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We previously observed that Turnip mosaic virus (TuMV) induces systemic necrosis in Arabidopsis ecotype Ler but not in Col-0. Sharing most of the common features of the hypersensitive reaction, this systemic necrosis has been found to be a result of a gene-for-gene interaction between the host TuNI gene and viral P3 gene. We here analyzed the TuNI locus in detail and identified three very similar candidates for TuNI gene(s). Our functional and expression analyses using transgenic plants expressing each of the candidates and a protoplast transient expression assay suggested that the expression of the best candidate, named RGX, is responsible for the systemic necrosis although concomitant expression with the other two candidates may be necessary. To understand the expression profile of RGX, we analyzed promoter activity by producing transgenic Col-0 plants that express the reporter GFP gene under the control of the 500–1400-bp upstream regions of RGX. The transgenic plants reproduced the expression patterns of RGX; GFP expression increased after TuMV infection but decreased in the shade treatment. The expression of two other candidates was also upregulated by TuMV infection, suggesting that transcriptional activation of the TuNI candidate genes has a role in controlling TuMV-mediated systemic necrosis.

The collinear holographic data storage system (CHDSS) is a very promising storage system due to its large storage capacities and high transfer rates in the era of big data. The digital micro-mirror device (DMD) as a spatial light modulator is the key device of the CHDSS due to its high speed, high precision, and broadband working range. To improve the system stability and performance, an optimal micro-mirror tilt angle was theoretically calculated and experimentally confirmed by analyzing the relationship between the tilt angle of the micro-mirror on the DMD and the power profiles of diffraction patterns of the DMD at the Fourier plane. In addition, we proposed a novel chess board sync mark design in the data page to reduce the system bit error rate in circumstances of reduced aperture required to decrease noise and median exposure amount. It will provide practical guidance for future DMD based CHDSS development.

Passive immunotherapy against HIV-1 will most likely require broadly neutralizing antibodies (bnAbs) with maximum breadth and potency to ensure therapeutic efficacy. Recently, the novel CD4 binding site antibody N6 demonstrated extraordinary neutralization breadth and potency against large panels of cross-clade pseudoviruses. We evaluated the in vivo antiviral activity of N6-LS, alone or in combination with the established V3-glycan antibody PGT121, in chronically simian-human immunodeficiency virus (SHIV)-SF162P3-infected macaques. A single dose of N6-LS suppressed plasma viral loads in 4 out of 5 animals at day 7, while the combination of both antibodies suppressed all animals. The combination of both antibodies had no additive antiviral effect compared to a single dose of PGT121, potentially reflecting the nearly 10-fold-higher potency of PGT121 against this SHIV. Viral rebound occurred in the majority of suppressed animals and was linked to declining plasma bnAb levels over time. In addition to the effect on plasma viremia, bnAb administration resulted in significantly reduced proviral DNA levels in PBMCs after 2 weeks and in lymph nodes after 10 weeks. Autologous neutralizing antibody (nAb) responses and CD8 + T-cell responses were not significantly enhanced in the bnAb-treated animals compared to control animals, arguing against their contribution to the viral effects observed. These results confirm the robust antiviral activity of N6-LS in vivo , supporting the further clinical development of this antibody. IMPORTANCE Monocloncal antibodies (MAbs) are being considered for passive immunotherapy of HIV-1 infection. A critical requirement for such strategies is the identification of MAbs that recognize the diversity of variants within circulating but also reservoir viruses, and MAb combinations might be needed to achieve this goal. This study evaluates the novel bnAb N6-LS alone or in combination with the bnAb PGT121, in rhesus macaques that were chronically infected with SHIV. The results demonstrate that N6-LS potently suppressed plasma viral loads in the majority of animals but that the combination with PGT121 was not superior to PGT121 alone in delaying time to viral rebound or reducing peripheral blood mononuclear cell (PBMC) or lymph node proviral DNA levels. The occurrence of viral escape variants in an N6-LS-monotreated animal, however, argues for the need to maximize breadth and antiviral efficacy by combining bnAbs for therapeutic indications.

Despite the clinical successes fostered by immune checkpoint inhibitors, mechanisms underlying PD-1 upregulation in tumor-infiltrating T cells remain an enigma. Here, we show that tumor-repopulating cells (TRCs) drive PD-1 upregulation in CD8

The complete genome of a novel virus from Nesidiocoris tenuis was determined by RNA-seq and rapid amplification of cDNA ends. This virus has a single-stranded RNA genome of 10633 nucleotides (nt) in length, not including the poly(A) tail, and contains two putative open reading frames (ORFs). ORF1 encodes a polypeptide of 1320 amino acids (aa) with a predicted molecular mass of 147.92 kDa and theoretical isoelectric point (pI) of 6.96. ORF2 encodes a polypeptide of 1728 aa with a predicted molecular mass of 197.09 kDa and pI of 6.73. Phylogenetic analysis with the deduced aa sequences of the conserved RNA dependent RNA polymerase domain as well as whole genome nt sequences indicated that the virus clusters with viruses classified within the genus Iflavirus, with a high bootstrap value in the maximum-likelihood and neighbor-joining trees. However, this virus has a distinct genome structure with two ORFs, iflaviruses normally having one, suggesting the virus might be a prototype of a new genus. We named the virus isolate Nesidiocoris tenuis virus 1 (NtV-1). The prevalence of NtV-1 infection in wild samples of N. tenuis was at a low level (7.32%, 6 positive in 82 samples), suggesting a possible harmful effect to its host.

The power MOSFETs are one of the widely used core components in power electronics, automotive electronics, consumer electronics, aerospace and other fields generally. There is a high requirement for stabilization performance of MOSFETs. The breakdown voltage which is the most important electrical parameter of MOSFETs is usually reduced by the punch-through or reach-through phenomena, which leads the system circuits not to work functionally. In this paper, the basic principle of them are introduced and analyzed respectively. In a p-n junction with the doping concentration distribution fixed, certain width of the semiconductor is depleted in the n-side and p-side respectively when avalanche breakdown occurs. As the designed geometry thickness of the lightly doped side is less than the corresponding depletion width, punch-though phenomenon comes up. It often happens in P+NP+ and P+N-N+ sandwich structure In numerical simulation for a typical P+NP+ sandwich structure with a breakdown voltage of 226.3 V in non-through case, the breakdown voltage of punch-through case is reduced to 100.5 V and decreased by 55.6%. The reach-through effect appears when the designed geometry thickness of the heavily doped side is less than the corresponding depletion width. Its sandwich structure is defined N+P+NN+ style for the convenience of simulation. And the breakdown voltage of reach-through case is reduced to 50.99 V which is just only 22.5% of breakdown voltage of non-through structure. The simulation results are obtained by SSE (Sentaurus Structure Editor) software.

