bluuebunny/crossref_metadata_2025_split huggingface dataset:
First Report of Downy Mildew on Nursery-Grown Hellebore Caused by Peronospora pulveracea in California
Authors: Warfield C. Y. , Blomquist C. L. , Lovig E. E. 
Published: February 2009

Hellebore or Lenten rose (Helleborus × hybridus) is an evergreen, herbaceous perennial in the family Ranunculaceae. Hellebores are sold as decorative, potted plants and as shade-loving landscape plants favored for their attractive and prolonged blooms in late winter or early spring. In April of 2008, downy mildew-like growth was observed on the foliage of approximately 60 containerized plants of Helleborus ‘Blue Lady’, ‘Pink Lady’, ‘White Lady’, and ‘Royal Heritage’ grown outdoors in a retail nursery in coastal San Mateo County, California. Infected foliage had angular, vein-delimited, dark brown-to-black speckled lesions on adaxial leaf surfaces turning dry and necrotic with age. Young leaves were small and distorted. Affected flowers were spotted and brown. The abaxial sides of affected leaves had light brown-to-purplish downy mildew-like growth. Subhyaline conidia, globose to ellipsoid in shape, ranged from 25 to 31 × 17 to 24 μm (average 28 × 21 μm). Conidiophores ranged from 265 to 375 × 5 to 11.5 μm (average 333 × 8.9 μm), branching dichotomously four to five times in the upper half. Morphological measurements fell within the range previously described for Peronospora pulveracea and P. alpicola, which were reported on Helleborus spp. and Ranunculus aconitifolius, respectively (1,2). DNA sequence of the internal transcribed spacer region of rDNA of our isolate (Genbank Accession No. FJ384778) matched sequences of P. pulveracea (Genbank Accession No. AY198270) and P. alpicola (Genbank Accession No. AY198271) with 100% identity. These two organisms are taxonomically indistinguishable by rDNA sequences and are likely to be the same species (3). To our knowledge, this is the first report of P. pulveracea on Helleborus × hybridus in California and the United States. Lenten rose is commercially propagated by seed, which is a potential pathway for introduction of this pathogen. Mature plants are sold and shipped intra- and interstate as decorative flowering plants or nursery stock. The importance and economic impact of this disease is limited, but significant economic losses could occur during production. References: (1) E. A. Gäumann. Beitr. Kryptogamenflora Schweiz 5:113, 1923. (2) G. Hall. Mycopathologia 126:57, 1994. (3) H. Voglmayr. Mycol. Res. 107:1132, 2003.
First Report of Mountain Hemlock Dwarf Mistletoe (Arceuthobium tsugense subsp. mertensianae) on Sugar Pine (Pinus lambertiana) from Oregon
Authors: Mathiasen R. , Daugherty C. 
Published: February 2009

Mountain hemlock dwarf mistletoe (Arceuthobium tsugense (Rosendahl) G.N. Jones subsp. mertensianae Hawksw. & Nickrent, Viscaceae) commonly parasitizes mountain hemlock (Tsuga mertensiana (Bong.) Carr.) from the central Sierra Nevada Mountains to the southern Cascades in Oregon (1,3). It has also been reported to commonly parasitize whitebark pine (Pinus albicaulis Engelm.) and occasionally western white pine (P. monticola Dougl. ex D. Don) (1,4). In September of 2008, we found mountain hemlock dwarf mistletoe infecting two sugar pines (P. lambertiana Dougl.) 4.5 km north of Windigo Pass, Oregon (42°24′40″N, 123°35′26″W, elevation 2,710 m). One of the sugar pines was 63.5 cm (25 inches) in diameter and had three infections. The other tree was 22.4 cm (9 inches) in diameter, but had 17 infections, many with mistletoe plants that allowed identification of the mistletoe using published descriptions (1,2). Mountain hemlock dwarf mistletoe can be distinguished from sugar pine dwarf mistletoe (A. californicum Hawksw. & Wiens) by its smaller plant size (mean height 5 cm versus 8 cm) and plant color (green-brown versus green to yellow) (1,2). An area (site) of approximately 1 ha around the infected sugar pines was examined and none of the other sugar pines we observed (33 trees) were found to be infected. Because mountain hemlock dwarf mistletoe also occurs in the principal range of sugar pine in the Sierra Nevada Mountains, it may also parasitize this tree there. However, our observations in several mountain hemlock stands infested with mountain hemlock dwarf mistletoe in California have failed to uncover infection of sugar pine by this mistletoe. Therefore, we would tentatively classify sugar pine as a rare host of mountain hemlock dwarf mistletoe (1). Specimens of mountain hemlock dwarf mistletoe on sugar pine were collected and deposited at the Deaver Herbarium (ASC), Northern Arizona University, Flagstaff (Accession No. 87122). To our knowledge, this is the first report of mountain hemlock dwarf mistletoe parasitizing sugar pine. References: (1) F. G. Hawksworth and D. Wiens. USDA For. Serv. Agric. Handb. 709, 1996. (2) F. G. Hawksworth et al. Novon 2:204, 1992. (3) R. L. Mathiasen and C. M. Daugherty. Novon 17:222, 2007. (4) R. L. Mathiasen and F. G. Hawksworth. For. Sci. 34:429, 1988.
First Report of Elm Yellows Phytoplasma Infecting Clover in China
Authors: Li Z. N. , Zheng X. , Wei H. J. , Yu X. Q. , Wu W. J. , Wu Y. F. 
Published: February 2009

