bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of the leucocyte common antigen (LCA, CD45) isoforms RA and RO in acute haematological malignancies: possible relevance in the definition of new overlap points between normal and leukaemic haemopoiesis
Authors: Schiavone Ettore Mariano , Pardo Catia Lo , Noto Rosa Di , Manzo Ciro , Ferrara Felicetto , Vacca Clemente , Vecchio Luigi Del 
Published: March 2008

Summary. The membrane expression of CD45RA and CD45RO on fresh leukaemic cells taken from 529 cases of acute haemopoietic malignancies, including 117 B‐origin acute lymphoblastic leukaemia (B‐origin ALL), 3 7 T‐origin acute lymphoblastic leukaemia (T‐origin ALL), 297 de novo acute myeloid leukaemia (AML), 42 refractory anaemia with excess of blasts in transformation (RAEB‐T) and 36 myeloid blastic phase of chronic myelogenous leukaemia (CML‐BP‐my), was analysed. B‐origin ALLs were characterized by the lack of the RO isoform along with the consistent presence of RA. Conversely, a differential expression of the two isoforms was detected in different subsets of T‐origin ALL, in that T‐stem cell leukaemias (T‐SCL: CD7+, CD4−, CD8−, CD1−) preferentially expressed CD45RA whereas conventional T‐acute lymphoblastic leukaemias (T‐ALL: CD7+, CD4+ and/or CD8+ and/or CD1+) were consistently marked by CD45RO. Within myeloid malignancies, most of AMLs displayed CD45RA, while a substantial group of CML‐BP‐my preferentially exhibited CD45RO. As a general rule, a reciprocal exclusion of the two isoforms was observed in AML as well as in ALL. Nevertheless, a frequent coexpression of CD45RA and CD45RO was observed in CD14+ AML. In vitro treatment with all‐trans retinoic acid (ATRA) was able to promote a switch from CD45RA to CD45RO expression in 2 7 de novo AML, independently from morphological subtyping.To our knowledge, this is the first report on CD45 isoform expression in a large series of patients with acute leukaemia. The knowledge of the differential expression of CD45RA and CD45RO can ameliorate our classificative approach to haematological malignancies, as well as disclose new multiple overlap points between normal and leukaemic cell differentiation.
Flow cytometric analysis of decay‐accelerating factor (CD55) on neutrophils from aplastic anaemia patients
Authors: FORES RAFAEL , ALCOCER MARIA , DIEZ‐MARTIN JOSE L. , FERNANDEZ MANUEL N. 
Published: March 2008

Summary. Using a flow cytometric analysis, CD55 (decay‐accelerating factor), CD59 and CD58 have been measured on neutrophils from 12 aplastic anaemia (AA) patients who were long‐term survivors after immunosuppressive therapy (IS), 17 healthy individuals, four patients with PNH, and six patients with other haematological disorders.The neutrophils from normal control patients and the six patients with other haematological disorders showed 98 ±2% (mean ±SD) positive granulocytes for CD55. Corresponding values were low (12%, 26%, 51% and 58%) on the primarily PNH patients. Among the 12 AA patients examined, seven had normal and five low values (59% in two, 70%, 71% and 82%).Among the five A A patients who showed CD 5 5 neutrophil deficiency, four had showed an incomplete response after the initial IS treatment and the other relapsed following an initial haematological complete response; three cases had a positive Ham's test and two were negative.Our data suggest that the development of PNH clones is a frequent finding in A A long‐term survivors, mainly in those who had shown an incomplete response following IS. Neutrophil CD55 expression analysis by flow cytometry could be useful to detect clonal evolution in these patients.
Frequent association of t(3;14) or variant with other lymphoma‐specific translocations
Authors: Horsman Douglas E. , McNeil B. Kelly , Anderson Michelle , Shenkier Tamara , Gascoyne Randy D. 
Published: March 2008

