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Polydiacetylenes are prepared from amphiphilic diacetylenes first through self-assembly and then polymerization. Different from common supramolecular assemblies, polydiacetylenes have stable structure and very special optical properties such as absorption, fluorescence, and Raman. The hydrophilic head of PDAs is easy to be chemically modified with functional groups for detection and imaging applications. PDAs will undergo a specific color change from blue to red, fluorescence enhancement and Raman spectrum changes in the presence of receptor ligands. These properties allow PDA-based sensors to have high sensitivity and specificity during analysis. Therefore, the PDAs have been widely used for detection of viruses, bacteria, proteins, antibiotics, hormones, sialic acid, metal ions and as probes for bioimaging in recent years. In this review, the preparation, polymerization, and detection mechanisms of PDAs are discussed, and some representative research advances in the field of bio-detection and bioimaging are highlighted.

The beneficial effect of quercetin in rheumatic diseases is unclear. Studies have already confirmed that human umbilical cord mesenchymal stem cells (hUCMSCs) alleviate some symptoms of rheumatoid arthritis (RA) by their immunosuppressive capacities. This study explored whether there are additive effects of quercetin and hUCMSCs on peripheral blood mononuclear cells (PBMCs) under simulated rheumatic conditions. hUCMSCs were pretreated with quercetin (10 μM) before coculture with TNF-α/IFN-γ-stimulated PBMCs at a ratio of 1:1 for 3 days. PBMC proliferation was inhibited, and the proportion of Th17 cells was shifted. These effects may be related to the effect of quercetin on functional molecules in hUCMSCs, including nitric oxide (NO), indoleamine 2,3-dioxygenase (IDO), interleukin 6 (IL-6) and Toll-like receptor-3 (TLR-3) and the Akt/IκB pathways. These results suggest that quercetin effectively promoted the immunoregulatory effect of hUCMSCs by inhibiting the Akt/IκB pathway, activating the Toll-like receptor-3 pathway, and regulating downstream cytokines.

As one of the important methods of solving the problem of computation over encrypted data under multiple public keys in cloud environment,public key encryption with equality test (PKEET) supports to check whether two ciphertexts encrypted under (possibly) different public keys contain the same message without decrypting the ciphertexts.Definitions,security models and six types of authorization modes of PKEET are introduced and summarized.Besides,the relationship between PKEET and public key encryption with keyword search (PKES) is discussed.Several typical public-key,identity-based and attribute-based encryption with equality test schemes proposed recently are analyzed and compared.Furthermore,some application scenarios and research directions are discussed.

Abstract Background Metabolic plasticity has been increasingly thought to be a determinant of tumor growth and metastasis. MACC1, a transcriptional regulator of MET, was recognized as an oncogene in gastric cancer (GC); however, its transcriptional or post-translational regulation was not clear. We previously reported the metabolic role of MACC1 in glycolysis to promote GC progression. MACC1-AS1 is the antisense lncRNA of MACC1, yet its function was previously unknown. Methods We profiled and analyzed the expression of MACC1-AS1 utilizing the TCGA database as well as in situ hybridization using 123 pairs of GC tissues and matched adjacent normal gastric mucosa tissues (ANTs). The biological role of MACC1-AS1 in cell growth and metastasis was determined by performing in vitro and in vivo functional experiments. Glycolysis and antioxidant capabilities were assayed to examine its metabolic function. Further, the specific regulatory effect of MACC1-AS1 on MACC1 was explored transcriptionally and post-transcriptionally. Results MACC1-AS1 was shown to be expressed significantly higher in GC tissues than in ANTs, which predicted poor prognosis in GC patients. MACC1-AS1 promoted GC cell proliferation and inhibited cell apoptosis under metabolic stress. Mechanistically, MACC1-AS1 stabilized MACC1 mRNA and post-transcriptionally augmented MACC1 expression. Further, MACC1-AS1 was shown to mediate metabolic plasticity through MACC1 upregulation and subsequent enhanced glycolysis and anti-oxidative capabilities, and this was suggested to be coordinated by the AMPK/Lin28 pathway. Conclusions Elevated expression of MACC1-AS1 in gastric cancer tissues is linked to poor prognosis and promotes malignant phenotype upon cancer cells. MACC1-AS1 is elevated under metabolic stress and facilitates metabolic plasticity by promoting MACC1 expression through mRNA stabilization. Our study implicates lncRNA MACC1-AS1 as a valuable biomarker for GC diagnosis and prognosis.