In the summer of 2008, phyllody and enlarged petioles resembling symptoms of phytoplasma infection were observed on clover (Trifolium repens) plants in lawns on the campus of Northwest A&F University. Typical phytoplasma-like bacteria were observed in the phloem cells when ultra-thin sections from leaf midrib tissues were examined with transmission electron microscopy. Nested PCR assays were used to verify the association of phytoplasma with the disease. Total DNA was extracted from the phloem of leaf midribs from 20 symptomatic plants and six symptomless plants using the modified CTAB method (1). Using the phytoplasma universal primer pair R16mF2/R16mR1 followed by specific primers R16F2n/R16R2 (4), PCR products of 1.4 and 1.2 kb were amplified, respectively, from symptomatic plants only. Jujube witches'-broom (JWB) and paulownia witches'-broom (PaWB) phytoplasma DNA samples served as controls and were used to study group relationships. After sequencing of the 16S rDNA fragment (GenBank Accession No. FJ436792), a BLAST search determined that the clover phytoplasma shared closest homology (99.6%) with JWB (GenBank Accession No. FJ154846) phytoplasmas compared with lesser identity (90.4%) with PaWB (GenBank Accession No. EF199937). Subsequent restriction fragment length polymorphism analysis of the PCR-amplified 1.2-kb 16S rDNA R16(1)F1/R1 fragment indicated that the phytoplasma associated with the disease belongs to subgroup 16SrV-B of the elm yellows phytoplasma group. Clover phyllody phytoplasma were previously reported to infect clover in Canada (GenBank Accession No. L33762) (3) and Italy (GenBank Accession No. X77482) (2). The phytoplasma reported here shared 86.7 and 90.0% identity with the clover phyllody phytoplasma above, respectively, much lower than that with Elm yellows phytoplasma group. To our knowledge, this is the first report of Elm yellows phytoplasma infecting clover in China. References:(1) E. Angelini et al. Vitis 40:79, 2001. (2) G. Firrao et al. Eur. J. Plant Pathol. 102:817, 1996. (3) N. A. Harrison et al. Plant Pathol. 52:147, 2003. (4) I.-M. Lee et al. Int. J. Syst. Bacteriol. 48:1153, 1998.
First Report of Syringa oblata and S. reticulata Leafroll Disease in China
Authors: Li Z. N. , Min H. , Yan Y. , Zhao Z. , Wu W. J. , Wu Y. F. 
Published: February 2009

Syringa oblata is an important ornamental tree widely grown in China. In September of 2008, S. oblata plants exhibiting symptoms of leafroll and yellowing were found in a garden on the Northwest A&F University campus. Samples were collected from this site. Total DNA was extracted from 0.5 g of phloem tissue from leaf midribs and stems of each sample. DNA samples were analyzed with a nested PCR assay using phytoplasma 16S rDNA universal primers R16mF2/R16mR1 followed by specific primers R16F2n/R16R2 (1), which amplified a 1,452- and 1,246-bp product, respectively. We tested all 30 lilac samples, 20 of which had symptoms of leafroll and yellowing. These produced the expected 1,452- and 1,246-bp PCR products In contrast, the remaining 10 samples from symptomless trees yielded no PCR products. We also surveyed another lilac variety (Syringa reticulata), which is widely grown on the campus, and tested 50 samples with the above method. Again, 1.4- and 1.2-kb PCR products were amplified from all 30 trees displaying leafroll and yellowing symptoms, but not from the other 20 samples from symptomless trees. A comparative analysis of sequences derived from the two hosts showed that the phytoplasmas infecting them were most similar (>99%) to paulownia witches'-broom (PaWB) phytoplasma (GenBank Accession No. EF199937). Restriction fragment length polymorphism (RFLP) analysis of the nested 1.2-kb 16S rDNA products with endonucleases AluI and MseI indicated that all symptomatic plants were infected by the phytoplasmas belonging to aster yellow group (16SrI) subgroup D (16SrI-D) PaWB phytoplasma (2). 16S rDNA sequence comparisons and RFLP analysis of the cloned 16S rDNA from S. oblata (GenBank Accession No. FJ445224) and S. reticulate (GenBank Accession No. FJ445225) indicated that the phytoplasmas infecting them were nearly identical (99.8% identity). To our knowledge, this is the first report of the presence of the phytoplasma associated with a leafroll disease of S. oblata and S. reticulata in China. References: (1) D. E. Gundersen and I.-M. Lee. Phytopathol. Mediterr. 35:144, 1996. (2) I.-M. Lee et al. Int. J. Syst. Bacteriol. 48:1153, 1998.
First Report of Fusarium Wilt Caused by Fusarium oxysporum on Strawberry in Spain
Authors: Arroyo F. T. , Llergo Y. , Aguado A. , Romero F. 
Published: February 2009