A coplanar waveguide (CPW) feeding circularly polarized (CP) ferrite antenna with rectangular slot and a microstrip feeding CP annular-ring antenna with a pair of identical meandered strips (U-shaped strip) are proposed in this paper They use the same ferrite substrate with e r = 7.5 (tanδ e = 0.01) and µ r = 7.2 (tanδ µ = 0.2). Ferrite can efficiently reduce the dimension of the antenna with respect to the dielectric substrate. Not only that, ferrite can also make the bandwidth of the antenna become wider and energy easier radiate. The rectangular slot antenna and annular-ring antenna can achieve CP easily by embedding arc-shaped strip and a pair of diagonal U-shaped strips, respectively. Electromagnetic simulation software Ansoft HFSS based on the finite element method has been used to make simulation and optimization for the proposed two designs. We contain the simulated results of two different designs in multiple parameters which include return loss, 3 dB axial ratio, radiation patterns and the gain. We found that the rectangular slot antenna has a wider 3 dB axis ratio bandwidth (from 865 MHz to 982 MHz, 12.7% @ 920 MHz) and larger peak gain (2.42 dBi) than annular-ring ferrite antenna (from 901MHz to 940MHz, 4% @ 920MHz; −23.5dBi). The annular-ring ferrite antenna has a wider return loss bandwidth (from 815 MHz to 1.29 GHz) than rectangular slot ferrite antenna (from 825 MHz to 1.0GHz, 18.9% @ 925MHz). The dimensions of the rectangular slot antenna and annular-ring antenna are 106∗94.5 mm2 and 60∗36 mm2 respectively, so annular-ring antenna has a smaller size. They both can be used for UHF RFID applications.

In some RFID applications, the reader needs to identify the staying tags within its interrogation zone repeatedly. Meanwhile, there are some arriving tags continually moving into the interrogation zone of the reader. For these scenes, the adaptive query splitting (AQS) algorithm, the semi-blocking AQS (SBA), and the slot allocated blocking anti-collision (SABA) algorithm are proposed. However, these algorithms all use query tree algorithm to identify arriving tags, which leads to lower identification efficiency. Therefore, the blocking collision tracking tree (BCTT) algorithm is proposed in this paper. BCTT allocates a unique slot number for each identified tag. The identification process of BCTT is divided into two phases. The staying tags are identified in the first phase according to the slot number, which reduce the bits transmitted by tags. In the second phase, the staying tags are blocked to respond the reader's query, so the collision between staying tags and arriving tags are thoroughly avoid. The arriving tags are identified by adopting collision tracking tree algorithm. The query prefix is generated according to the first collided bit, so BCTT can completely eliminate the idle slots, and also significantly reduce the number of collision slots. Especially, if there is only one collided bit in the response, BCTT can identify two tags in a slot. The simulation results indicate that the identification efficiency, identification speed, and communication load of BCTT are obviously superior to other similar algorithms such as SABA.

Melanoma-associated antigen (MAGE)-A3 and MAGE-C2 are antigens encoded by cancer-germline genes, and have been recognized as potential prognostic biomarkers and attractive targets for immunotherapy in multiple types of cancer. The present study aimed to analyze the clinicopathological significance of MAGE-A3/C2 expression in non-small cell lung cancer (NSCLC). The association between MAGE-A3/C2 mRNA and protein expression, and the pathological characteristics and overall survival of patients with NSCLC was analyzed. In addition, the functional role of MAGE-A3 in human NSCLC cell line A549 was examined in vitro. MAGE-A3/C2 mRNA expression was identified in 73% (151/206) and 53% (109/206) of patients with NSCLC, respectively. MAGE-A3/C2 protein expression was identified in 58% (44/76) and 53% (40/76) of NSCLC cases, respectively. MAGE-A3 mRNA expression was observed to be associated with smoking history, disease stage and lymph node metastasis. However, no association was identified between MAGE-C2 mRNA expression and the clinicopathological characteristics of patients with NSCLC. MAGE-A3/C2-positive patients had a poorer survival rate compared with MAGE-A3/C2-negative patients. Multivariate analysis identified that MAGE-A3 expression may serve as an independent marker of poor prognosis in patients with NSCLC. Downregulation of MAGE-A3 mRNA expression in A549 cells resulted in lower migration and colony formation rates, and a higher amount of epithelial marker and lower amount of mesenchymal marker expression compared with the control group. These results indicate that MAGE-A3 serves a role in NSCLC cell metastasis through the induction of epithelial-mesenchymal transition. In conclusion, MAGE-A3 may serve as a diagnostic and prognostic biomarker for patients with NSCLC, due to its association with tumor progression and poor clinical outcome.

Peritoneal fibrosis resulting from long-term clinical peritoneal dialysis has been the main reason of dropout from peritoneal dialysis. Peritonitis as a common complication of peritoneal dialysis treatment may lead to the occurrences of peritoneal fibrosis. We cultured peritoneal mesothelial cells with lipopolysaccharides (LPS) in order to stimulate the environment of peritonitis and investigate whether lipopolysaccharides could induce epithelial-to-mesenchymal transition (EMT). Oxidative stress could stimulate fibrogenesis while selenium has antioxidant properties. So, this study also explored whether selenium supplementation affects lipopolysaccharide-induced EMT and fibrosis. We found that lipopolysaccharides could activate EMT changes such as the loss of E-cadherin and the increase of α-smooth muscle actin (α-SMA), collagen I, vimentin, and fibronectin (FN), while selenium inhibits EMT by modulating reactive oxygen species (ROS) generation and ROS/MMP-9 signaling pathways in peritoneal mesothelial cells. Moreover, it was revealed that selenium decreased the EMT events of peritoneal mesothelial cells via inhibition of PI3k/AKT pathways. In conclusion, these findings enable a better understanding of the mechanism of peritoneal fibrosis and explore a new idea for the prevention and treatment.

