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  • 1
    Publication Date: 2018-01-28
    Description: Objectives Workplace violence is relatively frequent among medical professionals who work in otorhinolaryngology units. This phenomenon reduces the quality of provided medical care and increases the incidence of depressive symptoms among physicians and nurses, seriously affecting their job satisfaction and work efficiency with a negative attitude towards providing treatment. Few existing studies have assessed workplace-violence-related factors associated with depressive symptoms among otorhinolaryngology physicians and nurses. Methods We conducted a cross-sectional study in grade A tertiary hospitals of Heilongjiang province in Northern China, to evaluate the occurrence and level of depressive symptoms among otorhinolaryngology physicians and nurses and to analyse the relationship between them and workplace-violence-related risk factors and demographic variables. Results Of all our participating professionals, (379 otorhinolaryngologists and 273 nurses), 57.2% were found to have depressive symptoms, whereas, of the respondents who had suffered from physical violence, 71.25% had depressive symptoms. Professionals with less than 1 year of experience, as well as professionals who more frequently worked alone, were more likely to suffer from depressive symptoms than their colleagues. Conclusions This research addresses an emerging issue of clinical practice, and its results differ from those of previous studies; specifically, it indicates that the frequency of depressive symptoms among otorhinolaryngology physicians and nurses may be influenced by physical violence, the number of coworkers they have for more than half of their working hours and other workplace-violence-related factors. To reduce the depressive symptoms caused by workplace violence and improve the quality of medical services, medical institutions should implement effective measures to prevent the occurrence of physical violence, strengthen team cooperation ability and increase peer support.
    Keywords: Open access, Public health
    Electronic ISSN: 2044-6055
    Topics: Medicine
    Published by BMJ Publishing
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  • 2
    Publication Date: 2018-05-07
    Description: Objectives Develop predictive models for a paediatric population that provide information for paediatricians and health authorities to identify children at risk of hospitalisation for conditions that may be impacted through improved patient care. Design Retrospective healthcare utilisation analysis with multivariable logistic regression models. Data Demographic information linked with utilisation of health services in the years 2006–2014 was used to predict risk of hospitalisation or death in 2015 using a longitudinal administrative database of 527 458 children aged 1–13 years residing in the Regione Emilia-Romagna (RER), Italy, in 2014. Outcome measures Models designed to predict risk of hospitalisation or death in 2015 for problems that are potentially avoidable were developed and evaluated using the C-statistic, for calibration to assess performance across levels of predicted risk, and in terms of their sensitivity, specificity and positive predictive value. Results Of the 527 458 children residing in RER in 2014, 6391 children (1.21%) were hospitalised for selected conditions or died in 2015. 49 486 children (9.4%) of the population were classified in the ‘At Higher Risk’ group using a threshold of predicted risk 〉2.5%. The observed risk of hospitalisation (5%) for the ‘At Higher Risk’ group was more than four times higher than the overall population. We observed a C-statistic of 0.78 indicating good model performance. The model was well calibrated across categories of predicted risk. Conclusions It is feasible to develop a population-based model using a longitudinal administrative database that identifies the risk of hospitalisation for a paediatric population. The results of this model, along with profiles of children identified as high risk, are being provided to the paediatricians and other healthcare professionals providing care to this population to aid in planning for care management and interventions that may reduce their patients’ likelihood of a preventable, high-cost hospitalisation.
