bluuebunny/crossref_metadata_2025_split huggingface dataset:
Zoonotic transmission of Cryptococcus neoformans from a magpie to an immunocompetent patient
Authors: LAGROU K. , VAN ELDERE J. , KEULEERS S. , HAGEN F. , MERCKX R. , VERHAEGEN J. , PEETERMANS W. E. , BOEKHOUT T. 
Published: August 2010

Abstract.  Lagrou K, Van Eldere J, Keuleers S, Hagen F, Merckx R, Verhaegen J, Peetermans WE, Boekhout T (University Hospital Leuven, Leuven, Belgium; and Centraalbureau voor Schimmelcultures, CT Utrecht, the Netherlands) Zoonotic transmission of Cryptococcus neoformans from a magpie to an immunocompetent patient (Case report). J Intern Med 2005; 257: 385–388.Abstract.
We report a case of cryptococcal meningitis in an immunocompetent female patient with exposure to a pet magpie (Pica pica). Genetically indistinguishable isolates were cultured from the cerebrospinal fluid of the patient and excreta of the bird. Our data strongly suggest zoonotic transmission of Cryptococcus neoformans var. grubii from a magpie to this patient.
Fracture risk associated with systemic and topical corticosteroids
Authors: VESTERGAARD P. , REJNMARK L. , MOSEKILDE L. 
Published: August 2010

Abstract.Objectives.  To study the fracture risk associated with the use of corticosteroids in any formulation and administration.Design.  Case–control study.Setting.  Community‐based study in Denmark.Subjects.  Cases were all subjects with any fracture sustained during the year 2000 (n = 124 655). For each case, three controls (n = 373 962) matched on age and gender were randomly drawn from the background population. Adjustments were made for concurrent diseases (lung diseases, rheumatic disorders), use of other drugs (inhaled bronchodilators), contacts to hospitals and general practitioners, and social variables.Results.  An increased risk of any fracture, hip, spine, and forearm fractures was present with use of more than 2.5 mg of prednisolone or equivalent orally per day. For inhaled corticosteroids a limited increase in the risk of any fracture was present in users of more than 7.5 mg prednisolone equivalents per day (equivalent to 1875 μg of budesonide per day). However, no increase in the risk of hip, spine or forearm fractures was present in users of inhaled corticosteroids. For other topical corticosteroids (dermal, rectal, nasal, local application in the mouth, the eyes or the ears) no increase in fracture risk could be demonstrated even at high doses after adjustment for confounders.Conclusions.  Ingestion of more than 2.5 mg of oral prednisolone equivalents per day is associated with an increase in fracture risk. No increase is associated with inhaled corticosteroids except at daily dosages above 7.5 mg of prednisolone equivalents. No increase in fracture risk is associated with other forms of topical corticosteroids.
Neutrophil serine proteases: potential key regulators of cell signalling during inflammation
Authors: WIEDOW O. , MEYER‐HOFFERT U. 
Published: August 2010

Abstract.  Wiedow O, Meyer‐Hoffert U (University Kiel, Kiel, Germany; and Karolinska Institute, Stockholm, Sweden). Neutrophil serine proteases: potential key regulators of cell signalling during inflammation (Review). J Intern Med 2005; 257: 319–328.The serine proteases cathepsin G, human leucocyte elastase and proteinase 3 are major contents of neutrophils and are released at sites of inflammation. The common picture of their function was that they do not degrade extracellular proteins specifically. Recent studies provided evidence that these proteases are able to activate specifically pro‐inflammatory cytokines and lead to the activation of different receptors. Neutrophil serine proteases might therefore be important regulators of inflammatory processes and are interesting targets for new therapeutic approaches against inflammatory disorders. This review summarizes the current knowledge on the regulation of cell signalling by neutrophil serine proteases.
Separating cause from effect: how does insulin/IGF signalling control lifespan in worms, flies and mice?
Authors: Piper M. D. W. , Selman C. , McElwee J. J. , Partridge L. 
Published: August 2010

Abstract.Ageing research has been revolutionized by the use of model organisms to discover genetic alterations that can extend lifespan. In the last 5 years alone, it has become apparent that single gene mutations in the insulin and insulin‐like growth‐factor signalling pathways can lengthen lifespan in worms, flies and mice, implying evolutionary conservation of mechanisms. Importantly, this research has also shown that these mutations can keep the animals healthy and disease‐free for longer and can alleviate specific ageing‐related pathologies. These findings are striking in view of the negative effects that disruption of these signalling pathways can also produce. Here, we summarize the body of work that has lead to these discoveries and point out areas of interest for future work in characterizing the genetic, molecular and biochemical details of the mechanisms to achieving a longer and healthier life.
SecY and integral membrane components of the Escherichia coli protein translocation system
Authors: Ito Koreaki 
Published: August 2010

