bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of the
Streptococcus pneumoniae
BgaC Protein as a Novel Surface β-Galactosidase with Specific Hydrolysis Activity for the Galβ1-3GlcNAc Moiety of Oligosaccharides
Authors: Jeong Jae Kap , Kwon Ohsuk , Lee Yun Mi , Oh Doo-Byoung , Lee Jung Mi , Kim Seonghun , Kim Eun-Hye , Le Tu Nhat , Rhee Dong-Kwon , Kang Hyun Ah 
Published: March 2009

ABSTRACT

Streptococcus pneumoniae
is a causative agent of high morbidity and mortality. Although sugar moieties have been recognized as ligands for initial contact with the host, only a few exoglycosidases have been reported to occur in
S. pneumoniae
. In this study, a putative β-galactosidase, encoded by the
bgaC
gene of
S. pneumoniae
, was characterized for its enzymatic activity and virulence. The recombinant BgaC protein, expressed and purified from
Escherichia coli
, was found to have a highly regiospecific and sugar-specific hydrolysis activity for the Galβ1-3-GlcNAc moiety of oligosaccharides. Interestingly, the BgaC hydrolysis activity was localized at the cell surface of
S. pneumoniae
, indicating that BgaC is expressed as a surface protein although it does not have a typical signal sequence or membrane anchorage motif. The surface localization of BgaC was further supported by immunofluorescence microscopy analysis using an antibody raised against BgaC and by a reassociation assay with fluorescein isothiocyanate-labeled BgaC. Although the
bgaC
deletion mutation did not significantly attenuate the virulence of
S. pneumoniae
in vivo, the
bgaC
mutant strain showed relatively low numbers of viable cells compared to the wild type after 24 h of infection in vivo, whereas the mutant showed higher colonization levels at 6 and 24 h postinfection in vivo. Our data strongly indicate for the first time that
S. pneumoniae bgaC
encodes a surface β-galactosidase with high substrate specificity that is significantly associated with the infection activity of pneumococci.
Residues of Heat-Labile Enterotoxin Involved in Bacterial Cell Surface Binding
Authors: Mudrak Benjamin , Rodriguez Daniel L. , Kuehn Meta J. 
Published: March 2009

ABSTRACT

Enterotoxigenic
Escherichia coli
(ETEC) is a leading cause of traveler's diarrhea worldwide. One major virulence factor released by this pathogen is the heat-labile enterotoxin LT, which upsets the balance of electrolytes in the intestine. After export, LT binds to lipopolysaccharide (LPS) on the bacterial surface. Although the residues responsible for LT's binding to its host receptor are known, the portion of the toxin which mediates LPS binding has not been defined previously. Here, we describe mutations in LT that impair the binding of the toxin to the external surface of
E. coli
without altering holotoxin assembly. One mutation in particular, T47A, nearly abrogates surface binding without adversely affecting expression or secretion in ETEC. Interestingly, T47A is able to bind mutant
E. coli
expressing highly truncated forms of LPS, indicating that LT binding to wild-type LPS may be due primarily to association with an outer core sugar. Consequently, we have identified a region of LT distinct from the pocket involved in eukaryotic receptor binding that is responsible for binding to the surface of
E. coli
.
Pseudomonas syringae
HrpP Is a Type III Secretion Substrate Specificity Switch Domain Protein That Is Translocated into Plant Cells but Functions Atypically for a Substrate-Switching Protein
Authors: Morello Joanne E. , Collmer Alan 
Published: March 2009

