bluuebunny/crossref_metadata_2025_split huggingface dataset:
The role of sugar, xylitol, toothbrushing frequency, and use of fluoride toothpaste in maintenance of adults’ dental health: findings from the Finnish National Health 2000 Survey
Authors: Tseveenjav Battsetseg , Suominen Anna L. , Hausen Hannu , Vehkalahti Miira M. 
Published: January 2011

Tseveenjav B, Suominen AL, Hausen H, Vehkalahti MM. The role of sugar, xylitol, toothbrushing frequency, and use of fluoride toothpaste in maintenance of adults’ dental health: findings from the Finnish National Health 2000 Survey.

Eur J Oral Sci 2011; 119: 40–47. © 2011 Eur J Oral Sci We assessed the effect of certain oral health‐related behaviours on adults’ dental health. As part of the Finnish nationwide Health 2000 Survey, dentate subjects, 30–64 yr of age, reported their frequency of consumption of eight sugar‐ and xylitol‐containing products, together with toothbrushing frequency and use of fluoride toothpaste, and underwent clinical oral examination (n = 4,361). The mean number of teeth present (NoT) was 24.2 and the mean numbers of sound teeth (ST), filled teeth (FT), and decayed teeth (DT) were 10.8, 12.1, and 1.1 for men and 9.6, 13.8, and 0.5 for women, respectively. Consumption of sugar‐sweetened beverages was more frequent than that of other sugar‐containing products, and greater in men than in women. Daily use of xylitol chewing gum was reported by 13% of the men and by 22% of the women. Toothbrushing at least twice daily was reported by 47% of the men and by 79% of the women; 86% and 96%, respectively, reported daily use of fluoride toothpaste. The frequency of consumption of sugar‐ and xylitol‐containing products and of toothbrushing, as well as use of fluoride toothpaste, play a role in the dental health of dentate adults, with the impact being weak on NoT, ST, and FT, but stronger on DT, especially concerning toothbrushing frequency (relative risk = 1.5) and use of fluoride toothpaste (relative risk = 1.8). Understanding the impact of certain oral health‐related behaviours on dental health in adults would facilitate better targeting of oral self‐care messages.
Insulin resistance and metabolic syndrome in prepubertal boys with Klinefelter syndrome
Authors: Bardsley Martha Z , Falkner Bonita , Kowal Karen , Ross Judith L 
Published: January 2011

AbstractAims:  To investigate risk factors for metabolic syndrome in prepubertal boys with Klinefelter syndrome.Methods:  Eighty‐nine boys with Klinefelter syndrome, ages 4–12.9 years, and 34 age‐matched control boys had height, weight, waist circumference and blood pressure measured and their parents completed a questionnaire about physical activity. The boys with Klinefelter syndrome also had measurement of lipids, fasting glucose and insulin. Insulin‐glucose homeostasis model assessment was calculated, and the boys were evaluated for childhood metabolic syndrome.Results:  The Klinefelter syndrome and control groups were similar ages (7.5 ± 2.4 vs. 8.1 ± 2.3 years). Body mass index measurements were similar, but waist circumference was >90 percentile in 30% of boys with Klinefelter syndrome versus 21% of controls. The mean daily time spent running was 42 min less in the Klinefelter syndrome versus control groups (p < 0.01). About 37% of the boys with Klinefelter syndrome had elevated LDL cholesterol, 24% had insulin resistance, and 7% met the three criteria for diagnosis of metabolic syndrome.Conclusions:  Truncal obesity, insulin resistance and metabolic syndrome are present in boys as young as 4–12 years with Klinefelter syndrome, and these occur in association with reduced running‐type activity.
Lactobacilli Reduce Cell Cytotoxicity Caused by
Streptococcus pyogenes
by Producing Lactic Acid That Degrades the Toxic Component Lipoteichoic Acid
Authors: Maudsdotter Lisa , Jonsson Hans , Roos Stefan , Jonsson Ann-Beth 
Published: January 2011