SummaryGenetic approaches can address the question of how integral membrane Sec factors interact with each other and facilitate protein translocation across the cytoplasmic membrane of E. coli. This review summarizes genetic analyses of SecY, SecE and some other protein translocation factors, utilizing ‘prl’ mutations,‘sec’ mutations, ‘suppressor‐directed inactivation’, ‘Sec titration’, dominant negative mutations and their suppressors. Evidence suggests that coordinate participation of SecY, SecE, SecD, SecF, and probably some other factors, is crucial for the process.
Evidence for global regulatory control of pilus expression in Escherichia coli by Lrp and DNA methylation: model building based on analysis of pap
Authors: van der Woude M. W. , Braaten B. A. , Low D. A. 
Published: August 2010

SummaryPyelonephritis‐associated pilus (Pap) expression is regulated by a phase variation control mechanism involving PapB, Papl, catabolite activator protein (CAP), leucine‐responsive regulatory protein (Lrp) and deoxyadenosine methylase (Dam). Lrp and Papl bind to a specific non‐methylated pap regulatory DNA region containing the sequence ‘GATC’ and facilitate the formation of an active transcriptional complex. Evidence indicates that binding of Lrp and Papl to this region inhibits methylation of the GATC site by Dam. However, if this GATC site is first methylated by Dam, binding of Lrp and Papl is inhibited. These events lead to the formation of two different pap methylation states characteristic of active (ON) and inactive (OFF) pap transcription states. The fae (K88), daa (F1845) and sfa (S) pilus operons share conserved ‘GATC‐box’ domains with pap and may be subject to a similar regulatory control mechanism involving Lrp and DNA methylation.
The DNA supercoiling‐sensitive expression of the Salmonella typhimurium his operon requires the his attenuator and is modulated by anaerobiosis and by osmolarity
Authors: O'Byrne Conor P. , Bhriain Niamh Ní , Dorman Charles J. 
Published: August 2010

SummaryBacterial cells possess a subset of genes whose expression correlates with changes in DNA supercoiling brought about by anaerobic growth and by growth at high osmolarity. It has been shown previously that expression of the histidine biosynthetic operon of Salmonella typhimurium is derepressed by relaxation of supercoiled DNA. Here, we confirm that a his:: MudJ operon fusion in S. typhimurium can be induced by treatment with the DNA gyrase inhibitor novobiocin in a dose‐dependent manner, and show that the level of derepression is higher in stationary phase than in mid‐exponential phase cultures. Furthermore, expression of his is repressed by anaerobiosis and by osmolarity, two environmental parameters which increase the negative supercoiling of bacterial DNA. Novobiocin induction of his is also repressed by growing the cells either at high osmolarity or anaerobically. Both environmental repression and novobiocin induction of his require the his attenuator. In addition, derepression of his expression by novobiocin and its repression by anaerobiosis or osmolarity are independent of the stringent response gene, relA.
Molecular dissection of structure and function in the lipopolysaccharide of Rhizobium leguminosarum strain 3841 using monoclonal antibodies and genetic analysis
Authors: Kannenberg E. L. , Rathbun E. A. , Brewin N. J. 
Published: August 2010

