bluuebunny/crossref_metadata_2025_split huggingface dataset:
The
Pseudomonas syringae
HopPtoV Protein Is Secreted in Culture and Translocated into Plant Cells via the Type III Protein Secretion System in a Manner Dependent on the ShcV Type III Chaperone
Authors: Wehling Misty D. , Guo Ming , Fu Zheng Qing , Alfano James R. 
Published: May 2004

ABSTRACT

The bacterial plant pathogen
Pseudomonas syringae
depends on a type III protein secretion system and the effector proteins that it translocates into plant cells to cause disease and to elicit the defense-associated hypersensitive response on resistant plants. The availability of the
P. syringae
pv. tomato DC3000 genome sequence has resulted in the identification of many novel effectors. We identified the
hopPtoV
effector gene on the basis of its location next to a candidate type III chaperone (TTC) gene,
shcV
, and within a pathogenicity island in the DC3000 chromosome. A DC3000 mutant lacking ShcV was unable to secrete detectable amounts of HopPtoV into culture supernatants or translocate HopPtoV into plant cells, based on an assay that tested whether HopPtoV-AvrRpt2 fusions were delivered into plant cells. Coimmunoprecipitation and
Saccharomyces cerevisiae
two-hybrid experiments showed that ShcV and HopPtoV interact directly with each other. The ShcV binding site was delimited to an N-terminal region of HopPtoV between amino acids 76 and 125 of the 391-residue full-length protein. Our results demonstrate that ShcV is a TTC for the HopPtoV effector. DC3000 overexpressing ShcV and HopPtoV and DC3000 mutants lacking either HopPtoV or both ShcV and HopPtoV were not significantly impaired in disease symptoms or bacterial multiplication in planta, suggesting that HopPtoV plays a subtle role in pathogenesis or that other effectors effectively mask the contribution of HopPtoV in plant pathogenesis.
The
Butyrivibrio fibrisolvens tet
(W) Gene Is Carried on the Novel Conjugative Transposon Tn
B1230
, Which Contains Duplicated Nitroreductase Coding Sequences
Authors: Melville Claire M. , Brunel Romain , Flint Harry J. , Scott Karen P. 
Published: May 2004

ABSTRACT

The
Butyrivibrio fibrisolvens tet
(W) gene is located on the conjugative transposon Tn
B1230
. Tn
B1230
encodes transfer proteins with 48 to 67% identity to some of those encoded by Tn
1549. tet
(W) is flanked by directly repeated sequences with significant homology to oxygen-insensitive nitroreductases. The 340 nucleotides upstream of
tet
(W) are strongly conserved and are required for tetracycline resistance.
An epidemiological study of the magnitude and consequences of work related violence: the Minnesota Nurses’ Study
Authors: Gerberich S G , Church T R , McGovern P M , Hansen H E , Nachreiner N M , Geisser M S , Ryan A D , Mongin S J , Watt G D 
Published: May 2004

Aims:To identify the magnitude of and potential risk factors for violence within a major occupational population.Methods:Comprehensive surveys were sent to 6300 Minnesota licensed registered (RNs) and practical (LPNs) nurses to collect data on physical and non-physical violence for the prior 12 months. Re-weighting enabled adjustment for potential biases associated with non-response, accounting for unknown eligibility.Results:From the 78% responding, combined with non-response rate information, respective adjusted rates per 100 persons per year (95% CI) for physical and non-physical violence were 13.2 (12.2 to 14.3) and 38.8 (37.4 to 40.4); assault rates were increased, respectively, for LPNs versus RNs (16.4 and 12.0) and males versus females (19.4 and 12.9). Perpetrators of physical and non-physical events were patients/clients (97% and 67%, respectively). Consequences appeared greater for non-physical than physical violence. Multivariate modelling identified increased rates for both physical and non-physical violence for working: in a nursing home/long term care facility; in intensive care, psychiatric/behavioural or emergency departments; and with geriatric patients.Conclusions:Results show that non-fatal physical assault and non-physical forms of violence, and relevant consequences, are frequent among both RNs and LPNs; such violence is mostly perpetrated by patients or clients; and certain environmental factors appear to affect the risk of violence. This serves as the basis for further analytical studies that can enable the development of appropriate prevention and control efforts.
Indices of asthma among atopic and non-atopic woodworkers
Authors: Schlünssen V , Schaumburg I , Heederik D , Taudorf E , Sigsgaard T 
Published: May 2004