ABSTRACT
Lactobacilli are known to prevent colonization by many pathogens; nevertheless, the mechanisms of their protective effect are largely unknown. In this work, we investigated the role of lactobacilli during infection of epithelial cells with group A streptococci (GAS). GAS cause a variety of illnesses ranging from noninvasive disease to more severe invasive infections, such as necrotizing fasciitis and toxic shock-like syndrome. Invasion of deeper tissues is facilitated by GAS-induced apoptosis and cell death. We found that lactobacilli inhibit GAS-induced host cell cytotoxicity and shedding of the complement regulator CD46. Further, survival assays demonstrated that lactic acid secreted by lactobacilli is highly bactericidal toward GAS. In addition, lactic acid treatment of GAS, but not heat killing, prior to infection abolishes the cytotoxic effects against human cells. Since lipoteichoic acid (LTA) of GAS is heat resistant and cytotoxic, we explored the effects of lactic acid on LTA. By applying such an approach, we demonstrate that lactic acid reduces epithelial cell damage caused by GAS by degrading both secreted and cell-bound LTA. Taken together, our experiments reveal a mechanism by which lactobacilli prevent pathogen-induced host cell damage.
GS-8374, a Novel HIV Protease Inhibitor, Does Not Alter Glucose Homeostasis in Cultured Adipocytes or in a Healthy-Rodent Model System
Authors: Hruz Paul W. , Yan Qingyun , Tsai Luong , Koster Joseph , Xu Lianhong , Cihlar Tomas , Callebaut Christian 
Published: January 2011

ABSTRACT

Adverse effects induced by HIV protease inhibitors (PIs) are a significant factor in limiting their clinical success. PIs directly contribute to peripheral insulin resistance and alterations in lipid metabolism. GS-8374 is a novel PI with potent antiretroviral activity and a favorable resistance profile. Here we report on the potential of GS-8374 to adversely affect glucose and lipid homeostasis. Acute effects of GS-8374 and control PIs on glucose uptake and lipid accumulation were assessed
in vitro
in mouse OP9 and primary human adipocytes, respectively. GS-8374 and atazanavir showed no effect on insulin-stimulated deoxyglucose uptake, whereas ritonavir and lopinavir caused significant reductions. Similarly,
in vitro
lipid accumulation was not significantly affected in adipocytes treated with either GS-8374 or atazanavir. In euglycemic-hyperinsulinemic clamp experiments performed in rats during acute infusion of therapeutic levels of PIs, sustained serum GS-8374 levels of 8 μM had no effect on peripheral glucose disposal (similar to the findings for atazanavir). Comparable serum levels of lopinavir and ritonavir produced acute 19% and 53% reductions in
in vivo
glucose disposal, respectively. In conclusion, similar to atazanavir, but unlike ritonavir and lopinavir, GS-8374 neither affects insulin-stimulated glucose uptake in adipocytes in culture nor acutely alters peripheral glucose disposal in a rodent model system. These results dissociate the antiretroviral activity of GS-8374 from adverse effects on insulin sensitivity observed with some of the first-generation PIs and provide further support for the use of these experimental systems in the preclinical evaluation of novel PIs.
Echinocandin Susceptibility Testing of
Candida
spp. Using EUCAST EDef 7.1 and CLSI M27-A3 Standard Procedures: Analysis of the Influence of Bovine Serum Albumin Supplementation, Storage Time, and Drug Lots
Authors: Arendrup Maiken Cavling , Rodriguez-Tudela Juan-Luis , Park Steven , Garcia-Effron Guillermo , Delmas Guillaume , Cuenca-Estrella Manuel , Gomez-Lopez Alicia , Perlin David S. 
Published: January 2011

ABSTRACT

The MICs of echinocandins against
Candida
isolates with
fks
mutations are higher than those for wild-type (WT) isolates. However, the MIC ranges for susceptible and mutant populations overlap or are poorly separated. It was recently reported that a greater separation could be achieved in the presence of serum. To more fully explore this possibility, we compared the performances of the reference microdilution methods by using standard and bovine serum albumin (BSA)-supplemented growth medium. Anidulafungin, caspofungin, and micafungin MICs were determined according to EUCAST and CLSI methods and with 50% BSA in the medium for 93 clinical isolates, including
Candida albicans
(20/10 [number of isolates/number of mutants]),
C. glabrata
(19/10),
C. dubliniensis
(2/1),
C. krusei
(16/3),
C. parapsilosis
(19), and
C. tropicalis
(19/4) isolates. Stability of the plates was tested after storage at −80°C for 2 and 6 months, and the performance of two different lots of caspofungin was investigated. The addition of BSA to the medium resulted in higher MICs (1 to 9 2-fold dilution steps) for all isolates and compounds. The increases were greatest for anidulafungin and micafungin and, among WT isolates, for
C. parapsilosis
. The number of very major errors (VMEs) was reduced (24% [20/84 isolates] versus ≤7% [6/84 isolates]) using BSA-supplemented EUCAST medium but not using BSA-supplemented CLSI medium (6% versus 9%). MIC results were unchanged after 6 months of storage of test plates. The two lots of caspofungin yielded identical results. Addition of BSA to the EUCAST medium increases the ability to differentiate between WT isolates and isolates harboring resistance mutations.
Properties and Therapeutic Efficacy of Broadly Reactive Chimeric and Humanized H5-Specific Monoclonal Antibodies against H5N1 Influenza Viruses
Authors: Zheng Qingbing , Xia Lin , Wu Wai Lan , Zheng Zhenhua , Huo Yongting , Wu Jun , Liu Yanning , Yu Hai , Chen Yixin , Lau Siu-Ying , Chen Honglin , Luo Wenxin , Xia Ningshao 
Published: January 2011