SummaryFollowing treatment with nitrosoguanidine, mutant derivatives of Rhizobium leguminosarum strain 3841 were isolated which failed to react with AFRC MAC 203. This monoclonal antibody normally recognizes a strain‐specific lipopolysaccharide epitope which is developmentally regulated during legume nodule differentiation. Structural modification of lipopolysaccharide (LPS) was analysed by examining reactivity with a range of monoclonal antibodies with different epitope specificities, and also by analysis of LPS mobility changes after electrophoresis on polyacrylamide gels. One class of these LPS‐defective mutants induced normal nitrogen‐fixing (Fix+) nodules on peas (Pisum sativum), while another two classes of Fix‐ mutants were also identified, suggesting that a component of the LPS antigen that is part of the MAC 203 epitope is essential for normal nodule development leading to symbiotic nitrogen fixation. When grown under low‐oxygen or low‐pH culture conditions, one class of Fix‐ mutants completely lacked LPS‐1 (the species that carries O antigen) and a second class showed a modified and truncated form of LPS‐1. Mutants with defective LPS structure were also obtained after Tn5 mutagenesis of R leguminosarum 3841 and all nine Fix‐ mutants were also found to lack the MAC 203 epitope. Three of these transposon‐induced mutants synthesized a truncated form of LPS‐1 that was structurally similar to that of the class of the NTG‐induced mutants described above. These transposon‐induced mutations, and the nitrosoguanidine‐induced Fix‐ mutations, were closely linked and could be suppressed by the same cloned fragment of chromosomal DNA. The data presented here suggest that a precondition for normal nodule development of R. leguminosarum 3841 within pea nodules is the ability to synthesize relatively long‐chain LPS–1 macromolecules under the physiological conditions encountered within the nodule. All mutants that lacked the ability to elongate LPS‐1 macromolecules also failed to express the MAC 203 epitope.
The class 1 outer membrane protein of Neisseria meningitidis produced in Bacillus subtilis can give rise to protective immunity
Authors: Nurminen Marjatta , Butcher Sarah , Idänpään‐Heikkilä IIona , Wahlström Eva , Muttilainen Susanna , Runeberg‐Nyman Kate , Sarvas Matti , Mäkelä P. Helena 
Published: August 2010

SummaryThe class 1 outer membrane protein of Neisseria meningitidis B:15:P1.7, 16 was expressed in Bacillus subtilis in high yield as intracellular aggregates. These were easy to isolate and the protein (called BacP1) could be solubilized under denaturing conditions. Sera of mice immunized with thus‐solubilized BacP1 contained high titres of antibodies that reacted with the class 1 protein of the meningococcal envelope in immunoblots but did not react with native meningococcal envelope in enzyme immunoassays (EIA) or with intact meningococci in bactericidal assays. However, when the BacP1 protein was complexed with heterologous (Salmonella) lipopolysaccharide, the ensuing sera reacted with meningococcal envelope preparations in both EIA and immunoblots, showed subtype‐specific bactericidal activity, and were protective in an infant rat meningitis model.
Sensing of 5′ monophosphate by Escherichia coli RNase G can significantly enhance association with RNA and stimulate the decay of functional mRNA transcripts in vivo
Authors: Jourdan Stefanie S. , McDowall Kenneth J. 
Published: August 2010

SummaryThe RNase E/G family of endoribonucleases has a central role in RNA degradation and processing. Previous work has shown that their cleavage of substrates in vitro can be stimulated by the presence of a 5′ monophosphate group. It has not however, established the importance of this activation for any natural RNA processing or decay pathway in vivo. Here we provide for Escherichia coli RNase G the first evidence that the sensing of a 5′ monophosphate is required in vivo for the normal rapid decay of functional mRNAs; moreover, we show in vitro that, in contrast to a previous study, the presence of a 5′ monophosphate can enhance the affinity of RNase G binding to RNA. The implications of these results along with our finding that the maturation of 16S rRNA is unaffected in cells containing an RNase G mutant impaired in 5′ end sensing are discussed with regard to current models of RNA processing and decay and the molecular mechanism that underlies RNA cleavage by the RNase E/G family.
The role of osmiophilic bodies and Pfg377 expression in female gametocyte emergence and mosquito infectivity in the human malaria parasite Plasmodium falciparum
Authors: De Koning‐Ward Tania F. , Olivieri Anna , Bertuccini Lucia , Hood Andrew , Silvestrini Francesco , Charvalias Konstantinos , Berzosa Díaz Pedro , Camarda Grazia , McElwain Terry F. , Papenfuss Tony , Healer Julie , Baldassarri Lucilla , Crabb Brendan S. , Alano Pietro , Ranford‐Cartwright Lisa C. 
Published: August 2010

