bluuebunny/crossref_metadata_2025_split huggingface dataset:
Assessment of malignant potential of small hypervascular hepatocellular carcinoma using B‐mode ultrasonography
Authors: Moribata Kosaku , Tamai Hideyuki , Shingaki Naoki , Mori Yoshiyuki , Enomoto Shotaro , Shiraki Tatsuya , Deguchi Hisanobu , Ueda Kazuki , Inoue Izumi , Maekita Takao , Iguchi Mikitaka , Yanaoka Kimihiko , Oka Masashi , Ichinose Masao 
Published: January 2011

Aim:  Evaluation of malignant potential is important to determine the treatment strategy for small hepatocellular carcinoma (HCC). The aim of the present study was to establish a method of assessing the malignant potential of small hypervascular HCC using B‐mode ultrasonography.Methods:  One hundred and thirteen arterial hypervascular HCC nodules under 3 cm diagnosed by biopsy or surgical resection (20.5 ± 6.3 mm) were classified into two groups ultrasonographically: type 1 with (n = 27) and type 2 without (n = 86) a halo. Type 2 was categorized into three subgroups: type 2a, homogenous hyperechoic (n = 9); type 2b, hypoechoic with a smooth margin (n = 35); and type 2c, hypoechoic with an irregular or unclear margin (n = 42).Results:  The mean diameter of type 2a nodules was significantly smaller than that of other HCC types (P < 0.05). Overall, moderately differentiated HCC was the predominant histological type, except for type 2a, all of which were well‐differentiated HCC. The percentage of poorly differentiated HCC was significantly higher in type 2c nodules (19%) than in other HCC types (P < 0.01). The percentage of Lens culinaris agglutinin‐reactive α‐fetoprotein (AFP‐L3) positivity was significantly higher in type 2c nodules (55%) than in other HCC types (P < 0.01). Classification on B‐mode ultrasonography was correlated with the histological differentiation and serum level, an indicator of a poor prognosis.Conclusion:  The malignant potential of type 2a is the lowest and that of type 2c is the highest, both histologically and serologically. Assessment of the malignant potential of small, hypervascular HCC is possible by B‐mode ultrasonography.
New insights into the mineralogy and weathering of the Meridiani Planum meteorite, Mars
Authors: FLEISCHER Iris , SCHRÖDER Christian , KLINGELHÖFER Göstar , ZIPFEL Jutta , MORRIS Richard V. , ASHLEY James W. , GELLERT Ralf , WEHRHEIM Simon , EBERT Sandro 
Published: January 2011

Abstract–Meridiani Planum is the first officially recognized meteorite find on the surface of Mars. It was discovered at and named after the landing site of the Mars Exploration Rover Opportunity. Based on its composition, it was classified as a IAB complex iron meteorite. Mössbauer spectra obtained by Opportunity are dominated by kamacite (α‐Fe‐Ni) and exhibit a small contribution of ferric oxide. Several small features in the spectra have been neglected to date. To shed more light on these features, five iron meteorite specimens were investigated as analogs to Meridiani Planum with a laboratory Mössbauer setup. Measurements were performed on (1) their metallic bulk, (2) troilite (FeS) inclusions, (3) cohenite ((Fe,Ni,Co)3C) and schreibersite ((Fe,Ni)3P), and (4) corroded rims. In addition to these room‐temperature measurements, a specimen from the Mundrabilla IAB‐ungrouped meteorite was measured at Mars‐equivalent temperatures. Based on these measurements, the features in Meridiani Planum spectra can be explained with the presence of small amounts of schreibersite and/or cohenite and iron oxides. The iron oxides can be attributed to a previously reported coating on Meridiani Planum. Their presence indicates weathering through the interaction of the meteorite with small amounts of water.
Recent advances in the management of diabetic distal symmetrical polyneuropathy
Authors: Tesfaye Solomon 
Published: January 2011

