bluuebunny/crossref_metadata_2025_split huggingface dataset:
Darkness visible: reflections on underground ecology
Authors: FITTER A. H. 
Published: March 2005

Summary

Soil science and ecology have developed independently, making it difficult for ecologists to contribute to urgent current debates on the destruction of the global soil resource and its key role in the global carbon cycle. Soils are believed to be exceptionally biodiverse parts of ecosystems, a view confirmed by recent data from the UK Soil Biodiversity Programme at Sourhope, Scotland, where high diversity was a characteristic of small organisms, but not of larger ones. Explaining this difference requires knowledge that we currently lack about the basic biology and biogeography of micro‐organisms.
It seems inherently plausible that the high levels of biological diversity in soil play some part in determining the ability of soils to undertake ecosystem‐level processes, such as carbon and mineral cycling. However, we lack conceptual models to address this issue, and debate about the role of biodiversity in ecosystem processes has centred around the concept of functional redundancy, and has consequently been largely semantic. More precise construction of our experimental questions is needed to advance understanding.
These issues are well illustrated by the fungi that form arbuscular mycorrhizas, the Glomeromycota. This ancient symbiosis of plants and fungi is responsible for phosphate uptake in most land plants, and the phylum is generally held to be species‐poor and non‐specific, with most members readily colonizing any plant species. Molecular techniques have shown both those assumptions to be unsafe, raising questions about what factors have promoted diversification in these fungi. One source of this genetic diversity may be functional diversity.
Specificity of the mycorrhizal interaction between plants and fungi would have important ecosystem consequences. One example would be in the control of invasiveness in introduced plant species: surprisingly, naturalized plant species in Britain are disproportionately from mycorrhizal families, suggesting that these fungi may play a role in assisting invasion.
What emerges from an attempt to relate biodiversity and ecosystem processes in soil is our extraordinary ignorance about the organisms involved. There are fundamental questions that are now answerable with new techniques and sufficient will, such as how biodiverse are natural soils? Do microbes have biogeography? Are there rare or even endangered microbes?
Liver histology of Asian patients with chronic hepatitis B on prolonged lamivudine therapy
Authors: Yuen M.‐F. , Chow D. H.‐F. , Tsui K. , Wong B. C.‐Y. , Yuen J. C.‐H. , Wong D. K.‐H. , Lai C.‐L. 
Published: March 2005

SummaryBackground : Long‐term effect of YMDD mutations on liver histology in Chinese hepatitis B patients is unknown.Aim : To examine the effect of prolonged lamivudine treatment on liver histology in Chinese patients with and without YMDD mutations.Methods : Liver histology was assessed in 85 patients on long‐term lamivudine at baseline and year 1, and at year 3 for 25 patients.Results : Comparing patients with and without YMDD mutations at year 1, the former had higher baseline median necroinflammatory (11 vs. six respectively, P = 0.014) and fibrosis scores (three vs. one respectively, P = 0.001). The proportion of patients with improvement in necroinflammation and worsening of fibrosis was comparable for patients with and without YMDD mutations at year 1 (57.1%, 14.3% vs. 55%, 15% respectively) and year 3 (57.9%, 26.3% vs. 50%, 16.7% respectively). Comparing the histology at year 1 and 3, more patients with YMDD mutations developing after year 1 had worsening of necroinflammation than patients with persistent YMDD wild type (53.8% vs. 25% respectively).Conclusions : Patients who developed YMDD mutations had higher baseline histological scores. With YMDD mutations, the liver histology became less favourable after 3 years than at the first year, although there was still improvement when compared with that at baseline.
A randomized, double blind, comparative trial of micafungin (FK463) vs. fluconazole for the treatment of oesophageal candidiasis
Authors: De Wet N. T. E. , Bester A. J. , Viljoen J. J. , Filho F. , Suleiman J. M. , Ticona E. , Llanos E. A. , Fisco C. , Lau W. , Buell D. 
Published: March 2005

