bluuebunny/crossref_metadata_2025_split huggingface dataset:
A New Lineage of Halophilic, Wall-Less, Contractile Bacteria from a Brine-Filled Deep of the Red Sea
Authors: Antunes André , Rainey Fred A. , Wanner Gerhard , Taborda Marco , Pätzold Jürgen , Nobre M. Fernanda , da Costa Milton S. , Huber Robert 
Published: March 2008

ABSTRACT

A novel strictly anaerobic bacterium designated strain SSD-17B
T
was isolated from the hypersaline brine-sediment interface of the Shaban Deep, Red Sea. Cells were pleomorphic but usually consisted of a central coccoid body with one or two “tentacle-like” protrusions. These protrusions actively alternated between a straight, relaxed form and a contracted, corkscrew-like one. A peptidoglycan layer was not detected by electron microscopy. The organism forms “fried-egg”-like colonies on MM-X medium. The organism is strictly anaerobic and halophilic and has an optimum temperature for growth of about 30 to 37°C and an optimum pH of about 7. Nitrate and nitrite are reduced; lactate is a fermentation product. The fatty acid profile is dominated by straight saturated and unsaturated chain compounds. Menaquinone 4 is the major respiratory quinone. Phylogenetic analysis demonstrated strain SSD-17B
T
represents a novel and distinct lineage within the radiation of the domain
Bacteria
. The branching position of strain SSD-17B
T
was equidistant to the taxa considered to be representative lineages of the phyla
Firmicutes
and
Tenericutes
(with its sole class
Mollicutes
). The phenotypic and phylogenetic data clearly show the distinctiveness of this unusual bacterium, and we therefore propose that strain SSD-17B
T
(= DSM 18853 = JCM 14575) represents a new genus and a new species, for which we recommend the name
Haloplasma contractile
gen. nov., sp. nov. We are also of the opinion that the organism represents a new order-level taxon, for which we propose the name
Haloplasmatales
.
Quantitative Analysis of Three Hydrogenotrophic Microbial Groups, Methanogenic Archaea, Sulfate-Reducing Bacteria, and Acetogenic Bacteria, within Plaque Biofilms Associated with Human Periodontal Disease
Authors: Vianna M. E. , Holtgraewe S. , Seyfarth I. , Conrads G. , Horz H. P. 
Published: March 2008

ABSTRACT

Human subgingival plaque biofilms are highly complex microbial ecosystems that may depend on H
2
-metabolizing processes. Here we investigated the ubiquity and proportions of methanogenic archaea, sulfate reducers, and acetogens in plaque samples from 102 periodontitis patients. In contrast to the case for 65 healthy control subjects, hydrogenotrophic groups were almost consistently detected in periodontal pockets, with the proportions of methanogens and sulfate reducers being significantly elevated in severe cases. In addition, antagonistic interactions among the three microbial groups indicated that they may function as alternative syntrophic partners of secondary fermenting periodontal pathogens.
Staphylococcus aureus
HrtA Is an ATPase Required for Protection against Heme Toxicity and Prevention of a Transcriptional Heme Stress Response
Authors: Stauff Devin L. , Bagaley Danielle , Torres Victor J. , Joyce Rose , Anderson Kelsi L. , Kuechenmeister Lisa , Dunman Paul M. , Skaar Eric P. 
Published: March 2008

ABSTRACT

During systemic infection,
Staphylococcus aureus
acquires nutrient iron from heme, the cofactor of vertebrate myoglobin and hemoglobin. Upon exposure to heme,
S. aureus
up-regulates the expression of the
h
eme-
r
egulated
t
ransporter, HrtAB. Strains lacking
hrtAB
exhibit increased sensitivity to heme toxicity, and upon heme exposure they elaborate a secreted protein response that interferes with the recruitment of neutrophils to the site of infection. Taken together, these results have led to the suggestion that
hrtAB
encodes an efflux system responsible for relieving the toxic effects of accumulated heme. Here we extend these observations by demonstrating that HrtA is the ATPase component of the HrtAB transport system. We show that HrtA is an Mn
2+
/Mg
2+
-dependent ATPase that functions at an optimal pH of 7.5 and exhibits in vitro temperature dependence uncommon to ABC transporter ATPases. Furthermore, we identify conserved residues within HrtA that are required for in vitro ATPase activity and are essential for the functionality of HrtA in vivo. Finally, we show that heme induces an alteration in the gene expression pattern of
S. aureus
Δ
hrtA
, implying the presence of a novel transcriptional regulatory mechanism responsible for the previously described immunomodulatory characteristics of
hrtA
mutants exposed to heme.
Phenolic Acid-Mediated Regulation of the
padC
Gene, Encoding the Phenolic Acid Decarboxylase of
Bacillus subtilis
Authors: Tran Ngoc Phuong , Gury Jerôme , Dartois Véronique , Nguyen Thi Kim Chi , Seraut Hélène , Barthelmebs Lise , Gervais Patrick , Cavin Jean-François 
Published: March 2008

