bluuebunny/crossref_metadata_2025_split huggingface dataset:
First Report of Alternaria Brown Spot of Citrus Caused by Alternaria alternata in Yunnan Province, China
Authors: Wang X. F. , Li Z. A. , Tang K. Z. , Zhou C. Y. , Yi L. 
Published: February 2010

Brown spot of citrus is considered a major problem on the fruit of many citrus cultivars grown for fresh markets including tangerines (Citrus reticulata) and their hybrids. It causes lesions on leaves, stems, and fruit and reduces yield and fruit quality (2). In 2003 in southern Wenshan Municipality, Yunnan Province in China, sporadic occurrence of Alternaria brown spot was observed on Tangfang mandarin, a local citrus cultivar identified preliminarily as a kind of mandarin hybrid. From 2006 to 2008, nearly 80% of local orchards were infected with the disease. Fruit symptoms typical of Alternaria brown spot ranging from light brown, slightly depressed spots to circular and dark brown areas were observed. Leaves showed small, brown, circular spots and irregular blighted areas with characteristic yellow halos. Tissues from the margin of fruit spots or infected leaf parts of eight different trees were surface sterilized in 1.5% sodium hypochlorite for 1 min, plated on potato dextrose agar (PDA), and then incubated at 27°C in the dark for 1 week. Dark brown mycelia and pigmented septate conidia with lengths of 10 to 35 μm and widths of 5 to 13 μm were produced. On the basis of conidial morphological characteristics, the pathogen was identified as Alternaria alternata (Fr.:Fr.) Keissl (1). Detached young healthy leaves of ‘Minneola’ tangelo (C. reticulata × C. paradisi) were sprayed with a conidial suspension of 105 conidia per ml and incubated in a moist chamber at 27°C. A control treatment with an equal number of leaves was sprayed with distilled water only. After 48 h, seven of these isolates caused necrotic lesions on detached leaves, characteristic of the disease, whereas there were no symptoms on leaves of the water control. Pure cultures were recovered on PDA from symptomatic tissues and the morphological characteristics of the conidia closely fit the description of A. alternata, confirming Koch's postulates. Currently, the distribution of Alternaria brown spot of citrus is confined to southern Wenshan Municipality in Yunnan Province where it is a serious disease problem on the most important commercial cultivar in this region. The identification of the pathogen now allows for appropriate field management and control measures. To our knowledge, this is the first report of Alternaria brown spot of citrus in China. References: (1) Z. Solel. Plant Pathol. 40:145, 1991. (2) J. O. Whiteside. Plant Dis. Rep. 60:326, 1976.
First Report of the Stubby Root Nematode, Paratrichodorus minor, in Mainland China
Authors: Li X. , Guo K. , Zhang Y. , Yan X. , Zheng J. 
Published: February 2010

