bluuebunny/crossref_metadata_2025 huggingface dataset:
Control of mammalian predators in game management and conservation
Authors: REYNOLDS J. C. , TAPPER S. C.
Published: April 2008

Wildlife management in modern environments has to contend with an inheritance of faunal and landscape changes caused by humans which affect the relationships between predatory and prey species. In both game management for harvesting, and in species preservation, this leads to difficult decisions about whether and how to manage predation.

Predator control by humans is as old as livestock husbandry. The deliberate, often organized, destruction of many mammalian predator species has been a feature of human development in Europe ‐ and later in countries to which Europeans spread ‐ for centuries. Destruction to the point of extinction was practised for a number of reasons (self‐protection, protection of domestic stock, protection of wild game, fur, adventure, sport) which were rarely distinguished. Reduction of predator numbers specifically to allow an increased harvest of some game species was mainly a nineteenth century development, while the adoption of predator control to benefit endangered species for their own sake belongs to recent decades.

We review scientific literature relevant to predator control in game management and in conservation. Understanding of the role of predation in prey population dynamics has changed considerably during the last 20 years, and predation is now credited with a much more powerful role than in the past. Increasingly it becomes possible not merely to understand what predator control achieves, but to predict when it might be valuable in management, and what strategy will best achieve the aims.

Examples of conservation problems involving predation illustrate the complexity of decision‐making in management. Because of habitat loss, habitat degradation, altered predator communities, or altered predator‐prey ratios, predation losses often have increased significance in modern environments.

Novel approaches potentially offer non‐lethal ways to manage mammalian predators. However, most are still in an exploratory phase and there have been no unqualified successes. The best tested approach, excluding predators from small areas by fencing, is discussed.

In Britain, predator control to benefit small game populations and allow harvesting has been practised for nearly 200 years, and has undoubtedly played a role in shaping the present‐day fauna. Although earlier gamekeeping severely reduced the geographical range of several mammalian (and avian) predator species, nowadays predator control is subject to legal restrictions based on species' conservation status and humaneness. However, illegal persecution of species protected by law remains a persistent and significant conservation problem. The predator species legitimately targeted are successful, common and increasing in the modem environment, while wild populations of gamebirds and many other ground‐nesting birds are declining seriously in most areas.
The LAMP‐like protein p67 plays an essential role in the lysosome of African trypanosomes
Authors: Peck Ronald F. , Shiflett April M. , Schwartz Kevin J. , McCann Amanda , Hajduk Stephen L. , Bangs James D.
Published: April 2008

RNAi knockdown was employed to study the function of p67, a lysosome‐associated membrane protein (LAMP)‐like type I transmembrane lysosomal glycoprotein in African trypanosomes. Conditional induction of p67 dsRNA resulted in specific ∼90% reductions in de novo p67 synthesis in both mammalian bloodstream and procyclic insect‐stage parasites. Bloodstream cell growth was severely retarded with extensive death after > 24 h of induction. Biosynthetic trafficking of residual p67, and of the soluble lysosomal protease trypanopain, were unimpaired. Endocytosis of tomato lectin, a surrogate receptor‐mediated cargo, was only mildly impaired (∼20%), but proper lysosomal targeting was unaffected. p67 ablation had dramatic effects on lysosomal morphology with gross enlargement (four‐ to fivefold) and internal membrane profiles reminiscent of autophagic vacuoles. Ablation of p67 expression rendered bloodstream trypanosomes refractory to lysis by human trypanolytic factor (TLF), a lysosomally activated host innate immune mediator. Similar effects on lysosomal morphology and TLF sensitivity were also obtained by two pharmacological agents that neutralize lysosomal pH – chloroquine and bafilomycin A1. Surprisingly, however, lysosomal pH was not affected in ablated cells suggesting that other physiological alterations must account for increased resistance to TLF. These results indicate p67 plays an essential role in maintenance of normal lysosomal structure and physiology in bloodstream‐stage African trypanosomes.
A novel autotransporter of uropathogenic Proteus mirabilis is both a cytotoxin and an agglutinin
Authors: Alamuri Praveen , Mobley Harry L. T.
Published: April 2008

One of the six predicted Proteus mirabilis autotransporters (ATs), ORF c2341, is predicted to contain a serine protease motif and was earlier identified as an immunogenic outer membrane protein in P. mirabilis. The 3.2 kb gene encodes a 117 kDa protein with a 58‐amino‐acid‐long signal peptide, a 75‐kDa‐long N‐terminal passenger domain and a 30‐kDa‐long C‐terminal translocator. Affinity‐purified 110 kDa AT exhibited chymotrypsin‐like activity and hydrolysed N‐Suc–Ala–Ala–Pro–Phe–pNa and N‐Suc–Ala–Ala–Pro–Leu–pNa with a KM of 22 μM and 31 μM, respectively, under optimal pH of 8.5–9.0 in a Ca2+‐dependent manner. Activity was inhibited by subtilase‐specific inhibitors leupeptin and chymostatin. Both the cell‐associated and purified form elicited cytopathic effects on cultured kidney and bladder epithelial cells. Substrate hydrolysis as well as cytotoxicity was associated with the passenger domain and was compromised upon mutation of any of the catalytic residues (Ser366, His147 and Asp533). At alkaline pH and optimal cell density, the AT also promoted autoaggregation of P. mirabilis and this function was independent of its protease activity. Cytotoxicity, autoaggregation and virulence were significantly reduced in an isogenic pta mutant of P. mirabilis. Proteus toxic agglutinin (Pta) represents a novel autotransported cytotoxin with no bacterial homologues that works optimally in the alkalinized urinary tract, a characteristic of urease‐mediated urea hydrolysis during P. mirabilis infection.
LysM, a widely distributed protein motif for binding to (peptido)glycans
Authors: Buist Girbe , Steen Anton , Kok Jan , Kuipers Oscar P.
Published: April 2008