ABSTRACT

In
Bacillus subtilis
, several phenolic acids specifically induce expression of
padC
, encoding a phenolic acid decarboxylase that converts these antimicrobial compounds into vinyl derivatives.
padC
forms an operon with a putative coding sequence of unknown function,
yveFG
, and this coding sequence does not appear to be involved in the phenolic acid stress response (PASR). To identify putative regulators involved in the PASR, random transposon mutagenesis, combined with two different screens, was performed. PadR, a negative transcriptional regulator of
padC
expression, was identified.
padR
is not located in the vicinity of
padC
, and the expression of
padR
is low and appears constitutive. This is in contrast with what occurs in other gram-positive bacteria, in which
padR
is autoregulated and induced by phenolic acids. Further screening of the transposon library failed to identify genes other than
padR
involved in the PASR. Modest inactivation of
padR
by phenolic acids was obtained in recombinant
Escherichia coli
expressing
padC
and
padR
, and this translates into induction of decarboxylase activity. Gel shift promoter binding assays performed with and without MgCl
2
, and with and without phenolic acids, demonstrated that phenolic acids were able to abolish the binding of PadR to the
yveFG
-
padC
promoter in the absence of MgCl
2
. Altogether, our results indicate that (i) PadR is inactivated directly by phenolic acids in vitro, (ii) inhibition of PadR in response to phenolic acids may occur without the need for a sensor-like effector in
B. subtilis
, and (iii) phenolic acids are able to modulate PadR activity in
E. coli
in the absence of any additional effector.
Characterization of the
Streptomyces lividans
PspA Response
Authors: Vrancken Kristof , Van Mellaert Lieve , Anné Jozef 
Published: March 2008

ABSTRACT

Phage shock protein (Psp) is induced by extracytoplasmic stress that may reduce the energy status of the cell. It is encoded in
Escherichia coli
by the phage shock protein regulon consisting of
pspABCDE
and by
pspF
and
pspG
. The phage shock protein system is highly conserved among a large number of gram-negative bacteria. However, many bacterial genomes contain only a
pspA
homologue but no homologues of the other genes of the Psp system. This conservation indicates that PspA alone might play an important role in these bacteria. In
Streptomyces lividans
, a soil-borne gram-positive bacterium, the phage shock protein system consists only of the
pspA
gene. In this report, we showed that
pspA
encodes a 28-kDa protein that is present in both the cytoplasmic and the membrane fractions of the
S. lividans
mycelium. We demonstrated that the
pspA
gene is strongly induced under stress conditions that attack membrane integrity and that it is essential for growth and survival under most of these conditions. The data reported here clearly show that PspA plays an important role in
S. lividans
under stress conditions despite the absence of other
psp
homologues, suggesting that PspA may be more important in most bacteria than previously thought.
Enterococcus faecalisPcfC, a Spatially Localized Substrate Receptor for Type IV Secretion of the pCF10 Transfer Intermediate
Authors: Chen Yuqing , Zhang Xiaolin , Manias Dawn , Yeo Hye-Jeong , Dunny Gary M. , Christie Peter J. 
Published: March 2008

ABSTRACTUpon sensing of peptide pheromone,Enterococcus faecalisefficiently transfers plasmid pCF10 through a type IV secretion (T4S) system to recipient cells. The PcfF accessory factor and PcfG relaxase initiate transfer by catalyzing strand-specific nicking at the pCF10 origin of transfer sequence (oriT). Here, we present evidence that PcfF and PcfG spatially coordinate docking of the pCF10 transfer intermediate with PcfC, a membrane-bound putative ATPase related to the coupling proteins of gram-negative T4S machines. PcfC and PcfG fractionated with the membrane and PcfF with the cytoplasm, yet all three proteins formed several punctate foci at the peripheries of pheromone-induced cells as monitored by immunofluorescence microscopy. A PcfC Walker A nucleoside triphosphate (NTP) binding site mutant (K156T) fractionated with theE. faecalismembrane and also formed foci, whereas PcfC deleted of its N-terminal putative transmembrane domain (PcfCΔN103) distributed uniformly throughout the cytoplasm. Native PcfC and mutant proteins PcfCK156T and PcfCΔN103 bound pCF10 but notpcfGor ΔoriTmutant plasmids as shown by transfer DNA immunoprecipitation, indicating that PcfC binds only the processed form of pCF10 in vivo. Finally, purified PcfCΔN103 bound DNA substrates and interacted with purified PcfF and PcfG in vitro. Our findings support a model in which (i) PcfF recruits PcfG tooriTto catalyze T-strand nicking, (ii) PcfF and PcfG spatially position the relaxosome at the cell membrane to stimulate substrate docking with PcfC, and (iii) PcfC initiates substrate transfer through the pCF10 T4S channel by an NTP-dependent mechanism.
The Early Kinetics of Cytomegalovirus-Specific CD8+T-Cell Responses Are Not Affected by Antigen Load or the Absence of Perforin or Gamma Interferon
Authors: Andrews Daniel M. , Andoniou Christopher E. , Fleming Peter , Smyth Mark J. , Degli-Esposti Mariapia A. 
Published: March 2008

