Erratum: Impact of Advanced Hearing Aid Technology on Speech Understanding for Older Listeners with Mild to Moderate, Adult-Onset, Sensorineural Hearing Loss

<b><i>Background:</i></b> Hearing loss is one of the most common chronic health conditions of older people. Hearing aids are the customary treatment and they improve quality of life in older adults. Even so, relatively few older adults with uncomplicated, mild to moderate, adult-onset, sensorineural hearing loss use hearing aids. One reason for this is a belief that hearing aids do not provide sufficient value to justify their expense. Although modern hearing aids are available at several price points, there is minimal evidence about the relative benefits of premium-level versus basic-level hearing aid technologies. <b><i>Objective:</i></b> This research was designed to demonstrate the relative effectiveness of premium hearing aids compared with basic hearing aids in improving speech understanding and quality of life. <b><i>Methods:</i></b> 25 participants, including both new and experienced hearing aid users, completed blinded month-long field trials with each of four pairs of hearing aids: two basic and two premium level. Outcomes were laboratory speech understanding tests, standardized questionnaires and open-ended diary items. <b><i>Results:</i></b> Participants reacted very positively to all the hearing aids. Both everyday speech understanding and quality of life were substantially improved with hearing aids. Results for both new and experienced users were consistent with a conclusion that there were no statistically significant or clinically important differences in improvement between the premium- and basic-level hearing aids. <b><i>Conclusions:</i></b> It should not be assumed that more costly hearing aids always produce better outcomes. With contemporary hearing aids from two major manufacturers, the subjects obtained as much improvement in speech understanding and quality of life from lower-cost basic-level instruments as from higher-cost premium-level instruments. Regardless of technology level, comprehensive best-practice fitting protocols should be followed to optimize results for every patient. © 2014 S. Karger AG, Base

Supplementary Material for: LncRNA HOXA-AS2 facilitates prostate cancer progression by inhibiting miR-885-5p to upregulate KDM5B

Background: The regulatory network of competing endogenous RNAs (ceRNAs) affects tumorigenesis. In this study, we aimed to investigate the mechanism by which long non-coding RNA (lncRNA) HOXA-AS2 promotes prostate cancer (PCa) progression. Methods: The expression levels of HOXA-AS2, miR-885-5p, and KDM5B in PCa tissues and cell lines were evaluated by qRT-PCR or western blotting. CCK-8 assay, caspase-3 activity assay, flow cytometry, and scratch test revealed changes in cell proliferation, caspase-3 activity, apoptosis, and migration, respectively. Luciferase and radioimmunoprecipitation assays were used to evaluate the correlation among HOXA-AS2, miR-885-5p, and KDM5B expression profiles. Results: HOXA-AS2 expression level was elevated in PCa tissues and cells. Silencing of HOXA-AS2 suppressed proliferation and migration and facilitated apoptosis in PCa cells. HOXA-AS2 competitively adsorbed miR-885-5p, thereby blocking the effect of HOXA-AS2 knockdown by the miR-885-5p inhibitor in PCa cells. Moreover, KDM5B, a target of miR-885-5p, neutralized the function of miR-885-5p in PCa cells. Conclusions: This study revealed a potential ceRNA regulatory pathway in which HOXA-AS2 affects KDM5B expression levels by sponging miR-885-5p to promote PCa development and progression

Supplementary Material for: Role of Epidermal Growth Factor Receptor Expression on Patient Survival in Pancreatic Cancer: A Meta-Analysis

<p><i>Background/Aims:</i> Epidermal growth factor receptor (EGFR) has been considered as an attractive and potential therapeutic target of pancreatic cancer. However, the clinical importance of EGFR expression remains controversial. <i>Methods:</i> We performed a meta-analysis of previous studies to quantitatively review the effects of EGFR expression on survival in patients with pancreatic cancer. <i>Results:</i> Eight studies (570 patients) were included to perform a meta-analysis of the survival results. Overall, positivity for EGFR expression was 45.1% in pancreatic carcinoma. The combined hazard ratio was 1.225 (95% CI 1.014–1.481; p = 0.035), indicating that EGFR expression has a significant impact on survival. Heterogeneity was absent between studies and publication bias, which suggests that the summary statistics obtained may approximate the actual average. Three trials reported a survival disadvantage for patients with EGFR expression while five trials reported no statistically significant difference. <i>Conclusion:</i> EGFR expression is a poor prognostic factor for survival in patients with pancreatic cancer.</p