Bacteria retain certain proteins at their cell envelopes by attaching them in a non‐covalent manner to peptidoglycan, using specific protein domains, such as the prominent LysM (Lysin Motif) domain. More than 4000 (Pfam PF01476) proteins of both prokaryotes and eukaryotes have been found to contain one or more Lysin Motifs. Notably, this collection contains not only truly secreted proteins, but also (outer‐)membrane proteins, lipoproteins or proteins bound to the cell wall in a (non‐)covalent manner. The motif typically ranges in length from 44 to 65 amino acid residues and binds to various types of peptidoglycan and chitin, most likely recognizing the N‐acetylglucosamine moiety. Most bacterial LysM‐containing proteins are peptidoglycan hydrolases with various cleavage specificities. Binding of certain LysM proteins to cells of Gram‐positive bacteria has been shown to occur at specific sites, as binding elsewhere is hindered by the presence of other cell wall components such as lipoteichoic acids. Interestingly, LysM domains of certain plant kinases enable the plant to recognize its symbiotic bacteria or sense and induce resistance against fungi. This interaction is triggered by chitin‐like compounds that are secreted by the symbiotic bacteria or released from fungi, demonstrating an important sensing function of LysMs.
The stellar population histories of early-type galaxies – III. The Coma cluster
Authors: Trager S. C. , Faber S. M. , Dressler Alan
Published: April 2008

We present stellar population parameters of 12 elliptical and S0 galaxies in the Coma cluster around and including the cD galaxy NGC 4874, based on spectra obtained using the Low Resolution Imaging Spectrograph on the Keck II Telescope. Our data are among the most precise and accurate absorption-line strengths yet obtained for cluster galaxies, allowing us to examine in detail the zero-point and scatter in the stellar population properties of Coma cluster early-type galaxies (ETGs). Recent observations of red sequence galaxies in the high-redshift Universe and generic hierarchical galaxy formation models lead to the following expectations for the stellar populations of local ETGs. (1) In all environments, bigger ETGs should have older stellar populations than smaller ETGs (‘downsizing’); (2) ETGs at fixed stellar mass form stars earlier and thus should have older stellar population ages in the highest density environments than those in lower density environments and (3) the most massive ETGs in the densest environments should have a small spread in stellar population ages. We find the following surprising results using our sample. (1) Our ETGs have single-stellar-population-equivalent (SSP-equivalent) ages of on average 5–8 Gyr with the models used here, with the oldest galaxies having SSP-equivalent ages of ≲10-Gyr old. This average age is identical to the mean age of field ETGs. (2) The ETGs in our sample span a large range in velocity dispersion (mass) but are consistent with being drawn from a population with a single age. Specifically, 10 of the 12 ETGs in our sample are consistent within their formal errors of having the same SSP-equivalent age, 5.2 ± 0.2 Gyr, over a factor of more than 750 in mass. We therefore find no evidence for downsizing of the stellar populations of ETGs in the core of the Coma cluster. We confirm the lack of a trend of SSP-equivalent age with mass in the core of the Coma cluster from all other samples of Coma cluster ETG absorption-line strengths available in the literature, but we do find from the largest samples that the dispersion in age increases with decreasing mass. These conclusions stand in stark contrast to the expectations from observations of high-redshift red sequence galaxies and model predictions. We suggest that Coma cluster ETGs may have formed the majority of their mass at high redshifts but suffered small but detectable star formation events at z≈ 0.1–0.3. In this case, previous detections of ‘downsizing’ from stellar populations of local ETGs may not reflect the same downsizing seen in look-back studies of RSGs, as the young ages of the local ETGs represent only a small fraction of their total masses.
Functional gastrointestinal disorders as a public health problem
Authors: Talley N. J.
Published: April 2008

Summary  The functional gastrointestinal disorders (FGIDs) are a heterogeneous group of chronic conditions that are considered to be important to public health because they are remarkably common, can be disabling, and induce a major social and economic burden. Despite the Rome consensus process, the line defining true abnormality from health is as yet imprecise. Furthermore, the concept that the FGIDs have no pathological or biochemical correlates is starting to unravel, and some candidate morphometric abnormalities (e.g. duodenal eosinophilia, colonic mastocytosis) have been documented. The quality of care that patients with FGIDs receive is not well understood, despite the high volume of patients seen in primary and specialty care. There are a remarkable number of symptom‐based and disease‐based co‐morbidities that appear to be more common in those with FGIDs that are not alone explained by coexistent somatization. Whether there is any means of preventing the development of FGIDs post‐infection is untested but has vast public health implications. Defining disease severity remains key to better understanding the public health impact of FGIDs; severity is probably influenced by the intestinal and extra‐intestinal symptom burden, psychological distress and the impact on quality of life, but how these factors interact remains uncertain. An important future research direction must be to quantify at what risk level it is reasonable to prescribe a medication that may be dangerous, and stratify which subsets of patients with FGIDs would qualify for such an approach using objective well validated tools (e.g. based on accurately defining gradations of severity of disease). Finally, there are some reasons to suspect that there may be an increase in mortality in FGID sufferers; for example, unnecessary surgery or invasive testing has a small but not zero associated mortality, and this should be a factor in view of the high prevalence of disease.
Functional development of the enteric nervous system – from migration to motility
Authors: Young H. M.
Published: April 2008

