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Abstract Background Ganoderma lucidum-derived polysaccharide (PS-G) can rapidly and effectively promote the activation and maturation of immature dendritic cells (DCs), suggesting that PS-G possesses the capacity to regulate immune responses. This study aimed to clarify the immunologic effect of PS-G on monocyte-derived dendritic cells (MD-DCs) from asthmatic children allergic to house dust mites. The MD-DCs were stimulated for 24 h with the related allergen, Der p 1, in the presence or absence of PS-G. Cell surface markers and phagocytic capacity were assessed by FACS analysis, and key polarizing cytokines (IL-12 p40, IL-12 p70, IL-6, IL-23, and IL-10) were quantified. The subsequent regulatory effect of pulsed MD-DCs on naïve T cells was evaluated by determining the T-cell cytokine profile. Results PS-G induced the maturation of MD-DCs and decreased phagocytic capacity, even if pulsed with Der p 1. After incubation with PS-G and Der p 1, MD-DCs produced higher amounts of IL-12 p70, IL-12 p40, IL-6, IL-23, and IL10 than Der p 1-pulsed DCs. Furthermore, type 1 helper T (Th1) cell cytokine (INF-γ) production was highly increased when naïve autologous T cells were co-cultured with Der p 1-pulsed MD-DCs. Naïve T cells stimulated by MD-DCs pulsed with Der p 1 failed to produce proliferation of T-cells, whereas the addition of PS-G to Der p 1 induced a significant proliferation of T-cells similar to that observed with PS-G alone. Conclusion The presence of PS-G in an allergen pulse promoted allergic MD-DCs to produce IL-12 p70, IL-12 p40, IL-6, IL-23, and IL-10, and exerted an effect on shifting the immune balance towards Th1 in children with allergic asthma.

Abstract Background Propolis, an ancient herbal medicine, has been reported the beneficial effect both in asthma patients and murine model of asthma, but the mechanism was not clearly understood. In this study, the effect of caffeic acid phenethyl ester (CAPE), the most extensively studied components in propolis, on the functions of human monocyte-derived dendritic cells (MoDCs) was investigated. Results CAPE significantly inhibited IL-12 p40, IL-12 p70, IL-10 protein expression in mature healthy human MoDCs stimulated by lipopolysaccharides (LPS) and IL-12 p40, IL-10, IP-10 stimulated by crude mite extract. CAPE significantly inhibited IL-10 and IP-10 but not IL-12 expression in allergic patients' MoDCs stimulated by crude mite extract. In contrast, the upregulation of costimulatory molecules in mature MoDCs was not suppressed by CAPE. Further, the antigen presenting ability of DCs was not inhibited by CAPE. CAPE inhibited IκBα phosphorylation and NF-κB activation but not mitogen-activated protein kinase (MAPK) family phosphorylation in human MoDCs. Conclusion These results indicated that CAPE inhibited cytokine and chemokine production by MoDCs which might be related to the NF-κB signaling pathway. This study provided a new insight into the mechanism of CAPE in immune response and the rationale for propolis in the treatment of asthma and other allergic disorders.

Adipocyte fatty acid binding protein is positively associated with atherosclerosis. Peripheral arterial disease is associated with an increased mortality in hemodialysis patients. This study aimed to evaluate the relationship between serum adipocyte fatty acid binding protein levels and peripheral arterial disease by ankle‐brachial index in hemodialysis patients. Among the 90 chronic hemodialysis recipients, 20 patients (22.2%) were in the low ankle‐brachial index group who had a higher prevalence of diabetes, hyperlipidemia, statin use, older age, higher body fat mass, higher serum adipocyte fatty acid binding protein level, and lower serum creatinine level compared with patients in the control group. After statistical analysis, body fat mass (P = 0.006) and creatinine level (P = 0.018) were shown to be the independent predictors of adipocyte fatty acid binding protein level. Serum adipocyte fatty acid binding protein (P = 0.021) was found to be positively associated with peripheral arterial disease in hemodialysis patients. [ABSTRACT FROM AUTHOR]

Introduction: Leptin is an adipokine secreted from adipocytes that mediate lipid metabolism and inflammation. This cross‐sectional study investigated the relationship between serum leptin level and nutrition status evaluated by malnutrition‐inflammation score (MIS) among patients undergoing hemodialysis (HD). Methods: This study included 100 patients on HD. Nutritional status was based on MIS (malnutrition ≥7 points). Body composition, biochemistry data, and serum leptin level were evaluated. Findings: Of 100 subjects, 33 (33.0%) were categorized as having malnutrition. Compared with subjects in the well‐nourished group, those in the malnutrition group had on average an older age, longer HD duration, and lower height, weight, body mass index, waist circumference, body fat mass, serum triglyceride level, and creatinine level. Serum leptin levels were also significantly lower in the malnutrition group (P < 0.001), whereas C‐reactive protein (CRP) levels were higher (P = 0.002). Multivariable linear regression analysis revealed that HD duration (β = 2.06, P = 0.009), serum leptin level (β = −5.16, P < 0.001), CRP level (β = 3.33, P < 0.001), and albumin level (β = −1.95, P = 0.008) were factors independently associated with MIS. The discriminative power of serum leptin level to predict malnutrition was 0.834 (95% confidence interval: 0.747‐0.901, P < 0.001). Discussion: Low serum leptin level was associated with malnutrition, and serum leptin level may be a valuable marker for nutrition assessment in patients undergoing HD. [ABSTRACT FROM AUTHOR]

