T cells. This study demonstrates differential regulation of B and T lymphocytes by HCV core and supports a mechanism by which lymphocyte dysregulation occurs in the course of persistent HCV infection.
Defective T‐cell function leading to reduced antibody production in a kleisin‐β mutant mouse
Authors: Gosling Katharine M. , Goodnow Christopher C. , Verma Naresh K. , Fahrer Aude M. 
Published: April 2008

SummaryThe recently described nessy (Ncaph2nes/nes) mutant mouse strain has a defect in T‐cell development caused by a mutation in the ubiquitous kleisin‐β (also known as Ncaph2). Kleisin‐β is a subunit of the condensin II complex involved in chromosome condensation during mitosis. The nessy phenotype is characterized by CD44hi CD8+ peripheral T cells, 10–20% of normal thymocyte numbers and 2·5‐fold fewer αβ T cells in the spleen compared with wild‐type mice. In this study we examined the effect of the nessy mutation in kleisin‐β on the immune response by challenging mice with an attenuated strain of Salmonella. Results showed that nessy mice control bacterial load as effectively as wild‐type mice but exhibit a reduced antibody titre. Further experiments revealed that while the T‐dependent antibody response was diminished in nessy mice the T‐independent response was normal, suggesting that the defect was the result of T‐cell function and not B‐cell function. In vitro activation assays showed that nessy T cells have a lower capacity to up‐regulate the early activation marker CD69 than wild‐type T cells. Upon transfer into RAG−/− mice, nessy and wild‐type CD4 T cells showed equivalent homeostatic proliferation, while nessy CD8 T cells proliferated more than their wild‐type counterparts. When cultured with anti‐T‐cell receptor β or concanavalin A, nessy T cells were found to die faster than wild‐type T cells. These data indicate that kleisin‐β is required for a normal immune response, and represent the first demonstration of a role for kleisin‐β in T‐cell function.
Human B cells express the orphan chemokine receptor CRAM‐A/B in a maturation‐stage‐dependent and CCL5‐modulated manner
Authors: Hartmann Tanja N. , Leick Marion , Ewers Susann , Diefenbacher Andrea , Schraufstatter Ingrid , Honczarenko Marek , Burger Meike 
Published: April 2008

SummaryChemokines orchestrate the organization of leucocyte recruitment during inflammation and homeostasis. Despite growing knowledge of chemokine receptors, some orphan chemokine receptors are still not characterized. The gene CCRL2 encodes such a receptor that exists in two splice variants, CRAM‐A and CRAM‐B. Here, we report that CRAM is expressed by human peripheral blood and bone marrow B cells, and by different B‐cell lines dependent on the B‐cell maturation stage. Intriguingly, CRAM surface expression on the pre‐B‐cell lines Nalm6 and G2 is specifically upregulated in response to the inflammatory chemokine CCL5 (RANTES), a chemokine that is well known to play an important role in modulating immune responses. Although Nalm6 cells do not express any of the known CCL5 binding receptors, extracellular signal‐regulated kinases 1 and 2 (ERK1/2) are phosphorylated upon CCL5 stimulation, suggesting a direct effect of CCL5 through the CRAM receptor. However, no calcium mobilization or migratory responses upon CCL5 stimulation are induced in B‐cell lines or in transfected cells. Also, ERK1/2 phosphorylation cannot be inhibited by pertussis toxin, suggesting that CRAM does not couple to Gi proteins. Our results describe the expression of a novel, non‐classical chemokine receptor on B cells that is potentially involved in immunomodulatory functions together with CCL5.
Managing change in an information systems development organization: understanding developer transitions from a structured to an object‐oriented development environment1
Authors: Shaft Teresa M. , Albert Leslie Jordan , Jasperson Jon (Sean) 
Published: April 2008

