Regulatory T cells (Tregs) and plasmacytoid dendritic cells (pDCs) play important roles in the immune escape of cancer. In this study, we investigated pDCs and pDC-induced inducible costimulator (ICOS)+ Treg populations in peripheral blood from gastric cancer (GC) patients and healthy donors by flow cytometry. The distribution of these cells in carcinoma tissue, peritumor tissue, and normal gastric mucosa was detected by immunohistochemistry. Plasma and tissue concentration of the cytokines such as interleukin-10 and transforming growth factor-β1 were also measured. We found that the numbers of pDCs, Tregs, and ICOS+ Tregs in peripheral blood were increased in GC patients compared with healthy donors. In tissue, Tregs and ICOS+ Tregs were found distributing mainly in carcinoma tissue, whereas pDCs were mainly found in peritumor tissue. Moreover, the Foxp3+ICOS+/Foxp3+ cell ratio in carcinoma and peritumor tissue were higher than that in normal tissue. There were more ICOS+ Tregs in tumor and peritumor tissue of late-stage GC patients. There was a positive correlation between pDCs and ICOS+ Tregs in peripheral blood and peritumor tissue from GC patients. In conclusion, pDCs may play a potential role in recruiting ICOS+ Tregs, and both participate in the immunosuppression microenvironment of GC.

The revolution of molecular techniques in the field of microbial ecology not only allows an in-depth exploration of abundant bacteria, but also confirms the existence of "rare biosphere." However, the mechanisms underlying the assembly process of abundant and rare bacteria in plateau lakes are still poorly understood. In the present study, distribution of abundant and rare bacteria in 21 lakes on Yungui Plateau, China and the relative importance of deterministic and neutral factors to their biogeographic patterns were examined. Results surprisingly showed that similar biogeographic patterns of rare and abundant taxa were generally shaped via similar assembly mechanisms. For both bacterial groups, deterministic process strongly influenced the distribution, while neutral process was not at play. In addition, they both exhibited a weak distance-decay relationship. Nevertheless, environmental drivers of rare and abundant taxa and their importance were not exactly the same. Water physicochemical property was the most dominant driver shaping the biogeographic pattern of rare taxa, followed by lake morphology and watershed land-use, while for abundant taxa, watershed land-use was the most dominant driver and lake morphology did not play a significant role. This study suggested that rare bacteria in high-altitude aquatic ecosystems might experience equally low extinction risk and respond to environmental changes in a similar manner to abundant ones, but their ecological niches and functions were not identical. To fully understand the assembly mechanism of bacterial community, it is necessary to differentiate the community by traits of taxa.Bacteria are typically diverse and complex organisms crucial to ecosystem function for their vital roles in global biogeochemical cycles (Xia et al. 2010;Newton et al. 2011;Liao et al. 2015a;Cao et al. 2016). The revolution of highthroughput sequencing and increasing sampling efforts have confirmed the existence of "rare bacterial biosphere," which is composed of massive species with a few individuals . These rare bacteria exhibit characteristic metabolic activities (Jones and Lennon 2010;Campbell et al. 2011), carry out particular metabolic functions important for the turnover of certain elements (Pester et al. 2010; Pedr osAli o 2012), and can be regarded as a propagule bank (Grime 1998). Compared to rare bacteria, abundant ones have been explored to a deeper degree. They appear to contribute a major function to ecosystems (Kim et al. 2013). Considering the importance of rare and abundant taxa, it is necessary to unveil their biogeographic patterns, which will provide more useful information for functional and ecological investigations (Herlemann et al. 2011;Hanson et al. 2012;Liu et al. 2015). However, it is still under debate whether rare bacterial taxa share similar biogeography with abundant ones. In order to resolve this dispute and also to interpret a global map of bacterial diversity, more efforts are in demand to characterize the biogeographic patterns of rare and ab...

A bunch of microRNAs (miRNAs) have been demonstrated to be aberrantly expressed in cancer tumor tissue and serum. The miRNA signatures identified from the serum samples could serve as potential noninvasive diagnostic markers for breast cancer. The role of the miRNAs in cancerigenesis is unclear. In this study, we generated the expression profiles of miRNAs from the paired breast cancer tumors, normal, tissue, and serum samples from eight patients using small RNA-sequencing. Serum samples from eight healthy individuals were used as normal controls. We identified total 174 significantly differentially expressed miRNAs between tumors and the normal tissues, and 109 miRNAs between serum from patients and serum from healthy individuals. There are only 10 common miRNAs. This suggests that only a small portion of tumor miRNAs are released into serum selectively. Interestingly, the expression change pattern of 28 miRNAs is opposite between breast cancer tumors and serum. Functional analysis shows that the differentially expressed miRNAs and their target genes form a complex interaction network affecting many biological processes and involving in many types of cancer such as prostate cancer, basal cell carcinoma, acute myeloid leukemia, and more.