Aims:To investigate the relation between wood dust exposure and different indices of asthma among woodworkers and non-exposed subjects.Methods:A total of 302 woodworkers and 71 non-exposed subjects answered a respiratory health questionnaire, underwent a non-specific bronchial provocation test using the Yan method, and received a skin prick test with 12 common inhalant allergens. Subgroups performed repeated peak flow monitoring and underwent a reversibility test. A total of 347 dust measurements among 234 woodworkers were performed with passive dust monitors.Results:The overall geometric mean (geometric standard deviation) exposure to inhalable dust was 0.96 (2.02) mg/m3. There was a tendency to increased risk of asthma among atopic woodworkers compared to atopic non-exposed subjects, with ORs between 3.0 (0.8–11.9) (symptomatic BHR) and 1.3 (0.5–4.2) (work related symptoms). In woodworkers, asthma was associated with atopy, with ORs between 7.4 (2.8–19.7) (symptomatic BHR) and 4.2 (2.4–7.7) (asthma symptoms). Asthma was related to dust level, most pronounced for symptomatic BHR among atopics, with OR 22.9 (1.0–523.6) for the highest compared to the lowest dust level. For work related asthma symptoms the association with dust level was seen only for non-atopics.Conclusions:Wood dust exposure was associated with asthma, despite a low dust level compared to other studies. Atopy was an important effect modifier in the association between asthma and wood dust exposure.
A descriptive study of work aggravated asthma
Authors: Goe S K , Henneberger P K , Reilly M J , Rosenman K D , Schill D P , Valiante D , Flattery J , Harrison R , Reinisch F , Tumpowsky C , Filios M S 
Published: May 2004

Background and Aims:Work related asthma (WRA) is one of the most frequently reported occupational lung diseases in a number of industrialised countries. A better understanding of work aggravated asthma (WAA), as well as work related new onset asthma (NOA), is needed to aid in prevention efforts.Methods:WAA and NOA in the United States were compared using cases reported to the National Institute for Occupational Safety and Health (NIOSH) from four state Sentinel Event Notification Systems for Occupational Risks (SENSOR) surveillance programmes for 1993–95.Results:A total of 210 WAA cases and 891 NOA cases were reported. WAA cases reported mineral and inorganic dusts as the most common exposure agent, as opposed to NOA cases, in which diisocyanates were reported most frequently. A similar percentage of WAA and NOA cases still experienced breathing problems at the time of the interview or had visited a hospital or emergency room for work related breathing problems. NOA cases were twice as likely to have applied for workers’ compensation compared with WAA cases. However, among those who had applied for worker compensation, approximately three-fourths of both WAA and NOA cases had received awards. The services and manufacturing industrial categories together accounted for the majority of both WAA (62%) and NOA (75%) cases. The risk of WAA, measured by average annual rate, was clearly the highest in the public administration (14.2 cases/105) industrial category, while the risk of NOA was increased in both the manufacturing (3.2 cases/105) and public administration (2.9 cases/105) categories.Conclusions:WAA cases reported many of the same adverse consequences as NOA cases. Certain industries were identified as potential targets for prevention efforts based on either the number of cases or the risk of WAA and NOA.
Mortality and cancer incidence among Lithuanian cement producing workers
Authors: Smailyte G , Kurtinaitis J , Andersen A 
Published: May 2004

Aims:To investigate mortality and cancer incidence of cement producing workers.Methods:A total of 2498 cement workers who have been employed at Portland cement producing departments for at least one year from 1956 to 2000 were followed up from 1 January 1978 to 31 December 2000. The cohort contributed 43 490 person-years to the study. Standardised incidence ratios (SIR) and standardised mortality ratios (SMR) were calculated as ratios between observed and expected numbers of cancers and deaths. The expected numbers were based on sex specific incidence and mortality rates for the total Lithuanian population.Results:Significantly increased SMRs were found for all malignant neoplasms (SMR 1.3, 95% CI 1.0 to 1.5) and for lung cancer (SMR 1.4, 95% CI 1.0 to 1.9) among male cement workers. SIR for all cancer sites was 1.2 (95% CI 1.0 to 1.4). Excess risk was found for cancer of the lung (SIR 1.5, 95% CI 1.1 to 2.1). The SIR for urinary bladder cancer was also increased (SIR 1.8, 95% CI 0.9 to 3.5). The overall cancer incidence was not increased among females (SIR 0.8, 95% CI 0.6 to 1.1). With increasing cumulated exposure to cement dust, there were indications of an increasing risk of lung and stomach cancers among males.Conclusions:This study supported the hypothesis that exposure to cement dust may increase the lung and bladder cancer risk. A dose related risk was found for stomach cancer, but no support was found for an increased risk of colorectal cancer.
Erythropoietin gene from a teleost fish, Fugu rubripes
Authors: Chou Chih-Fong , Tohari Sumanty , Brenner Sydney , Venkatesh Byrappa 
Published: May 2004