Abstract.  Object‐oriented systems development has attracted great interest in the information systems (IS) field because of a belief that using object‐oriented development (OD) makes it easier to develop and maintain software plus achieve software reuse. However, the transition from structured to OD may be especially challenging for IS developers. In fact, some argue that structured development (SD) knowledge may interfere with the ability to learn OD approaches because of a form of proactive interference.To understand how knowledge of SD concepts influences the ability to gain OD knowledge, we assessed a team of IS developers' understanding of structured and object‐oriented concepts at the beginning of their first OD project and repeated our assessment 1 year later. Developers increased their understanding of some object‐oriented concepts, but these changes were associated with increases in understanding of one of the SD concepts. Further, at the beginning and end of the project, developers' mental models were highly consistent with one another and that of an OD expert with regard to most OD concepts. It appears that the formal training that developers received allowed them to attain a good understanding of most object‐oriented concepts. These findings challenge the idea that structured developers must ‘unlearn’ SD to adopt OD approaches. Future research may wish to examine the different types of software development knowledge to ascertain which are amenable to positive transfer and which are more likely to suffer from proactive interference.
Cardiac involvement in adults with Pompe disease
Authors: Soliman O. I. I. , Van Der Beek N. A. M. E. , Van Doorn P. A. , Vletter W. B. , Nemes A. , Van Dalen B. M. , Ten Cate F. J. , Van Der Ploeg A. T. , Geleijnse M. L. 
Published: April 2008

Abstract.Background.  Glycogen storage disease type II or Pompe disease is a neuromuscular disorder caused by deficiency of lysosomal acid α‐ glucosidase. Classic infantile Pompe disease results in massive left ventricular (LV) hypertrophy and failure. Although Pompe disease is often included in the differential diagnosis of LV hypertrophy the true frequency of cardiac involvement in adults with Pompe disease is not known.Methods.  Forty‐six consecutive adult patients (mean age 48 ± 12, 22 men) with Pompe disease were included. Each patient underwent a clinical examination, electrocardiography, and rest and low‐dose dobutamine (in 20 patients) two‐dimensional echocardiography including contrast and tissue Doppler imaging.Results.  All patients had limited exercise tolerance; a rollator walking aid was used in seven patients (15%), a wheelchair in 13 patients (28%), and assisted ventilation in 14 patients (30%). Prior to this study, one patient was known with permanent atrial fibrillation, His‐bundle ablation and a VVI pacemaker and another patient was known with fluid retention. The first patient had increased LV end‐diastolic diameter, impaired LV ejection fraction, low systolic mitral annular velocities and diastolic dysfunction grade II. The patient with fluid retention was wheelchair bound and dependent on 24‐h assisted ventilation and showed right ventricular and LV hypertrophy (septum 16 mm, posterior wall 15 mm). LV hypertrophy was not seen in any of the other patients. One woman of advanced age had isolated low systolic mitral annular velocities. Mean global systolic LV function, including contractile reserve, was not decreased in patients with Pompe disease. Eight patients (17%) had mild diastolic dysfunction grade I, related to hypertension in four and advanced age in seven.Conclusions.  In adult patients with Pompe disease without objective signs of cardiac affection by 12‐leads electrocardiography or physical examination, echocardiographic screening for LV hypertrophy seems not effective.
Developing Antibacterial Vaccines in Genomics and Proteomics Era
Authors: Kaushik D. K. , Sehgal D. 
Published: April 2008