SummaryAim:  To determine efficacy and safety of intravenous micafungin vs. intravenous fluconazole in the treatment of oesophageal candidiasis.Methods:  A total of 523 patients ≥16 years with documented oesophageal candidiasis were randomized (1:1) in this controlled, non‐inferiority study to receive either micafungin (150 mg/day) or fluconazole (200 mg/day). Response was evaluated clinically and endoscopically. Post‐treatment assessments were performed at 2 and 4 weeks after discontinuation of therapy.Results:  Median duration of therapy was 14 days. For the primary end‐point of endoscopic cure, treatment difference was −0.3% (micafungin 87.7%, fluconazole 88.0%). Documented persistent invasive disease at the end of therapy was reported in 2.7% and 3.9% of patients, respectively. Both 84.8% of micafungin and 88.7% of fluconazole patients remained recurrence free at 4‐weeks post‐treatment. The overall therapeutic response rate was 87.3% for micafungin and 87.2% for fluconazole. The incidence of drug‐related adverse events was 27.7% for micafungin and 21.3% for fluconazole. Six (2.3%) micafungin‐ and two (0.8%) fluconazole‐treated patients discontinued therapy; rash was the most common event leading to discontinuation.Conclusion:  Intravenous micafungin (150 mg daily) is well tolerated and as efficacious as intravenous fluconazole (200 mg daily) in the primary treatment of oesophageal candidiasis, achieving high rates of clinical and endoscopic cure.
Gene expression profiling in polycythaemia vera: overexpression of transcription factor NF‐E2
Authors: Goerttler Philipp S. , Kreutz Clemens , Donauer Johannes , Faller Daniel , Maiwald Thomas , März Edith , Rumberger Brigitta , Sparna Titus , Schmitt‐Gräff Annette , Wilpert Jochen , Timmer Jens , Walz Gerd , Pahl Heike L. 
Published: March 2005

SummaryThe molecular aetiology of polycythaemia vera (PV) remains unknown and the differential diagnosis between PV and secondary erythrocytosis (SE) can be challenging. Gene expression profiling can identify candidates involved in the pathophysiology of PV and generate a molecular signature to aid in diagnosis. We thus performed cDNA microarray analysis on 40 PV and 12 SE patients. Two independent data sets were obtained: using a two‐step training/validation design, a set of 64 genes (class predictors) was determined, which correctly discriminated PV from SE patients. Separately 253 genes were identified to be upregulated and 391 downregulated more than 1·5‐fold in PV compared with healthy controls (P < 0·01). Of the genes overexpressed in PV, 27 contained Sp1 sites: we therefore propose that altered activity of Sp1‐like transcription factors may contribute to the molecular aetiology of PV. One Sp1 target, the transcription factor NF‐E2 [nuclear factor (erythroid‐derived 2)], is overexpressed 2‐ to 40‐fold in PV patients. In PV bone marrow, NF‐E2 is overexpressed in megakaryocytes, erythroid and granulocytic precursors. It has been shown that overexpression of NF‐E2 leads to the development of erythropoietin‐independent erythroid colonies and that ectopic NF‐E2 expression can reprogram monocytic cells towards erythroid and megakaryocytic differentiation. Transcription factor concentration may thus control lineage commitment. We therefore propose that elevated concentrations of NF‐E2 in PV patients lead to an overproduction of erythroid and, in some patients, megakaryocytic cells/platelets. In this model, the level of NF‐E2 overexpression determines both the severity of erythrocytosis and the concurrent presence or absence of thrombocytosis.
The human leucocyte antigen‐DRB1*1302‐DQB1*0609‐DPB1*0201 haplotype may be a strong genetic marker for aspirin‐induced urticaria
Authors: Kim S.‐H. , Choi J.‐H. , Lee K.‐W. , Kim S.‐H. , Shin E.‐S. , Oh H.‐B. , Suh C.‐H. , Nahm D.‐H. , Park H.‐S. 
Published: March 2005