    Keywords: Open access, Health services research
    Electronic ISSN: 2044-6055
    Topics: Medicine
    Published by BMJ Publishing
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  • 3
    Publication Date: 2018-05-15
    Description: Author Correction: Magnetism and high magnetic-field-induced stability of alloy carbides in Fe-based materials Author Correction: Magnetism and high magnetic-field-induced stability of alloy carbides in Fe-based materials, Published online: 15 May 2018; doi:10.1038/s41598-018-25978-5 Author Correction: Magnetism and high magnetic-field-induced stability of alloy carbides in Fe-based materials
    Electronic ISSN: 2045-2322
    Topics: Natural Sciences in General
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  • 4
    Keywords: ESTRADIOL ; SERUM ; TWINS ; PREMENOPAUSAL WOMEN ; SEX-HORMONE LEVELS ; STEROID-HORMONES ; LOCI ; GENOME-WIDE ASSOCIATION
    Abstract: Introduction: We have previously shown that a tag single nucleotide polymorphism (rs10235235), which maps to the CYP3A locus (7q22.1), was associated with a reduction in premenopausal urinary estrone glucuronide levels and a modest reduction in risk of breast cancer in women age 〈= 50 years. Methods: We further investigated the association of rs10235235 with breast cancer risk in a large case control study of 47,346 cases and 47,570 controls from 52 studies participating in the Breast Cancer Association Consortium. Genotyping of rs10235235 was conducted using a custom Illumina Infinium array. Stratified analyses were conducted to determine whether this association was modified by age at diagnosis, ethnicity, age at menarche or tumor characteristics. Results: We confirmed the association of rs10235235 with breast cancer risk for women of European ancestry but found no evidence that this association differed with age at diagnosis. Heterozygote and homozygote odds ratios (ORs) were OR = 0.98 (95% CI 0.94, 1.01; P = 0.2) and OR = 0.80 (95% CI 0.69, 0.93; P = 0.004), respectively (P-trend = 0.02). There was no evidence of effect modification by tumor characteristics. rs10235235 was, however, associated with age at menarche in controls (P-trend = 0.005) but not cases (P-trend = 0.97). Consequently the association between rs10235235 and breast cancer risk differed according to age at menarche (P-het = 0.02); the rare allele of rs10235235 was associated with a reduction in breast cancer risk for women who had their menarche age 〉= 15 years (ORhet = 0.84, 95% CI 0.75, 0.94; ORhom = 0.81, 95% CI 0.51, 1.30; P-trend = 0.002) but not for those who had their menarche age 〈= 11 years (ORhet = 1.06, 95% CI 0.95, 1.19, ORhom = 1.07, 95% CI 0.67, 1.72; P-trend = 0.29). Conclusions: To our knowledge rs10235235 is the first single nucleotide polymorphism to be associated with both breast cancer risk and age at menarche consistent with the well-documented association between later age at menarche and a reduction in breast cancer risk. These associations are likely mediated via an effect on circulating hormone levels.
    Type of Publication: Journal article published
    PubMed ID: 24887515
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  • 5
    Abstract: Large-scale genome-wide association studies (GWAS) have likely uncovered all common variants at the GWAS significance level. Additional variants within the suggestive range (0.0001〉 P 〉 5x10(-8)) are, however, still of interest for identifying causal associations. This analysis aimed to apply novel variant prioritization approaches to identify additional lung cancer variants that may not reach the GWAS level. Effects were combined across studies with a total of 33456 controls and 6756 adenocarcinoma (AC; 13 studies), 5061 squamous cell carcinoma (SCC; 12 studies) and 2216 small cell lung cancer cases (9 studies). Based on prior information such as variant physical properties and functional significance, we applied stratified false discovery rates, hierarchical modeling and Bayesian false discovery probabilities for variant prioritization. We conducted a fine mapping analysis as validation of our methods by examining top-ranking novel variants in six independent populations with a total of 3128 cases and 2966 controls. Three novel loci in the suggestive range were identified based on our Bayesian framework analyses: KCNIP4 at 4p15.2 (rs6448050, P = 4.6x10(-7)) and MTMR2 at 11q21 (rs10501831, P = 3.1x10(-6)) with SCC, as well as GAREM at 18q12.1 (rs11662168, P = 3.4x10(-7)) with AC. Use of our prioritization methods validated two of the top three loci associated with SCC (P = 1.05x10(-4) for KCNIP4, represented by rs9799795) and AC (P = 2.16x10(-4) for GAREM, represented by rs3786309) in the independent fine mapping populations. This study highlights the utility of using prior functional data for sequence variants in prioritization analyses to search for robust signals in the suggestive range.