BACKGROUND: Ferroptosis is a recently discovered form of iron-dependent nonapoptotic cell death. It is characterized by loss of the activity of the lipid repair enzyme, glutathione peroxidase 4 (GPX4), and accumulation of lethal reactive lipid oxygen species. However, we still know relatively little about ferroptosis and its molecular mechanism in gastric cancer (GC) cells. Here, we demonstrate that erastin, a classic inducer of ferroptosis, induces this form of cell death in GC cells and that cysteine dioxygenase 1 (CDO1) plays an important role in this process. METHODS: We performed quantitative real-time polymerase chain reaction, Western blotting, cell viability assay, reactive oxygen species (ROS) assay, glutathione assay, lipid peroxidation assay, RNAi and gene transfection, immunofluorescent staining, dual-luciferase reporter assay, transmission electron microscopy, and chromatin immunoprecipitation assay to study the regulation of ferroptosis in GC cells. Mouse xenograft assay was used to figure out the mechanism in vivo. RESULTS: Silencing CDO1 inhibited erastin-induced ferroptosis in GC cells both in vitro and in vivo. Suppression of CDO1 restored cellular GSH levels, prevented ROS generation, and reduced malondialdehyde, one of the end products of lipid peroxidation. In addition, silencing COO1 maintained mitochondrial morphologic stability in erastin-treated cells. Mechanistically, c-Myb transcriptionally regulated CDO1, and inhibition of CDO1 expression upregulated GPX4 expression. CONCLUSIONS: Our findings give a better understanding of ferroptosis and its molecular mechanism in GC cells, gaining insight into ferroptosis-mediated cancer treatment.

Clubroot disease caused by the obligate parasite Plasmodiophora brassicae is a serious threat to cabbage production worldwide. Current clubroot control primarily relies on a fungicide, but this has a negative impact on the environment and the use of a single biocontrol agent cannot efficiently control the disease. Thus, the combined application of different biocontrol agents has been proposed as a promising alternative. In this study, we used bacterial biocontrol agents as a co-culture (inter-genus and intra-genus) and mono-culture to mitigate the clubroot disease of Chinese cabbage. We evaluated their biocontrol effect and plant growth promoter (PGP) traits in in vitro and in vivo experiments. This study revealed that the inter-genus bacterial co-culture significantly suppresses the incidence of clubroot disease and enhances plant growth compared with intra-genus and mono-culture. In pairwise interaction, we observed that Bacillus cereus BT-23 promotes the growth of Lysobacter antibioticus 13-6 (inter-genus bacterial co-culture), whereas L. capsici ZST1-2 and L. antibioticus 13-6 (intra-genus microbial co-culture) are antagonists to each other. Furthermore, a total of 5575 metabolites, 732 differentially expressed metabolites (DEMs), and 510 unique metabolites were detected through the LC-MS/MS technique in the bacterial co-culture. The number of unique metabolites in inter-genus bacterial co-culture (393 metabolites) was significantly higher than in the intra-genus bacterial co-culture (117 metabolites). Further analysis of DEMs showed that the DEMs were mainly involved in four kinds of metabolism pathways, i.e., carbohydrate metabolism, amino metabolism, nucleotide metabolism, and metabolism of cofactors and vitamins. The contents of some secondary metabolites with biocontrol activity and plant growth-promoting functions were increased in inter-genus bacterial co-culture, indicating that inter-genus bacterial co-culture has a solid potential to suppress clubroot disease. We conclude that the inter-genus bacterial interaction changes the community metabolism and improves several secondary metabolites functions with respect to disease control and PGP ability.

Accurately counting the number of insect pests from digital images captured on yellow sticky traps remains a challenge in the field of insect pest monitoring. In this study, we develop a new approach to counting the number of insect pests using a saliency map and improved non-maximum suppression. Specifically, as the background of a yellow sticky trap is simple and the insect pest object is small, we exploit a saliency map to construct a region proposal generator including saliency map building, activation region formation, background–foreground classifier, and tune-up boxes involved in region proposal generation. For each region proposal, a convolutional neural network (CNN) model is used to classify it as a specific insect pest class, resulting in detection bounding boxes. By considering the relationship between detection bounding boxes, we thus develop an improved non-maximum suppression to sophisticatedly handle the redundant detection bounding boxes and obtain the insect pest number through counting the handled detection bounding boxes, each of which covers one insect pest. As this insect pest counter may miscount insect pests that are close to each other, we further integrate the widely used Faster R-CNN with the mentioned insect pest counter to construct a dual-path network. Extensive experimental simulations show that the two proposed insect pest counters achieve significant improvement in terms of F1 score against the state-of-the-art object detectors as well as insect pest detection methods.

Background/Aims: This study investigated signaling pathways via which extracellular histones induce the pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) release from the macrophage cell line RAW 264.7 and the anti-inflammatory efficacy of the antioxidant alpha-lipoic acid (ALA). Methods: ELISA and western blotting analyses were conducted to detect the release of TNF-α from histone-stimulated RAW 264.7 macrophages and the associated phospho-activation of MAPKs (ERK and p38) and NF-κB p65. The effects of ALA on the release of TNF-α and phospho-activation of the MAPKs and NF-κB p65 were studied. P < 0.05 was considered statistically significant. Results: Extracellular histones dose-dependently induced TNF-α release from RAW 264.7 cells and increased the phosphorylation of p38, ERK, and NF-κB p65. TNF-α release was markedly suppressed by p38, ERK, and NF-kB inhibitors. ALA reduced histone-induced TNF-α release, ERK/p38 MAPK activation, and NF-kB activation without affecting macrophage viability. Conclusion: Histones induce TNF-α release from macrophages by activating the MAPK and NF-kB signaling pathways, while ALA suppresses this response by inhibiting ERK, p38 and NF-kB. These findings identify potentially critical inflammatory signaling pathways in sepsis and molecular targets for sepsis treatment.