SummaryOsmiophilic bodies are membrane‐bound vesicles, found predominantly in Plasmodium female gametocytes, that become progressively more abundant as the gametocyte reaches full maturity. These vesicles lie beneath the subpellicular membrane of the gametocyte, and the release of their contents into the parasitophorous vacuole has been postulated to aid in the escape of gametocytes from the erythrocyte after ingestion by the mosquito. Currently, the only protein known to be associated with osmiophilic bodies in Plasmodium falciparum is Pfg377, a gametocyte‐specific protein expressed at the onset of osmiophilic body development. Here we show by targeted gene disruption that Pfg377 plays a fundamental role in the formation of these organelles, and that female gametocytes lacking the full complement of osmiophilic bodies are significantly less efficient both in vitro and in vivo in their emergence from the erythrocytes upon induction of gametogenesis, a process whose timing is critical for fertilization with the short‐lived male gamete. This reduced efficiency of emergence explains the significant defect in oocyst formation in mosquitoes fed blood meals containing Pfg377‐negative gametocytes, resulting in an almost complete blockade of infection.
Reciprocal oxylipin‐mediated cross‐talk in the Aspergillus–seed pathosystem
Authors: Brodhagen Marion , Tsitsigiannis Dimitrios I. , Hornung Ellen , Goebel Cornelia , Feussner Ivo , Keller Nancy P. 
Published: August 2010

SummaryIn Aspergilli, mycotoxin production and sporulation are governed, in part, by endogenous oxylipins (oxygenated, polyunsaturated fatty acids and metabolites derived therefrom). In Aspergillus nidulans, oxylipins are synthesized by the dioxygenase enzymes PpoA, PpoB and PpoC. Structurally similar oxylipins are synthesized in seeds via the action of lipoxygenase (LOX) enzymes. Previous reports have shown that exogenous application of seed oxylipins to Aspergillus cultures alters sporulation and mycotoxin production. Herein, we explored whether a plant oxylipin biosynthetic gene (ZmLOX3) could substitute functionally for A. nidulans ppo genes. We engineered ZmLOX3 into wild‐type A. nidulans, and into a ΔppoAC strain that was reduced in production of oxylipins, conidia and the mycotoxin sterigmatocystin. ZmLOX3 expression increased production of conidia and sterigmatocystin in both backgrounds. We additionally explored whether A. nidulans oxylipins affect seed LOX gene expression during Aspergillus colonization. We observed that peanut seed pnlox2–3 expression was decreased when infected by A. nidulansΔppo mutants compared with infection by wild type. This result provides genetic evidence that fungal oxylipins are involved in plant LOX gene expression changes, leading to possible alterations in the fungal/host interaction. This report provides the first genetic evidence for reciprocal oxylipin cross‐talk in the Aspergillus–seed pathosystem.
Intracellular levels and activity of PvdS, the major iron starvation sigma factor of Pseudomonas aeruginosa
Authors: Tiburzi Federica , Imperi Francesco , Visca Paolo 
Published: August 2010

SummaryIn Pseudomonas aeruginosa the iron starvation sigma factor PvdS directs the transcription of pyoverdine and virulence genes under iron limitation. PvdS activity is modulated by pyoverdine through the surface signalling cascade involving the FpvA receptor and the inner membrane‐spanning sensor FpvR. To gain insight into the molecular mechanisms enabling PvdS to compete with the major sigma RpoD for RNA polymerase (RNAP) binding, we determined the intracellular levels of RNAP, RpoD and PvdS in P. aeruginosa PAO1, and the effect of pyoverdine signalling on PvdS activity. Under iron limitation, P. aeruginosa contains 2221 and 933 molecules of RNAP and RpoD per cell respectively. PvdS attains 62% of RpoD levels. The high PvdS content is partly offset by retention of 30% of PvdS on the membrane, lowering the concentration of cytosolic PvdS to 45% of RpoD levels. RNAP purification from iron‐starved P. aeruginosa cells demonstrated that PvdS–RNAP is poorly represented compared with RpoD–RNAP (1 and 27% of total RNAP respectively). Pyoverdine signalling does not affect the PvdS cellular content but facilitates PvdS release from the membrane, increasing its cytosolic concentration from 35% in both pvdF and fpvA signalling mutants to 70% in the wild type and 83% in the fpvR mutant.
Inadequate inhibition of host RNA polymerase restricts T7 bacteriophage growth on hosts overexpressing udk
Authors: Qimron Udi , Kulczyk Arkadiusz W. , Hamdan Samir M. , Tabor Stanley , Richardson Charles C. 
Published: August 2010