ABSTRACTBoth innate and adaptive immune responses participate in the control of murine cytomegalovirus (mCMV) infection. In some mouse strains, like BALB/c, the control of infection relies on the activities of CD8+T cells. mCMV-specific CD8+T-cell responses are unusual in that, even after mCMV has been controlled in the periphery, the numbers of circulating virus-specific CD8+T cells remain high compared to those observed in other viral infections. To better understand the generation and maintenance of mCMV-specific CD8+T-cell responses, we evaluated how antigen load and effector molecules, such as perforin (Prf) and gamma interferon (IFN-γ), influence these responses during acute infection in vivo. Viral burden affected the magnitude, but not the early kinetics, of antigen-specific CD8+T-cell responses. Similarly, the magnitude of virus-specific CD8+T-cell expansion was affected by Prf and IFN-γ, but contraction of antigen-specific responses occurred normally in both Prf- and IFN-γ-deficient mice. These data indicate that control of mCMV-specific CD8+T-cell expansion and contraction is more complex than anticipated and, despite the role of Prf or IFN-γ in controlling viral replication, a full program of T-cell expansion and contraction can occur in their absence.
Polyomavirus Middle T Antigen Induces the Transcription of Osteopontin, a Gene Important for the Migration of Transformed Cells
Authors: Whalen Kerry A. , Weber Georg F. , Benjamin Thomas L. , Schaffhausen Brian S. 
Published: March 2008

ABSTRACT

Middle T antigen (MT) is the principal oncoprotein of murine polyomavirus. Experiments on the acute immediate effects of MT expression on cellular RNA levels showed that expression of osteopontin (OPN) was strongly induced by MT expression. Osteopontin is a protein known to be associated with cancer. It has a role in tumor progression and invasion. Protein analysis confirmed that MT induced the secretion of OPN into the extracellular medium. Expression of antisense OPN RNA had no effect on the growth of MT-transformed cells. However, it had a strong effect on the ability of MT transformants to migrate or to fill a wound. Analysis of MT mutants implicated both the SHC and phosphatidylinositol 3-kinase pathways in OPN induction. Reporter assays showed that MT regulated the OPN promoter through two of its PEA3 (
p
olyoma
e
nhancer
a
ctivator
3
) sites. As critical PEA3 sites are also part of the polyomavirus enhancer, the same signaling important for viral replication also contributes to virally induced metastatic potential.
Weak and Strong Convergence Theorems for Nonexpansive Mappings in Banach Spaces
Authors: Zhao Jing , He Songnian , Su Yongfu 
Published: March 2008

AbstractThe purpose of this paper is to introduce two implicit iteration schemes for approximating fixed points of nonexpansive mapping "Equation missing" and a finite family of nonexpansive mappings "Equation missing", respectively, in Banach spaces and to prove weak and strong convergence theorems. The results presented in this paper improve and extend the corresponding ones of H.-K. Xu and R. Ori, 2001, Z. Opial, 1967, and others.
A Prospective Study of Injury Patterns in High School Pole Vaulters
Authors: Rebella Gregory S. , Edwards Jamie O. , Greene Joseph J. , Husen Mark T. , Brousseau David C. 
Published: March 2008