AbstractIn this paper we report the cloning and characterization of the erythropoietin (Epo) gene from the pufferfish, Fugu rubripes. This is the first nonmammalian Epo gene to be cloned. The Fugu Epo comprises 5 exons and 4 introns similar to the human EPO, and encodes a 185–amino acid protein that is 32% to 34% identical to Epo from various mammals. The synteny of genes at the Epo locus is conserved between the Fugu and humans. Unlike in mammals in which adult kidney is the primary Epo-producing organ, the heart is the main Epo-producing organ in adult Fugu. In addition to the heart, Fugu Epo is also expressed in the liver and brain similar to the human EPO. Interestingly, the transcripts in the Fugu brain are generated from a distal promoter and include an alternatively spliced first coding exon. No such brain-specific alternative splicing of Epo has been reported in mammals so far. Transient transfection studies in a fish hepatoma cell line (PLHC-1) and a human hepatoma cell line (HepG2) suggest that although the Fugu Epo promoter many not be hypoxia inducible, the gene may be regulated by hypoxia.
Apoptotic resistance to ionizing radiation in pediatric B-precursor acute lymphoblastic leukemia frequently involves increased NF-κB survival pathway signaling
Authors: Weston Victoria J. , Austen Belinda , Wei Wenbin , Marston Eliot , Alvi Azra , Lawson Sarah , Darbyshire Philip J. , Griffiths Mike , Hill Frank , Mann Jill R. , Moss Paul A. H. , Taylor A. Malcolm R. , Stankovic Tatjana 
Published: May 2004

AbstractTo investigate possible causes of the variable response to treatment in pediatric B-precursor acute lymphoblastic leukemia (ALL) and to establish potential novel therapeutic targets, we used ionizing radiation (IR) exposure as a model of DNA damage formation to identify tumors with resistance to p53-dependent apoptosis. Twenty-one of 40 ALL tumors responded normally to IR, exhibiting accumulation of p53 and p21 proteins and cleavage of caspases 3, 7, and 9 and of PARP1. Nineteen tumors exhibited apoptotic resistance and lacked PARP1 and caspase cleavage; although 15 of these tumors had normal accumulation of p53 and p21 proteins, examples exhibited abnormal expression of TRAF5, TRAF6, and cIAP1 after IR, suggesting increased NF-κB prosurvival signaling as the mechanism of apoptotic resistance. The presence of a hyperactive PARP1 mutation in one tumor was consistent with such increased NF-κB activity. PARP1 inhibition restored p53-dependent apoptosis after IR in these leukemias by reducing NF-κB DNA binding and transcriptional activity. In the remaining 4 ALL tumors, apoptotic resistance was associated with a TP53 mutation or with defective activation of p53. We conclude that increased NF-κB prosurvival signaling is a frequent mechanism by which B-precursor ALL tumors develop apoptotic resistance to IR and that PARP1 inhibition may improve the DNA damage response of these leukemias.
Effects of lethal irradiation in zebrafish and rescue by hematopoietic cell transplantation
Authors: Traver David , Winzeler Alissa , Stern Howard M. , Mayhall Elizabeth A. , Langenau David M. , Kutok Jeffrey L. , Look A. Thomas , Zon Leonard I. 
Published: May 2004

Abstract
The study of hematopoiesis has been greatly facilitated by transplantation of blood cell populations into recipient animals. Efficient engraftment of donor cells generally requires ablation of the host hematopoietic system. The zebrafish has recently emerged as a developmental and genetic system to study hematopoiesis. To enable the study of hematopoietic stem cell (HSC) biology, immune cell function, and leukemogenesis in zebrafish, we have developed hematopoietic cell transplantation (HCT) into adult recipient animals conditioned by γ irradiation. Dose-response experiments showed that the minimum lethal dose (MLD) of 40 Gy led to the specific ablation of hematolymphoid cells and death by 14 days after irradiation. Sublethal irradiation doses of 20 Gy predominantly ablated lymphocytes and permitted transplantation of a lethal T-cell leukemia. Finally, transplantation of hematopoietic cells carrying transgenes yielding red fluorescent erythrocytes and green fluorescent leukocytes showed that HCT is sufficient to rescue the MLD, that recipient hematolymphoid tissues were repopulated by donor-derived cells, and that donor blood cell lineages can be independently visualized in living recipients. Together, these results establish transplantation assays to test for HSC function and oncogenic transformation in zebrafish.
Anti-α4 integrin antibody suppresses the development of multiple myeloma and associated osteoclastic osteolysis
Authors: Mori Yoshihisa , Shimizu Nobuaki , Dallas Mark , Niewolna Maryla , Story Beryl , Williams Paul J. , Mundy Gregory R. , Yoneda Toshiyuki 
Published: May 2004