The stubby root nematode, Paratrichodorus minor (Colbran, 1956) Siddiqi, 1974, is an economically important species. It not only causes direct damage to the meristemic tissues of plants, but also can be a vector of Tobacco rattle virus and Pepper ringspot virus (2). It has been documented in Afghanistan, Argentina, Australia, Brazil, Canary Islands, Cuba, Egypt, Fiji, India, Israel, Ivory Coast, Japan, Java, Mauritania, New Zealand, Nicaragua, Philippines, Puerto Rico, Senegal, South Africa, Taiwan, Upper Volta, the United States, the former USSR, and Venezuela (1). During a recent investigation on Trichodoridae occurring in China, eight stubby root nematode populations were detected in Hainan, Yunnan, and Fujian provinces in the rhizospheres of eggplant (Solanum melongena), Chinaberry (Melia azedarach), lettuce (Lactuca sativa), longan (Dimocarpus longan), peach (Prunus persica), pear (Pyrus sp.), and walnut (Juglans regia) in soils ranging from clay to sand. The eight populations had similar morphological and molecular characters. The females were cigar shaped with rod-shaped vaginal sclerotization parallel to the longitudinal body axis with a quadrangular vagina in side view having a short vulval slit. The key morphometrics of females were consistent with those of P. minor: body length, 631 to 757 μm; body diameter, 27 to 43 μm; onchiostyle, 35 to 36 μm; a, 18 to 24; b, 4.9 to 5.5; v%, 53 to 55; length of vagina, 10.8 to 11.1 μm; and size of vaginal pieces, 1.7 to 1.9 μm. Males in P. minor are rare and were not found in any of the eight populations. Partial sequences of the 18s RNA gene of each population were amplified with forward primer 5′-AAA GAT TAA GCC ATG CAT G-3′ (2), and reverse primer 5′-AGT CAA ATT AAG CCG CAG-3′ (3), which yielded a PCR fragment of 1,153 bp. PCR products from all eight populations were sequenced and submitted to GenBank and assigned Accession Nos. GQ995703, GQ995704, GQ995705, GQ995706, GQ995707, GQ995708, GQ995709, and GQ995710. The sequences exhibited 99.8 to 100% similarity with those of P. minor isolates DQ345526, AM269897, AJ438052, AJ438053, and AJ438058 from GenBank. Morphological and molecular identification confirmed that all populations were P. minor. To our knowledge, this is the first report of P. minor in mainland China. References: (1) K. Boutsika et al. Nematology 6:145, 2004. (2) W. Decramer. The Family Trichodiridae: Stubby Root and Virus Vector Nematodes. Kluwer Academic Publishers, Dordrecht, the Netherlands, 1995. (3) I. S. Waite et al. Soil Biol. Biochem. 35:1165, 2003.
Occurrence of Potato Soft Rot Caused by Erwinia carotovora (synonym Pectobacterium carotovorum) in Nepal: A First Report
Authors: Lamichhane J. R. , Balestra G. M. , Varvaro L. 
Published: February 2010

Potato (Solanum tuberosum L.) is the fourth most important major crop of Nepal after rice, corn, and wheat, with an annual production of 1.94 million t and 153,000 ha of harvested area. It is a staple food crop in the remote hilly areas and the main vegetable in other parts of the country. Potato is grown in all three major agricultural zones (high hills, mid hills, and plain land) of Nepal, at an altitude ranging from 60 m to more than 4,000 m. Erwinia carotovora causes soft rot worldwide on a wide range of hosts including potato, carrot, and cabbage. During the spring of 2009, a soft rot with a foul smell was noted in stored potato tubers of different local cultivars, especially Rato Alu and Seto Alu, in the Kathmandu District, central region of Nepal. Symptoms on tubers appeared as tan, water-soaked areas with watery ooze. The rotted tissues were white-to-cream colored. Seven different potato fields, where the stored tubers originated, were surveyed and 23 samples consisting of approximately three symptomatic tubers were collected. Bacteria were successfully isolated from all diseased tissues on nutrient agar supplemented with 5% sucrose and incubated at 26 ± 1°C. After purification on tripticase soy agar medium, 17 isolates were identified as E. carotovora by the following deterministic tests: all strains were gram-negative rods; oxidase negative; facultatively anaerobic; able to degrade pectate; sensitive to erythromycin; negative for phosphatase; unable to produce acid from α-methyl-glucoside; and produced acid from trehalose. Pathogenicity of the strains was evaluated by depositing a bacterial suspension (106 CFU/ml) on potato slices (cv. Monalisa) and incubating at 30 ± 1°C. A reference strain of E. carotovora subsp. carotovora (NCPPB 2577) and sterile distilled water were used, respectively, as positive and negative controls. All strains caused soft rot within a week. Bacteria were reisolated from the slices and were shown to be identical to the original strains according to the above morphological, cultural, and biochemical tests. A 1,430-bp region of the 16S rDNA from all strains was amplified with primers NOC 1F (AGAGTTTGATCATGGCTCAG) and NOC 3R (ACGGTTACCTTGTTACGACTT) and sequenced (GenBank Accession No. GU075708; strain NEP ECC09). A BlastN search of GenBank revealed that the strains had 100% nt identity with the 16S rDNA sequence of E. carotovora subsp. carotovora type strain ATCC 15713 (GenBank Accession No. U80197). The finding of this pathogen is of fundamental value since this crop represents one of the economically important crops of Nepal. This pathogen has already been reported in the countries of China and India (1) with whom Nepal shares its boundaries. The pathogen may have been introduced to this region of Nepal via seed potato tubers from other countries. Reference: (1) G. S. Shekhawat et al. Potato Res. 19:241, 1976.
Analysis of DOK‐6 function in downstream signaling of RET in human neuroblastoma cells
Authors: Kurotsuchi Ai , Murakumo Yoshiki , Jijiwa Mayumi , Kurokawa Kei , Itoh Yasutomo , Kodama Yoshinori , Kato Takuya , Enomoto Atsushi , Asai Naoya , Terasaki Hiroko , Takahashi Masahide 
Published: February 2010