AbstractInfectious diseases are the greatest cause of global morbidity and mortality. About half of this burden is caused by pathogenic bacteria. One of the most effective ways to prevent infectious diseases is to use vaccines. Limitations in the traditional approaches may be one of the reasons why vaccines are yet not available against some infectious bacterial agents. Recent advancements in high‐throughput ‘omics’ technologies and the availability of complete genome sequences of microbial pathogens and multiple isolates of the same species have dramatically changed the time frame and scope for identifying novel vaccine candidates. At present, 582 microbial genomes have been sequenced and sequencing of 1733 is in progress. There are more than 50 bacterial species for which the genome sequence is available for three or more isolates. Development of tools for in silico analysis has led to the identification of novel virulence genes, metabolic pathways and cell surface proteins that represent potential new targets for anti‐microbial drug and vaccine strategies. In this review, we provide an overview of the ‘omics’‐based techniques that can be used to advance and accelerate the discovery of vaccine candidates against extracellular bacterial pathogens. By citing specific examples, we discuss how high‐throughput molecular profiling techniques, such as genomics, transcriptomics and proteomics have contributed to the discovery of novel vaccine candidates. We end by contemplating on the emerging technologies that are likely to have a high impact on the field of vaccinology in the near future.
Plant virus infection‐induced persistent host gene downregulation in systemically infected leaves
Authors: Havelda Zoltán , Várallyay Éva , Válóczi Anna , Burgyán József 
Published: April 2008

SummaryUnderstanding of virus infection‐induced alterations in host plant gene expression and metabolism leading to the development of virus disease symptoms is both scientifically and economically important. Here, we show that viruses belonging to various RNA virus families are able to induce efficient host gene mRNA downregulation (shut‐off) in systemically infected leaves. We demonstrate that the host gene mRNA shut‐off overlaps spatially with virus‐occupied sectors, indicating the direct role of virus accumulation in this phenomenon. The establishment of shut‐off was not directly connected to active viral replication or the RNA‐silencing machinery. Importantly, the induced shut‐off phenomenon persisted for several weeks, resulting in severe deficiency of mRNA for important housekeeping genes in the infected plants. Interestingly, we found that some other RNA viruses do not induce or only slightly induce the shut‐off phenomenon for the same set of genes, implicating genetic determination in this process. Nuclear run‐on experiments suggest that plant viruses, similarly to animal viruses, mediate suppression of host mRNA synthesis in the nucleus. By investigating various host–virus interactions, we revealed a correlation between the intensity of the shut‐off phenomenon and the severity of disease symptoms. Our data suggest that efficient and persistent downregulation of host genes may be an important component of symptom development in certain host–virus interactions.
Cytokinins negatively regulate the root iron uptake machinery in Arabidopsis through a growth‐dependent pathway
Authors: Séguéla Mathilde , Briat Jean‐François , Vert Grégory , Curie Catherine 
Published: April 2008

SummaryPlants display a number of biochemical and developmental responses to low iron availability in order to increase iron uptake from the soil. The ferric‐chelate reductase FRO2 and the ferrous iron transporter IRT1 control iron entry from the soil into the root epidermis. In Arabidopsis, expression of IRT1 and FRO2 is tightly controlled to maintain iron homeostasis, and involves local and long‐distance signals, as well as transcriptional and post‐transcriptional events. FIT encodes a putative basic helix‐loop‐helix (bHLH) transcription factor that regulates iron uptake responses in Arabidopsis. Here, we uncover a new regulation of the root iron uptake genes. We show that IRT1, FRO2 and FIT are repressed by the exogenous addition of cytokinins (CKs), and that this repression acts at the level of transcript accumulation, and depends on the AHK3 and CRE1 CK receptors. The CKs and iron‐deficiency signals act through distinct pathways to regulate the soil iron uptake genes, as (i) CK repression is independent of the iron status, (ii) IRT1 and FRO2 downregulation is unchanged in a fit loss‐of‐function mutant, indicating that FIT does not mediate CK repression, and (iii) the iron‐regulated genes AtNRAMP3 and AtNRAMP4 are not downregulated by CKs. We show that root growth‐inhibitory conditions, such as abiotic stresses (mannitol, NaCl) and hormonal treatments (auxin, abscissic acid), repress the iron starvation response genes. We propose that CKs control the root iron uptake machinery through a root growth dependent pathway in order to adapt nutrient uptake to the demand of the plant.
RLM3, a TIR domain encoding gene involved in broad‐range immunity of Arabidopsis to necrotrophic fungal pathogens
Authors: Staal Jens , Kaliff Maria , Dewaele Ellen , Persson Mattias , Dixelius Christina 
Published: April 2008