Malignant lymphomas (ML) with t(3;14) or variant t(2;3) and t(3;22) have recently been recognized. These translocations have been shown to associate predominantly with B‐cell diffuse large cell lymphoma (DLCL) and less frequently with follicular lymphoma (FL). The molecular alterations associated with these translocations involve one of the immunoglobulin gene (Ig) loci and a recently cloned gene, bcl‐6 located at 3q27 which codes for a zinc‐finger protein that may function as a transcription factor.We have identified by cytogenetic analysis 22 cases of ML with a 3q27/Ig translocation. The pathologic diagnoses of these cases include DLCL, FL, small non‐cleaved non‐Burkitt lymphoma and chronic lymphocytic leukaemia. Molecular analysis confirmed a bcl‐6 rearrangement in 10/12 cases tested.The karyotype in 5/22 cases revealed the t(3;14) or variant in association with another lymphoma‐specific translocation, t(14;18) in three cases and t(8;14) in two cases. ML with dual translocations that implicate Ig genes in the deregulation of proto‐oncogenes are being increasingly recognized and may represent distinct subtypes or ‘hybrid’forms of malignant lymphoma.
Attenuated platelet sensitivity to collagen in patients with neurofibromatosis type 1
Authors: Rasko John E. J. , North Kathryn N. , Favaloro Emmanuel J. , Grispo Linda , Berndt Michael C. 
Published: March 2008

Haemostatis has not previously been studied in patients with neurofibromatosis 1 (NF‐1), despite case reports of an association with von Willebrand disease and reported excessive bleeding in those undergoing surgery for neurofibromas. Platelets from NF‐1 patients (n= 28) were tested for aggregation and ATP release with agonists including ADP, arachidonic acid, thrombin and collagen. Mepacrine staining of platelets and three different assays for von Willebrand factor (VWF) were also performed.In response to collagen as the platelet agonist, tested at both 2 and 1 μg/ml, NF‐1 patients had an attenuated rate of aggregation (P < 0.007), aggregation lag phase (P < 0.005) and ATP release (P < 0.045), as well as requiring higher collagen concentrations to attain threshold aggregation response (P= 0.041). Normal platelets resuspended in selected NF‐1 plasma exhibited significantly reduced platelet aggregation and release compared to controls, which was not corrected by mixing 1:1 with normal plasma. Collagen binding activity was reduced in NF‐1 patients compared with controls (127% v 161%, P= 0.05).As a group, patients with NF‐1 display defective platelet function characterized by in vitro evidence of impaired responsiveness to collagen. It is suggested that a plasma factor, present in a significant proportion of NF‐1 patients, may interfere with the ability of collagen to interact with other proteins such as von Willebrand factor and the platelet collagen receptor.
Experiences in controlling resistant pollen beetle by type I ether pyrethroid Trebon 30 EC in Germany
Authors: Glattkowski H. , Saggau B. , Goebel G. 
Published: March 2008

Oil seed rape (OSR) is an important crop in Germany with a long growing history. Due to the prevalence of various springtime pests an average of two pyrethroid applications are made. Pyrethroid resistance in Germany was found locally in 2003, widespread distribution of resistance was observed in 2006, a year of very strong pest pressure. Field trials in 2005 and the following years and laboratory analysis showed good control of resistant pollen beetle (Meligethes aeneus) by type I ether pyrethroid etofenprox, the active substance of Trebon 30 EC. Etofenprox differs significantly from common pyrethroids, which are usually ester pyrethroids including an α‐amino‐group and halogen substitutions. Trebon 30 EC has comparable efficacy on all important OSR pests but it has superior efficacy on resistant pollen beetle compared to common pyrethroids. To cope with pyrethroid resistance of pollen beetle, three different modes of action (MOA)s are postulated, which may be type I pyrethroids, neonicotinoids and organophosphates (OPs). Because type I pyrethroids, such as Trebon 30 EC, perform well at low temperatures, have a broad spectrum of activity, are considered as not to be toxic to bees, and give a high level of control of resistant pollen beetle, they will have an important role in the insecticide spraying regime of OSR.
Calcium intake and its relationship with adiposity and insulin resistance in post‐pubertal adolescents
Authors: Dos Santos L. C. , De Pádua Cintra I. , Fisberg M. , Martini L. A. 
Published: March 2008

AbstractBackground Dietary calcium intake has been described as being a negative contributor to adiposity. In adolescents, this relationship is not well established. The objectives of the present study were to compare the calcium intake of normal‐weight and obese adolescents and to evaluate its relationship with adiposity and insulin resistance.Methods A cross‐sectional analysis of 96 post‐pubertal adolescents; 47 normal weight and 49 obese, mean age 16.6 (SD ± 1.3) years. Body composition was assessed by dual‐energy X‐ray absorptiometry. Dietary intake was evaluated using a 3‐day dietary record. The biochemical evaluation comprised the measurements of serum lipids, lipoproteins, glucose and insulin. Insulin resistance was calculated using the Homeostasis Model Assessment of Insulin resistance (HOMA‐IR).Results The mean calcium intake, adjusted for energy, was lower in obese adolescents, 585.2 (±249.9) mg, than in normal weight adolescents, 692.1 (±199.5) mg. Only 4% of adolescents had an adequate intake of calcium. Calcium intake was inversely associated with body trunk fat, insulin and HOMA‐IR in the obese group. The quartile analysis of calcium intake provided evidence that girls in the highest quartile had decreased adiposity and insulin resistance.Conclusions This study showed a negative relationship between calcium intake and body fat and insulin resistance, mainly in obese girls, and demonstrates the importance of an increased dietary calcium intake.
Cardiovascular disease‐risk factors in middle‐aged osteopaenic women treated with calcium alone or combined to three nutrients essential to artery and bone collagen
Authors: Massé P. G. , Tranchant C. C. , Jougleux J. L. , Coburn S. P. , Cole D. E. 
Published: March 2008