The viral reservoir represents a critical challenge for human immunodeficiency virus type 1 (HIV-1) eradication strategies. However, it remains unclear when and where the viral reservoir is seeded during acute infection and the extent to which it is susceptible to early antiretroviral therapy (ART). Here we show that the viral reservoir is seeded rapidly after mucosal simian immunodeficiency virus (SIV) infection of rhesus monkeys and before systemic viraemia. We initiated suppressive ART in groups of monkeys on days 3, 7, 10 and 14 after intrarectal SIVMAC251 infection. Treatment with ART on day 3 blocked the emergence of viral RNA and proviral DNA in peripheral blood and also substantially reduced levels of proviral DNA in lymph nodes and gastrointestinal mucosa as compared with treatment at later time points. In addition, treatment on day 3 abrogated the induction of SIV-specific humoral and cellular immune responses. Nevertheless, after discontinuation of ART following 24 weeks of fully suppressive therapy, virus rebounded in all animals, although the monkeys that were treated on day 3 exhibited a delayed viral rebound as compared with those treated on days 7, 10 and 14. The time to viral rebound correlated with total viraemia during acute infection and with proviral DNA at the time of ART discontinuation. These data demonstrate that the viral reservoir is seeded rapidly after intrarectal SIV infection of rhesus monkeys, during the 'eclipse' phase, and before detectable viraemia. This strikingly early seeding of the refractory viral reservoir raises important new challenges for HIV-1 eradication strategies.

We address the problem of providing shared-path protection for a set of connection requests in a flexible bandwidth optical network under the constraint that the joint failure probability of the primary path and backup path of each request is below a given maximum joint failure probability threshold. The overall objective of the problem is to minimize spectrum consumption while meeting the maximum joint failure probability requirements. We propose the minimum free spectrum–block consumption algorithm (MFSB) for providing shared-path protection with joint failure probability requirements in flexible bandwidth optical networks, and we introduce two additional algorithms, named the conventional shared spectrum–block (CSSB) consumption algorithm and the maximum shared spectrum–block (MSSB) consumption algorithm, for comparison. Simulation results show that MFSB not only achieves better performance in terms of blocking probability, spectrum consumption, spectrum redundancy, and hop counts compared to the CSSB and MSSB algorithms, but also guarantees a joint failure probability that is lower than the MSSB algorithm. Furthermore, the spectrum efficiency of these three algorithms increases with the growth of the maximum shared degree, especially for the MFSB algorithm. Therefore, the MFSB algorithm provides a better tradeoff between the minimum spectrum–block consumption and the average joint failure probability.

Fe3O4-embedded graphene oxide was developed as a magnetic adsorbent for removal of methylene blue from aqueous solution. Fe3O4 nanoparticles were embedded on the surface of the as-prepared graphene oxide via a co-precipitation procedure with cheap and environmentally friendly iron salts. The weight percentage of graphene oxide was estimated by calcination to be about 18.5 %. In the aqueous solution of methylene blue at 20 °C, the adsorption data agreed well with the Langmuir adsorption model with a maximum adsorption capacity of 246 mg/g and a Langmuir adsorption equilibrium constant of 8.926 mL/mg. The adsorption amount increased with the increase of the solution pH (3–11), decreased with the increase of KCl concentration until it was up to 60 mM. The adsorbed methylene blue could be desorbed by using the methanol solution of acetic acid. In addition, both the adsorption and desorption rate were very quick that the equilibrium was achieved within 5 min due to the absence of the internal diffusion resistance. Fe3O4-embedded graphene oxide with large adsorption capacity and easy separation could be regarded as a potential adsorbent for removal of cationic dye in wastewater treatment process.

The early research found that the spiderlings of black widow spider (Latrodectus tredecimguttatus) exhibited obvious toxicity to animals. The present work performed a systematical analysis of the aqueous extract of newborn black widow spiderlings. The extract was shown to contain 69.42% of proteins varying in molecular weights and isoelectric points. Abdominal injection of the extract into mice and cockroaches caused obvious poisoning symptoms as well as death, with LD50 being 5.30 mg/kg in mice and 16.74 µg/g in Periplaneta americana. Electrophysiological experiments indicated that the extract at a concentration of 10 µg/mL could completely block the neuromuscular transmission in isolated mouse nerve-hemidiaphragm preparations within 21 ± 1.5 min, and 100 µg/mL extract could inhibit a certain percentage of voltage-activated Na(+) , K(+) , and Ca(2+) channel currents in rat dorsal root ganglion neurons. These results demonstrate that the spiderlings are rich in neurotoxic components, which play important roles in the spiderling toxicity. Language: en

Hepatocyte growth factor activator inhibitor type 2 (SPINT2), a Kunitz-type serine proteinase inhibitor, has been identified as a putative tumor suppressor gene silenced by promoter methylation. We aimed to investigate whether SPINT2 might act as an esophageal squamous cell carcinoma (ESCC) tumor suppressor gene. Four ESCC cell lines, Fifty-two ESCC tissues and twenty-nine neighboring non-cancerous tissues were included in this study. The expression of SPINT2 was monitored by real time PCR. Bisulfite genomic sequencing and methylation-specific PCR were used to analyze methylation status. The effect of SPINT2 on cell proliferation and apoptosis in EC109 and EC9706 cells was observed by CCK-8 assay and flow cytometric analysis. We found that silencing of SPINT2 was associated with promoter methylation in ESCC cell lines. The densely methylated SPINT2 promoter region was confirmed by bisulfite genomic sequencing. Ectopic expression of SPINT2 inhibited cell proliferation through inducing cell apoptosis in vitro. Furthermore, methylation-specific PCR analysis revealed that SPINT2 promoter methylation was prominent in carcinoma tissues (52.08%) compared with neighboring non-cancerous tissues (22.58%). Kaplan-Meier analysis showed that patients with SPINT2 hypermethylation had shorter survival time. The tumor suppressor gene of SPINT2 is commonly silenced by promoter hypermethylation in human ESCC and SPINT2 hypermethylation is correlated with poor overall survival, implicating SPINT2 is an underlying prognostic marker for human ESCC.

It is well known that different crystal facets of TiO2 have different surface electronic and atomic structures, which can influence the photocatalytic performance, and appropriate noble metal-loading usually improves the photocatalytic activity. Herein we demonstrate that Pt-loading can reverse the photocatalytic activity order of anatase TiO2 {0 0 1} facets (TiO2-0 0 1) and {0 1 0} facets (TiO2-0 1 0) for the photoreduction of CO2 to CH4. This new phenomenon was discussed on the bases of the experimental data including attenuated total reflectance Fourier transform infrared (ATR-IR) spectra, CO2 temperature programmed desorption (CO2-TPD) curves, transmission electron microscopy (TEM) images and time-resolved photoluminescence (PL) spectra. It is found that the higher photocatalytic CO2 reduction activity of TiO2-0 1 0 without Pt-loading can be attributed to its larger CO2 adsorbed amount and longer charge lifetime as compared with TiO2-0 0 1, while the Pt nanoparticles loaded on TiO2-0 0 1 can more efficiently enhance the photoinduced carrier separation efficiency than that on TiO2-0 1 0, and therefore resulting in a photoactivity higher than the Pt-loaded TiO2-0 0 1. The above results provide an important indication about the effects of Pt-loading on the photocatalytic CO2 reduction activity of anatase TiO2 with different exposed facets, and shed light on the fabrication of novel nanostructured photocatalysts through morphological control for high conversion efficiency in the CO2 resource utilization.