SummaryBackground
Urticaria/angioedema is a common aspirin‐induced allergy; however, its pathogenic mechanism is not understood.Objective
In order to uncover the genetic mechanism, we studied the associations of the human leucocyte antigen (HLA) genotypes in patients with aspirin‐induced urticaria compared with aspirin‐intolerant asthma and normal control in a Korean population.Methods
Ninety‐four aspirin‐induced urticaria patients presenting urticaria/angioedema‐induced by both ASA and NSAID (50 had underlying chronic urticaria) and showing positive responses on oral aspirin challenge test, 76 aspirin‐intolerant asthmatics with positive responses on lysine–aspirin bronchoprovocation test, and 185 normal healthy controls were enrolled. HLA‐DRB1, DQB1, and DPB1 genotypings were performed by direct DNA sequencing analysis.Results
The allele frequencies of HLA‐DRB1*1302 (18.1%) and HLA‐DQB1*0609 (10.1%) in aspirin‐induced urticaria were significantly higher than in aspirin‐intolerant asthma (5.3%, P=0.0004; 2.0%, P=0.0024) and in normal controls (8.1%, P=0.0005; 3.2%, P=0.0008), and they remained significant after correcting for multiple comparisons. The patients with these two HLA markers had a significantly younger age than patients without, while no associations were found in with respect to atopic status, a history of previous allergic diseases, total IgE level, or presence of underlying chronic urticaria (P>0.05, respectively). In haplotype analysis, the HLA‐DRB1*1302‐DQB1*0609‐DPB1*0201 was significantly higher in the aspirin‐induced urticaria (8.0%) than in the aspirin‐intolerant asthma (0.7%, P=0.0014) and normal controls (2.0%, P=0.0006).Conclusion
These findings suggest that the HLA‐DRB1*1302‐DQB1*0609‐DPB1*0201 may be a strong genetic marker to determine the aspirin‐induced urticaria phenotype.
Characterization of the human T cell response to antigen 5 from Vespula vulgaris (Ves v 5)
Authors: Bohle B. , Zwölfer B. , Fischer G. F. , Seppälä U. , Kinaciyan T. , Bolwig C. , Spangfort M. D. , Ebner C. 
Published: March 2005

SummaryBackground
The T cell reactivity to the major allergen of bee venom, phospholipase A2, has been thoroughly characterized. In contrast, only little is known about the human cellular response to major allergens from wasp venom.Objective
To characterize the human T cell response to antigen 5 from Vespula vulgaris, Ves v 5.Methods
Recombinant Ves v 5 was used to establish allergen‐specific T cell lines (TCL) and T cell clones (TCC) from the peripheral blood of vespid‐allergic and non‐allergic individuals. Ves v 5‐specific TCL were mapped for T cell epitopes using overlapping synthetic peptides representing the complete amino acid sequence of Ves v 5. Ves v 5‐specific TCC were analysed for antigen‐induced secretion of IL‐4, IFN‐γ and IL‐10.Results
Seventeen distinct T cell epitopes were recognized by allergic individuals among which Ves v 5181–192 was identified as a dominant T cell epitope. Partially different epitopes were observed in TCL from non‐allergic subjects and the dominant epitope Ves v 5181–192 was not prevalent in these cultures. Ves v 5‐specific TCC isolated from allergic individuals did not show the typical T helper type 2 (Th2)‐like cytokine profile in response to specific stimulation, i.e. high amounts of IL‐4 and low IFN‐γ. TCC from non‐allergic individuals showed a Th1‐like cytokine pattern.Conclusions
Our findings provide evidence that the allergic T cell response to Ves v 5 is not Th2‐dominated and that different immunogenic sites on this major wasp venom allergen are recognized by allergic and non‐allergic individuals.
Relationship of thyroid function with body mass index, leptin, insulin sensitivity and adiponectin in euthyroid obese women
Authors: Iacobellis Gianluca , Cristina Ribaudo Maria , Zappaterreno Alessandra , Valeria Iannucci Concetta , Leonetti Frida 
Published: March 2005

SummaryBackground   A possible relationship between thyroid hormones and adipose tissue metabolism in humans has been suggested.Aim of the study   We sought to evaluate thyroid function and its possible relationship with body mass index (BMI), leptin, adiponectin and insulin sensitivity in euthyroid obese women.Materials and methods   Eighty‐seven uncomplicated obese women (mean age 34·7 ± 9 years, mean BMI 40·1 ± 7 kg/m2) were studied. Levels of TSH, free thyroxine (FT4), free triiodothyronine (FT3), plasma adiponectin and leptin were evaluated. Insulin sensitivity was assessed by euglycaemic hyperinsulinaemic clamp (M index), fasting insulin and HOMA‐IR.Results   Uncomplicated obese women with BMI > 40 kg/m2 showed higher serum TSH than obese subjects with BMI < 40 kg/m2 (P < 0·01). TSH was correlated with BMI (r = 0·44, P = 0·01) leptin (r = 0·41, P = 0·01), leptin/BMI ratio (r = 0·33, P = 0·03), body surface area (r = 0·26, P = 0·05), HOMA‐IR (r = 0·245, P = 0·05) and inversely with adiponectin (r =−0·25, P = 0·05) and M index (r =−0·223 P = 0·05).Conclusions   Our data show that, although thyroid function was normal in the studied obese population, TSH and BMI were positively related. TSH has been found to be correlated also with leptin adjusted for BMI. TSH could represent a marker of altered energy balance in severe, but uncomplicated obese women.
PROGINS Alu sequence insertion is associated with hyperprolactinaemia but not leiomyoma susceptibility
Authors: Hsieh Yao‐Yuan , Chan Ian‐Pan , Wang Hsin‐I. , Chang Chi‐Chen , Huang Ching‐Wei , Lin Chich‐Sheng 
Published: March 2005