Privacy-preserving optimistic fair exchange (P2OFE) is a kind of protocols which aim to solve the fairness problem in the exchange of digital signatures between two parties and in the meanwhile protect their privacy. In P2OFE, no one else including the semi-trusted third party in charge of arbitration can confirm an exchange even after resolving a dispute. In this paper we present a black-box construction of P2OFE based on a tag-based public key encryption scheme and a standard digital signature scheme. Our construction follows the ‘sign-then-encrypt’ paradigm, and is secure in the standard model. Our construction is generic and admits more instantiations of P2OFE.

Abstract Cancer cells are frequently confronted with metabolic stress in tumor microenvironments due to their rapid growth and limited nutrient supply. Metabolic stress induces cell death through ROS-induced apoptosis. However, cancer cells can adapt to it by altering the metabolic pathways. AMPK and AKT are two primary effectors in response to metabolic stress: AMPK acts as an energy-sensing factor which rewires metabolism and maintains redox balance. AKT broadly promotes energy production in the nutrient abundance milieu, but the role of AKT under metabolic stress is in dispute. Recent studies show that AMPK and AKT display antagonistic roles under metabolic stress. Metabolic stress-induced ROS signaling lies in the hub between metabolic reprogramming and redox homeostasis. Here, we highlight the cross-talk between AMPK and AKT and their regulation on ROS production and elimination, which summarizes the mechanism of cancer cell adaptability under ROS stress and suggests potential options for cancer therapeutics.

Abstract BTK plays a critical role in the B cell receptor mediated inflammatory signaling in the rheumatoid arthritis (RA). Through a rational design approach we discovered a highly selective and potent BTK kinase inhibitor (CHMFL-BTK-11) which exerted its inhibitory efficacy through a covalent bond with BTK Cys481. CHMFL-BTK-11 potently blocked the anti-IgM stimulated BCR signaling in the Ramos cell lines and isolated human primary B cells. It significantly inhibited the LPS stimulated TNF-α production in the human PBMC cells but only weakly affecting the normal PBMC cell proliferation. In the adjuvant-induced arthritis rat model, CHMFL-BTK-11 ameliorated the inflammatory response through blockage of proliferation of activated B cells, inhibition of the secretion of the inflammatory factors such as IgG1, IgG2, IgM, IL-6 and PMΦ phagocytosis, stimulation of secretion of IL-10. The high specificity of CHMFL-BTK-11 makes it a useful pharmacological tool to further detect BTK mediated signaling in the pathology of RA.

The complete mitochondrial genome of the black citrus aphid from Sichuan Province of China, Aphis aurantii, was sequenced and analyzed. The mitochondrial genome was a double strand, circular molecule with 15,296 bp and an A + T content of 83.5%, comprising 13 PCGs, 22 tRNA genes, and two rRNA genes. Gene arrangement was conserved in the mitogenome of A. aurantii. A 631-bp long control region was found, with a high A + T content of 82.6%. All PCGs used standard ATN start codons and most PCGs ended with complete TAA stop codons. The phylogenetic analysis supported that A. aurantii was closely related to other five congeners of the genus Aphis.

Background: Sepsis and septic shock are common in noninvasive ventilation (NIV) patients. However, studies on the association between sepsis and NIV failure are lacking. Methods: A prospective multi-center observational study was performed in 16 Chinese intensive care units (ICUs). Patients who used NIV due to hypoxemic respiratory failure were enrolled. Sepsis and septic shock were diagnosed according to the guideline of sepsis-3. Results: A total of 519 patients were enrolled. Sepsis developed in 365 patients (70%) and septic shock developed in 79 patients (15%). However, 75 patients (14%) had no sepsis. NIV failure was 23%, 38%, and 61% in patients, with no sepsis, sepsis, and septic shock, respectively. Multivariate analysis found that sepsis [odds ratio (OR) = 1.95, 95% confidence interval (CI): 1.06–3.61] and septic shock (OR = 2.47, 95% CI: 1.12–5.45) were independently associated with NIV failure. In sepsis and septic shock population, the NIV failure was 13%, 31%, 37%, 53%, and 67% in patients with sequential organ failure assessment (SOFA) scores of ⩽2, 3–4, 5–6, 7–8, and ⩾9, respectively. Patients with nonpulmonary induced sepsis had similar NIV failure rate compared with those with pulmonary induced sepsis, but had higher proportion of septic shock (37% versus 10%, p ⩽ 0.01) and lower ICU mortality (10% versus 22%, p ⩽ 0.01). Conclusions: Sepsis was associated with NIV failure in patients with hypoxemic respiratory failure, and the association was stronger in septic shock patients. NIV failure increased with the increase of organ dysfunction caused by sepsis. The reviews of this paper are available via the supplemental material section .

