bluuebunny/crossref_metadata_2025_split huggingface dataset:
The invisible work with tobacco cessation – strategies among dental hygienists
Authors: Andersson P , Westergren A , Johannsen A 
Published: October 2011

To cite this article:

Int J Dent Hygiene
10, 2012; 54–60  DOI: 10.1111/j.1601‐5037.2011.00530.x  Andersson P, Westergren A, Johannsen A. The invisible work with tobacco cessation – strategies among dental hygienists.Abstract:  Objective:  This study elucidates dental hygienists’ experiences of work with tobacco cessation among patients who smoke or use snuff.Methods:  Data were obtained and categorized by interviewing 12 dental hygienists, who worked actively with tobacco cessation interventions. Qualitative content analysis was used for analysis.Results:  The latent content was formulated into the core category ‘the invisible oral health promotion work’. The informants thought that they had a responsibility to work with tobacco cessation. They perceived the financial system in which they perform the activity as frustrating, because tobacco cessation has no treatment code in the dental care insurance. This was one of several reasons why they had to integrate it in other treatment procedures. The results identified three categories: ‘balance in the meeting’, ‘possibilities and hindrance’ and ‘procedures’. In the narratives, both positive and negative aspects were displayed.Conclusions:  The financial conditions for tobacco cessation interventions need to be reformed and the activity has to be given a higher priority in the organization of dental care. Practical training in performing tobacco cessation interventions is important during the dental hygiene education; otherwise, tobacco cessation interventions will remain invisible in oral health promotion in the future.
A spoonful of sugar makes the melanoma go: the role of heparan sulfate proteoglycans in melanoma metastasis
Authors: O’Connell M. P. , Weeraratna A. T. 
Published: October 2011

SummaryHeparan sulfate proteoglycans (HSPGs) have been shown to regulate signaling in many systems and are of increasing interest in cancer. While these are not the only sugars to drive melanoma metastasis, HSPGs play important roles in driving metastatic signaling cascades in melanoma. The ability of these proteins to modulate ligand–receptor interactions in melanoma has been quite understudied. Recent data from several groups indicate the importance of these ligands in modulating key signaling pathways including Wnt and fibroblast growth factor (FGF) signaling. In this review, we summarize the current knowledge regarding the structure and function of these proteoglycans and their role in melanoma. Understanding how HSPGs modulate signaling in melanoma could lead to new therapeutic approaches via the dampening or heightening of key signaling pathways.
Detection of Staphylococcus aureus Isolates with Heterogeneous Intermediate-Level Resistance to Vancomycin in the United States
Authors: Richter Sandra S. , Satola Sarah W. , Crispell Emily K. , Heilmann Kristopher P. , Dohrn Cassie L. , Riahi Fathollah , Costello Andrew J. , Diekema Daniel J. , Doern Gary V. 
Published: October 2011

ABSTRACT

The prevalence of heterogeneous intermediate-level resistance to vancomycin (hVISA) in
Staphylococcus aureus
was assessed by screening a large collection of recent isolates. Susceptibility testing by the Clinical and Laboratory Standards Institute broth microdilution method and the Etest GRD (glycopeptide resistance detection) method (bioMérieux) was performed on 4,210 clinically significant
S. aureus
isolates obtained in 2009 from 43 U.S. centers. Isolates with Etest GRD-positive results for hVISA were evaluated further by repeat GRD testing and population analysis profiling–area under the curve (PAP-AUC) analysis. No VISA (vancomycin MIC, 4 to 8 μg/ml) or vancomycin-resistant (MIC ≥ 16 μg/ml) strains were detected. The Etest GRD screen for hVISA was initially positive for 68 isolates (1.6%; all by teicoplanin MIC ≥ 8 μg/ml at 24 or 48 h). Among those 68 isolates, 45 were reproducibly GRD positive. PAP-AUC testing confirmed only 11 isolates as hVISA (all had reproducible GRD-positive results). The 11 hVISA isolates were from nine medical centers and appeared genetically diverse (ten different PFGE types). The rates of resistance (including intermediate) for hVISA were as follows: oxacillin, 82%; erythromycin, 82%; clindamycin, 73%; levofloxacin, 73%; trimethoprim-sulfamethoxazole, 9%; and daptomycin, 9%. All hVISA isolates were susceptible to linezolid, tigecycline, and ceftaroline. Our data suggest that the overall prevalence of hVISA in the United States is low (0.3%). The hVISA isolates represented 10.5% of isolates with vancomycin MICs of 2 μg/ml and 0.1% of isolates with vancomycin MICs of 1 μg/ml. The positive predictive value of GRD Etest for hVISA was 16.2% for initial screen positive and 24.4% for reproducibly positive results.
A Novel Flucytosine-Resistant Yeast Species, Candida pseudoaaseri, Causes Disease in a Cancer Patient
Authors: Pfüller Roland , Gräser Yvonne , Erhard Marcel , Groenewald Marizeth 
Published: October 2011