BiOBr-g-C3N4 inorganic–organic composite photocatalysts were synthesized by a one-step chemical bath method at low temperature and characterized by X-ray diffraction patterns (XRD), Fourier transform infrared (FT-IR), thermo gravimetric (TG), X-ray photoelectron spectroscopy (XPS), transmission electron microscopy (TEM), high-resolution transmission electron microscopy (HRTEM) and UV–vis diffuse reflectance spectra (DRS). The BiOBr-g-C3N4 composite showed much higher visible-light-driven (VLD) photocatalytic activity than pure g-C3N4 and BiOBr for rhodamine B (RhB) degradation. The photocatalytic mechanism analysis revealed that the interreaction between BiOBr and g-C3N4 is a kind of facet coupling between BiOBr-{0 0 1} and g-C3N4-{0 0 2}. The active species trapping and quantification experiments indicated that the photoinduced charges transfer between these facets resulted in the efficient charge separation.

Highly biocompatible superparamagnetic Fe 3 O 4 nanoparticles were synthesized by amide of folic acid (FA) ligands and the NH 2 -group onto the surface of Fe 3 O 4 nanoparticles. The as-synthesized folate-conjugated Fe 3 O 4 nanoparticles were characterized by X-ray diffraction diffractometer, transmission electron microscope, FT-IR spectrometer, vibrating sample magnetometer, and dynamic light scattering instrument. The in vivo labeling effect of folate-conjugated Fe 3 O 4 nanoparticles on the hepatoma cells was investigated in tumor-bearing rat. The results demonstrate that the as-prepared nanoparticles have cubic structure of Fe 3 O 4 with a particle size of about 8 nm and hydrated diameter of 25.7 nm at a saturation magnetization of 51 A·m 2 /kg. These nanoparticles possess good physiological stability, low cytotoxicity on human skin fibroblasts and negligible effect on Wistar rats at the concentration as high as 3 mg/kg body mass. The folate-conjugated Fe 3 O 4 nanoparticles could be effectively mediated into the human hepatoma Bel 7402 cells through the binding of folate and folic acid receptor, enhancing the signal contrast of tumor tissue and surrounding normal tissue in MRI imaging. It is in favor of the tumor cells labeling, tracing, magnetic resonance imaging (MRI) target detection and magnetic hyperthermia.

Anatase TiO2 crystals with {1 0 1}–{0 0 1} and {0 1 0}–{0 0 1} two facets coexistence were synthesized by (NH4)2TiF6 acting as titanium and fluorine sources and the photocatalytic activity of the samples were investigated. The replacement of {1 0 1} by {0 1 0} facets inhibits the photocatalytic activity of anatase TiO2. The mechanism was examined by photoluminescence spectrum, time-resolved photoluminescence spectra, field emission scanning electron microscope (FESEM) images of selected deposition of Ag, surface atoms structures and electronic band structures of anatase TiO2 facets. The results demonstrated that photoinduced charge transfer properties between {1 0 1} facets and {0 0 1} facets resulted in the efficient charge separation. Replacing {1 0 1} by {0 1 0}, the charge transfer mechanism was altered and the photoinduced electron–hole pairs cannot be separated well. The photocatalytic activity of it has thus been inhibited.

The aim of this study was to explore the etiology and diagnosis of multiple intracranial hemorrhages (ICHs) following severe burns, with a retrospective review of 16 cases of severe burns further complicated by multiple ICHs. Using cranial CT scans of the brains, we identified that all patients presented with low platelet counts and coagulation abnormalities prior to intracranial hemorrhaging. Following conventional treatment and various supporting treatments, five cases succumbed following a progressive reduction in blood platelet levels and the ICHs were cured in 11 cases following the restoration of normal platelet levels. We conclude that low platelet counts and coagulation abnormalities may cause multiple ICHs following severe burns and early diagnosis and treatment is the key to successful treatment.

BiOI thin film (BiOI TF) was prepared via a low temperature chemical vapor transport (CVT) route for the first time, and characterized by X-ray diffraction, X-ray photoelectron spectroscopy, field emission scanning electron microscopy, transmission electron microscopy, high-resolution transmission electron microscopy, fast-Fourier transform pattern and UV–vis diffuse reflectance. As-synthesized BiOI thin film was composed of high symmetrical BiOI nanosheets with dominant exposed {0 0 1} facets. It displayed better photocatalytic activity, durability and selectivity than benchmark P25 TiO 2 thin film and the origin come from the layered structure and good photoelectrochemical performance, CVT immobilization, the 100% terminal oxygen atoms of {0 0 1} facets, respectively. At end, the photocatalytic mechanism with O 2 − production was studied.

Antigens encoded by cancer-germline genes are attractive targets for cancer immunotherapy. In this study, we aimed to evaluate the mRNA expression of cancer-germline genes, expression of the encoded proteins in patients with esophageal squamous cell carcinoma (ESCC) and their correlations with clinical characteristics. In addition, the effects of downregulation cancer-germline genes on ESCC cells were assessed in vitro. Our results showed that cancer-germline genes were frequently expressed in ESCC samples. The positive rates of in ESCC samples were: 87% of MAGE-A3, 60% of MAGE-A4, 65% of MAGE-C2, and 20% of NY-ESO-1 at mRNA level. MAGE-A3 expression was associated with age, lymph node metastasis and tumor stage (all P0.05), while MAGE-C2 expression was only associated with tumor stage (P0.05). Furthermore, the MAGE-A3 expressing patients had a poorer overall survival (P0.05). Multivariate analysis identified MAGE-A3 as an independent poor prognostic marker in ESCC. In vitro assay, ESCC cell lines treated with specific siRNAs to down-regulate MAGE-A3 and MAGE-C2 resulted in decreased colony-formation and migration ability (P0.05). Epithelial marker E-cadherin was up-regulated in siRNA-MAGE-A3/C2 cells compared to controls, whereas mesenchymal markers Vimentin, N-cadherin and Slug were downregulated (all P0.05), suggesting a role for MAGE-A3/C2 in ESCC metastasis through inducing epithelial-mesenchymal transition. The present study revealed that cancer-germline genes and their encoded proteins were frequently expressed in ESCC tumor samples and were related to poor prognosis. Thus, cancer-germline genes may serve as useful biomarkers and potential targets for ESCC patients.