Background: The differentiation of large vessel occlusion caused by intracranial atherosclerotic stenosis (ICAS) or intracranial embolism significantly impacts the course of treatment (i.e., intravenous thrombolysis versus mechanical thrombectomy) for acute cerebral infarction. Currently, there is no objective evidence to indicate ICAS-related middle cerebral artery M1 segment occlusion before treatment. In cases of ICAS, it is often observed that the infarct core caused by ICAS-related M1 segment middle cerebral artery occlusion (MCAO) is located in deeper parts of the brain (basal ganglia or semiovoid region).Objective: To evaluate whether the location of the infarct core, identified using diffusion-weighted imaging (DWI), can be used to differentiate ICAS from intracranial embolism.Methods: Thirty-one consecutive patients diagnosed with acute cerebral infarction caused by middle cerebral artery M1 segment occlusion were retrospectively included based on angiographic findings to distinguish ICAS from embolic occlusion. Patients were divided into two groups based on the location of the infarct core on DWI: in the deep part of the brain (basal ganglia or semiovoid region) or more superficially (i.e., cortex).Results: In 16 patients, the infarct core was mainly in the deep part of the brain on DWI [14 of 16 patients in the ICAS group and only 2 in the non-ICAS group (93.3 vs. 6.7%, respectively; P < 0.001)]. The diagnostic sensitivity of DWI for ICAS was 93.3%, with a specificity of 87.5%, a Positive predictive value (PPV) of 87.5%, and an Negative predictive value (NPV) of 93.3%, the accuracy was 88.5%.Conclusion: Intracranial atherosclerotic disease-related acute MCAO can be predicted using DWI.

Histone deacetylase inhibitors (HDACi) are a promising therapeutic intervention for stroke. The involvement of the anti-inflammatory effects of HDACi in their neuroprotection has been reported, but the underlying mechanisms are still uncertain. Given the post-stroke inflammation is a time-dependent process, starting with acute and intense inflammation, and followed by a prolonged and mild one, we proposed whether target the early inflammatory response could achieve the neuroprotection of HDACi? To test this hypothesis, a single dose of suberoylanilide hydroxamic acid (SAHA) (50 mg/kg), a pan HDACi, was intraperitoneally (i.p.) injected immediately or 12 h after ischemia onset in a transient middle cerebral artery occlusion (tMCAO) mouse model. Compared with delayed injection, immediate SAHA treatment provided more protection, evidenced by smaller infarction volume, and a better outcome. This protection was accompanied by suppression of pro-inflammatory cytokines and reduction of activated microglia in the early stage of post-stroke inflammation. Moreover, SAHA treatment suppressed M1 cytokine expression (IL-6, TNF-α, and iNOS) while promoted the transcription of M2 cytokines (Arg-1 and IL-10) in LPS-challenged mouse microglia, and enhanced CD206 (M2 marker) but decreased CD86 (M1 markers) levels in microglia isolated from the ipsilateral hemisphere of MCAO mice. Collectively, our data suggested that the protection of SAHA on ischemic brain injury was closely associated with its inhibition on the early inflammatory response, and this inhibition was related to its reducing microglia activation and priming the activated microglia toward a more protective phenotype.

China has been the largest vehicle market in the world since 2009. The stalemate between the rapid development of the vehicle industry and delayed vehicle emission control has become increasingly prominent. Vehicle emission has become a significant source of air pollution in China’s cities. Understanding the current barriers in the vehicle industry is necessary for the development of effective and sustainable measures and policy to manage vehicle-induced air pollution. This review provides insight into the circumstances and causes of vehicle-induced air pollution and outlines recent progress in policy-makers’ long-term strategies and regulations. The development of an integrated mechanism of social participation, technical revolution, and regulatory innovation in vehicles, fuel, and roads is suggested to break the stalemate between air pollution and the automobile boom in China; the implications of this review extend to other countries facing the similar atmospheric pollution problems.

Zinc level in the body is finely regulated to maintain cellular function. Dysregulation of zinc metabolism may induce a variety of diseases, e.g., diabetes. Zinc participates in insulin synthesis, storage, and secretion by functioning as a “cellular second messenger” in the insulin signaling pathway and glucose homeostasis. The highest zinc concentration is in the pancreas islets. Zinc accumulation in cell granules is manipulated by ZnT8, a zinc transporter expressed predominately in pancreatic α and β cells. A common ZnT8 gene (SLC30A8) polymorphism increases the risk of type 2 diabetes mellitus (T2DM), and rare mutations may present protective effects. In type 1 diabetes mellitus (T1DM), autoantibodies show specificity for binding two variants of ZnT8 (R or W at amino acid 325) dictated by a polymorphism in SLC30A8. In this review, we summarize the structure, feature, functions, and polymorphisms of ZnT8 along with its association with diabetes and explore future study directions.