AbstractSupporting roles of stromal cells in preferential colonization of myeloma cells in bone marrow and development of associated osteoclastic osteolysis through cell-cell interactions have been indicated. Here we examined the effects of a monoclonal antibody to α4 integrin (anti-α4 Ab) that disrupts myeloma cell-stromal cell interactions mediated via α4β1 integrin and vascular cell adhesion molecule-1 (VCAM-1) on myeloma cell growth in bone marrow and accompanying osteolysis. The anti-α4 Ab decreased VCAM-1-stimulated 5TGM1/luc cell growth in culture. The 5TGM1 murine myeloma cells stably transfected with the firefly luciferase (5TGM1/luc) were inoculated from tail vein in bg/xid/nd mice. Preventative administration of the anti-α4 Ab suppressed the elevation of serum IgG2b levels, decreased 5TGM1/luc tumor burden with increased apoptosis in bone and spleen, reduced bone destruction with diminished number of osteoclasts, and prolonged survival of 5TGM1/luc-bearing mice. In contrast, therapeutic administration of the antibody failed to show these effects. However, therapeutic administration of the antibody combined with melphalan significantly suppressed serum IgG2b levels and tumor burden in bone. Our results suggest that the interactions with stromal cells via α4β1/VCAM-1 are critical to the development of myeloma and associated osteolysis and that disruption of these interactions using anti-α4 Ab is a potential therapeutic approach for myeloma. (Blood. 2004;104:2149-2154)
Mutations of AML1 are common in therapy-related myelodysplasia following therapy with alkylating agents and are significantly associated with deletion or loss of chromosome arm 7q and with subsequent leukemic transformation
Authors: Christiansen Debes H. , Andersen Mette K. , Pedersen-Bjergaard Jens 
Published: May 2004

Abstract
The AML1 transcription factor is essential for normal hematopoiesis and is the target of several chromosomal translocations in acute leukemia. Acquired somatic AML1 mutations were recently demonstrated sporadically in de novo myelodysplasia (MDS) and acute myeloid leukemia (AML) including a few cases of therapy-related disease (t-MDS/t-AML). We examined 140 patients with t-MDS or t-AML for AML1 mutations by direct sequencing. We identified 9 missense, 3 nonsense, and 10 frameshift mutations, all heterozygous, in 22 patients (15.7%). Thirteen mutations were located in the N-terminal Runt homology domain (RHD), whereas 9 mutations were located in the C-terminal region including the transactivation domain (TAD). Nineteen patients with AML1 mutations had previously received alkylating agents whereas 2 patients had received radiotherapy only. AML1 mutations were highly significantly associated with presentation of the disease as t-MDS (P = .003), with deletion or loss of chromosome arm 7q (P = .001) and with subsequent transformation to overt t-AML (P = .0001). Patients with missense mutations presented a shorter survival compared with patients with nonsense/frameshift mutations (P = .03). Our results suggest that AML1 mutations and deletion of genes on chromosome arm 7q cooperate in leukemogenesis and predispose to leukemic transformation.
Platelet surface glutathione reductase-like activity
Authors: Essex David W. , Li Mengru , Feinman Richard D. , Miller Anna 
Published: May 2004

AbstractWe previously found that reduced glutathione (GSH) or a mixture of GSH/glutathione disulfide (GSSG) potentiated platelet aggregation. We here report that GSSG, when added to platelets alone, also potentiates platelet aggregation. Most of the GSSG was converted to GSH by a flavoprotein-dependent platelet surface mechanism. This provided an appropriate redox potential for platelet activation. The addition of GSSG to platelets generated sulfhydryls in the β subunit of the αIIbβ3 fibrinogen receptor, suggesting a mechanism for facilitation of agonist-induced platelet activation.
Prevalence and incidence of severe sepsis in Dutch intensive care units
Authors: van Gestel Aukje , Bakker Jan , Veraart Christiaan PWM , van Hout Ben A 
Published: May 2004

Abstract
Introduction
Severe sepsis is a dreaded consequence of infection and necessitates intensive care treatment. Severe sepsis has a profound impact on mortality and on hospital costs, but recent incidence data from The Netherlands are not available. The purpose of the present study was to determine the prevalence and incidence of severe sepsis occurring during the first 24 hours of admission in Dutch intensive care units (ICUs).