Background : The prognostic nutritional index (PNI) is a useful parameter that indicates the immunonutritional status of patients with malignant tumors. In this retrospective study, we aimed to investigate the value of PNI to predict the outcome of gastrointestinal stromal tumors (GISTs). Material and methods : This study enrolled 431 GIST patients who underwent curative resection from January 2000 to December 2012. A receiver operating characteristic (ROC) curve analysis was used to identify the cutoff value of PNI, neutrophil to lymphocyte ratio (NLR) and platelet to lymphocyte ratio (PLR). Survival curves were produced using the Kaplan-Meier method and were compared using a log-rank test. The Cox proportional hazards model was used to identify independent prognostic factors. Results : Of the 431 patients, 209 (48.5%) were male and 222 (51.5%) were female. The median age was 56 (range 20-80 years old). The PNI cutoff value was 47.45, with a sensitivity of 61.1 % and a specificity of 69.9 %. Compared to the PNI-low group (PNI < 47.45), the PNI-high group (PNI ≥47.45) had a significantly longer recurrence-free survival (RFS) (5-year RFS rate 89.9% versus 70.8%, p<0.001). Patients with higher PNI (p<0.001), lower NLR (p<0.001) and lower PLR (p=0.002) had significant better prognosis. PNI was found to be an independent prognostic factor of RFS (hazard ratio [HR] =1.967, 95% confidence interval [95% CI]: 1.243-3.114, p=0.004). Conclusions : PNI is a simple and useful marker that can predict the prognosis of GIST.

We utilize the variational method to study the Kondo screening of a spin-1/2 magnetic impurity in a three-dimensional (3D) Weyl semimetal with two Weyl nodes along the kz-axis. The model reduces to a 3D Dirac semimetal when the separation of the two Weyl nodes vanishes. When the chemical potential lies at the nodal point, µ = 0, the impurity spin is screened only if the coupling between the impurity and the conduction electron exceeds a critical value. For finite but small µ, the impurity spin is weakly bound due to the low density of state, which is proportional to µ 2 , contrary to that in a 2D Dirac metal such as graphene and 2D helical metal where the density of states is proportional to |µ|. The spin-spin correlation function Juv(r) between the spin v-component of the magnetic impurity at the origin and the spin u-component of a conduction electron at spatial point r, is found to be strongly anisotropic due to the spin-orbit coupling, and it decays in the power-law. The main difference of the Kondo screening in 3D Weyl semimetals and in Dirac semimetals is in the spin x-(y-) component of the correlation function in the spatial direction of the z-axis.

Interleukin-17 (IL-17) is prevalent in tumor tissue and suppresses effective anti-tumor immune responses. However, the source of the increased tumor-infiltrating IL-17 and its contribution to tumor progression in human gastric cancer remain poorly understood. In this study, we enrolled 112 gastric cancer patients, immunofluorescence was used to evaluate the colocalization of CD3, CD4, CD56, CD20, CD68, and mast cell tryptase (MCT) with IL-17. Immunohistochemistry was used to evaluate the distribution of microvessel density (CD34), CD66b+, CD68+, and FoxP3+ cells in different microanatomical areas. Prognostic value was determined by Kaplan-Meier analysis and a Cox regression model. The results showed that mast cells, but not T cells or macrophages, were the predominant cell type producing IL-17 in gastric cancer. Significant positive correlations were detected between densities of mast cell-derived IL-17 and microvessels, neutrophils, and regulatory T cells (Tregs). Futhermore, we found that the majority of vascular endothelial cells expressing Interleukin-17 receptor (IL-17R). Kaplan-Meier analysis revealed that increasing intratumor infiltrated mast cells and IL-17+ cells, as well as MCT+ IL-17+ cells, were significantly associated with worse overall survival. These findings indicated that mast cells were the major source of IL-17 in gastric cancer, and intratumor IL-17 infiltration may have promoted tumor progression by enhancing angiogenesis in the tumor microenvironment through the axis of IL-17/IL-17R. IL-17-positive mast cells showed a prognostic factor in gastric cancer, indicating that immunotherapy targeting mast cells might be an effective strategy to control intratumor IL-17 infiltration, and consequently reverse immunosuppression in the tumor microenvironment, facilitating cancer immunotherapy.

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Objective: Dysfunction of endothelial progenitor cells (EPCs) leads to impaired endothelial repair capacity in patients with hypertension, but the mechanisms remain incompletely understood. Mitochondrial oxidative stress is involved in endothelial injury in hypertension. In this study, we aim to investigate the role of mitochondrial oxidative stress in the deficient endothelial reparative capacity of EPCs and identify enhanced SIRT3 (sirtuin 3)-mediated SOD2 (superoxide dismutase 2) deacetylation as a novel endothelial protective mechanism in hypertension. Approach and Results: Hypertension-EPCs displayed increased mitochondrial reactive oxygen species and mitochondrial damage, including loss of mitochondrial membrane potential, abnormal mitochondrial ultrastructure, and mtDNA oxidative injury, which was coincided with impaired in vitro function and in vivo reendothelialization capacity. The harmful effects of hypertension on mitochondrial function of EPCs were in vitro mimicked by angiotensin II coincubation. Scavenging of mitochondrial reactive oxygen species with mitoTEMPO attenuated mitochondrial oxidative damage and rescued reendothelialization capacity. Enzymatic activity and deacetylation level of SOD2 were significantly reduced in hypertension-EPCs, which was accompanied with decreased SIRT3 expression. Knockdown of SIRT3 in EPCs resulted in mitochondrial oxidative damage, hyperacetylation of SOD2, and suppression of reendothelialization capacity. SIRT3 physically interacted with SOD2 and eliminated excess mitochondrial reactive oxygen species, restored mitochondrial function through enhancing SOD2 activity by deacetylation of K68. Upregulation of SIRT3/SOD2 signaling improved reendothelialization capability of EPCs. Conclusions: The present study demonstrated for the first time that mitochondrial oxidative damage because of deficient SIRT3/SOD2 signaling contributes to the decline in reendothelialization capacity of EPCs in hypertension. Maintenance of mitochondrial redox homeostasis in EPCs may be a novel therapeutic target for endothelial injury.