We used active and passive surveillance to estimate nontyphoidal Salmonella (NTS) infection during 2012 in Guangdong Province, China. Under passive surveillance, for every reported NTS infection, an estimated 414.8 cases occurred annually. Under active surveillance, an estimated 35.8 cases occurred. Active surveillance provides remarkable advantages in incidence estimate.

Numerous gut microbes are associated with insects, but their composition remains largely unknown for many insect groups, along with factors influencing their composition. Here, we compared gut bacterial microbiota of two co-occurring agricultural pests, the peach fruit moth (PFM), Carposina sasakii, and the oriental fruit moth (OFM), Grapholita molesta, collected from different orchards and host plant species. Gut microbiota of both species was mainly composed of bacteria from Proteobacteria, followed by Firmicutes. The two species shared bacteria from the genera Pseudomonas, Gluconobacter, Acetobacter, and Pantoea. When we compared two pairs of PFM and OFM populations collected from the same host species and the same orchard, there is no difference in alpha and beta diversity in gut microbiota. When we compared gut microbiota of the same species and host plant from different orchards, alpha and beta diversity was different in populations of PFM collected from two pear orchards but not in other comparisons. Our study suggests that the two pests share many features of gut microbiota and environment in orchards is a main factor influencing their gut microbiota.

The immune contexture, a composition of the tumor microenvironment, plays multiple important roles in cancer stem cell (CSC) and epithelial–mesenchymal transition (EMT), and hence critically influences tumor initiation, progression and patient outcome. Tumor-associated macrophages (TAMs) are abundant in immune contexture, however their roles in CSC, EMT and prognosis of colorectal cancer (CRC) have not been elucidated. In 419 colorectal carcinomas, immune cell types (CD68+ macrophages, CD3+, CD4+ or CD8+ T lymphocytes, CD20+ B lymphocytes), EMT markers (E-cadherin and Snail) as well as the stem cell marker (CD44v6) were detected in tumor center (TC) and tumor invasive front (TF) respectively by immunohistochemistry. Tumor buds, that represent EMT phenotype, were also counted. It was found CD68+ macrophages were the most infiltrating immune cells in CRC. By correlation analysis, more CD68+TF macrophages were associated with more CD44v6 expression (p < 0.001), lower SnailTF expression (p = 0.08) and fewer tumor buds (p < 0.001). More CD68+TF macrophages were significantly related to more CD3+TF T lymphocytes (p = 0.002), CD8+TF T lymphocytes (p < 0.001) and CD20+TF B lymphocytes counts (p = 0.004). Strong CD68+TF macrophages infiltration also predicted long term overall survival. CRC patients with more tumor buds had worse survival. However, strong CD68+TF macrophages infiltration could reverse the unfavorable results since patients with more tumor buds but increasing CD68+TF macrophages infiltration had the favorable outcome, similar to lower tumor buds groups. This study provided direct morphological evidence that tumor-associated macrophages in the invasive front play critical roles in fighting with the unfavorable results of tumor buds, thus resulting favorable outcomes for CRC patients.

Researchers have shown that the level of immunoglobulin D (IgD) is often elevated in patients with autoimmune diseases. The possible roles of IgD on the function of human T cell activation are still unclear. Paeoniflorin-6′-O-benzene sulfonate (code: CP-25), the chemistry structural modifications of paeoniflorin, was a novel drug of anti-inflammation and immunomodulation. The aims of this study were to determine if human CD4+ T cells could be activated by IgD via the IgD receptor (IgDR)-Lck pathway and whether the novel compound CP-25 could affect the activation of T cells by regulating Lck. Human CD4+ T cells were purified from peripheral blood mononuclear cells using microbeads. T cell viability and proliferation were detected by Cell Counting Kit-8 and CFSE Cell Proliferation Kit. Cytokines secreted by T cells were assessed with the Quantibody Human Inflammation Array. The binding affinity and expression of IgDR on T cells were detected by flow cytometry, and protein expression of IgDR, Lck, and P-Lck were analyzed by western blot. IgD was shown to bind to IgDR on CD4+ T cells in a concentration-dependent manner and stimulate the activation and proliferation of these cells by enhancing phosphorylation of the activating tyrosine residue of Lck (Tyr394). CP-25 inhibited the IgD-stimulated activation and proliferation of CD4+ T cells, as well as the production of inflammatory cytokines; it was thus suggested that this process might be related to the downregulation of Lck (Tyr394) phosphorylation. These results demonstrate that IgD amplifies the activation of CD4+ T cells, which could be mediated by Lck phosphorylation. Further, CP-25, via its ability to modulate Lck, is a novel potential therapeutic agent for the treatment of human autoimmune diseases.