Background The pole vault is a track and field event that has witnessed a large increase in participants during the past 5 years. Currently there are no prospective studies that have evaluated injury patterns in pole vaulters. Objectives To determine the injury rate and to describe injury patterns in high school pole vaulters. Study Design Descriptive epidemiological study. Methods This was a prospective cohort study of 140 Wisconsin high school athletes who participated in pole vaulting during the 2005 and 2006 track and field seasons. Baseline athlete information was obtained at the beginning of each season. When an injury occurred, an injury report form was completed to document diagnosis and circumstances of the incident. Injury rates were expressed as injuries per 100 athletes per season as well as injuries per 1000 athletic exposures. Risk factors were analyzed by calculating relative risks for baseline athlete variables. Results The injury rates were 26.4 injuries per 100 athletes per season (95% confidence interval, 18.6–36.4) and 7.1 injuries per 1000 athletic exposures (95% confidence interval, 5.0–9.8). Trauma to the lower extremities accounted for 71.5% of injuries. The most common injury types were ligament sprains (31.6%). Landing incorrectly was the most frequent mechanism of injury (26.3%). A history of pole-vault injury was associated With increased risk of injury (relative risk, 2.4; 95% confidence interval, 1.4–4.1). Conclusion Injuries are common in young vaulters. Injury mechanisms indicate that many could be avoided by using proper technique, particularly during the landing phase. Coaches should focus on vaulters with prior injuries to identify risky behavior and to help correct poor technique.
The Effects of Generalized Joint Laxity on Risk of Anterior Cruciate Ligament Injury in Young Female Athletes
Authors: Myer Gregory D. , Ford Kevin R. , Paterno Mark V. , Nick Todd G. , Hewett Timothy E. 
Published: March 2008

Background Women who participate in high-risk sports suffer anterior cruciate ligament injury at a 4- to 6-fold greater rate than men. Purpose To prospectively determine if female athletes with decreased passive knee joint restraint (greater joint laxity) and greater side-to-side differences in knee laxity would be at increased risk of anterior cruciate ligament injury. Study Design Case control study; Level of evidence, 3. Methods From 1558 female soccer and basketball players who were prospectively screened, 19 went on to tear their anterior cruciate ligaments. Four height- and mass-matched control subjects were selected from the uninjured screened athletes for comparison with each of the 19 injured subjects, making a total of 95 subjects (19 injured; 76 uninjured). Generalized joint-laxity tests and anterior-posterior tibiofemoral translation were quantified using the CompuKT knee arthrometer. A multivariable logistic regression model was constructed to determine predictors of anterior cruciate ligament injury status from recorded laxity measures. Results A multivariable logistic regression model (chi-square = 18.6; P = .002) used the independent variables laxity measures of knee hyperextension ( P = .02), wrist and thumb to forearm opposition ( P = .80), fifth-finger hyperextension > 90° ( P = .71), side-to-side differences in anterior-posterior tibiofemoral translation ( P = .002), and prior knee injury ( P = .22) to predict anterior cruciate ligament-injury status. The validated C statistic, or validated area under the receiver operating characteristic curve, was 0.72. For every 1.3-mm increase in side-to-side differences in anterior-posterior knee displacement, the odds of anterior cruciate ligament–injured status increased 4-fold (95% confidence interval, 1.68–9.69). A positive measure of knee hyperextension increased the odds of anterior cruciate ligament-injured status 5-fold (95% confidence interval, 1.24–18.44). Conclusion The current results indicate that increased knee-laxity measures may contribute to increased risk of anterior cruciate ligament injury. The methods to quantify knee joint laxity in this report may be used in conjunction with measures of neuromuscular control of the knee joint to identify high-risk female athletes with high accuracy. Once high-risk female athletes are identified, they may be targeted to the appropriate interventions to reduce injury risk.
Can Platelet-Rich Plasma Enhance Tendon Repair?
Authors: de Mos Marieke , van der Windt Anna E. , Jahr Holger , van Schie Hans T. M. , Weinans Harrie , Verhaar Jan A. N. , van Osch Gerjo J. V. M. 
Published: March 2008