ABSTRACT

Some members of the genus
Candida
are among the most common human fungal pathogens and cause serious diseases especially in immunocompromised people. A yeast was isolated from a blood culture from an immunocompromised cancer patient who suffered from acute pneumonia. The growth characteristics of the yeast on CHROMagar Candida were similar to those of
Candida tropicalis
, whereas the API ID 32C system identified the yeast as
Candida silvicola
. On the basis of the nucleotide divergence in the D1/D2 domain of the 26S nuclear rRNA (nrRNA) gene, as well as the internal transcribed spacer (ITS) domain of the nrRNA gene region, a new species,
Candida pseudoaaseri
sp. nov. with type strain VK065094 (CBS 11170
T
), which was found to be closely related to
Candida aaseri
, is proposed. While
C. aaseri
strains were susceptible to all tested antifungals, the new species is resistant to flucytosine and may also be distinguished from
C. aaseri
by its ability to assimilate
l
-rhamnose, whereas its colony morphology on CHROMagar Candida may be helpful for differentiation.
Confirmation and Follow-Up of Neurocysticercosis by Real-Time PCR in Cerebrospinal Fluid Samples of Patients Living in France
Authors: Yera H. , Dupont D. , Houze S. , Ben M'Rad M. , Pilleux F. , Sulahian A. , Gatey C. , Andrieu F. Gay , Dupouy-Camet J. 
Published: October 2011

ABSTRACT
Neurocysticercosis diagnosis is based on a combination of clinical, epidemiological, radiological, and immunological findings. We describe a real-time PCR assay for the confirmation of neurocysticercosis diagnosis in cerebrospinal fluid. The assay, tested on samples from nine patients living in France and diagnosed with neurocysticercosis, had a detection rate of 83.3% and 100% specificity.
White Spot Syndrome Virus Induces Metabolic Changes Resembling the Warburg Effect in Shrimp Hemocytes in the Early Stage of Infection
Authors: Chen I-Tung , Aoki Takashi , Huang Yun-Tzu , Hirono Ikuo , Chen Tsan-Chi , Huang Jiun-Yan , Chang Geen-Dong , Lo Chu-Fang , Wang Han-Ching 
Published: October 2011

ABSTRACT
The Warburg effect is an abnormal glycolysis response that is associated with cancer cells. Here we present evidence that metabolic changes resembling the Warburg effect are induced by a nonmammalian virus. When shrimp were infected with white spot syndrome virus (WSSV), changes were induced in several metabolic pathways related to the mitochondria. At the viral genome replication stage (12 h postinfection [hpi]), glucose consumption and plasma lactate concentration were both increased in WSSV-infected shrimp, and the key enzyme of the pentose phosphate pathway, glucose-6-phosphate dehydrogenase (G6PDH), showed increased activity. We also found that at 12 hpi there was no alteration in the ADP/ATP ratio and that oxidative stress was lower than that in uninfected controls. All of these results are characteristic of the Warburg effect as it is present in mammals. There was also a significant decrease in triglyceride concentration starting at 12 hpi. At the late stage of the infection cycle (24 hpi), hemocytes of WSSV-infected shrimp showed several changes associated with cell death. These included the induction of mitochondrial membrane permeabilization (MMP), increased oxidative stress, decreased glucose consumption, and disrupted energy production. A previous study showed that WSSV infection led to upregulation of the voltage-dependent anion channel (VDAC), which is known to be involved in both the Warburg effect and MMP. Here we show that double-stranded RNA (dsRNA) silencing of the VDAC reduces WSSV-induced mortality and virion copy number. For these results, we hypothesize a model depicting the metabolic changes in host cells at the early and late stages of WSSV infection.
Vaginal Langerhans Cells Nonproductively Transporting HIV-1 Mediate Infection of T Cells
Authors: Ballweber Lamar , Robinson Barry , Kreger Allison , Fialkow Michael , Lentz Gretchen , McElrath M. Juliana , Hladik Florian 
Published: October 2011