Abstract  The enteric nervous system (ENS) consists of many different types of enteric neurones forming complex reflex circuits that underlie or regulate many gut functions. Studies of humans with Hirschsprung’s disease (distal aganglionosis), and of animal models of Hirschsprung’s disease, have led to the identification of many of the genetic, molecular and cellular mechanisms responsible for the colonization of the gut by enteric neurone precursors. However, later events in the ENS development are still poorly understood, including the development of functioning ENS circuits. This article is a personal view of the current state of play in our understanding of the ENS development and of the future of the field.
Lower gastrointestinal functions
Authors: Bharucha A. E.
Published: April 2008

Abstract  The human colon serves to absorb water and electrolytes, store intraluminal contents until elimination is socially convenient, and salvage nutrients by bacterial metabolism of carbohydrates that have not been absorbed in the small intestine. The anorectum is responsible for fecal continence and defecation. This article is a broad perspective of the current status and a personal perspective of future challenges in understanding lower gastrointestinal functions in health and disease in humans.
Breeding cereals for rust resistance in Australia
Authors: Park R. F.
Published: April 2008

Rust diseases have caused significant losses to Australian cereal crops, and continue to pose a serious threat. Because Australian cereal crop yields are generally low, genetic resistance remains the most economical means of rust control. Resistant cultivars also contribute significantly to reducing over‐summer rust survival. A policy of releasing only rust resistant wheats in northern New South Wales and Queensland has resulted in industry‐wide protection from rust in this region for the past 40 years. The Australian Cereal Rust Control Program conducts annual pathogenicity surveys for all cereal rust pathogens, undertakes genetic research to identify and characterize new sources of resistance, and provides a germplasm screening and enhancement service to all Australian cereal breeding groups. These three activities are interdependent, and are closely integrated with particular emphasis on linking pathology and genetics to ensure breeding outcomes. Recent changes in the wheat rust pathogens, including the development of virulences for Yr17, Lr24, Lr37 and Sr38 resistance genes, and the introduction of a new pathotype of the wheat stripe rust pathogen, have provided new and significant challenges for wheat rust resistance breeding. Similar challenges exist in breeding barley and oats for rust resistance. Examples are discussed to illustrate the ways in which rust isolates are providing information that can be used in breeding for rust resistance. In future, as more markers linked to durable rust resistance sources become available, it is likely that the use of marker‐assisted selection will become more common‐place in rust resistance breeding.
CD8α+βlow Effector T Cells in Systemic Lupus Erythematosus
Authors: Werwitzke S. , Tiede A. , Jacobs R. , Zielinska‐Skowronek M. , Buyny S. , Schmidt R. E. , Witte T.
Published: April 2008

Systemic lupus erythematosus (SLE) is a complex autoimmune disorder characterized by the loss of self‐tolerance to nuclear antigens. Aberrant T‐cell function plays a central role in lupus pathogenesis. We and others previously demonstrated that peripheral TCRαβ+CD3+ T cells express CD8β either at a high (CD8βhigh) or low density (CD8βlow), thereby defining two functionally distinct subsets. CD8βlow T cells express predominantly CD8αα and less CD8αβ as a coreceptor, display a differentiated phenotype and exert effector function. CD8βhigh T cells appear to be the precursors expressing predominantly the heterodimeric efficient CD8αβ coreceptor, exhibiting a naïve phenotype and high proliferative capacity. In the present study, the distribution and functional properties of CD8βhigh and CD8βlow T cells of SLE patients were compared (n = 20) with those of healthy subjects (n = 16). It was found that expansion of CD8βlow T‐cell subset correlated with disease activity indicating chronic antigenic stimulation leading to a major lack of naïve CD8βhigh precursor T cells in SLE. Functional characteristics of CD8βlow T cells including production of cytokines and cytotoxic granules were not significantly different between patients with SLE and healthy individuals. We speculate that unbalanced CD8βhigh/CD8βlow T‐cell relation reflects a skewed homeostasis within the CD8+ T‐cell compartment towards fully differentiated effector T cells possibly due to persistent antigen stimulation in SLE.
Cerebral Gene Expression of Superantigen Encephalitis in the Lewis Rat Induced by Staphylococcal Enterotoxin A
Authors: Emmer A. , Gerlach K. , Staege M. S. , Kornhuber M. E.
Published: April 2008

Superantigens were suggested to play a role in the pathogenesis of different autoimmune diseases including multiple sclerosis (MS). Previously, it was demonstrated that local expression of the superantigen, staphylococcal enterotoxin A (SEA) in the brain of rats may lead to encephalitis which was amplified by using intravenous injection of concanavalin A (ConA)‐activated splenocytes. In the present investigation, gene expression was studied in the rat brain 8 days after an injection of 50 μl of 1 mg/ml SEA or saline and 5 days after an intravenous injection of 1 × 107 ConA‐activated spleen cells. Of 8800 genes investigated (Affymetrix, rat genome U34A), the expression of 106 genes was significantly and at least threefold increased with SEA, while the expression of 29 genes was decreased at least threefold. Increased gene expression was compatible with an intracerebral inflammatory response mediated by antigen‐presenting cells and CD8+ T lymphocytes. Elevated chemokines comprised RANTES (CCL5), osteopontin, MCP‐1 (CCL2) and CXCL10. Further, genes with increased expression were assigned to the extracellular matrix, microglia/macrophage cell elements, astrocytes (GFAP) and phagocytosis. There was considerable conformity between previously reported gene expression profiles for experimental autoimmune encephalomyelitis (EAE) or MS and the present findings. Our data are in line with the concept that T‐cell superantigen locally expressed in the central nervous system induces an inflammatory response. Therefore, the study of gene expression profiles does not seem to allow clear conclusions with respect to the aetiology of central nervous system autoimmune diseases.
CCR5 Δ32 Polymorphism: Associated with Gallbladder Cancer Susceptibility
Authors: Srivastava A. , Pandey S. N. , Choudhuri G. , Mittal B.
Published: April 2008