ABSTRACT

Pseudomonas syringae
delivers virulence effector proteins into plant cells via an Hrp1 type III secretion system (T3SS).
P. syringae
pv. tomato DC3000 HrpP has a C-terminal, putative T3SS substrate specificity switch domain, like
Yersinia
YscP. A Δ
hrpP
DC3000 mutant could not cause disease in tomato or elicit a hypersensitive response (HR) in tobacco, but the HR could be restored by expression of HrpP in
trans
. Though HrpP is a relatively divergent protein in the T3SS of different
P. syringae
pathovars,
hrpP
from
P. syringae
pv. syringae 61 and
P. syringae
pv. phaseolicola 1448A restored HR elicitation and pathogenicity to DC3000 Δ
hrpP
. HrpP was translocated into
Nicotiana benthamiana
cells via the DC3000 T3SS when expressed from its native promoter, but it was not secreted in culture. N- and C-terminal truncations of HrpP were tested for their ability to be translocated and to restore HR elicitation activity to the Δ
hrpP
mutant. No N-terminal truncation completely abolished translocation, implying that HrpP has an atypical T3SS translocation signal. Deleting more than 20 amino acids from the C terminus abolished the ability to restore HR elicitation. HrpP fused to green fluorescent protein was no longer translocated but could restore HR elicitation activity to the Δ
hrpP
mutant, suggesting that translocation is not essential for the function of HrpP. No T3SS substrates were detectably secreted by DC3000 Δ
hrpP
except the pilin subunit HrpA, which unexpectedly was secreted poorly. HrpP may function somewhat differently than YscP because the
P. syringae
T3SS pilus likely varies in length due to differing plant cell walls.
ThecinandraiQuorum-Sensing Regulatory Systems inRhizobium leguminosarumAre Coordinated by ExpR and CinS, a Small Regulatory Protein Coexpressed with CinI
Authors: Edwards Anne , Frederix Marijke , Wisniewski-Dyé Florence , Jones Jacob , Zorreguieta Angeles , Downie J. Allan 
Published: March 2009

ABSTRACTTo understand how theRhizobium leguminosarum raiI-raiRquorum-sensing system is regulated, we identified mutants with decreased levels of RaiI-madeN-acyl homoserine lactones (AHLs). A LuxR-type regulator, ExpR, is required forraiRexpression, and RaiR is required to induceraiI. SinceraiR(andraiI) expression is also reduced incinIandcinRquorum-sensing mutants, we thought CinI-made AHLs may activate ExpR to induceraiR. However, added CinI-made AHLs did not induceraiRexpression in acinImutant. The reducedraiRexpression incinIandcinRmutants was due to lack of expression ofcinSimmediately downstream ofcinI. cinSencodes a 67-residue protein, translationally coupled to CinI, andcinSacts downstream ofexpRforraiRinduction. ClonedcinSinR. leguminosarumcaused an unusual collapse of colony structure, and this was delayed by mutation ofexpR. The phenotype looked like a loss of exopolysaccharide (EPS) integrity; mutations incinI, cinR, cinS, andexpRall reduced expression ofplyB, encoding an EPS glycanase, and mutation ofplyBabolished the effect of clonedcinSon colony morphology. We conclude that CinS and ExpR act to increase PlyB levels, thereby influencing the bacterial surface. CinS is conserved in other rhizobia, includingRhizobium etli; the previously observed effect ofcinIandcinRmutations decreasing swarming in that strain is primarily due to a lack of CinS rather than a lack of CinI-made AHL. We conclude that CinS mediates quorum-sensing regulation because it is coregulated with an AHL synthase and demonstrate that its regulatory effects can occur in the absence of AHLs.
vfr
, a Novel Locus Affecting Cysteine Protease Production in
Streptococcus pyogenes
Authors: Ma Yongsheng , Bryant Amy E. , Salmi Dan B. , McIndoo Eric , Stevens Dennis L. 
Published: March 2009

ABSTRACT

A gene unique to
Streptococcus pyogenes
, called
vfr
, that negatively regulates
speB
, an important extracellular proteinase, has been identified. Disruption of
vfr
markedly increased SpeB production in a clinical strain of
S. pyogenes
and relieved its growth phase dependency. These findings may provide important insights into the pathogenesis of invasive
S. pyogenes
infections.
The
Bacillus subtilis ywjI
(
glpX
) Gene Encodes a Class II Fructose-1,6-Bisphosphatase, Functionally Equivalent to the Class III Fbp Enzyme
Authors: Jules Matthieu , Le Chat Ludovic , Aymerich Stéphane , Le Coq Dominique 
Published: March 2009