AbstractBackground  Recent research suggests that cardiovascular disease (CVD) and bone loss are functionally interwoven. This study examined the concomitant effects of a nutritional treatment of osteopaenia on CVD‐risk factors.Methods  A 1‐year placebo‐controlled trial was conducted on middle‐aged women with normal (group A) or low (groups B and C) bone mineral density. Subjects (n = 20 per group) took daily either a placebo, calcium carbonate alone or combined to a vitamin (C and B6)‐proline capsule, respectively. Urinary pyridoxic acid (used to assess treatment compliance), plasma homocysteine, serum lipids and lipoproteins were measured before and after nutritional intervention.Results  Groups were comparable at baseline in most parameters of interest. No changes occurred in groups A and B. The 4%, 7% and 25% reductions of total cholesterol, LDL and triglycerides, and 14% elevation of HDL were all significant in group C. A trend toward reduction was observed for homocysteine in this group.Conclusions  Vitamins C (500 mg) and B6 (75 mg) combined with proline had consistent beneficial effects on CVD‐risk factors, whereas calcium alone did not. This study also underlined the importance of considering vitamin B6 status as a potential CVD risk factor.
Dietary intervention in chronic fatigue syndrome
Authors: Hobday R. A. , Thomas S. , O’Donovan A. , Murphy M. , Pinching A. J. 
Published: March 2008

AbstractBackground  Anecdotal reports and books have been published linking an over growth of Candida Albicans with chronic fatigue syndrome (CFS), suggesting dietary change as a treatment option. Little scientific data has been published to validate this controversial theory. This study aims to determine the efficacy of dietary intervention on level of fatigue and quality of life (QoL) in individuals with CFS.Methods  A 24‐week randomized intervention study was conducted with 52 individuals diagnosed with CFS. Patients were randomized to either a low sugar low yeast (LSLY) or healthy eating (HE) dietary interventions. Primary outcome measures were fatigue as measured by the Chalder Fatigue Score and QoL measured by Medical Outcomes Survey Short Form‐36.Results  A high drop out rate occurred with 13 participants not completing the final evaluation (7HE/6LSLY). Intention to treat analysis showed no statistically significant differences on primary outcome measurements.Conclusion  In this randomized control trial, a LSLY diet appeared to be no more efficacious on levels of fatigue or QoL compared to HE. Given the difficulty with dietary compliance experienced by participants, especially in the LSLY group, it would appear HE guidance is a more pragmatic approach than advocating a complicated dietary regime.
A new liquid intravenous immunoglobulin with three dedicated virus reduction steps: virus and prion reduction capacity
Authors: Poelsler G. , Berting A. , Kindermann J. , Spruth M. , Hämmerle T. , Teschner W. , Schwarz H. P. , Kreil T. R. 
Published: March 2008