Inflammation of gallbladder is an established risk factor for gallbladder cancer (GBC) pathogenesis. Chemokine receptors play crucial role in antitumour immunity and are involved in inflammation and pathogenesis of cancers. Present study was aimed to examine the role of CCR5 Δ32 polymorphism in conferring genetic susceptibility to GBC. Present case–control study included 144 proven GBC patients and 210 healthy controls. Genotyping was done by polymerase chain reaction–restriction fragment length polymorphism (PCR‐RFLP) method. Statistically significant difference was observed in distribution of CCR5+/Δ32 genotype (P = 0.028) [odds ratio (OR) = 2.850; 95% confidence interval (CI) = 1.1–7.2] and CCR5 Δ32 allele (P = 0.012) (OR = 3.145, 95% CI = 1.2–7.7) in GBC patients which was conferring high risk. Stratification of GBC patients showed significant association of CCR5+/Δ32 genotype and CCR5 Δ32 allele with GBC patients with and without gallstones. Analysis based on age of onset and gender suggested significant association of CCR5 Δ32 allele with early onset (<50 years) of the disease but only marginal influence of gender in CCR5 Δ32‐mediated risk of cancer. Risk was further modulated by tobacco usage and significantly increased risk was observed in tobacco users with CCR5+/Δ32 genotype. In conclusion, CCR5+/Δ32 genotype and CCR5 Δ32 allele confer significant risk for GBC particularly in patients with early onset and tobacco usage. Role of CCR5+/Δ32 polymorphism in GBC susceptibility is independent of gallstone formation.
Auto‐antibodies to Receptor Tyrosine Kinases TrkA, TrkB and TrkC in Patients with Chronic Chagas’ Disease
Authors: Lu B. , Petrola Z. , Luquetti A. O. , PereiraPerrin M.
Published: April 2008

The Chagas’ disease parasite Trypanosoma cruzi promotes survival and differentiation of neurones by binding and activating nerve growth factor (NGF) receptor TrkA. The functional mimic of NGF in T. cruzi is a surface‐bound and shed immunogenic protein [neurotrophic factor/trans‐sialidase (TS)], which raised the possibility that immune response to T. cruzi in general and to neurotrophic factor/TS in particular leads to loss of immunological tolerance to host NGF and/or the NGF‐binding partner TrkA. In testing this hypothesis, we found that sera of individuals with chronic Chagas’ disease bear unique IgG2 autoantibodies that bind TrkA and TrkA family members TrkB and TrkC (ATA). Binding of ATA to Trk receptors is specific because the autoantibodies did not cross‐react with five other growth factor receptors, NGF and other neurotrophins, and T. cruzi. Thus, individuals with chronic Chagas’ disease produce unique antibodies that react with pan‐Trk receptors, one of which (TrkA) T. cruzi exploits to inhibit host cell apoptosis and to promote cellular invasion.
Structural models of primary cell walls in flowering plants: consistency of molecular structure with the physical properties of the walls during growth
Authors: Carpita Nicholas C. , Gibeaut David M.
Published: April 2008

Advances in determination of polymer structure and in preservation of structure for electron microscopy provide the best view to date of how polysaccharides and structural proteins are organized into plant cell walls. The walls that form and partition dividing cells are modified chemically and structurally from the walls expanding to provide a cell with its functional form. In grasses, the chemical structure of the wall differs from that of all other flowering plant species that have been examined. Nevertheless, both types of wall must conform to the same physical laws. Cell expansion occurs via strictly regulated reorientation of each of the wall's components that first permits the wall to stretch in specific directions and then lock into final shape. This review integrates information on the chemical structure of individual polymers with data obtained from new techniques used to probe the arrangement of the polymers within the walls of individual cells. We provide structural models of two distinct types of walls in flowering plants consistent with the physical properties of the wall and its components.
The evolution and future of haemophilia therapy
Authors: Bloom A. L.
Published: April 2008

Summary. Lane (1840) first noted the beneficial effect of blood transfusion in controlling haemophilic bleeding following ophthalmic surgery. The appreciation that haemophilia is due to a plasma defect, at first thought to be prothrombin, coincided with the discovery of blood groups. This led in due course to the discovery of citrate anti‐coagulant and the ability to store blood. The beneficial effect of citrated plasma in haemophilia led to the exploitation of stored blood, fresh frozen plasma, and the subsequent development of cryoprecipitate and factor concentrates. All this would not have been possible, however, without the selfless contribution of blood donors and the development of an organized blood transfusion service. In the United Kingdom, P. L. Oliver pioneered the development of blood donor panels, the London Blood Transfusion Service and the British Red Cross Society Blood Transfusion Service leading directly to the National Blood Transfusion Service; recognized as the World's senior service. The development of haemophilia therapy owes much, therefore, to Oliver's energetic and pioneering work and it is entirely appropriate that the first Oliver Memorial Lecture be directed to the evolution and future of haemophilia therapy. It is indeed an honour to be invited to deliver this Oliver Memorial Lecture at the combined meeting of the British Blood Transfusion Society and the British Society for Haematology here in Wembley.
Antibody to hepatitis C virus in blood donors found positive for other agents. II. Anti‐HIV‐1
Authors: Moore M. C. , Barbara J. A. J. , Hewitt P. E.
Published: April 2008