A user interest-aware content replica optimized placement algorithm (UIARP) is proposed.Firstly,the interest subjects of the user-collective are extracted from their content access logs by clustering algorithms,and according to the weighting of the individual interest degree,their collective interest degree would be got and updated in real time; then under the nonlinear optimization model,replicas of larger collective interest degree have priority to be placed,with the goal of minimizing the average response time,which achieves the maximum match between placing replicas and users’ content demand.This algorithm not only ensures that users get interested replicas quickly,but also improves the system efficiency.From four aspects including average response time,the matching degree of request response,load balancing and the utilization rate of adjacent replicas,using 1-Greedy-Insert or others as compared algorithms,the simulation re-sults show that each metric improves by 30% on average,which verifies the effectiveness of the proposed algorithm.

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Apoptosis of lymphocytes is associated with immunosuppression and poor prognosis in sepsis. Our previous report showed that histones, nuclear proteins released from damaged or dying cells in sepsis, can mediate lymphocyte apoptosis via mitochondria damage. Grape seed proanthocyanidin extract (GSPE), a natural substance with protective properties against oxidative stress, plays a vital role in cell and mitochondria protection. We thus hypothesized that GSPE may play a protective role in histone-induced lymphocyte apoptosis through its anti-oxidative properties. In this study, we investigated the protective efficacy of GSPE on lymphocyte apoptosis induced by extracellular histones, a main contributor of death in sepsis. Human blood lymphocytes were treated with 50 μg/ml histones, 2 μg/ml GSPE, or a combination of both. A total of 100 μM N-acetylcysteine (NAC), a reactive oxygen species (ROS) inhibitor, was used as a positive control for GSPE. Apoptosis, intracellular ROS levels, mitochondrial membrane potential, Bcl-2 expression, and caspase-3 cleavage were measured. Our data clearly indicate that GSPE significantly inhibited lymphocyte apoptosis, generation of ROS, the loss of mitochondrial membrane potential, the decrease in Bcl-2 expression, and caspase-3 activation induced by extracellular histones. In conclusion, we show that GSPE has a protective effect on lymphocyte apoptosis induced by extracellular histones. This study suggests GSPE as a potential therapeutic agent that could help reduce lymphocyte apoptosis, and thus the state of immunosuppression was observed in septic patients.

During the RFID tag identification process, the tree-based anti-collision algorithms usually incur large amount of redundant data due to an excess of long query commands,which increases the communication overhead. To resolve this problem, a searching tree anti-collision algorithm with low-redundancy on the basis of regressive-style dynamic searching tree algorithm was proposed. In order to reduce the number of queries, a novel query mode was developed, i.e., single query with duo responses. Depending on the most significant collided bit, the collided tags respond in the first or second slot separately. In order to reduce the length of query command, the prefix matching circuit in tag was replaced with a counter, which eliminated the prefix as the parameter of query command. The predictive identification and block-ing technique were also introduced to avoid unnecessary queries. Theoretical analysis and simulation results show that the communication overhead is greatly reduced.

Gerschgorin disk theorem (GDT) based wideband spectrum sensing methods, namely Gerschgorin likelihood estimate(GLE) algorithm and Gerschgorin disk radii iteration(GDRI) algorithm, were proposed for cognitive radios. By means of exploring the possibility of utilizing GDT in wideband spectrum sensing, the occupied and the idle licensed subbands was distingwished by respectively identifying the cardinalities of the corresponding subband sets. With an aim to strengthen the performance of GLE and GDRI, a subband continuity based wideband sensing algorithm was further proposed. Simulation results show that GLE sensing performance remains consistent when the SNR is low, whereas GDRI requires no a priori knowledge of the noise power and the PU signal and it overcomes the practical problem of small spectrum observation samples. With salient performance and practical feasibility, the proposed GLE and GDRI may serve as candidate wideband sensing technologies for cognitive radios.

In this work we describe the establishment of mesenchymal stem cells (MSCs) derived from embryonic stem cells (ESCs) and the role of bFGF in adipocyte differentiation. The totipotency of ESCs and MSCs was assessed by immunofluorescence staining and RT-PCR of totipotency factors. MSCs were successfully used to induce osteoblasts, chondrocytes and adipocytes. MSCs that differentiated into adipocytes were stimulated with and without bFGF. The OD/DNA (optical density/content of total DNA) and expression levels of the specific adipocyte genes PPARγ2 (peroxisome proliferator activated receptor γ2) and C/EBPs were higher in bFGF cells. Embryonic bodies had a higher adipocyte level compared with cells cultured in plates. These findings indicate that bFGF promotes adipocyte differentiation. MSCs may be useful cells for seeding in tissue engineering and have enormous therapeutic potential for adipose tissue engineering.