Point mutations and structural alterations of the RET tyrosine kinase gene cause multiple endocrine neoplasia type 2 (MEN 2) and papillary thyroid carcinoma, respectively. RET activation by glial cell line‐derived neurotrophic factor (GDNF) is essential for the development of the enteric nervous system and the kidney. The signal through RET tyrosine kinase requires several adaptor proteins including the DOK (downstream of kinase) family of proteins. Of the seven members of the DOK protein family, DOK‐1, ‐4, ‐5, and ‐6 have been reported to play roles in the GDNF–RET signaling pathway. Although DOK‐6 has been shown to bind to RET and promote GDNF‐induced neurite outgrowth in mouse Neuro2A cells, DOK‐6 function in human cells remains unclear. In the present study, we investigated the role of DOK‐6 in GDNF–RET signaling in human cells including neuroblastoma cells. DOK‐6 was constitutively localized to the plasma membrane via its pleckstrin homology (PH) domain, and was phosphorylated following RET activation via a MEN2A mutation or GDNF stimulation. However, DOK‐6 could not significantly affect downstream signaling and neurite outgrowth in human neuroblastoma cells. The binding affinity of the DOK‐6 phosphotyrosine‐binding (PTB) domain to RET was much lower than that of the DOK‐1, DOK‐4, and SHC PTB domains to RET. These findings indicate that DOK‐6 is involved in RET signaling with less influence when compared with DOK‐1, DOK‐4, and SHC.(Cancer Sci 2010; 101: 1047–1155)
Herbivore‐induced plant responses in Brassica oleracea prevail over effects of constitutive resistance and result in enhanced herbivore attack
Authors: POELMAN ERIK H. , VAN LOON JOOP J. A. , VAN DAM NICOLE M. , VET LOUISE E. M. , DICKE MARCEL 
Published: February 2010

1. Plant responses to herbivore attack may have community‐wide effects on the composition of the plant‐associated insect community. Thereby, plant responses to an early‐season herbivore may have profound consequences for the amount and type of future attack.2. Here we studied the effect of early‐season herbivory by caterpillars of Pieris rapae on the composition of the insect herbivore community on domesticated Brassica oleracea plants. We compared the effect of herbivory on two cultivars that differ in the degree of susceptibility to herbivores to analyse whether induced plant responses supersede differences caused by constitutive resistance.3. Early‐season herbivory affected the herbivore community, having contrasting effects on different herbivore species, while these effects were similar on the two cultivars. Generalist insect herbivores avoided plants that had been induced, whereas these plants were colonised preferentially by specialist herbivores belonging to both leaf‐chewing and sap‐sucking guilds.4. Our results show that community‐wide effects of early‐season herbivory may prevail over effects of constitutive plant resistance. Induced responses triggered by prior herbivory may lead to an increase in susceptibility to the dominant specialists in the herbivorous insect community. The outcome of the balance between contrasting responses of herbivorous community members to induced plants therefore determines whether induced plant responses result in enhanced plant resistance.
The permease genenagE2is the key toN‐acetylglucosamine sensing and utilization inStreptomyces coelicolorand is subject to multi‐level control
Authors: Nothaft Harald , Rigali Sébastien , Boomsma Bart , Swiatek Magdalena , McDowall Kenneth J. , Van Wezel Gilles P. , Titgemeyer Fritz 
Published: February 2010