ABSTRACTHighly pathogenic H5N1 virus infection causes severe disease and a high rate of fatality in humans. Development of humanized monoclonal antibodies may provide an efficient therapeutic regime for H5N1 virus infection. In the present study, broadly cross-reactive monoclonal antibodies (MAbs) derived from mice were humanized to minimize immunogenicity. One chimeric antibody (cAb) and seven humanized antibodies (hAbs) were constructed. These antibodies retained broad-spectrum reactivity to H5N1 viruses, binding to recombinant H5-subtype HA1 molecules expressed in CHO cells in a dose-dependent manner and exhibiting similar reactivities against antigenically distinct H5N1 viruses in hemagglutination inhibition (HI) assays. One humanized antibody, 37 hAb, showed HI and neutralization activities comparable to that of the parental murine antibody, 13D4 MAb, while the other six antibodies were less reactive to H5N1 viruses. Analysis of amino acid sequences in the variable region frameworks of the seven humanized antibodies found that Q5 and Y27 in the VH region are highly conserved murine residues. Comparison of the three-dimensional structures derived from the variable regions of MAbs 37 hAb, H1202-34, and 13D4 revealed that residue substitutions at sites 70 and 46 may be the major cause for the observed differences in binding affinity. Examination of the chimeric antibody and one of the humanized antibodies, 37 hAb, showed that both antibodies offered postinfection protection against lethal challenge with antigenically diverse H5N1 viruses in the mouse model. Chimeric and humanized antibodies which retain the broadly reactive and protective properties of murine H5-specific monoclonal antibodies have great potential for use in the treatment of human H5N1 infection.
Regulation of Innate Immune Response toCandida albicansInfections by αMβ2-Pra1p Interaction
Authors: Soloviev Dmitry A. , Jawhara Samir , Fonzi William A. 
Published: January 2011

ABSTRACTCandida albicansis a common opportunistic fungal pathogen and is the leading cause of invasive fungal diseases in immunocompromised individuals. The induction of cell-mediated immunity toC. albicansis one of the main tasks of cells of the innate immune system, andin vitroevidence suggests that integrin αMβ2(CR3, Mac-1, and CD11b/CD18) is the principal leukocyte receptor involved in recognition of the fungus. Using αMβ2-KO mice and mutated strains ofC. albicansin two models of murine candidiasis, we demonstrate that neutrophils derived from mice deficient in αMβ2have a reduced ability to killC. albicansand that the deficient mice themselves exhibit increased susceptibility to fungal infection. Disruption of thePRA1gene ofC. albicans, the primary ligand for αMβ2, protects the fungus against leukocyte killingin vitroandin vivo, impedes the innate immune response to the infection, and increases fungal virulence and organ invasionin vivo. Thus, recognition of pH-regulated antigen 1 protein (Pra1p) by αMβ2plays a pivotal role in determining fungal virulence and host response and protection againstC. albicansinfection.
Identification of a Putative Chaperone Involved in Stress Resistance and Virulence in
Francisella tularensis
Authors: Dieppedale Jennifer , Sobral Daniel , Dupuis Marion , Dubail Iharilalao , Klimentova Jana , Stulik Jiri , Postic Guillaume , Frapy Eric , Meibom Karin L. , Barel Monique , Charbit Alain 
Published: January 2011