We present a secure multi-party quantum summation protocol based on quantum teleportation, in which a malicious, but non-collusive, third party (TP) helps compute the summation. In our protocol, TP is in charge of entanglement distribution and Bell states are shared between participants. Users encode the qubits in their hand according to their private bits and perform Bell-state measurements. After obtaining participants’ measurement results, TP can figure out the summation. The participants do not need to send their encoded states to others, and the protocol is therefore congenitally free from Trojan horse attacks. In addition, our protocol can be made secure against loss errors, because the entanglement distribution occurs only once at the beginning of our protocol. We show that our protocol is secure against attacks by the participants as well as the outsiders.

According to the tendency of development for digital media convergence and management of massive data, a fine-grained hypermedia document description model and its implementation were proposed, basing the analysis of the relationship between the related multidimensional digital media. The method for access control was given, as well as its XML description grammar system. The model could satisfy the demands of convenient and effective management.

Bubali Cornu (water buffalo horn, WBH) has been used for thousands of years in traditional Chinese medicine (TCM) as an effective treatment for heat. In the present study, we have carried out a metabolomics profiling study on plasma and urine samples to explore potential biomarkers and determine how WBH exerts its antipyretic effects in yeast-induced pyrexia at a metabolomic level. Ultra-high performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry (UPLC-Q-TOF-MS), together with multivariate statistical analysis, was used to detect and identify potential biomarkers associated with pyrexia and with WBH treatment. In total, sixteen endogenous metabolites were identified in plasma samples and twenty-one metabolites were detected in urine samples. The biomarkers identified in this study, using metabolic pathway analysis (MetPA), are involved in glycerophospholipid, arachidonic acid, amino acid, sphingolipid, and purine metabolism, all of which are disturbed in rats with pyrexia. As a result, WBH affect arachidonic acid metabolism and oxidative stress in yeast-induced pyrexia rats chiefly. The present study determines the important substances underlying the antipyretic efficacy of WBH at a metabolic level. It might pave the way for further investigations into the mechanisms of action of other animal horn-derived traditional Chinese medicines (TCMs).

Immunoglobulin D (IgD) is a surface immunoglobulin that is expressed as either membrane IgD (mIgD) or secreted IgD (sIgD). Researchers have shown that sIgD is often elevated in patients with autoimmune diseases. The possible roles of sIgD on the function of peripheral blood mononuclear cells (PBMCs) in rheumatoid arthritis (RA) are still unclear. In this study, we compared the expression of sIgD, mIgD and IgD receptor (IgDR) in RA patients and healthy controls, and investigated the effect of sIgD on the function of PBMCs. We found that the levels of sIgD, mIgD and IgDR were significantly higher in RA patients compared with healthy controls. The concentrations of sIgD were positively correlated with soluble receptor activator of nuclear factor-κB ligand (sRANKL), rheumatoid factor (RF) and C-reactive protein (CRP) in RA patients. Strikingly, IgD could enhance the proliferation of PBMCs and induce IL-1α, IL-1β, TNF-α, IL-6 and IL-10 production from PBMCs. Moreover, the percentage of activated T cell subsets (CD4+CD69+, CD4+CD154+) and activated B cell subsets (CD19+CD23+, CD19+CD21+, CD19+IgD+ and CD19-CD138+) were increased by IgD. The percentage of unactivated T cell subset (CD4+CD62L+) and immature B cell subset (CD19+IgM+IgD-) were decreased by IgD in PBMCs. Furthermore, the expressions of IgDR on T and B cells were significantly increased by treatment with IgD. Our results demonstrate that IgD enhanced the activation of PBMCs, which may contribute to RA pathogenesis. Therefore, IgD could be a potential novel immunotherapeutic target for the management of RA.

We report a unique case of multicentric reticulohistiocytosis (MRH) associated with liver carcinoma. A 61-year-old man presented with a 4-month history of nonpruritic, generalized, ruby-red papules and nodules, accompanied by fever, joint swelling and difficulty in swallowing. Skin histology showed polymorphic histiocyte infiltration with typical ‘ground glass’ cytoplasm. Further immunohistochemical studies characterized the lesions as positive for leukocyte common antigen, HLA-DR and CD68. The patient had a history of hepatitis B, and systemic examination, including carcinoma index and type-B ultrasonic examination, revealed high levels of AFP and a solid tumor, which was considered malignant, localized on the right lobe of the liver. Treatment of the liver carcinoma resulted in a significant improvement of the skin symptoms. This is the first case study to report an association between MRH and liver carcinoma. A review of the English-language literature reveals the close linkage between MRH and malignancy. All patients with MRH should be evaluated and monitored carefully to determine the underlying neoplasm.

The experience showed that the predicted delay's accuracy was improved when the nodes were chosen around the given delay as anchors.Thus a distance range-aware IP network coordinate system(R-Vivaldi) was proposed.The main idea was:according to the approximate range of the predicted delay,the anchors were re-selected in the radius area of the approximate range to compute the new range.In accordance with the above process,the coordinate system constantly iterated the network distance and dynamically chose anchors until the prediction accuracy meet the requirement.Experiments show that the approach can not only effectively improve the prediction accuracy of delay but also overcome inconsistencies of the prediction accuracy to a certain extent.