Supplementary Material for: Reproductive Performance after Surgery for Endometriosis: Predictive Value of the Revised American Fertility Society Classification and the Endometriosis Fertility Index

<b><i>Background/Aims:</i></b> To determine whether the revised American Fertility Society (rAFS) classification and endometriosis fertility index (EFI) predict pregnancy rates (PRs) in patients with surgically confirmed endometriosis attempting natural conception. <b><i>Methods:</i></b> We retrospectively assessed 194 women with endometriosis who underwent laparoscopic surgery; 161 women completed the follow-up. Pregnancy outcomes, rAFS stages and EFI scores were documented. Cumulative PRs were compared using Kaplan-Meier survival analysis. <b><i>Results:</i></b> The cumulative PR 36 months after surgery was 46.6% (stage I, 53.6%; stage II, 36.0%; stage III, 51.7%, and stage IV, 41.7%; log-rank test, χ² = 4.143, p = 0.246). In the 1st year, PRs significantly differed between patients with rAFS stage IV and those with stages I-III (Pearson's χ² test, χ² = 6.024, p = 0.014). Significant differences in cumulative PRs were observed among EFI scores (group 1, EFI score 0-3, 8.3%; group 2, EFI score 4-7 41.2%, and group 3, EFI score 8-10 60.9%; log-rank test, χ² = 16.254, p < 0.001). <b><i>Conclusions:</i></b> EFI scores, but not rAFS stage, predict PRs in patients with endometriosis-associated infertility. EFI scores may be used to guide postoperative treatment

Supplementary Material for: Demineralized Dentin Matrix Induces Odontoblastic Differentiation of Dental Pulp Stem Cells

<br>The aim of this study was to investigate the effect of demineralized dentin matrix (DDM) on dental pulp stem cells (DPSCs) and the potential of complexes with DPSCs and DDM for mineralized tissue formation. Stem cells derived from the dental pulp of healthy pigs aged 18 months were isolated and cultured. DPSCs were incubated with alpha-minimum essential medium treated with DDM extract at 1 mg/ml (DDM1) or 10 mg/ml (DDM10). The concentrations of 3 growth factors in DDM extract was measured by enzyme-linked immunosorbent assay. Adhesion of DPSCs on DDM and hydroxyapatite-tricalcium phosphate (HA-TCP) surfaces was observed using scanning electron microscopy. Cell proliferation was evaluated with cell counting kit-8 and migration by Transwell migration assays. Odontoblastic differentiation was assessed by alkaline phosphatase (ALP) and alizarin red staining, ALP activity and real-time polymerase chain reaction analysis of markers of ALP, runt-related transcription factor 2, type I collagen, dentin matrix acidic phosphoprotein-1, osteonectin and dentin sialophosphoprotein (DSPP). Finally, DPSCs were combined with DDM and placed subcutaneously in nude mice for 12 weeks; DPSCs combined with HA-TCP and DDM alone served as controls. DDM could promote DPSC adhesion, migration and odontoblastic differentiation. Mineralized tissue formation was observed with the DPSC and DDM combination and the DPSC and HA-TCP combination. The mineralized tissue of the DPSC + DDM combination stained positive for DSPP, similar to the dentin tissue. These results indicate that DDM induces DPSC odontoblastic differentiation, suggesting applications for dentin regeneration

Supplementary Material for: Downregulation of the Cl^-/HCO₃^-Exchanger Pendrin in Kidneys of Mice with Cystic Fibrosis: Role in the Pathogenesis of Metabolic Alkalosis