Dimensionality reduction is an important issue in information processing and has popular applications in many fields, where locally linear embedding (LLE) is widely used due to accuracy and simple to implement. However, LLE is lack of robustness, and sensitive to local structure that can't preserve neighborhood character sometimes. Instead, Laplacian eigenmaps (LE) can overcome these weaknesses. In this paper, a new dimensionality reduction algorithm, called locally linear embedding preserving neighborhood (NLLE) is proposed. It takes the advantage of LLE and LE, and can keep the intrinsic character of high-dimensional data. Several experiments are employed to confirm the effectiveness and robustness of the algorithm.

A pediatric human immunodeficiency virus type 1 (HIV-1) vaccine would be desirable to protect infants against HIV-1 transmission from breast-feeding. Such a vaccine would need to induce protective immunity at mucosal surfaces in neonates as soon as possible after birth. Recombinant adenovirus (rAd) vectors have been shown to elicit potent systemic and mucosal virus-specific immune responses in adult nonhuman primates and humans, but these vectors have not previously been comprehensively studied in infants. In this study, we demonstrate that a single injection of rAd26 encoding simian immunodeficiency virus mac239 (SIVmac239) Gag on the day of birth elicited detectable Gag-specific cellular immune responses in rhesus monkeys, but these responses were transient and waned quickly. In contrast, an accelerated heterologous prime-boost regimen involving administration of rAd35 at birth and rAd26 at 4 weeks of life elicited potent and durable Gag-specific cellular and humoral immune responses in neonatal rhesus monkeys, including mucosal responses that remained detectable at 1 year of age. These results suggest the potential of an accelerated heterologous rAd prime-boost regimen as a candidate HIV-1 vaccine for newborns.

Ag/AgX/BiOX (X = Cl, Br) three-component visible-light-driven (VLD) photocatalysts were synthesized by a low-temperature chemical bath method and characterized by X-ray diffraction patterns, X-ray photoelectron spectroscopy, field emission scanning electron microscopy, transmission electron microscopy, high-resolution transmission electron microscopy, and UV–vis diffuse reflectance spectra. The Ag/AgX/BiOX composites showed enhanced VLD photocatalytic activity for the degradation of rhodamine B, which was much higher than Ag/AgX and BiOX. The photocatalytic mechanisms were analyzed by active species trapping and superoxide radical quantification experiments. It revealed that metallic Ag played a different role for Ag/AgX/BiOX VLD photocatalysts, surface plasmon resonance for Ag/AgCl/BiOCl, and the Z-scheme bridge for Ag/AgBr/BiOBr.

The CNTs–WO3 hybrid nanostructures were fabricated by solvothermal synthesis. The morphologies, phase structures and optical properties of the nanostructures were investigated by TEM, XRD, UV–vis DRS and XPS respectively. The CNTs–WO3 hybrid nanostructures exist higher photocatalytic activity than pure WO3 nanosheets and the mechanical mixture of WO3 and CNTs for the degradation of methyl blue (MB) under visible light. This is attributed to their large surface area, absorption enhancement in visible light region and effective separation of electrons and holes. The presence of radical scavengers such as KI, Fe3 + and methanol in photocatalytic experiments demonstrates that photogenerated electrons are responsible for the photocatalytic degradation of MB on CNTs–WO3.

In Fig. 4b of this Article, the x-axis labels ‘PGT121’ and ‘GS-9620’ were inadvertently swapped in both graphs. In Fig. 5a, b, ‘TLR7’ should have been ‘GS-9620’. These figures have been corrected online.

Post hoc analysis of the phase 2b Step study evaluating a recombinant adenovirus serotype 5 (rAd5)-based HIV-1 vaccine candidate suggested a potential increased risk of HIV-1 acquisition in subjects who were baseline Ad5 seropositive and uncircumcised. These concerns had a profound impact on the HIV-1 vaccine development field, although the mechanism underlying this observation remains unknown. It has been hypothesized that rAd5 vaccination of baseline Ad5-seropositive individuals may have resulted in anamnestic, vector-specific CD4 + T lymphocytes that could have trafficked to mucosal sites and served as increased targets for HIV-1 infection. Here we show that Ad5-specific CD4 + T lymphocyte responses at mucosal sites following rAd5-Gag/Pol/Nef vaccination were comparable in rhesus monkeys with and without baseline Ad5 immunity. Moreover, the total cellular inflammatory infiltrates and the CD3 + , CD4 + , HLA-DR + , Ki67 + , and langerin + cellular subpopulations in colorectal and foreskin mucosa were similar in both groups. Thus, no greater trafficking of Ad5-specific CD4 + T lymphocytes to mucosal target sites was observed following rAd5 vaccination of rhesus monkeys with baseline Ad5 immunity. These findings from this nonhuman primate model provide evidence against the hypothesis that recruitment of vector-specific target cells to mucosal sites led to increased HIV-1 acquisition in Ad5-seropositive, uncircumcised vaccinees in the Step study.

Resetting tumor-associated macrophages (TAMs) is a promising strategy to ameliorate the immunosuppressive tumor microenvironment and improve innate and adaptive antitumor immunity. Here we show that chloroquine (CQ), a proven anti-malarial drug, can function as an antitumor immune modulator that switches TAMs from M2 to tumor-killing M1 phenotype. Mechanistically, CQ increases macrophage lysosomal pH, causing Ca2+ release via the lysosomal Ca2+ channel mucolipin-1 (Mcoln1), which induces the activation of p38 and NF-κB, thus polarizing TAMs to M1 phenotype. In parallel, the released Ca2+ activates transcription factor EB (TFEB), which reprograms the metabolism of TAMs from oxidative phosphorylation to glycolysis. As a result, CQ-reset macrophages ameliorate tumor immune microenvironment by decreasing immunosuppressive infiltration of myeloid-derived suppressor cells and Treg cells, thus enhancing antitumor T-cell immunity. These data illuminate a previously unrecognized antitumor mechanism of CQ, suggesting a potential new macrophage-based tumor immunotherapeutic modality., Tumour-associated macrophages (TAMs) display an M2 phenotype that promote tumour immune escape. Here the authors show that Chloroquine (CQ), a lysosome inhibitor used against malaria, inhibits tumour growth by switching TAMs into an M1 tumor-killing phenotype by repolarizing macrophages metabolism.