AbstractThere is now little doubt that poor blood glucose control is an important risk factor for the development of diabetic peripheral neuropathy (DPN). Furthermore, traditional cardiovascular risk factors for macrovascular disease appear to be associated with an increased risk of DPN. The recently established International Expert Group on Diabetic Neuropathy has recommended new criteria for the diagnosis of DPN in the context of clinical and research settings. Studies in experimental diabetes examining the pathogenesis of DPN have identified a number of metabolic abnormalities including polyol pathway hyperactivity, increased advanced glycation end‐point formation, alterations in the protein kinase C beta pathway through diacylglycerol and oxidative stress. There is now strong evidence implicating nerve ischemia as the cause of DPN. Studies in human and animal models have shown reduced nerve perfusion and endoneurial hypoxia. These endoneurial microvascular changes strongly correlate with clinical severity and the degree of nerve‐fiber pathology. Unfortunately, many compounds that have been effective in animal models of neuropathy have not been successful in human diabetic neuropathy. The only compounds found to be efficacious in human diabetic neuropathy, and are in clinical use, are the anti‐oxidant, α‐lipoic acid and the aldose reductase inhibitor, epalrestat. Overall, the evidence emphasizes the importance of vascular dysfunction, driven by metabolic change, in the etiology of DPN, and highlights potential therapeutic approaches. Epidemiological data on diabetic painful neuropathic pain (DPNP) are limited. In one population‐based study, the prevalence of DPNP, as assessed by a structured questionnaire and examination, was estimated at 16%. It was notable that, of these patients, 12.5% had never reported symptoms to their doctor and 39% had never received treatment for their pain. Thus, despite being common, DPNP continues to be underdiagnosed and undertreated. Pharmacological treatment of DPNP include tricyclic compounds, serotonin noradrenalin reuptake inhibitors, the anti‐oxidant α‐lipoic acid, anticonvulsants, opiates, membrane stabilizers, topical capsaicin and so on. Management of the patient with DPNP must be tailored to individual requirements and will depend on the presence of other comorbidities. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2010.00083.x)
Fine‐scale environmental variation in species distribution modelling: regression dilution, latent variables and neighbourly advice
Authors: McInerny Greg J. , Purves Drew W. 
Published: January 2011

Summary1. Developing the next‐generation of species distribution modelling (SDM) requires solutions to a number of widely recognised problems. Here, we address the problem of uncertainty in predictor variables arising from fine‐scale environmental variation.2. We explain how this uncertainty may cause scale‐dependent ‘regression dilution’, elsewhere a well‐understood statistical issue, and explain its consequences for SDM. We then demonstrate a simple, general correction for regression dilution based on Bayesian methods using latent variables. With this correction in place, unbiased estimates of species occupancy vs. the true environment can be retrieved from data on occupancy vs. measured environment, where measured environment is correlated with the true environment, but subject to substantial measurement error.3. We then show how applying our correction to multiple co‐occurring species simultaneously increases the accuracy of parameter estimates for each species, as well as estimates for the true environment at each survey plot – a phenomenon we call ‘neighbourly advice’. With a sufficient number of species, the estimates of the true environment at each plot can become extremely accurate.4. Our correction for regression dilution could be integrated with models addressing other issues in SDM, e.g. biotic interactions and/or spatial dynamics. We suggest that Bayesian analysis, as employed here to address uncertainty in predictor variables, might offer a flexible toolbox for developing such next‐generation species distribution models.
Watch your time step: trapping and tracking dispersal in autocorrelated environments
Authors: Skarpaas Olav , Shea Katriona , Jongejans Eelke 
Published: January 2011