<b><i>Background/Aims:</i></b> Patients with cystic fibrosis (CF) are prone to the development of metabolic alkalosis; however, the pathogenesis of this life threatening derangement remains unknown. We hypothesized that altered acid base transport machinery in the kidney collecting duct underlies the mechanism of impaired bicarbonate elimination in the CF kidney. <b><i>Methods:</i></b> Balance studies in metabolic cages were performed in WT and CFTR knockout (CF) mice with the intestinal rescue in response to bicarbonate loading or salt restriction, and the expression levels and cellular distribution of acid base and electrolyte transporters in the proximal tubule, collecting duct and small intestine were examined by western blots, northern blots and/or immunofluorescence labeling. <b><i>Results:</i></b> Baseline parameters, including acid-base and systemic vascular volume status were comparable in WT and CF mice, as determined by blood gas, kidney renin expression and urine chloride excretion. Compared with WT animals, CF mice demonstrated a significantly higher serum HCO₃^- concentration (22.63 in WT vs. 26.83 mEq/l in CF mice; n=4, p=0.013) and serum pH (7.33 in WT vs. 7.42 in CF mice; n=4, p=0.00792) and exhibited impaired kidney HCO₃^- excretion (urine pH 8.10 in WT vs. 7.35 in CF mice; n=7, p=0.00990) following a 3-day oral bicarbonate load. When subjected to salt restriction, CF mice developed a significantly higher serum HCO₃^- concentration vs. WT animals (29.26 mEq/L in CF mice vs. 26.72 in WT; n=5, p=0.0291). Immunofluorescence labeling demonstrated a profound reduction in the apical expression of the Cl^-/HCO₃^- exchanger pendrin in cortical collecting duct cells and western and northern blots indicated diminished plasma membrane abundance and mRNA expression of pendrin in CF kidneys. <b><i>Conclusions:</i></b> We propose that patients with cystic fibrosis are prone to the development of metabolic alkalosis secondary to the inactivation of the bicarbonate secreting transporter pendrin, specifically during volume depletion, which is a common occurrence in CF patients

Supplementary Material for: Plasma sACE-2 and risk of recurrent stroke: a nested case-control analysis

Abstract Introduction The angiotensin-converting enzyme-2 (ACE-2) and its shedding product [soluble ACE-2 (sACE-2)] are implicated in adverse cardiovascular outcomes. However, the relationship between sACE-2 and stroke recurrence is unknown. Herein, we examined the relationship of sACE-2 with stroke recurrence in patients with ischemic stroke or transient ischemic attack (TIA). Methods Data were obtained from the Third China National Stroke Registry (CNSR-Ⅲ). Eligible cases consisted of 494 patients who developed recurrent stroke within 1-year follow-up, 494 controls were selected using age- and sex- matched with a 1:1 case-control ratio. Conditional logistic regressions were used to evaluate the association between sACE-2 and recurrent stroke. The main outcomes were recurrent stroke within 1 year. Results Among 988 patients included in this study, the median (interquartile range) of sACE-2 was 25.17 (12.29-45.56) ng/mL. After adjustment for conventional confounding factors, the odds ratio with 95% confidence interval in the highest quartile versus the lowest quartile was 1.68 (1.12-2.53) for recurrent stroke within 1-year follow-up. Subgroup analysis showed that the association between elevated plasma level of sACE-2 and stroke recurrence was significant in patients with higher systemic inflammation, as indicated by high sensitivity C reactive protein (hsCRP) ≥ 2 mg/L (adjusted OR: 2.33 [95% CI, 1.15–4.72]) and neutrophil (NEUT) counts ≥ median (adjusted OR: 2.66 [95% CI, 1.35–5.23]), but not significant in patients with lower systemic inflammation. Discussion Elevated plasma sACE-2 concentration was associated with increased risk of recurrent stroke

Supplementary Material for: Genome-Wide Association Study and Transcriptome Analysis Provide New Insights into the White/Red Earlobe Color Formation in Chicken