Summary Despite the clinical successes fostered by immune checkpoint inhibitors, mechanisms underlying PD-1 upregulation in tumor-infiltrating T cells remain an enigma. Here, we show that tumor-repopulating cells (TRCs) drive PD-1 upregulation in CD8 + T cells through a transcellular kynurenine (Kyn)-aryl hydrocarbon receptor (AhR) pathway. Interferon-γ produced by CD8 + T cells stimulates release of high levels of Kyn produced by TRCs, which is transferred into adjacent CD8 + T cells via the transporters SLC7A8 and PAT4. Kyn induces and activates AhR and thereby upregulates PD-1 expression. This Kyn-AhR pathway is confirmed in both tumor-bearing mice and cancer patients and its blockade enhances antitumor adoptive T cell therapy efficacy. Thus, we uncovered a mechanism of PD-1 upregulation with potential tumor immunotherapeutic applications.

We evaluated whether weaned piglets were protected from bacterial endotoxins by placing the animals on a taurine-supplemented diet. A total of 40 weaned Landrace × Yorkshire piglets (5.75 ± 0.58 kg, weaned at 21 days) were allocated to four groups with 10 barrows per group, following a 2 × 2 factorial design with two inclusion levels of lipopolysaccharide (LPS) (no or one time peritoneal injection by the dose of 100 µg/kg bodyweight on Day 7 of the trial) and two inclusion levels of dietary taurine (no or 0.1% taurine in a basal diet in the whole trial). There was a significant interaction between LPS and taurine with regard to growth and small intestinal mucosal membrane integrity, morphology, immune parameters, and antioxidant capacity (P < 0.05). Feed conversion, daily weight gain, daily feed intake, villus height, and the villus to crypt ratio, vascular endothelial growth factor, regenerating islet-derived protein 3 gamma, trefoil factor-3, transforming growth factor β-1 expression, number of goblet cells and the least amount of claudin-1, occludin, zonula occludens-1, serum glutathione peroxidase, nitrogen oxide synthase, superoxide dismutase, peroxidase, and total antioxidant was lowest in LPS-challenged animals. Furthermore, animals in the LPS group had the highest serum diamine oxidase concentration, number of lymphocytes, concentrations of calprotectin, sIgA, toll-like receptor-4, mRNA levels of interleukin-1β, interleukin-8, toll-like receptor-4, and tumour necrosis factor-α (P < 0.05). These data suggested that the peritoneal injection administration of LPS decreased growth performance and disrupted small intestinal mucosal membrane integrity and triggered an inflammatory response in the small intestinal mucosal membrane. Dietary administration of taurine improved growth performance, increased small intestinal villus height, stimulated immune and antioxidant function and improved small intestinal mucosal membrane integrity in weaned piglets challenged without or with LPS (P < 0.05). The beneficial effects of taurine were likely due to decreased stimulation of the immune response to LPS and an improvement in intestinal epithelial barrier function. Dietary administration of taurine could prevent weaned piglets from intestinal damage by LPS of Gram-negative bacteria.

We propose four-level phase pair encoding and decoding with single interferometric phase retrieval for holographic data storage. Inherent with phase pair encoding, phase shifting is generated by assigning a certain phase difference between two pixels of the phase pair. Multiple phase shifting operations are not required. In addition, a phase-readout reference beam can be a plane beam with an arbitrary phase in our method because phase shifting can be encoded on the phase-only spatial light modulator easily and accurately. Therefore, our method can not only increase the data transfer rate, but also improve the robustness of the holographic data storage system. Although the code rate of our method needs to be sacrificed by half, the code rate is still twice that of amplitude code when four-level phase encoding is used. We demonstrated experimentally that there is only a 1×10−2 order of bit error rate before error correcting, which is acceptable. We believe our method will further advance the phase-modulated holographic data storage technique.

The mixture of the anionic O,O′-bis(sodium 2-lauricate)- p -benzenediol (C 11 p PHCNa) and cationic (oligoona)alkanediyl-α, ω-bis(dimethyldodecylammonium bromide) (C 12 -2-E x -C 12 ·2Br) gemini surfactants has been investigated by surface tension and pyrene fluorescence. The results show that the surface tension γ drops faster with total surfactant concentration C T for α 1 = 0.1 or 0.3 than for α 1 = 0.7 or 0.9, where α 1 is the mole fraction of C 11 p PHCNa in the bulk solution on a surfactant-only basis. The fast drop in γ for α 1 γ for α 1 > 0.5 is attributed to the pre-aggregation in the solution before the critical micelle concentration cmc . A possible mechanism is proposed.

The viscosity of aqueous micellar solutions depends on the size and shape of the aggregates and thus can be adjusted by addition of another surfactant interacting with the original component, which alters the geometry of the molecule-pair consisting of two surfactants and influences strongly the size and shape of the mixed micelles. Ethanediyl-α,ω-bis(dimethyl dodecyl ammonium bromide), referred to as C12-2-C12·2Br, forms generally large micelles. Addition of a cationic surfactant (dodecyltrimethylammonium bromide, C12TMABr) or a nonionic surfactant (alkyl polyoxyethylene ether, C m E n ), the mixed micelle size is reduced violently since the electrostatic repulsion between the same charged heads of C12-2-C12·2Br and C12TMABr or the steric hindrance of the PEO chain of C m E n in the palisade layers of the mixed micelle, which leads to a decrease in the packing parameter P of the molecule-pair. As a result, the zero-shear viscosity (η 0) of the mixed solution reduces rapidly. In contrast, on adding an oppositely charged surfactant, η 0 of the mixed solution increases strongly since the P of the molecule-pair increases through electrostatic attraction between the oppositely charged heads. The typical cases occur in the mixtures of the anionic gemini surfactant, O,O′-bis(sodium 2-lauricate)-p-benzenediol C11pPHCNa, and the cationic surfactant C12-2-C12·2Br, C12TMABr or its homologue with a different size of heads.

The purpose of the present study was to correlate the in vitro level of HIV Env expression by recombinant modified vaccinia virus Ankara (rMVA) with immunogenicity in mice. A 5-fold difference in Env synthesis was achieved at the translational level by the presence or absence of an out-of-frame initiation codon upstream of the env gene. This perturbation had no effect on the size or processing of Env. In contrast to the variation in Env synthesis, the rMVAs produced similar amounts of HIV Gag, which were expressed from identical cassettes. Mice immunized with the higher Env expressing rMVAs had about 15-fold higher titers of Env antibodies and several fold higher frequencies of Env-specific CD8+ and CD4+ T cells than mice immunized with the low expresser. The greater immune response achieved by high expression was maintained over a 100-fold dose range. Importantly, enhanced Env immune responses did not come at the expense of lower Gag T cell responses. These data suggest that for high immunogenicity, rMVAs should be engineered to produce the most recombinant protein that can be achieved without compromising the growth and stability of the rMVA.