Summary. Stored serum samples from 24 blood donors confirmed positive for anti‐HIV‐1 were tested for antibody to hepatitis C virus (HCV). Those repeatedly reactive using the anti‐HCV ELISA screening test were retested by the HCV recombinant immunoblot (RIBA). Risk‐factors for the contraction of HIV infection that had been elicited at formal counselling sessions were evaluated in relation to HCV/HIV modes of infection. The only two donors confirmed to be anti‐HCV positive both admitted to intravenous drug use.
Decreasing transfusion exposure risk during extracorporeal membrane oxygenation (ECMO)
Authors: Scott Bjerke H. , Kelly R. E. , Foglia R. P. , Barcliff L. , Petz L.
Published: April 2008

SUMMARY. Extracorporeal membrane oxygenation (ECMO) is a lifesaving therapy for neonatal pulmonary hypertension but carries a significant risk for transfusion‐related complications. Packed red blood cell (PRBC) and platelet exposure were quantified and reviewed in 17 ECMO survivors prior (Group I, n= 9) and subsequent to (Group II, n= 8) changes in transfusion protocols. Blood product requirements included ECMO circuit priming, maintenance of haematocrit >0.40 or platelet count > 50 times 109/1, and colloid volume expansion. Group I was exposed to 13.8±10.2 (x±SD) different PRBC units. In Group II, multiple transfusions from single donor units decreased exposure 71% to 3.9±0.7 units (P<0.05). Decreases in blood withdrawn (11%) and transfusion volume (7%) were coincident with a 15% reduction in mean bypass time. Platelet volume transfusion decreased from 159±213 to 93±64 ml using volume‐reduced platelet packs. Total transfusion exposure decreased 59% from 20.8±17.8 units to 8.6±2.4 donor units. No transfusion complications occurred during the aggregate 1,926 h on bypass.

We conclude that neonates on ECMO have a significant transfusion exposure risk increasing with prolonged duration of ECMO therapy. In addition we noted that concentrated platelet packs decreased transfusion volume by 41%, and multiple PRBC transfusions from single donor units decreased donor exposure by 71% while both strategies decreased the overall transfusion exposure risk by 59%.
Bv: a distinct category of B sub‐group among Chinese blood donors in Hong Kong
Authors: Mak K. H. , Voak D. , Chu R. W. , Leong S. , Chua K. M.
Published: April 2008

SUMMARY. During the period 1984–1989, a total of 46 examples of Bv phenotype were encountered out of a total of 567,210 donors, giving an incidence of 1 in 12,330 among the Chinese in Hong Kong.

The Bv determinant corresponds to the portion of the B antigen that is present on rabbit red cells, and gives a negative reaction with polyclonal anti‐B reagents absorbed with rabbit red cells that still react with B3. Some potent monoclonal anti‐B reagents confirm the absence of a B epitope from Bv red cells even by adsorption and elution techniques. The failure of some monoclonal anti‐B reagents to detect Bv demonstrates the need to select or blend monoclonal anti‐B reagents for use in typing Oriental bloods. Cell‐conversion techniques failed to convert O cells to B cells using Bv serum with the appropriate substrate, whereas sera from most of the other B variants were capable of doing so. The Bv phenotype, therefore, represents a distinct category of B subgroups that is easily distinguishable from B3 and other B variants.
Serological and clinical aspects of granulocyte antibodies leading to alloimmune neonatal neutropenia
Authors: BUX J. , Jung K. D. , Kauth T. , Mueller‐Eckhardt C.
Published: April 2008

SUMMARY. Eighteen cases of alloimmune neonatal neutropenia (ANN) were analysed for their clinical and serological properties. Pregnancy was normal in all cases, but a 50% incidence of abortion is recorded. With the exception of two premature babies, all newborns were delivered at term. Omphalitis and mild infections of the skin were predominantly present. None of the new‐borns died by overwhelming sepsis. The average duration of neutropenia was 11 weeks (range 3–28 weeks). Intravenous IgG therapy was followed by transient remission in 2 of 4 affected newborns. Antibody differentiation revealed in five sera NA1‐, in four sera NA2‐ and in two sera NB1‐specific antibodies. In two sera only HLA antibodies were detectable. Complement activating antibodies were determined in 72% of the sera. Screening for granulocyte‐specific antibodies in 1016 postpartum sera of unselected women revealed a total of 11 sera (1.1%) reacting selectively with granulocytes, but only four (0.4%) were directed against a known granulocyte‐specific antigen. None of the new‐born of mothers alloimmunized to granulocyte antigens developed neutropenia, which suggests an incidence of ANN below 0.1%.
Immunomodulatory activity of different blood products on the mitogen‐induced human lymphocyte transformation
Authors: Sibrowski W. , Wegner W. , Kühnl P.
Published: April 2008

SUMMARY. Blood transfusions have an immunosuppressive effect on the recipient and induce changes in several immunological parameters. We studied the effect of homologous and autologous fresh plasma (FP), fresh frozen plasma (FFP), heparinized plasma, as well as the influence of red blood cells (RBC), CPDA‐1, CPD, heparin, PAGGS‐mannitol, SAG‐mannitol and ADSOL on mitogen‐induced lymphocyte transformation.