    Type of Publication: Journal article published
    PubMed ID: 26363033
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  • 6
    Publication Date: 2018-01-04
    Description: Purpose: The objectives of the study were to evaluate the safety of daily oral PX-866 in combination with twice daily vemurafenib and to identify potential predictive biomarkers for this novel combination. Experimental Design: We conducted a phase I, open-label, dose-escalation study in patients with advanced BRAF V600–mutant solid tumors. PX-866 was administered on a continuous schedule in combination with vemurafenib. Patients underwent a baseline and on-treatment biopsy after 1-week of PX-866 monotherapy for biomarker assessment. Results: Twenty-four patients were enrolled. The most common treatment-related adverse events were gastrointestinal side effects. One dose-limiting toxicity (DLT) of grade 3 rash and one DLT of grade 3 pancreatitis were observed in cohort 2 (PX-866 6 mg daily; vemurafenib 960 mg twice daily) and cohort 3 (PX-866 8 mg daily; vemurafenib 960 mg twice daily), respectively. Of 23 response-evaluable patients, seven had confirmed partial responses (PR), 10 had stable disease, and six had disease progression. Decreases in intratumoral pAKT expression were observed following treatment with PX-866. Patients who achieved PRs had higher rates of PTEN loss by IHC (80% vs. 58%) and pathogenic PTEN mutations and/or deletions (57% vs. 25%). Two patients with durable PRs had an increase in intratumoral CD8 + T-cell infiltration following treatment with PX-866. Conclusions: PX-866 was well tolerated at its maximum tolerated single-agent dose when given in combination with a modified dose of vemurafenib (720 mg twice daily). Response to treatment appeared to be associated with PTEN loss and treatment with PX-866 seemed to increase CD8 + T-cell infiltration in some patients. Clin Cancer Res; 24(1); 22–32. ©2017 AACR .
    Print ISSN: 1078-0432
    Electronic ISSN: 1557-3265
    Topics: Medicine
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  • 7
    Publication Date: 2018-01-17
    Description: Purpose: Emerging studies demonstrate that long noncoding RNAs (lncRNA) participate in the regulation of various cancers. In the current study, a novel lncRNA-TTN-AS1 has been identified and explored in esophageal squamous cell carcinoma (ESCC). Experimental Design: To discover a new regulatory circuitry in which RNAs crosstalk with each other, the transcriptome of lncRNA-miRNA-mRNA from ESCC and adjacent nonmalignant specimens were analyzed using multiple microarrays and diverse bioinformatics platforms. The functional role and mechanism of a novel lncRNA-TTN-AS1 were further investigated by gain-of-function and loss-of-function assays in vivo and in vitro . An ESCC biomarker panel, consisting of lncRNA-TTN-AS1 , miR-133b , and FSCN1 , was validated by qRT-PCR and in situ hybridization using samples from 148 patients. Results: lncRNA-TTN-AS1 as an oncogene is highly expressed in ESCC tissues and cell lines, and promotes ESCC cell proliferation and metastasis. Mechanistically, lncRNA-TTN-AS1 promotes expression of transcription factor Snail1 by competitively binding miR-133b , resulting in the epithelial–mesenchymal transition (EMT) cascade. Moreover, lncRNA-TTN-AS1 also induces FSCN1 expression by sponging miR-133b and upregulation of mRNA-stabilizing protein HuR, which further promotes ESCC invasion cascades. We also discovered and validated a clinically applicable ESCC biomarker panel, consisting of lncRNA-TTN-AS1 , miR-133b , and FSCN1 , that is significantly associated with overall survival and provides additional prognostic evidence for ESCC patients. Conclusions: As a novel regulator, lncRNA-TTN-AS1 plays an important role in ESCC cell proliferation and metastasis. The lncRNA-TTN-AS1/miR133b/FSCN1 regulatory axis provides bona fide targets for anti-ESCC therapies. Clin Cancer Res; 24(2); 486–98. ©2017 AACR .