SummaryThe availability of nutrients is a major determinant for the timing of morphogenesis and antibiotic production in the soil‐dwelling bacteriumStreptomyces coelicolor. Here we show thatN‐acetylglucosamine transport, the first step of an important nutrient signalling cascade, is mediated by the NagE2 permease of the phosphotransferase system, and that the activity of this permease is linked to nutritional control of development and antibiotic production. The permease serves as a high‐affinity transporter forN‐acetylglucosamine (Kmof 2.6 µM). The permease complex was reconstituted with individually purified components. This showed that uptake ofN‐acetylglucosamine requires a phosphoryl group transfer from phosphoenolpyruvate via the phosphotransferases EI, HPr and IIACrrto NagF, which in turn phosphorylatesN‐acetylglucosamine during transport. Transcription of thenagFandnagE2genes is induced byN‐acetylglucosamine. Nutrient signalling byN‐acetylglucosamine that triggers the onset of development was abolished in thenagE2andnagFmutants.nagE2is subject to multi‐level control by the global transcription factor DasR and the activator AtrA that also stimulates genes for antibiotic actinorhodin biosynthesis. Hence, it is apparent that streptomycetes tightly control the nutritional state in a complex manner to ensure the correct timing for the developmental programme.
Error‐prone initiation factor 2 mutations reduce the fitness cost of antibiotic resistance
Authors: Zorzet Anna , Pavlov Michael Y. , Nilsson Annika I. , Ehrenberg Måns , Andersson Dan I. 
Published: February 2010

SummaryMutations in the fmt gene (encoding formyl methionine transferase) that eliminate formylation of initiator tRNA (Met‐tRNAi) confer resistance to the novel antibiotic class of peptide deformylase inhibitors (PDFIs) while concomitantly reducing bacterial fitness. Here we show in Salmonella typhimurium that novel mutations in initiation factor 2 (IF2) located outside the initiator tRNA binding domain can partly restore fitness of fmt mutants without loss of antibiotic resistance. Analysis of initiation of protein synthesis in vitro showed that with non‐formylated Met‐tRNAi IF2 mutants initiated much faster than wild‐type IF2, whereas with formylated fMet‐tRNAi the initiation rates were similar. Moreover, the increase in initiation rates with Met‐tRNAi conferred by IF2 mutations in vitro correlated well with the increase in growth rate conferred by the same mutations in vivo, suggesting that the mutations in IF2 compensate formylation deficiency by increasing the rate of in vivo initiation with Met‐tRNAi. IF2 mutants had also a high propensity for erroneous initiation with elongator tRNAs in vitro, which could account for their reduced fitness in vivo in a formylation‐proficient strain. More generally, our results suggest that bacterial protein synthesis is mRNA‐limited and that compensatory mutations in IF2 could increase the persistence of PDFI‐resistant bacteria in clinical settings.
Pediatric orthotopic living‐donor liver transplantation cures pulmonary hypertension caused by Abernethy malformation type Ib
Authors: Hori Tomohide , Yonekawa Yukihide , Okamoto Shinya , Ogawa Kohei , Ogura Yasuhiro , Oike Fumitaka , Takada Yasutsugu , Egawa Hiroto , Nguyen Justin H. , Uemoto Shinji 
Published: February 2010