SummaryObjective  Leiomyoma and hyperprolactinaemia are both progesterone‐dependent diseases. Hormone‐related genes, such as the progesterone receptor (PGR), might be involved in their pathogenesis.Design and measurements  Subjects were divided into three groups: (i) leiomyoma (n = 120); (ii) hyperprolactinaemia (n = 101); (iii) normal controls (n = 140). We investigated the Alu (306‐bp DNA) insertion in intron G of the PGR gene in all individuals. PGR gene polymorphisms [T1 (wild‐type); T2 (PROGINS, with Alu insertion)] were determined by PCR and electrophoresis. Genotype and allele frequencies of the PROGINS in each group were detected and compared.Results  We observed no significant difference of the PGR*T1/T2 genotypes and allele frequencies between leiomyoma and other two groups. The proportions of T1 homozygote/heterozygote/T2 homozygote in each group were (i) 90/8·3/1·7%; (ii) 84·2/9·9/5·9%; (iii) 92·9/6·4/0·7%. In contrast, a higher percentage of T2‐related genotype and allele were noted in hyperprolactinaemic women compared to other two groups. The proportions of T1/T2 alleles in each group were: (i) 94·2/5·8%; (ii) 89·1/10·9%; (iii) 96·1/3·9%.Conclusions  The PROGIN*T2‐related genotype and allele are related to a higher susceptibility to hyperprolactinaemia. The PROGINS polymorphism is not associated with leiomyoma development.
The role of coastal ecotones: a case study of the salt marsh/upland transition zone in California
Authors: TRAUT BIBIT HALLIDAY 
Published: March 2005

Summary

Ecotones, the transition zones between adjacent ecological systems, may intensify or concentrate the flow and processing of materials and organisms between systems.
To determine whether the salt marsh/upland transition zone is an ecotone, both in functioning as a habitat, as well as concentrating materials and organisms, I conducted an extensive survey of 12 marsh/upland transition zones in the Pt Reyes area of California.
The high saltmarsh was identified as an ecotone, with biological and physical conditions distinct from the adjacent marsh plain and upland. It supports a unique plant assemblage and greater total soil nitrogen than the adjacent upland.
Taxonomic richness patterns did not reflect changes in habitat spatial characteristics (e.g. ecotone area, ecotone area/perimeter), instead showing a quadratic correlation along the gradient, with increased diversity of both plants and spiders in the ecotone. Spider richness was enhanced with increased vegetation complexity, which was greatest in the ecotone.
This study presents empirical evidence that suggests coastal marsh/upland ecotones harbour increased diversity and may concentrate nitrogen pools, thereby highlighting the need for further research investigating the relationship between landscape connections and the coupling of species and biogeochemical processes.
Improving competition representation in theoretical models of self‐thinning: a critical review
Authors: REYNOLDS JOEL H. , FORD E. DAVID 
Published: March 2005

SummaryMany theoretical models have been proposed to explain the empirical self‐thinning relationship given by Yodaet al. in 1963 for even‐aged, monospecific stands of plants, but the models are inadequate to allow consensus on the processes driving variation in density‐dependent mortality and self‐thinning.Most non‐individual based models (non‐IBMs), and many IBMs, employ a common representation of competition in which a finite amount of potential crown area remains completely allocated throughout self‐thinning, making stand density inversely proportional to mean projected crown area.This representation entails four assumptions regarding the competition process: the population is adequately represented by the mean plant; total stand resource utilization is constant throughout self‐thinning; competition is a horizontal packing process; and differences in initial stand conditions may affect the rate of competition but not the process itself.Reviewing published empirical data, the competition literature and the logical implications for the self‐thinning process shows that all four assumptions are untenable as generalizations. Unfortunately, their application provides neither a mortality‐inducing mechanism nor insight into the relationship between stand growth and mortality.Explaining the observed variation in self‐thinning relationships therefore requires improved representation of the competition process. This improvement is likely to require IBMs that explicitly represent variation in plant size or resource acquisition, two‐dimensional stand distribution, dynamic rather than static stand resource utilization, and, perhaps, explicit three‐dimensional stand development. Most importantly, the requirement for explicitly modelling mortality mechanisms implies that whole plant models may be insufficient for insight into the self‐thinning process.The review reinforces the need to assess mechanistic models for more than their ability to reproduce a single, high‐level pattern. Such models should be assessed for their ability to simultaneously reproduce multiple features selected from the levels of both the modelled mechanisms and the high‐level patterns.Progress in understanding the observed variation in self‐thinning currently requires a shift from searching for universal insight into the modelling of specific mechanisms for specific plant types, eventually leading to a broader theory explaining how variation in plants affects the competition process.
The gene NCE103 (YNL036w) from Saccharomyces cerevisiae encodes a functional carbonic anhydrase and its transcription is regulated by the concentration of inorganic carbon in the medium
Authors: Amoroso Gabriele , Morell‐Avrahov Lola , Müller Dominik , Klug Katharina , Sültemeyer Dieter 
Published: March 2005