Summary 1. Reliable estimates of dispersal kernels are needed for many applications in ecology. For both plants and animals, and for passive and active dispersal, the two most common methods for obtaining dispersal kernel estimates from direct measurements are following individual propagules (tracking) and counting propagules at fixed locations (trapping). 2. We consider the effect of the chosen sampling method on the estimation of dispersal kernels and highlight reasons why we should not necessarily expect estimates from the two methods to be the same. We illustrate this point using data from field experiments for three wind‐dispersed plant species (Carduus nutans, Carduus acanthoides and Crepis praemorsa) and a mechanistic dispersal model (WALD). 3. The field experiments demonstrate that the two sampling methods lead to different dispersal kernel estimates. Although estimated mean dispersal distances may be similar, short‐term tracking studies with random seed release generally lead to more peaked distributions with greater modal dispersal distances than long‐term trapping of naturally dispersing seeds. 4. Wind speed data and dispersal distributions estimated using the mechanistic dispersal model suggest that differences between the sampling methods arise from temporally autocorrelated environmental conditions interacting with study time frame and dispersal initiation processes. Single tracking events tend to provide biased estimates of wind statistics because of short‐term autocorrelation in wind speeds. Depending on the long‐term autocorrelation structure of wind speeds, and the sampling of wind speeds compared to natural seed release, single short‐term tracking studies may result in distributions that differ strongly from the ‘true’ distribution sampled by trapping over the dispersal season. Distributions from several tracking studies, weighted according to natural dispersal initiation, may therefore be needed to recapture the true dispersal distribution. 5. This study demonstrates that commonly used sampling methods for dispersal can result in dramatically different distributions under temporally autocorrelated environmental conditions. As autocorrelated environments are ubiquitous, this could lead to marked biases in predictions of movement and spread. These results are relevant for a wide range of ecological systems and to theoretical and applied problems relying on measurements and models of dispersal, for instance, conservation in fragmented landscapes, biological invasions and species re‐introductions. The measurement process should be taken into account in such applications.
Resistance and Tolerance to Tropodithietic Acid, an Antimicrobial in Aquaculture, Is Hard To Select
Authors: Porsby Cisse Hedegaard , Webber Mark A. , Nielsen Kristian Fog , Piddock Laura J. V. , Gram Lone 
Published: January 2011

ABSTRACT

The antibacterial compound tropodithietic acid (TDA) is produced by bacteria of the marine
Roseobacter
clade and is thought to explain the fish probiotic properties of some roseobacters. The aim of the present study was to determine the antibacterial spectrum of TDA and the likelihood of development of TDA resistance. A bacterial extract containing 95% TDA was effective against a range of human-pathogenic bacteria, including both Gram-negative and Gram-positive bacteria. TDA was bactericidal against
Salmonella enterica
serovar Typhimurium SL1344 and
Staphylococcus aureus
NCTC 12493 and killed both growing and nongrowing cells. Several experimental approaches were used to select mutants resistant to TDA or subpopulations of strains with enhanced tolerance to TDA. No approach (single exposures to TDA extract administered via different methods, screening of a transposon library for resistant mutants, or prolonged exposure to incremental concentrations of TDA) resulted in resistant or tolerant strains. After more than 300 generations exposed to sub-MIC and MIC concentrations of a TDA-containing extract, strains tolerant to 2× the MIC of TDA for wild-type strains were selected, but the tolerance disappeared after one passage in medium without TDA extract.
S.
Typhimurium mutants with nonfunctional efflux pump and porin genes had the same TDA susceptibility as wild-type strains, suggesting that efflux pumps and porins are not involved in innate tolerance to TDA. TDA is a promising broad-spectrum antimicrobial in part due to the fact that enhanced tolerance is difficult to gain and that the TDA-tolerant phenotype appears to confer only low-level resistance and is very unstable.
Antimicrobial Susceptibilities and Molecular Epidemiology of Clinical Isolates of
Clostridium difficile
in Taiwan
Authors: Lin Yi-Chun , Huang Yu-Tsung , Tsai Pei-Jane , Lee Tai-Fen , Lee Nan-Yao , Liao Chun-Hsing , Lin Shyr-Yi , Ko Wen-Chien , Hsueh Po-Ren 
Published: January 2011