SummaryHere, we describe the rapid cloning of a plant gene, Leptosphaeria maculans 3 (RLM3Col), which encodes a putative Toll interleukin‐1 receptor‐nucleotide binding (TIR‐NB) class protein, which is involved in defence against the fungal pathogen L. maculans and against three other necrotrophic fungi. We have, through microarray‐based case control bulk segregant comparisons of transcriptomes in pools of Col‐0 × An‐1 progeny, identified the absence of a locus that causes susceptibility in An‐1. The significance of this locus on chromosome 4 for L. maculans resistance was supported by PCR‐based mapping, and denoted resistance to RLM3Col. Differential susceptible phenotypes in four independent T‐DNA insertion lines support the hypothesis that At4g16990 is required for RLM3Col function. The mutants in RLM3Col also exhibited an enhanced susceptibility to Botrytis cinerea, Alternaria brassicicola and Alternaria brassicae. Complementations of An‐1 and T‐DNA mutants using overexpression of a short transcript lacking the NB‐ARC domain, or a genomic clone, restored resistance to all necrotrophic fungi. The elevated expression of RLM3Col on B. cinerea‐susceptible mutants further suggested convergence in signalling and gene regulation between defence against B. cinerea and L. maculans. In the case of L. maculans, RLM3Col is required for efficient callose deposition downstream of RLM1Col.
Mixed‐linkage β‐glucan : xyloglucan endotransglucosylase, a novel wall‐remodelling enzyme from Equisetum (horsetails) and charophytic algae
Authors: Fry Stephen C. , Mohler Kyle E. , Nesselrode Bertram H.W.A. , Franková Lenka 
Published: April 2008

SummaryMixed‐linkage (1→3,1→4)‐β‐d‐glucan (MLG), a hemicellulose long thought to be confined to certain Poales, was recently also found in Equisetum; xyloglucan occurs in all land plants. We now report that Equisetum possesses MLG:xyloglucan endotransglucosylase (MXE), which is a unique enzyme that grafts MLG to xyloglucan oligosaccharides (e.g. the heptasaccharide XXXGol). MXE occurs in all Equisetum species tested (Equisetum arvense, Equisetum fluviatile, Equisetum hyemale, Equisetum scirpoides, Equisetum telmateia and Equisetum variegatum), sometimes exceeding xyloglucan endotransglucosylase (XET) activity. Charophytic algae, especially Coleochaete, also possess MXE, which may therefore have been a primordial feature of plant cell walls. However, MXE was negligible in XET‐rich extracts from grasses, dicotyledons, ferns, Selaginella and bryophytes. This and the following four additional observations indicate that MXE activity is not the result of a conventional xyloglucan endotransglucosylase/hydrolase (XTH): (i) XET, but not MXE, activity correlates with the reaction rate on water‐soluble cellulose acetate, hydroxyethylcellulose and carboxymethylcellulose, (ii) MXE and XET activities peak in old and young Equisetum stems, respectively, (iii) MXE has a higher affinity for XXXGol (Km ∼ 4 μM) than any known XTH, (iv) MXE and XET activities differ in their oligosaccharide acceptor‐substrate preferences. High‐molecular‐weight (Mr) xyloglucan strongly competes with [3H]XXXGol as the acceptor‐substrate of MXE, whereas MLG oligosaccharides are poor acceptor‐substrates. Thus, MLG‐to‐xyloglucan grafting appears to be the favoured activity of MXE. In conclusion, Equisetum has evolved MLG plus MXE, potentially a unique cell wall remodelling mechanism. The prominence of MXE in mature stems suggests a strengthening/repairing role. We propose that cereals, which possess MLG but lack MXE, might be engineered to express this Equisetum enzyme, thereby enhancing the crop mechanical properties.