ABSTRACT

Although implied by other models, proof that Langerhans cells (LCs) in the human vagina participate in dissemination of infectious human immunodeficiency virus type 1 (HIV-1) has been lacking. Here, we show that LCs migrate from HIV-1-exposed vaginal epithelia and pass infectious virus to CD4
+
T cells without being productively infected themselves, and we point to a pathway that might enable HIV-1 to avoid degradation in vaginal LCs. Transport by migratory LCs to local lymphatics in a nonproductive but infectious form may aid HIV-1 in evasion of topical microbicides that target its intracellular productive life cycle.
The Cytomegaloviral Protein pUL138 Acts as Potentiator of Tumor Necrosis Factor (TNF) Receptor 1 Surface Density To Enhance ULb′-Encoded Modulation of TNF-α Signaling
Authors: Le Vu Thuy Khanh , Trilling Mirko , Hengel Hartmut 
Published: October 2011

ABSTRACTHuman cytomegalovirus is a ubiquitous herpesvirus that establishes lifelong latent infection. Changes in immune homeostasis induce the reactivation of lytic infection, which is mostly inapparent in healthy individuals but often causes overt disease in immunocompromised hosts. Based on discrepant tumor necrosis factor receptor 1 surface disposition between human cytomegalovirus AD169 variants differing in the ULb′ region, we identified the latency-associated gene product pUL138, which also is expressed during productive infection, as a selective potentiator of tumor necrosis factor receptor 1, one of the key receptors of innate immunity. Ectopically expressed pUL138 coprecipitated with tumor necrosis factor receptor 1, extended the protein half-life, and enhanced its signaling responses, thus leading to tumor necrosis factor receptor 1 hyperresponsiveness. Conversely, the targeted deletion ofUL138from the human cytomegaloviral genome strongly reduced tumor necrosis factor receptor 1 surface densities of infected cells. Remarkably, the comparison ofUL138deficiency to ULb′ deficiency revealed the presence of further positive modulators of tumor necrosis factor alpha signal transduction encoded within the human cytomegalovirus ULb′ region, identifying this region as a hub for multilayered tumor necrosis factor alpha signaling regulation.
Coagulation Factor IX Mediates Serotype-Specific Binding of Species A Adenoviruses to Host Cells
Authors: Lenman Annasara , Müller Steffen , Nygren Mari I. , Frängsmyr Lars , Stehle Thilo , Arnberg Niklas 
Published: October 2011

ABSTRACT
Human species A adenoviruses (HAdVs) comprise three serotypes: HAdV-12, -18, and -31. These viruses are common pathogens and cause systemic infections that usually involve the airways and/or intestine. In immunocompromised individuals, species A adenoviruses in general, and HAdV-31 in particular, cause life-threatening infections. By combining binding and infection experiments, we demonstrate that coagulation factor IX (FIX) efficiently enhances binding and infection by HAdV-18 and HAdV-31, but not by HAdV-12, in epithelial cells originating from the airways or intestine. This is markedly different from the mechanism for HAdV-5 and other human adenoviruses, which utilize coagulation factor X (FX) for infection of host cells. Surface plasmon resonance experiments revealed that the affinity of the HAdV-31 hexon-FIX interaction is higher than that of the HAdV-5 hexon-FX interaction and that the half-lives of these interactions are profoundly different. Moreover, both HAdV-31–FIX and HAdV-5–FX complexes bind to heparan sulfate-containing glycosaminoglycans (GAGs) on target cells, but binding studies utilizing cells expressing specific GAGs and GAG-cleaving enzymes revealed differences in GAG dependence and specificity between these two complexes. These findings add to our understanding of the intricate infection pathways used by human adenoviruses, and they may contribute to better design of HAdV-based vectors for gene and cancer therapy. Furthermore, the interaction between the HAdV-31 hexon and FIX may also serve as a target for antiviral treatment.
Chemotherapy Enhances Metastasis Formation via VEGFR-1–Expressing Endothelial Cells
Authors: Daenen Laura G.M. , Roodhart Jeanine M.L. , van Amersfoort Miranda , Dehnad Mantre , Roessingh Wijnand , Ulfman Laurien H. , Derksen Patrick W.B. , Voest Emile E. 
Published: October 2011