ABSTRACT

We present here experimental evidence that the
Bacillus subtilis ywjI
gene encodes a class II fructose-1,6-bisphosphatase, functionally equivalent to the
fbp
-encoded class III enzyme, and constitutes with the upstream gene,
murAB
, an operon transcribed at the same level under glycolytic or gluconeogenic conditions.
Molecular Analysis of an Extrachromosomal Element Containing the C2 Toxin Gene Discovered inClostridium botulinumType C
Authors: Sakaguchi Yoshihiko , Hayashi Tetsuya , Yamamoto Yumiko , Nakayama Keisuke , Zhang Kai , Ma Shaobo , Arimitsu Hideyuki , Oguma Keiji 
Published: March 2009

ABSTRACTClostridium botulinumcultures are classified into seven types, types A to G, based on the antigenicity of the neurotoxins produced. Of these seven types, only types C and D produce C2 toxin in addition to the neurotoxin. The C2 toxin consists of two components designated C2I and C2II. The genes encoding the C2 toxin components have been cloned, and it has been stated that they might be on the cell chromosome. The present study confirmed by using pulsed-field gel electrophoresis and subsequent Southern hybridization that these genes are on a large plasmid. The complete nucleotide sequence of this plasmid was determined by using a combination of inverse PCR and primer walking. The sequence was 106,981 bp long and contained 123 potential open reading frames, including thec2Iandc2IIgenes. The 57 products of these open reading frames had sequences similar to those of well-known proteins. It was speculated that 9 these 57 gene products were related to DNA replication, 2 were responsible for the two-component regulatory system, and 3 were σ factors. In addition, a total of 20 genes encoding proteins related to diverse processes in purine catabolism were found in two regions. In these regions, there were 9 and 11 genes rarely found in plasmids, indicating that this plasmid plays an important role in purine catabolism, as well as in C2 toxin production.
The French Musculoskeletal Disorders Surveillance Program: Pays de la Loire network
Authors: Ha C , Roquelaure Y , Leclerc A , Touranchet A , Goldberg M , Imbernon E 
Published: March 2009

Objectives:An epidemiological surveillance system for work-related musculoskeletal disorders (MSDs) was implemented in 2002 in France’s Pays de la Loire region to assess the incidence and prevalence of MSDs in the general and working populations, identify levels of exposure to occupational risk factors and investigate the proportion of cases attributable to work exposure.Methods:The program combines (1) surveillance of sentinel health events in the general population (carpal tunnel syndrome (CTS) was the sentinel event for upper limb MSDs), (2) assessment of the prevalence of the main upper limb MSDs and their risk factors in the workplace based on a network of occupational physicians and (3) registration of the notification of work-related diseases (WRDs).Results:1168 incident cases of CTS were included over a 3 year period. The estimated incidence of CTS was 1.00 per 1000 person-years in those aged 20–59 years (0.60 in men and 1.40 in women). The incidence rate was higher in employed than unemployed persons in the year of diagnosis (0.6 per 1000 vs 0.3 in men and 1.7 vs 0.8 in women). The occupational physician network noted high prevalence rates: 11% of men and 15% of women had at least one of the six main upper limb clinically-diagnosed MSDs. The WRD survey showed that MSDs represented 65% of notified WRDs.Conclusion:The Pays de la Loire program plays a significant role in informing the authorities and the public about the state of current MSDs. It is planned to extend it to a routine national surveillance program.
DESIGN AND PERFORMANCE EVALUATION OF A FUZZY-BASED TRAFFIC CONDITIONER FOR MOBILE AD HOC NETWORKS
Authors: TORSHIZ MASOOD NIAZI , MOVAGHAR ALI 
Published: March 2009