Background Autologous platelet-rich plasma (PRP) application appears to improve tendon healing in traumatic tendon injuries, but basic knowledge of how PRP promotes tendon repair is needed. Hypothesis Platelet-rich plasma has a positive effect on cell proliferation and collagen production and induces the production of matrix-degrading enzymes and endogenous growth factors by human tenocytes. Study Design Controlled laboratory study. Methods Human tenocytes were cultured 14 days in 2% fetal calf serum medium complemented with 0%, 10%, or 20% vol/vol platelet-rich clot releasate ([PRCR] the active releasate of PRP) or platelet-poor clot releasate (PPCR). At day 4,7, and 14, cell amount, total collagen, and gene expression of collagen Iα1 (COL1) and Mod (COL3), matrix metalloproteinases ([MMPs] MMP1, MMP3, and MMP13), vascular endothelial-derived growth factor (VEGF)-A, and transforming growth factor (TGF)-β1 were analyzed. Results Platelet numbers in PRP increased to 2.55 times baseline. Growth-factor concentrations of VEGF and platelet-derived growth factor (PDGF)-BB were higher in PRCR than PPCR. Both PRCR and PPCR increased cell number and total collagen, whereas they decreased gene expression of COL1 and COL3 without affecting the COL3/COL1 ratio. PRCR, but not PPCR, showed upregulation of MMP1 and MMP3 expression. Matrix metalloproteinase 13 expression was not altered by either treatment. PRCR increased VEGF-A expression at all time points and TGF-β1 expression at day 4. Conclusion In human tenocyte cultures, PRCR, but also PPCR, stimulates cell proliferation and total collagen production. PRCR, but not PPCR, slightly increases the expression of matrix-degrading enzymes and endogenous growth factors. Clinical Relevance In vivo use of PRP, but also of PPP to a certain extent, in tendon injuries might accelerate the catabolic demarcation of traumatically injured tendon matrices and promote angiogenesis and formation of a fibrovascular callus. Whether this will also be beneficial for degenerative tendinopathies remains to be elucidated.
Twelve-Year Follow-up on Anterior Cruciate Ligament Reconstruction
Authors: Hanypsiak Bryan T. , Spindler Kurt P. , Rothrock Christopher R. , Calabrese Gary J. , Richmond Brad , Herrenbruck Todd M. , Parker Richard D. 
Published: March 2008

Background Although successful at restoring near normal laxity to the knee in the short term, anterior cruciate ligament reconstructions have not been shown to prevent the development of posttraumatic arthritis. Hypothesis Bone bruises and articular cartilage injuries sustained at the time of initial injury (1991) would not resolve. Our secondary hypothesis was that the presence of a bone bruise or articular cartilage injury originally identified on magnetic resonance imaging would not be associated with long-term outcomes after anterior cruciate ligament reconstruction evaluated by the International Knee Documentation Committee questionnaire. Study Design Cohort study (prognosis); Level of evidence, 1. Methods We attempted to contact all patients from an original cohort (N = 54) for follow-up evaluation, which included repeat radiographs, magnetic resonance images, physical examination, and International Knee Documentation Committee questionnaire more than a decade postoperatively. Results Forty-four patients (82% of the original cohort) returned for on-site follow-up. No patient with a bone bruise identified on original magnetic resonance imaging had one identified at 12-year follow-up. The mean (±SD) International Knee Documentation Committee score at follow-up with no bone bruise originally present was 70.6 (±12.7) versus 70.0 (±8.1) when a bone bruise was observed ( P > .05). No consistent association was observed between the presence of an initial articular cartilage lesion with a lesion on follow-up magnetic resonance images. The mean (±SD) International Knee Documentation Committee score at follow-up with no articular cartilage injury was 69.0 (±11.9) versus 72.8 (±12.0) with articular cartilage lesion ( P > .05). Conclusion All bone bruises identified in our study with magnetic resonance imaging at the time of initial injury had resolved at 12-year follow-up. The presence of a bone bruise at the time of initial injury did not significantly alter the patient-oriented outcome by International Knee Documentation Committee after anterior cruciate ligament reconstruction. Additionally, articular cartilage abnormality on magnetic resonance imaging did not influence the International Knee Documentation Committee score.
Erythropoietin mediates hepcidin expression in hepatocytes through EPOR signaling and regulation of C/EBPα
Authors: Pinto Jorge P. , Ribeiro Sara , Pontes Helena , Thowfeequ Shifaan , Tosh David , Carvalho Félix , Porto Graça 
Published: March 2008

Abstract
Hepcidin is the principal iron regulatory hormone, controlling the systemic absorption and remobilization of iron from intracellular stores. Recent in vivo studies have shown that hepcidin is down-regulated by erythropoiesis, anemia, and hypoxia, which meets the need of iron input for erythrocyte production. Erythropoietin (EPO) is the primary signal that triggers erythropoiesis in anemic and hypoxic conditions. Therefore, a direct involvement of EPO in hepcidin regulation can be hypothesized. We report here the regulation of hepcidin expression by EPO, in a dose-dependent manner, in freshly isolated mouse hepatocytes and in the HepG2 human hepatocyte cell model. The effect is mediated through EPOR signaling, since hepcidin mRNA levels are restored by pretreatment with an EPOR-blocking antibody. The transcription factor C/EBPα showed a pattern of expression similar to hepcidin, at the mRNA and protein levels, following EPO and anti-EPOR treatments. Chromatin immunoprecipitation experiments showed a significant decrease of C/EBPα binding to the hepcidin promoter after EPO supplementation, suggesting the involvement of this transcription factor in the transcriptional response of hepcidin to EPO.