Objective: Adiponectin is a fat-derived hormone that secretes exclusively by adipocytes and has antiatherosclerotic effects. Peripheral arterial occlusive disease (PAOD) is associated with an increased risk of death in hemodialysis (HD) patients. The aim of this study was to evaluate the relationship between serum adiponectin levels and PAOD by ankle–brachial index (ABI) in HD patients. Materials and Methods: Blood samples were obtained from 100 HD patients. Serum adiponectin levels were measured using a commercial enzyme-linked immunosorbent assay kit. ABI values were measured using the automated oscillometric method (VaSera VS-1000). ABI values that <0.9 were included in the low ABI group. Results: Among the 100 HD patients, 18 of them (18.0%) were in the low ABI group. Compared with patients in the normal ABI group, the patients in the low ABI group had a higher prevalence of diabetes (P = 0.043), older age (P = 0.027), and lower serum adiponectin level (P = 0.003). In addition, the multivariable logistic regression analysis showed that adiponectin (Odds ratio [OR]: 0.927, 95% confidence interval [CI]: 0.867–0.990, P = 0.025) and age (OR: 1.054, 95% CI: 1.002–1.109, P = 0.043) were the independently associated with PAOD in HD patients. Conclusion: In this study, serum adiponectin level was found to be associated with PAOD in HD patients. [ABSTRACT FROM AUTHOR]

Background: Overtreatment is a common concern for patients with ductal carcinoma in situ (DCIS), but this entity is difficult to distinguish from invasive breast cancers in administrative claims data sets because DCIS often is coded as invasive breast cancer. Therefore, the authors developed and validated algorithms to select DCIS cases from administrative claims data to enable outcomes research in this type of data.Methods: This retrospective cohort using invasive breast cancer and DCIS cases included women aged 66 to 70 years in the 2004 through 2011 Texas Cancer Registry (TCR) data linked to Medicare administrative claims data. TCR records were used as "gold" standards to evaluate the sensitivity, specificity, and positive predictive value (PPV) of 2 algorithms. Women with a biopsy enrolled in Medicare parts A and B at 12 months before and 6 months after their first biopsy without a second incident diagnosis of DCIS or invasive breast cancer within 12 months in the TCR were included. Women in 2010 Medicare data were selected to test the algorithms in a general sample.Results: In the TCR data set, a total of 6907 cases met inclusion criteria, with 1244 DCIS cases. The first algorithm had a sensitivity of 79%, a specificity of 89%, and a PPV of 62%. The second algorithm had a sensitivity of 50%, a specificity of 97%. and a PPV of 77%. Among women in the general sample, the specificity was high and the sensitivity was similar for both algorithms. However, the PPV was approximately 6% to 7% lower.Conclusions: DCIS frequently is miscoded as invasive breast cancer, and thus the proposed algorithms are useful to examine DCIS outcomes using data sets not linked to cancer registries. Cancer 2018;124:2815-2823. © 2018 American Cancer Society. [ABSTRACT FROM AUTHOR]

Enterovirus D68 (EV-D68), belonging to the genus Enterovirus of the Picornavirus family, is an emerging pathogen that can cause neurological and respiratory diseases in children. However, there is little understanding of the pathogenesis of EV-D68, and no effective vaccine or drug for the prevention or treatment of the diseases caused by this virus is available. Autophagy is a cellular process that targets cytoplasmic proteins or organelles to the lysosomes for degradation. Enteroviruses strategically harness the host autophagy pathway to facilitate the completion of their life cycle. Therefore, we selected an autophagy compound library to screen for autophagy-related compounds that may affect viral growth. By using the neutralization screening assay, we identified a compound, 'licochalcone A' that significantly inhibited EV-D68 replication. To investigate the mechanism by which licochalcone A inhibits EV-D68 replication and to identify the viral life cycle stage it inhibits, the time-of-addition, viral attachment, viral entry, and dual-luciferase reporter assays were performed. The results of the time-of-addition assay showed that licochalcone A, a characteristic chalcone found in liquorice roots and widely used in traditional Chinese medicine, inhibits EV-D68 replication during the early stages of the viral life cycle, while those of the dual-luciferase reporter assay showed that licochalcone A does not regulate viral attachment and entry, but inhibits EV-D68 IRES-dependent translation. Licochalcone A also inhibited enterovirus A71 and coxsackievirus B3 but did not significantly inhibit dengue virus 2 or human coronavirus 229E replication. Licochalcone A regulates IRES translation to inhibit EV-D68 viral replication. • Licochalcone A inhibits EV-D68 replication. • Licochalcone A regulates the translation of IRES to hinder EV-D68 replication. • Licochalocne A inhibits different genotypes of enterovirus replication. • Licochalcone A didn't significantly inhibit DNEV2 and hCoV-229 E replication. [ABSTRACT FROM AUTHOR]