Methods
Forty-seven ICUs in The Netherlands participated in a point prevalence survey and included patients with infection at the time of ICU admission. Clinical symptoms of severe sepsis during the first 24 hours of each patient's ICU stay were recorded and the prevalence of severe sepsis was calculated. Then, the annual incidence of severe sepsis in The Netherlands was estimated, based on the prevalence, the estimated length of stay, and the capacity of the participating ICUs relative to the national intensive care capacity.

Results
The participating ICUs had 442 beds available for admissions, which was estimated to be 42% of the national ICU capacity. At the time of the survey, 455 patients were currently admitted and 151 were included in the analysis; 134 (29.5%) patients met criteria for severe sepsis. The most common failing organ system was the respiratory system (90%), and most patients were admitted following surgery (37%) and were admitted because of acute infection (62%). The most prevalent source of infection was the lung (47%). The estimated duration of ICU stay for severe sepsis patients was 13.3 ± 1.1 days.

Conclusion
The annual number of admissions for severe sepsis in Dutch ICUs was calculated at 8643 ± 929 cases/year, which is 0.054% of the population, 0.61% of hospital admissions and 11% of ICU admissions.
Epidemiology of sepsis in Norway in 1999
Authors: Flaatten Hans 
Published: May 2004

Abstract
Introduction
Sepsis and severe sepsis are asociated with high hospital mortality. Little is known about the occurrence of sepsis in general hospital populations. The goal of the present study was to reveal the epidemiology of sepsis in Norwegian hospitals over 1 year.

Methods
Patients admitted to all Norwegian hospitals during 1999 (n = 700,107) were analyzed by searching the database of the Norwegian Patient Registry for markers of sepsis, using International Classification of Diseases (ICD)-10 codes for sepsis and severe infections. In patients with such diagnoses, demographic data, hospital outcome data and ICD-10 codes for organ dysfunction were also retrieved. Sepsis was further classified as primary or secondary, and severe (sepsis with vital organ dysfunction) or nonsevere. The age-adjusted mortality rate, and the sepsis rates for all hospital admissions and in the Norwegian population were calculated.

Results
A total of 6665 patients were classified as having sepsis, and of these 2121 (31.8%) had severe sepsis. The most frequent failing organ system was the circulatory system, and 1562 had septic shock. Mortality increased from 7.1% (in those with no documented organ dysfunction) to 71.8% (in those with three or more organ dysfunctions). The mean mortality was 13.5%, and the mortality of severe sepsis was 27%. The incidence of sepsis was 9.5/1000 hospital admissions and 1.49/1000 inhabitants in 1999.

Conclusion
Sepsis is not uncommon in Norwegian hospitals and is associated with high hospital mortality, which is similar to recent findings from the USA. Awareness of sepsis and its appropriate treatment is mandatory in Norway if we are to reduce mortality from sepsis by 25% in the next 5 years.
Tumor Necrosis Factor α Stimulates MUC1 Synthesis and Ectodomain Release in a Human Uterine Epithelial Cell Line
Authors: Thathiah Amantha , Brayman Melissa , Dharmaraj Neeraja , Julian JoAnne J. , Lagow Errin L. , Carson Daniel D. 
Published: May 2004

AbstractRegulation of MUC1 expression and removal is a salient feature of embryo implantation, bacterial clearance, and tumor progression. In some species, embryo implantation is accompanied by a transcriptional decline in uterine epithelial expression of MUC1. In other species, MUC1 is locally removed at blastocyst attachment sites, suggesting a proteolytic activity. Previously, we demonstrated that MUC1 is proteolytically released from the surface of a human uterine epithelial cell line, HES, and identified TNFα converting enzyme/a disintegrin and metalloprotease 17 as a constitutive and phorbol ester-stimulated MUC1 sheddase. The aims of the current study were to test the ability of soluble factors elevated during the periimplantation interval in vivo to stimulate ectodomain shedding of MUC1 from HES uterine epithelial cells and to characterize the nature of this proteolytic activity(ies). We identified TNFα as a prospective endogenous stimulus of MUC1 ectodomain release and of MUC1 and TNFα converting enzyme/a disintegrin and metalloprotease 17 expression. Moreover, we established that TNFα-stimulated MUC1 shedding occurs independently of increased de novo protein synthesis and demonstrated that the TNFα-induced increase in MUC1 gene expression is mediated through the κB site in the MUC1 promoter. Finally, we determined that the TNFα-sensitive MUC1 sheddase is inhibited by the metalloprotease inhibitor, TNFα protease inhibitor (TAPI), and the endogenous tissue inhibitor of metalloprotease-3. Collectively, these studies provide the initial in vitro characterization of a putative physiological stimulus of MUC1 ectodomain release and establish the nature of the metalloproteolytic activity(ies) involved.