Porokeratosis (PK) is a heterogeneous group of keratinization disorders. No causal genes except MVK have been identified, even though the disease was linked to several genomic loci. Here, we performed massively parallel sequencing and exonic CNV screening of 12 isoprenoid genes in 134 index PK patients (61 familial and 73 sporadic) and identified causal mutations in three novel genes (PMVK, MVD, and FDPS) in addition to MVK in the mevalonate pathway. Allelic expression imbalance (AEI) assays were performed in 13 lesional tissues. At least one mutation in one of the four genes in the mevalonate pathway was found in 60 (98%) familial and 53 (73%) sporadic patients, which suggests that isoprenoid biosynthesis via the mevalonate pathway may play a role in the pathogenesis of PK. Significantly reduced expression of the wild allele was common in lesional tissues due to gene conversion or some other unknown mechanism. A G-to-A RNA editing was observed in one lesional tissue without AEI. In addition, we observed correlations between the mutations in the four mevalonate pathway genes and clinical manifestations in the PK patients, which might support a new and simplified classification of PK under the guidance of genetic testing.

ObjectivesDiabetic retinopathy (DR) is a common diabetic eye disease which is well-known as the result of microvascular retinal changes. Although the potential biological functions of astragaloside IV (AS IV) have long been described in traditional system of medicine, its protective effect on DR remains unclear. This study aims to investigate the function and mechanism of AS IV on type 2 diabetic db/db mice.MethodsDb/db mice were treated with AS IV (4.5 mg/kg or 9 mg/kg) or physiological saline by oral gavage for 20 weeks along with db/m mice. In each group, retinal ganglion cell (RGC) function was measured by pattern electroretinogram (ERG) and apoptosis was determined by Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. Blood and retina aldose reductase (AR) activity were quantified by chemiluminescence analysis. The expressions of phosporylated-ERK1/2, NF-κB were determined by Western blot analysis. Furthermore, the expression of related downstream proteins were quantified by Label-based Mouse Antibody Array.ResultsAdministration of AS IV significantly improved the amplitude in pattern ERG and reduced the apoptosis of RGCs.in db/db mice. Furthermore, downregulation of AR activity, ERK1/2 phosphorylation, NF-κB and related cytokine were observed in AS IV treatment group.ConclusionsOur study indicated that AS IV, as an inhibitor of AR, could prevent the activation of ERK1/2 phosporylation and NF-kB and further relieve the RGCs disfunction in db/db mice with DR. It has provided a basis for investigating the clinical efficacy of AR inhibitors in preventing DR.

Astrocytes are macroglial cells that have a crucial role in development of the retinal vasculature and maintenance of the blood-retina-barrier (BRB). Diabetes affects the physiology and function of retinal vascular cells including astrocytes (AC) leading to breakdown of BRB. However, the detailed cellular mechanisms leading to retinal AC dysfunction under high glucose conditions remain unclear. Here we show that high glucose conditions did not induce the apoptosis of retinal AC, but instead increased their rate of DNA synthesis and adhesion to extracellular matrix proteins. These alterations were associated with changes in intracellular signaling pathways involved in cell survival, migration and proliferation. High glucose conditions also affected the expression of inflammatory cytokines in retinal AC, activated NF-κB, and prevented their network formation on Matrigel. In addition, we showed that the attenuation of retinal AC migration under high glucose conditions, and capillary morphogenesis of retinal endothelial cells on Matrigel, was mediated through increased oxidative stress. Antioxidant proteins including heme oxygenase-1 and peroxiredoxin-2 levels were also increased in retinal AC under high glucose conditions through nuclear localization of transcription factor nuclear factor-erythroid 2-related factor-2. Together our results demonstrated that high glucose conditions alter the function of retinal AC by increased production of inflammatory cytokines and oxidative stress with significant impact on their proliferation, adhesion, and migration.

AIM: To determine the pharmacogenetics of platinum-based chemotherapy in Non Small Cell Lung Cancer (NSCLC) patients. METHODS: Publications were selected from PubMed, Cochrane Library and ISI Web of Knowledge. A meta-analysis was conducted to determine the association between genetic polymorphisms and platinum-based chemotherapy by checking odds ratio (OR) and 95% confidence interval (CI). RESULTS: Data were extracted from 24 publications, which included 11 polymorphisms in 8 genes for meta-analysis. MDR1 C3435T (OR = 1.97, 95% CI: 1.11-3.50, P = 0.02), G2677A/T (OR = 2.61, 95% CI: 1.44-4.74, P = 0.002) and GSTP1 A313G (OR = 0.32, 95% CI: 0.17-0.58, P = 0.0002) were significantly correlated with platinum-based chemotherapy in Asian NSCLC patients. CONCLUSION: Attention should be paid to MDR1 C3435T, G2677A/T and GSTP1 A313G for personalized chemotherapy treatment for NSCLC patients in Asian population in the future.