Hori T, Yonekawa Y, Okamoto S, Ogawa K, Ogura Y, Oike F, Takada Y, Egawa H, Nguyen JH, Uemoto S. Pediatric orthotopic living‐donor liver transplantation cures pulmonary hypertension caused by Abernethy malformation type Ib. Pediatr Transplantation 2011: 15:e47–e52. © 2010 John Wiley & Sons A/S.Abstract:  A 3.3‐yr‐old boy was diagnosed with PH caused by a PSS of Abernethy malformation type Ib. After control of PH, he underwent OLDLT at 4.9 yr. His PV flowed directly into the confluence of the CCLMHV and the IVC. To shorten the anhepatic phase, hepatic arterial flow was partially maintained. Removal of the native liver began simultaneously with the graft harvest. The proximal PV was cut at the optimal point for reconstruction. The distal PV was cut at the concrescence of the PV and the CCLMHV. After IVC‐plasty, the LHV of the graft was attached with an anterior patch by venous grafting and was then anastomosed to the IVC. Although the mPAP temporarily increased above the mean arterial pressure, mPAP was stable during OLDLT. FNH and steatosis were confirmed histopathologically. In summary, pediatric OLDLT was performed successfully in PH caused by PSS.
Genetic polymorphism of methylenetetrahydrofolate reductase G1793A, hyperhomocysteinemia, and folate deficiency correlate with ulcerative colitis in central China
Authors: Jiang Yi , Zhao Jie , Jiang Ting , Ge Liuqing , Zhou Feng , Chen Zhitao , Lei Yuan , Huang Sha , Xia Bing 
Published: February 2010

AbstractBackground and Aims:  Methylenetetrahydrofolate reductase (MTHFR) encoding genes were associated with ulcerative colitis in Chinese in our previous study. We further studied association of a new polymorphism of MTHFR G1793A with ulcerative colitis and assessed relationship of this polymorphism with hyperhomocysteinemia (HHcy, ≥ 15 mmol/L) and deficiency of folate (≤ 7 nmol/L) and vitamin B12 (≤ 150 pmol/L) in a cohort of patients with ulcerative colitis in central China.Methods:  A total of 252 patients and 654 healthy controls were recruited. Polymorphism of MTHFR G1793A was examined using a polymerase chain reaction‐restriction fragment length polymorphism method. Plasma levels of homocysteine (Hcy), folate and vitamin B12 were determined by enzymatic cycling assay and corpuscle immune chemiluminescence assay, respectively.Results:  Frequencies of alleles and genotypes in MTHFR G1793A gene differed significantly between ulcerative colitis patients and the healthy controls (20.83% vs 10.47%, 95% confidence interval [CI]: 1.703–2.972, P = 0.0006; 40.48% vs 19.88%, 95% CI: 1.997–3.761, P = 0.0002, respectively). Plasma Hcy levels were higher and folate and vitamin B12 concentrations were lower in the patients than in the healthy controls (21.72 ± 6.59 vs 12.47 ± 5.02, 95% CI: −10.93–−7.58, P < 0.0001; 11.25 ± 6.19 vs 15.28 ± 7.72, 95% CI: 2.03–6.04; P < 0.001; 322.81 ± 128.47 vs 442.59 ± 129.36, 95% CI: 62.61–136.95, P < 0.0001, respectively). HHcy and folate deficiency were more prevalent in patients with ulcerative colitis (45.32% vs 26.17%, 95% CI: 1.285–4.378, P = 0.005; 30.68% vs 13.0%, 95% CI: 1.416–6.197, P = 0.003, respectively).Conclusions:  MTHFR G1793A gene polymorphism, HHcy, folate deficiency and low vitamin B12 concentration were associated with ulcerative colitis in central China. Our findings demonstrate that the Hcy‐related gene and metabolites are involved in pathogenesis of ulcerative colitis.
Taspoglutide, a novel human once‐weekly analogue of glucagon‐like peptide‐1, improves glucose homeostasis and body weight in the Zucker diabetic fatty rat
Authors: Sebokova E. , Bénardeau A. , Sprecher U. , Sewing S. , Tobalina L. , Migliorini C. 
Published: February 2010