    Print ISSN: 1078-0432
    Electronic ISSN: 1557-3265
    Topics: Medicine
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  • 8
    Publication Date: 2018-09-05
    Description: Small therapeutic proteins represent a promising novel approach to treat cancer. Nevertheless, their clinical application is often adversely impacted by their short plasma half-life. Controlled long-term delivery of small biologicals has become a challenge because of their hydrophilic properties and in some cases their limited stability. Here, an in situ forming depot-injectable polymeric system was used to deliver BiJ591, a bispecific T-cell engager (BiTE) targeting both prostate-specific membrane antigen (PSMA) and the CD3 T-cell receptor in prostate cancer. BiJ591 induced T-cell activation, prostate cancer–directed cell lysis, and tumor growth inhibition. The use of diblock (DB) and triblock (TB) biodegradable polyethylene glycol–poly(lactic acid; PEG-PLA) copolymers solubilized in tripropionin, a small-chain triglyceride, allowed maintenance of BiJ591 stability and functionality in the formed depot and controlled its release. In mice, after a single subcutaneous injection, one of the polymeric candidates, TB1/DB4, provided the most sustained release of BiJ591 for up to 21 days. Moreover, the use of BiJ591-TB1/DB4 formulation in prostate cancer xenograft models showed significant therapeutic activity in both low and high PSMA–expressing tumors, whereas daily intravenous administration of BiJ591 was less efficient. Collectively, these data provide new insights into the development of controlled delivery of small therapeutic proteins in cancer. Mol Cancer Ther; 17(9); 1927–40. ©2018 AACR .
    Print ISSN: 1535-7163
    Electronic ISSN: 1538-8514
    Topics: Medicine
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  • 9
    Publication Date: 2018-10-02
    Description: Purpose: Triple-negative breast cancer (TNBC) is a clinically aggressive disease with poor prognosis. Conventional chemotherapeutics are generally able to shrink the tumor mass, but often fail to completely eradicate cancer stem–like cells (CSCs) that are responsible for high risk of relapse and frequent metastases. In this study, we examined thermal sensibility of CSCs, developed an approach that enabled concurrent elimination of both the bulk of cancer cells and CSCs, and investigated the underlying mechanism. Experimental Design: We designed a platform consisting of gold nanoparticle-coated porous silicon microparticle (AuPSM) that was also loaded with docetaxel micelles (mDTXs) to enable concurrent killing of the bulk of cancer cells by released mDTX and CSCs by mild hyperthermia upon stimulation of AuPSM with near infrared. In addition, we examined the role of heat shock proteins in sensitizing CSC killing. Finally, we applied mDTX-loaded AuPSM to treat mice with SUM159 and 4T1 orthotopic tumors and evaluated tumor growth and tumor metastasis. Results: MDA-MB-231 and SUM159 TNBC cells treated with mDTX-loaded AuPSM and mild hyperthermia displayed significantly reduced efficiencies in mammosphere formation than those treated with mDTX alone or mild hyperthermia alone. Combination treatment also completely inhibited SUM159 orthotopic tumor growth and 4T1 tumor metastasis. Mechanistically, DTX treatment suppressed expression of heat shock protein 27 in cancer cells including the CSCs, rendering cells sensitive to mild hyperthermia. Conclusions: Our results indicate that chemotherapy sensitizes CSC to mild hyperthermia. We have developed an effective therapeutic approach to eliminate therapy-resistant cells in TNBC. Clin Cancer Res; 24(19); 4900–12. ©2018 AACR .
    Print ISSN: 1078-0432
    Electronic ISSN: 1557-3265
    Topics: Medicine
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  • 10
    Publication Date: 2018-10-02
    Description: Neoangiogenesis plays a key role in diverse pathophysiological conditions, including liver regeneration. Yet, the source of new endothelial cells (ECs) remains elusive. By analyzing the regeneration of the liver vasculature in irradiation-based myeloablative and nonmyeloablative bone marrow transplantation mouse models, we discovered that neoangiogenesis in livers with intact endothelium was solely mediated by proliferation of resident ECs. However, following irradiation-induced EC damage, bone marrow–derived mononuclear cells were recruited and incorporated into the vasculature. Further experiments with direct bone marrow infusion or granulocyte colony–stimulating factor (G-CSF)–mediated progenitor cell mobilization, which resembles clinically relevant stem cell therapy, demonstrated that bone marrow–derived cells did not contribute to the regeneration of liver vasculature after two-thirds partial hepatectomy (PHx). Taken together, the data reconcile many of the discrepancies in the literature and highlight that the cellular source of regenerating endothelium depends on the fitness of the residual vasculature.
    Keywords: Cardiovascular Biology, Stem Cells & Regeneration
    Print ISSN: 0022-1007
    Electronic ISSN: 1540-9538
    Topics: Medicine
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