SummaryOverexpression of udk, an Escherichia coli gene encoding a uridine/cytidine kinase, interferes with T7 bacteriophage growth. We show here that inhibition of T7 phage growth by udk overexpression can be overcome by inhibition of host RNA polymerase. Overexpression of gene 2, whose product inhibits host RNA polymerase, restores T7 phage growth on hosts overexpressing udk. In addition, rifampicin, an inhibitor of host RNA polymerase, restores the burst size of T7 phage on udk‐overexpressing hosts to normal. In agreement with these findings, suppressor mutants that overcome the inhibition arising from udk overexpression gain the ability to grow on hosts that are resistant to inhibition of RNA polymerase by gene 2 protein, and suppressor mutants that overcome a lack of gene 2 protein gain the ability to grow on hosts that overexpress udk. Mutations that eliminate or weaken strong promoters for host RNA polymerase in T7 DNA, and mutations in T7 gene 3.5 that affect its interaction with T7 RNA polymerase, also reduce the interference with T7 growth by host RNA polymerase. We propose a general model for the requirement of host RNA polymerase inhibition.
Osmiophilic bodies and the odd organelles of alveolates
Authors: Hayton Karen , Templeton Thomas J. 
Published: August 2010

SummaryThe apicomplexa are parasitic protozoa that are responsible for important human and animal diseases, including malaria, toxoplasmosis, cryptosporidiosis, coccidiosis and babesiosis. Like other members of the superphylum Alveolata, apicomplexans have regulated exocytosis of specialized secretory organelles, such as the apicomplexan‐specific rhoptries and micronemes that are required for host cell invasion. The secretions of another class of organelles, the dense granules and osmiophilic bodies, are proposed to be required for maintenance of the parasitophorous vacuole and host cell egress. Little is known about the osmiophilic bodies and to date only one protein, P377, has been localized to this organelle. In this issue, de Koning‐Ward et al. describe the disruption of pfg377 in the virulent human malaria parasite, Plasmodium falciparum, which results in reduced osmiophilic body formation, a marked decrease in female fitness, and dramatically impaired infectivity to mosquitoes. These findings suggest that targeting PFG377 may be a strategy to block parasite transmission.
Electron tomography of the Maurer's cleft organelles of Plasmodium falciparum‐infected erythrocytes reveals novel structural features
Authors: Hanssen Eric , Sougrat Rachid , Frankland Sarah , Deed Samantha , Klonis Nectarios , Lippincott‐Schwartz Jennifer , Tilley Leann 
Published: August 2010

SummaryDuring intraerythrocytic development, the human malaria parasite, Plasmodium falciparum, establishes membrane‐bound compartments, known as Maurer's clefts, outside the confines of its own plasma membrane. The Maurer's compartments are thought to be a crucial component of the machinery for protein sorting and trafficking; however, their ultrastructure is only partly defined. We have used electron tomography to image Maurer's clefts of 3D7 strain parasites. The compartments are revealed as flattened structures with a translucent lumen and a more electron‐dense coat. They display a complex and convoluted morphology, and some regions are modified with surface nodules, each with a circular cross‐section of ∼25 nm. Individual 25 nm vesicle‐like structures are also seen in the erythrocyte cytoplasm and associated with the red blood cell membrane. The Maurer's clefts are connected to the red blood cell membrane by regions with extended stalk‐like profiles. Immunogold labelling with specific antibodies confirms differential labelling of the Maurer's clefts and the parasitophorous vacuole and erythrocyte membranes. Spot fluorescence photobleaching was used to demonstrate the absence of a lipid continuum between the Maurer's clefts and parasite membranes and the host plasma membrane.
Trigger enzymes: bifunctional proteins active in metabolism and in controlling gene expression
Authors: Commichau Fabian M. , Stülke Jörg 
Published: August 2010

SummaryAll regulatory processes require components that sense the environmental or metabolic conditions of the cell, and sophisticated sensory proteins have been studied in great detail. During the last few years, it turned out that enzymes can control gene expression in response to the availability of their substrates. Here, we review four different mechanisms by which these enzymes interfere with regulation in bacteria. First, some enzymes have acquired a DNA‐binding domain and act as direct transcription repressors by binding DNA in the absence of their substrates. A second class is represented by aconitase, which can bind iron responsive elements in the absence of iron to control the expression of genes involved in iron homoeostasis. The third class of these enzymes is sugar permeases of the phosphotransferase system that control the activity of transcription regulators by phosphorylating them in the absence of the specific substrate. Finally, a fourth class of regulatory enzymes controls the activity of transcription factors by inhibitory protein–protein interactions. We suggest that the enzymes that are active in the control of gene expression should be designated as trigger enzymes. An analysis of the occurrence of trigger enzymes suggests that the duplication and subsequent functional specialization is a major pattern in their evolution.