ABSTRACT

The antimicrobial susceptibility and virulence factors of
Clostridium difficile
clinical isolates in Taiwan have not previously been reported. One hundred and thirteen isolates were collected from two major teaching hospitals in Taiwan from 2001 to 2009. Molecular typing was performed by an automated repetitive extragenic palindromic sequence-based PCR (rep-PCR) method (DiversiLab; Bacterial Barcodes, Inc., Athens, GA) and PCR ribotyping. Detection of
tcdA
,
tcdB
,
cdtA
, and
cdtB
genes was performed using a multiplex PCR assay, and
gyrA
and
gyrB
genes of moxifloxacin-nonsusceptible isolates were sequenced. All isolates were susceptible to vancomycin and metronidazole. Ninety-five (84%) isolates were susceptible to moxifloxacin, and the MIC
90
for nemonoxacin was 4 μg/ml. Tigecycline showed favorable antibacterial activity (MIC
90
of 0.06 μg/ml). Thirteen rep-PCR types were identified as a predominant rep-PCR type (type A; non-North American pulsed-field gel electrophoresis type 1 [NAP1], -NAP7, or -NAP8) accounting for 52.2% (59 isolates). Nine of 18 moxifloxacin-nonsusceptible isolates belonged to the rep-PCR type A. The rep-PCR type A and C isolates were distinct from NAP1 (ribotype 027) and NAP8 (ribotype 078) as determined by PCR ribotyping. Seventy-four (65%) isolates harbored
tcdA
and
tcdB
, and 15 (13%) harbored
cdtAB
encoding binary toxin. Eleven isolates had a gene deletion in
tcdC
, including a 39-bp deletion (9 isolates) and an 18-bp deletion (2). In conclusion, dissemination of a predominant
C. difficile
clone in southern and northern Taiwan was noted. However, no NAP1 (ribotype 027) isolate could be discovered in this study.
Experimental Infection withSchistosoma mansoniin CCR5-Deficient Mice Is Associated with Increased Disease Severity, as CCR5 Plays a Role in Controlling Granulomatous Inflammation
Authors: Souza Adriano L. S. , Souza Patrícia R. S. , Pereira Cíntia A. , Fernandes Adriana , Guabiraba Rodrigo , Russo Remo C. , Vieira Leda Q. , Corrêa Ary , Teixeira Mauro M. , Negrão-Corrêa Deborah 
Published: January 2011

ABSTRACTThe plasma level of the chemokine CCL3 is elevated in patients with chronic severe schistosomiasis mansoni. We have previously shown that CCL3−/−mice with experimental infection showed diminished pathology and worm burden compared to those of wild-type (WT) mice. To elucidate further the role of CC chemokines during schistosomiasis mansoni infection, we evaluated the course of infection in C57BL/6J mice deficient in CCR5, one of the receptors for CCL3. The CCR5 deficiency proved to be remarkably deleterious to the host, since mortality rates reached 70% at 14 weeks postinfection in CCR5−/−mice and 19% in WT mice. The increased lethality was not associated with an increased parasite burden, since similar numbers of eggs and adult worms were found in mice from both groups. Liver granulomas of chronically infected CCR5−/−mice were larger and showed greater numbers of cells and collagen deposition than liver granulomas from WT mice. This was associated with higher levels of production of intereleukin-5 (IL-5), IL-13, CCL3, and CCL5 in infected CCR5−/−mice than in infected WT mice. Moreover, at 8 weeks after infection, just before changes in pathology and mortality, the numbers of FoxP3-positive cells were lower in liver granulomas of CCR5−/−mice than in WT mice. In conclusion, the CCR5 deletion is deleterious to mice infected withSchistosoma mansoni, and this is associated with enhanced fibrosis and granulomatous inflammation.
Lipoxin A
4
Inhibits
Porphyromonas gingivalis
-Induced Aggregation and Reactive Oxygen Species Production by Modulating Neutrophil-Platelet Interaction and CD11b Expression
Authors: Börgeson Emma , Lönn Johanna , Bergström Ida , Brodin Veronika Patcha , Ramström Sofia , Nayeri Fariba , Särndahl Eva , Bengtsson Torbjörn 
Published: January 2011