The micellization of C11pPHCNa, a carboxylated gemini surfactant with an p-Oxybenzene residue in the spacer, in aqueous solution at pH 12 was characterized by the absorption and the fluorescence spectra of the p-Oxybenzene residue. The critical micelle concentration of C11pPHCNa was determined by the absorption spectra to be 0.0940 mmol L−1, which agreed well with that measured by surface tension technique. The fluorescent intensity of C11pPHCNa aqueous solution rapidly increased with increasing C11pPHCNa concentration (C) then reduced when C was beyond 0.45 mmol L−1, which meant the self-quenching occurring. At fixed C, the time-resolved and the steady-state fluorescence quenching with the p-Oxybenzene residue as the intrinsic probe and with methyl viologen (MV2+) as the extrinsic quencher could be used to measure the aggregation number (N) of C11pPHCNa micelle. The results showed the N for the micelle formed at C = 1.5 mmol L−1 was 14.5 and gradually increased with further increasing C. This indicated the more and more molecules packed within a micelle with increasing C, which explained well the fluorescence self-quenching when C was beyond 0.45 mmol L−1.

The earliest events following mucosal HIV-1 infection, prior to measurable viremia, remain poorly understood. Here we show by detailed necropsy studies that the virus can disseminate rapidly following mucosal SIV infection of rhesus monkeys and trigger components of the inflammasome, both at the site of inoculation and at early sites of distal virus spread. By 24 hours following inoculation, a proinflammatory signature that lacked antiviral restriction factors was observed in viral RNA positive tissues. The early innate response included expression of NLRX1, which inhibits antiviral responses, and activation of the TGF-β pathway, which negatively regulates adaptive immune responses. These data suggest a model in which the virus triggers specific host mechanisms that suppress the generation of antiviral innate and adaptive immune responses in the first few days of infection, thus facilitating its own replication. These findings have important implications for the development of vaccines and other strategies to prevent infection.

To defeat SIV, add a protein boost Despite 30 years of effort, no HIV-1 vaccine exists. Barouch et al. evaluated one promising strategy in rhesus macaques, a preclinical model commonly used to test potential HIV-1 vaccine candidates. They immunized monkeys with adenovirus-36 vectors engineered to express SIV (simian immunodeficiency virus) genes and then boosted them with a recombinant gp120 envelope glycoprotein (Env) from SIV. This regimen afforded greater protection than a strategy that instead used a viral vector–based boost. A parallel trial using a SHIV (simian/human immunodeficiency virus)–based vaccine and challenge model produced similar results. Whether this particular approach will be equally successful in humans remains to be tested. Science , this issue p. 320

// Jinyan Liu 1, * , Feng Li 1, * , Yu Ping 1 , Liping Wang 2 , Xinfeng Chen 1 , Dan Wang 1 , Ling Cao 1 , Song Zhao 3 , Bing Li 3 , Pawel Kalinski 5 , Stephen H. Thorne 5 , Bin Zhang 6 , Yi Zhang 1, 2, 4 1 Biotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China 2 Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China 3 Department of Thoracic surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China 4 Engineering Key Laboratory for Cell Therapy of Henan Province, Zhengzhou, Henan, P.R. China 5 Department of Surgery, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA, USA 6 Robert H. Lurie Comprehensive Cancer Center, Department of Medicine-Division of Hematology/Oncology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA * These authors have contributed equally to this work Correspondence to: Yi Zhang, e-mail: yizhang@zzu.edu.cn Keywords: esophageal squamous cell carcinoma, T lymphocyte, chemotaxis, CCL5, CXCL10 Received: April 01, 2015 Accepted: July 06, 2015 Published: July 16, 2015 ABSTRACT Esophageal squamous cell carcinoma (ESCC) is a very common malignant tumor with poor prognosis in China. Chemokines secreted by tumors are pivotal for the accumulation of CD8 + T lymphocytes within malignant lesions in several types of cancers, but the exact mechanism underlying CD8 + T lymphocyte homing is still unknown in ESCC. In this study, we revealed that, compared with marginal tissues, the expression of both chemokine (C-C motif) ligand 5 (CCL5) and (C-X-C motif) ligand 10 (CXCL10) was upregulated in ESCC tissues. CCL5 expression was positively associated with the overall survival of patients. Meanwhile, RT-PCR data showed that the expression of CCL5 and CXCL10 was positively correlated with the local expressions of the CD8 + T lymphocyte markers ( CD8 and Granzyme B ) in tumor tissues. Correspondingly, CD8 + T lymphocytes were more frequently CCR5- and CXCR3-positive in tumor than in peripheral blood. Transwell analysis showed both CCL5 and CXCL10 were important for the chemotactic movement of CD8 + T lymphocytes. Our data indicate that CCL5 and CXCL10 serve as the key chemokines to recruit CD8 + T lymphocytes into ESCC tissue and may play a role in patient survival.

A series of carbon-coated Ni (Ni@C)-Cd0.8Zn0.2S nanocomposites were fabricated via a facile hydrothermal process using pre-prepared Ni@C as a starting material. The obtained products were characterized by X-ray diffraction, UV-Vis diffuse reflectance absorption spectroscopy, X-ray photoelectron spectroscopy and electron microscopy. It was found that the introduction of Ni@C nanoparticles can improve both the visible light-induced photocatalytic H2 production activity and stability of the Cd0.8Zn0.2S solid solution, and the Ni nanoparticles encapsulated by several graphite-like carbon layers show high chemical and thermal stability. Among those products with various Ni@C contents, the 5 wt% Ni@C-Cd0.8Zn0.2S nanocomposite exhibits the maximum photoactivity (969.5 μmol h(-1)) for H2 production, which is ∼3.10 times higher than that (312.6 μmol h(-1)) of pristine Cd0.8Zn0.2S. This significant enhancement in the photoactivity by loading Ni@C nanoparticles can be attributed to the metallic Ni in the Ni@C acting as a co-catalyst, while the graphite-like carbon shells acting as the Cd0.8Zn0.2S nanoparticles' support and electron acceptor, which causes an effective photogenerated carrier separation in space and an improvement in the photoactivity and stability for H2 production. The present findings demonstrate a cost reduction strategy by using a non-noble metal co-catalyst for efficient and stable light-to-hydrogen energy conversion.