<b><i>Background/Aims:</i></b> Earlobe color is a typical external trait in chicken. There are some previous studies showing that the chicken white/red earlobe color is a polygenic and sex-linked trait in some breeds, but its molecular genetic and histological mechanisms still remain unclear. <b><i>Methods:</i></b> We herein utilized histological section, genome-wide association study (GWAS) and RNA-seq, further to investigate the potential histological and molecular genetic mechanisms of white/red earlobe formation in Qiangyuan Partridge chicken (QYP). <b><i>Results:</i></b> through histological section analysis, we found the dermal papillary layer of red earlobes had many more blood vessels than that of white earlobes. And we identified a total of 44 SNPs from Chromosome 1, 2, 3, 4, 9, 10, 11, 13, 19, 20, 23 and Z, that was significantly associated with the chicken white/red earlobe color from GWAS, along with 73 significantly associated genes obtained (e.g., <i>PIK3CB, B4GALT1</i> and <i>TP63</i>), supporting the fact that the white/red earlobe color was also polygenic and sex-linked in QYP. Importantly, <i>PIK3CB</i> and <i>B4GALT1</i> are both involved in the biological process of angiogenesis, which may directly give rise to the chicken white earlobe formation through regulating blood vessel density in chicken earlobe. Additionally, through contrast of RNA-seq profiles between white earlobe skins and red earlobe skins, we further identified <i>TP63</i> and <i>CDH1</i> differentially expressed. Combined with the existing knowledge of TP63 in epithelial development and tumor angiogenesis, we propose that down-regulated <i>TP63</i> in white earlobes may play roles in thickening the skin and decreasing the vessel numbers in dermal papillary layer, thereby contributing to the white earlobe formation via paling the redness of the skin in QYP, but the specific mechanism remains to be further clarified. <b><i>Conclusion:</i></b> our findings advance the existing understanding of the white earlobe formation, as well as provide new clues to understand the molecular mechanism of chicken white/red earlobe color formation

Supplementary Material for: One-Year Survival and Renal Function Recovery of Acute Kidney Injury Patients with Chronic Heart Failure

<b><i>Objective:</i></b> To describe and analyze the clinical characteristics of acute kidney injury (AKI) patients with preexisting chronic heart failure (CHF) and to identify the prognostic factors of the 1-year outcome. <b><i>Methods:</i></b> A total of 120 patients with preexisting CHF who developed AKI between January 2005 and December 2010 were enrolled. CHF was diagnosed according to the European Society of Cardiology guidelines, and AKI was diagnosed using the RIFLE criteria. Clinical characteristics were recorded, and nonrecovery from kidney dysfunction as well as mortality were analyzed. <b><i>Results:</i></b> The median age of the patients was 70 years, and 58.33% were male. 60% of the patients had an advanced AKI stage (‘failure') and 90% were classified as NYHA class III/IV. The 1-year mortality rate was 35%. 25.83% of the patients progressed to end-stage renal disease after 1 year. Hypertension, anemia, coronary atherosclerotic heart disease and chronic kidney disease were common comorbidities. Multiple organ dysfunction syndrome (MODS; OR, 35.950; 95% CI, 4.972-259.952), arrhythmia (OR, 13.461; 95% CI, 2.379-76.161), anemia (OR, 6.176; 95% CI, 1.172-32.544) and RIFLE category (OR, 5.353; 95% CI, 1.436-19.952) were identified as risk factors of 1-year mortality. For 1-year nonrecovery from kidney dysfunction, MODS (OR, 8.884; 95% CI, 2.535-31.135) and acute heart failure (OR, 3.281; 95% CI, 1.026-10.491) were independent risk factors. <b><i>Conclusion:</i></b> AKI patients with preexisting CHF were mainly elderly patients who had an advanced AKI stage and NYHA classification. Their 1-year mortality and nonrecovery from kidney dysfunction rates were high. Identifying risk factors may help to improve their outcome