SummaryCarbonic anhydrase (CA) catalyses the rapid interconversion between CO2 and HCO3–. Despite its wide distribution among living organisms, the presence of CA in fungi has been controversially discussed. Using mass spectrometric analysis of 18O exchange from doubly labelled CO2, we were able to measure CA activity in intact cells of Saccharomyces cerevisiae. Intracellular CA activity was lacking in the Δnce103 mutant, indicating that NCE103 encodes a functional CA. This was proven by overexpressing and purification of the NCE103 gene product showing a specific activity of around 6900 units per mg protein. Interestingly, the in vivo CA activity was 10–20 times higher in cells grown on low inorganic carbon (Ci; air containing 0.035% CO2) than in high‐Ci cells (grown on 5% CO2). The enhanced CA activity of low‐Ci cells was inducible after transferring high‐Ci cells to air. Northern blot analysis revealed that that expression of NCE103 is transcriptionally regulated by low Ci which was also demonstrated by fusing the NCE103 promoter to β‐galactosidase as a reporter gene. Inactivation of NCE103 results in a high CO2 requiring mutant indicating that a functional CA is an important prerequisite for S. cerevisiae to grow under low‐Ci conditions
Measure for measure in the control of type III secretion hook and needle length
Authors: Minamino Tohru , Pugsley Anthony P. 
Published: March 2005

SummaryBacterial flagella and injectisomes are supramolecular structures that are responsible for motility and for delivering toxic proteins into the cytosol of eukaryotic cells, respectively. They look very similar to each other. Both systems are called type III secretion pathways, and their components share substantial sequence similarities. One remarkable feature of the type III systems is that the length of their substructure is fairly well controlled by a secretion switching machinery, which consists of at least two proteins, a length control protein and an integral membrane secretion component. Here, we review how and why the length of these structures must be accurately controlled.
N‐terminal signal region of FliK is dispensable for length control of the flagellar hook
Authors: Hirano Takanori , Shibata Satoshi , Ohnishi Kouhei , Tani Tomomi , Aizawa Shin‐Ichi 
Published: March 2005

SummaryThe length of the flagellar hook is regulated; it is 55 ± 6 nm long in Salmonella. Five genes involved in hook‐length regulation are fliK, flhB, fliG, fliM and fliN. The last four genes encode structural components of the protein export apparatus in the flagellar base, whereas FliK is soluble and secreted during flagellar assembly. The role of FliK, however, remains ambiguous. We constructed two kinds of FliK variants: N‐terminally truncated FliK protein and FliK N‐terminally fused with cyan fluorescent protein (CFP‐FliK). Both N‐terminally truncated FliK missing the first 99 amino acids (aa) and CFP‐FliK fusion variants partially complemented a fliK null (polyhook) mutant to produce cells with filaments, allowing cells to swim; the hooks, however, were not normal but were polyhooks. When the N‐terminally defective FliK variants were expressed at high levels, the average polyhook length was shortened coming close to the length of the wild‐type hook, independently of the sizes of the FliK variants. These FliK variants were not secreted. CFP‐FliK fusion proteins were observed to homogeneously distribute in the cytoplasm. We conclude that FliK does not need to be exported to control hook length and is unlikely to be a ruler; instead, we conclude that FliK controls hook length by the timely switching of secretion modes of the flagellar type III secretion system  by  the  FliK  C‐terminal  domain,  and  that  the  N‐terminal region is dispensable for hook length control.