ABSTRACT

Francisella tularensis
is a highly infectious bacterium causing the zoonotic disease tularemia. This facultative intracellular bacterium replicates
in vivo
mainly inside macrophages and therefore has developed strategies to resist this stressful environment. Here, we identified a novel genetic locus that is important for stress resistance and intracellular survival of
F. tularensis. In silico
and transcriptional analyses suggest that this locus (genes
FTL_0200
to
FTL_0209
in the live vaccine strain [LVS]) constitutes an operon controlled by the alternative sigma factor σ
32
. The first gene,
FTL_0200
, encodes a putative AAA+ ATPase of the MoxR subfamily. Insertion mutagenesis into genes
FTL_0200
,
FTL_0205
, and
FTL_0206
revealed a role for the locus in both intracellular multiplication and
in vivo
survival of
F. tularensis
. Deletion of gene
FTL_0200
led to a mutant bacterium with increased vulnerability to various stress conditions, including oxidative and pH stresses. Proteomic analyses revealed a pleiotropic impact of the Δ
FTL_0200
deletion, supporting a role as a chaperone for FTL_0200. This is the first report of a role for a MoxR family member in bacterial pathogenesis. This class of proteins is remarkably conserved among pathogenic species and may thus constitute a novel player in bacterial virulence.
The Pathogenicity of an EntericCitrobacter rodentiumInfection Is Enhanced by Deficiencies in the Antioxidants Selenium and Vitamin E
Authors: Smith Allen D. , Botero Sebastian , Shea-Donohue Terez , Urban Joseph F. 
Published: January 2011

ABSTRACTThe pathogenesis of aCitrobacter rodentiuminfection was evaluated in mice fed diets with a single deficiency in either selenium or vitamin E or with a double deficiency in both selenium and vitamin E compared to mice on nutritionally adequate diets. Mice fed the selenium- and vitamin E-deficient diet for 6 weeks had increased loads ofC. rodentiumin the colon and spleen, which were not observed in mice fed either of the singly deficient diets or the adequate diet. Infected mice fed the doubly deficient diet had increased colon crypt hyperplasia and an influx of infiltrating cells along with gross changes to crypt architecture, including ulceration and denuding of the epithelial layer. Cytokine and chemokine mRNA levels in the colon were measured by real-time PCR. Expression of proinflammatory cytokines and chemokines was upregulated on day 12 after infection withC. rodentiumin mice fed the doubly deficient diet compared to mice fed the control diet. Heme oxygenase 1, an enzyme upregulated by oxidative stress, also was more highly induced in infected mice fed the doubly deficient diet. Production ofC. rodentiumantigen-specific IgM and IgG antibodies was not affected by feeding the doubly deficient diet. The results indicated that selenium and vitamin E play an important role in host resistance and in the pathology induced byC. rodentium, an infection that mimics disease caused by common food-borne bacterial pathogens in humans.
Acupuncture Prevents Relapses of Recurrent Otitis in Dogs: A 1-Year Follow-Up of a Randomised Controlled Trial
Authors: Sánchez-Araujo Max , Puchi Alfredo 
Published: January 2011

BackgroundRecurrent infections within a particular, well-localised body location are often seen in veterinary and medical practice. This condition could represent a localised or segmental immune deficiency. Recurrent canine otitis seems to be one example of this problem. It has been reported that acupuncture increased the efficacy of conventional treatment for canine otitis by >50%.ObjectiveTo assess whether the relapse rate of recurrent canine otitis over 1 year can be modified by acupuncture in adult dogs.MethodsOne-year follow-up of a randomised controlled trial. 31 dogs with a history of recurring otitis were randomised into two groups. In addition to conventional treatment, each group received four sessions of either real acupuncture, group A (n=16), or sham acupuncture, group B (n=15). The main outcome for the follow-up was the rate of acute otitis episodes in each group over 1 year, with blinded evaluation. A χ2test was used for statistical analysis.ResultsThere was one dropout in each group. Fourteen (93%) dogs in group A: were free of otitis relapses, compared with 7 (50%) in group B (p<0.01).ConclusionAcupuncture seems effective for preventing relapses in cases of recurrent canine otitis. This result suggests that acupuncture could be tested as a treatment of other recurrent localised infections. Given the ability of acupuncture to modulate neurotransmitters and opioid peptides, which can in turn modulate the immune system, the immune response to acupuncture also seems worth exploring.
Associations of hip osteoarthritis with history of recurrent exposure to manual handling of loads over 20 kg and work participation: a population-based study of men and women
Authors: Kaila-Kangas Leena , Arokoski Jari , Impivaara Olli , Viikari-Juntura Eira , Leino-Arjas Päivi , Luukkonen Ritva , Heliövaara Markku 
Published: January 2011