ABSTRACT

Porphyromonas gingivalis
is an etiological agent that is strongly associated with periodontal disease, and it correlates with numerous inflammatory disorders, such as cardiovascular disease. Circulating bacteria may contribute to atherogenesis by promoting CD11b/CD18-mediated interactions between neutrophils and platelets, causing reactive oxygen species (ROS) production and aggregation. Lipoxin A
4
(LXA
4
) is an endogenous anti-inflammatory and proresolving mediator that is protective of inflammatory disorders. The aim of this study was to investigate the effect of LXA
4
on the
P. gingivalis
-induced activation of neutrophils and platelets and the possible involvement of Rho GTPases and CD11b/CD18 integrins. Platelet/leukocyte aggregation and ROS production was examined by lumiaggregometry and fluorescence microscopy. Integrin activity was studied by flow cytometry, detecting the surface expression of CD11b/CD18 as well as the exposure of the high-affinity integrin epitope, whereas the activation of Rac2/Cdc42 was examined using a glutathione
S
-transferase pulldown assay. The study shows that
P. gingivalis
activates Rac2 and Cdc42 and upregulates CD11b/CD18 and its high-affinity epitope on neutrophils, and that these effects are diminished by LXA
4
. Furthermore, we found that LXA
4
significantly inhibits
P. gingivalis
-induced aggregation and ROS generation in whole blood. However, in platelet-depleted blood and in isolated neutrophils and platelets, LXA
4
was unable to inhibit either aggregation or ROS production, respectively. In conclusion, this study suggests that LXA
4
antagonizes
P. gingivalis
-induced cell activation in a manner that is dependent on leukocyte-platelet interaction, likely via the inhibition of Rho GTPase signaling and the downregulation of CD11b/CD18. These findings may contribute to new strategies in the prevention and treatment of periodontitis-induced inflammatory disorders, such as atherosclerosis.
Actin Polymerization Drives Septation of
Listeria monocytogenes namA
Hydrolase Mutants, Demonstrating Host Correction of a Bacterial Defect
Authors: Alonzo Francis , McMullen P. David , Freitag Nancy E. 
Published: January 2011

ABSTRACT

The Gram-positive bacterial cell wall presents a structural barrier that requires modification for protein secretion and large-molecule transport as well as for bacterial growth and cell division. The Gram-positive bacterium
Listeria monocytogenes
adjusts cell wall architecture to promote its survival in diverse environments that include soil and the cytosol of mammalian cells. Here we provide evidence for the enzymatic flexibility of the murein hydrolase NamA and demonstrate that bacterial septation defects associated with a loss of NamA are functionally complemented by physical forces associated with actin polymerization within the host cell cytosol.
L. monocytogenes
Δ
namA
mutants formed long bacterial chains during exponential growth in broth culture; however, normal septation could be restored if mutant cells were cocultured with wild-type
L. monocytogenes
bacteria or by the addition of exogenous NamA. Surprisingly, Δ
namA
mutants were not significantly attenuated for virulence in mice despite the pronounced exponential growth septation defect. The physical force of
L. monocytogenes
-mediated actin polymerization within the cytosol was sufficient to sever Δ
namA
mutant intracellular chains and thereby enable the process of bacterial cell-to-cell spread so critical for
L. monocytogenes
virulence. The inhibition of actin polymerization by cytochalasin D resulted in extended intracellular bacterial chains for which septation was restored following drug removal. Thus, despite the requirement for NamA for the normal septation of exponentially growing
L. monocytogenes
cells, the hydrolase is essentially dispensable once
L. monocytogenes
gains access to the host cell cytosol. This phenomenon represents a notable example of eukaryotic host cell complementation of a bacterial defect.
Role of
Salmonella
Pathogenicity Island 1 Protein IacP in
Salmonella enterica
Serovar Typhimurium Pathogenesis
Authors: Kim Jin Seok , Eom Jeong Seon , Jang Jung Im , Kim Hyeon Guk , Seo Doo Won , Bang Iel-Soo , Bang Seong Ho , Lee In Soo , Park Yong Keun 
Published: January 2011

ABSTRACT

Gram-negative bacteria, including
Salmonella enterica
serovar Typhimurium, exploit type III secretion systems (T3SSs) through which virulence proteins are delivered into the host cytosol to reinforce invasive and replicative niches in their host. Although many secreted effector proteins and membrane-bound structural proteins in the T3SS have been characterized, the functions of many cytoplasmic proteins still remain unknown. In this study, we found that IacP, encoded by
Salmonella
pathogenicity island 1, was important for nonphagocytic cell invasion and bacterial virulence. When the
iacP
gene was deleted from several
Salmonella
serovar Typhimurium strains, the invasion into INT-407 epithelial cells was significantly decreased compared to that of their parental strains, and retarded rearrangements of actin fibers were observed for the
iacP
mutant-infected cells. Although IacP had no effect on the secretion of type III translocon proteins, the levels of secretion of the effector proteins SopB, SopA, and SopD into the culture medium were decreased in the
iacP
mutant. In a mouse infection model, mice infected with the
iacP
mutant exhibited alleviated pathological signs in the intestine and survived longer than did wild-type-infected mice. Taken together, IacP plays a key role in
Salmonella
virulence by regulating the translocation of T3SS effector proteins.