Spider venom is a complex mixture of bioactive peptides to subdue their prey. Early estimates suggested that over 400 venom peptides are produced per species. In order to investigate the mechanisms responsible for this impressive diversity, transcriptomics based on second generation high throughput sequencing was combined with peptidomic assays to characterize the venom of the tarantula Haplopelma hainanum. The genes expressed in the venom glands were identified, and the bioactivity of their protein products was analyzed using the patch clamp technique. A total of 1,136 potential toxin precursors were identified that clustered into 90 toxin groups, of which 72 were novel. The toxin peptides clustered into 20 cysteine scaffolds that included between 4 and 12 cysteines, and 14 of these groups were newly identified in this spider. Highly abundant toxin peptide transcripts were present and resulted from hypermutation and/or fragment insertion/deletion. In combination with variable post-translational modifications, this genetic variability explained how a limited set of genes can generate hundreds of toxin peptides in venom glands. Furthermore, the intraspecies venom variability illustrated the dynamic nature of spider venom and revealed how complex components work together to generate diverse bioactivities that facilitate adaptation to changing environments, types of prey, and milking regimes in captivity. Background: Spider venom is a complex mixture and contains over 400 venom peptides/species. Results: Highly abundant hypermutation, fragment insertion/deletion, and variable post-translational modifications were observed in venom gland, and the highly diverse toxins exhibit diverse functions. Conclusion: Spider toxins are abundant and variable, factors that work together to generate diverse bioactivities. Significance: Our study reveals the mechanism of structural and functional diversity of peptide toxins from Ornithoctonus hainana.

MicroRNAs (miRs), a class of non‑coding RNAs 18‑25 nucleotides in length, generally serve suppressive role in the regulation of gene expression via directly binding to the 3'‑untranslated region (UTR) of their target mRNA. Previous studies have identified several miRs to be involved in thermal injury repair. However, the role of miR let‑7b during the recovery of thermal injury, in addition to the underlying mechanisms, has not previously been studied. In the present study, the expression of let‑7b was observed to be significantly increased in skin tissue shortly following thermal injury, however, gradually reduced during the recovery of thermal injury. Notably, similar findings were observed in heat‑denatured skin fibroblasts. Furthermore, collagen, type I, alpha 1 (COL1A1) and collagen, type I, alpha 2 (COL1A2), which are associated with the synthesis of type I collagen, were identified as two targets of let‑7b in skin fibroblasts. The overexpression of let‑7b was observed to upregulate the protein expression levels of COL1A1 and COL1A2, while knockdown of let‑7b reduced the levels of COL1A1 and COL1A2 in skin fibroblasts. Furthermore, COL1A1 and COL1A2 were significantly downregulated shortly following thermal injury, while gradually upregulated during healing, in heat‑damaged skin tissue and skin fibroblasts, with the expression profiles opposite to that of let‑7b. Taken together, this suggests that the downregulation of let‑7b in heat‑damaged dermis promotes the synthesis of type I collagen and thus aids in burn wound repair.

To investigate the expression and significance of CCL5 in patients with esophageal carcinoma.Using reverse transcriptase polymerase chain reaction (RT-PCR), the expressions of CCL5/CD8/granzyme B/perforin in tumor and corresponding adjacent tissues from esophageal carcinoma patients were examined. Flow cytometry (FACS) was used to detect the percentages of CD8(+) T cells and CCR5(+)CD8(+) T cells in TIL and PBMC from the patients. Transwell assay was performed to study the effect of CCL5 on the migration of T cells in vitro. T test and Spearman correlation analysis were performed.The mRNA expressions of CCL5 and perforin were 0.348 2 ± 0.300 1 and 0.181 9 ± 0.118 6, respectively, in the tumor samples, while their expressions in adjacent samples were 0.279 6 ± 0.138 0 and 0.118 0 ± 0.109 8, respectively, with no statistically significant differences between them (P0.05 for both). The mRNA expressions of CD8 and granzyme B were significantly higher in the tumor tissues than in adjacent tissues (0.464 9 ± 0.300 8 vs. 0.279 0 ± 0.173 4, 0.648 7 ± 0.516 0 vs. 0.469 7 ± 0.259 1; P0.05 for both). The relative expression of CCL5 was positively correlated with that of CD8, perforin and granzyme B (r(CD8) = 0.272, P = 0.034; r(perforin) = 0.305, P = 0.026; r(granzymeB) = 0.108, P = 0.012) in the tumor sites. FACS data revealed that the proportions of CD8(+) T cells in TIL and PBMC were (45.86 ± 16.09)% and (34.05 ± 15.07)%, respectively, showing a significant difference (P = 0.022). Similarly, CCR5(+)CD8(+) T cells fraction in TIL (48.12 ± 26.75)% was much higher than that in PBMC (19.53 ± 13.67) % (P0.001). Transwell assay showed that CCL5 protein enhanced the migration of T cells, supporting that CCL5 is crucial for CD8(+) T cells recruitment in vivo. Intriguingly, CCL5 expression was down-regulated in advanced patients (stage IIb-IV). The accumulation of CD8(+) T cells and CCR5(+)CD8(+) T cells was strongly reduced in advanced patients, suggesting that CCL5 expression may be involved in the local control of the disease and its reduction may be involved in disease progression.The current data indicate the involvement of CCL5 in the regulation of CD8(+) T cell entry into tumor lesions in esophageal carcinoma patients. This process may affect the disease status and potentially as a prognostic factor for cancer patients. Enhancing local CCL5 expression in tumor lesions may represent a novel strategy in esophageal cancer therapy.

When a quaternary ammonium surfactant has a suitable solubility in a polar solvent, it can induce the phase self-separation of mutually soluble polar and apolar mixed solvents and a stable interface between the two phases can be formed. This phenomenon is attributed to the quaternary ammonium surfactant reaching suitable solubility in the polar solvent and driving out the most part of the apolar solvent in which the surfactant is insoluble. As a result, phase separation appears. Using aqueous surfactant two-phase as reference, we suggest that it be termed nonaqueous surfactant two-phase and also as two oil phases for short.

Here we conduct dose-response studies for in vitro expression and in vivo immunogenicity for a recombinant modified vaccinia Ankara (MVA) vaccine that expresses HIV Gag, Pol, and Env proteins. The dose-response studies for in vitro expression used fluorescent-activated cell sorting to score Gag- and Env-expressing cells and showed good increases for antigen expression with increasing MVA dose. In these studies, a 1000-fold increase in the dose of MVA resulted in a 300-fold increase in the frequency of antigen-expressing cells. In contrast, dose-response studies for in vivo immunogenicity showed