ObjectivesWe reviewed work histories of manual handling of loads >20 kg in relation to hip osteoarthritis by age, exposure and work participation.MethodsA nationally representative sample of 3110 Finnish men and 3446 women aged 30–97 was recruited. Diagnosis of hip osteoarthritis was based on standardised clinical examination by trained physicians. Previous exposure to physically loading work was evaluated through interviews. Logistic regression was used to estimate associations between work factors and hip osteoarthritis.Results1.9% of men and 2.1% of women had hip osteoarthritis. Almost half the men and a quarter of the women had recurrently handled heavy loads at work. Subjects who had manually handled loads >20 kg had a 1.8-fold increased risk of hip osteoarthritis compared to non-exposed references, when age, body mass index, traumatic fractures and smoking were accounted for. Results were similar for men (OR 2.0; 95% CI 1.0 to 4.0) and women (1.8; 1.1 to 2.8). In a sub-analysis of subjects with hip replacement, the OR was 1.7 (1.0 to 2.9). Risk increased first after 12 years' exposure: among men it was 2.2 (0.8 to 5.9) for 13–24 years' exposure, and 2.3 (1.2 to 4.3) for >24 years' exposure. Among women it was 3.8 (1.7 to 8.1) for 13–24 years' exposure. Work participation among men aged <60 years with hip osteoarthritis was 20% lower compared with subjects without osteoarthritis.ConclusionsA work history of manual handling of loads >20 kg showed a strong association with hip osteoarthritis in all age groups except the youngest.
Smad4 Inactivation Promotes Malignancy and Drug Resistance of Colon Cancer
Authors: Papageorgis Panagiotis , Cheng Kuanghung , Ozturk Sait , Gong Yi , Lambert Arthur W. , Abdolmaleky Hamid M. , Zhou Jin-Rong , Thiagalingam Sam 
Published: January 2011

Abstract
SMAD4 is localized to chromosome 18q21, a frequent site for loss of heterozygosity in advanced stage colon cancers. Although Smad4 is regarded as a signaling mediator of the TGFβ signaling pathway, its role as a major suppressor of colorectal cancer progression and the molecular events underlying this phenomenon remain elusive. Here, we describe the establishment and use of colon cancer cell line model systems to dissect the functional roles of TGFβ and Smad4 inactivation in the manifestation of a malignant phenotype. We found that loss of function of Smad4 and retention of intact TGFβ receptors could synergistically increase the levels of VEGF, a major proangiogenic factor. Pharmacologic inhibition studies suggest that overactivation of the TGFβ-induced MEK-Erk and p38-MAPK (mitogen-activated protein kinase) auxiliary pathways are involved in the induction of VEGF expression in SMAD4 null cells. Overall, SMAD4 deficiency was responsible for the enhanced migration of colon cancer cells with a corresponding increase in matrix metalloprotease 9 enhanced hypoxia-induced GLUT1 expression, increased aerobic glycolysis, and resistance to 5′-fluoruracil–mediated apoptosis. Interestingly, Smad4 specifically interacts with hypoxia-inducible factor (HIF) 1α under hypoxic conditions providing a molecular basis for the differential regulation of target genes to suppress a malignant phenotype. In summary, our results define a molecular mechanism that explains how loss of the tumor suppressor Smad4 promotes colorectal cancer progression. These findings are also consistent with targeting TGFβ-induced auxiliary pathways, such as MEK-ERK, and p38-MAPK and the glycolytic cascade, in SMAD4-deficient tumors as attractive strategies for therapeutic intervention. Cancer Res; 71(3); 998–1008. ©2011 AACR.
Tumor Cell Invasion Is Promoted by Interstitial Flow-Induced Matrix Priming by Stromal Fibroblasts
Authors: Shieh Adrian C. , Rozansky Hallie A. , Hinz Boris , Swartz Melody A. 
Published: January 2011

Abstract
Interstitial flow emanates from tumors into the microenvironment where it promotes tumor cell invasion. Fibroblasts are key constituents of the tumor stroma that modulate the mechanical environment by matrix remodeling and contraction. Here, we explore how interstitial fluid flow affects fibroblast–tumor cell interactions. Using a 3-dimensional invasion assay and MDA-MB-435S cells cocultured with dermal fibroblasts in a collagen matrix, we showed a synergistic enhancement of tumor cell invasion by fibroblasts in the presence of interstitial flow. Interstitial flow also drove transforming growth factor (TGF)-β1 and collagenase-dependent fibroblast migration, consistent with previously described mechanisms in which flow promotes invasion through autologous chemotaxis and increased motility. Concurrently, migrating fibroblasts enhanced tumor cell invasion by matrix priming via Rho-mediated contraction. We propose a model in which interstitial flow promotes fibroblast migration through increased TGF-β1 activation and collagen degradation, positioning fibroblasts to locally reorganize collagen fibers via Rho-dependent contractility, in turn enhancing tumor cell invasion via mechanotactic cues. This represents a novel mechanism in which interstitial flow causes fibroblast-mediated stromal remodeling that facilitates tumor invasion. Cancer Res; 71(3); 790–800. ©2011 AACR.