Background and Objectives  A new 10% liquid human intravenous immunoglobulin (US trade name: Gammagard Liquid; European trade name: KIOVIG) manufactured by a process with three dedicated pathogen inactivation/removal steps (solvent/detergent treatment, 35‐nm nanofiltration and low pH/elevated temperature incubation) was developed. The ability of the manufacturing process to inactivate/remove viruses and prions was investigated.Materials and Methods  Virus and prion removal capacities were assessed with down‐scale spiking experiments, validated for equivalence to the large‐scale process.Results  Lipid‐enveloped viruses were completely inactivated/removed by each of the three dedicated virus clearance steps, and for human immunodeficiency virus 1 (HIV‐1) and pseudorabies virus (PRV), also by the upstream cold ethanol fractionation step. Relevant non‐enveloped viruses [i.e. hepatitis A virus (HAV) and parvovirus B19 (B19V)] were effectively removed by nanofiltration and the cold ethanol fractionation step, and partial inactivation of non‐enveloped viruses was achieved by low pH incubation. Overall log reduction factors were > 20·0 for HIV‐1, > 18·1 for bovine viral diarrhoea virus, > 16·3 for West Nile virus, > 10·0 for influenza A virus subtype H5N1, > 21·8 for PRV, 12·0 for HAV, > 12·1 for encephalomyocarditis virus, 10·6 for B19V and 10·3 for mice minute virus. Prions (Western blot assay) were completely removed (≥ 3·2 mean log reduction) by a step of the cold ethanol fractionation process.Conclusions  Introducing three dedicated virus‐clearance steps in the manufacturing process of immunoglobulins from human plasma provides high margins of safety.
The construction of a novel kind of non‐viral gene delivery vector based on protein as core backbone
Authors: Li D. , Kong Y. , Yu H. , Lehtinen A. , Huang H. , Shen F. , Min L. , Zhou J. , Tang G. , Wang Q. 
Published: March 2008

Background and Objectives  A novel kind of non‐viral gene delivery vector based on transferrin (Tf) as the core component was constructed with high transfection efficiency and low toxicity.Materials and Methods  The synthesis vector of Tf‐PEI600 was confirmed by different physicochemical methods, including 1H nuclear magnetic resonance, gel permeation chromatography, X‐ray and thermogravimetric analysis. The cytotoxicity and gene delivery efficiency of the synthesized vector were verified by in vitro experiments.Results  The agarose gel electrophoresis assay indicated that the novel copolymer Tf‐PEI600 could efficiently condense plasmid DNA and the condensed nanoparticles exhibited a spherical shape. As the weight ratio of Tf‐PEI600 to DNA reached 15·0, the particle size (about 200 nm) and the zeta potential (about 20 mV) of the nanoparticles became optimal for gene delivery. The methylthiazolyl tetrazolium (MTT) assay showed the cytotoxicity of Tf‐PEI600 to be similar to that of PEI600 and much lower than that of PEI25kDa. In gene‐delivery experiments with COS‐7 cells and HepG2 cells, the Tf‐PEI600 showed about a 30‐ to 53‐fold higher efficiency than PEI600 and nearly equal to that of PEI25kDa.Conclusions  These data suggest that Tf‐PEI600, with the advantages of low toxicity and high gene‐delivery efficiency, might have great prospects in the practice of gene delivery. The core‐shell structure of Tf‐PEI600 also provided a novel strategy for the construction of non‐viral gene delivery vectors.
Dissection of endoplasmic reticulum stress signaling in alcoholic and non‐alcoholic liver injury
Authors: Ji Cheng 
Published: March 2008

AbstractAccumulation of unfolded or malfolded proteins induces endoplasmic reticulum (ER) stress which elicits a complex network of interacting and parallel responses that dampen the stress. The ER stress response in the liver is controlled by intrinsic feedback effectors and is initially protective. However, delayed or insufficient responses or interplay with mitochondrial dysfunction may turn physiological mechanisms into pathological consequences including apoptosis, fat accumulation and inflammation all of which have an important role in the pathogenesis of liver disorders such as genetic mutations, viral hepatitis, insulin resistance, ischemia/reperfusion injury, and alcoholic and non‐alcoholic steatosis. In both alcohol and non‐alcohol‐induced ER stress, a common candidate is hyperhomocysteinemia. Betaine supplementation and/or expression of betaine‐homocysteine methyltransferase (BHMT) promote removal of homocysteine and alleviate ER stress, fatty accumulation and apoptosis in cultured hepatocytes and mouse models. The rapidity and magnitude of homocysteine‐induced activation of each of the main ER resident transmembrane sensors including inositol requiring enzyme 1 (IRE‐lα), activating transcription factor 6 (ATF‐6) and RNA‐activated protein kinase (PKR)‐like ER kinase (PERK) appear different in different experimental models. Dissection and differentiation of ER stress signaling may reveal clues on the specific importance of the ER stress response in contributing to liver injury and thus provide better strategies on prevention and treatment of liver disease.
Ca2+‐induced pancreatic cell death: Roles of the endoplasmic reticulum, zymogen granules, lysosomes and endosomes
Authors: Petersen Ole H 
Published: March 2008