A mobile ad hoc network is a collection of mobile hosts forming a temporary network on the fly, without using any fixed infrastructure. Characteristics of mobile ad hoc networks such as lack of central coordination, mobility of hosts, dynamically varying network topology, and limited availability of resources make QoS provisioning very challenging in such networks. In this paper, we introduce a fuzzy QoS traffic conditioner for mobile ad hoc networks. The proposed traffic conditioner consists of fuzzy admission control (FAC), fuzzy traffic rate controller (FTRC), and fuzzy scheduler (FS). The proposed FAC monitors the delay and available bandwidth and decides whether to accept or reject the request. The FTRC uses the additive increase multiplicative decrease (AIMD) rate control algorithm as a base, in which a node increments its transmission rate when the observed delay is below the predefined threshold, with an increment rate of c Kbps and decreases its transmission rate by r% when the delay passes the threshold. FTRC accepts the packet delay and the "delay-threshold d" as inputs and calculates c and r by using a set of fuzzy rules. The third part of the proposed traffic conditioner is FS, which is based on the traditional weighted round robin (WRR) mechanism. FS monitors the packet drop and delay of each queue and adjusts the queue weights by using a fuzzy inference engine.
Aflatoxin B1 Exposure, Hepatitis B Virus Infection, and Hepatocellular Carcinoma in Taiwan
Authors: Wu Hui-Chen , Wang Qiao , Yang Hwai-I , Ahsan Habibul , Tsai Wei-Yann , Wang Li-Yu , Chen Shu-Yuan , Chen Chien-Jen , Santella Regina M. 
Published: March 2009

Abstract
To evaluate the role of aflatoxin B1 (AFB1) exposure on risk of hepatocellular carcinoma (HCC), a case-control study nested within a community-based cohort was conducted. Baseline blood and urine samples were used to determine the level of AFB1-albumin adducts and urinary AFB1 metabolites. Conditional logistic regression analysis was used to calculate odds ratios (OR) and 95% confidence intervals (95% CI) to assess the effect of AFB1 exposure on risk of HCC. The adjusted ORs (95% CIs) were 1.54 (1.01-2.36) and 1.76 (1.18-2.58), respectively, for those with AFB1-albumin adducts and urinary AFB1 metabolite levels above the mean compared with those with levels below the mean. When compared with subjects in the lowest quartile of urinary AFB1 metabolites, there was an increase in risk of HCC, with adjusted ORs (95% CIs) of 0.57 (0.14-2.43), 1.43 (0.32-6.42), and 4.91 (1.18-20.48; Ptrend = 0.02), respectively, among noncarriers of hepatitis B virus (HBV) infection. The adjusted OR (95% CI) was 7.49 (5.13-10.93) for carriers of hepatitis B surface antigen compared with noncarriers, regardless of AFB1 status. The ORs (95% CI) were 10.38 (5.73-18.82) and 15.13 (7.83-29.25) for carriers of hepatitis B surface antigens with levels of AFB1-albumin adducts and urinary AFB1 metabolites above the mean, respectively. The combined effect of aflatoxin exposure and HBV infection did not differ by duration of follow-up. Consistent with our previous study with fewer subjects, these data show that AFB1 exposure is a risk factor for HCC risk. However, in this larger study, the effect of combined AFB1 exposure and HBV infection is more consistent with an additive than a multiplicative model. (Cancer Epidemiol Biomarkers Prev 2009;18(3):846–53)
IGF-IandIGFBP-3Polymorphisms in Relation to Circulating Levels among African American and Caucasian Women
Authors: D'Aloisio Aimee A. , Schroeder Jane C. , North Kari E. , Poole Charles , West Suzanne L. , Travlos Gregory S. , Baird Donna D. 
Published: March 2009