AbstractRecent studies suggest that chemotherapy, in addition to its cytotoxic effects on tumor cells, can induce a cascade of host events to support tumor growth and spread. Here, we used an experimental pulmonary metastasis model to investigate the role of this host response in metastasis formation. Mice were pretreated with chemotherapy and after clearance of the drugs from circulation, tumor cells were administered intravenously to study potential “protumorigenic” host effects of chemotherapy. Pretreatment with the commonly used chemotherapeutic agents cisplatin and paclitaxel significantly enhanced lung metastasis in this model. This corresponded to enhanced adhesion of tumor cells to an endothelial cell monolayer that had been pretreated with chemotherapy in vitro. Interestingly, chemotherapy exposure enhanced the expression of VEGF receptor 1 (VEGFR-1) on endothelial cells both in vitro and in vivo. Administration of antibodies targeting VEGFR-1 reversed the early retention of tumor cells in the lungs, thereby preventing the formation of chemotherapy-induced pulmonary metastases. The data indicate that chemotherapy-induced expression of VEGFR-1 on endothelial cells can create an environment favorable to tumor cell homing. Inhibition of VEGFR-1 function may therefore be used to counteract chemotherapy-induced retention of tumor cells within the metastatic niche, providing a novel level of tumor control in chemotherapy. Cancer Res; 71(22); 6976–85. ©2011 AACR.
Sonic Hedgehog Pathway Promotes Metastasis and Lymphangiogenesis via Activation of Akt, EMT, and MMP-9 Pathway in Gastric Cancer
Authors: Yoo Young A. , Kang Myoung Hee , Lee Hyun Joo , Kim Baek-hui , Park Jong Kuk , Kim Hyun Koo , Kim Jun Suk , Oh Sang Cheul 
Published: October 2011

Abstract
Activation of sonic hedgehog (Shh) signaling has been implicated in progression of a variety of tumors. In this study, we elucidated a role for Shh in the invasion of gastric tumors and determined the mechanism by which Shh is regulated. Immunohistochemical analysis of 178 primary human gastric tumor biopsies indicated that Shh expression was positively correlated with lymph node metastasis, high lymphatic vessel density, and poor prognosis. In mouse xenograft models of human gastric cancer, enforced expression of Shh significantly enhanced the incidence of lung metastasis compared with nonexpressing controls. Mechanistic investigations revealed that phosphoinositide 3-kinase (PI3K)/Akt inhibition blocked Shh-induced epithelial–mesenchyme transition, the activity of matrix metalloproteinase 9 (MMP-9), and lymphangiogenesis, reducing tumor invasiveness and metastasis. Taken together, our findings establish that Shh signaling promotes the metastasis of gastric cancer through activation of the PI3K/Akt pathway, which leads to mesenchymal transition and MMP-9 activation. These findings offer preclinical validation of Shh as a candidate therapeutic target for treatment of metastatic gastric cancers. Cancer Res; 71(22); 7061–70. ©2011 AACR.
Design and Conduct of Intervention-Based Research among Cancer Survivors
Authors: Wolin Kathleen Y. , Colditz Graham A. 
Published: October 2011

Abstract
Intervention trials in cancer survivors play an important and growing role in complementing the wealth of knowledge obtained from observational studies about how lifestyle can improve clinical, physiologic, and psychological outcomes. As the number of intervention trials grows, attention to study design and reporting is essential to establishing a high-quality data pool from which to make evidence-based recommendations and guidelines. We highlight several key issues important to the design and interpretation of intervention trials in cancer survivors. Intervention dose and duration both matter in trials of cancer survivors, yet few trials have evaluated different intervention doses and few intervention trials with multiyear follow-up exist. Finally, there is a need for interventions both of longer duration and those that take a practical trials approach and reflect clinical practice to speed implementation within practice and improve outcomes for cancer survivors. Cancer Epidemiol Biomarkers Prev; 20(10); 2078–84. ©2011 AACR.
Role of Genetic Susceptibility in Development of Treatment-Related Adverse Outcomes in Cancer Survivors
Authors: Bhatia Smita 
Published: October 2011

Abstract
Clear and unambiguous associations have been established between therapeutic exposures and specific complications. However, considerable interindividual variability is observed in the risk of developing an outcome for a given therapeutic exposure. Genetic predisposition and especially its interaction with therapeutic exposures can potentially exacerbate the toxic effect of treatment on normal tissues and organ systems, and can possibly explain the interindividual variability. This article provides a brief overview of the current knowledge about the role of genomic variation in the development of therapy-related complications. Relatively common outcomes with strong associations with therapeutic exposures, including cardiomyopathy, obesity, osteonecrosis, ototoxicity, and subsequent malignancies are discussed here. To develop a deeper understanding of the molecular underpinnings of therapy-related complications, comprehensive and near-complete collection of clinically annotated samples is critical. Methodologic issues such as study design, definition of the endpoints or phenotypes, identification of appropriate and adequately sized study population together with a reliable plan for collecting and maintaining high-quality DNA, and selection of an appropriate approach or platform for genotyping are also discussed. Understanding the etiopathogenetic pathways that lead to the morbidity is critical to developing targeted prevention and intervention strategies, optimizing risk-based health care of cancer survivors, thus minimizing chronic morbidities and improving quality of life. Cancer Epidemiol Biomarkers Prev; 20(10); 2048–67. ©2011 AACR.
Biologic and Clinical Activity of Tivozanib (AV-951, KRN-951), a Selective Inhibitor of VEGF Receptor-1, -2, and -3 Tyrosine Kinases, in a 4-Week-On, 2-Week-Off Schedule in Patients with Advanced Solid Tumors
Authors: Eskens Ferry A.L.M. , de Jonge Maja J.A. , Bhargava Pankaj , Isoe Toshiyuki , Cotreau Monette M. , Esteves Brooke , Hayashi Kunihiko , Burger Herman , Thomeer Maarten , van Doorn Leni , Verweij Jaap 
Published: October 2011