AbstractAlcohol induces Ca2+‐dependent intracellular trypsinogen activation in the apical granular area via non‐oxidative metabolites, such as fatty acid ethyl esters and fatty acids. Intracellular trypsinogen activation is a crucial initiating event in the development of acute pancreatitis, but the specific organelle in which this process takes place has been unknown. Recent data demonstrate that the Ca2+‐dependent trypsinogen activation occurs in postexocytotic endocytic vacuoles. These vacuoles are acid due to a bafilomycin‐sensitive vacuolar H+ ATPase and have a very Ca2+‐permeable membrane. Acid endocytic structures, together with lysosomes, zymogen granules and elements of the endoplasmic reticulum, also play an important role in the physiological Ca2+ signal generation that normally regulates enzyme and fluid secretion from the exocrine pancreas.
Mechanisms for the anti‐inflammatory effects of adiponectin in macrophages
Authors: Huang Honglian , Park Pil‐Hoon , McMullen Megan R , Nagy Laura E 
Published: March 2008

AbstractAdiponectin is an adipokine with potent anti‐inflammatory properties. The development of alcoholic liver disease is thought to involve increased pro‐inflammatory activity, mediated in part by the activation of hepatic macrophages (Kupffer cells). Chronic ethanol feeding sensitizes hepatic macrophages to activation by lipopolysaccharide (LPS), leading to increased production of reactive oxygen species and tumor necrosis factor‐α (TNF‐α). Adiponectin can normalize Toll‐like receptor‐4 (TLR‐4) mediated signaling in hepatic macrophages after ethanol feeding, likely contributing to the hepatoprotective effect of adiponectin in the progression of alcoholic liver disease. However, the mechanisms by which adiponectin suppress TLR‐4 mediated responses are not well understood. Using the macrophage‐like cell line, RAW264.7, we have investigated the molecular mechanisms by which adiponectin suppresses LPS‐stimulated TNF‐α production. Globular adiponectin (gAcrp)‐mediated desensitization of LPS‐stimulated responses in RAW264.7 macrophages was dependent on the production of the anti‐inflammatory cytokine interleukin (IL)‐10. gAcrp initially increased TNF‐α expression in RAW264.7 macrophages; this TNF‐α then contributed to increased expression of IL‐10. This initial gAcrp‐mediated increase in TNF‐α production by macrophages was mediated via activation of ERK1/2→Egr‐1 and nuclear factor (NF)‐κB‐dependent mechanisms. gAcrp‐stimulated IL‐10 expression was also dependent on the phosphorylation of cAMP response element‐binding protein and the cAMP response element in the IL‐10 promoter. In summary, these studies reveal a complex, integrated response of macrophages to gAcrp. gAcrp initially activated signaling pathways considered to be pro‐inflammatory, with a subsequent increase in the expression of the potent, anti‐inflammatory cytokine, IL‐10. Increased IL‐10 expression was ultimately required for the suppression of TLR4‐mediated signaling by gAcrp.
New role of plasminogen activator inhibitor‐1 in alcohol‐induced liver injury
Authors: Arteel Gavin E 
Published: March 2008

AbstractPlasminogen activator inhibitor‐1 (PAI‐1) is the main inhibitor of plasminogen activators, thereby playing a major role in fibrinolysis. Whereas hyperfibrinolysis is common in alcoholic cirrhosis, hypofibrinolysis (driven mostly by elevated levels of PAI‐1) is common during the development of alcoholic liver disease (ALD). However, whether or not PAI‐1 plays a causal role in the development of ALD has been unclear. The role of PAI‐1 was therefore investigated in models of early (steatosis), intermediate (inflammation/necrosis) and late (fibrosis) stages of alcoholic liver disease. For example, hepatic steatosis caused by both acute and chronic ethanol was blunted by inhibiting PAI‐1 activation. This effect of inhibiting PAI‐1 appears to be mediated, at least in part, by an increase in very low‐density lipoprotein (VLDL) synthesis in the absence of PAI‐1. The results from that study also indicated that PAI‐1 plays a critical role in both acute and chronic hepatic inflammation. Lastly, knocking out PAI‐1 potently protected against experimental hepatic fibrosis; the mechanism of this protective effect appears to be mediated predominantly by extracellular matrix (ECM) resolution by matrix metalloproteases, which are indirectly inhibited by PAI‐1. In summary, targeting PAI‐1 protects against all three stages of ALD in model systems. The mechanisms by which PAI‐1 contributes to these disease stages appear to not only involve the ‘classical’ function of PAI‐1 (i.e. in mediating fibrinolysis), but also other functions of this protein. These data support a role of PAI‐1 in the initiation and progression of ALD, and suggest that PAI‐1 may be a useful target for clinical therapy to halt or blunt disease progression.