AbstractCirculating insulin-like growth factor-I (IGF-I) and IGF-binding protein-3 (IGFBP-3) levels have been associated with common diseases. Although family-based studies suggest that genetic variation contributes to circulating IGF-I and IGFBP-3 levels, analyses of associations with multiple IGF-I and IGFBP-3 single nucleotide polymorphisms (SNP) have been limited, especially among African Americans. We evaluated 30 IGF-I and 15 IGFBP-3 SNPs and estimated diplotypes in association with plasma IGF-I and IGFBP-3 among 984 premenopausal African American and Caucasian women. In both races, IGFBP-3 rs2854746 (Ala32Gly) was positively associated with plasma IGFBP-3 (CC versus GG mean difference among Caucasians, 631 ng/mL; 95% confidence interval, 398-864; African Americans, 897 ng/mL; 95% confidence interval, 656-1,138), and IGFBP-3 diplotypes with the rs2854746 GG genotype had lower mean IGFBP-3 levels than reference diplotypes with the CG genotype, whereas IGFBP-3 diplotypes with the CC genotype had higher mean IGFBP-3 levels. IGFBP-3 rs2854744 (-202 A/C) was in strong linkage disequilibrium with rs2854746 in Caucasians only, but was associated with plasma IGFBP-3 in both races. Eight additional IGFBP-3 SNPs were associated with ≥5% differences in mean IGFBP-3 levels, with generally consistent associations between races. Twelve IGF-I SNPs were associated with ≥10% differences in mean IGF-I levels, but associations were generally discordant between races. Diplotype associations with plasma IGF-I did not parallel IGF-I SNP associations. Our study supports that common IGFBP-3 SNPs, especially rs2854746, influence plasma IGFBP-3 levels among African Americans and Caucasians but provides less evidence that IGF-I SNPs affect plasma IGF-I levels. (Cancer Epidemiol Biomarkers Prev 2009;18(3):954–66)
Human Papillomavirus Types by Age in Cervical Cancer Precursors: Predominance of Human Papillomavirus 16 in Young Women
Authors: Porras Carolina , Rodríguez Ana Cecilia , Hildesheim Allan , Herrero Rolando , González Paula , Wacholder Sholom , Burk Robert D. , Schiffman Mark 
Published: March 2009

Abstract
In a population-based study conducted in Guanacaste, Costa Rica, we investigated the human papillomavirus (HPV) types detected in 233 cases of cervical intraepithelial neoplasia (CIN) 2/3 and cancer by age. CIN2+ and CIN3+ in young women were significantly more likely to be associated with HPV 16 than the same lesions in older women (80% of CIN3+ were associated with HPV 16 among women ages 18-26 years compared with only 32% among women older than 55 years; Ptrend = 0.018). There were no differences by age in HPV 18 positivity. Lesions in older women were mainly caused by other carcinogenic types. This association was present for both prevalent and incident lesions and supports the notion that HPV 16 is a stronger carcinogen than other HPV types. It also has implications for prevention, including the need to vaccinate young women before exposure to HPV vaccine–containing types (HPV 16 and HPV 18) to prevent the majority of cervical cancer precursors. (Cancer Epidemiol Biomarkers Prev 2009;18(3):863–5)
Persistence of an Incident Human Papillomavirus Infection and Timing of Cervical Lesions in Previously Unexposed Young Women
Authors: Trottier Helen , Mahmud Salaheddin M. , Lindsay Lisa , Jenkins David , Quint Wim , Wieting Susan L. , Schuind Anne , Franco Eduardo L. ,   on behalf of the GSK HPV-001 Vaccine Study Group
Published: March 2009

Abstract
Background: We analyzed data from a cohort of 553 women enrolled in the placebo arm of a randomized controlled trial of the human papillomavirus (HPV) 16/18 vaccine to study the timing of the occurrence of squamous intraepithelial lesions (SIL) or cervical intraepithelial neoplasia (CIN) following incident HPV infection and its relation to persistence of the infection.
Methods: At entry, women were cytologically negative, HPV 16/18 seronegative, and high-risk HPV (HR-HPV) DNA negative. Cervicovaginal samples were initially collected at 3-month and cervical samples at 6-month intervals. We estimated the mean time to SIL/CIN, relative risks of SIL/CIN following incident HPV, and odds ratios between persistent HPV and SIL/CIN.
Results: The mean time for SIL/CIN detection was 43.3 [95% confidence interval (95% CI), 36.4-50.1] and 46.4 (95% CI, 42.0-50.7) months from first infection with HPV 16/18 and other HR-HPVs, respectively. Relative risks of SIL/CIN following incident HPV infection were 66.2 (95% CI, 14.9-295.1) for HPV 16/18 and 50.9 (95% CI, 11.5-225.4) for other HR-HPVs. The odds ratios of SIL/CIN for persistent HPV 16/18 infection, defined as a minimum of two and three (6 monthly) visits, were, respectively, 169.0 (95% CI, 37.2-768.6) and 169.1 (95% CI, 31.5-907.4). The majority of women with cervical infection with HPV 16/18 lasting &gt;6 months (33 of 51, 65%) developed SIL and/or CIN.
Conclusions: These analyses provide the first actuarial estimate of mean time between incident HR-HPV infection in previously uninfected women and onset of cervical lesion development. Persistent HR-HPV infection, particularly HPV 16/18, is a strong predictor of cervical lesion risk and potentially a reliable end point for clinical HPV research. (Cancer Epidemiol Biomarkers Prev 2009;18(3):854–62)
Polymorphic Variation in NFKB1 and Other Aspirin-Related Genes and Risk of Hodgkin Lymphoma
Authors: Chang Ellen T. , Birmann Brenda M. , Kasperzyk Julie L. , Conti David V. , Kraft Peter , Ambinder Richard F. , Zheng Tongzhang , Mueller Nancy E. 
Published: March 2009