Abstract
Purpose: To assess the maximum tolerated dose (MTD)/dose-limiting toxicities (DLT), safety, pharmacokinetics, and pharmacodynamics of tivozanib, a potent and selective oral VEGF receptor (VEGFR) tyrosine kinase inhibitor.
Experimental Design: Dose levels of 1.0, 1.5, and 2.0 mg/d tivozanib for 28 days followed by 14 days of medication were explored in patients with advanced solid tumors.
Results: Forty-one patients were enrolled. Animal data incorrectly predicted toxicity, resulting in DLTs at the starting dose (2.0 mg) consisting of grade 3 proteinuria and hypertension and grade 3 ataxia. At 1.0 mg, no DLT was observed. At an intermediate dose (1.5 mg), 1 patient experienced DLT consisting of grade 3 hypertension. This dose was determined as the MTD. Of 10 additional patients treated at 1.5 mg, 1 patient each experienced grade 3 hypertension and grade 3 fatigue, and 2 patients experienced grade 3 and 4 transaminase elevation. In 12 additional patients treated at 1.0 mg, no DLT was observed. Pharmacokinetics displayed long absorption time, dose proportional exposure, and a half-life of 4.7 days. Plasma levels of VEGF-A and soluble VEGFR-2 showed dose-dependent increases and decreases, respectively. Dynamic contrast-enhanced MRI indicated reduction in tumor perfusion. Clinical activity was observed in renal cell cancer, colorectal cancer, and other tumors.
Conclusion: Tivozanib was well tolerated with manageable side effects. The pharmacokinetics profile revealed that tivozanib was suitable for once-daily dosing. Encouraging and durable clinical activity was observed. The recommended daily dose of tivozanib in a 4-week-on and 2-week-off dosing regimen is 1.5 mg. Clin Cancer Res; 17(22); 7156–63. ©2011 AACR.
Achieving Sufficient Accrual to Address the Primary Endpoint in Phase III Clinical Trials from U.S. Cooperative Oncology Groups
Authors: Schroen Anneke T. , Petroni Gina R. , Wang Hongkun , Thielen Monika J. , Gray Robert , Benedetti Jacqueline , Wang Xiaofei F. , Sargent Daniel J. , Wickerham Donald L. , Cronin Walter , Djulbegovic Benjamin , Slingluff Craig L. 
Published: October 2011

Abstract
Purpose: Assessing impact of poor accrual on premature trial closure requires a relevant metric. We propose defining accrual sufficiency on apparent ability to address primary endpoints (PE) rather than attaining accrual targets.
Experimental Design: All phase III trials open January 1, 1993, to December 31, 2002, by five U.S. oncology Clinical Trials Cooperative Groups (CTCG) were evaluated for accrual sufficiency and scientific results. Sufficient accrual included meeting accrual target, CTCGs documentation attesting adequate accrual, or conclusive results at interim analysis; insufficient accrual included poor accrual as cited closure reason or other reasons rendering a trial unable to address its primary endpoints. Closure rates based on our accrual sufficiency definition are compared with rates of meeting accrual targets and addressing the primary endpoints. A percentage of target accrual above which trials commonly answer the intended scientific question was identified to serve as an alternative to meeting full target accrual in designating accrual success.
Results: Of 238 eligible trials, 158 (66%) closed with sufficient accrual. Among 80 trials with insufficient accrual, 70 (29%) closed specifically because of poor accrual. Inadequate accrual rates are overemphasized when defining accrual success solely by meeting accrual targets. Nearly 75% of trials conclusively addressed the primary endpoints with positive results in 39% of trials. Exceeding 80% of target accrual serves as a reliable proxy for answering the intended scientific question.
Conclusions: Approximately one third of phase III trials closed with insufficient accrual to address the primary endpoints, primarily due to poor accrual. Defining accrual sufficiency broader than meeting accrual targets represents a fairer account of trial closures. Clin Cancer Res; 18(1); 256–62. ©2011 AACR.