In the spring of 2007, wilted and dead strawberry plants (Fragaria × ananassa Duch. cvs. Camarosa and Ventana) were observed in a soilless culture system in Huelva, southwestern Spain. Approximately 8% of the plants in the field died. Isolations from necrotic crowns and roots and necrotic flowers were made on potato dextrose agar after disinfestation in 0.6% NaOCl for 30 s. Colonies with light purple mycelia and beige or orange reverse colony colors developed after 9 days of incubation at 25°C. Colonies produced abundant microconidia, macroconidia, and chlamydospores. Microconidia were hyaline and oval-ellipsoid to cylindrical (5.9 to 9.2 × 2.1 to 3.4 μm). Macroconidia were 3 to 5 septate and fusoid-subulate with a pedicellate base (28.8 to 37.3 × 3.2 to 4.3 μm). Morphology and growth matched descriptions of Fusarium oxysporum Schlechtend emend. Snyder & Hansen (2). A PCR assay for amplification of r-DNA using primers PFO2 and PFO3 established the identity of the isolate as F. oxysporum (1). To confirm the pathogenicity of the fungus, roots of 30-day-old strawberry cvs. Camarosa and Ventana (20 plants each) were inoculated by dipping the roots into a conidial suspension (107 conidia per ml) for 15 min. The inoculated plants were transplanted into plastic pots containing sterilized peat and maintained at 25°C and 100% relative humidity in a growth chamber with a daily 12-h photoperiod of fluorescent light. The pathogenicity test was conducted twice. Within 30 days, all inoculated plants developed wilt symptoms similar to that observed in the field and eventually 75% of the plants died. No symptoms were observed on plants dipped in distilled water. The fungus was successfully reisolated from crowns, roots, and necrotic flowers, fulfilling Koch's postulates. To our knowledge, this is the first report of the occurrence of Fusarium wilt caused by F. oxysporum on strawberry plants in Spain. References: (1) V. Edel et al. Mycol. Res. 104:518, 2000. (2) W. C. Snyder and H. N. Hansen. Am. J. Bot. 27:64, 1940.
Evaluation of Alternative Decay Control Products for Control of Postharvest Rhizopus Soft Rot of Sweetpotatoes
Authors: Edmunds Brooke A. , Holmes Gerald J. 
Published: February 2009

Postharvest Rhizopus soft rot of sweetpotato, caused by Rhizopus stolonifer, is managed by minimizing injuries incurred during harvesting and packing, curing roots immediately after harvest, and applying fungicide during packing. The United States sweetpotato industry relies heavily on a single fungicide (dicloran) to control Rhizopus soft rot, however, many markets (export, infant food, and organic) no longer allow dicloran residues. Dicloran is currently the only fungicide labeled for control of Rhizopus soft rot. Thirty-three products were tested in nine individual experiments over a 5-year period to identify alternative control products. The reduced-risk fungicides boscalid plus pyraclostrobin (Pristine) and fludioxonil (Scholar) significantly reduced Rhizopus soft rot and performed similarly to dicloran. The biological products Bio-Save 10LP and 11LP suppressed Rhizopus soft rot although results were variable among tests. Generally recognized as safe (GRAS) treatments were ineffective in controlling soft rot by our methods. Accepted for publication 1 December 2008. Published 6 February 2009.
Altered early infant gut microbiota in children developing allergy up to 5 years of age
Authors: Sjögren Y. M. , Jenmalm M. C. , Böttcher M. F. , Björkstén B. , Sverremark‐Ekström E. 
Published: February 2009