Abstract
We found that regular use of aspirin may reduce the risk of Hodgkin lymphoma (HL), a common cancer of adolescents and young adults in the United States. To explore possible biological mechanisms underlying this association, we investigated whether polymorphic variation in genes involved in nuclear factor-κB (NF-κB) activation and inhibition, other inflammatory pathways, and aspirin metabolism influences HL risk. Twenty single nucleotide polymorphisms (SNP) in seven genes were genotyped in DNA from 473 classical HL cases and 373 controls enrolled between 1997 and 2000 in a population-based case-control study in the Boston, Massachusetts, metropolitan area and the state of Connecticut. We selected target genes and SNPs primarily using a candidate-SNP approach and estimated haplotypes using the expectation-maximization algorithm. We used multivariable logistic regression to estimate odds ratios (OR) for associations with HL risk. HL risk was significantly associated with rs1585215 in NFKB1 (AG versus AA: OR, 2.1; 95% confidence interval, 1.5-2.9; GG versus AA: OR, 3.5; 95% confidence interval, 2.2-5.7, Ptrend = 1.7 × 10−8) and with NFKB1 haplotypes (Pglobal = 6.0 × 10−21). Similar associations were apparent across categories of age, sex, tumor EBV status, tumor histology, and regular aspirin use, although statistical power was limited for stratified analyses. Nominally significant associations with HL risk were detected for SNPs in NFKBIA and CYP2C9. HL risk was not associated with SNPs in IKKA/CHUK, PTGS2/COX2, UDP1A6, or LTC4S. In conclusion, genetic variation in the NF-κB pathway seems to influence risk of HL. Pooled studies are needed to detect any heterogeneity in the association with NF-κB across HL subgroups, including aspirin users and nonusers. (Cancer Epidemiol Biomarkers Prev 2009;18(3):976–86)
Modafinil for the treatment of fatigue in lung cancer: a pilot study
Authors: Spathis A , Dhillan R , Booden D , Forbes K , Vrotsou K , Fife K 
Published: March 2009

Cancer-related fatigue is the most prevalent and distressing symptom experienced by patients with advanced cancer. Central nervous system stimulants have been shown to relieve fatigue in nonmalignant disease. Modafinil is a stimulant with a selective site of action in the brain that is better tolerated than traditional stimulants, such as methylphenidate. The aim of this study was to determine the feasibility of conducting a randomised controlled trial to assess the efficacy and safety of modafinil for the treatment of fatigue in patients with lung cancer. Twenty patients with non-small cell lung cancer were recruited to this open-label study. Modafinil was taken in a fixed dose-titration schedule of 100 mg daily for 7 days followed by 200 mg daily for 7 days. Fifteen patients completed the study. During the study period, there was a rapid and statistically significant reduction in the primary outcome, fatigue ( P = 0.001) and the secondary outcomes of daytime sleepiness and depression/anxiety. This improvement in fatigue was also clinically significant. Ten patients chose to continue modafinil after the study and the drug was well-tolerated. It would be both feasible and worthwhile to conduct a definitive randomised controlled trial to determine the role of modafinil in the treatment of cancer-related fatigue.