Both homologous and autologous FP and FFP decreased the PHA and ConA response of human lympocytes (P<0.05). The PWM response was reduced by FP (P<0.05). The mean t1/2 of plasma‐induced suppression was approximately 38 h. Dose‐dependent suppression rates were observed with pure CPDA‐1 and CPD solutions. In contrast, heparinized plasma showed an elevated PHA‐ and ConA‐induced transformation rate (P<0.025), whereas PWM induction was unaffected. In addition, washed RBC, pure PAGGS‐M, SAG‐M and ADSOL solutions revealed no effect on the PHA response. Freezing, heating or recalcification of plasma resulted in an increase in the PHA response. Adenine was not immunosuppressive in vitro.

We conclude that, in addition to unspecific mechanisms by CPDA‐1 or CPD, an unknown plasma factor, which is susceptible to changes in temperature or storage conditions, suppresses the PHA‐, PWM‐ or ConA‐induced T‐cell immune response. Further clinical studies are needed to correlate these observations with clinical phenomena.
Fetal and neonatal alloimmune thrombocytopenia: current trends in diagnosis and therapy
Authors: Kaplan C. , Morel‐Kopp M.‐C. , Clemenceau S. , Daffos F. , Forestier F. , Tchernia G.
Published: April 2008

SUMMARY. Neonatal thrombocytopenia affects 20–40% of the infants in intensive care units. The frequency of neonatal alloimmune thrombocytopenia (NAIT) is estimated at 1/1500 to 1/5000 live births. The risk of morbidity is significant with 20% neurological sequelae and the death rate is estimated at 10% of affected infants. During recent years considerable efforts have been made to prevent fetal bleeding and to avoid birth trauma, which have significantly changed the natural history of NAIT.
Confidential unit exclusion: the North London Blood Transfusion Centre's experience
Authors: Brennan M. T. , Hewitt P. E. , Moore C. , Hall G. , Barbara J. A. J.
Published: April 2008

SUMMARY. A ‘Confidential AIDS Questionnaire’ has been used at North London Blood Transfusion Centre (NLBTC) donor sessions since July, 1985. The aim of the questionnaire is to encourage self‐exclusion by those donors whose behaviour puts them at risk of HIV infection. In a situation where such individuals cannot avoid donating they can indicate, in confidence, that their blood should not be used for transfusion. Since the introduction of this procedure, an average of 10 donors per month, who admitted relevant risk behaviour, have been permanently excluded and a number of prospective donors have excluded themselves when faced with the questionnaire. We have found the questionnaire to be well accepted by donors. It is a useful adjunct to routine donor selection and microbiological testing of donations in our efforts to minimize transfusion‐transmitted infection.
Bacterial contamination of single‐donor blood components
Authors: Illert W. E. , Sänger W. , Weise W.
Published: April 2008

SUMMARY. An analysis was performed of the microbiological laboratory quality control data for the past 9 years (1985–1993). Bacterial contamination was detected in 100 of 25,171 tested blood components. Single‐donor platelet concentrates had a contamination incidence of 25 in 5889 (0.42%); whole blood samples were contaminated at a rate of 1 in 2973 (0.03%) and red cell concentrates at a rate of 73 in 15, 317 (0.48%); of 992 samples of fresh frozen plasma only 1 was contaminated (0.1%). Gram‐positive staphylococci comprised 75% of cases and Gram‐negative rods 10%. This frequency of laboratory‐detected bacterial contamination contrasts with the low rate of transfusion‐associated septicaemic events.
Quantification of IgG anti‐D bound to D‐positive red cells infused into D‐negative subjects after intramuscular injection of monoclonal anti‐D
Authors: Kumpel B. M. , Judson P. A.
Published: April 2008

SUMMARY. A flow‐cytometric method was developed to determine the number of molecules of IgG bound to D‐positive red blood cells (RBC) when sensitized with low plasma concentrations of IgG anti‐D in the presence of an excess of D‐negative RBC. D‐positive RBC were infused into 12 D‐negative male volunteers 2 days after intramuscular injection of monoclonal anti‐D (BRAD‐3, IgG3 or BRAD‐5, IgG1). Blood samples were taken immediately before, 3 min and 3 h after injection of the RBC, incubated for 1 h at 37°C, washed, then incubated sequentially with FITC‐conjugated anti‐IgG, IgM monoclonal anti‐D, biotin‐conjugated anti‐IgM, and R‐phycoerythrin‐conjugated streptavidin. To prepare a standard curve, O R1R2 RBC were incubated in duplicate with varying dilutions of BRAD‐3 or BRAD‐5, and RBC from one set were mixed with an excess of D‐negative RBC (1:100) and labelled as above, while cell‐bound IgG on the other set was quantified by ELISA. The test samples and standards were analysed by flow cytometry and the mean channel (FITC) fluorescence was plotted against molecules IgG/cell, from which the sensitization level of D‐positive RBC in the test samples was determined. The use of IgM anti‐D enhanced the discrimination between D‐positive and D‐negative RBC, especially when fewer than about 3000 molecules IgG/cell were bound. The assay was sensitive to about 1000 molecules IgG/cell. The sensitization levels of the D‐positive RBC in samples taken 3 h after injection were found to be in the range 1500‐10,000 molecules IgG anti‐D per cell.
Evaluation of a combined lysate/recombinant antigen anti‐HTLV‐I/II ELISA in high and low endemic areas of HTLV‐I/II infection
Authors: Vrielink H. , Sisay Y. , Reesink H. W. , Woerdeman M. , Winkel C. , de Leeuw S. J. , Lelie P. N. , van der Poel C. L.
Published: April 2008