SummaryBackground
Early colonization with bifidobacteria and lactobacilli is postulated to protect children from allergy, while Clostridium (C.) difficile colonization might be associated with allergic disease. Previous studies of infant gut microbiota in relation to subsequent allergy development have mostly employed culture‐dependent techniques, studied genera of bacteria and the follow‐up period was limited to 2 years.Objective
To relate gut microbiota in early infancy, notably bifidobacteria and lactobacilli at species level, to allergy development during the first 5 years of life and study if environmental factors influence the early infant gut microbiota.Methods
Fecal samples were collected at 1 week, 1 month and 2 months after birth from 47 Swedish infants, followed prospectively to 5 years of age. Bacterial DNA was analysed with real‐time PCR and related to allergy development, family size as well as endotoxin and Fel d 1 levels in house dust samples. Primers binding to C. difficile, four species of bifidobacteria, two lactobacilli groups and Bacteroides fragilis were used. Children regarded as allergic manifested allergic symptoms and were skin prick test positive during their first 5 years while non‐allergic children were neither.Results
Children who developed allergy were significantly less often colonized with lactobacilli group I (Lactobacillus (L.) rhamnosus, L. casei, L. paracasei), Bifidobacterium adolescentis and C. difficile during their first 2 months. Infants colonized with several Bifidobacterium species had been exposed to higher amounts of endotoxin and grew up in larger families than infants harbouring few species.Conclusion
A more diverse gut microbiota early in life might prevent allergy development and may be related to the previously suggested inverse relationship between allergy, family size and endotoxin exposure.
Interleukin‐12 is sufficient to promote antigen‐independent interferon‐γ production by CD8 T cells in old mice
Authors: Rottinghaus Erin K. , Vesosky Bridget , Turner Joanne 
Published: February 2009

SummaryNumerous functional defects have been identified in naive T cells from aged mice, including deficiencies in proliferation, cytokine production and signal transduction. It is well documented that the ratio of naïve to memory T cells significantly decreases with age resulting in the majority of T cells from aged hosts expressing activated/memory T‐cell markers (CD44hi), yet it is unclear whether T cells with a CD44hi phenotype in aged hosts are functionally equivalent to T cells with a similar phenotype in young hosts. We have identified a population of CD44hi CD8 T cells in old mice that are capable of secreting interferon‐γ (IFN‐γ) in response to interleukin‐12 (IL‐12) stimulation. This occurred in the absence of T‐cell receptor engagement, a function that was not observed in CD8 T cells from young mice. This phenotype was associated with increased IL‐12 receptor β2 gene expression and IL‐12 induced signal transducer and activator of transcription 4 (STAT‐4) activation, even when CD8 T‐cell numbers from young and old mice were normalized for CD44hi expression. Furthermore, we demonstrate that IL‐12‐induced STAT‐4 activation was required for T helper type 1 (Th1) cytokine‐induced IFN‐γ production in CD8 T cells. These data illustrate that old mice possess a specialized subset of CD44hi CD8 T cells with an enhanced responsiveness to IL‐12, enabling these cells to produce substantial amounts of IFN‐γ in response to Th1 cytokine stimulation. We have therefore identified a functional difference in the populations of CD44hi CD8 T cells from young and old mice, and believe that understanding age‐associated immunological changes is essential for helping the elderly combat deadly diseases.
Astrocyte elevated gene‐1 (AEG‐1) is induced by lipopolysaccharide as toll‐like receptor 4 (TLR4) ligand and regulates TLR4 signalling
Authors: Khuda Imtiaz I‐E. , Koide Naoki , Noman Abu S. M. , Dagvadorj Jargalsaikhan , Tumurkhuu Gantsetseg , Naiki Yoshikazu , Komatsu Takayuki , Yoshida Tomoaki , Yokochi Takashi 
Published: February 2009

SummaryAstrocyte elevated gene‐1 (AEG‐1) is induced by human immunodeficiency virus 1 (HIV‐1) infection and involved in tumour progression, migration and invasion as a nuclear factor‐κB (NF‐κB) ‐dependent gene. The involvement of AEG‐1 on lipopolysaccharide (LPS) ‐induced proinflammatory cytokine production was examined. AEG‐1 was induced via NF‐κB activation in LPS‐stimulated U937 human promonocytic cells. AEG‐1 induced by LPS subsequently regulated NF‐κB activation. The prevention of AEG‐1 expression inhibited LPS‐induced tumour necrosis factor‐α and prostaglandin E2 production. The AEG‐1 activation was not induced by toll‐like receptor ligands other than LPS. Therefore, AEG‐1 was suggested to be a LPS‐responsive gene and involved in LPS‐induced inflammatory response.
Suppression of antitumour protective cytotoxic T lymphocyte responses to a human papillomavirus 16 E7 DNA vaccine by coinjection of interleukin‐12 complementary DNA: involvement of nitric oxide in immune suppression
Authors: Sin Jeong‐Im 
Published: February 2009