Aim: Glucagon‐like peptide‐1 (GLP‐1) receptor agonists are a novel class of pharmacotherapy for type 2 diabetes. We investigated the effects of a novel, long‐acting human GLP‐1 analogue, taspoglutide, in the Zucker diabetic fatty (ZDF) rat, an animal model of type 2 diabetes. Methods: Blood glucose and plasma levels of insulin, peptide YY (PYY), glucose‐dependent insulinotropic polypeptide (GIP) and triglycerides were measured during oral glucose tolerance tests (oGTT) conducted in ZDF rats treated acutely or chronically with a single long‐acting dose of taspoglutide. Pioglitazone was used as a positive control in the chronic study. Postprandial glucose, body weight, glycaemic control and insulin sensitivity were assessed over 21 days in chronically treated animals. Results: Acute treatment with taspoglutide reduced glucose excursion and increased insulin response during oGTT. In chronically treated rats, glucose excursion and levels of GIP, PYY and triglycerides during oGTT on day 21 were significantly reduced. Postprandial glucose levels were significantly lower than vehicle controls by day 15. A significant reduction in body weight gain was noticed by day 8, and continued until the end of the study when body weight was approximately 7% lower in rats treated with taspoglutide compared to vehicle. Glycaemic control (increased levels of 1,5‐anhydroglucitol) and insulin sensitivity (Matsuda index) were improved by taspoglutide treatment. Conclusions: Taspoglutide showed typical effects of native GLP‐1, with improvement in glucose tolerance, postprandial glucose, body weight, glycaemic control and insulin sensitivity.
Adding insulin glargine vs. NPH insulin to metformin results in a more efficient postprandial β‐cell protection in individuals with type 2 diabetes
Authors: Forst T. , Larbig M. , Hohberg C. , Forst S. , Diessel S. , Borchert M. , Roth W. , Pfützner A. 
Published: February 2010

Aim: Postprandial release of intact proinsulin (IP) is an independent marker for β‐cell dysfunction in patients with type 2 diabetes. This open‐label, parallel‐group, two‐arm, pilot study compared the β‐cell protective effect of adding insulin glargine (GLA) vs. NPH insulin to ongoing metformin. Material and methods: Overall, 28 insulin‐naive type 2 diabetes subjects (mean ± SD age, 61.5 ± 6.7 years; diabetes duration, 9.8 ± 6.5 years; HbA1c, 7.1 ± 0.5%; BMI, 30.7 ± 4.3 kg/m2) treated with metformin and sulfonylurea were randomized to add once‐daily GLA or NPH at bedtime. At baseline and after 3 months, subjects received a standardized breakfast, lunch and dinner, with pre‐ and postprandial blood sampling to measure plasma IP, total insulin and blood glucose (BG). Results: Insulin dose after 3 months was comparable in both groups (GLA vs. NPH: 23.6 ± 13.4 vs. 23.3 ± 12.7; p = NS ). Both treatments significantly reduced fasting BG levels (GLA: 158 ± 19 to 121 ± 23 mg/dl; NPH: 156 ± 34 to 119 ± 29 mg/dl; both p < 0.01 vs. baseline). Fasting and postprandial BG levels did not differ between groups. IP levels decreased in both groups (p < 0.05 at all timepoints). Although IP release after breakfast did not differ between treatments, GLA induced a greater reduction in IP release after lunch (p = 0.08) and dinner (p = 0.04). Total plasma insulin levels did not differ between groups. Conclusions: Adding basal insulin to metformin reduces postprandial β‐cell load. While GLA and NPH had comparable effects at breakfast, GLA reduces β‐cell stress more effectively at dinner, and with a trend at lunch, most probably because of its longer lasting pharmacodynamic profile.