SUMMARY. The Wellcozyme HTLV‐I/II ELISA (Murex Diagnostics) was evaluated in 7800 samples of various serum panels. Repeat reactivity was found by Wellcozyme in (A) 1/2181 (0.05%) Dutch blood donors, (B) 44/3036 (1.4%) Curaçao (Caribbean area) blood donors, (C) 46/2533 (1.8%) individuals of different Ethiopian population subsets, (D) 30/30 (100%) confirmed anti‐HTLV‐I positive samples and (E) 20/20 (100%) HTLV‐II PCR‐positive samples. All 91 Wellcozyme‐positive samples were tested for confirmation by Western blot (WB, Diagnostic Biotechnology). Among Wellcozyme HTLV‐I/II ELISA‐positive individuals, HTLV‐I/II WB positivity was found in 0/1 Dutch blood donors, 40/44 (88.9%) Curaçao blood donors and 20/46 (43.5%) Ethiopian individuals. HTLV‐I positivity was found in 40 (1.3%) WB‐positive Curaçao blood donors and in 9 (0.35%) Ethiopian individuals. HTLV‐II positivity was found in 11 (0.43%) WB‐positive Ethiopian individuals. The Wellcozyme HTLV‐I/II ELISA had a specificity of 99.95% in Dutch blood donors and a sensitivity of 100% in confirmed HTLV‐I‐ and HTLV‐II‐positive samples. In Ethiopia 55% of the HTLV‐I/II WB‐positive individuals were exclusively HTLV‐II positive, whereas in Curaçao no HTLV‐II infections were found.
ISBT Code 128 and code changes as part of the implementation of a national IT system for the English National Blood Service
Authors: DOUGHTY R. , FLANAGAN P.
Published: April 2008

The implementation of PULSE within the NBS will bring considerable advantages to the Service and to hospitals. A system of dual labelling has been developed to overcome intrinsic constraints identified with the ABC Codabar system. This should not, however, impact directly on hospitals which will be able to continue to utilize the ABC Codabar system.

The dual labelling system incorporates the use of the ISBT Code 128 barcode system for transfusion centre use. This must be clearly differentiated from the implementation of ISBT code 128 within the UK. This latter development would bring considerable benefit to transfusion practice, increasing the overall safety of blood transfusion. It is, however, recognized that extensive discussion with appropriate stakeholders will be necessary before any implementation date can be determined for this initiative, particularly so given the significant logistical and financial implications inherent in such a change.
The evidence for the use of recombinant factor VIIa in massive bleeding: development of a transfusion policy framework
Authors: Moltzan C. J. , Anderson D. A. , Callum J. , Fremes S. , Hume H. , Mazer C. D. , Poon M. C. , Rivard G. , Rizoli S. , Robinson S.
Published: April 2008

summary A review of the recent randomized control trial evidence of the use of recombinant factor VIIa (rFVIIa) in massive bleeding. rFVIIa is a recombinant genetically engineered clotting factor that has been used for the management of haemophilia patients with inhibitors. There has been increasing use in patients with massive bleeding, even when there is no underlying coagulation disorder present. In November 2006, the Canadian National Advisory Committee on Blood and Blood Products engaged in a consultation and review process with several leading Canadian experts to review and discuss the current evidence up to November 2006. There is little evidence to support the routine use of rFVIIa in massive bleeding on review of 13 randomized controlled trials. rFVIIa should only be considered as part of a transfusion policy framework for massive bleeding after all other transfusion and supportive measures are considered. An example of a policy framework is presented.
Procleix Ultrio transcription‐mediated amplification vs. serological blood screening in south‐western Greece
Authors: Sgourou A. , Karakantza M. , Theodori E. , Papadimitriou C. , Theodorou G. L. , Davanos N. , Thymianou S. , Zoumbos N. C. , Mouzaki A.
Published: April 2008

summary We present here our overall experience after 27 months of performance of the Procleix Ultrio [HIV‐1, hepatitis C virus (HCV), hepatitis B virus (HBV)] transcription‐mediated amplification (TMA) assay.

The aim of this report is to assess the impact of nucleic acid testing (NAT) implementation in blood screening of south‐western Greek blood donors.

We processed 38 264 units of blood as neat samples with the Procleix Ultrio TMA assay (Chiron/GenProbe, Emeryville/San Diego, CA, USA) between 1 January 2005 and 31 March 2007. NAT results were compared to those obtained from routine serology tests and quantitative polymerase chain reaction (PCR) assays.

Overall, 52 units of blood tested positive for HBV (1·4‰), 8 for HCV (0·2‰) and none for HIV or multiple infections. The yield of TMA was 0·183‰ for HBV (7/38 264) and 0 for HCV. The TMA HBV‐positive donations were tested for HBV DNA by a quantitative PCR assay and were found negative (below the detection limit of the method, 200 copies/mL). Follow‐up testing showed that the TMA HBV‐positive donations were positive for anti‐hepatitis B core antigen immunoglobulin G antibodies.

Implementation of the TMA assay in the individual donation configuration increased HBV detection compared to serological screening or a commonly used quantitative PCR assay. Follow‐up studies will determine the impact of NAT implementation in HBV transmission in countries with an intermediate HBV incidence.
Microbial complexes in supragingival plaque
Authors: Haffajee A. D. , Socransky S. S. , Patel M. R. , Song X.
Published: April 2008

Background/aims:  To examine microbial communities in supragingival biofilm samples.

Methods:  Supragingival plaque samples were taken from 187 subjects at baseline (n = 4745). Fifty‐five subjects provided supragingival plaque samples at 1–7 days after professional tooth cleaning (n = 1456); 93 subjects provided 8044 samples between 3 and 24 months post‐therapy. All samples were individually analyzed for their content of 40 bacterial species using checkerboard DNA–DNA hybridization. Microbial associations among species were sought using cluster analysis and community ordination techniques for the three groups separately.