SummaryInterleukin‐12 (IL‐12) has been shown to enhance cellular immunity in vitro and in vivo. The beneficial roles of IL‐12 as a DNA vaccine adjuvant have been commonly observed. Here the impact of IL‐12 complementary DNA (cDNA) as an adjuvant for a human papillomavirus (HPV) type 16 E7 DNA vaccine is investigated in a mouse tumour model. Coinjection of E7 DNA vaccine with IL‐12 cDNA completely suppressed antigen‐specific cytotoxic T‐lymphocyte (CTL) responses, leading to a complete loss of antitumour protection from a tumour cell challenge. In addition, antigen‐specific antibody and T helper cell proliferative responses were also suppressed by IL‐12 cDNA coinjection. This inhibition was observed over different IL‐12 cDNA doses. Furthermore, separate leg injections of IL‐12 and E7 cDNAs suppressed antigen‐specific CTL and tumour protective responses, but not antibody and T helper cell proliferative responses, suggesting different pathways for suppression of these two separate responses. Further knockout animal studies demonstrated that interferon‐γ and nitric oxide are not directly associated with suppression of antigen‐specific antibody responses by IL‐12 cDNA coinjection. However, nitric oxide was found to be involved in suppression of antigen‐specific CTL and tumour protective responses by IL‐12 cDNA coinjection. These data suggest that coinjection of IL‐12 cDNA results in suppression of E7‐specific CTL responses through nitric oxide, leading to a loss of antitumour resistance in this DNA vaccine model. This study further shows that the adjuvant effect of IL‐12 is dependent on the antigen types tested.
A central role for monocytes in Toll‐like receptor‐mediated activation of the vasculature
Authors: Ward Jon R. , Francis Sheila E. , Marsden Luke , Suddason Tesha , Lord Graham M. , Dower Steven K. , Crossman David C. , Sabroe Ian 
Published: February 2009

SummaryThere is increasing evidence that activation of inflammatory responses in a variety of tissues is mediated co‐operatively by the actions of more than one cell type. In particular, the monocyte has been implicated as a potentially important cell in the initiation of inflammatory responses to Toll‐like receptor (TLR)‐activating signals. To determine the potential for monocyte‐regulated activation of tissue cells to underpin inflammatory responses in the vasculature, we established cocultures of primary human endothelial cells and monocytes and dissected the inflammatory responses of these systems following activation with TLR agonists. We observed that effective activation of inflammatory responses required bidirectional signalling between the monocyte and the tissue cell. Activation of cocultures was dependent on interleukin‐1 (IL‐1). Although monocyte‐mediated IL‐1β production was crucial to the activation of cocultures, TLR specificity to these responses was also provided by the endothelial cells, which served to regulate the signalling of the monocytes. TLR4‐induced IL‐1β production by monocytes was increased by TLR4‐dependent endothelial activation in coculture, and was associated with increased monocyte CD14 expression. Activation of this inflammatory network also supported the potential for downstream monocyte‐dependent T helper type 17 activation. These data define co‐operative networks regulating inflammatory responses to TLR agonists, identify points amenable to targeting for the amelioration of vascular inflammation, and offer the potential to modify atherosclerotic plaque instability after a severe infection.
Multiple Tissue Markers in Human Malignant Testicular Tumours
Authors: HEYDERMAN E. 
Published: February 2009

Using an indirect immunoperoxidase technique, the localization of human chorionic gonadotrophin (HCG), human placental lactogen (HPL), carcinoembryonic antigen (CEA) and alphafoetoprotein (AFP) has been achieved in paraffin embedded sections of human malignant testicular tumours. HCG was localized in the syncytiotrophoblast of trophoblastic teratomas, in morphologically distinctive cells of many teratomas classified as ‘non‐trophoblastic’ and in some seminomas. The presence of such cells showed good correlation with the development of elevated serum/urine HCG levels on or before overt tumour recurrence. HPL had a similar but more restricted distribution. CEA was demonstrated in areas showing intestinal‐like differentiation. AFP could be readily demonstrated in tumours with yolk sac differentiation, although widespread diffusion made accurate localization difficult.The routine localization of these tumour products may be of potential value in improving the diagnosis and classification of malignant testicular disease. Preliminary results also indicate that such an approach may have a role in predicting suitable serum markers with which to monitor disease activity and in providing further prognostic criteria.