Results:  Six complexes were formed for the baseline samples. Similar complexes were formed for the samples taken 3–24 months post‐therapy. However, distinct changes were observed in microbial communities in samples taken during the 7 days of plaque redevelopment. The complexes related to clinical parameters of periodontal disease.

Conclusion:  There were specific microbial complexes in supragingival plaque that were similar to those found in subgingival plaque samples with a few minor differences. The relation of previously unclustered taxa to the complexes was also described.
Actinobacillus actinomycetemcomitans lipopolysaccharide stimulates collagen phagocytosis by human gingival fibroblasts
Authors: Takahashi N. , Kobayashi M. , Takaki T. , Takano K. , Miyata M. , Okamatsu Y. , Hasegawa K. , Nishihara T. , Yamamoto M.
Published: April 2008

Introduction:  Collagen phagocytosis by fibroblasts is involved in the intracellular pathway related to collagen breakdown in soft connective tissues. The possible role of lipopolysaccharide (LPS) in regulating this fibroblast function has not been elucidated so we investigated the effect of LPS from Actinobacillus actinomycetemcomitans, a periodontopathic bacterium, on collagen phagocytic activity in human gingival fibroblasts and associated regulatory mechanisms.

Methods:  LPS pretreatment stimulated binding of collagen‐coated beads to cells and, subsequently, their internalization.

Results:  The LPS‐activated collagen phagocytic process was enhanced in the presence of the soluble form of CD14 (sCD14) or LPS‐binding protein (LBP), while the LPS/LBP treatment activated Akt and induced actin reorganization. Furthermore, these LPS/LBP‐induced effects were partially suppressed by adding phosphatidyl‐inositol‐3 kinase (PI3K) inhibitors.

Conclusion:  These results suggest that A. actinomycetemcomitans LPS disturbs the homeostasis of collagen metabolism within gingival tissue by facilitating collagen phagocytosis by gingival fibroblasts, and serum sCD14 and LBP positively regulate the action of LPS. In addition, the PI3K/Akt signaling is thought to partially mediate the LPS/LBP‐stimulated collagen phagocytic pathway, which may be dependent on actin cytoskeletal rearrangement.
Adherence of Aggregatibacter actinomycetemcomitans via serotype‐specific polysaccharide antigens in lipopolysaccharides
Authors: Fujise O. , Wang Y. , Chen W. , Chen C.
Published: April 2008

Introduction:  Gram‐negative Aggregatibacter actinomycetemcomitans is recognized as an important periodontal pathogen. A striking property of this bacterium is its ability to form a tenacious biofilm adhering to abiotic surfaces. Both fimbrial and non‐fimbrial adhesins are believed to be responsible for this ability. In our study, specific markerless mutants in the biosynthesis genes of cell surface polysaccharides were constructed with the Cre‐loxP recombination system to identify non‐fimbrial adhesin(s).

Methods:  Non‐fimbriated A. actinomycetemcomitans strain ATCC29523 (serotype a) was used to construct a deletion mutant of serotype‐a specific polysaccharide antigen (SPA‐a) in lipopolysaccharide (LPS). The LPS was purified through a polymyxin B column following phenol extraction, and verified by silver staining following sodium dodecyl sulfate–polyacrylamide gel electrophoresis and by immunoblot analysis using rabbit antisera raised against SPA‐a. Strains were grown in broth for 2 days and examined for the adherence of bacterial cells on the glass surface.

Results:  Strain ATCC29523 formed a thin film of bacterial growth on the glass surface. The deletion of SPA‐a affected its ability to form this thin film. When this mutant was rescued with the wild‐type SPA‐a gene cluster, its adherence‐positive phenotype was restored.

Conclusion:  SPA‐a in the LPS molecule appears to promote the adherence of A. actinomycetemcomitans cells to abiotic surfaces.
Insights into the evolution of CCMs from comparisons with other resource acquisition and assimilation processes
Authors: Raven John A. , Giordano Mario , Beardall John
Published: April 2008

Regarding inorganic carbon as ‘just another’ chemical resource used in the growth of aquatic photolithotrophs, we ask three questions and then attempt to answer them. (1) How common are catalysed chemical changes of the resource outside the cell, and accumulation of the resource inside the cell prior to assimilation, for the diverse chemical resources used? (2) Do acquisition and assimilation meet evolutionary optimality criteria with respect to the use of other resources? (3) Are there clues to the evolutionary origin of inorganic carbon concentrating mechanism (CCMs) in the mechanisms of acquisition of other resources and vice versa? Evidence considered includes molecular genetic similarities between CCM components and components of other resource acquisition mechanisms, and palaeogeochemical evidence on the timing of restrictions on the availability of the resources such that extracellular transformation of materials, and their accumulation within cells prior to assimilation, are needed. Provisional answers to the questions are as follows: (1) Many common chemical resources other than inorganic carbon are subject to extracellular chemical conversion and/or accumulation prior to assimilation, e.g. ammonium, nitrate, urea, amino acids, organic and inorganic phosphate and iron; (2) There is some evidence for optimality of CCMs and of less complex resource acquisition processes, exemplified by NH4+ entry and assimilation, though many more data are needed and (3) There are molecular genetic similarities between CCM components and transporters for other solutes and components of respiratory NADH dehydrogenases that are consistent with their use in CCMs representing a derived evolutionary state. Palaeogeochemical evidence suggests that CCMs evolved later than did at least some of the extracellular chemical transformation and/or accumulation mechanisms for other resources.